Tal Hasin

Prompt benefit of early immunosuppressive therapy in acute lymphocytic myocarditis with persistent heart failure.

Myocarditis resolves in about 50 % of cases during 2–4 weeks, but 25 % develop persistent cardiac dysfunction and 12–25 % may deteriorate leading to death or endstage dilated cardiomyopathy [1]. Presentation with heart failure and ventricular dysfunction are strong predictors of adverse outcome [2]. Viral infection is the most commonly identified cause of myocarditis. Mechanisms of injury include direct viral damage or inappropriate immune response. While the initial immune response limits the degree of viral cellular invasion and myocardial damage, non-replicating viral genomic fragments and cardiac epitopes such as myosin and beta-1 receptors might drive an ongoing adverse autoimmune response leading to inflammation through ‘‘anti-heart auto-antibodies’’ [3, 4]. Treatment of myocarditis includes supportive measures, heart failure therapy and treatment of arrhythmias according to current position statements [1]. Immunosuppression is advised with specific rare etiologies such as giant cell and eosinophilic myocarditis, but controversial in the prevalent lymphocytic subtype. A 28-year-old woman was admitted with weakness, dyspnea and nausea for a few days and gastroenteritis 2 weeks earlier. Otherwise, she had no history pertinent to the current illness. On admission, she was pale and nauseous, blood pressure was 90/60, pulse was 130 and ECG showed sinus tachycardia with small complexes. Troponin I was 0.22 mcg/L (normal range\ 0.04), Leukocytes were 10,600 (75 % neutrophils) and hemoglobin was 13 g/dL. She had moderate hepatic transaminase elevation (in the hundreds) and normal renal function; BNP was 2760 pgr/ ml, lactate was 1.29 mmol/L and CRP was 3.5 mg%. Chest X-ray demonstrated mild bilateral congestion. Echocardiogram showed mildly enlarged left ventricle with severe biventricular failure, left ventricular ejection fraction 23 %, normal wall thickness and severe mitral and tricuspid regurgitation. Cardiac MRI showed marked lateral wall edema without late gadolinium enhancement. On catheterization, right atrial pressure was 16 mmHg, pulmonary pressure was 45/25, mean was 30 mmHg, wedge pressure was 20 mmHg and cardiac index was 1.55 l/min/ m. Right ventricular endomyocardial biopsy revealed active lymphocytic myocarditis (CD3? T lymphocyte predominant with CD68? histiocytes and without eosinophils or giant cells) associated with ongoing and wellestablished perivascular and interstitial replacing fibrosis. Electron microscopy showed no viral capsids, no evidence of myofilament loss or mitochondrial pathology. She continued to suffer from persistent weakness and nausea needing continued hospitalization with ongoing tachycardia and low blood pressures, tolerating only low doses of heart failure treatment (Losartan 12.5 mg BID, Bisoprolol 1.25 mg BID, Spironolactone 25 mg and Furosemide). The patient occasionally missed heart failure medication due to low blood pressure, but did not need inotropic support. Repeat echocardiography showed no improvement in ventricular function with a new apical thrombus (treated with anticoagulation). Evaluation for etiologic cause was negative. After 1 month in the hospital, catheterization was repeated without improvement. Repeat biopsy revealed & Tatyana Weitsman tweitsman@gmail.com

Advanced heart failure: a position statement of the Heart Failure Association of the European Society of Cardiology: Advanced heart failure: HFA position statement

This article updates the Heart Failure Association of the European Society of Cardiology (ESC) 2007 classification of advanced heart failure and describes new diagnostic and treatment options for these patients. Recognizing the patient with advanced heart failure is critical to facilitate timely referral to advanced heart failure centres. Unplanned visits for heart failure decompensation, malignant arrhythmias, co‐morbidities, and the 2016 ESC guidelines criteria for the diagnosis of heart failure with preserved ejection fraction are included in this updated definition. Standard treatment is, by definition, insufficient in these patients. Inotropic therapy may be used as a bridge strategy, but it is only a palliative measure when used on its own, because of the lack of outcomes data. Major progress has occurred with short‐term mechanical circulatory support devices for immediate management of cardiogenic shock and long‐term mechanical circulatory support for either a bridge to transplantation or as destination therapy. Heart transplantation remains the treatment of choice for patients without contraindications. Some patients will not be candidates for advanced heart failure therapies. For these patients, who are often elderly with multiple co‐morbidities, management of advanced heart failure to reduce symptoms and improve quality of life should be emphasized. Robust evidence from prospective studies is lacking for most therapies for advanced heart failure. There is an urgent need to develop evidence‐based treatment algorithms to prolong life when possible and in accordance with patient preferences, increase life quality, and reduce the burden of hospitalization in this vulnerable patient population.

