Damian McNamara

JACKSONVILLE, FLA. — Financial and logistic barriers will limit the implementation and impact of human papillomavirus vaccine, Dr. Lance Rodewald said at a conference on STD prevention sponsored by the Centers for Disease Control and Prevention.

New vaccines incorporated into the child immunization schedule are typically adopted quickly across the nation. “For adolescents, we don't do as well,” Dr. Rodewald said. “For example, there is 74% coverage for the three shots for hepatitis B. It is better for MMR and Td [tetanus-diphtheria], but our adolescent platform is not well established now.”

To improve distribution to those at highest risk, family physicians, obstetricians and gynecologists, and other primary care providers will be encouraged to join the federal government's Vaccines for Children (VFC) program. VFC pays for vaccinations for certain vulnerable children through age 18 years, including those on Medicaid, Native Americans or Alaska natives, the uninsured, and those insured without a vaccine benefit.

Underinsured children are not covered by VFC, nor are they covered in most cases by a smaller federal program—Section 317—or state funding. “My confidence in government funding starts and stops at the VFC program,” said Dr. Rodewald, a pediatrician and director of the Immunization Services Division, National Immunization Program, at the Centers for Disease Control and Prevention.

“HPV [human papillomavirus] vaccine is certainly going to be delivered in a two-tiered system. There is no way around it unless something changes,” he said.

Because of inadequate state and Section 317 funding, many states cannot purchase vaccine for underinsured children, resulting in the two-tiered policy. “There is some indication the president might increase funding to include underinsured children who could get vaccinated at federal public health sites—but it's unlikely to happen this year,” he said.

Financing the HPV vaccine for women over age 18 is another challenge. “The provider may have to purchase adult vaccines up front and get reimbursed later. So there is a financial risk if the vaccine is not used,” Dr. Rodewald said.

The vast majority of Section 317 program funding, 95%, goes to vaccines for children. However, this means only 5% of Section 317 money pays for adult immunization, and state funding for adults is discretionary.

The financial considerations are not unique to HPV prevention. Other new vaccines likely coming soon include a second-dose varicella product and protection against shingles/postherpetic neuralgia, Dr. Rodewald said. “These new vaccines are great, but they come at a cost,” he said. The cost to protect each child has grown from $45 in 1985 to $155 in 1995 to $837 in 2006.

“The U.S. immunization system is highly effective and highly successful at protecting children from vaccine-preventable diseases,” Dr. Rodewald said. “But the most important stress in the U.S. system is financing access to the many new vaccines.”

JACKSONVILLE, FLA. — Financial and logistic barriers will limit the implementation and impact of human papillomavirus vaccine, Dr. Lance Rodewald said at a conference on STD prevention sponsored by the Centers for Disease Control and Prevention.

New vaccines incorporated into the child immunization schedule are typically adopted quickly across the nation. “For adolescents, we don't do as well,” Dr. Rodewald said. “For example, there is 74% coverage for the three shots for hepatitis B. It is better for MMR and Td [tetanus-diphtheria], but our adolescent platform is not well established now.”

To improve distribution to those at highest risk, family physicians, obstetricians and gynecologists, and other primary care providers will be encouraged to join the federal government's Vaccines for Children (VFC) program. VFC pays for vaccinations for certain vulnerable children through age 18 years, including those on Medicaid, Native Americans or Alaska natives, the uninsured, and those insured without a vaccine benefit.

Underinsured children are not covered by VFC, nor are they covered in most cases by a smaller federal program—Section 317—or state funding. “My confidence in government funding starts and stops at the VFC program,” said Dr. Rodewald, a pediatrician and director of the Immunization Services Division, National Immunization Program, at the Centers for Disease Control and Prevention.

“HPV [human papillomavirus] vaccine is certainly going to be delivered in a two-tiered system. There is no way around it unless something changes,” he said.

Because of inadequate state and Section 317 funding, many states cannot purchase vaccine for underinsured children, resulting in the two-tiered policy. “There is some indication the president might increase funding to include underinsured children who could get vaccinated at federal public health sites—but it's unlikely to happen this year,” he said.

Financing the HPV vaccine for women over age 18 is another challenge. “The provider may have to purchase adult vaccines up front and get reimbursed later. So there is a financial risk if the vaccine is not used,” Dr. Rodewald said.

The vast majority of Section 317 program funding, 95%, goes to vaccines for children. However, this means only 5% of Section 317 money pays for adult immunization, and state funding for adults is discretionary.

The financial considerations are not unique to HPV prevention. Other new vaccines likely coming soon include a second-dose varicella product and protection against shingles/postherpetic neuralgia, Dr. Rodewald said. “These new vaccines are great, but they come at a cost,” he said. The cost to protect each child has grown from $45 in 1985 to $155 in 1995 to $837 in 2006.

“The U.S. immunization system is highly effective and highly successful at protecting children from vaccine-preventable diseases,” Dr. Rodewald said. “But the most important stress in the U.S. system is financing access to the many new vaccines.”

JACKSONVILLE, FLA. — Financial and logistic barriers will limit the implementation and impact of human papillomavirus vaccine, Dr. Lance Rodewald said at a conference on STD prevention sponsored by the Centers for Disease Control and Prevention.

New vaccines incorporated into the child immunization schedule are typically adopted quickly across the nation. “For adolescents, we don't do as well,” Dr. Rodewald said. “For example, there is 74% coverage for the three shots for hepatitis B. It is better for MMR and Td [tetanus-diphtheria], but our adolescent platform is not well established now.”

To improve distribution to those at highest risk, family physicians, obstetricians and gynecologists, and other primary care providers will be encouraged to join the federal government's Vaccines for Children (VFC) program. VFC pays for vaccinations for certain vulnerable children through age 18 years, including those on Medicaid, Native Americans or Alaska natives, the uninsured, and those insured without a vaccine benefit.

Underinsured children are not covered by VFC, nor are they covered in most cases by a smaller federal program—Section 317—or state funding. “My confidence in government funding starts and stops at the VFC program,” said Dr. Rodewald, a pediatrician and director of the Immunization Services Division, National Immunization Program, at the Centers for Disease Control and Prevention.

“HPV [human papillomavirus] vaccine is certainly going to be delivered in a two-tiered system. There is no way around it unless something changes,” he said.

Because of inadequate state and Section 317 funding, many states cannot purchase vaccine for underinsured children, resulting in the two-tiered policy. “There is some indication the president might increase funding to include underinsured children who could get vaccinated at federal public health sites—but it's unlikely to happen this year,” he said.

Financing the HPV vaccine for women over age 18 is another challenge. “The provider may have to purchase adult vaccines up front and get reimbursed later. So there is a financial risk if the vaccine is not used,” Dr. Rodewald said.

The vast majority of Section 317 program funding, 95%, goes to vaccines for children. However, this means only 5% of Section 317 money pays for adult immunization, and state funding for adults is discretionary.

The financial considerations are not unique to HPV prevention. Other new vaccines likely coming soon include a second-dose varicella product and protection against shingles/postherpetic neuralgia, Dr. Rodewald said. “These new vaccines are great, but they come at a cost,” he said. The cost to protect each child has grown from $45 in 1985 to $155 in 1995 to $837 in 2006.

“The U.S. immunization system is highly effective and highly successful at protecting children from vaccine-preventable diseases,” Dr. Rodewald said. “But the most important stress in the U.S. system is financing access to the many new vaccines.”

SAN JUAN, P.R. — New data—especially on bipolar depression—are starting to emerge from randomized studies conducted within a bipolar disorder observational treatment study, according to an update presented at the annual meeting of the American College of Psychiatrists.

Researchers have been busy with analysis of three randomized trials embedded within the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study since recruitment ended in September 2005. With a total of 4,361 patients at 19 centers, STEP-BD is the largest prospective cohort study of this patient population.

One randomized study compares bupropion, paroxetine (Paxil), and placebo added to a standard mood stabilizer for acute bipolar depression. “It is not yet published. This probably will be the most interesting data to come out,” Dr. S. Nassir Ghaemi predicted.

Results of one study just published favor lamotrigine vs. inositol or risperidone (Risperdal) for treatment of resistant bipolar depression (Am. J. Psychiatry 2006;163:210–6). Researchers randomized 66 patients unresponsive to a mood stabilizer plus antidepressant to either lamotrigine (150–250 mg/day), inositol (10–25 g/day), or risperidone (up to 6 mg/day) for 16 weeks. They defined recovery as two or fewer DSM-IV mood criteria for 2 months, and “lamotrigine looked more favorable,” said Dr. Ghaemi, director of the Bipolar Disorder Research Program at Emory University, Atlanta.

The third randomized trial is not yet published. Researchers will compare psychosocial therapies for maintenance: cognitive-behavioral therapy, family-focused treatment, interpersonal and social rhythm therapy, and collaborative care/psychoeducation. “This is the hardest to conduct, getting people into psychosocial therapy and randomizing them,” said Dr. Ghaemi.

Many other researchers have mined the rich STEP-BD data to study the natural history, diagnosis, and treatment of bipolar disorder. For example, Dr. Ghaemi and his associates assessed treatment patterns among a cohort of 500 STEP-BD participants. They found that most were taking mood stabilizers (72%), and the next most common class of medication was antidepressants (41%). Anticonvulsants came in third, at 32%.

“We also looked at rapid vs. nonrapid cyclers,” Dr. Ghaemi said. “And we found no difference in medication use, including antidepressants.

“We're doing an open, randomized, long-term study of antidepressant outcome in bipolar disorder” based on a sample of STEP-BD participants, Dr. Ghaemi said. He presented an interim analysis based on 69 patients with acute bipolar depression who responded to a mood stabilizer and antidepressant for 2 months. Dr. Ghaemi and his associates then randomized participants to continue both agents or only the mood stabilizer for 1 year.

“On our clinical monitoring form, we found no difference between the two groups, meaning that continuing antidepressants had no effect on mood criteria, after adjusting for other variables,” Dr. Ghaemi said. In addition, there was no significant increased relapse to depression in the group that discontinued antidepressant therapy. “This conflicts with the Stanley Foundation [Bipolar Network] data published two years ago, but that was observational and this was randomized,” Dr. Ghaemi said (Bipolar Disord. 2003;5:396–406).

Predictors of increased morbidity in the study included rapid cycling, a negative patient attitude toward the regimen to which the patient was assigned, and prior psychosis. “Rapid cyclers who continued on antidepressants trended toward greater depressive morbidity, suggesting we should use these medications even less in this subpopulation,” Dr. Ghaemi said.

STEP-BD is sponsored by the National Institute of Mental Health.

Visit www.stepbd.org

SAN JUAN, P.R. — New data—especially on bipolar depression—are starting to emerge from randomized studies conducted within a bipolar disorder observational treatment study, according to an update presented at the annual meeting of the American College of Psychiatrists.

Researchers have been busy with analysis of three randomized trials embedded within the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study since recruitment ended in September 2005. With a total of 4,361 patients at 19 centers, STEP-BD is the largest prospective cohort study of this patient population.

One randomized study compares bupropion, paroxetine (Paxil), and placebo added to a standard mood stabilizer for acute bipolar depression. “It is not yet published. This probably will be the most interesting data to come out,” Dr. S. Nassir Ghaemi predicted.

