Relationship between left ventricular longitudinal deformation and clinical heart failure during admission for acute...

Heart failure (HF) complicating acute myocardial infarction (MI) is an ominous prognostic sign frequently caused by left ventricular (LV) systolic dysfunction. However, many patients develop HF despite preserved LV ejection fractions. The aim of this study was to test the hypothesis that LV longitudinal function is a stronger marker of in-hospital HF than traditional echocardiographic indices.

A total of 548 patients with acute MIs were evaluated (mean age, 63.2 ± 11.7 years; 71.6% men). Within 48 hours of admission, comprehensive echocardiography with assessment of global longitudinal strain (GLS) was performed, along with measurements of N-terminal pro-brain natriuretic peptide.

A total 89 patients (16.2%) had in-hospital HF assessed by Killip class > 1 in whom GLS was significantly impaired compared with patients without in-hospital HF (Killip class 1) (-14.6 ± 3.3% vs -10.1 ± 3.5%, P < .0001). In stepwise multiple logistic regression analysis including age, known HF, three-vessel disease, involvement of the left anterior descending coronary artery, episodes of atrial fibrillation, renal function, N-terminal pro-brain natriuretic peptide, troponin T level, LV ejection fraction, wall motion score index, and diastolic dysfunction indices, GLS emerged as the strongest marker of clinical HF (odds ratio, 1.47; 95% confidence interval [CI], 1.33-1.62; P < .0001). GLS remained independently associated with in-hospital HF in patients with LV ejection fractions > 40% (odds ratio, 1.33; 95% CI, 1.14-1.54; P < .05) and improved the C-statistic over other important covariates significantly (0.87 [95% CI, 0.82-0.91] vs 0.82 [95% CI, 0.76-0.89], P = .02).

Global longitudinal function assessed by GLS is significantly impaired in patients with MIs with in-hospital HF, and multivariate analysis suggests that reduced GLS is the single most powerful marker of manifest LV hemodynamic deterioration in the acute phase of MI.