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The prevalence of overweight and obesity has reached pandemic proportions, affecting more than 1 billion people worldwide; it represents a major driver of cardiovascular morbidity, mortality, and health-care costs. 1 Excess adiposity triggers a complex cascade of metabolic and vascular disturbances which increase the risk of atherosclerotic cardiovascular disease, heart failure, and mortality. 2,3 GLP-1 receptor agonists have emerged as an important therapy at an intersection of obesity and cardiovascular disease. [...]mediation analysis suggested that waist circumference reduction explained approximately 33% of semaglutide treatment effect, whereas it was not significantly affected by early weight loss. [...]a question remains about the mechanisms driving disease-modifying effects of semaglutide, that should be further explored.

Inflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology. Inflammatory cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, protozoal or fungal infections as well as a wide variety of toxic substances and drugs and systemic immune-mediated diseases. Despite extensive research, inflammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmia is associated with a poor prognosis. At present, the reason why some patients recover without residual myocardial injury whereas others develop dilated cardiomyopathy is unclear. The relative roles of the pathogen, host genomics and environmental factors in disease progression and healing are still under discussion, including which viruses are active inducers and which are only bystanders. As a consequence, treatment strategies are not well established. In this Review, we summarize and evaluate the available evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy, with a special focus on virus-induced and virus-associated myocarditis. Furthermore, we identify knowledge gaps, appraise the available experimental models and propose future directions for the field. The current knowledge and open questions regarding the cardiovascular effects associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are also discussed. This Review is the result of scientific cooperation of members of the Heart Failure Association of the ESC, the Heart Failure Society of America and the Japanese Heart Failure Society.In this Review, Tschöpe and colleagues summarize and evaluate the available evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy, with special focus on virus-induced and virus-associated myocarditis. The authors also identify knowledge gaps, appraise available experimental models and propose future directions for the field.

The present study defined the short- and long-term effects of left ventricular assist device (LVAD) implantation and heart transplantation (HT) on physical activity and quality of life (QoL). Forty patients (LVAD, n = 14; HT, n = 12; and heart failure [HF], n = 14) and 14 matched healthy subjects were assessed for physical activity, energy expenditure, and QoL. The LVAD and HT groups were assessed postoperatively at 4 to 6 weeks (baseline) and 3, 6, and 12 months. At baseline, LVAD, HT, and HF patients demonstrated low physical activity, reaching only 15%, 28%, and 51% of that of healthy subjects (1,603 ± 302 vs 3,036 ± 439 vs 5,490 ± 1,058 vs 10,756 ± 568 steps/day, respectively, p <0.01). This was associated with reduced energy expenditure and increased sedentary time (p <0.01). Baseline QoL was not different among LVAD, HT, and HF groups (p = 0.44). LVAD implantation and HT significantly increased daily physical activity by 60% and 52%, respectively, from baseline to 3 months (p <0.05), but the level of activity remained unchanged at 3, 6, and 12 months. The QoL improved from baseline to 3 months in LVAD implantation and HT groups (p <0.01) but remained unchanged afterward. At any time point, HT demonstrated higher activity level than LVAD implantation (p <0.05), and this was associated with better QoL. In contrast, physical activity and QoL decreased at 12 months in patients with HF (p <0.05). In conclusion, patients in LVAD and HT patients demonstrate improved physical activity and QoL within the first 3 months after surgery, but physical activity and QoL remain unchanged afterward and well below that of healthy subjects. Strategies targeting low levels of physical activity should now be explored to improve recovery of these patients.

Cardiac tamponade is a medical emergency caused by the progressive accumulation of pericardial fluid (effusion), blood, pus or air in the pericardium, compressing the heart chambers and leading to haemodynamic compromise, circulatory shock, cardiac arrest and death. Pericardial diseases of any aetiology as well as complications of interventional and surgical procedures or chest trauma can cause cardiac tamponade. Tamponade can be precipitated in patients with pericardial effusion by dehydration or exposure to certain medications, particularly vasodilators or intravenous diuretics. Key clinical findings in patients with cardiac tamponade are hypotension, increased jugular venous pressure and distant heart sounds (Beck triad). Dyspnoea can progress to orthopnoea (with no rales on lung auscultation) accompanied by weakness, fatigue, tachycardia and oliguria. In tamponade caused by acute pericarditis, the patient can experience fever and typical chest pain increasing on inspiration and radiating to the trapezius ridge. Generally, cardiac tamponade is a clinical diagnosis that can be confirmed using various imaging modalities, principally echocardiography. Cardiac tamponade is preferably resolved by echocardiography-guided pericardiocentesis. In patients who have recently undergone cardiac surgery and in those with neoplastic infiltration, effusive–constrictive pericarditis, or loculated effusions, fluoroscopic guidance can increase the feasibility and safety of the procedure. Surgical management is indicated in patients with aortic dissection, chest trauma, bleeding or purulent infection that cannot be controlled percutaneously. After pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be considered to prevent recurrence and effusive–constrictive pericarditis. Cardiac tamponade is a potentially life-threatening emergency involving compression of the heart caused by accumulation of fluid in the pericardial sac. This Primer by Adler and colleagues provides an overview of the epidemiology, pathophysiology, diagnosis, treatment and effect on patient quality of life of cardiac tamponade as well as of areas requiring further research.

