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Cardiac function refers to the physiological performance and efficiency of the heart as a pump, encompassing its ability to deliver oxygenated blood to the systemic circulation and deoxygenated blood to the lungs [1, 3]. It is determined by the integration of myocardial contractility, heart rate, preload, and afterload, which collectively define cardiac output [1, 5]. Impaired cardiac function is the primary hallmark of cardiovascular diseases such as heart failure, where the heart cannot meet the body's metabolic demands [2, 9]. Clinically, it is frequently assessed via parameters like the left ventricular ejection fraction (LVEF) and monitored through biomarkers like B-type natriuretic peptide (BNP) [2, 10]. While improving cardiac function is a central therapeutic goal in medicine, it is considered a physiological phenotype or clinical endpoint rather than a single molecular target [6, 11]. Pharmacological agents such as beta-blockers or ACE inhibitors improve cardiac performance by targeting specific molecular pathways—including adrenergic signaling, calcium handling, or the renin-angiotensin-aldosterone system—rather than binding to a discrete 'cardiac function' molecule [7, 8].
N/A - Cardiac function is a physiological outcome resulting from the integration of multiple molecular pathways, not a specific target molecule. Drugs modulate this function by interacting with specific receptors, enzymes, or ion channels.
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