TY - JOUR
T1 - Mechanisms precipitating acute cardiac events
T2 - Review and recommendations of an NHLBI workshop
AU - Muller, James E.
AU - Kaufmann, Peter G.
AU - Luepker, Russell V
AU - Weisfeldt, Myron L.
AU - Deedwania, Prakash C.
AU - Willerson, James T.
PY - 1997/11/4
Y1 - 1997/11/4
N2 - The following specific recommendations were highlighted. Monitoring trends. It is clear that population patterns of cardiovascular diseases are changing. The majority of mortal cardiovascular events occur out of hospital. Better methods are needed to monitor events and classify the cimumstances under which they occur. In addition, population studies that include tracking of the widespread use of medications such as aspirin, B-blockers, and other therapies can provide an estimate of their effects. Retrospective patient studies. It is likely that new factors that may be triggers of acute events will be discovered from systematic retrospective studies of patients. Both short-term (hours) and long-term (days to weeks) influences may be involved. There may be differences between triggers of first and subsequent events. Autopsy studies. Detailed postmortem examinations of coronary pathology provide important data that cannot be obtained otherwise. When linked with detailed behavioral data, it can also lead to better understanding of the relationship between triggers and plaque morphology. Prospective patient studies. A variety of factors that are potential precipitants could he studied either in retrospective cohort studies or nested case-control studies or in prospective studies of survivors of a CHD event. Factors such as acute- phase reactants, autonomic status, sleep apnea, depression, and fatigue are among the many factors whose role requires further investigation. Transient ischemia. The availability of methods to measure transient myocardial ischemia, which is often nor associated with pain, provides a unique opportunity to study precipitating events. Monitoring of patients under various sources of stress, with systematic study of the occurrence of ischemia, has considerable potential. Treatment strategies. As more information accumulates on precipitating factors or triggers, clinical trials may be indicated, particularly among identified high-risk individuals. These trials could include behavioral, pharmacological, or other treatment approaches. End points should include hard events and may include intermediate markers such as transient ischemia. Sex differences. Relatively little is known about specific factors that precipitate events in women, and more population information is needed. Differences may involve the biology of the pathophysiological mechanisms leading to ischemia, such as platelet reactivity, endothelial dysfunction, or autonomic nervous system function. They could also result from different external influences, such as psychophysiological differences in response to stress or anger. Observational studies indicating sex differences in the triggers of ischemia may lead to insight into different mechanisms of disease in men and women. Psychosocial factors. Although the importance of mental stress and negative emotions such as depression and hostility have been described, their specific importance as precipitants of cardiac events requires clarification. Little is known about triggers of sudden cardiac death and even less about triggers of stroke. These are of interest in their own right and may provide additional insights into myocardial infarction and transient ischemic events. The workshop participants support three primary recommendations: First, psychological factors are likely to play a major role in acute disease onset and deserve increased study. Second, efforts should be accelerated to identify vulnerable plaques before they cause disease onset. Plaques that are vulnerable to rupture and cause thrombosis, vasoconstriction, and rapid proliferation represent a major health threat to the population. Current technology identifies stenotic plaques but cannot identify nonstenotic, vulnerable plaques or early signs of endothelial disease. Once vulnerable regions can he identified prospectively, intervention studies can be conducted to determine the feasibility of altering fatal and nonfatal cardiac events by use of systemically or locally delivered therapies. Third, opportunities for interdisciplinary dialogue, such as provided by this workshop, should be encouraged in order to provide the necessary communication between researchers studying the numerous aspects of this new research area. It was the conclusion of workshop participants that pursuit of the above goals and the specific recommendations listed in each section would lead to considerable advances in treatment and prevention of cardiovascular disease.
AB - The following specific recommendations were highlighted. Monitoring trends. It is clear that population patterns of cardiovascular diseases are changing. The majority of mortal cardiovascular events occur out of hospital. Better methods are needed to monitor events and classify the cimumstances under which they occur. In addition, population studies that include tracking of the widespread use of medications such as aspirin, B-blockers, and other therapies can provide an estimate of their effects. Retrospective patient studies. It is likely that new factors that may be triggers of acute events will be discovered from systematic retrospective studies of patients. Both short-term (hours) and long-term (days to weeks) influences may be involved. There may be differences between triggers of first and subsequent events. Autopsy studies. Detailed postmortem examinations of coronary pathology provide important data that cannot be obtained otherwise. When linked with detailed behavioral data, it can also lead to better understanding of the relationship between triggers and plaque morphology. Prospective patient studies. A variety of factors that are potential precipitants could he studied either in retrospective cohort studies or nested case-control studies or in prospective studies of survivors of a CHD event. Factors such as acute- phase reactants, autonomic status, sleep apnea, depression, and fatigue are among the many factors whose role requires further investigation. Transient ischemia. The availability of methods to measure transient myocardial ischemia, which is often nor associated with pain, provides a unique opportunity to study precipitating events. Monitoring of patients under various sources of stress, with systematic study of the occurrence of ischemia, has considerable potential. Treatment strategies. As more information accumulates on precipitating factors or triggers, clinical trials may be indicated, particularly among identified high-risk individuals. These trials could include behavioral, pharmacological, or other treatment approaches. End points should include hard events and may include intermediate markers such as transient ischemia. Sex differences. Relatively little is known about specific factors that precipitate events in women, and more population information is needed. Differences may involve the biology of the pathophysiological mechanisms leading to ischemia, such as platelet reactivity, endothelial dysfunction, or autonomic nervous system function. They could also result from different external influences, such as psychophysiological differences in response to stress or anger. Observational studies indicating sex differences in the triggers of ischemia may lead to insight into different mechanisms of disease in men and women. Psychosocial factors. Although the importance of mental stress and negative emotions such as depression and hostility have been described, their specific importance as precipitants of cardiac events requires clarification. Little is known about triggers of sudden cardiac death and even less about triggers of stroke. These are of interest in their own right and may provide additional insights into myocardial infarction and transient ischemic events. The workshop participants support three primary recommendations: First, psychological factors are likely to play a major role in acute disease onset and deserve increased study. Second, efforts should be accelerated to identify vulnerable plaques before they cause disease onset. Plaques that are vulnerable to rupture and cause thrombosis, vasoconstriction, and rapid proliferation represent a major health threat to the population. Current technology identifies stenotic plaques but cannot identify nonstenotic, vulnerable plaques or early signs of endothelial disease. Once vulnerable regions can he identified prospectively, intervention studies can be conducted to determine the feasibility of altering fatal and nonfatal cardiac events by use of systemically or locally delivered therapies. Third, opportunities for interdisciplinary dialogue, such as provided by this workshop, should be encouraged in order to provide the necessary communication between researchers studying the numerous aspects of this new research area. It was the conclusion of workshop participants that pursuit of the above goals and the specific recommendations listed in each section would lead to considerable advances in treatment and prevention of cardiovascular disease.
KW - Cardiovascular diseases
KW - Coronary disease
KW - Epidemiology
KW - NHLBI
KW - Prevention
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U2 - 10.1161/01.CIR.96.9.3233
DO - 10.1161/01.CIR.96.9.3233
M3 - Review article
C2 - 9386197
AN - SCOPUS:0030717447
SN - 0009-7322
VL - 96
SP - 3233
EP - 3239
JO - Circulation
JF - Circulation
IS - 9
ER -