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ABBREVIATIONS

Abbreviations

ACE: angiotensin-converting enzyme

ACEI: angiotensin-converting enzyme inhibitor

ACS: acute coronary syndrome

ALDH2: mitochondrial aldehyde dehydrogenase

ARB: angiotensin receptor blocker

AV: atrioventricular

CAD: coronary artery disease

COX-1: cyclooxygenase isoform 1

CYP: cytochrome P450

ECG: electrocardiogram

EMA: European Medicines Agency

eNOS: endothelial NOS

FFA: free fatty acid

GI: gastrointestinal

Gp: glycoprotein

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

LDL: low-density lipoprotein

MI: myocardial infarction

NET: neutrophil extracellular trap

nNOS: neuronal NOS

NO: nitric oxide

NOS: nitric oxide synthase

PAD: peripheral arterial disease

PDE: cyclic nucleotide phosphodiesterase

Pgp: P-glycoprotein

PLC: phospholipase C

rTPA: recombinant tissue plasminogen activator

SA: sinoatrial

STEMI: ST-segment elevation myocardial infarction

TxA2: thromboxane A2

ISCHEMIC HEART DISEASE: A SHORT INTRODUCTION

Ischemic heart disease comprises pathologies that lead to myocardial ischemia, a pathological reduction in blood supply and, by extension, oxygenation of myocardial tissue. The main symptom of myocardial ischemia is angina pectoris. This stage of cell injury is, in principle, reversible. Myocardial infarction (MI) refers to the complete stoppage of blood supply and oxygenation, resulting in the onset of irreversible cell injury, also called cell death or necrosis (Oakes, 2021).

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 (thus the name coronary artery disease [CAD]). 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 (concept of the “vulnerable plaque”; Libby et al., 2002).

Atherosclerosis encompasses increased lipid deposition in the subendothelial space (early plaque), endothelial dysfunction with decreased production of nitric oxide (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 the plaque or the cell layer enclosing the necrotic core of the plaque disrupts, thrombogenic materials such as collagen are presented to the bloodstream, causing platelet adhesion, fibrin deposition, thrombus formation, and closure of the blood vessel. It is increasingly recognized that platelets not only play a (mechanical) role in thrombus formation but also are an integral part of the immune response by stimulating neutrophil function (e.g., the formation of neutrophil extracellular traps [NETs]; Döring et al., 2017).

Triggering factors can be not only acute inflammation ...

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