Results of one study just published favor lamotrigine vs. inositol or risperidone (Risperdal) for treatment of resistant bipolar depression (Am. J. Psychiatry 2006;163:210–6). Researchers randomized 66 patients unresponsive to a mood stabilizer plus antidepressant to either lamotrigine (150–250 mg/day), inositol (10–25 g/day), or risperidone (up to 6 mg/day) for 16 weeks. They defined recovery as two or fewer DSM-IV mood criteria for 2 months, and “lamotrigine looked more favorable,” said Dr. Ghaemi, director of the Bipolar Disorder Research Program at Emory University, Atlanta.

The third randomized trial is not yet published. Researchers will compare psychosocial therapies for maintenance: cognitive-behavioral therapy, family-focused treatment, interpersonal and social rhythm therapy, and collaborative care/psychoeducation. “This is the hardest to conduct, getting people into psychosocial therapy and randomizing them,” said Dr. Ghaemi.

Many other researchers have mined the rich STEP-BD data to study the natural history, diagnosis, and treatment of bipolar disorder. For example, Dr. Ghaemi and his associates assessed treatment patterns among a cohort of 500 STEP-BD participants. They found that most were taking mood stabilizers (72%), and the next most common class of medication was antidepressants (41%). Anticonvulsants came in third, at 32%.

“We also looked at rapid vs. nonrapid cyclers,” Dr. Ghaemi said. “And we found no difference in medication use, including antidepressants.

“We're doing an open, randomized, long-term study of antidepressant outcome in bipolar disorder” based on a sample of STEP-BD participants, Dr. Ghaemi said. He presented an interim analysis based on 69 patients with acute bipolar depression who responded to a mood stabilizer and antidepressant for 2 months. Dr. Ghaemi and his associates then randomized participants to continue both agents or only the mood stabilizer for 1 year.

“On our clinical monitoring form, we found no difference between the two groups, meaning that continuing antidepressants had no effect on mood criteria, after adjusting for other variables,” Dr. Ghaemi said. In addition, there was no significant increased relapse to depression in the group that discontinued antidepressant therapy. “This conflicts with the Stanley Foundation [Bipolar Network] data published two years ago, but that was observational and this was randomized,” Dr. Ghaemi said (Bipolar Disord. 2003;5:396–406).

Predictors of increased morbidity in the study included rapid cycling, a negative patient attitude toward the regimen to which the patient was assigned, and prior psychosis. “Rapid cyclers who continued on antidepressants trended toward greater depressive morbidity, suggesting we should use these medications even less in this subpopulation,” Dr. Ghaemi said.

STEP-BD is sponsored by the National Institute of Mental Health.

Visit www.stepbd.org

SAN JUAN, P.R. — New data—especially on bipolar depression—are starting to emerge from randomized studies conducted within a bipolar disorder observational treatment study, according to an update presented at the annual meeting of the American College of Psychiatrists.

Researchers have been busy with analysis of three randomized trials embedded within the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study since recruitment ended in September 2005. With a total of 4,361 patients at 19 centers, STEP-BD is the largest prospective cohort study of this patient population.

One randomized study compares bupropion, paroxetine (Paxil), and placebo added to a standard mood stabilizer for acute bipolar depression. “It is not yet published. This probably will be the most interesting data to come out,” Dr. S. Nassir Ghaemi predicted.

Results of one study just published favor lamotrigine vs. inositol or risperidone (Risperdal) for treatment of resistant bipolar depression (Am. J. Psychiatry 2006;163:210–6). Researchers randomized 66 patients unresponsive to a mood stabilizer plus antidepressant to either lamotrigine (150–250 mg/day), inositol (10–25 g/day), or risperidone (up to 6 mg/day) for 16 weeks. They defined recovery as two or fewer DSM-IV mood criteria for 2 months, and “lamotrigine looked more favorable,” said Dr. Ghaemi, director of the Bipolar Disorder Research Program at Emory University, Atlanta.

The third randomized trial is not yet published. Researchers will compare psychosocial therapies for maintenance: cognitive-behavioral therapy, family-focused treatment, interpersonal and social rhythm therapy, and collaborative care/psychoeducation. “This is the hardest to conduct, getting people into psychosocial therapy and randomizing them,” said Dr. Ghaemi.

Many other researchers have mined the rich STEP-BD data to study the natural history, diagnosis, and treatment of bipolar disorder. For example, Dr. Ghaemi and his associates assessed treatment patterns among a cohort of 500 STEP-BD participants. They found that most were taking mood stabilizers (72%), and the next most common class of medication was antidepressants (41%). Anticonvulsants came in third, at 32%.

“We also looked at rapid vs. nonrapid cyclers,” Dr. Ghaemi said. “And we found no difference in medication use, including antidepressants.

“We're doing an open, randomized, long-term study of antidepressant outcome in bipolar disorder” based on a sample of STEP-BD participants, Dr. Ghaemi said. He presented an interim analysis based on 69 patients with acute bipolar depression who responded to a mood stabilizer and antidepressant for 2 months. Dr. Ghaemi and his associates then randomized participants to continue both agents or only the mood stabilizer for 1 year.

“On our clinical monitoring form, we found no difference between the two groups, meaning that continuing antidepressants had no effect on mood criteria, after adjusting for other variables,” Dr. Ghaemi said. In addition, there was no significant increased relapse to depression in the group that discontinued antidepressant therapy. “This conflicts with the Stanley Foundation [Bipolar Network] data published two years ago, but that was observational and this was randomized,” Dr. Ghaemi said (Bipolar Disord. 2003;5:396–406).

Predictors of increased morbidity in the study included rapid cycling, a negative patient attitude toward the regimen to which the patient was assigned, and prior psychosis. “Rapid cyclers who continued on antidepressants trended toward greater depressive morbidity, suggesting we should use these medications even less in this subpopulation,” Dr. Ghaemi said.

STEP-BD is sponsored by the National Institute of Mental Health.

Visit www.stepbd.org

MIAMI — Compulsive hoarding occurs across disorders, according to a community-solicited study of people who reported hoarding behaviors and a wide range of comorbidities.

Traditionally, researchers assess a group of people with obsessive-compulsive disorder (OCD) and determine which ones endorse compulsive hoarding. In fact, hoarding is the most consistent and distinct subtype of OCD reported, Randy O. Frost, Ph.D., said at the annual conference of the Anxiety Disorders Association of America.

Studies using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) find that 7%–54% of OCD patients endorse hoarding, but more recent evidence suggests a distinction between the two (Clin. Psychol. Rev. 2004;24:283–313). A stronger co-occurrence of certain OCD symptoms, such as contamination and rituals, relative to hoarding, supports this theory (Behav. Res. Ther. 2005;43:897–921).

Dr. Frost and an associate performed a previous study and found “anxiety plays a smaller role in hoarding than in OCD, which is another reason we think they might be distinct” (Behav. Res. Ther. 2003;41:179–94). Dr. Frost is the Harold Edward and Elsa Siipola Israel Professor of Psychology at Smith College in Northampton, Mass.

Frequency of hoarding in populations with DSM-IV diagnoses is pretty high (OCD, dementia, schizophrenia, brain injury, etc.).

“No studies have examined diagnoses in samples of people who hoard—flipping it the other way around,” Dr. Frost said. So instead of looking for compulsive hoarding within a subset of people with OCD, he and his associates assessed a sample of 75 self-reported compulsive hoarders for OCD and other comorbidities. They specifically looked for anxiety, impulse control, and personality disorders in a sample not recruited from an anxiety clinic.

Most of the participants (75%) were female, and the mean age was 53 years. “We frequently see an older population when we solicit for hoarding versus other anxiety disorders,” Dr. Frost said.

In addition to a home visit, researchers assessed all participants with the expanded Anxiety Disorder Interview Schedule (ADIS-Lifetime) and the Saving Inventory-Revised (SI-R). In 35 of the patients, they also used the Structured Clinical Interview for DSM-III-R (SCID-II) and the Minnesota Impulsive Disorders Interview (MIDI).

“Only 31% of this hoarding sample had any clinically significant OCD symptoms, and another 16% had subclinical symptoms,” Dr. Frost said. “The rest look like what we might call 'pure hoarders.'”

A total of 31% met criteria for major depressive disorder, 25% for general anxiety disorder, and 16% for generalized social phobia, “which was still significant,” Dr. Frost said.

“When we look at the frequency of axis II diagnoses in hoarding, it is much smaller than we might expect given the general assumptions about hoarding,” Dr. Frost said. In this study, for example, 31% had an axis II personality disorder, such as obsessive-compulsive personality disorder.

More than 70% of the sample endorsed compulsive acquisition. This finding was a composite of 60% who reported compulsive buying behavior and 51% who reported compulsive acquisition of free items.

A total of 92% scored high for compulsive acquisition on a subscale of the SI-R (SI-R-acquisition). This was the percentage that exceeded by at least one standard deviation the mean acquisition score of 6.9 among a normal sample. Regarding the SI-R-clutter subscale, 96% of the participants exceeded the mean score of 12.8. Regarding the SI-R-difficulty discarding measure, 95% exceeded the mean score of 8.2. “We are seeing these things are very prevalent in this sample who hoard,” Dr. Frost said.

MIAMI — Compulsive hoarding occurs across disorders, according to a community-solicited study of people who reported hoarding behaviors and a wide range of comorbidities.

Traditionally, researchers assess a group of people with obsessive-compulsive disorder (OCD) and determine which ones endorse compulsive hoarding. In fact, hoarding is the most consistent and distinct subtype of OCD reported, Randy O. Frost, Ph.D., said at the annual conference of the Anxiety Disorders Association of America.

Studies using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) find that 7%–54% of OCD patients endorse hoarding, but more recent evidence suggests a distinction between the two (Clin. Psychol. Rev. 2004;24:283–313). A stronger co-occurrence of certain OCD symptoms, such as contamination and rituals, relative to hoarding, supports this theory (Behav. Res. Ther. 2005;43:897–921).

Dr. Frost and an associate performed a previous study and found “anxiety plays a smaller role in hoarding than in OCD, which is another reason we think they might be distinct” (Behav. Res. Ther. 2003;41:179–94). Dr. Frost is the Harold Edward and Elsa Siipola Israel Professor of Psychology at Smith College in Northampton, Mass.

Frequency of hoarding in populations with DSM-IV diagnoses is pretty high (OCD, dementia, schizophrenia, brain injury, etc.).

“No studies have examined diagnoses in samples of people who hoard—flipping it the other way around,” Dr. Frost said. So instead of looking for compulsive hoarding within a subset of people with OCD, he and his associates assessed a sample of 75 self-reported compulsive hoarders for OCD and other comorbidities. They specifically looked for anxiety, impulse control, and personality disorders in a sample not recruited from an anxiety clinic.

Most of the participants (75%) were female, and the mean age was 53 years. “We frequently see an older population when we solicit for hoarding versus other anxiety disorders,” Dr. Frost said.

In addition to a home visit, researchers assessed all participants with the expanded Anxiety Disorder Interview Schedule (ADIS-Lifetime) and the Saving Inventory-Revised (SI-R). In 35 of the patients, they also used the Structured Clinical Interview for DSM-III-R (SCID-II) and the Minnesota Impulsive Disorders Interview (MIDI).

