Patients who have had a myocardial infarction experience faster cognitive decline over time than immediately after the event, new research suggests.

Although cognition in the acute phase after MI was not different than those without an MI in large observational cohorts, cognitive decline became significantly different over a median 6.5 years of follow-up.

The results reinforce the idea that heart health is closely tied to brain health, lead study author Michelle C. Johansen, MD, PhD, assistant professor of neurology cerebrovascular division, Johns Hopkins University, Baltimore, said in an interview. “From a clinical standpoint, heart health affects brain health and there may be effective interventions to prevent heart attack from happening that could reduce the rate of cognitive decline.”

The study was presented during the International Stroke Conference sponsored by the American Heart Association.

Researchers are increasingly recognizing the vascular contribution to cognitive impairment, said Dr. Johansen. This could involve “silent” or subclinical strokes that go unrecognized until seen on imaging.

The study included 31,377 adults free of MI and dementia from six large, well-known cohort studies: the Atherosclerosis Risk in Communities Study, the Coronary Artery Risk Development in Young Adults Study, the Cardiovascular Health Study, the Framingham Offspring Study, the Multi-Ethnic Study of Atherosclerosis, and the Northern Manhattan Study

About 56% of study participants were women, 23% were Black, 8% were Hispanic, and 69% were White.

They were followed from 1971 to 2017 with investigators repeatedly measuring vascular risk factors. The median study follow-up was 6.5 years, but some were followed for up to 20 years. During that time, there were 1,047 incident MIs.

The researchers performed a pooled analysis from these studies “using some fancy statistical techniques,” said Dr. Johansen. “The unique thing about this study was we were able to harmonize the cognitive measures.”

This allowed the researchers to determine if incident MI affected cognitive decline soon after the event and then long-term after the event. The primary outcome was change in global cognition. Additional outcomes were memory and executive function.

The median time between the first MI and the cognitive assessment was about 1.8 years but ranged from about 6 months to 4 years, said Dr. Johansen. Participants were a median age of 60 years at the time of the first cognitive assessment.

The researchers adjusted results for demographic factors, heart disease risk factors, and cognitive test results prior to the MI. Participants who had a stroke during the follow-up period were excluded from the analysis as stroke can affect cognition.

The study showed incident MI was associated with significant decline in global cognition (–0.71; 95% confidence interval, –1.02 to 0.42; P < .0001) and executive function (–0.68; 95% CI, –0.97 to 0.39; P < .004), but not memory, after the MI.

As cognition naturally declines with age, the researchers took that into consideration. “We anticipated cognition over time was going to go down, which it did, but the question we asked was: ‘How did the slope, which we knew was going to decline over time, compare in people who did not have a MI versus those that did?’ ” said Dr. Johansen.

After adjusting the model accordingly, the effect estimates indicating declines in global cognition and executive function were not significant.

However, another model that looked at the effect of incident MI on decline in cognitive function over the years following the event found significant differences.

Compared with participants without MI, those with incident MI had significantly faster declines in global cognition (–0.15 points/year faster, 95% CI, –0.21 to –0.10; P < .002), memory (–0.13 points/year faster, 95% CI, –0.23 to –0.04; P = .004), and executive function (–0.14 points/year faster, 95% CI, –0.20 to –0.08; P < .0001).

Dr. Johansen surmised that MI may result in subclinical infarcts or inflammation, or that MI and cognitive decline have shared vascular risk factors.

She said she can only speculate about why there was not more of a cognitive decline surrounding the MI. “It may be that right after the event, subjects are kind of sick from other things so it’s hard to see exactly what’s going on. Sometimes people can have other problems just from being in the hospital and having a heart attack may make cognition difficult to assess.”

The researchers also looked at those who had a second MI. “We asked whether the decline we saw after the first heart attack among those who had two heart attacks was explained by the fact they had more than one heart attack, and the answer to that question is no,” Dr. Johansen said.

The next research steps for Dr. Johansen and associates are to look at differences in race and sex.

Karen L. Furie, MD, chair, department of neurology, Brown University, and chief of neurology at Rhode Island Hospital, the Miriam Hospital, and the Bradley Hospital, all in Providence, provided a comment on the research.

MI and cognitive decline have a number of common risk factors, including hypertension, diabetes, high cholesterol, smoking, physical inactivity, and poor diet that can lead to obesity, said Dr. Furie.

“It’s critically important to identify these risk factors as early as possible,” she said. “People in early and middle life may not be receiving optimal medical management or engaging in ideal lifestyle choices and these contribute to the development and progression of atherosclerotic disease over the subsequent decades.”

In theory, she said, if these risk factors were eliminated or adequately treated earlier in life, “both the heart and brain could age naturally and in a healthy manner, enabling a higher functioning and better quality of life.”

The study was funded by the National Institute of Neurological Disorders and Stroke and the National Institute of Aging of the National Institutes of Health. Dr. Johansen receives research funding from NINDS.

A version of this article first appeared on Medscape.com.

 Patients who have had a myocardial infarction experience faster cognitive decline over time than immediately after the event, new research suggests.

Although cognition in the acute phase after MI was not different than those without an MI in large observational cohorts, cognitive decline became significantly different over a median 6.5 years of follow-up.

The results reinforce the idea that heart health is closely tied to brain health, lead study author Michelle C. Johansen, MD, PhD, assistant professor of neurology cerebrovascular division, Johns Hopkins University, Baltimore, said in an interview. “From a clinical standpoint, heart health affects brain health and there may be effective interventions to prevent heart attack from happening that could reduce the rate of cognitive decline.”

