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SNOWMASS, COLO. – By far the most-important contributor to improved outcomes following out-of-hospital cardiac arrest during the past decade has been therapeutic hypothermia, Dr. N.A. Mark Estes III said at the Annual Cardiovascular Conference at Snowmass.
The No. 1 cause of in-hospital death in patients who arrive at the hospital with a perfusable rhythm following resuscitation from out-of-hospital cardiac arrest isn’t sepsis, hepatic or renal failure, or cardiogenic shock. It’s neurologic death caused by anoxic brain injury, which begins several hours after cardiac arrest and continues for about 48 hours. This is where therapeutic hypothermia has made a huge difference, said Dr. Estes, professor of medicine and director of cardiac arrhythmia services at Tufts University, Boston.
“One-half of out-of-hospital cardiac arrest survivors experience secondary anoxic brain damage of varying degrees. Until recently, there was no treatment with documented efficacy in preventing this damage. Despite multiple agents being looked at for neuroprevention, none really has worked. But therapeutic hypothermia has drastically improved outcomes. More than half of patients who arrive at the hospital with a perfusable rhythm and receive therapeutic hypothermia are discharged relatively neurologically intact. That’s a huge difference from what we used to see,” the electrophysiologist observed.
Indeed, the proportion of U.S. patients who experience out-of-hospital cardiac arrest and survive to hospital discharge neurologically intact is “dismal” at about 10%, he noted.
Virtually all specialized cardiac arrest centers now provide therapeutic hypothermia using various protocols. The demonstrated effectiveness of this postresuscitation therapy was an impetus for the American Heart Association policy statement calling for creation of regional cardiac resuscitation systems of care (Circulation. 2010 Feb 9;121[5]:709-29). To date, however, such organized systems exist in only a handful of states or portions of states.
Nonetheless, when an out-of-hospital cardiac arrest patient arrives at a community hospital that can’t provide emergency coronary angiography and therapeutic hypothermia, it’s appropriate to stabilize that patient in the emergency department and then transfer to a hospital that can, according to Dr. Estes.
The mechanism by which therapeutic hypothermia works has been well elucidated. The treatment curbs the process by which ischemia as a second blow triggers formation of oxygen free radicals, glutamate release, calcium shifts, and mitochondrial dysfunction, with resultant destruction of brain tissue.
Roughly 250,000 sudden cardiac deaths (SCDs) occur annually in this country. In addition to more widespread availability of therapeutic hypothermia and other forms of specialized postresuscitation care through creation of regional systems of care for out-of-hospital cardiac arrest, there are other opportunities for improving outcomes. These include earlier activation of the chain of survival that begins with a bystander dialing 911 as well as greater availability of public access defibrillation.
Dr. Estes emphasized that while these measures will further improve outcomes of cardiac arrest, they won’t actually reduce its frequency. By far the greatest opportunity in that realm lies in primordial prevention of coronary artery disease; that is, prevention of the risk factors for CAD. After all, he noted, 80% of all SCDs are associated with underlying ischemic heart disease. In 30% of SCDs, the fatal event is the first manifestation of previously unrecognized CAD. Another one-third of SCDs occur in patients with known CAD, but who weren’t considered at high risk for SCD because of their preserved left ventricular ejection fraction.
“There are a number of luminaries in the field who feel that if we’re really going to make an impact on sudden cardiac death, it’s going to be through primordial prevention of CAD,” the cardiologist said.
For this reason, he was thrilled to hear Dr. Robert A. Vogel elsewhere at the conference describe research by investigators at Affiris AG in Vienna who’ve created a peptide-based vaccine that inhibits PCSK9. Moreover, they showed it to be effective in sharply lowering LDL in mice (PLoS One. 2014 Dec 4;9[12]:e114469).
“I believe that in my lifetime, we will have an antiatherosclerotic vaccine that will lower LDL to an extent where this disease will not disappear but may get to a manageable extent, perhaps a 10% lifetime risk instead of the 55% lifetime risk of MI or stroke that we as Americans currently have,” predicted Dr. Vogel of the University of Colorado, Denver.
Dr. Vogel reported serving as a consultant to the National Football League and the Pritikin Longevity Center as well as acting as the national coordinator for the Sanofi-sponsored ODYSSEY Outcomes trial studying the PCSK9 inhibitor alirocumab (Praluent).
Dr. Estes reported serving as a consultant to Boston Scientific, Medtronic, and St. Jude Medical.