“Only 31% of this hoarding sample had any clinically significant OCD symptoms, and another 16% had subclinical symptoms,” Dr. Frost said. “The rest look like what we might call 'pure hoarders.'”

A total of 31% met criteria for major depressive disorder, 25% for general anxiety disorder, and 16% for generalized social phobia, “which was still significant,” Dr. Frost said.

“When we look at the frequency of axis II diagnoses in hoarding, it is much smaller than we might expect given the general assumptions about hoarding,” Dr. Frost said. In this study, for example, 31% had an axis II personality disorder, such as obsessive-compulsive personality disorder.

More than 70% of the sample endorsed compulsive acquisition. This finding was a composite of 60% who reported compulsive buying behavior and 51% who reported compulsive acquisition of free items.

A total of 92% scored high for compulsive acquisition on a subscale of the SI-R (SI-R-acquisition). This was the percentage that exceeded by at least one standard deviation the mean acquisition score of 6.9 among a normal sample. Regarding the SI-R-clutter subscale, 96% of the participants exceeded the mean score of 12.8. Regarding the SI-R-difficulty discarding measure, 95% exceeded the mean score of 8.2. “We are seeing these things are very prevalent in this sample who hoard,” Dr. Frost said.

MIAMI — Compulsive hoarding occurs across disorders, according to a community-solicited study of people who reported hoarding behaviors and a wide range of comorbidities.

Traditionally, researchers assess a group of people with obsessive-compulsive disorder (OCD) and determine which ones endorse compulsive hoarding. In fact, hoarding is the most consistent and distinct subtype of OCD reported, Randy O. Frost, Ph.D., said at the annual conference of the Anxiety Disorders Association of America.

Studies using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) find that 7%–54% of OCD patients endorse hoarding, but more recent evidence suggests a distinction between the two (Clin. Psychol. Rev. 2004;24:283–313). A stronger co-occurrence of certain OCD symptoms, such as contamination and rituals, relative to hoarding, supports this theory (Behav. Res. Ther. 2005;43:897–921).

Dr. Frost and an associate performed a previous study and found “anxiety plays a smaller role in hoarding than in OCD, which is another reason we think they might be distinct” (Behav. Res. Ther. 2003;41:179–94). Dr. Frost is the Harold Edward and Elsa Siipola Israel Professor of Psychology at Smith College in Northampton, Mass.

Frequency of hoarding in populations with DSM-IV diagnoses is pretty high (OCD, dementia, schizophrenia, brain injury, etc.).

“No studies have examined diagnoses in samples of people who hoard—flipping it the other way around,” Dr. Frost said. So instead of looking for compulsive hoarding within a subset of people with OCD, he and his associates assessed a sample of 75 self-reported compulsive hoarders for OCD and other comorbidities. They specifically looked for anxiety, impulse control, and personality disorders in a sample not recruited from an anxiety clinic.

Most of the participants (75%) were female, and the mean age was 53 years. “We frequently see an older population when we solicit for hoarding versus other anxiety disorders,” Dr. Frost said.

In addition to a home visit, researchers assessed all participants with the expanded Anxiety Disorder Interview Schedule (ADIS-Lifetime) and the Saving Inventory-Revised (SI-R). In 35 of the patients, they also used the Structured Clinical Interview for DSM-III-R (SCID-II) and the Minnesota Impulsive Disorders Interview (MIDI).

“Only 31% of this hoarding sample had any clinically significant OCD symptoms, and another 16% had subclinical symptoms,” Dr. Frost said. “The rest look like what we might call 'pure hoarders.'”

A total of 31% met criteria for major depressive disorder, 25% for general anxiety disorder, and 16% for generalized social phobia, “which was still significant,” Dr. Frost said.

“When we look at the frequency of axis II diagnoses in hoarding, it is much smaller than we might expect given the general assumptions about hoarding,” Dr. Frost said. In this study, for example, 31% had an axis II personality disorder, such as obsessive-compulsive personality disorder.

More than 70% of the sample endorsed compulsive acquisition. This finding was a composite of 60% who reported compulsive buying behavior and 51% who reported compulsive acquisition of free items.

A total of 92% scored high for compulsive acquisition on a subscale of the SI-R (SI-R-acquisition). This was the percentage that exceeded by at least one standard deviation the mean acquisition score of 6.9 among a normal sample. Regarding the SI-R-clutter subscale, 96% of the participants exceeded the mean score of 12.8. Regarding the SI-R-difficulty discarding measure, 95% exceeded the mean score of 8.2. “We are seeing these things are very prevalent in this sample who hoard,” Dr. Frost said.

MIAMI — Higher self-reported alcohol consumption among men with panic attacks carries important implications for patient screening, according to a poster presentation at the annual conference of the Anxiety Disorders Association of America.

“The take-home message for physicians is to look for comorbidity in men with panic attacks for alcohol use and other substances,” Erin Marshall said in an interview.

Previous research indicated a relationship between panic attacks and drinking behaviors. “It could be a coping mechanism—people with panic attacks drink more than people without panic attacks,” said Ms. Marshall, doctoral student in clinical psychology at the University of Vermont at Burlington.

To assess associations between panic attacks, alcohol consumption, and gender, Ms. Marshall and her colleagues studied 413 college students in Mexico City. One of the collaborators, Samuel J. Cardenas, Ph.D., of the Universidad Nacional Autonoma de Mexico, facilitated recruitment of participants.

A total of 61% of participants were female. Each student completed self-report measures about substance use patterns and panic attack history.

“We found men with panic are drinking the most,” Ms. Marshall said.

As predicted, individuals experiencing panic attacks were significantly more likely to drink alcohol (P less than .01), as were males (P less than .001). In addition, “the interaction of panic attacks and gender incrementally predicted levels of alcohol consumption (P less than .001), such that the association between panic attacks and alcohol consumption was stronger in men than women,” the authors wrote.

MIAMI — Higher self-reported alcohol consumption among men with panic attacks carries important implications for patient screening, according to a poster presentation at the annual conference of the Anxiety Disorders Association of America.

“The take-home message for physicians is to look for comorbidity in men with panic attacks for alcohol use and other substances,” Erin Marshall said in an interview.

Previous research indicated a relationship between panic attacks and drinking behaviors. “It could be a coping mechanism—people with panic attacks drink more than people without panic attacks,” said Ms. Marshall, doctoral student in clinical psychology at the University of Vermont at Burlington.

To assess associations between panic attacks, alcohol consumption, and gender, Ms. Marshall and her colleagues studied 413 college students in Mexico City. One of the collaborators, Samuel J. Cardenas, Ph.D., of the Universidad Nacional Autonoma de Mexico, facilitated recruitment of participants.

A total of 61% of participants were female. Each student completed self-report measures about substance use patterns and panic attack history.

“We found men with panic are drinking the most,” Ms. Marshall said.

As predicted, individuals experiencing panic attacks were significantly more likely to drink alcohol (P less than .01), as were males (P less than .001). In addition, “the interaction of panic attacks and gender incrementally predicted levels of alcohol consumption (P less than .001), such that the association between panic attacks and alcohol consumption was stronger in men than women,” the authors wrote.

MIAMI — Higher self-reported alcohol consumption among men with panic attacks carries important implications for patient screening, according to a poster presentation at the annual conference of the Anxiety Disorders Association of America.

“The take-home message for physicians is to look for comorbidity in men with panic attacks for alcohol use and other substances,” Erin Marshall said in an interview.

Previous research indicated a relationship between panic attacks and drinking behaviors. “It could be a coping mechanism—people with panic attacks drink more than people without panic attacks,” said Ms. Marshall, doctoral student in clinical psychology at the University of Vermont at Burlington.

To assess associations between panic attacks, alcohol consumption, and gender, Ms. Marshall and her colleagues studied 413 college students in Mexico City. One of the collaborators, Samuel J. Cardenas, Ph.D., of the Universidad Nacional Autonoma de Mexico, facilitated recruitment of participants.

A total of 61% of participants were female. Each student completed self-report measures about substance use patterns and panic attack history.

“We found men with panic are drinking the most,” Ms. Marshall said.

As predicted, individuals experiencing panic attacks were significantly more likely to drink alcohol (P less than .01), as were males (P less than .001). In addition, “the interaction of panic attacks and gender incrementally predicted levels of alcohol consumption (P less than .001), such that the association between panic attacks and alcohol consumption was stronger in men than women,” the authors wrote.

SAN JUAN, P.R. – Growing evidence points to an association between inflammation and depression, according to a presentation at the annual meeting of the American College of Psychiatrists.

For example, depressed patients have elevated inflammatory markers–such as interleukin-6 and C-reactive protein. In fact, the levels of proinflammatory cytokines correlate with the severity of depressive symptoms in studies. In addition, administration of cytokine antagonists can effectively reverse depressive symptoms in patients, Dr. Andrew H. Miller said.

“We really stand at a point that is very exciting in terms of novel therapies and translation of research,” Dr. Miller said. “The notion quite simply is that stress or depression affects the HPA [hypothalamic-pituitary-adrenal] axis, [affects] the endocrine system, alters the immune system, and leaves patients open to diseases.”

Physicians from many specialties already recognize that inflammation plays a key role in cardiovascular disease, diabetes, metabolic syndrome, and cancer, said Dr. Miller, professor in the department of psychiatry and behavioral sciences at Emory University, Atlanta.

“We did not want to be left out in terms of psychiatry,” said Dr. Miller, who also is director of the psychiatric oncology program at the Winship Cancer Institute at Emory.

There are multiple possible mechanisms whereby inflammation could cause depression. Inflammatory cytokines released peripherally might reach the brain through active transport, passage through leaky regions in the blood-brain barrier, or transmission through afferent nerve fibers (vagus nerve), Dr. Miller said. There is a cytokine network in the central nervous system, and glia and microglia are the richest source of cytokines in the brain. Neurons also produce and express cytokines.

“We've learned these cytokines have access to the brain and … ultimately can change behavior,” Dr. Miller said. Inflammatory cytokines cause anhedonia, fatigue, cognitive dysfunction, and other flu-like symptoms in sick patients. In addition, researchers induced behavioral changes that resemble major depression in human and animal studies with administration of proinflammatory cytokines.

Some therapeutic cytokines cause depression. For example, interferon-α (IFN-α) is used to treat viral infections and cancer because it is a potent inducer of the inflammatory cytokine network, especially interleukin-6, Dr. Miller said. “Oncologists told us early on this drug causes a lot of depression.”

A total of 60% of patients treated with IFN-α reported depressed mood in one study (Neuropsychopharmacology 2002;26:643–52). Dr. Miller and his associates also found a 45% incidence of major depression among patients with malignant melanoma treated with IFN-α (N. Engl. J. Med. 2001;344:961–6).

The good news is that paroxetine (Paxil) aggressively blocked development of depression. “Just 11% developed depression, so there was a fourfold reduction with this pretreatment.

“There is a caveat. If you give a drug that causes release of dopamine–for example, paroxetine–that dopamine becomes oxidized and in the long term can damage basal ganglia,” Dr. Miller said in response to a question from a person attending the meeting. “So we're using dopamine antagonists to block this until we get more information about what we are doing to patients.”