The study was presented during the International Stroke Conference sponsored by the American Heart Association.

Researchers are increasingly recognizing the vascular contribution to cognitive impairment, said Dr. Johansen. This could involve “silent” or subclinical strokes that go unrecognized until seen on imaging.

The study included 31,377 adults free of MI and dementia from six large, well-known cohort studies: the Atherosclerosis Risk in Communities Study, the Coronary Artery Risk Development in Young Adults Study, the Cardiovascular Health Study, the Framingham Offspring Study, the Multi-Ethnic Study of Atherosclerosis, and the Northern Manhattan Study

About 56% of study participants were women, 23% were Black, 8% were Hispanic, and 69% were White.

They were followed from 1971 to 2017 with investigators repeatedly measuring vascular risk factors. The median study follow-up was 6.5 years, but some were followed for up to 20 years. During that time, there were 1,047 incident MIs.

The researchers performed a pooled analysis from these studies “using some fancy statistical techniques,” said Dr. Johansen. “The unique thing about this study was we were able to harmonize the cognitive measures.”

This allowed the researchers to determine if incident MI affected cognitive decline soon after the event and then long-term after the event. The primary outcome was change in global cognition. Additional outcomes were memory and executive function.

The median time between the first MI and the cognitive assessment was about 1.8 years but ranged from about 6 months to 4 years, said Dr. Johansen. Participants were a median age of 60 years at the time of the first cognitive assessment.

The researchers adjusted results for demographic factors, heart disease risk factors, and cognitive test results prior to the MI. Participants who had a stroke during the follow-up period were excluded from the analysis as stroke can affect cognition.

The study showed incident MI was associated with significant decline in global cognition (–0.71; 95% confidence interval, –1.02 to 0.42; P < .0001) and executive function (–0.68; 95% CI, –0.97 to 0.39; P < .004), but not memory, after the MI.

As cognition naturally declines with age, the researchers took that into consideration. “We anticipated cognition over time was going to go down, which it did, but the question we asked was: ‘How did the slope, which we knew was going to decline over time, compare in people who did not have a MI versus those that did?’ ” said Dr. Johansen.

After adjusting the model accordingly, the effect estimates indicating declines in global cognition and executive function were not significant.

However, another model that looked at the effect of incident MI on decline in cognitive function over the years following the event found significant differences.

Compared with participants without MI, those with incident MI had significantly faster declines in global cognition (–0.15 points/year faster, 95% CI, –0.21 to –0.10; P < .002), memory (–0.13 points/year faster, 95% CI, –0.23 to –0.04; P = .004), and executive function (–0.14 points/year faster, 95% CI, –0.20 to –0.08; P < .0001).

Dr. Johansen surmised that MI may result in subclinical infarcts or inflammation, or that MI and cognitive decline have shared vascular risk factors.

She said she can only speculate about why there was not more of a cognitive decline surrounding the MI. “It may be that right after the event, subjects are kind of sick from other things so it’s hard to see exactly what’s going on. Sometimes people can have other problems just from being in the hospital and having a heart attack may make cognition difficult to assess.”

The researchers also looked at those who had a second MI. “We asked whether the decline we saw after the first heart attack among those who had two heart attacks was explained by the fact they had more than one heart attack, and the answer to that question is no,” Dr. Johansen said.

The next research steps for Dr. Johansen and associates are to look at differences in race and sex.

Karen L. Furie, MD, chair, department of neurology, Brown University, and chief of neurology at Rhode Island Hospital, the Miriam Hospital, and the Bradley Hospital, all in Providence, provided a comment on the research.

MI and cognitive decline have a number of common risk factors, including hypertension, diabetes, high cholesterol, smoking, physical inactivity, and poor diet that can lead to obesity, said Dr. Furie.

“It’s critically important to identify these risk factors as early as possible,” she said. “People in early and middle life may not be receiving optimal medical management or engaging in ideal lifestyle choices and these contribute to the development and progression of atherosclerotic disease over the subsequent decades.”

In theory, she said, if these risk factors were eliminated or adequately treated earlier in life, “both the heart and brain could age naturally and in a healthy manner, enabling a higher functioning and better quality of life.”

The study was funded by the National Institute of Neurological Disorders and Stroke and the National Institute of Aging of the National Institutes of Health. Dr. Johansen receives research funding from NINDS.

A version of this article first appeared on Medscape.com.

 Patients who have had a myocardial infarction experience faster cognitive decline over time than immediately after the event, new research suggests.

Although cognition in the acute phase after MI was not different than those without an MI in large observational cohorts, cognitive decline became significantly different over a median 6.5 years of follow-up.

The results reinforce the idea that heart health is closely tied to brain health, lead study author Michelle C. Johansen, MD, PhD, assistant professor of neurology cerebrovascular division, Johns Hopkins University, Baltimore, said in an interview. “From a clinical standpoint, heart health affects brain health and there may be effective interventions to prevent heart attack from happening that could reduce the rate of cognitive decline.”

The study was presented during the International Stroke Conference sponsored by the American Heart Association.

Researchers are increasingly recognizing the vascular contribution to cognitive impairment, said Dr. Johansen. This could involve “silent” or subclinical strokes that go unrecognized until seen on imaging.

The study included 31,377 adults free of MI and dementia from six large, well-known cohort studies: the Atherosclerosis Risk in Communities Study, the Coronary Artery Risk Development in Young Adults Study, the Cardiovascular Health Study, the Framingham Offspring Study, the Multi-Ethnic Study of Atherosclerosis, and the Northern Manhattan Study

About 56% of study participants were women, 23% were Black, 8% were Hispanic, and 69% were White.

