One patient with a history of hypertension, but not coronary artery disease, myocardial infarction or valvular heart disease, had resolution of cardiomyopathy after ablation, which suggests that the tachycardia was the main mechanism for ventricular dysfunction rather than chronic hypertension. Another patient with hypertension and a history of an inferior wall myocardial infarction also showed resolution of dilated cardiomyopathy, also suggesting tachycardia-induced cardiomyopathy as the main mechanism for ventricular dysfunction. The echocardiogram in this patient showed global hypokinesia before ablation, with an LVEF of 35%; the postablation echocardiogram showed only inferior wall hypokinesia and an LVEF of 50%, supporting the assertion that the inferior wall myocardial infarction was not the main etiology of the LV dysfunction. These observations suggest that tachycardia should be considered a possible underlying cause of dilated cardiomyopathy in those patients with ventricular dysfunction or a ventricular motion pattern, out of proportion to the underlying anatomic substrate. A recent review of tachycardia-induced cardiomyopathy (1) introduced the concept of pure and impure tachycardia-induced cardiomyopathy, the former existing in those cases in which the tachycardia is the sole explanation for the ventricular dysfunction and the latter occurring in cases in which other factors may contribute to the reduction in LVEF. The patients in our series who showed improvement in LV function without achieving normalization and had a diagnosis other than idiopathic dilated cardiomyopathy could be classified as having impure tachycardia-induced cardiomyopathy, and all those with normalized ventricular function could be classified as having pure tachycardia-induced cardiomyopathy, even the patient with a history of hypertension because the latter diagnosis probably had no bearing on the preablation LV dysfunction. The example mentioned previously stresses the need to consider correction of the arrhythmias, even in the presence of seemingly logical causes for cardiomyopathy, because of the possibility of several simultaneous underlying mechanisms of dilated cardiomyopathy.