Ischemic heart disease: clinical and pathological mismatch

Area of Science:

• Cardiology
• Pathology
• Medical Imaging

Background:

• Discrepancies exist between dynamic and postmortem findings in cardiovascular disease.
• Severe coronary artery stenosis and multivessel disease are frequent in non-cardiac patients and accident victims, questioning direct causality with ischemic heart disease.
• Enlarged collaterals may compensate for stenosis, and occlusion may be ineffective if bypassed.

Purpose of the Study:

• To investigate the relationship between coronary artery morphology, inflammation, and ischemic heart disease.
• To explore alternative pathogenic mechanisms beyond ischemia and infarct expansion.
• To evaluate the role of inflammation in coronary atherosclerotic plaques and its potential impact on cardiac function.

Main Methods:

• Comparative analysis of dynamic imaging and postmortem morphological data.
• Examination of coronary atherosclerotic plaques for inflammation (lympho-plasmacellular infiltrate).
• Correlation of plaque inflammation with clinical outcomes including acute infarct, chronic ischemia, sudden coronary death, and healthy controls.

Main Results:

• The degree and number of stenoses do not reliably predict ischemic heart disease outcomes.
• Three distinct types of myocardial damage suggest varied pathogenic mechanisms.
• Lympho-plasmacellular inflammation of coronary atherosclerotic plaques is significantly more prevalent and severe in patients with ischemic heart disease and sudden coronary death compared to controls.
• Inflammation's location near pericoronary nerves suggests a role in spasm and altered cardiac contractility.

Conclusions:

• Ischemic heart disease pathogenesis involves multiple mechanisms, potentially including metabolic disorders and adrenergic imbalance.
• Coronary artery inflammation, particularly around nerves, may cause vasospasm and affect cardiac function, explaining imaging findings like coronary 'cut off' rather than thrombus.
• Postmortem findings highlight inflammation as a critical factor in cardiovascular events, challenging the sole focus on stenosis severity.