They were followed from 1971 to 2017 with investigators repeatedly measuring vascular risk factors. The median study follow-up was 6.5 years, but some were followed for up to 20 years. During that time, there were 1,047 incident MIs.

The researchers performed a pooled analysis from these studies “using some fancy statistical techniques,” said Dr. Johansen. “The unique thing about this study was we were able to harmonize the cognitive measures.”

This allowed the researchers to determine if incident MI affected cognitive decline soon after the event and then long-term after the event. The primary outcome was change in global cognition. Additional outcomes were memory and executive function.

The median time between the first MI and the cognitive assessment was about 1.8 years but ranged from about 6 months to 4 years, said Dr. Johansen. Participants were a median age of 60 years at the time of the first cognitive assessment.

The researchers adjusted results for demographic factors, heart disease risk factors, and cognitive test results prior to the MI. Participants who had a stroke during the follow-up period were excluded from the analysis as stroke can affect cognition.

The study showed incident MI was associated with significant decline in global cognition (–0.71; 95% confidence interval, –1.02 to 0.42; P < .0001) and executive function (–0.68; 95% CI, –0.97 to 0.39; P < .004), but not memory, after the MI.

As cognition naturally declines with age, the researchers took that into consideration. “We anticipated cognition over time was going to go down, which it did, but the question we asked was: ‘How did the slope, which we knew was going to decline over time, compare in people who did not have a MI versus those that did?’ ” said Dr. Johansen.

After adjusting the model accordingly, the effect estimates indicating declines in global cognition and executive function were not significant.

However, another model that looked at the effect of incident MI on decline in cognitive function over the years following the event found significant differences.

Compared with participants without MI, those with incident MI had significantly faster declines in global cognition (–0.15 points/year faster, 95% CI, –0.21 to –0.10; P < .002), memory (–0.13 points/year faster, 95% CI, –0.23 to –0.04; P = .004), and executive function (–0.14 points/year faster, 95% CI, –0.20 to –0.08; P < .0001).

Dr. Johansen surmised that MI may result in subclinical infarcts or inflammation, or that MI and cognitive decline have shared vascular risk factors.

She said she can only speculate about why there was not more of a cognitive decline surrounding the MI. “It may be that right after the event, subjects are kind of sick from other things so it’s hard to see exactly what’s going on. Sometimes people can have other problems just from being in the hospital and having a heart attack may make cognition difficult to assess.”

The researchers also looked at those who had a second MI. “We asked whether the decline we saw after the first heart attack among those who had two heart attacks was explained by the fact they had more than one heart attack, and the answer to that question is no,” Dr. Johansen said.

The next research steps for Dr. Johansen and associates are to look at differences in race and sex.

Karen L. Furie, MD, chair, department of neurology, Brown University, and chief of neurology at Rhode Island Hospital, the Miriam Hospital, and the Bradley Hospital, all in Providence, provided a comment on the research.

MI and cognitive decline have a number of common risk factors, including hypertension, diabetes, high cholesterol, smoking, physical inactivity, and poor diet that can lead to obesity, said Dr. Furie.

“It’s critically important to identify these risk factors as early as possible,” she said. “People in early and middle life may not be receiving optimal medical management or engaging in ideal lifestyle choices and these contribute to the development and progression of atherosclerotic disease over the subsequent decades.”

In theory, she said, if these risk factors were eliminated or adequately treated earlier in life, “both the heart and brain could age naturally and in a healthy manner, enabling a higher functioning and better quality of life.”

The study was funded by the National Institute of Neurological Disorders and Stroke and the National Institute of Aging of the National Institutes of Health. Dr. Johansen receives research funding from NINDS.

A version of this article first appeared on Medscape.com.

Key clinical point: Patients with multiple sclerosis (pwMS) who participated in a web-based mindfulness-based intervention (MBI) showed significant improvements in depressive symptoms and health-related quality of life (HRQoL).

Major finding: The MBI group showed a significant improvement in depressive symptoms compared with the waitlist (Cohen’s d 0.39; 95% CI, 0.034-0.742), with patients with recurrent depressive symptoms benefitting the most (P = .034). MBI had a positive effect on HRQoL regardless of previous depressive history (P = .009).

Study details: The findings come from a randomized controlled trial involving 132 pwMS with or without a history of recurrent depression, and who received either an internet-delivered MBI (n = 69) or were assigned to a waitlist (n = 63).

Disclosures: This study was supported by the National Health and Medical Research Council and Multiple Sclerosis Research, Australia. The authors declared no conflict of interests.

Source: Sesel AL et al. Mult Scler. 2022 (Feb 7). Doi:  10.1177/13524585211068002.

Key clinical point: Patients with multiple sclerosis (pwMS) who participated in a web-based mindfulness-based intervention (MBI) showed significant improvements in depressive symptoms and health-related quality of life (HRQoL).

Major finding: The MBI group showed a significant improvement in depressive symptoms compared with the waitlist (Cohen’s d 0.39; 95% CI, 0.034-0.742), with patients with recurrent depressive symptoms benefitting the most (P = .034). MBI had a positive effect on HRQoL regardless of previous depressive history (P = .009).

Study details: The findings come from a randomized controlled trial involving 132 pwMS with or without a history of recurrent depression, and who received either an internet-delivered MBI (n = 69) or were assigned to a waitlist (n = 63).

