PATHOPHYSIOLOGY OF PRECORDIAL ST-SEGMENT DEPRESSION IN INFERIOR WALL ACUTE MYOCARDIAL-INFARCTION - AN ECHOCARDIOGRAPHIC APPRAISAL

Precordial ST-segment depression (PSD) in inferior wall acute myocardi al infarction (IAMI), especially when maximal in leads V4-V6, has been shown to portend a higher rate of heart failure and mortality. To bet ter understand the pathophysiology behind this phenomenon, we evaluate d patients with a first IAMI by echocardiography 48-72 h after the acu te event, using segmental scoring (0 = normal to 3 = dyskinesia) of le ft ventricle wall motion, and a dichotomous assessment of right ventri cle involvement. Patients were categorized into 3 groups: I = no PSD ( n = 14); II = maximal PSD in leads V1-V3 (n = 28); III = maximal PSD i n leads V4-V6 (n = 8). As compared with group I, patients in groups II -III had more severe wall motion abnormalities in inferior segments (1 .36 +/- 0.97 vs. 2.19 +/- 1.74, p = 0.04), and a similar trend for pos terior and lateral segments (1 +/- 1.75 vs. 2 +/- 2.41, p = 0.11), tra nslating into a worse total left ventricle score (2.36 +/- 2.34 vs. 4. 25 +/- 4.05, p < 0.05). Frequency of right ventricle involvement was s imilar in patients with and without PSD (6 (43%) vs. 9 (25%), p = 0.37 ). Segmental scores for groups I, II, and III, respectively, were not different for inferior (1.36 +/- 1,2.25 +/- 1.82 and 2 +/- 1.51, p = 0 .24), posterior and lateral (1 +/- 1.75, 1.96 +/- 2.32 and 2.13 +/- 2. 9, p = 0.38), and septal, anteroseptal and anterior segments (0 +/- 0, 0.04 +/- 0.19 and 0.13 +/- 0.35, p = 0.28). Right ventricle abnormali ties occurred in 43, 21 and 38% of patients in groups I, II and III, r espectively, p = 0.3. Thus, IAMI with PSD is associated with worse lef t ventricle wall motion. However, since patients with maximal PSD in l eads V4-V6 do not have greater wall motion abnormalities or higher rat e of right ventricle involvement, their poorer prognosis cannot be exp lained by worse systolic dysfunction. We propose that maximal PSD in l eads V4-V6 reflects transient diffuse ischemia and altered diastolic d istensibility due to extensive coronary artery disease, causing increa sed left ventricle end-diastolic pressure.