Rest angina is the predominant presentation of unstable angina and shares a pathophysiologic mechanism of plaque disruption with threatened vessel closure following percutaneous coronary angioplasty.
Rest angina predominates in unstable angina; supports plaque disruption mechanisms but leaves open modern risk stratification needs.
Unstable angina is part of the acute coronary syndrome (ACS) spectrum and is adjacent to non-Q-wave myocardial infarction (MI) and slightly more distantly related to Q-wave MI. The diversity of conditions leading to unstable angina, as well as the varying symptoms upon presentation, have made the definition and classification of unstable angina difficult (1). The Global Unstable Angina Registry And Treatment Evaluation (GUARANTEE) study reported that one-third of hospitalized patients had new or accelerated symptoms associated with exertion, whereas two-thirds had rest angina (2). This distinction is important because patients with exertional angina may have a gradual worsening of an underlying atherosclerotic coronary arterial narrowing as opposed to those with rest angina who have an abrupt reduction in myocardial perfusion because of a ruptured plaque (Chapter 1). Angina at rest is often associated with electrocardiographic changes of ischemia and shares a similar underlying pathophysiologic mechanism to threatened vessel closure following percutaneous coronary angioplasty, i.e., plaque disruption. Whether spontaneous or as a result of angioplasty, plaque rupture leads to exposure of the coronary arterial subendothelial components, platelet activation, and thrombus formation.
No takes yet. Share an insight, caveat, or question.
Moliterno et al. (1999) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: