Triggers of acute coronary syndromes

doi:10.1053/pcad.2002.123470

Progress in Cardiovascular Diseases

Volume 44, Issue 5, March–April 2002, Pages 369-380

https://doi.org/10.1053/pcad.2002.123470 Get rights and content

Abstract

Despite recent progress in prevention of coronary heart disease, approximately 50% of the deaths from coronary artery disease continue to occur out of hospital, and many major cardiac events occur in individuals not previously known to be at risk. These facts create the need to identify the acute causes of myocardial infarction (MI) and sudden death, which has led to a rapid growth in interest over the last 15 years in the field of triggering research. Since initial observations that the incidence of MI onset was time and activity dependent with circadian, circaseptan, and circannual variation, triggering of MI by heavy exertion, sexual activity, anger, mental stress, cocaine and marijuana use, and exposure to air pollution has been demonstrated. Study of the pathophysiological changes produced by these triggers may provide novel therapeutic and preventive targets by a more thorough understanding of vulnerable plaque disruption and coronary thrombosis. Copyright 2002, Elsevier Science (USA). All rights reserved.

Section snippets

General theory for triggering of acute coronary syndromes

It is proposed that the onset of an acute coronary syndrome can result from an interaction between a vulnerable plaque, a trigger, and acute risk factors. (Fig 1) As noted, the coronary plaque suspected to be most vulnerable to rupture is lipid rich and has a thin fibrous cap that is weakest at its junction with the intima,¹⁴ probably caused by increased inflammatory cellular activity with elaboration of metalloproteinases.¹⁵

. Illustration of a hypothetical method by which daily activities and

Circadian variation of MI

The onset of MI has a distinct daily pattern with a peak incidence in the hours after awakening and arising. Serum creatine kinase (CK) measurements obtained from 703 subjects in the Multicenter Investigation of Limitation of Infarct Size study²⁷ were used to demonstrate a marked circadian variation in the incidence of MI, with a threefold increase at 9 AM compared with 11 PM (Fig 2).

. Hourly frequency of onset of MI as determined by the creatine kinase-MB method. The number of infarctions

Cardiovascular triggers

The circadian, circaseptan, and circannual variations in the incidence of onset of MI suggest that the onset of acute cardiac events is not random but rather can be triggered by endogenous rhythms in combination with external activities and exposures. The Myocardial Infarction Onset Study (MIOS) investigators have identified several activities/exposures that serve as triggers of MI onset including heavy physical exertion, anger, mental stress, sexual activity, cocaine use, marijuana use, and

Physical activity

Physical activity has a favorable effect on the lipid profile by lowering total serum cholesterol and triglycerides and raising high-density lipoprotein cholesterol. In addition, physical activity is associated with reduced blood pressure, improved glucose tolerance, increased insulin sensitivity, and reduced blood coagulability.⁷² The higher rate of infarction in the morning hours has raised concerns about the desirability of physical activity during this time period. Murray and colleagues⁷³

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Citation Excerpt :
Specifically, we need to understand and potentially to predict the response of the coagulation system to stimuli occurring with atherosclerotic plaque alterations. Variability in the coagulation system’s performance depends on numerous hormonal, dietary, and environmental influences, hampering our ability to predict its function at a given time, for example, when plaque ruptures (90–92). Thus, we must strive for comprehensive risk assessment that integrates specific information on the atherosclerotic plaque burden and systemic factors that increase the risk for disease activity and vascular thrombosis and is tailored to specific patient populations and individual patients.
The cardiovascular science community has pursued the quest to identify vulnerable atherosclerotic plaque in patients for decades, hoping to prevent acute coronary events. However, despite major advancements in imaging technology that allow visualization of rupture-prone plaques, clinical studies have not demonstrated improved risk prediction compared with traditional approaches. Considering the complex relationship between plaque rupture and acute coronary event risk suggested by pathology studies and confirmed by clinical investigations, these results are not surprising. This review summarizes the evidence supporting a multifaceted hypothesis of the natural history of atherosclerotic plaque rupture. Managing patients at risk of acute coronary events mandates a greater focus on the atherosclerotic disease burden rather than on features of individual plaques.

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^☆: Address reprint requests to James E. Muller, MD, Cardiology Division, Massachusetts General Hospital, Boston, Massachusetts, 02114.

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Triggers of acute coronary syndromes☆

Abstract

Section snippets

General theory for triggering of acute coronary syndromes

Circadian variation of MI

Cardiovascular triggers

Physical activity

Am J Cardiol

J Am Coll Cardiol

Lancet

Am J Cardiol

J Am Coll Cardiol

Am J Cardiol

Lancet

Am Heart J

J Am Coll Cardiol

J Am Coll Cardiol

Am J Cardiol

Lancet

Am J Cardiol

Am J Cardiol

Cardiol Clin

Am J Cardiol

Am J Med

Lancet

Lancet

Am J Cardiol

Am J Cardiol

Coronary plaque disruption

Circulation

Plaque rupture, thrombosis, and therapeutic implications

Haemostasis

Plaque rupture and sudden death related to exertion in men with coronary artery disease

JAMA

Pre-existing coronary stenoses in patients with first myocardial infarction are not necessarily severe

Eur Heart J

Angiographic assessment of the culprit coronary artery lesion before acute myocardial infarction

Am J Cardiol

Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators

N Engl J Med

Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators

Circulation

Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion. Determinants of Myocardial Infarction Onset Study Investigators

JAMA

Triggering of myocardial infarction by cocaine

Circulation

Triggering myocardial infarction by marijuana

Circulation

Increased particulate air pollution and the triggering of myocardial infarction

Circulation

Molecular bases of the acute coronary syndromes

Circulation

Rupture of coronary vasa vasorum as a trigger of acute myocardial infarction

Am J Cardiol

Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels

Circ Res

Endothelin in coronary endothelial dysfunction and early atherosclerosis in humans

Circulation

Infection and atherosclerosis: emerging mechanistic paradigms

Circulation