Left ventricular mass index (LVMI) increase has been described in hypertension (HTN), but less is known about its association with type 2 diabetes (T2DM). As these conditions frequently co-exist, we investigated the association of T2DM, HTN and both with echocardiographic parameters, and hypothesized that patients with both had highest LVMI, followed by patients with only T2DM or HTN. Study population included 101 T2DM patients, 62 patients with HTN and no T2DM, and 76 patients with T2DM and HTN, excluded for ischemic heart disease. Demographic and clinical data, biochemical measurements, stress echocardiography, transthoracic 2D Doppler and tissue Doppler echocardiography were performed. Multivariable logistic regression was used to determine the independent association with T2DM. Linear regression models and Pearson’s correlation were used to assess the correlations between LVMI and other parameters. Patients with only T2DM had significantly greater LVMI (84.9 ± 20.3 g/m 2 ) compared to patients with T2DM and HTN (77.9 ± 16 g/m 2 ) and only HTN (69.8 ± 12.4 g/m 2 ). In multivariate logistic regression analysis, T2DM was associated with LVMI (OR 1.033, 95%CI 1.003–1.065, p = 0.029). A positive correlation of LVMI was found with fasting glucose (p < 0.001) and HbA1c (p = 0.0003). Increased LVMI could be a potential, pre-symptomatic marker of myocardial structural change in T2DM.

In the recent years, there has been a burgeoning interest in Takotsubo syndrome (TTS), which is renowned as a specific form of reversible myocardial dysfunction. Despite the extensive literature available on TTS, clinicians still face several practical challenges associated with the diagnosis and management of this phenomenon. This potentially results in the underdiagnosis and improper management of TTS in clinical practice. The present paper, the first part (part-1) of the consensus report, aims to cover diagnostic and therapeutic challenges associated with TTS along with certain recommendations to combat these challenges.

Contrast-induced nephropathy (CIN) is the impairment of kidney function defined as a serum creatinine increase of 25% or 44 µmol/L compared with baseline, usually occurring 24 to 48 hours after the use of intravenous contrast. Important risk factors for CIN include female sex, advanced age (>65 years), type 2 diabetes (T2D), kidney disease, advanced heart failure, and intravascular volume depletion. We herein present a male patient with T2D, moderately reduced renal function, no albuminuria, and a positive echocardiography stress test. He underwent percutaneous coronary intervention (PCI), and two drug-eluting stents (in the left anterior descending coronary artery) and three bare-metal stents (in the right coronary artery) were implanted. Despite adequate rehydration (0.9% intravenous NaCl with 8.4% sodium bicarbonate) before and after the procedures, he developed irreversible kidney injury after coronary angiography and PCI. This case report demonstrates the unpredictable clinical course of CIN. Patients with T2D are at high risk for the occurrence of CIN, so careful clinical assessment is recommended with global renal functional reserve evaluation.

Takotsubo syndrome (TTS) still remains as an enigmatic phenomenon. In particular, long-term challenges (including clinical recurrence and persistent symptoms) and specific entities in the setting of TTS have been the evolving areas of interest. On the other hand, a significant gap still exists regarding the proper risk-stratification of this phenomenon in the short and long terms. The present paper, the second part (part-2) of the consensus report, aims to discuss less well-known aspects of TTS including specific entities, challenges after recovery and risk-stratification.

Hospital readmissions remain a continued challenge in the care of patients with heart failure (HF). This study aims to examine the rates, temporal trends, predictors and causes of 30-day unplanned readmissions after admission with HF. Patients hospitalized with a primary or secondary diagnosis of HF in the U.S. Nationwide Readmission Database were included. We examined the incidence, trends, predictors and causes of unplanned all-cause readmissions at 30-days. A total of 2,635,673 and 8,342,383 patients were included in the analyses for primary and secondary diagnoses of HF, respectively. The 30-day unplanned readmission rate was 15.1% for primary HF and 14.6% for secondary HF. Predictors of readmission in primary HF included renal failure (OR 1.27 (1.25 to 1.28)), cancer (OR 1.26 (1.22 to 1.29)), receipt of circulatory support (OR 2.81 (1.64 to 4.81)) and discharge against medical advice (OR 2.29 (2.20 to 2.39)). In secondary HF, the major predictors were receipt of circulatory support (OR 1.43 (1.12 to 1.84)) and discharge against medical advice (OR 2.01 95%CI (1.95 to 2.07)). In primary HF 52.4% of patients were readmitted for a noncardiac cause while for secondary HF 73.9% were readmitted for a noncardiac cause. For secondary HF, the strongest predictor of readmission was discharge against medical advice (OR 2.06 95%CI 2.01 to 2.12, p < 0.001). Early unplanned readmissions are common among patients hospitalized with HF, and a majority of readmissions are due to causes other than HF. Our results highlight the need to better manage comorbidities in patients with HF.

Right ventricular function has long been neglected by heart failure specialists. We have now learnt that it is strongly associated with morbidity and mortality in all patients with heart failure, regardless of the degree of left ventricular dysfunction. Importantly, right ventricular function is tightly linked with pulmonary hypertension, and only a thorough understanding of how the right ventricle couples with the pulmonary circulation can provide an improved knowledge of the pathophysiology and possibly a more efficient treatment and a better prognosis in patients with heart failure.