Physician reaction to his study varied, Dr. Miller said. “The people who got on us the most for that study with paroxetine were the ones who were treating hepatitis C. They said we'd expose a lot of people to antidepressants who don't really need them.” However, “with melanoma, many patients will not go back on interferon therapy, and giving antidepressant prophylaxis might help.”

In another study, patients with psoriasis treated with the cytokine antagonist etanercept experienced reversal of their depressive symptoms (Lancet 2006;367:29–35). Improvement in depression was independent of the drug's effect on disease progress.

The wider picture may be a link between stress, depression, and illness, Dr. Miller said. In one study in review, patients with major depressive disorder exhibited an exaggerated inflammatory response to stress.

“There is an interesting possible link between depression and a wide variety of medical disorders where inflammation plays a role,” Dr. Miller said. It “may explain high comorbidity of some medical conditions with depression.

“Psychiatry is now catching up to other medical specialties in recognizing the adverse effects of inflammation,” Dr. Miller added. “Psychiatrists need to keep an eye on this. The idea that the immune system might affect the brain and vice versa presents a lot of novel targets for treating psychiatric disorders.”

SAN JUAN, P.R. – Growing evidence points to an association between inflammation and depression, according to a presentation at the annual meeting of the American College of Psychiatrists.

For example, depressed patients have elevated inflammatory markers–such as interleukin-6 and C-reactive protein. In fact, the levels of proinflammatory cytokines correlate with the severity of depressive symptoms in studies. In addition, administration of cytokine antagonists can effectively reverse depressive symptoms in patients, Dr. Andrew H. Miller said.

“We really stand at a point that is very exciting in terms of novel therapies and translation of research,” Dr. Miller said. “The notion quite simply is that stress or depression affects the HPA [hypothalamic-pituitary-adrenal] axis, [affects] the endocrine system, alters the immune system, and leaves patients open to diseases.”

Physicians from many specialties already recognize that inflammation plays a key role in cardiovascular disease, diabetes, metabolic syndrome, and cancer, said Dr. Miller, professor in the department of psychiatry and behavioral sciences at Emory University, Atlanta.

“We did not want to be left out in terms of psychiatry,” said Dr. Miller, who also is director of the psychiatric oncology program at the Winship Cancer Institute at Emory.

There are multiple possible mechanisms whereby inflammation could cause depression. Inflammatory cytokines released peripherally might reach the brain through active transport, passage through leaky regions in the blood-brain barrier, or transmission through afferent nerve fibers (vagus nerve), Dr. Miller said. There is a cytokine network in the central nervous system, and glia and microglia are the richest source of cytokines in the brain. Neurons also produce and express cytokines.

“We've learned these cytokines have access to the brain and … ultimately can change behavior,” Dr. Miller said. Inflammatory cytokines cause anhedonia, fatigue, cognitive dysfunction, and other flu-like symptoms in sick patients. In addition, researchers induced behavioral changes that resemble major depression in human and animal studies with administration of proinflammatory cytokines.

Some therapeutic cytokines cause depression. For example, interferon-α (IFN-α) is used to treat viral infections and cancer because it is a potent inducer of the inflammatory cytokine network, especially interleukin-6, Dr. Miller said. “Oncologists told us early on this drug causes a lot of depression.”

A total of 60% of patients treated with IFN-α reported depressed mood in one study (Neuropsychopharmacology 2002;26:643–52). Dr. Miller and his associates also found a 45% incidence of major depression among patients with malignant melanoma treated with IFN-α (N. Engl. J. Med. 2001;344:961–6).

The good news is that paroxetine (Paxil) aggressively blocked development of depression. “Just 11% developed depression, so there was a fourfold reduction with this pretreatment.

“There is a caveat. If you give a drug that causes release of dopamine–for example, paroxetine–that dopamine becomes oxidized and in the long term can damage basal ganglia,” Dr. Miller said in response to a question from a person attending the meeting. “So we're using dopamine antagonists to block this until we get more information about what we are doing to patients.”

Physician reaction to his study varied, Dr. Miller said. “The people who got on us the most for that study with paroxetine were the ones who were treating hepatitis C. They said we'd expose a lot of people to antidepressants who don't really need them.” However, “with melanoma, many patients will not go back on interferon therapy, and giving antidepressant prophylaxis might help.”

In another study, patients with psoriasis treated with the cytokine antagonist etanercept experienced reversal of their depressive symptoms (Lancet 2006;367:29–35). Improvement in depression was independent of the drug's effect on disease progress.

The wider picture may be a link between stress, depression, and illness, Dr. Miller said. In one study in review, patients with major depressive disorder exhibited an exaggerated inflammatory response to stress.

“There is an interesting possible link between depression and a wide variety of medical disorders where inflammation plays a role,” Dr. Miller said. It “may explain high comorbidity of some medical conditions with depression.

“Psychiatry is now catching up to other medical specialties in recognizing the adverse effects of inflammation,” Dr. Miller added. “Psychiatrists need to keep an eye on this. The idea that the immune system might affect the brain and vice versa presents a lot of novel targets for treating psychiatric disorders.”

SAN JUAN, P.R. – Growing evidence points to an association between inflammation and depression, according to a presentation at the annual meeting of the American College of Psychiatrists.

For example, depressed patients have elevated inflammatory markers–such as interleukin-6 and C-reactive protein. In fact, the levels of proinflammatory cytokines correlate with the severity of depressive symptoms in studies. In addition, administration of cytokine antagonists can effectively reverse depressive symptoms in patients, Dr. Andrew H. Miller said.

“We really stand at a point that is very exciting in terms of novel therapies and translation of research,” Dr. Miller said. “The notion quite simply is that stress or depression affects the HPA [hypothalamic-pituitary-adrenal] axis, [affects] the endocrine system, alters the immune system, and leaves patients open to diseases.”

Physicians from many specialties already recognize that inflammation plays a key role in cardiovascular disease, diabetes, metabolic syndrome, and cancer, said Dr. Miller, professor in the department of psychiatry and behavioral sciences at Emory University, Atlanta.

“We did not want to be left out in terms of psychiatry,” said Dr. Miller, who also is director of the psychiatric oncology program at the Winship Cancer Institute at Emory.

There are multiple possible mechanisms whereby inflammation could cause depression. Inflammatory cytokines released peripherally might reach the brain through active transport, passage through leaky regions in the blood-brain barrier, or transmission through afferent nerve fibers (vagus nerve), Dr. Miller said. There is a cytokine network in the central nervous system, and glia and microglia are the richest source of cytokines in the brain. Neurons also produce and express cytokines.

“We've learned these cytokines have access to the brain and … ultimately can change behavior,” Dr. Miller said. Inflammatory cytokines cause anhedonia, fatigue, cognitive dysfunction, and other flu-like symptoms in sick patients. In addition, researchers induced behavioral changes that resemble major depression in human and animal studies with administration of proinflammatory cytokines.

Some therapeutic cytokines cause depression. For example, interferon-α (IFN-α) is used to treat viral infections and cancer because it is a potent inducer of the inflammatory cytokine network, especially interleukin-6, Dr. Miller said. “Oncologists told us early on this drug causes a lot of depression.”

A total of 60% of patients treated with IFN-α reported depressed mood in one study (Neuropsychopharmacology 2002;26:643–52). Dr. Miller and his associates also found a 45% incidence of major depression among patients with malignant melanoma treated with IFN-α (N. Engl. J. Med. 2001;344:961–6).

The good news is that paroxetine (Paxil) aggressively blocked development of depression. “Just 11% developed depression, so there was a fourfold reduction with this pretreatment.

“There is a caveat. If you give a drug that causes release of dopamine–for example, paroxetine–that dopamine becomes oxidized and in the long term can damage basal ganglia,” Dr. Miller said in response to a question from a person attending the meeting. “So we're using dopamine antagonists to block this until we get more information about what we are doing to patients.”

Physician reaction to his study varied, Dr. Miller said. “The people who got on us the most for that study with paroxetine were the ones who were treating hepatitis C. They said we'd expose a lot of people to antidepressants who don't really need them.” However, “with melanoma, many patients will not go back on interferon therapy, and giving antidepressant prophylaxis might help.”

In another study, patients with psoriasis treated with the cytokine antagonist etanercept experienced reversal of their depressive symptoms (Lancet 2006;367:29–35). Improvement in depression was independent of the drug's effect on disease progress.

The wider picture may be a link between stress, depression, and illness, Dr. Miller said. In one study in review, patients with major depressive disorder exhibited an exaggerated inflammatory response to stress.

“There is an interesting possible link between depression and a wide variety of medical disorders where inflammation plays a role,” Dr. Miller said. It “may explain high comorbidity of some medical conditions with depression.

“Psychiatry is now catching up to other medical specialties in recognizing the adverse effects of inflammation,” Dr. Miller added. “Psychiatrists need to keep an eye on this. The idea that the immune system might affect the brain and vice versa presents a lot of novel targets for treating psychiatric disorders.”

MIAMI – Anxiety in men may be a robust and independent predictor of the 10-year incidence of myocardial infarction, according to a study presented at the annual conference of the Anxiety Disorders Association of America.

“This is kind of exciting because most work has been done with psychosocial factors like depression and hostility,” Yael E. Avivi said in an interview during the meeting.

Depression and negative affect have been the focus of most of the literature addressing a possible association between psychosocial factors and heart disease. Other researchers have reported evidence suggesting that anxiety contributes to coronary heart disease (Ann. Behav. Med. 1998;20:47–58) and to an elevated risk of fatal coronary heart disease (Circulation 1994;90:2225–9). But these investigators used relatively short assessment scales to measure anxiety, noted Ms. Avivi, a doctoral student in the department of psychology at the University of Miami.

Her associates, including lead author Biing-Jiun Shen, Ph.D., analyzed data that included a more comprehensive assessment to look for a possible association between anxiety and subsequent MI. The study assessed follow-up data for 740 healthy men who entered the Veterans Administration Normative Aging Study in 1986. Initial assessments included the Minnesota Multiphasic Personality Inventory, a comprehensive physical examination, and a cardiovascular disease risk profile. The participants did not have diabetes or a history of MI. The mean age at study entry was 60 years.

The researchers calculated an overall anxiety factor for each participant based on a combined score from four anxiety scales used in the Minnesota Multiphasic Personality Inventory. Those included measures for psychasthenia and social introversion, as well scores from the Wiggins phobia scale and the Taylor Manifest Anxiety Scale.

During the 10 years of follow-up, there were 60 new-onset myocardial infarctions, including two fatal heart attacks. The researchers used hierarchical logistic regression to predict the likelihood of an MI using the composite score and each of the four anxiety constructs.

“We looked at the odds ratios for predicting new MI incidence when controlling for age, education, marital status, weight, blood pressure, glucose, cholesterol, drinking, smoking, and caloric intake,” Ms. Avivi said. “We could control for those and still see a significant effect.”

The overall anxiety factor was an independent and significant predictor of subsequent MI in the sample population (odds ratio, 1.46). Also, each of the four anxiety components independently and significantly predicted MI: psychasthenia (odds ratio, 1.42), social inhibition (odds ratio, 1.36), phobia (odds ratio, 1.44), and Taylor Manifest Anxiety (odds ratio, 1.50). In addition, being single and having lower HDL cholesterol levels predicted onset of MI in a multivariate analysis.