Associated Risk of Malignancy in Patients with Cardiovascular Disease: Evidence and Possible Mechanism

Cardiovascular disease and malignancy are leading causes of morbidity and mortality. Increased risk of malignancy was identified in patients with cardiovascular disease, including patients with heart failure, heart failure after myocardial infarction, patients undergoing cardiac intervention, and patients after a thrombotic event. Common risk factors and biological pathways can explain this association and are explored in this review. Further research is needed to establish the causes of malignancy in this population and direct possible intervention.

Prevalence, Echocardiographic Correlations and clinical outcome of Tricuspid Regurgitation in patients with significant Left Ventricular Dysfunction

PURPOSE We initiated this study to evaluate the prevalence and clinical significance of tricuspid regurgitation in patients with left ventricular dysfunction. METHODS A single-center analysis of all echocardiographic studies between 2000 and 2013 was performed. Patients with ejection fraction <35% were included, and those with mechanical valves, mitral stenosis, or significant aortic valve pathology were excluded. Patients were grouped based on tricuspid regurgitation severity (nonsignificant, moderate, and severe). Demographic and echocardiographic findings and survival were compared. RESULTS The study included 3943 patients (74% male, age 69 ± 14 years); 70% had nonsignificant, 24% had moderate, and 6% had severe tricuspid regurgitation. In a multivariate model, tricuspid regurgitation was independently associated with older age (odds ratio [OR] 1.009; 95% confidence interval [CI], 1.001-1.017; P = .022), female sex (OR 1.644; 95% CI, 1.329-2.035; P < .001), atrial fibrillation (OR 1.764; 95% CI, 1.429-2.134; P < .001), tricuspid regurgitation gradient (OR 1.051; 95% CI, 1.045-1.058; P < .001 per mm Hg), right ventricular dysfunction (OR 3.492; 95% CI, 2.870-4.248; P < .001), left atrial area (cm2, OR 1.031; 95% CI, 1.013-1.049; P < .001), mitral regurgitation severity (P < .001), and lack of hypertension (OR 0.760; 95% CI, 0.616-0.936; P = .010) or obesity (OR 0.583; 95% CI, 0.427-0.796; P < .001). Patients were followed for a median of 8.15 years (interquartile range 4.75-11.42). Median survival was 4.88 years for nonsignificant, 2.3 years for moderate, and 1.6 years for patients with severe tricuspid regurgitation, significantly associated with tricuspid regurgitation severity (hazard ratio 1.513; 95% CI, 1.383-1.656 for moderate, hazard ratio 1.857; 95% CI, 1.606-2.148 for severe tricuspid regurgitation; P < .001), the association persisted after multiple adjustments. CONCLUSIONS Significant tricuspid regurgitation is common in patients with left ventricular dysfunction. It is linked to various cardiac pathologies and independently associated with increased mortality.

Hemodynamic Assessment of Patients With and Without Heart Failure Symptoms Supported by a Continuous-Flow Left Ventricular Assist Device

