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ACE: angiotensin-converting enzyme

ACEI: angiotensin-converting enzyme inhibitor

ACS: acute coronary syndrome

ALDH2: mitochondrial aldehyde dehydrogenase

ARB: angiotensin receptor blocker

AV: atrioventricular

CABG: coronary artery bypass grafting

CAD: coronary artery disease

COX-1: cyclooxygenase isoform 1

CYP: cytochrome P450

EC50: half-maximal effective concentration

EMA: European Medicines Agency

eNOS: endothelial NOS

FDA: U.S. Food and Drug Administration

FFA: free fatty acid

GI: gastrointestinal

GTN: glyceryl trinitrate (nitroglycerin)

HCM: hypertrophic cardiomyopathy

HCN: hyperpolarization-activated cyclic nucleotide–gated

HMG-CoA: 3-hydroxy-3-methylglutaryl coenzyme A

iNOS: inducible NOS

IP3: inositol 1,4,5-trisphosphate

ISDN: isosorbide dinitrate

ISMN: isosorbide-5-mononitrate

MI: myocardial infarction

nNOS: neuronal NOS

NO: nitric oxide

NOS: nitric oxide synthase

NSTEMI: non–ST-elevation myocardial infarction

PDE: cyclic nucleotide phosphodiesterase

Pgp: P-glycoprotein

PLC: phospholipase C

rTPA: recombinant tissue plasminogen activator

SA: sinoatrial

SNS: sympathetic nervous system

STEMI: ST-segment elevation myocardial infarction

Tn: troponin

TxA2: thromboxane A2




The pathophysiological understanding of ischemic heart disease has seen major changes over the past two decades—from a concept of localized calcification causing progressive constrictions of coronary arteries, ischemia, and exercise-induced angina pectoris to a systemic inflammatory disease of the arteries, including the coronaries (therefore the CAD name). A key finding in this change of paradigm was that most infarct-causing occlusions occur at small-to-medium plaques (“active plaques”) by thrombosis rather than at hemodynamically relevant stenoses by progressive narrowing. Thus, in addition to the mere size of an obstructing plaque, the inflammatory activity of the atherosclerotic process, the stability of the plaque, and platelet reactivity appear to determine the prognosis (Libby et al., 2002).


Atherosclerosis encompasses increased lipid deposition in the subendothelial space (early plaque), endothelial dysfunction with decreased production of NO, less vasodilation and increased risk of platelet adhesion, influx of lipid scavenger cells (mainly macrophages), necrosis, sterile inflammation, proliferation of smooth muscle cells, and calcification and narrowing of the blood vessel by increasing plaque formation. If the endothelium covering of the plaque or the cell layer enclosing the necrotic core of the plaque disrupt, thrombogenic materials such as collagen are presented to the bloodstream, causing platelet adhesion, fibrin deposition, thrombus formation, and closure of the blood vessel.


Triggering factors can be not only acute inflammation (e.g., influenza), but also blood pressure peaks during physical exercise or emotional stress (e.g., demonstrated during a life-threatening emergency and in avid fans during football games). Importantly, the process is dynamic, and the net thrombus formation is the result of the balance between thrombosis and thrombolysis by the fibrinolytic system (plasminogen). The degree and the duration of coronary obstruction and thereby of the ischemia of downstream myocardium (and its size) determine the degree of necrosis of muscle tissue, that is, infarct size.


Taken together, important factors that determine the progress of CAD are the concentration of lipids in the blood, endothelial function, blood pressure (as a mechanical factor predisposing to plaque rupture), the ...

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