SNOWMASS, COLO. – By far the most-important contributor to improved outcomes following out-of-hospital cardiac arrest during the past decade has been therapeutic hypothermia, Dr. N.A. Mark Estes III said at the Annual Cardiovascular Conference at Snowmass.
The No. 1 cause of in-hospital death in patients who arrive at the hospital with a perfusable rhythm following resuscitation from out-of-hospital cardiac arrest isn’t sepsis, hepatic or renal failure, or cardiogenic shock. It’s neurologic death caused by anoxic brain injury, which begins several hours after cardiac arrest and continues for about 48 hours. This is where therapeutic hypothermia has made a huge difference, said Dr. Estes, professor of medicine and director of cardiac arrhythmia services at Tufts University, Boston.
“One-half of out-of-hospital cardiac arrest survivors experience secondary anoxic brain damage of varying degrees. Until recently, there was no treatment with documented efficacy in preventing this damage. Despite multiple agents being looked at for neuroprevention, none really has worked. But therapeutic hypothermia has drastically improved outcomes. More than half of patients who arrive at the hospital with a perfusable rhythm and receive therapeutic hypothermia are discharged relatively neurologically intact. That’s a huge difference from what we used to see,” the electrophysiologist observed.
Indeed, the proportion of U.S. patients who experience out-of-hospital cardiac arrest and survive to hospital discharge neurologically intact is “dismal” at about 10%, he noted.
Virtually all specialized cardiac arrest centers now provide therapeutic hypothermia using various protocols. The demonstrated effectiveness of this postresuscitation therapy was an impetus for the American Heart Association policy statement calling for creation of regional cardiac resuscitation systems of care (Circulation. 2010 Feb 9;121[5]:709-29). To date, however, such organized systems exist in only a handful of states or portions of states.
Nonetheless, when an out-of-hospital cardiac arrest patient arrives at a community hospital that can’t provide emergency coronary angiography and therapeutic hypothermia, it’s appropriate to stabilize that patient in the emergency department and then transfer to a hospital that can, according to Dr. Estes.
The mechanism by which therapeutic hypothermia works has been well elucidated. The treatment curbs the process by which ischemia as a second blow triggers formation of oxygen free radicals, glutamate release, calcium shifts, and mitochondrial dysfunction, with resultant destruction of brain tissue.
Roughly 250,000 sudden cardiac deaths (SCDs) occur annually in this country. In addition to more widespread availability of therapeutic hypothermia and other forms of specialized postresuscitation care through creation of regional systems of care for out-of-hospital cardiac arrest, there are other opportunities for improving outcomes. These include earlier activation of the chain of survival that begins with a bystander dialing 911 as well as greater availability of public access defibrillation.
Dr. Estes emphasized that while these measures will further improve outcomes of cardiac arrest, they won’t actually reduce its frequency. By far the greatest opportunity in that realm lies in primordial prevention of coronary artery disease; that is, prevention of the risk factors for CAD. After all, he noted, 80% of all SCDs are associated with underlying ischemic heart disease. In 30% of SCDs, the fatal event is the first manifestation of previously unrecognized CAD. Another one-third of SCDs occur in patients with known CAD, but who weren’t considered at high risk for SCD because of their preserved left ventricular ejection fraction.
“There are a number of luminaries in the field who feel that if we’re really going to make an impact on sudden cardiac death, it’s going to be through primordial prevention of CAD,” the cardiologist said.
For this reason, he was thrilled to hear Dr. Robert A. Vogel elsewhere at the conference describe research by investigators at Affiris AG in Vienna who’ve created a peptide-based vaccine that inhibits PCSK9. Moreover, they showed it to be effective in sharply lowering LDL in mice (PLoS One. 2014 Dec 4;9[12]:e114469).
“I believe that in my lifetime, we will have an antiatherosclerotic vaccine that will lower LDL to an extent where this disease will not disappear but may get to a manageable extent, perhaps a 10% lifetime risk instead of the 55% lifetime risk of MI or stroke that we as Americans currently have,” predicted Dr. Vogel of the University of Colorado, Denver.
Dr. Vogel reported serving as a consultant to the National Football League and the Pritikin Longevity Center as well as acting as the national coordinator for the Sanofi-sponsored ODYSSEY Outcomes trial studying the PCSK9 inhibitor alirocumab (Praluent).
Dr. Estes reported serving as a consultant to Boston Scientific, Medtronic, and St. Jude Medical.