Disclosures: This study was supported by the National Health and Medical Research Council and Multiple Sclerosis Research, Australia. The authors declared no conflict of interests.

Source: Sesel AL et al. Mult Scler. 2022 (Feb 7). Doi:  10.1177/13524585211068002.

Key clinical point: Patients with multiple sclerosis (pwMS) who participated in a web-based mindfulness-based intervention (MBI) showed significant improvements in depressive symptoms and health-related quality of life (HRQoL).

Major finding: The MBI group showed a significant improvement in depressive symptoms compared with the waitlist (Cohen’s d 0.39; 95% CI, 0.034-0.742), with patients with recurrent depressive symptoms benefitting the most (P = .034). MBI had a positive effect on HRQoL regardless of previous depressive history (P = .009).

Study details: The findings come from a randomized controlled trial involving 132 pwMS with or without a history of recurrent depression, and who received either an internet-delivered MBI (n = 69) or were assigned to a waitlist (n = 63).

Disclosures: This study was supported by the National Health and Medical Research Council and Multiple Sclerosis Research, Australia. The authors declared no conflict of interests.

Source: Sesel AL et al. Mult Scler. 2022 (Feb 7). Doi:  10.1177/13524585211068002.

Key clinical point: A significant reduction in absolute lymphocyte counts (ALC) early after the initiation of dimethyl fumarate (DMF) was strongly associated with the development of severe lymphopenia in patients with relapsing multiple sclerosis (MS).

Major finding: A decline in mean ALC of ≥21.2% within the first 3 months of treatment increased the risk for DMF associated-lymphopenia by 6.5-fold (adjusted hazard risk [aHR] 6.503), whereas a decline of ≥40.2% increased the risk for severe lymphopenia by 12.67-fold (aHR 12.67; both P < .001).

Study details: The findings come from a multicenter, noninterventional, prospective real-world study involving 532 patients with relapsing MS who initiated taking DMF.

Disclosures: No funding was received for conducting this study. The authors, including the lead author, declared serving on the advisory board or receiving research/travel grants and speaker/consultancy fees from various sources.

Source: Sainz de la Maza S et al. Mult Scler Relat Disor. 2022;59:103669 (Feb 4). Doi:  10.1016/j.msard.2022.103669.

Key clinical point: A significant reduction in absolute lymphocyte counts (ALC) early after the initiation of dimethyl fumarate (DMF) was strongly associated with the development of severe lymphopenia in patients with relapsing multiple sclerosis (MS).

Major finding: A decline in mean ALC of ≥21.2% within the first 3 months of treatment increased the risk for DMF associated-lymphopenia by 6.5-fold (adjusted hazard risk [aHR] 6.503), whereas a decline of ≥40.2% increased the risk for severe lymphopenia by 12.67-fold (aHR 12.67; both P < .001).

Study details: The findings come from a multicenter, noninterventional, prospective real-world study involving 532 patients with relapsing MS who initiated taking DMF.

Disclosures: No funding was received for conducting this study. The authors, including the lead author, declared serving on the advisory board or receiving research/travel grants and speaker/consultancy fees from various sources.

Source: Sainz de la Maza S et al. Mult Scler Relat Disor. 2022;59:103669 (Feb 4). Doi:  10.1016/j.msard.2022.103669.

Key clinical point: A significant reduction in absolute lymphocyte counts (ALC) early after the initiation of dimethyl fumarate (DMF) was strongly associated with the development of severe lymphopenia in patients with relapsing multiple sclerosis (MS).

Major finding: A decline in mean ALC of ≥21.2% within the first 3 months of treatment increased the risk for DMF associated-lymphopenia by 6.5-fold (adjusted hazard risk [aHR] 6.503), whereas a decline of ≥40.2% increased the risk for severe lymphopenia by 12.67-fold (aHR 12.67; both P < .001).

Study details: The findings come from a multicenter, noninterventional, prospective real-world study involving 532 patients with relapsing MS who initiated taking DMF.

Disclosures: No funding was received for conducting this study. The authors, including the lead author, declared serving on the advisory board or receiving research/travel grants and speaker/consultancy fees from various sources.

Source: Sainz de la Maza S et al. Mult Scler Relat Disor. 2022;59:103669 (Feb 4). Doi:  10.1016/j.msard.2022.103669.

Key clinical point: The time to confirmed disability progression (CDP) and serum neurofilament light chain levels (sNfL) was not significantly different in patients with primary progressive multiple sclerosis (pwPPMS), who received treatment with rituximab or ocrelizumab.

Major finding: After a mean follow-up of 18.3 months, rituximab vs. ocrelizumab groups showed no significant difference in the proportion of patients with CDP (30.6% vs. 23.9%; P = .356). The mean sNfL level was not significantly different between the groups (P = .192).

Study details: The findings come from a multicentric observational study involving 111 pwPPMS who started treatment with ocrelizumab or rituximab.

Disclosures: This study was supported by the Health Institute Carlos III and FEDER funding. Four authors reported receiving travel grants and consulting/speaker fees from various sources.

Source: Alcalá C et al. J Neurol. 2022 (Feb 2). Doi: 10.1007/s00415-022-10989-0

Key clinical point: The time to confirmed disability progression (CDP) and serum neurofilament light chain levels (sNfL) was not significantly different in patients with primary progressive multiple sclerosis (pwPPMS), who received treatment with rituximab or ocrelizumab.

Major finding: After a mean follow-up of 18.3 months, rituximab vs. ocrelizumab groups showed no significant difference in the proportion of patients with CDP (30.6% vs. 23.9%; P = .356). The mean sNfL level was not significantly different between the groups (P = .192).

