Identifying a previous myocardial infarction in patients with hypertensive heart disease: lights and shadows.

E lectrocardiography and echocardiography are widely used in hypertensive patients with the aim of identifying left-ventricular hypertrophy and its serial changes, because such changes have important prognostic implications. Detection of left-ventricular hypertrophy is, however, only one of the many applications of these diagnostic techniques. In this issue of the Journal, Cicala et al address an important related issue (ie, the power of electrocardiography and echocardiography to detect a previous clinically symptomatic myocardial infarction in a cohort of hypertensive patients with left-ventricular hypertrophy). In this analysis of the echocardiographic study of the Losartan Intervention For Endpoint reduction (LIFE) study, the appearance of new Q waves on the surface electrocardiogram had a 29% sensitivity and 95% specificity, whereas the presence of new or worsened wall motion abnormalities on the echocardiogram had a higher sensitivity (68%) with a lower specificity (84%). In contrast, development of repolarization abnormalities did not correlate with the previous occurrence of myocardial infarction. Both methods provided valuable information in this regard, but the contribution of echocardiography appeared to be somewhat greater than that of electrocardiography. The ability of electrocardiography and echocardiography to identify a previous myocardial infarction had been assessed before in a number of studies. However, data of the present study are both novel and clinically relevant under at least two viewpoints. This is the first attempt to quantify the accuracy of the electrocardiogram and echocardiogram in identifying a previous infarction in a cohort of subjects with left-ventricular hypertrophy, which can have a masking effect on both pathologic Q waves and wall motion abnormalities. The lack of a relationship between newly developed repolarization abnormalities and previous myocardial infarction in the specific setting of electrocardiographic left-ventricular hypertrophy is in part an expected finding, as repolarization changes in those patients are often due to ventricular strain rather than to