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Evaluation of biventricular involvement in hypotensive patients with transmural inferior infarction by
Hypotension in inferior myocardial infarction (IMI) may be due to extensive involvement of the right ventricle (RV), left ventricle (LV), or both. We verified this hypothesis in 24 patients with IMI and hypotension (systolic blood pressure less than 100 mm Hg), within 48 hours of admission, by means of two-dimensional echocardiography (2DE). We measured the extent of regional RV and LV asynergy (akinesis and/or dyskinesis) in parasternal short-axis sections at mitral, chordal, midpapillary muscle, and low papillary muscle levels. Initial right heart catheterization revealed predominant RV dysfunction in 16 patients (group 1) and predominant LV dysfunction in eight patients (group 2). For all patients, the initial 2DE revealed: (1) biventricular asynergy involving the posterior RV, posterior LV, and posterior interventricular septum; (2) a wide range of values for the extent of asynergy (RV 21% to 90%; LV 19% to 48%); and (3) a direct correlation between peak creatine kinase levels and percentage of LV asynergy (r = 0.80, p less than 0.001) or percentage of RV plus LV asynergy (r = 0.72, p less than 0.001). Although the extent of LV asynergy was similar in the two groups (34% vs 34%, NS), the extent of RV asynergy was greater in group 1 than in group 2 (57% vs 30%, p less than 0.001). More important, the ratio of RV/LV asynergy was greater for group 1 than group 2 (1.75 vs 0.89, p less than 0.001), and this difference in ratios between the two groups was also found in 2DE studies at 10 days and 6 months. A RV/LV asynergy ratio value of 1.1 provided clear separation between the groups. Thus, the RV/LV asynergy ratio on an initial 2DE can clarify the clinical syndrome of hypotension in patients with IMI. An increased asynergy ratio might identify those patients with predominant RV involvement.
Hypotension in inferior myocardial infarction (IMI) may be due to extensive involvement of the right ventricle (RV), left ventricle (LV), or both. We verified this hypothesis in 24 patients with IMI and hypotension (systolic blood pressure less than 100 mm Hg), within 48 hours of admission, by means of two-dimensional echocardiography (2DE). We measured the extent of regional RV and LV asynergy (akinesis and/or dyskinesis) in parasternal short-axis sections at mitral, chordal, midpapillary muscle, and low papillary muscle levels. Initial right heart catheterization revealed predominant RV dysfunction in 16 patients (group 1) and predominant LV dysfunction in eight patients (group 2). For all patients, the initial 2DE revealed: (1) biventricular asynergy involving the posterior RV, posterior LV, and posterior interventricular septum; (2) a wide range of values for the extent of asynergy (RV 21% to 90%; LV 19% to 48%); and (3) a direct correlation between peak creatine kinase levels and percentage of LV asynergy (r = 0.80, p less than 0.001) or percentage of RV plus LV asynergy (r = 0.72, p less than 0.001). Although the extent of LV asynergy was similar in the two groups (34% vs 34%, NS), the extent of RV asynergy was greater in group 1 than in group 2 (57% vs 30%, p less than 0.001). More important, the ratio of RV/LV asynergy was greater for group 1 than group 2 (1.75 vs 0.89, p less than 0.001), and this difference in ratios between the two groups was also found in 2DE studies at 10 days and 6 months. A RV/LV asynergy ratio value of 1.1 provided clear separation between the groups. Thus, the RV/LV asynergy ratio on an initial 2DE can clarify the clinical syndrome of hypotension in patients with IMI. An increased asynergy ratio might identify those patients with predominant RV involvement.