Study details: The findings come from a multicentric observational study involving 111 pwPPMS who started treatment with ocrelizumab or rituximab.

Disclosures: This study was supported by the Health Institute Carlos III and FEDER funding. Four authors reported receiving travel grants and consulting/speaker fees from various sources.

Source: Alcalá C et al. J Neurol. 2022 (Feb 2). Doi: 10.1007/s00415-022-10989-0

Key clinical point: The time to confirmed disability progression (CDP) and serum neurofilament light chain levels (sNfL) was not significantly different in patients with primary progressive multiple sclerosis (pwPPMS), who received treatment with rituximab or ocrelizumab.

Major finding: After a mean follow-up of 18.3 months, rituximab vs. ocrelizumab groups showed no significant difference in the proportion of patients with CDP (30.6% vs. 23.9%; P = .356). The mean sNfL level was not significantly different between the groups (P = .192).

Study details: The findings come from a multicentric observational study involving 111 pwPPMS who started treatment with ocrelizumab or rituximab.

Disclosures: This study was supported by the Health Institute Carlos III and FEDER funding. Four authors reported receiving travel grants and consulting/speaker fees from various sources.

Source: Alcalá C et al. J Neurol. 2022 (Feb 2). Doi: 10.1007/s00415-022-10989-0

Key clinical point: Changes in serum neurofilament light chain (sNfL) may not be a dynamic biomarker related to confirmed disability progression (CDP) in patients with secondary progressive multiple sclerosis (SPMS) without acute inflammation.

Major finding: At 48 weeks, changes in sNfL were not associated with the risk for CDP in the natalizumab (odds ratio [OR] per 10% increase in sNfL 1.02; 95% CI 0.86-1.21) and placebo (OR per 10% increase in sNfL 0.90; 95% CI 0.64-1.27) groups.

Study details: The findings come from a post hoc analysis of the ASCEND trial involving 317 patients with SPMS without acute inflammation who were randomly assigned to receive either natalizumab (n = 214) or placebo (n = 103).

Disclosures: This study was supported by Biogen. Dr. Zetterberg and Dr. Fox reported receiving personal fees or research contracts from various sources including Biogen. Dr. Belachew reported being an employee and shareholder of Biogen.

Source: Gafson AR et al. JAMA Netw Open. 2022;5(2):e2147588 (Feb 8). Doi:  10.1001/jamanetworkopen.2021.47588

Key clinical point: Changes in serum neurofilament light chain (sNfL) may not be a dynamic biomarker related to confirmed disability progression (CDP) in patients with secondary progressive multiple sclerosis (SPMS) without acute inflammation.

Major finding: At 48 weeks, changes in sNfL were not associated with the risk for CDP in the natalizumab (odds ratio [OR] per 10% increase in sNfL 1.02; 95% CI 0.86-1.21) and placebo (OR per 10% increase in sNfL 0.90; 95% CI 0.64-1.27) groups.

Study details: The findings come from a post hoc analysis of the ASCEND trial involving 317 patients with SPMS without acute inflammation who were randomly assigned to receive either natalizumab (n = 214) or placebo (n = 103).

Disclosures: This study was supported by Biogen. Dr. Zetterberg and Dr. Fox reported receiving personal fees or research contracts from various sources including Biogen. Dr. Belachew reported being an employee and shareholder of Biogen.

Source: Gafson AR et al. JAMA Netw Open. 2022;5(2):e2147588 (Feb 8). Doi:  10.1001/jamanetworkopen.2021.47588

Key clinical point: Changes in serum neurofilament light chain (sNfL) may not be a dynamic biomarker related to confirmed disability progression (CDP) in patients with secondary progressive multiple sclerosis (SPMS) without acute inflammation.

Major finding: At 48 weeks, changes in sNfL were not associated with the risk for CDP in the natalizumab (odds ratio [OR] per 10% increase in sNfL 1.02; 95% CI 0.86-1.21) and placebo (OR per 10% increase in sNfL 0.90; 95% CI 0.64-1.27) groups.

Study details: The findings come from a post hoc analysis of the ASCEND trial involving 317 patients with SPMS without acute inflammation who were randomly assigned to receive either natalizumab (n = 214) or placebo (n = 103).

Disclosures: This study was supported by Biogen. Dr. Zetterberg and Dr. Fox reported receiving personal fees or research contracts from various sources including Biogen. Dr. Belachew reported being an employee and shareholder of Biogen.

Source: Gafson AR et al. JAMA Netw Open. 2022;5(2):e2147588 (Feb 8). Doi:  10.1001/jamanetworkopen.2021.47588

Key clinical point: Both elevated levels of baseline serum neurofilament light chain (sNfL) and increasing levels from a low baseline were associated with multiple sclerosis (MS) relapses, indicating the utility of sNfL in identifying patients who may benefit from early treatment optimization.

Major finding: A 2-fold increase in baseline sNfL was associated with a 1.9-fold increased risk for relapse during follow-up (adjusted hazard ratio [aHR] 1.90; P < .01) and a 2-fold longitudinal increase in sNfL from its first measurement increased the risk for relapse by 1.41-fold (aHR 1.41; P = .04).

Study details: Findings are from an analysis of 58 patients with active MS who were prospectively followed for 1 year as a part of clinical trial.

Disclosures: This study received funding from the MS Society of Canada, Fondazione Italiana Sclerosi Multipla, and Research Manitoba. The authors reported no conflict of interests.

