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Viable myocardial cells, primarily cardiomyocytes, are the functional muscle cells of the heart responsible for its contractile force and electrical conduction (StatPearls [1]). These cells are characterized by their ability to maintain metabolic activity, membrane integrity, and contractile function, which distinguishes them from necrotic or fibrotic tissue (NIH [2]). In clinical practice, the assessment of myocardial viability is a critical diagnostic step to determine if patients with chronic ischemic heart disease will benefit from revascularization procedures (American College of Cardiology [3]). While not a single molecular target, these cells contain numerous therapeutic targets such as beta-adrenergic receptors, ion channels, and metabolic enzymes (StatPearls [1]). Preserving the health and function of these cells is the primary goal of many cardiovascular therapies, including those for myocardial infarction and heart failure (AHA/ACC Guidelines [4]). Pharmacological interventions often aim to protect these cells from oxidative stress, apoptosis, and further ischemic damage to maintain overall cardiac performance (PubMed [5]).
Drugs typically act on specific receptors (e.g., beta-adrenergic receptors) or ion channels (e.g., calcium channels) located on or within these cells to modulate contractility, heart rate, or survival (StatPearls [1], AHA/ACC Guidelines [4]).
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