Abstract

We sought to identify prognostic factors of long-term mortality, specific for the underlying etiology of chronic systolic heart failure (CHF). Between 1995 and 2009 baseline characteristics, treatment and follow-up data from 2318 CHF-patients due to ischemic (ICM, 1100 patients) or dilated cardiomyopathy (DCM, 1218 patients) were prospectively compared. To calculate hazard ratios with 95%-confidence intervals cox regression was used. We respectively established etiology-specific multivariable models of independent prognostic factors. During the follow-up period of up to 14.8 years (mean = 53.1 ± 43.5 months, 10, 264 patient-years) 991 deaths (42.8%) occurred. In the ICM-cohort, 5-year-survival was 53.4% (95% CI: 49.9–56.7%), whereas in DCM-patients it was higher (68.1% (95% CI: 65.1–71.0%)). Age, ejection fraction, or hyponatremia were independent predictors for mortality in both cohorts, whereas diabetes, COPD, atrial fibrillation and a heart rate of ≥ 80/min carried independent predictive power only in ICM-patients. This study demonstrates the disparity of prognostic value of clinically derived risk factors between the two main causes of CHF. The effects of covariables in DCM-patients were lower, suggesting a less modifiable disease through risk factors considering mortality risk. An etiology-specific prognostic model may improve accuracy of survival estimations in CHF.

Abstract

Left ventricular (LV) systolic dysfunction is the most frequent initial presentation of patient with LV noncompaction (NC). Our objectives were to evaluate myocardial contraction properties in patients with LVNC and the relationship of non-compacted segments with the degree of global and regional systolic deformation. We included 50 LVNC with an echocardiography and speckle imaging calculation of peak longitudinal strain (PLS). Each of the 16 LV myocardial segments was defined as NC (ratio NC/compacted layer > 2), borderline (NC/C 0–2) and compacted (NC/C = 0). Basal, median and apical strain values were calculated as the average of segmental strain values. For comparison a group of 50 patients with dilated cardiomyopathy (DCM) underwent the same measurements. There was no statistical difference between the 2 groups for any conventional LV systolic parameters. A characteristic deformation pattern was observed in LVNC with higher strain values in the LV apical segments (− 12.8 ± 5.9 vs − 10.7 ± 5.7) and an apical–basal ratio (1.52 ± 0.73 vs 1.12 ± 0.42, p < 0.001). There was no correlation between LV function and the degree of NC. Among 726 segments, compacta thickness was thinner in NC vs C segments (6.4 ± 1.4 vs 7.7 ± 1.8 mm, p < 0.05). There was no difference in WMS but regional strain values were significantly higher in NC compared to C segments (− 13.1 ± 6.1 vs − 10.2 ± 6.3, p < 0.05). Compared to DCM, LVNC presented with relatively preserved apical deformation as compared to basal segments. Lower regional deformation values in compacted segments confirm the concept that LVNC is a phenotypic marker of an underlying diffuse cardiomyopathy involving both C and NC myocardium.