The macrophage is exquisitely sensitive to its microenvironment, as demonstrated primarily through in vitro study. Changes in macrophage phenotype and function within the atherosclerotic plaque have profound consequences for plaque biology, including rupture and arterial thrombosis leading to clinical events such as myocardial infarction. We review the evidence for dynamic changes in macrophage numbers and macrophage differentiation within the atherosclerotic plaque microenvironment and discuss potential approaches to target macrophage differentiation for therapeutic benefit in cardiovascular disease.

CMR identified a likely pathogenesis for sudden cardiac arrest in nearly half of survivors in whom coronary artery disease had been excluded. One in 3 subjects had MACE; risk doubled in those with a CMR diagnosis and some CMR parameters-late gadolinium enhancement, left ventricular ejection fraction, and especially right ventricular ejection fraction-associated with prognosis.

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