Objective: To investigate differences in invasive hemodynamic parameters and outcomes in patients with and without heart failure (HF) symptoms after left ventricular assist device (LVAD) implantation. Patients and Methods: We performed a single‐center retrospective analysis of 51 symptomatic patients and 50 patients with resolved HF symptoms who underwent right‐sided heart catheterization (RHC) after LVAD implantation from March 1, 2007, through June 30, 2016. Patient characteristics and outcomes including all‐cause mortality and right ventricular (RV) failure were compared between groups. Results: Fifty‐one patients had development of HF symptoms after LVAD implantation and underwent RHC a mean ± SD of 243.7±288 days postoperatively. Fifty asymptomatic LVAD recipients underwent routine RHC 278.6±205 days after implantation. Compared with patients who had resolved HF symptoms, symptomatic patients were older, more likely to be male, and more likely to have ischemic cardiomyopathy. Symptomatic patients had higher right atrial pressure (P<.001), mean pulmonary arterial pressure (P<.001), and pulmonary capillary wedge pressure (P<.001). Improvements in right atrial pressure, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure before and after LVAD implantation were less remarkable in symptomatic patients. The frequency of RV dysfunction was significantly higher among symptomatic patients than patients with resolved HF symptoms (P=.001). Symptomatic patients displayed significantly higher risk of all‐cause mortality (hazard ratio, 3.0; 95% CI, 1.3‐6.5; P=.007) and RV failure (hazard ratio, 6.2; 95% CI, 1.3‐29.7; P=.02) independent of other predictors of outcome. Conclusion: Patients with recurrent HF symptoms after LVAD implantation display more profound hemodynamic derangements, greater burden of RV failure, and increased rates of all‐cause mortality compared with LVAD recipients with resolved HF symptoms.

Pulmonary Congestion Complicating Atrial Fibrillation Cardioversion

Acute pulmonary congestion (APC) may occur within hours after electrical cardioversion of atrial fibrillation (AF). There is scarce data about its incidence, risk factors, and the outcome. In the present study, data of consecutive patients admitted for first electrical cardioversion for AF between 2007 and 2016 were retrospectively reviewed. APC within the 48 hours following cardioversion was defined as dyspnea and at least one of the following: drop in saturation to <90%, administration of intravenous diuretic or an emergent chest X-ray with new pulmonary congestion. All-cause mortality was determined from the national registry. Total of 1,696 patients had first cardioversion for AF, of whom 66 (3.9%) had APC. In a multivariate logistic regression model independent predictors of APC included (OR [CI], p): older age (odds ratio [OR] 1.05, 95% confidence interval [CI] 1.02 to 1.08, p = 0.001), rapid ventricular response (OR 1.98, 95% CI 1.17 to 3.34, 0.010), previous heart failure (OR 3.53, 95% CI 2.09 to 5.97, p <0.001), Amiodarone loading (OR 2.38, 95% CI 1.18 to 4.79, p = 0.016) and diabetes mellitus (OR 1.77 95% CI 1.05 to 3.00, p = 0.033). There was no difference in cardioversion success rate (overall 94%). In-hospital mortality was 1.5% within the APC group and 0.5% without (p = 0.301). Patients with APC had higher rate of 6-month readmissions (28.8% vs 18.1% p <0.028). Within a median follow-up of 2.9 years, APC following cardioversion was an independent predictor of overall mortality (hazard ratio 1.73, 95% CI (1.17 to 2.56) p = 0.006). In conclusion, APC occurs in 3.9% of hospitalized patients following electrical AF cardioversion. Risk factors include increased age, diabetes mellitus, heart failure, Amiodarone loading and rapid ventricular response. APC following cardioversion is associated with increased rates of readmissions and mortality.

Sexual Function in Adults with Implantable Cardioverter-Defibrillators/Pacemaker Recipients

Sexual function is an important component of quality of life. The present chapter examines issues concerning sex and implantable electronic devices, including sexual dysfunction and safety concerns. Performing sex involves a 3–5 metabolic equivalent effort, a gradual increase in catecholamines with a modest and short increase in heart rate and blood pressure. Overall sexual activity is safe, especially if response to moderate physical activity tested normal. Pathology based research suggests a mild increased in the incidence of myocardial infarction, specifically in men performing extra-marital sex. However, significant arrhythmia that may lead to activation of an implanted defibrillator is extremely rare. Sexual dysfunction is prevalent in patients with a cardiovascular disease including those with implantable devices. Patients with pacemakers may have sexual dysfunctions which seem attributable to older age, and not to the device. Heart failure patients implanted with a resynchronization device may benefit from improved sexual function and consequently better quality of life. Despite these low risks, “sexual avoidance” is prevalent among patients with implanted defibrillators and has several causes such as fear, anxiety and altered body image. Sex and sexuality should be actively addressed during medical consultation to relieve unjustified fears and provide patients with adequate information and treatment.