Source: Thebault S et al. Mult Scler Relat Disord. 2022;59:103535 (Jan 18). Doi:  10.1016/j.msard.2022.103535

Key clinical point: Both elevated levels of baseline serum neurofilament light chain (sNfL) and increasing levels from a low baseline were associated with multiple sclerosis (MS) relapses, indicating the utility of sNfL in identifying patients who may benefit from early treatment optimization.

Major finding: A 2-fold increase in baseline sNfL was associated with a 1.9-fold increased risk for relapse during follow-up (adjusted hazard ratio [aHR] 1.90; P < .01) and a 2-fold longitudinal increase in sNfL from its first measurement increased the risk for relapse by 1.41-fold (aHR 1.41; P = .04).

Study details: Findings are from an analysis of 58 patients with active MS who were prospectively followed for 1 year as a part of clinical trial.

Disclosures: This study received funding from the MS Society of Canada, Fondazione Italiana Sclerosi Multipla, and Research Manitoba. The authors reported no conflict of interests.

Source: Thebault S et al. Mult Scler Relat Disord. 2022;59:103535 (Jan 18). Doi:  10.1016/j.msard.2022.103535

Key clinical point: Both elevated levels of baseline serum neurofilament light chain (sNfL) and increasing levels from a low baseline were associated with multiple sclerosis (MS) relapses, indicating the utility of sNfL in identifying patients who may benefit from early treatment optimization.

Major finding: A 2-fold increase in baseline sNfL was associated with a 1.9-fold increased risk for relapse during follow-up (adjusted hazard ratio [aHR] 1.90; P < .01) and a 2-fold longitudinal increase in sNfL from its first measurement increased the risk for relapse by 1.41-fold (aHR 1.41; P = .04).

Study details: Findings are from an analysis of 58 patients with active MS who were prospectively followed for 1 year as a part of clinical trial.

Disclosures: This study received funding from the MS Society of Canada, Fondazione Italiana Sclerosi Multipla, and Research Manitoba. The authors reported no conflict of interests.

Source: Thebault S et al. Mult Scler Relat Disord. 2022;59:103535 (Jan 18). Doi:  10.1016/j.msard.2022.103535

Key clinical point: Patients with multiple sclerosis (MS) who were untreated or received immunomodulatory disease-modifying treatments (IM-DMT) showed excellent seroconversion rates after SARS-CoV-2 vaccination; however, immunosuppressive DMT (IS-DMT) was associated with lower seroconversion rates.

Major finding: For these patients 3 months after vaccine dose seroconversion occurred in 96.7% of untreated, 97.1% of IM-DMT treated, and 61.1% of IS-DMT treated patients vs. 97.4% of healthy control individuals (P < .001), with IS-DMT being the only significant predictor of seroconversion (odds ratio 0.04; P < .001).

Study details: The finding comes from a multicenter, prospective study involving 456 patients with MS who were either untreated (n = 91) or treated with DMT (IM-DMT, n = 139; IS-DMT, n = 226) and 116 healthy control individuals, all of whom were willing to be vaccinated against SARS-CoV-2.

Disclosures: This study was supported by the Austrian Multiple Sclerosis Society and others. Some of the authors declared serving as an advisor or receiving speaker honoraria, scientific grants, travel funding, and consulting from various sources.

Source: Bsteh G et al. Eur J Neurol. 2022 (Feb 1). Doi: 10.1111/ene.15265

Key clinical point: Patients with multiple sclerosis (MS) who were untreated or received immunomodulatory disease-modifying treatments (IM-DMT) showed excellent seroconversion rates after SARS-CoV-2 vaccination; however, immunosuppressive DMT (IS-DMT) was associated with lower seroconversion rates.

Major finding: For these patients 3 months after vaccine dose seroconversion occurred in 96.7% of untreated, 97.1% of IM-DMT treated, and 61.1% of IS-DMT treated patients vs. 97.4% of healthy control individuals (P < .001), with IS-DMT being the only significant predictor of seroconversion (odds ratio 0.04; P < .001).

Study details: The finding comes from a multicenter, prospective study involving 456 patients with MS who were either untreated (n = 91) or treated with DMT (IM-DMT, n = 139; IS-DMT, n = 226) and 116 healthy control individuals, all of whom were willing to be vaccinated against SARS-CoV-2.

Disclosures: This study was supported by the Austrian Multiple Sclerosis Society and others. Some of the authors declared serving as an advisor or receiving speaker honoraria, scientific grants, travel funding, and consulting from various sources.

Source: Bsteh G et al. Eur J Neurol. 2022 (Feb 1). Doi: 10.1111/ene.15265

Key clinical point: Patients with multiple sclerosis (MS) who were untreated or received immunomodulatory disease-modifying treatments (IM-DMT) showed excellent seroconversion rates after SARS-CoV-2 vaccination; however, immunosuppressive DMT (IS-DMT) was associated with lower seroconversion rates.

Major finding: For these patients 3 months after vaccine dose seroconversion occurred in 96.7% of untreated, 97.1% of IM-DMT treated, and 61.1% of IS-DMT treated patients vs. 97.4% of healthy control individuals (P < .001), with IS-DMT being the only significant predictor of seroconversion (odds ratio 0.04; P < .001).

Study details: The finding comes from a multicenter, prospective study involving 456 patients with MS who were either untreated (n = 91) or treated with DMT (IM-DMT, n = 139; IS-DMT, n = 226) and 116 healthy control individuals, all of whom were willing to be vaccinated against SARS-CoV-2.