“The next question we had was, can depression and other psychosocial factors explain this association?” she said. Interestingly, these other psychosocial factors could not explain the link between anxiety and the new cases of MI that emerged in this study. After controlling for depression, anger, hostility, type A personality, and perceived stress, anxiety remained an independent predictor of a subsequent MI.

The researchers divided participants into quartiles based on their anxiety scores. “We also saw a dose-response effect,” Ms. Avivi said. “People with the highest anxiety scores had the highest incidence of MI.”

The association between anxiety and acute myocardial infarction was not surprising to Dr. James J. Ferguson, chairman of the Research Committee at the Texas Heart Institute, Houston. Still, he commented, the results could have important implications for any physician treating patients with anxiety.

“Yes, these people are at risk, but what can we do about it?” he asked. He described the findings as an important first step, but added that “there is a long ways to go before we understand how changing anxiety or stress can affect outcomes” and noted that the study did not address that point.

Mechanisms that would explain the relationship between anxiety and subsequent MI remain unknown and require further study, Ms. Avivi said. Anxiety might adversely affect health behaviors, promote atherogenesis, or trigger fatal coronary events through arrythmia, plaque rupture, coronary vasospasm, or thrombosis (Ann. Behavior. Med. 1998;20:47–58).

General distress across a range of negative emotions might play an important role in the relationship between psychosocial factors and coronary heart disease, according to a recently published study that also was based on follow-up data from the Veterans Administration Normative Aging Study (Ann. Behavior. Med. 2006;31:21–9).

Those researchers also concluded that aspects of anxiety may independently increase the risk for coronary heart disease. However, they also assessed anger and depression in their cohort, and they urged future researchers to consider a shared component of these features as a possible explanation for the elevated coronary disease risk.

MIAMI – Anxiety in men may be a robust and independent predictor of the 10-year incidence of myocardial infarction, according to a study presented at the annual conference of the Anxiety Disorders Association of America.

“This is kind of exciting because most work has been done with psychosocial factors like depression and hostility,” Yael E. Avivi said in an interview during the meeting.

Depression and negative affect have been the focus of most of the literature addressing a possible association between psychosocial factors and heart disease. Other researchers have reported evidence suggesting that anxiety contributes to coronary heart disease (Ann. Behav. Med. 1998;20:47–58) and to an elevated risk of fatal coronary heart disease (Circulation 1994;90:2225–9). But these investigators used relatively short assessment scales to measure anxiety, noted Ms. Avivi, a doctoral student in the department of psychology at the University of Miami.

Her associates, including lead author Biing-Jiun Shen, Ph.D., analyzed data that included a more comprehensive assessment to look for a possible association between anxiety and subsequent MI. The study assessed follow-up data for 740 healthy men who entered the Veterans Administration Normative Aging Study in 1986. Initial assessments included the Minnesota Multiphasic Personality Inventory, a comprehensive physical examination, and a cardiovascular disease risk profile. The participants did not have diabetes or a history of MI. The mean age at study entry was 60 years.

The researchers calculated an overall anxiety factor for each participant based on a combined score from four anxiety scales used in the Minnesota Multiphasic Personality Inventory. Those included measures for psychasthenia and social introversion, as well scores from the Wiggins phobia scale and the Taylor Manifest Anxiety Scale.

During the 10 years of follow-up, there were 60 new-onset myocardial infarctions, including two fatal heart attacks. The researchers used hierarchical logistic regression to predict the likelihood of an MI using the composite score and each of the four anxiety constructs.

“We looked at the odds ratios for predicting new MI incidence when controlling for age, education, marital status, weight, blood pressure, glucose, cholesterol, drinking, smoking, and caloric intake,” Ms. Avivi said. “We could control for those and still see a significant effect.”

The overall anxiety factor was an independent and significant predictor of subsequent MI in the sample population (odds ratio, 1.46). Also, each of the four anxiety components independently and significantly predicted MI: psychasthenia (odds ratio, 1.42), social inhibition (odds ratio, 1.36), phobia (odds ratio, 1.44), and Taylor Manifest Anxiety (odds ratio, 1.50). In addition, being single and having lower HDL cholesterol levels predicted onset of MI in a multivariate analysis.

“The next question we had was, can depression and other psychosocial factors explain this association?” she said. Interestingly, these other psychosocial factors could not explain the link between anxiety and the new cases of MI that emerged in this study. After controlling for depression, anger, hostility, type A personality, and perceived stress, anxiety remained an independent predictor of a subsequent MI.

The researchers divided participants into quartiles based on their anxiety scores. “We also saw a dose-response effect,” Ms. Avivi said. “People with the highest anxiety scores had the highest incidence of MI.”

The association between anxiety and acute myocardial infarction was not surprising to Dr. James J. Ferguson, chairman of the Research Committee at the Texas Heart Institute, Houston. Still, he commented, the results could have important implications for any physician treating patients with anxiety.

“Yes, these people are at risk, but what can we do about it?” he asked. He described the findings as an important first step, but added that “there is a long ways to go before we understand how changing anxiety or stress can affect outcomes” and noted that the study did not address that point.

Mechanisms that would explain the relationship between anxiety and subsequent MI remain unknown and require further study, Ms. Avivi said. Anxiety might adversely affect health behaviors, promote atherogenesis, or trigger fatal coronary events through arrythmia, plaque rupture, coronary vasospasm, or thrombosis (Ann. Behavior. Med. 1998;20:47–58).

General distress across a range of negative emotions might play an important role in the relationship between psychosocial factors and coronary heart disease, according to a recently published study that also was based on follow-up data from the Veterans Administration Normative Aging Study (Ann. Behavior. Med. 2006;31:21–9).

Those researchers also concluded that aspects of anxiety may independently increase the risk for coronary heart disease. However, they also assessed anger and depression in their cohort, and they urged future researchers to consider a shared component of these features as a possible explanation for the elevated coronary disease risk.

MIAMI – Anxiety in men may be a robust and independent predictor of the 10-year incidence of myocardial infarction, according to a study presented at the annual conference of the Anxiety Disorders Association of America.

“This is kind of exciting because most work has been done with psychosocial factors like depression and hostility,” Yael E. Avivi said in an interview during the meeting.

Depression and negative affect have been the focus of most of the literature addressing a possible association between psychosocial factors and heart disease. Other researchers have reported evidence suggesting that anxiety contributes to coronary heart disease (Ann. Behav. Med. 1998;20:47–58) and to an elevated risk of fatal coronary heart disease (Circulation 1994;90:2225–9). But these investigators used relatively short assessment scales to measure anxiety, noted Ms. Avivi, a doctoral student in the department of psychology at the University of Miami.

Her associates, including lead author Biing-Jiun Shen, Ph.D., analyzed data that included a more comprehensive assessment to look for a possible association between anxiety and subsequent MI. The study assessed follow-up data for 740 healthy men who entered the Veterans Administration Normative Aging Study in 1986. Initial assessments included the Minnesota Multiphasic Personality Inventory, a comprehensive physical examination, and a cardiovascular disease risk profile. The participants did not have diabetes or a history of MI. The mean age at study entry was 60 years.

The researchers calculated an overall anxiety factor for each participant based on a combined score from four anxiety scales used in the Minnesota Multiphasic Personality Inventory. Those included measures for psychasthenia and social introversion, as well scores from the Wiggins phobia scale and the Taylor Manifest Anxiety Scale.

During the 10 years of follow-up, there were 60 new-onset myocardial infarctions, including two fatal heart attacks. The researchers used hierarchical logistic regression to predict the likelihood of an MI using the composite score and each of the four anxiety constructs.

“We looked at the odds ratios for predicting new MI incidence when controlling for age, education, marital status, weight, blood pressure, glucose, cholesterol, drinking, smoking, and caloric intake,” Ms. Avivi said. “We could control for those and still see a significant effect.”

The overall anxiety factor was an independent and significant predictor of subsequent MI in the sample population (odds ratio, 1.46). Also, each of the four anxiety components independently and significantly predicted MI: psychasthenia (odds ratio, 1.42), social inhibition (odds ratio, 1.36), phobia (odds ratio, 1.44), and Taylor Manifest Anxiety (odds ratio, 1.50). In addition, being single and having lower HDL cholesterol levels predicted onset of MI in a multivariate analysis.

“The next question we had was, can depression and other psychosocial factors explain this association?” she said. Interestingly, these other psychosocial factors could not explain the link between anxiety and the new cases of MI that emerged in this study. After controlling for depression, anger, hostility, type A personality, and perceived stress, anxiety remained an independent predictor of a subsequent MI.

The researchers divided participants into quartiles based on their anxiety scores. “We also saw a dose-response effect,” Ms. Avivi said. “People with the highest anxiety scores had the highest incidence of MI.”

The association between anxiety and acute myocardial infarction was not surprising to Dr. James J. Ferguson, chairman of the Research Committee at the Texas Heart Institute, Houston. Still, he commented, the results could have important implications for any physician treating patients with anxiety.

“Yes, these people are at risk, but what can we do about it?” he asked. He described the findings as an important first step, but added that “there is a long ways to go before we understand how changing anxiety or stress can affect outcomes” and noted that the study did not address that point.

Mechanisms that would explain the relationship between anxiety and subsequent MI remain unknown and require further study, Ms. Avivi said. Anxiety might adversely affect health behaviors, promote atherogenesis, or trigger fatal coronary events through arrythmia, plaque rupture, coronary vasospasm, or thrombosis (Ann. Behavior. Med. 1998;20:47–58).

General distress across a range of negative emotions might play an important role in the relationship between psychosocial factors and coronary heart disease, according to a recently published study that also was based on follow-up data from the Veterans Administration Normative Aging Study (Ann. Behavior. Med. 2006;31:21–9).

Those researchers also concluded that aspects of anxiety may independently increase the risk for coronary heart disease. However, they also assessed anger and depression in their cohort, and they urged future researchers to consider a shared component of these features as a possible explanation for the elevated coronary disease risk.

SCOTTSDALE, ARIZ. – Existing data suggest that a subset of migraine patients may benefit from closure of their patent foramen ovale, Dr. David W. Dodick said during a symposium sponsored by the American Headache Society.

However, any clinical decision of the merits of surgical closure of a patent foramen ovale for patients with migraine should await the results of a number of ongoing safety and efficacy trials, he stressed.

Closures are being done with regularity as a treatment for migraines in the United States and Europe despite the lack of safety and efficacy data. “This [procedure] is gathering momentum, to say the least. We have a responsibility to know the data and give patients proper and appropriate advice,” said Dr. Dodick, professor of neurology at Mayo Clinic Arizona. “This is something patients will come into your office wanting to talk about, if they haven't already.”

Physicians are in a tough spot between patient demand and a dearth of data to support patent foramen ovale (PFO) closure for migraine relief, he acknowledged.

Some research indicates an association between a PFO and migraines with aura, particularly in patients with a large left-to-right shunt. In one study, patients with migraine with aura were three times more likely to have a PFO than those who experienced migraines without aura (Neurology 1999;53:2213–4).

The main take-home message for now remains that PFO appears to be more prevalent in patients whose migraines involve aura, Dr. Dodick said.

A left-to-right shunt is also more common among migraine-with-aura patients. In addition, both large atrial shunts and large PFOs are dominantly inherited and might therefore share a genetic origin (Heart 2004;90:1315–20).

