The progress of contemporary cardiovascular therapy has led to improved survival in patients with myocardial disease. However, the development of heart failure (HF) represents a common clinical challenge, regardless of the underlying myocardial pathology, due to the severely impaired quality of life and increased mortality comparable with malignant neoplasms. Left ventricular ejection fraction (LVEF) is the main index of systolic function and a key predictor of mortality among HF patients, hence its improvement represents the main indicator of response to instituted therapy. The introduction of complex pharmacotherapy for HF, increased availability of cardiac-implantable electronic devices and advances in the management of secondary causes of HF, including arrhythmia-induced cardiomyopathy, have led to significant increase in the proportion of patients with prominent improvement or even normalization of LVEF, paving the way for the identification of a new subgroup of HF with an improved ejection fraction (HFimpEF). Accumulating data has indicated that these patients share far better long-term prognoses than patients with stable or worsening LVEF. Due to diverse HF aetiology, the prevalence of HFimpEF ranges from roughly 10 to 40%, while the search for reliable predictors and genetic associations corresponding with this clinical presentation is under way. As contemporary guidelines focus mainly on the management of HF patients with clearly defined LVEF, the present review aimed to characterize the definition, epidemiology, predictors, clinical significance and principles of therapy of patients with HFimpEF.

Aortic stenosis (AS) is a progressive valvular heart disease characterized by fibrocalcific remodeling, inflammation, and hemodynamic disturbances. Serum biomarkers may indirectly reflect these processes. Autotaxin (ATX) and lysophosphatidic acid (LPA) have been implicated in osteogenic differentiation of valvular interstitial cells, while growth differentiation factor-15 (GDF-15) reflects cellular stress and vascular changes. Thrombomodulin (TM) indicates endothelial injury and interacts with thrombin. This study aimed to evaluate biomarkers focusing on serum ATX, LPA, GDF-15, and TM levels and flow-mediated dilatation (FMD) in patients with AS. Overall, 149 patients were included in the study: 86 consecutive patients with AS hospitalized due to qualification for invasive treatment of AS and 63 controls. The clinical characteristics, echocardiographic data, FMD, and the following biomarkers—ATX, LPA, GDF-15, and TM—were included in the analysis. AS patients presented increased serum levels of ATX, GDF-15, and TM as compared to the controls. Differences in LPA levels were not statistically significant. FMD values were significantly lower in AS patients. The biomarkers mentioned above and FMD correlated with AS severity. There were no differences in both biomarkers’ serum levels and FMD regarding the hemodynamic AS phenotype. GDF-15 serum level was a risk factor for all-cause mortality and MACCE in the 12-month follow-up.

In patients with acute onset dilated cardiomyopathy (DCM) an improvement of left ventricular ejection fraction (LVEF) can occur as an effect of complex therapy. The aim of the study was to evaluate a pharmacotherapeutic impact on LVEF recovery in newly diagnosed DCM heart failure (HF) patients. A total of 2436 patients hospitalized due to acute decompensated HF were retrospectively analyzed. Finally, 24 patients with newly diagnosed DCM (51.4 ± 16.3 years, New York Heart Association 2.3 ± 0.7, LVEF 25 ± 10%) were observed (13.4 ± 16.0 months) in terms of the result of complex therapy. Patients were divided according to LVEF improvement on follow-up echocardiography: “recovery group” (LVEF improvement > 5%; n = 13) and “nonrecovery group” (∆LVEF ≤ 5%; n = 11). Evaluation of baseline parameters showed lower LVEF (19 ± 6 vs 31 ± 10%; P = .0048) and lower incidence of arterial hypertension (27% vs 73%; P = .043) in “recovery” group. After follow-up period LVEF was similar in both groups; however, significant LVEF improvement was demonstrated only in the “recovery group” (19 ± 6% to 34 ± 8%; P < .001). Only the “recovery group” showed significant HF symptoms reduction (New York Heart Association class: 2.5 ± 0.7 to 1.6 ± 0.6; P = .003). The “recovery group” had prescribed higher doses of loop diuretic (equivalent dose of furosemidum: 80 ± 38 mg vs 43 ± 24 mg; P = .025). Despite optimal therapy, significant LVEF improvement is observed only in the half of the patients with newly diagnosed DCM with HF with reduced EF. Prescription of higher doses of loop diuretics may have positive effect on the reduction of symptoms in newly diagnosed DCM HF patients. Lack of other risk factors such as arterial hypertension may increase the chance of LVEF recovery.