Cardiovascular protection denotes the concerted action of endogenous mediators, pharmacological agents, or lifestyle interventions that confer resistance to injury and preserve function across the cardiac and vascular systems ^[1]. Its targets encompass the myocardium, the coronary microcirculation, and the vascular endothelium, with protective effects directed toward limiting infarct size, attenuating ischaemia–reperfusion injury, and preventing the initiation and progression of atherosclerotic disease ^[1][2]. Mechanistically, cardiovascular protection is effected through the activation of intracellular signalling cascades—including sarcolemmal receptor activation, cytosolic kinase signalling, and inhibition of mitochondrial permeability transition pore opening—as well as through antioxidant, anti-inflammatory, and endothelial-modulating pathways that reduce oxidative stress, vascular inflammation, and endothelial dysfunction ^[2][3]. The concept spans primary prevention, which aims to avert the onset of cardiovascular disease by modifying risk factors, secondary prevention, which reduces the recurrence of cardiovascular events, and acute cardioprotection, which seeks to salvage jeopardised myocardium during ischaemic syndromes ^[2][4]. Cardiovascular protection therefore designates the integrated set of mechanisms and interventions—molecular, pharmacological, and behavioural—through which the structural and functional integrity of the heart and vasculature is maintained or restored ^[1].