REN and endothelial dysfunction: The latter may be further augmented through localized microvascular effects, endotheliitis,71 associated microthrombi, and altered renin–angiotensin homeostasis.72 Elevated cytokines73,74 [e.g. interleukins (IL)-1, IL-16, IL-17, IL-22, interferon (IFN)-γ, tumour necrosis factor (TNF)-α] could also contribute to myocardial injury by inducing endothelial dysfunction, activation of platelets, recruitment of neutrophils, and eventually triggering a hypercoagulable state.