Despite efforts to restore tissue perfusion after myocardial infarction, coronary no-reflow--a failure to achieve adequate reperfusion of the cardiac microcirculation--is a common complication, which correlates with an increased incidence of death and disability. The treatment of ischaemic stroke is also plagued by no-reflow and, in the brain, a major cause of this phenomenon has been shown to be contractile microvascular pericytes irreversibly constricting capillaries and dying. We propose that cardiac pericytes, which are the second most-common cell type in the heart, impede reperfusion of coronary capillaries in a similar fashion to those in the brain after a stroke. Pericyte constriction might contribute to morbidity in patients by causing microvascular obstruction, even after successful treatment of coronary artery block. The similarity of the no-reflow phenomenon in the brain and in the heart suggests that cardiac pericytes are a novel therapeutic target for coronary no-reflow after myocardial infarction.