One of the large, prospective trials underway is the Migraine Intervention with STARFlex Technology (MIST) study. Patients with migraine with aura will be assessed by a cardiologist and then randomized to closure or no closure.

Although results are not finalized, enrollment data show 60% of 370 participants having a right-to-left shunt (versus 27% of the general population) and 38% having a large PFO (versus 7% of the general population).

Updates and an animation that shows a possible role of PFO in migraine can be viewed on www.migraine-mist.org

PFO closure might effectively treat migraine in a subgroup of patients, Dr. Dodick proposed. A number of studies suggest that closure eliminates migraines in about one-third of migraineurs, reduces frequency in another third, and does not alter attacks in another third of patients.

“Are there factors that will reliably predict which patients will benefit? If these studies are positive, how will we know that a patient in front of us in the future will benefit significantly from this invasive procedure?” he asked.

Many headache specialists are taking a conservative stance. “While many patients have disabling migraines, many people think migraines are not life threatening. They are life altering but not life threatening,” Dr. Dodick. “And the surgery is invasive.”

There is an overall peri-interventional adverse-event rate of about 6% (Catheter Cardiovasc. Interv. 2004;62:512–6).

SCOTTSDALE, ARIZ. – Existing data suggest that a subset of migraine patients may benefit from closure of their patent foramen ovale, Dr. David W. Dodick said during a symposium sponsored by the American Headache Society.

However, any clinical decision of the merits of surgical closure of a patent foramen ovale for patients with migraine should await the results of a number of ongoing safety and efficacy trials, he stressed.

Closures are being done with regularity as a treatment for migraines in the United States and Europe despite the lack of safety and efficacy data. “This [procedure] is gathering momentum, to say the least. We have a responsibility to know the data and give patients proper and appropriate advice,” said Dr. Dodick, professor of neurology at Mayo Clinic Arizona. “This is something patients will come into your office wanting to talk about, if they haven't already.”

Physicians are in a tough spot between patient demand and a dearth of data to support patent foramen ovale (PFO) closure for migraine relief, he acknowledged.

Some research indicates an association between a PFO and migraines with aura, particularly in patients with a large left-to-right shunt. In one study, patients with migraine with aura were three times more likely to have a PFO than those who experienced migraines without aura (Neurology 1999;53:2213–4).

The main take-home message for now remains that PFO appears to be more prevalent in patients whose migraines involve aura, Dr. Dodick said.

A left-to-right shunt is also more common among migraine-with-aura patients. In addition, both large atrial shunts and large PFOs are dominantly inherited and might therefore share a genetic origin (Heart 2004;90:1315–20).

One of the large, prospective trials underway is the Migraine Intervention with STARFlex Technology (MIST) study. Patients with migraine with aura will be assessed by a cardiologist and then randomized to closure or no closure.

Although results are not finalized, enrollment data show 60% of 370 participants having a right-to-left shunt (versus 27% of the general population) and 38% having a large PFO (versus 7% of the general population).

Updates and an animation that shows a possible role of PFO in migraine can be viewed on www.migraine-mist.org

PFO closure might effectively treat migraine in a subgroup of patients, Dr. Dodick proposed. A number of studies suggest that closure eliminates migraines in about one-third of migraineurs, reduces frequency in another third, and does not alter attacks in another third of patients.

“Are there factors that will reliably predict which patients will benefit? If these studies are positive, how will we know that a patient in front of us in the future will benefit significantly from this invasive procedure?” he asked.

Many headache specialists are taking a conservative stance. “While many patients have disabling migraines, many people think migraines are not life threatening. They are life altering but not life threatening,” Dr. Dodick. “And the surgery is invasive.”

There is an overall peri-interventional adverse-event rate of about 6% (Catheter Cardiovasc. Interv. 2004;62:512–6).

SCOTTSDALE, ARIZ. – Existing data suggest that a subset of migraine patients may benefit from closure of their patent foramen ovale, Dr. David W. Dodick said during a symposium sponsored by the American Headache Society.

However, any clinical decision of the merits of surgical closure of a patent foramen ovale for patients with migraine should await the results of a number of ongoing safety and efficacy trials, he stressed.

Closures are being done with regularity as a treatment for migraines in the United States and Europe despite the lack of safety and efficacy data. “This [procedure] is gathering momentum, to say the least. We have a responsibility to know the data and give patients proper and appropriate advice,” said Dr. Dodick, professor of neurology at Mayo Clinic Arizona. “This is something patients will come into your office wanting to talk about, if they haven't already.”

Physicians are in a tough spot between patient demand and a dearth of data to support patent foramen ovale (PFO) closure for migraine relief, he acknowledged.

Some research indicates an association between a PFO and migraines with aura, particularly in patients with a large left-to-right shunt. In one study, patients with migraine with aura were three times more likely to have a PFO than those who experienced migraines without aura (Neurology 1999;53:2213–4).

The main take-home message for now remains that PFO appears to be more prevalent in patients whose migraines involve aura, Dr. Dodick said.

A left-to-right shunt is also more common among migraine-with-aura patients. In addition, both large atrial shunts and large PFOs are dominantly inherited and might therefore share a genetic origin (Heart 2004;90:1315–20).

One of the large, prospective trials underway is the Migraine Intervention with STARFlex Technology (MIST) study. Patients with migraine with aura will be assessed by a cardiologist and then randomized to closure or no closure.

Although results are not finalized, enrollment data show 60% of 370 participants having a right-to-left shunt (versus 27% of the general population) and 38% having a large PFO (versus 7% of the general population).

Updates and an animation that shows a possible role of PFO in migraine can be viewed on www.migraine-mist.org

PFO closure might effectively treat migraine in a subgroup of patients, Dr. Dodick proposed. A number of studies suggest that closure eliminates migraines in about one-third of migraineurs, reduces frequency in another third, and does not alter attacks in another third of patients.

“Are there factors that will reliably predict which patients will benefit? If these studies are positive, how will we know that a patient in front of us in the future will benefit significantly from this invasive procedure?” he asked.

Many headache specialists are taking a conservative stance. “While many patients have disabling migraines, many people think migraines are not life threatening. They are life altering but not life threatening,” Dr. Dodick. “And the surgery is invasive.”

There is an overall peri-interventional adverse-event rate of about 6% (Catheter Cardiovasc. Interv. 2004;62:512–6).

MIAMI – Children with comorbid oppositional-defiant and obsessive-compulsive disorders may be more likely to engage in and benefit from cogni-tive-behavioral therapy if the oppositional defiant disorder is treated first, according to preliminary findings from an ongoing study.

Such comorbid children are at increased risk for early, more severe obsessive-compulsive disorder (OCD).

“Children with oppositional defiant behavior tend to develop OCD more rapidly,” Jennifer Adkins, Ph.D., said at the annual conference of the Anxiety Disorders Association of America.

“They engage in rituals more than other children might be able to, and that allows OCD symptoms to get more severe more rapidly,” she noted. “There is a strong importance to this work in children–80% of adults with OCD exhibited the disorder in childhood,” said Dr. Adkins, of the department of psychiatry at the University of Florida, Gainesville.

Dr. Adkins and her associates studied 40 pediatric patients at the University of Florida in Tallahassee. The goal was to determine whether oppositional defiant disorder and/or family accommodation alter cognitive-behavioral therapy (CBT) outcomes immediately after treatment and/or at follow-up.

All participants actively sought treatment for OCD. An independent evaluator performed a preassessment.

Patients had 15 CBT sessions. Those sessions were followed by an assessment immediately after treatment and at 3 months' follow-up.

Clinicians assessed the participants with a diagnostic clinical interview and the Children's Yale-Brown Obsessive-Compulsive Scale.

Parents provided input using the Child Behavior Checklist and the Family Accommodation Scale.

“We don't expect full clinical remission; we expect alleviation of symptoms,” Dr. Adkins said.

The investigators defined a treatment responder as someone who experienced a 70% or more reduction in total score on the obsessive-compulsive scale, “so we set a higher standard for clinical response than most researchers,” Dr. Adkins said.

Mean age was 13 years (range 8–18 years), most patients were white, and annual family income ranged from $30,000 to $350,000.

Twenty-five of the patients were taking concurrent selective serotonin reuptake inhibitors.

The CBT protocol included exposure and response prevention, psychoeducation, and attempted cognitive restructuring. There is active family involvement, “so parents become the treatment after we are done,” Dr. Adkins said.

Age and onset severity were not predictive of treatment outcome. The presence of oppositional defiant disorder, however, significantly predicted poorer outcome immediately after treatment but not at follow-up.

The disorder correctly predicted outcomes in 58% of the patients. There was excellent specificity with no false positives, although “the false negatives brought down” the accuracy, according to Dr. Adkins.

“Treatment may be more effective if oppositional defiant disorder is addressed before starting CBT for OCD, especially if they are extremely oppositional,” Dr. Adkins said.

“Patients must be agreeable to engage in exposure therapy for it to be effective.”

Dr. Adkins and her colleagues also examined the effect of family accommodation on treatment outcomes.

“Interestingly, family accommodation did not predict outcome at this immediate time measurement,” Dr. Adkins said. At the 3-month follow-up, though, family accommodation proved to be 70% predictive.

Parents may be less stringent about adhering to no-accommodation rules following the end of active treatment, she proposed.

“This is an early study. We only have 40 participants so far,” Dr. Adkins said. “More significant predictors of outcome may be identified as we recruit and assess more patients.”

MIAMI – Children with comorbid oppositional-defiant and obsessive-compulsive disorders may be more likely to engage in and benefit from cogni-tive-behavioral therapy if the oppositional defiant disorder is treated first, according to preliminary findings from an ongoing study.

Such comorbid children are at increased risk for early, more severe obsessive-compulsive disorder (OCD).

“Children with oppositional defiant behavior tend to develop OCD more rapidly,” Jennifer Adkins, Ph.D., said at the annual conference of the Anxiety Disorders Association of America.

“They engage in rituals more than other children might be able to, and that allows OCD symptoms to get more severe more rapidly,” she noted. “There is a strong importance to this work in children–80% of adults with OCD exhibited the disorder in childhood,” said Dr. Adkins, of the department of psychiatry at the University of Florida, Gainesville.

Dr. Adkins and her associates studied 40 pediatric patients at the University of Florida in Tallahassee. The goal was to determine whether oppositional defiant disorder and/or family accommodation alter cognitive-behavioral therapy (CBT) outcomes immediately after treatment and/or at follow-up.

All participants actively sought treatment for OCD. An independent evaluator performed a preassessment.

Patients had 15 CBT sessions. Those sessions were followed by an assessment immediately after treatment and at 3 months' follow-up.

Clinicians assessed the participants with a diagnostic clinical interview and the Children's Yale-Brown Obsessive-Compulsive Scale.

Parents provided input using the Child Behavior Checklist and the Family Accommodation Scale.

“We don't expect full clinical remission; we expect alleviation of symptoms,” Dr. Adkins said.

The investigators defined a treatment responder as someone who experienced a 70% or more reduction in total score on the obsessive-compulsive scale, “so we set a higher standard for clinical response than most researchers,” Dr. Adkins said.

