Heart and Metabolism n° 75 – Editorial

Mario Marzilli, MD, PhD

Correspondence: Professor Mario Marzilli, Professor and Chairman, Cardiovascular Medicine
Division, Pisa University Medical School, Via Paradisa, 2, 56100 Pisa, Italy
E-mail: mario.marzilli@med.unipi.it

Mario Marzilli, MD, PhD
Cardiovascular Medicine Division, Pisa University Medical School, Pisa, Italy

Acute coronary syndromes:
changing face

Since the beginning of this century, an overwhelming body of evidence has prompted a deep revision of our understanding of ischemic heart disease, which was traditionally based on the misconception that myocardial ischemia is closely linked with coronary artery atherosclerotic obstructions. The revision was initially focused on chronic ischemic syndromes or “stable angina” and, with it, the acknowledgment of the multifactorial nature of this condition with a number of possible precipitating mechanisms, including severe stenosis, coronary vasospasm, and microvascular dysfunction. It was also acknowledged that multiple mechanisms might be present at the same time or alternate in time. In addition, the diagnostic and therapeutic implications of this new understanding have yet to be fully implemented in clinical practice.

More recently, the traditional concepts on the pathogenesis of acute ischemic syndrome have also been strongly challenged. The classic model was based on the assumption that acute ischemic syndromes are precipitated by plaque rupture, fissure, or erosion. However, recent reports do not support this concept. In summary, most vulnerable plaques identified in patients with acute ischemic syndrome are located in nonculprit vessels, not all patients with acute ischemic syndrome have vulnerable plaques at coronary angiography, and vulnerable plaques are a common observation, also in stable or asymptomatic patients.

Longitudinal studies with repeat intracoronary imaging have shown that plaques are dynamic structures with rapid changes from a vulnerable pattern to a stable pattern and vice versa, and these changes are not associated with clinical events. The most recent reports on the subject have concluded that, of the more than 82 patients with acute ischemic syndrome analyzed, 31 had no evidence of erosion or rupture at optical coherence tomography, and the latest guidelines from the European Society of Cardiology on non–ST-segment elevation myocardial infarction acute coronary syndrome (NSTEMI-ACS) admit that up to 20% of patients have normal coronary angiography.

This issue of Heart and Metabolism, with its suggestive title, aims to offer the readers some useful hints on being an active participant in this process. Readers will find cases of acute ischemic syndrome in patients with clean coronary arteries, will learn how to interpret the biochemical markers of cardiac damage, will be helped by experts to manage acute ischemic syndromes in patients with no coronary obstruction, will be informed on the role of cardiac energy metabolism as a possible cause of acute ischemic syndrome and, at the same time, a possible therapeutic target, and will also find a critical appraisal of current therapeutic results.

The invited authors have done a spectacular job and I am personally indebted to them for their outstanding contributions. ■