Disclosures: This study was supported by the Austrian Multiple Sclerosis Society and others. Some of the authors declared serving as an advisor or receiving speaker honoraria, scientific grants, travel funding, and consulting from various sources.

Source: Bsteh G et al. Eur J Neurol. 2022 (Feb 1). Doi: 10.1111/ene.15265

Key clinical point: Spike receptor-binding domain (RBD) immunoglobulin G (IgG) levels following SARS-CoV-2 vaccination were higher in patients with multiple sclerosis (MS) treated with dimethyl fumarate or natalizumab vs. healthy controls; however, the levels were significantly lower in patients receiving sphingosine-1-phosphate receptor modulators (S1P) or anti-CD20 monoclonal antibody (mAb).

Major finding: Postvaccination spike RBD IgG levels were significantly higher in patients treated with dimethyl fumarate (P = .038) and natalizumab (P < .0001) than in healthy controls, whereas patients receiving S1P (P = .01), rituximab (P = .002), or ocrelizumab (P = .0004) showed significantly reduced levels.

Study details: The findings come from a prospective observational study including healthy controls (n =  13) and patients with MS who were either untreated (n = 9) or received treatment with glatiramer acetate (n = 5), dimethyl fumarate (n = 5), natalizumab (n = 6), S1P (n = 7), or anti-CD20 mAbs, including rituximab (n = 13) or ocrelizumab (n = 22).

Disclosures: The study was supported by the National Institutes of Health and others. Some of the authors declared serving on Data Safety Monitoring Boards for or receiving research grant funding and consulting/speaking honoraria from various sources.

Source: Sabatino JJ Jr et al. JCI Insight. 2022 (Jan 14). Doi: 10.1172/jci.insight.156978

Key clinical point: Spike receptor-binding domain (RBD) immunoglobulin G (IgG) levels following SARS-CoV-2 vaccination were higher in patients with multiple sclerosis (MS) treated with dimethyl fumarate or natalizumab vs. healthy controls; however, the levels were significantly lower in patients receiving sphingosine-1-phosphate receptor modulators (S1P) or anti-CD20 monoclonal antibody (mAb).

Major finding: Postvaccination spike RBD IgG levels were significantly higher in patients treated with dimethyl fumarate (P = .038) and natalizumab (P < .0001) than in healthy controls, whereas patients receiving S1P (P = .01), rituximab (P = .002), or ocrelizumab (P = .0004) showed significantly reduced levels.

Study details: The findings come from a prospective observational study including healthy controls (n =  13) and patients with MS who were either untreated (n = 9) or received treatment with glatiramer acetate (n = 5), dimethyl fumarate (n = 5), natalizumab (n = 6), S1P (n = 7), or anti-CD20 mAbs, including rituximab (n = 13) or ocrelizumab (n = 22).

Disclosures: The study was supported by the National Institutes of Health and others. Some of the authors declared serving on Data Safety Monitoring Boards for or receiving research grant funding and consulting/speaking honoraria from various sources.

Source: Sabatino JJ Jr et al. JCI Insight. 2022 (Jan 14). Doi: 10.1172/jci.insight.156978

Key clinical point: Spike receptor-binding domain (RBD) immunoglobulin G (IgG) levels following SARS-CoV-2 vaccination were higher in patients with multiple sclerosis (MS) treated with dimethyl fumarate or natalizumab vs. healthy controls; however, the levels were significantly lower in patients receiving sphingosine-1-phosphate receptor modulators (S1P) or anti-CD20 monoclonal antibody (mAb).

Major finding: Postvaccination spike RBD IgG levels were significantly higher in patients treated with dimethyl fumarate (P = .038) and natalizumab (P < .0001) than in healthy controls, whereas patients receiving S1P (P = .01), rituximab (P = .002), or ocrelizumab (P = .0004) showed significantly reduced levels.

Study details: The findings come from a prospective observational study including healthy controls (n =  13) and patients with MS who were either untreated (n = 9) or received treatment with glatiramer acetate (n = 5), dimethyl fumarate (n = 5), natalizumab (n = 6), S1P (n = 7), or anti-CD20 mAbs, including rituximab (n = 13) or ocrelizumab (n = 22).

Disclosures: The study was supported by the National Institutes of Health and others. Some of the authors declared serving on Data Safety Monitoring Boards for or receiving research grant funding and consulting/speaking honoraria from various sources.

Source: Sabatino JJ Jr et al. JCI Insight. 2022 (Jan 14). Doi: 10.1172/jci.insight.156978

Key clinical point: Disease-modifying treatments (DMT) do not influence the risk for neoplasms in patients with multiple sclerosis (MS), indicating either a low carcinogenic potential of DMTs or neoplasia latencies exceeding the typical trial observation periods.

Major finding: The pooled analysis of trials conducted between 1991 and 2020 showed no increased risk for neoplasm between active-DMT treated vs. placebo arms (incidence rate ratio 1.0797; P = .5711).

Study details: This was a meta-analysis of 42 randomized controlled trials of DMTs published between 1991 and 2020, involving 16,360 active-DMT treated and 10,638 placebo-treated patients with MS.

Disclosures: This study received no external funding. D Papadopoulos, DD Mitsikostas, and R Nicholas reported receiving speaker/consultancy fees and travel grants from various sources.

Source: Papadopoulos D et al. J Neurol. 2022 (Jan 23). Doi: 10.1007/s00415-021-10932-9

Key clinical point: Disease-modifying treatments (DMT) do not influence the risk for neoplasms in patients with multiple sclerosis (MS), indicating either a low carcinogenic potential of DMTs or neoplasia latencies exceeding the typical trial observation periods.

