Hypothesis: is congestive cardiomyopathy caused by a hyperreactive myocardial microcirculation (microvascular spasm)?

In most congested, dilated cardiomyopathies, pathologic analysis reveals focal myocardial necrosis, microscopic scarring, interstitial fibrosis, and myocellular hypertrophy. The focal nature of these processes indicates that the cardiomyopathies may not be due to diffuse abnormalities of cardiac muscle cells, at least in the early stages, but that the changes may represent focal events affecting discrete, small volumes of tissue. Experimental evidence of microvascular hyperreactivity (spasm), both in the hereditary cardiomyopathy of the Syrian hamster and in the acquired cardiomyopathy of the hypertensive-diabetic rat, suggests that transient spasm of the myocardial microcirculation may lead to focal myocellular necrosis and scarring, which then causes the unaffected myocardial cells to undergo compensatory hypertrophy in order to normalize the increased load per unit of myocardium. When enough myocardium is lost and the compensatory hypertrophy results in decreased contractility, congestive heart failure ensues as a systemic response to altered ventricular function. The efficacy of verapamil therapy in the Syrian hamster in preventing microvascular spasm, cell necrosis, and the subsequent development of a cardiomyopathy has provided hope that similar preventive treatment can be applied to patients with early stages of cardiomyopathy.