Springer Science and Business Media LLC

Heart failure (HF) is a common and growing health problem with high morbidity and mortality rates. Thromboembolism is a major contributor to the poor prognosis of HF patients. HF independently increases the risk of thromboembolism, and the high incidence of atrial fibrillation (AF) in HF patients further adds to the risk of thromboembolic events. The reviewed evidence for the efficacy of anticoagulation in HF patients shows a potential preventive effect of oral anticoagulation in thromboembolism—in particular, risk reduction for stroke—but this is offset by an increased risk of major bleeding. However, given the inhomogeneity of the HF cohorts, the diagnosis of AF warranting oral anticoagulation, the increasing awareness of the potential of bleeding risk assessment, and the advantages of the new oral anticoagulants, the future of thromboembolic prevention in HF patients could very well be brighter than it appears and help improve outcomes for this large group of patients.

An acute myocardial infarction causes a loss of contractile fibers which reduces systolic function. Parallel to the effect on systolic function, a myocardial infarction also impacts diastolic function, but this relationship is not as well understood. The two physiologic phases of diastole, active relaxation and passive filling, are both influenced by myocardial ischemia and infarction. Active relaxation is delayed following a myocardial infarction, whereas left ventricular stiffness changes depending on the extent of infarction and remodeling. Interstitial edema and fibrosis cause an increase in wall stiffness which is counteracted by dilation. The effect on diastolic function is correlated to an increased incidence of adverse outcomes. Moreover, patients with comorbid conditions that are associated with worse diastolic function tend to have more adverse outcomes after infarction. There are currently no treatments aimed specifically at treating diastolic dysfunction following a myocardial infarction, but several new drugs, including aldosterone antagonists, may offer promise.

The purpose of this review is to provide an overview of recent evidence on female-specific risk factors related to reproductive status or pregnancy. Pregnancy-related factors, including hypertensive disorders and gestational diabetes, increase the risk of heart failure in women, while breastfeeding and hormone therapy may offer protection. Hypertensive disorders of pregnancy, gestational diabetes, polycystic ovarian syndrome, placental abruption, younger maternal age at first live birth, younger maternal age at last live birth, number of stillbirths, number of pregnancies, onset of menstruation before 12 years of age, shorter reproductive age, ovariectomy, and prolonged absence of ovarian hormones may increase the risk of heart failure in women. Conversely, breastfeeding status and hormone therapy (for menopause or contraception) may serve as protective factors, while fertility treatments have no discernible effect on the risk of heart failure.

Chronic heart failure (CHF) is a complex clinical syndrome leading to exercise intolerance due to muscular fatigue and dyspnea. Hemodynamics fail to explain the reduced exercise capacity, while a significant skeletal muscular pathology seems to constitute the main underlying mechanism for exercise intolerance in CHF patients. There have been proposed several metabolic, neurohormonal and immune system abnormalities leading to an anabolic/catabolic imbalance that plays a central role in the pathogenesis of the wasting process of skeletal muscle myopathy. The impairment of the anabolic axes is associated with the severity of symptoms and the poor outcome in CHF, whereas increased cortisol levels are predictive of exercise intolerance, ventilatory inefficiency and chronotropic incompetence, suggesting a significant contributing mechanism to the limited functional status. Exercise training and device therapy could have beneficial effects in preventing and treating muscle wasting in CHF. However, specific anabolic treatment needs more investigation to prove possible beneficial effects.

Despite significant advances in the management of heart failure, short-term mortality due to advanced heart failure and cardiogenic shock remains high. Developed over the past few decades, percutaneous circulatory support devices offer a rapid and effective approach to slow the downward spiral of hemodynamic instability in patients presenting with decompensated heart failure until a more definitive strategy is pursued or patients recover. This review will discuss the goals of percutaneous circulatory support, the types of devices currently available, and the most recent clinical datasets examining the utility of these devices.

The incidence and prevalence of heart failure is increasing, especially heart failure with preserved ejection fraction (HFpEF) relative to heart failure with reduced ejection fraction (HFrEF). For both HFrEF and HFpEF, there is need to shift our focus from secondary to primary prevention. Detailed epidemiologic data on both HFpEF and HFrEF are needed to allow early identification of at-risk subjects. Current cohorts with new onset heart failure lack uniformity with respect to diagnosis, follow-up, and population characteristics, but most important, fail to distinguish between HFpEF and HFrEF. Studies on prevalent heart failure show ischemic heart disease as the predominant risk factor for HFrEF, while hypertension, atrial fibrillation, and diabetes are risk factors for HFpEF. As it becomes increasingly clear that both subtypes of heart failure are different syndromes, new cohorts and trials are necessary to obtain separate data on both subtypes of heart failure.

The purpose of this review is to provide an update on the recent advances in the research and clinical care of patients with the major phenotypes of inherited cardiomyopathies—hypertrophic, dilated, and arrhythmogenic. Developments in genetics, risk stratification, therapies, and disease modeling will be discussed. Diagnostic, prognostic, and therapeutic tools which incorporate genetic and genomic data are being steadily incorporated into the routine clinical care of patients with genetic cardiomyopathies. Human pluripotent stem cells are a breakthrough model system for the study of genetic variation associated with inherited cardiovascular disease. Next-generation sequencing technology and molecular-based diagnostics and therapeutics have emerged as valuable tools to improve the recognition and care of patients with hypertrophic, dilated, and arrhythmogenic cardiomyopathies. Improved adjudication of variant pathogenicity and management of genotype-positive/phenotype-negative individuals are imminent challenges in this realm of precision medicine.

The right ventricle (RV) has a complex geometry and physiology which is distinct from the left. RV dysfunction and failure can be the aftermath of volume- and/or pressure-loading conditions, as well as myocardial and pericardial diseases. Echocardiography, magnetic resonance imaging and right heart catheterisation can assess RV function by using several qualitative and quantitative parameters. In pulmonary hypertension (PH) in particular, RV function can be impaired and is related to survival. An accurate assessment of RV function is crucial for the early diagnosis and management of these patients. This review focuses on the different modalities and indices used for the evaluation of RV function with an emphasis on PH.