Left ventricular (LV) dysfunction after acute myocardial infarction (AMI) is associated with an increased risk of heart failure (HF) development. Diverse microRNAs (miRNAs) have been shown to appear in the bloodstream following various cardiovascular events. The aim of this study was to identify prognostic miRNAs associated with LV dysfunction following AMI. Patients were divided into subgroups comprising patients who developed or not LV dysfunction within six months of the infarction. miRNA profiles were determined in plasma and serum samples of the patients on the first day of AMI. Levels of 14 plasma miRNAs and 16 serum miRNAs were significantly different in samples from AMI patients who later developed LV dysfunction compared to those who did not. Two miRNAs were up-regulated in both types of material. Validation in an independent group of patients, using droplet digital PCR (ddPCR) confirmed that miR-30a-5p was significantly elevated on admission in those patients who developed LV dysfunction and HF symptoms six months after AMI. A bioinformatics analysis indicated that miR-30a-5p may regulate genes involved in cardiovascular pathogenesis. This study demonstrates, for the first time, a prognostic value of circulating miR-30a-5p and its association with LV dysfunction and symptoms of HF after AMI.

In hypertrophic cardiomyopathy (HCM), the following five risk factors have a major role in the primary prevention of sudden death (SD): family history of SD (FHSD), syncope, massive wall thickness (MWTh) >30 mm, non-sustained ventricular tachycardia (nsVT) in Holter monitoring of electrocardiography, and abnormal blood pressure response to exercise (aBPRE). In HCM, as a genetic cardiac disease, the risk for SD may also exist from birth. The aim of the study was to compare the survival curves constructed for each of the five risk factors in a traditional follow-up model (started at the first presentation of a patient at the institution) and in a novel follow-up model (started at the date of birth). In an additional analysis, we compared the survival rate in three subgroups (without FHSD, with one SD, and with two or more SDs in a family). A total of 1306 consecutive HCM patients (705 males, 601 females, mean age of 47 years, and 193 patients were <18 years) evaluated at 15 referral centres in Poland were enrolled in the study. In a novel method of follow-up, all the five risk factors confirmed its prognostic power (FHSD: P = 0.0007; nsVT: P < 0.0001; aBPRE: P = 0.0081; syncope: P < 0.0001; MWTh P> 0.0001), whereas in a traditional method, only four factors predicted SD (except aBPRE). In a novel model of follow-up, FHSD in a single episode starts to influence the prognosis with a delay to the fifth decade of life (P = 0.0007). Multiple FHSD appears to be a very powerful risk factor (P < 0.0001), predicting frequent SDs in childhood and adolescence. The proposed concept of a lifelong calculated follow-up is a useful strategy in the risk stratification of SD. Multiple FHSD is a very ominous risk factor with strong impact, predicting frequent SD episodes in the early period of life.

Personalized management involving heart failure (HF) etiology is crucial for better prognoses for HF patients. This study aimed to compare patients with ischemic cardiomyopathy (ICM) and patients with non-ischemic dilated cardiomyopathy (NIDCM) in terms of baseline characteristics and prognosis. We assessed 895 patients with HF with reduced left ventricular ejection fraction participating in the Polish part of the European Society of Cardiology (ESC)-HF registries. ICM was present in 583 patients (65%), NIDCM in 312 patients (35%). The ICM patients were older (p < 0.001) and had more comorbidities. The NIDCM patients more frequently had atrial fibrillation (p = 0.04) and lower LVEF (p = 0.01); therefore, they were treated more often with anticoagulants (p = 0.01) and digitalis (p < 0.001). The NIDCM patients were prescribed aldosterone antagonists more often (p = 0.01). There were no other differences as regards the use of HF guideline-recommended medications, implantable cardioverter defibrillators or cardiac resynchronization therapy. The ICM patients were more likely to be treated with statins (p < 0.001) and antiplatelet agents (p < 0.001). All-cause death, as well as all-cause death and readmissions for HF at 12 months, occurred more often in the ICM group compared with the NIDCM group (15.9% vs. 10%, p = 0.016; and 40.9% vs. 28.6%, p = 0.00089, respectively). ICM etiology was an independent predictor of the composite endpoint in the total cohort (p = 0.003). The ICM patients were older and had more comorbidities, whereas the NIDCM patients had lower LVEF. One-year prognosis was worse in the ICM patients than in the NIDCM patients. ICM etiology was independently associated with a worse one-year outcome.