Ischemic MR in STEMI is frequent, even despite effective primary PCI. The regurgitation grade and lower LVEF assessed at hospital discharge and lack of abciximab administration could predict development of LVR at 6 months.
Background: Cardiac resynchronization therapy (CRT) improves outcome in patients with heart failure (HF) however approximately 30% of patients still remain non-responsive. We propose a novel index—Regional Strain Pattern Index (RSPI)—to prospectively evaluate response to CRT. Methods: Echocardiography was performed in 49 patients with HF (66.5 ± 10 years, LVEF 24.9 ± 6.4%, QRS width 173.1 ± 19.1 ms) two times: before CRT implantation and 15 ± 7 months after. At baseline, dyssynchrony was assessed including RSPI and strain pattern. RSPI was calculated from all three apical views across 12 segments as the sum of dyssynchronous components. From every apical view, presence of four components were assessed: (1) contraction of the early-activated wall; (2) prestretching of the late activated wall; (3) contraction of the early-activated wall in the first 70% of the systolic ejection phase; (4) peak contraction of the late-activated wall after aortic valve closure. Each component scored 1 point, thus the maximum was 12 points. Results: Responders reached higher mean RSPI values than non-responders (5.86 ± 2.9 vs. 4.08 ± 2.4; p = 0.044). In logistic regression analysis value of RSPI ≥ 7 points was a predictor of favorable CRT effect (OR: 12; 95% CI = 1.33–108.17; p = 0.004). Conclusions: RSPI could be a valuable predictor of positive outcome in HF patients treated with CRT.
The aim of the study was: (1) to verify the hypothesis that left ventricular global longitudinal strain (LVGLS) may be of additive prognostic value in prediction CRT response and (2) to obtain such a LVGLS value that in the best optimal way enables to characterize potential CRT responders. Forty-nine HF patients (age 66.5 ± 10 years, LVEF 24.9 ± 6.4%, LBBB 71.4%, 57.1% ischemic aetiology of HF) underwent CRT implantation. Transthoracic echocardiography was performed prior to and 15 ± 7 months after CRT implantation. Speckle-tracking echocardiography was performed to assess longitudinal left ventricular function as LVGLS. The response to CRT was defined as a ≥ 15% reduction in the left ventricular end-systolic volume (∆LVESV). Thirty-six (73.5%) patients responded to CRT. There was no linear correlation between baseline LVGLS and ∆LVESV (r = 0.09; p = 0.56). The patients were divided according to the percentile of baseline LVGLS: above 80th percentile; between 80 and 40th percentile; below 40th percentile. Two peripheral groups (above 80th and below 40th percentile) formed “peripheral LVGLS” and the middle group was called “mid-range LVGLS”. The absolute LVGLS cutoff values were − 6.07% (40th percentile) and − 8.67% (80th percentile). For the group of 20 (40.8%) “mid-range LVGLS” patients mean ΔLVESV was 33.3 ± 16.9% while for “peripheral LVGLS” ΔLVESV was 16.2 ± 18.8% (p < 0.001). Among non-ischemic HF etiology, all “mid-range LVGLS” patients (100%) responded positively to CRT (in “peripheral LVGLS”—55% responders; p = 0.015). Baseline LVGLS may have a potential prognostic value in prediction CRT response with relationship of inverted J-shaped pattern. “Mid-range LVGLS” values should help to select CRT responders, especially in non-ischemic HF etiology patients.
Summary
Introduction
ST elevation myocardial infarction (STEMI) is one of the main causes of congestive heart failure (CHF). The main symptom of CHF is exercise tolerance impairment. The aim of the study was to evaluate the prevalence and risk factors for impaired exercise tolerance in patients after STEMI.
Methods and Results
A total of 84 patients with STEMI were analysed in the study. Cardiopulmonary exercise test (CPET) was performed 6 months after STEMI. Impaired exercise tolerance defined as peak VO2 < 84% predicted for age and sex was present in 49 (58%) patients and was connected with lack of abciximab administration (91.4 versus 69%, P = 0·02) and the presence of mitral regurgitation (47 versus 23%, P = 0·02). In univariate analysis, the troponin I level at admission (OR 1·89, P = 0·047), the use of abciximab (OR 0·21, P = 0·03), the presence of mitral regurgitation (OR 2·98, P = 0·03) and NT‐proBNP concentration (OR 2·17, P = 0·021) were related to impaired exercise tolerance. The best multivariate model for predicting impaired exercise tolerance included mitral regurgitation and lack of abciximab administration.
Conclusions
Impaired exercise tolerance after STEMI is common. Mitral regurgitation and lack of abciximab administration are the best predicting factors of impaired exercise tolerance after STEMI.
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