SNOWMASS, COLO. – By far the most-important contributor to improved outcomes following out-of-hospital cardiac arrest during the past decade has been therapeutic hypothermia, Dr. N.A. Mark Estes III said at the Annual Cardiovascular Conference at Snowmass.
The No. 1 cause of in-hospital death in patients who arrive at the hospital with a perfusable rhythm following resuscitation from out-of-hospital cardiac arrest isn’t sepsis, hepatic or renal failure, or cardiogenic shock. It’s neurologic death caused by anoxic brain injury, which begins several hours after cardiac arrest and continues for about 48 hours. This is where therapeutic hypothermia has made a huge difference, said Dr. Estes, professor of medicine and director of cardiac arrhythmia services at Tufts University, Boston.
“One-half of out-of-hospital cardiac arrest survivors experience secondary anoxic brain damage of varying degrees. Until recently, there was no treatment with documented efficacy in preventing this damage. Despite multiple agents being looked at for neuroprevention, none really has worked. But therapeutic hypothermia has drastically improved outcomes. More than half of patients who arrive at the hospital with a perfusable rhythm and receive therapeutic hypothermia are discharged relatively neurologically intact. That’s a huge difference from what we used to see,” the electrophysiologist observed.
Indeed, the proportion of U.S. patients who experience out-of-hospital cardiac arrest and survive to hospital discharge neurologically intact is “dismal” at about 10%, he noted.
Virtually all specialized cardiac arrest centers now provide therapeutic hypothermia using various protocols. The demonstrated effectiveness of this postresuscitation therapy was an impetus for the American Heart Association policy statement calling for creation of regional cardiac resuscitation systems of care (Circulation. 2010 Feb 9;121[5]:709-29). To date, however, such organized systems exist in only a handful of states or portions of states.
Nonetheless, when an out-of-hospital cardiac arrest patient arrives at a community hospital that can’t provide emergency coronary angiography and therapeutic hypothermia, it’s appropriate to stabilize that patient in the emergency department and then transfer to a hospital that can, according to Dr. Estes.
The mechanism by which therapeutic hypothermia works has been well elucidated. The treatment curbs the process by which ischemia as a second blow triggers formation of oxygen free radicals, glutamate release, calcium shifts, and mitochondrial dysfunction, with resultant destruction of brain tissue.
Roughly 250,000 sudden cardiac deaths (SCDs) occur annually in this country. In addition to more widespread availability of therapeutic hypothermia and other forms of specialized postresuscitation care through creation of regional systems of care for out-of-hospital cardiac arrest, there are other opportunities for improving outcomes. These include earlier activation of the chain of survival that begins with a bystander dialing 911 as well as greater availability of public access defibrillation.
Dr. Estes emphasized that while these measures will further improve outcomes of cardiac arrest, they won’t actually reduce its frequency. By far the greatest opportunity in that realm lies in primordial prevention of coronary artery disease; that is, prevention of the risk factors for CAD. After all, he noted, 80% of all SCDs are associated with underlying ischemic heart disease. In 30% of SCDs, the fatal event is the first manifestation of previously unrecognized CAD. Another one-third of SCDs occur in patients with known CAD, but who weren’t considered at high risk for SCD because of their preserved left ventricular ejection fraction.
“There are a number of luminaries in the field who feel that if we’re really going to make an impact on sudden cardiac death, it’s going to be through primordial prevention of CAD,” the cardiologist said.
For this reason, he was thrilled to hear Dr. Robert A. Vogel elsewhere at the conference describe research by investigators at Affiris AG in Vienna who’ve created a peptide-based vaccine that inhibits PCSK9. Moreover, they showed it to be effective in sharply lowering LDL in mice (PLoS One. 2014 Dec 4;9[12]:e114469).
“I believe that in my lifetime, we will have an antiatherosclerotic vaccine that will lower LDL to an extent where this disease will not disappear but may get to a manageable extent, perhaps a 10% lifetime risk instead of the 55% lifetime risk of MI or stroke that we as Americans currently have,” predicted Dr. Vogel of the University of Colorado, Denver.
Dr. Vogel reported serving as a consultant to the National Football League and the Pritikin Longevity Center as well as acting as the national coordinator for the Sanofi-sponsored ODYSSEY Outcomes trial studying the PCSK9 inhibitor alirocumab (Praluent).
Dr. Estes reported serving as a consultant to Boston Scientific, Medtronic, and St. Jude Medical.
EXPERT ANALYSIS FROM THE CARDIOVASCULAR CONFERENCE AT SNOWMASS
