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Coronary Microcirculation Remodelling in Dilated Cardiomyopathy: Another Brick in the Wall

reserve and, as the patient enters the final phase of the disease, an actual fall in coronary blood flow and perfusion [4–8] . As blood flow to various organs becomes compromised with varying degrees of organ dysfunction (e.g. renal failure, cerebral dysfunction), a reduction in coronary blood flow can lead to further ventricular dysfunction and accelerate end-stage failure. The heart is not spared. At this stage, the autoregulatory mechanisms of the coronary arteries, along with those of other organ systems, are overwhelmed and become nonfunctional and nearly irrelevant [7] . A low grade rise in serum troponin, often occurring at this time, reflects the anguish of the DCM heart at this stage [9–11] . Some of the reduced coronary blood flow can be explained on the basis of hemodynamic derangements that occur during the advanced stage of DCM. Any rise in left intraventricular end-diastolic pressure with or without a concomitant fall in aortic diastolic pressure, both rather common in advanced DCM, reduces the coronary artery perfusion pressure [5] . Any increase in heart rate will reduce the coronary diastolic perfusion time [12, 13] . Both coronary perfusion pressure and coronary perfusion time are compromised in DCM, especially as it enters the advanced stages. Some of the beneficial effects of current therapies act in reversing some of these adverse mechaDespite the advances in pharmacologic therapeutics and device interventions, the clinical outlook and prognosis for idiopathic dilated cardiomyopathy (DCM), although greatly improved, remain poor and fall far short of the life expectancy of the general population even when matched for age, gender, and comorbidites. As DCM proceeds through its natural course, near term, it enters the functional class IV stage and unless the patient is fortunate enough to be a transplant recipient, undergoes placement of a ventricular assist device, or experiences sudden death, the terminal phase of DCM is characterized by marked impairment, suffering, repeated hospitalizations, and finally hospice care. What is the mechanism of this intractable clinical deterioration? Why, after doing so well for years, do these patents appear to hit a ‘brick wall’? There are many considerations including a rise in circulating cytokines (TNF , certain interleukins) [1, 2] , which can lead to further reduction in ventricular function and recruitment of the mechanisms of apoptosis leading to a loss of cardiomyocytes [2] , intractable depression [3] , and others. No doubt, these mechanisms contribute to a variable degree to the end-stage phase of DCM. Our group and others have long proposed that the natural course of DCM involves loss of coronary blood flow Received and accepted: August 31, 2011 Published online: October 6, 2011