Major finding: The pooled analysis of trials conducted between 1991 and 2020 showed no increased risk for neoplasm between active-DMT treated vs. placebo arms (incidence rate ratio 1.0797; P = .5711).

Study details: This was a meta-analysis of 42 randomized controlled trials of DMTs published between 1991 and 2020, involving 16,360 active-DMT treated and 10,638 placebo-treated patients with MS.

Disclosures: This study received no external funding. D Papadopoulos, DD Mitsikostas, and R Nicholas reported receiving speaker/consultancy fees and travel grants from various sources.

Source: Papadopoulos D et al. J Neurol. 2022 (Jan 23). Doi: 10.1007/s00415-021-10932-9

Key clinical point: Disease-modifying treatments (DMT) do not influence the risk for neoplasms in patients with multiple sclerosis (MS), indicating either a low carcinogenic potential of DMTs or neoplasia latencies exceeding the typical trial observation periods.

Major finding: The pooled analysis of trials conducted between 1991 and 2020 showed no increased risk for neoplasm between active-DMT treated vs. placebo arms (incidence rate ratio 1.0797; P = .5711).

Study details: This was a meta-analysis of 42 randomized controlled trials of DMTs published between 1991 and 2020, involving 16,360 active-DMT treated and 10,638 placebo-treated patients with MS.

Disclosures: This study received no external funding. D Papadopoulos, DD Mitsikostas, and R Nicholas reported receiving speaker/consultancy fees and travel grants from various sources.

Source: Papadopoulos D et al. J Neurol. 2022 (Jan 23). Doi: 10.1007/s00415-021-10932-9

Key clinical point: At 1 year postpartum, clinically meaningful disability from pregnancy-related multiple sclerosis (MS) relapses after natalizumab cessation was retained by over 10% of patients with neither restarting natalizumab shortly after delivery nor solely breastfeeding the infant, providing protection against relapse.

Major finding: Overall, 10.58% of pregnancies accrued significant relapse-related disability at 1 year postpartum. Exclusive breastfeeding (adjusted hazard ratio [aHR] 1.34; 95% CI 0.86-2.10) or restarting natalizumab within 4 weeks postpartum (aHR 1.06; 95% CI 0.48-2.36) was not linked to a lower risk for early postpartum relapses 6 months after delivery.

Study details: The findings come from a prospective cohort study that evaluated 274 successful pregnancies in 255 women with MS from the German MS and Pregnancy Registry. The patients stopped natalizumab before pregnancy or in the first trimester.

Disclosures: The registry was partly supported by the German Federal Joint Committee's Innovation Fund and various pharmaceutical companies. Some authors reported receiving speaker fees, honoraria, research support, and travel grants from or serving on advisory boards for various sources.

Source: Hellwig K et al. JAMA Netw Open. 2022;5(1):e2144750 (Jan 24). Doi:  10.1001/jamanetworkopen.2021.44750

Key clinical point: At 1 year postpartum, clinically meaningful disability from pregnancy-related multiple sclerosis (MS) relapses after natalizumab cessation was retained by over 10% of patients with neither restarting natalizumab shortly after delivery nor solely breastfeeding the infant, providing protection against relapse.

Major finding: Overall, 10.58% of pregnancies accrued significant relapse-related disability at 1 year postpartum. Exclusive breastfeeding (adjusted hazard ratio [aHR] 1.34; 95% CI 0.86-2.10) or restarting natalizumab within 4 weeks postpartum (aHR 1.06; 95% CI 0.48-2.36) was not linked to a lower risk for early postpartum relapses 6 months after delivery.

Study details: The findings come from a prospective cohort study that evaluated 274 successful pregnancies in 255 women with MS from the German MS and Pregnancy Registry. The patients stopped natalizumab before pregnancy or in the first trimester.

Disclosures: The registry was partly supported by the German Federal Joint Committee's Innovation Fund and various pharmaceutical companies. Some authors reported receiving speaker fees, honoraria, research support, and travel grants from or serving on advisory boards for various sources.

Source: Hellwig K et al. JAMA Netw Open. 2022;5(1):e2144750 (Jan 24). Doi:  10.1001/jamanetworkopen.2021.44750

Key clinical point: At 1 year postpartum, clinically meaningful disability from pregnancy-related multiple sclerosis (MS) relapses after natalizumab cessation was retained by over 10% of patients with neither restarting natalizumab shortly after delivery nor solely breastfeeding the infant, providing protection against relapse.

Major finding: Overall, 10.58% of pregnancies accrued significant relapse-related disability at 1 year postpartum. Exclusive breastfeeding (adjusted hazard ratio [aHR] 1.34; 95% CI 0.86-2.10) or restarting natalizumab within 4 weeks postpartum (aHR 1.06; 95% CI 0.48-2.36) was not linked to a lower risk for early postpartum relapses 6 months after delivery.

Study details: The findings come from a prospective cohort study that evaluated 274 successful pregnancies in 255 women with MS from the German MS and Pregnancy Registry. The patients stopped natalizumab before pregnancy or in the first trimester.

Disclosures: The registry was partly supported by the German Federal Joint Committee's Innovation Fund and various pharmaceutical companies. Some authors reported receiving speaker fees, honoraria, research support, and travel grants from or serving on advisory boards for various sources.

Source: Hellwig K et al. JAMA Netw Open. 2022;5(1):e2144750 (Jan 24). Doi:  10.1001/jamanetworkopen.2021.44750