Mean age was 13 years (range 8–18 years), most patients were white, and annual family income ranged from $30,000 to $350,000.

Twenty-five of the patients were taking concurrent selective serotonin reuptake inhibitors.

The CBT protocol included exposure and response prevention, psychoeducation, and attempted cognitive restructuring. There is active family involvement, “so parents become the treatment after we are done,” Dr. Adkins said.

Age and onset severity were not predictive of treatment outcome. The presence of oppositional defiant disorder, however, significantly predicted poorer outcome immediately after treatment but not at follow-up.

The disorder correctly predicted outcomes in 58% of the patients. There was excellent specificity with no false positives, although “the false negatives brought down” the accuracy, according to Dr. Adkins.

“Treatment may be more effective if oppositional defiant disorder is addressed before starting CBT for OCD, especially if they are extremely oppositional,” Dr. Adkins said.

“Patients must be agreeable to engage in exposure therapy for it to be effective.”

Dr. Adkins and her colleagues also examined the effect of family accommodation on treatment outcomes.

“Interestingly, family accommodation did not predict outcome at this immediate time measurement,” Dr. Adkins said. At the 3-month follow-up, though, family accommodation proved to be 70% predictive.

Parents may be less stringent about adhering to no-accommodation rules following the end of active treatment, she proposed.

“This is an early study. We only have 40 participants so far,” Dr. Adkins said. “More significant predictors of outcome may be identified as we recruit and assess more patients.”

MIAMI – Children with comorbid oppositional-defiant and obsessive-compulsive disorders may be more likely to engage in and benefit from cogni-tive-behavioral therapy if the oppositional defiant disorder is treated first, according to preliminary findings from an ongoing study.

Such comorbid children are at increased risk for early, more severe obsessive-compulsive disorder (OCD).

“Children with oppositional defiant behavior tend to develop OCD more rapidly,” Jennifer Adkins, Ph.D., said at the annual conference of the Anxiety Disorders Association of America.

“They engage in rituals more than other children might be able to, and that allows OCD symptoms to get more severe more rapidly,” she noted. “There is a strong importance to this work in children–80% of adults with OCD exhibited the disorder in childhood,” said Dr. Adkins, of the department of psychiatry at the University of Florida, Gainesville.

Dr. Adkins and her associates studied 40 pediatric patients at the University of Florida in Tallahassee. The goal was to determine whether oppositional defiant disorder and/or family accommodation alter cognitive-behavioral therapy (CBT) outcomes immediately after treatment and/or at follow-up.

All participants actively sought treatment for OCD. An independent evaluator performed a preassessment.

Patients had 15 CBT sessions. Those sessions were followed by an assessment immediately after treatment and at 3 months' follow-up.

Clinicians assessed the participants with a diagnostic clinical interview and the Children's Yale-Brown Obsessive-Compulsive Scale.

Parents provided input using the Child Behavior Checklist and the Family Accommodation Scale.

“We don't expect full clinical remission; we expect alleviation of symptoms,” Dr. Adkins said.

The investigators defined a treatment responder as someone who experienced a 70% or more reduction in total score on the obsessive-compulsive scale, “so we set a higher standard for clinical response than most researchers,” Dr. Adkins said.

Mean age was 13 years (range 8–18 years), most patients were white, and annual family income ranged from $30,000 to $350,000.

Twenty-five of the patients were taking concurrent selective serotonin reuptake inhibitors.

The CBT protocol included exposure and response prevention, psychoeducation, and attempted cognitive restructuring. There is active family involvement, “so parents become the treatment after we are done,” Dr. Adkins said.

Age and onset severity were not predictive of treatment outcome. The presence of oppositional defiant disorder, however, significantly predicted poorer outcome immediately after treatment but not at follow-up.

The disorder correctly predicted outcomes in 58% of the patients. There was excellent specificity with no false positives, although “the false negatives brought down” the accuracy, according to Dr. Adkins.

“Treatment may be more effective if oppositional defiant disorder is addressed before starting CBT for OCD, especially if they are extremely oppositional,” Dr. Adkins said.

“Patients must be agreeable to engage in exposure therapy for it to be effective.”

Dr. Adkins and her colleagues also examined the effect of family accommodation on treatment outcomes.

“Interestingly, family accommodation did not predict outcome at this immediate time measurement,” Dr. Adkins said. At the 3-month follow-up, though, family accommodation proved to be 70% predictive.

Parents may be less stringent about adhering to no-accommodation rules following the end of active treatment, she proposed.

“This is an early study. We only have 40 participants so far,” Dr. Adkins said. “More significant predictors of outcome may be identified as we recruit and assess more patients.”

MIAMI — A cognitive-behavioral therapy program designed for children aged 4–7 years significantly improves anxiety symptoms over 6 months, according to a randomized, controlled trial.

Many pediatric cognitive-behavioral therapy (CBT) programs are geared toward older children and teenagers. The typical age range is between 8 and 14 years, for example. “But anxiety disorders have an earlier onset than age 8,” Dina R. Hirshfeld-Becker, Ph.D., said in an interview at her poster at the annual conference of the Anxiety Disorders Association of America.

“People thought for a while that CBT was not suitable for younger children. They thought kids did not have enough perception into their cognition and would not be compliant enough with their homework,” said Dr. Hirshfeld-Becker, director of anxiety research in the pediatric psychopharmacology program at Massachusetts General Hospital, Boston.

However, the findings of this study counter that perception. Dr. Hirshfeld-Becker and her associates assessed 65 children. All but one had a DSM-IV anxiety disorder; the other child was at high risk for anxiety. A total of 71% had multiple anxiety diagnoses. More than half of the children had a parent with an anxiety disorder, and 20% had comorbid oppositional defiant disorder. Mean age was 5 years, 54% were female, 80% were white, and 88% came from intact families.

The researchers randomized 35 participants to CBT treatment—up to 20 sessions over 6 months—and an additional 30 to a monitoring-only group as a control. The CBT protocol is called “Being Brave: A Program for Coping With Anxiety,” adapted from the Coping Cat program for children aged 8–13 years developed by Philip C. Kendall, Ph.D., at Temple University in Philadelphia. The first six sessions are a parent-only module, in which parents learn anxiety management and how to coach their children to cope in feared situations. A child-parent module for an additional 8–13 sessions incorporates effective techniques for preschoolers with phobia analogs, in vivo exposure, modeling, and reinforced practice. A final session for parents is designed to maintain gains and continue progress.

“We teach relaxation exercises and coping self-statements like, 'I'm a brave boy,' and that can help,” Dr. Hirshfeld-Becker said. All attempts at success are rewarded, for example, with stickers or extra time with the parent. “We do graded exposure therapy, but we make it fun.”

A total of 58 children completed the study. At 6 months, a blinded clinician rated 70% of the 30 CBT completers as having much or maximal improvement on global ratings of improvement for anxiety compared with 32% of the 28 control group completers. An intent-to-treat analysis yielded similar findings: 60% achievement with CBT, vs. 30% for controls.

“I was happy the improvement rates they showed were comparable to CBT protocols in older kids,” Dr. Hirshfeld-Becker said.

Initially, parents were concerned with the graded exposure, Dr. Hirshfeld-Becker said. “Parents might expect the kid will suffer, but they come to respect their children when they show resiliency.” The protocol helped parents too, she added. “The parents tended to benefit as well as the child.”

MIAMI — A cognitive-behavioral therapy program designed for children aged 4–7 years significantly improves anxiety symptoms over 6 months, according to a randomized, controlled trial.

Many pediatric cognitive-behavioral therapy (CBT) programs are geared toward older children and teenagers. The typical age range is between 8 and 14 years, for example. “But anxiety disorders have an earlier onset than age 8,” Dina R. Hirshfeld-Becker, Ph.D., said in an interview at her poster at the annual conference of the Anxiety Disorders Association of America.

“People thought for a while that CBT was not suitable for younger children. They thought kids did not have enough perception into their cognition and would not be compliant enough with their homework,” said Dr. Hirshfeld-Becker, director of anxiety research in the pediatric psychopharmacology program at Massachusetts General Hospital, Boston.

However, the findings of this study counter that perception. Dr. Hirshfeld-Becker and her associates assessed 65 children. All but one had a DSM-IV anxiety disorder; the other child was at high risk for anxiety. A total of 71% had multiple anxiety diagnoses. More than half of the children had a parent with an anxiety disorder, and 20% had comorbid oppositional defiant disorder. Mean age was 5 years, 54% were female, 80% were white, and 88% came from intact families.

The researchers randomized 35 participants to CBT treatment—up to 20 sessions over 6 months—and an additional 30 to a monitoring-only group as a control. The CBT protocol is called “Being Brave: A Program for Coping With Anxiety,” adapted from the Coping Cat program for children aged 8–13 years developed by Philip C. Kendall, Ph.D., at Temple University in Philadelphia. The first six sessions are a parent-only module, in which parents learn anxiety management and how to coach their children to cope in feared situations. A child-parent module for an additional 8–13 sessions incorporates effective techniques for preschoolers with phobia analogs, in vivo exposure, modeling, and reinforced practice. A final session for parents is designed to maintain gains and continue progress.

“We teach relaxation exercises and coping self-statements like, 'I'm a brave boy,' and that can help,” Dr. Hirshfeld-Becker said. All attempts at success are rewarded, for example, with stickers or extra time with the parent. “We do graded exposure therapy, but we make it fun.”

A total of 58 children completed the study. At 6 months, a blinded clinician rated 70% of the 30 CBT completers as having much or maximal improvement on global ratings of improvement for anxiety compared with 32% of the 28 control group completers. An intent-to-treat analysis yielded similar findings: 60% achievement with CBT, vs. 30% for controls.

“I was happy the improvement rates they showed were comparable to CBT protocols in older kids,” Dr. Hirshfeld-Becker said.

Initially, parents were concerned with the graded exposure, Dr. Hirshfeld-Becker said. “Parents might expect the kid will suffer, but they come to respect their children when they show resiliency.” The protocol helped parents too, she added. “The parents tended to benefit as well as the child.”

MIAMI — A cognitive-behavioral therapy program designed for children aged 4–7 years significantly improves anxiety symptoms over 6 months, according to a randomized, controlled trial.

Many pediatric cognitive-behavioral therapy (CBT) programs are geared toward older children and teenagers. The typical age range is between 8 and 14 years, for example. “But anxiety disorders have an earlier onset than age 8,” Dina R. Hirshfeld-Becker, Ph.D., said in an interview at her poster at the annual conference of the Anxiety Disorders Association of America.

“People thought for a while that CBT was not suitable for younger children. They thought kids did not have enough perception into their cognition and would not be compliant enough with their homework,” said Dr. Hirshfeld-Becker, director of anxiety research in the pediatric psychopharmacology program at Massachusetts General Hospital, Boston.

However, the findings of this study counter that perception. Dr. Hirshfeld-Becker and her associates assessed 65 children. All but one had a DSM-IV anxiety disorder; the other child was at high risk for anxiety. A total of 71% had multiple anxiety diagnoses. More than half of the children had a parent with an anxiety disorder, and 20% had comorbid oppositional defiant disorder. Mean age was 5 years, 54% were female, 80% were white, and 88% came from intact families.

