Table 1.

Potential mechanisms that may trigger acute coronary syndrome during respiratory tract infection. Adapted from Bazaz et al. [30].

Process	Effect
Systemic host response to infection	Systemic inflammation and intense cytokine release
Local host response to infection	Local vascular inflammation- inflammatory cells infiltrating atherosclerotic plaques;
	Plaque vulnerability- macrophage polarization, differentiation of T-helper lymphocytes, macrophage apoptosis
Thrombosis	Activation of coagulation system and platelets;
	Endothelial dysfunction
Haemodynamic effects	Peripheral vasodilatation especially in sepsis;
	Coronary vasoconstriction due to catecholamine release;
	Altered (increased) myocardial metabolic demand and hypoxaemia which may result in increased myocardial region vulnerable to ischaemia