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Coronary Heart Disease Syndromes: Pathophysiology and Clinical Recognition

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Coronary Artery Disease

Part of the book series: Cardiovascular Medicine ((CVM))

Abstract

Atherosclerotic plaque fissuring or ulceration generally causes the development of the acute coronary artery disease syndromes. Vulnerable, or “unstable,” atherosclerotic plaques have temperature and pH heterogeneity, thin fibrous caps, inflammatory cells (primarily macrophages), and activated T cells on their surfaces, as well as an adjacent lipid pool. Some patients have multiple unstable atherosclerotic plaques simultaneously. Several serum markers, when elevated, help identify patients at increased risk for future vascular events. These markers include C-reactive protein, CD40SL, pregnancy-associated protein, serum amyloid protein, brain natriuretic peptide, vascular cell adhesion molecules, intracellular adhesion molecules, and interleukin-6. Unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI) are associated with atherosclerotic plaque fissuring or ulceration; adherence of platelets at the same sites; the accumulation of thromboxane A2, serotonin, adenosine diphosphate, thrombin, tissue factor, and oxygen-derived free radicals; and endothelin, promoting growth of the thrombus and dynamic vasoconstriction with transient coronary artery occlusion (unstable angina or NSTEMI) or sustained coronary artery occlusion (ST-segment elevation MI [STEMI]). The functional absence or diminished effect of nitric oxide, tissue-type plasminogen activator, and prostacyclin at sites of vascular injury contributes to dynamic thrombosis, vasoconstriction, fibroproliferation, and inflammation at sites of coronary artery atherosclerosis and plaque fissuring and ulceration.

Unstable angina, NSTEMI, and STEMI represent a continuum of thrombosis and vasoconstriction, in that unstable angina is often caused by transient and recurrent coronary artery thrombosis and vasoconstriction; NSTEMI by slightly more prolonged (but still usually transient) thrombosis and vasoconstriction or subtotal coronary artery occlusion; and STEMI by prolonged and often permanent coronary artery occlusion. Power-failure complications of MIs occur in patients with ≥40 % irreversible damage to the left ventricle and include cardiogenic shock, medically refractory congestive heart failure, and medically refractory arrhythmias.

Even with relatively small MIs, mechanical problems, such as acute mitral regurgitation, ventricular septal defects, and ventricular aneurysms, may lead to shock and congestive heart failure.

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Authors and Affiliations

  1. Cardiology Division, Texas Heart Institute, Houston, TX, USA

    James T. Willerson MD (President)

  2. Division of Cardiology, Canadian VIGOUR Centre, 2-132 Li Ka Shing Centre for Health Research Innovation, University of Alberta, Edmonton, AB, Canada

    Paul W. Armstrong MD

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  1. Cardiology Division, President, Texas Heart Institute, Houston, Texas, USA

    James T. Willerson

  2. Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota, USA

    David R. Holmes, Jr.

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Willerson, J.T., Armstrong, P.W. (2015). Coronary Heart Disease Syndromes: Pathophysiology and Clinical Recognition. In: Willerson, J., Holmes, Jr., D. (eds) Coronary Artery Disease. Cardiovascular Medicine. Springer, London. https://doi.org/10.1007/978-1-4471-2828-1_15

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