The researchers randomized 35 participants to CBT treatment—up to 20 sessions over 6 months—and an additional 30 to a monitoring-only group as a control. The CBT protocol is called “Being Brave: A Program for Coping With Anxiety,” adapted from the Coping Cat program for children aged 8–13 years developed by Philip C. Kendall, Ph.D., at Temple University in Philadelphia. The first six sessions are a parent-only module, in which parents learn anxiety management and how to coach their children to cope in feared situations. A child-parent module for an additional 8–13 sessions incorporates effective techniques for preschoolers with phobia analogs, in vivo exposure, modeling, and reinforced practice. A final session for parents is designed to maintain gains and continue progress.

“We teach relaxation exercises and coping self-statements like, 'I'm a brave boy,' and that can help,” Dr. Hirshfeld-Becker said. All attempts at success are rewarded, for example, with stickers or extra time with the parent. “We do graded exposure therapy, but we make it fun.”

A total of 58 children completed the study. At 6 months, a blinded clinician rated 70% of the 30 CBT completers as having much or maximal improvement on global ratings of improvement for anxiety compared with 32% of the 28 control group completers. An intent-to-treat analysis yielded similar findings: 60% achievement with CBT, vs. 30% for controls.

“I was happy the improvement rates they showed were comparable to CBT protocols in older kids,” Dr. Hirshfeld-Becker said.

Initially, parents were concerned with the graded exposure, Dr. Hirshfeld-Becker said. “Parents might expect the kid will suffer, but they come to respect their children when they show resiliency.” The protocol helped parents too, she added. “The parents tended to benefit as well as the child.”

SAN JUAN, P.R. — Low heart rate variability is significantly associated with an increased risk of death in depressed versus nondepressed patients after an acute myocardial infarction, Robert M. Carney, Ph.D., said at the annual meeting of the American College of Psychiatrists.

Depression is common among patients with a recent, acute myocardial infarction (MI)—incidence of major depression ranges from 15% to 23% in the literature. Other researchers found that low 24-hour heart rate variability is a strong predictor of cardiac mortality in patients with a recent MI (Ann. Noninvasive Electrocardiol. 2005;10:88–101). Heart rate variability was as robust a predictor as ventricular dysfunction or the size of the infarction in this review article.

The aim of the current study was to determine whether 24-hour heart rate variability is lower in depressed patients, and if so, whether this finding explains why depression reduces cardiovascular mortality after an MI, said Dr. Carney, professor of psychiatry and director of the behavioral medicine center at Washington University, St. Louis.

Researchers assessed 305 depressed patients (135 with major depression and 170 with minor depression) with 24-hour ambulatory ECG readings 1–3 weeks post MI. Another group of 366 nondepressed, post-MI patients was included for comparison.

The investigators measured frequency domain heart rate variability using very-low-frequency (VLF) power spectral analysis. “VLF reflects parasympathetic modulation and is one of the best predictors of post-MI mortality,” Dr. Carney said.

Dr. Carney and his associates found a difference in log of VLF power (LnVLF) measurements: 6.32 in the depressed group, compared with 6.59 in the nondepressed patients.

“This was statistically significant, but is it clinically significant?” Dr. Carney asked.

In the study, 16% of depressed patients and 7% of nondepressed controls had a VLF below 180 squared milliseconds. The estimated probability of survival over 30 months of follow-up was statistically lower among depressed patients.

“So low heart rate variability is a significant and important factor post MI,” Dr. Carney said.

After adjustment for other risk factors, including left ventricular ejection fraction, smoking, older age, and diabetes, the low heart rate variability hazard ratio “goes from 3.1 to 2.8—a tiny difference,” he said.

“About 27% of the mortality risk in these patients can be accounted for by low heart rate variability,” Dr. Carney said. “So there are other things that are important here—including platelet function and inflammation.”

The literature is conflicting about whether treatment of depression provides a beneficial increase in heart rate variability. For example, 10 studies with tricyclic antidepressants yielded mixed results, Dr. Carney said, “and the six SSRI studies are more confusing.”

Three SSRI studies reported increased heart rate variability, and three reported no change. Studies with other antidepressants offer no clear answer, either. No change in heart rate variability was seen in a nefazodone study, while lower heart rate variability was observed in a bupropion study and a venlafaxine trial.

Dr. Carney assessed the effect of psychotherapy among depressed congestive heart disease (CHD) patients. After 12 sessions of cognitive-behavioral therapy, mean heart rate decreased 5 beats/min and root mean squared successive difference increased. There were no changes in other heart rate variability indices. “Whether any treatment can reduce risk in CHD patients is unclear,” he said.

Depression is associated with autonomic nervous system dysfunction, and heart rate variability is a noninvasive method for studying cardiac autonomic nervous system modification, Dr. Carney explained. Heart rate variability reflects the intrinsic firing rate of sinoatrial pacemaker cells, an action that the autonomic nervous system modulates.

SAN JUAN, P.R. — Low heart rate variability is significantly associated with an increased risk of death in depressed versus nondepressed patients after an acute myocardial infarction, Robert M. Carney, Ph.D., said at the annual meeting of the American College of Psychiatrists.

Depression is common among patients with a recent, acute myocardial infarction (MI)—incidence of major depression ranges from 15% to 23% in the literature. Other researchers found that low 24-hour heart rate variability is a strong predictor of cardiac mortality in patients with a recent MI (Ann. Noninvasive Electrocardiol. 2005;10:88–101). Heart rate variability was as robust a predictor as ventricular dysfunction or the size of the infarction in this review article.

The aim of the current study was to determine whether 24-hour heart rate variability is lower in depressed patients, and if so, whether this finding explains why depression reduces cardiovascular mortality after an MI, said Dr. Carney, professor of psychiatry and director of the behavioral medicine center at Washington University, St. Louis.

Researchers assessed 305 depressed patients (135 with major depression and 170 with minor depression) with 24-hour ambulatory ECG readings 1–3 weeks post MI. Another group of 366 nondepressed, post-MI patients was included for comparison.

The investigators measured frequency domain heart rate variability using very-low-frequency (VLF) power spectral analysis. “VLF reflects parasympathetic modulation and is one of the best predictors of post-MI mortality,” Dr. Carney said.

Dr. Carney and his associates found a difference in log of VLF power (LnVLF) measurements: 6.32 in the depressed group, compared with 6.59 in the nondepressed patients.

“This was statistically significant, but is it clinically significant?” Dr. Carney asked.

In the study, 16% of depressed patients and 7% of nondepressed controls had a VLF below 180 squared milliseconds. The estimated probability of survival over 30 months of follow-up was statistically lower among depressed patients.

“So low heart rate variability is a significant and important factor post MI,” Dr. Carney said.

After adjustment for other risk factors, including left ventricular ejection fraction, smoking, older age, and diabetes, the low heart rate variability hazard ratio “goes from 3.1 to 2.8—a tiny difference,” he said.

“About 27% of the mortality risk in these patients can be accounted for by low heart rate variability,” Dr. Carney said. “So there are other things that are important here—including platelet function and inflammation.”

The literature is conflicting about whether treatment of depression provides a beneficial increase in heart rate variability. For example, 10 studies with tricyclic antidepressants yielded mixed results, Dr. Carney said, “and the six SSRI studies are more confusing.”

Three SSRI studies reported increased heart rate variability, and three reported no change. Studies with other antidepressants offer no clear answer, either. No change in heart rate variability was seen in a nefazodone study, while lower heart rate variability was observed in a bupropion study and a venlafaxine trial.

Dr. Carney assessed the effect of psychotherapy among depressed congestive heart disease (CHD) patients. After 12 sessions of cognitive-behavioral therapy, mean heart rate decreased 5 beats/min and root mean squared successive difference increased. There were no changes in other heart rate variability indices. “Whether any treatment can reduce risk in CHD patients is unclear,” he said.

Depression is associated with autonomic nervous system dysfunction, and heart rate variability is a noninvasive method for studying cardiac autonomic nervous system modification, Dr. Carney explained. Heart rate variability reflects the intrinsic firing rate of sinoatrial pacemaker cells, an action that the autonomic nervous system modulates.

SAN JUAN, P.R. — Low heart rate variability is significantly associated with an increased risk of death in depressed versus nondepressed patients after an acute myocardial infarction, Robert M. Carney, Ph.D., said at the annual meeting of the American College of Psychiatrists.

Depression is common among patients with a recent, acute myocardial infarction (MI)—incidence of major depression ranges from 15% to 23% in the literature. Other researchers found that low 24-hour heart rate variability is a strong predictor of cardiac mortality in patients with a recent MI (Ann. Noninvasive Electrocardiol. 2005;10:88–101). Heart rate variability was as robust a predictor as ventricular dysfunction or the size of the infarction in this review article.

The aim of the current study was to determine whether 24-hour heart rate variability is lower in depressed patients, and if so, whether this finding explains why depression reduces cardiovascular mortality after an MI, said Dr. Carney, professor of psychiatry and director of the behavioral medicine center at Washington University, St. Louis.

Researchers assessed 305 depressed patients (135 with major depression and 170 with minor depression) with 24-hour ambulatory ECG readings 1–3 weeks post MI. Another group of 366 nondepressed, post-MI patients was included for comparison.

The investigators measured frequency domain heart rate variability using very-low-frequency (VLF) power spectral analysis. “VLF reflects parasympathetic modulation and is one of the best predictors of post-MI mortality,” Dr. Carney said.

Dr. Carney and his associates found a difference in log of VLF power (LnVLF) measurements: 6.32 in the depressed group, compared with 6.59 in the nondepressed patients.

“This was statistically significant, but is it clinically significant?” Dr. Carney asked.

In the study, 16% of depressed patients and 7% of nondepressed controls had a VLF below 180 squared milliseconds. The estimated probability of survival over 30 months of follow-up was statistically lower among depressed patients.

“So low heart rate variability is a significant and important factor post MI,” Dr. Carney said.

After adjustment for other risk factors, including left ventricular ejection fraction, smoking, older age, and diabetes, the low heart rate variability hazard ratio “goes from 3.1 to 2.8—a tiny difference,” he said.

“About 27% of the mortality risk in these patients can be accounted for by low heart rate variability,” Dr. Carney said. “So there are other things that are important here—including platelet function and inflammation.”

The literature is conflicting about whether treatment of depression provides a beneficial increase in heart rate variability. For example, 10 studies with tricyclic antidepressants yielded mixed results, Dr. Carney said, “and the six SSRI studies are more confusing.”

Three SSRI studies reported increased heart rate variability, and three reported no change. Studies with other antidepressants offer no clear answer, either. No change in heart rate variability was seen in a nefazodone study, while lower heart rate variability was observed in a bupropion study and a venlafaxine trial.

Dr. Carney assessed the effect of psychotherapy among depressed congestive heart disease (CHD) patients. After 12 sessions of cognitive-behavioral therapy, mean heart rate decreased 5 beats/min and root mean squared successive difference increased. There were no changes in other heart rate variability indices. “Whether any treatment can reduce risk in CHD patients is unclear,” he said.

Depression is associated with autonomic nervous system dysfunction, and heart rate variability is a noninvasive method for studying cardiac autonomic nervous system modification, Dr. Carney explained. Heart rate variability reflects the intrinsic firing rate of sinoatrial pacemaker cells, an action that the autonomic nervous system modulates.