Objectives: Our study aimed at conducting a systematic review and meta-analysis, with the objective of evaluating the prognostic value of T1 mapping techniques via cardiac magnetic resonance (CMR) in heart failure with preserved ejection fraction (HFpEF) patients. Materials and methods: The protocol was prospectively registered in the international prospective register of systematic reviews PROSPERO (registration number CRD42022300991). We searched PubMed, Google Scholar, and EMBASE for studies examining the prognostic value of characterizing myocardial tissue via CMR imaging with T1 mapping in HFpEF. Hazard ratios (HRs) for uniformly defined predictors were pooled for meta-analysis. Results: In total, 7 studies were retrieved from 351 publications for this systematic review and meta-analysis. A total of 1930 patients (mean age of 69.4 years, mean follow-up duration of 25.6 months) was included in the analysis. The meta-analysis demonstrated that higher extracellular volume (ECV) was associated with an increased risk of death and/or hospitalization with heart failure (HF) (HR:1.12; 95% CI: 1.06–1.18; p < 0.0001). After adjusting for baseline characteristics, the higher extent of ECV remained strongly associated with the risk of death and/or hospitalization with HF (HR_adjusted: 1.08; 95% CI: 1.04–1.13; p = 0.0001). However, no significant association of native T1 value with risk of death or adverse cardiovascular events was found (HR:1.01; 95% CI: 1.00–1.02; p = 0.21). Conclusion: Assessment of ECV via CMR has an important prognostic value for outcomes of death and/or hospitalization with HF, and can therefore be used as an effective tool for risk stratification of patients with HFpEF.

The abrupt cessation of effective cardiac function that is generally due to heart rhythm disorders can cause sudden and unexpected death at any age and is referred to as a syndrome called sudden cardiac death (SCD). Annually, about 400,000 cases of SCD occur in the United States alone. Less than 5% of the resuscitation techniques are effective. The prevalence of SCD in a population rises with age according to the prevalence of coronary artery disease, which is the most common cause of sudden cardiac arrest. However, there is a peak in SCD incidence for the age below 5 years, which is equal to 17 cases per 100,000 of the population. This peak is due to congenital monogenic arrhythmic canalopathies. Despite their relative rarity, these cases are obviously the most tragic. The immediate causes, or mechanisms, of SCD are comprehensive. Generally, it is arrhythmic death due to ventricular tachyarrythmias - sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Bradyarrhythmias and pulseless electrical activity account for no more than 40% of all registered cardiac arrests, and they are more often the outcome of the abovementioned arrhythmias. Our current understanding of the mechanisms responsible for SCD has emerged from decades of basic science investigation into the normal electrophysiology of the heart, the molecular physiology of cardiac ion channels, the fundamental cellular and tissue events associated with cardiac arrhythmias, and the molecular genetics of monogenic disorders of the heart rhythm (for example, the long QT syndrome). This review presents an overview of the molecular and genetic basis of SCD in the long QT syndrome, Brugada syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia and idiopathic ventricular fibrillation, and arrhythmogenic right ventricular dysplasia, and sudden cardiac death prevention strategies by modern techniques (including implantable cardioverter-defibrillator).