Project description:Reliable estimates of heart failure are lacking in India because of the absence of a surveillance programme to track incidence, prevalence, outcomes and key causes of heart failure. Nevertheless, we propose that the incidence and prevalence rates of heart failure are rising due to population, epidemiological and health transitions. Based on disease-specific estimates of prevalence and incidence rates of heart failure, we conservatively estimate the prevalence of heart failure in India due to coronary heart disease, hypertension, obesity, diabetes and rheumatic heart disease to range from 1.3 to 4.6 million, with an annual incidence of 491 600-1.8 million. The double burden of rising cardiovascular risk factors and persistent 'pre-transition' diseases such as rheumatic heart disease, limited healthcare infrastructure and social disparities contribute to these estimates. Staging of heart failure, introduced in 2005, provides a framework to target preventive strategies in patients at risk for heart failure (stage A), with structural disease alone (B), with heart failure symptoms (C) and with end-stage disease (D). Policy-level interventions, such as regulations to limit salt and tobacco consumption, are effective for primordial prevention and would have a wider impact on prevention of heart failure. Clinical preventive interventions and clinical quality improvement interventions, such as treatment of hypertension, atherosclerotic disease, diabetes and acute decompensated heart failure are effective for primary, secondary and even tertiary prevention.
Project description:Aim of this project was the evaluation of the effect of flushing (intraportal and intraoperative) hepatic allografts with tacrolimus before transplantation. Group A was administered tacrolimus, 20ng/ml in 1500ml albumin solution; and Group B was administered only albumin solution. Wedge biopsie of the allograft were harvested after 15 min flushing time and the gene expression profile were determined. The primary study objective was to determine on a genome-wide basis whether intraoperative and intraportal treatment of the allograft with tacrolimus reduces inflammatory signature in the liver. The secondary objective was the causally test, whether suppression of genes belongong to the ontologies of inflammation and immune response by tacrolimus will lead to a better initial function of the liver. randomized double-blind, placebo-controlled trial
Project description:ObjectiveThe left ventricle remodels from an ellipsoidal/conical shape to a spherical shape after a myocardial infarction. The spherical ventricle is inefficient as a pumping chamber, has higher wall stresses, and can lead to congestive heart failure. We sought to investigate if restoring physiological ventricular shape with a beating heart implant improves pump function.MethodsRats were induced with a myocardial infarction, developing left ventricular dilatation and dysfunction, and becoming spherical over 3 weeks. Thereafter, they were randomized to undergo left ventricular reshaping with a beating heart implant (n = 19) or continue follow-up without an implant (n = 19). Biweekly echocardiography was performed until 12 weeks, with half the rats euthanized at 6 weeks and remaining at 12 weeks. At termination, invasive hemodynamic parameters and histopathology were performed.ResultsAt 3 weeks after the infarction, rats had a 22% fall in ejection fraction, 31% rise in end diastolic volume, and 23% rise in sphericity. Transventricular implant reshaping reduced the volume by 12.6% and sphericity by 21%, restoring physiologic ventricular shape and wall stress. Over the 12-week follow-up, pump function improved significantly with better ventricular-vascular coupling in the reshaped hearts. In this group, cardiomyocyte cross-section area was higher and the cells were less elongated.ConclusionsReshaping a postinfarction, failing left ventricle to restore its physiological conical shape significantly improves long-term pump function.
Project description:Isoproterenol (ISO), is a non-selective beta-adrenergic agonist, that is used widely to induce cardiac injury in mice. While the acute model mimics stress-induced cardiomyopathy, the chronic model, administered through an osmotic pump, mimics advanced heart failure in humans. The purpose of the described protocol is to create the chronic ISO-induced heart failure model in mice using an implanted mini-pump. This protocol has been used to induce heart failure in 100+ strains of inbred mice. Techniques on surgical pump implantation are described in detail and may be relevant to anyone interested in creating a heart failure model in mice. In addition, the weekly cardiac remodeling changes based on echocardiographic parameters for each strain and expected time to model development are presented. In summary, the method is simple and reproducible. Continuous ISO administered via the implanted mini-pump over 3 to 4 weeks is sufficient to induce cardiac remodeling. Finally, the success for ISO model creation may be assessed in vivo by serial echocardiography demonstrating hypertrophy, ventricular dilation, and dysfunction.
Project description:There is increasing interest in the concept of personalised medicine, whereby conditions with common pathophysiologies are targeted together, and also using biomarkers to identify patients who will most benefit from certain interventions. Several data sets indicate that natriuretic peptides are effective in refining risk prediction for heart failure and cardiovascular disease and add predictive power to conventional risk factors. To date two trials have tested the approach of using natriuretic peptides as part of a strategy to identify those at highest risk of cardiovascular events: St. Vincent's Screening to Prevent Heart Failure (STOP-HF) and N-terminal Pro-brain Natriuretic Peptide Guided Primary Prevention of Cardiovascular Events in Diabetic Patients (PONTIAC). These have shown natriuretic peptide-based screening and targeted prevention can reduce heart failure and left ventricular dysfunction and other major cardiovascular events. This approach is now part of North American guidelines.
Project description:Success with oncologic treatment has allowed cancer patients to experience longer cancer-free survival gains. Unfortunately, this success has been tempered by unintended and often devastating cardiac complications affecting overall patient outcomes. Cardiac toxicity, specifically the association of several cancer therapy agents with the development of left ventricular dysfunction and cardiomyopathy, is an issue of growing concern. Although the pathophysiologic mechanisms behind cardiac toxicity have been characterized, there is currently no evidence-based approach for monitoring and management of these patients. In the first of a 2-part review, we discuss the epidemiologic, pathophysiologic, risk factors, and imaging aspects of cancer therapy-related cardiac dysfunction and heart failure. In this second part, we discuss the prevention and treatment aspects in these patients and conclude with highlighting the evidence gaps and future directions for research in this area.
Project description:Purpose of reviewArrhythmias are common in patients with heart failure (HF) and are associated with a significant risk of mortality and morbidity. Optimal antiarrhythmic treatment is therefore essential. Here, we review current approaches to antiarrhythmic treatment in patients with HF.Recent findingsIn atrial fibrillation, rhythm control and ventricular rate control are accepted therapeutic strategies. In recent years, clinical trials have demonstrated a prognostic benefit of early rhythm control strategies and AF catheter ablation, especially in patients with HF with reduced ejection fraction. Prevention of sudden cardiac death with ICD therapy is essential, but optimal risk stratification is challenging. For ventricular tachycardias, recent data support early consideration of catheter ablation. Antiarrhythmic drug therapy is an adjunctive therapy in symptomatic patients but has no prognostic benefit and well-recognized (proarrhythmic) adverse effects. Antiarrhythmic therapy in HF requires a systematic, multimodal approach, starting with guideline-directed medical therapy for HF and integrating pharmacological, device, and interventional therapy.