Background: Cardiac resynchronization therapy (CRT) improves both morbidity and mortality in selected patients with heart failure and increased QRS duration. However, chronic kidney disease (CKD) may have an adverse effect on patient outcome. The aim of this systematic review was to analyze the existing data regarding the impact of baseline renal function on all‐cause mortality in patients who underwent CRT.Methods: Medline database was searched systematically, and studies evaluating the effect of baseline renal function on all‐cause mortality in patients who underwent CRT were retrieved. We performed three separate analyses according to the comparison groups included in each study. Data were analyzed using Review Manager software (RevMan version 5.3; Oxford, UK).Results: We included 16 relevant studies in our analysis. Specifically, 13 studies showed a statistically significant higher risk of all‐cause mortality in patients with impaired baseline renal function who underwent CRT. The remaining three studies did not show a statistically significant result. The quantitative synthesis of five studies showed a 19% decrease in all‐cause mortality per 10‐unit increment in estimated glomerular filtration rate (eGFR) [HR: 0.81, 95% CI (0.73–0.90), p<0.01, 86% I²]. Additionally, we demonstrated that patients with an eGFR<60 mL/min/1.73 m² had an all‐cause mortality rate of 66% [HR: 1.66, 95% CI (1.37–2.02), p<0.01, 0% I²], which was higher than in those with an eGFR≥60 mL/min/1.73 m².Conclusion: Baseline renal dysfunction has an adverse effect on‐all cause mortality in patients who underwent CRT.

Atrial arrhythmias are common in patients with diabetes mellitus (DM), and despite recent advances in pharmaceutical and invasive treatments, atrial fibrillation (AF) and atrial flutter (AFl) are still associated with substantial mortality and morbidity. Clinical trial data imply a protective effect of sodium-glucose cotransporter-2 inhibitors (SGLT2is) on the occurrence of AF and AFl. This review summarizes the state of knowledge regarding DM-mediated mechanisms responsible for AF genesis and recurrence but also discusses the recent data from experimental studies, published trials and metanalyses.

Current data indicate that in the community, approximately 50% of patients with heart failure (HF) have preserved left ventricular (LV) ejection fraction (LVEF)—the so-called HFpEF. Treatment of HFpEF has been considered an unmet need for decades. We believe that the main underlying reasons have been (a) the ever-changing LVEF cut-offs used for HF classification; (b) controversies regarding the definition of the LVEF normal range; (c) the fact that HFpEF does not represent a phenotype, but a category of diseases with entirely different characteristics (hypertensive heart disease, valvular heart disease (VHD), hypertrophic cardiomyopathy (HCM) etc.); (d) the lack of recognition that hypertensive HFpEF is the most common and important HFpEF phenotype; (e) the assumption that neurohormonal overactivity is absent in HF patients with a LVEF > 45–50% which has been proven to be wrong. Current HFpEF trials, in which the vast majority of the participants suffered from hypertension (HTN), whereas VHD and HCM were absent, demonstrated that neurohormonal and sodium-glucose cotransporter 2 (SGLT2) inhibitors are effective in HF patients over a wide LVEF range. Thus, restricting these lifesaving treatments to HF patients with reduced LVEF is not justified anymore and it should be additionally considered for HFpEF patients suffering from HTN.