The association of coronary heart disease (CHD) and human immunodeficiency virus (HIV) infection has been well recognized for many years. The etiology of the increased prevalence of CHD in HIV-infected populations is the result of complex interactions among the viral infection, host factors, traditional risk factors, and therapies for HIV. As the HIV population is living longer, largely attributable to combination antiretroviral therapy, there is concern about the effect of the rising prevalence of CHD on morbidity and mortality, as well its effect on health systems around the world. This review will highlight the epidemiological evidence linking HIV infection and CHD. It will also focus on our current understanding of the pathogenesis and factors associated with HIV infection and CHD. In addition, the review will highlight modes of presentation and management strategies for mitigating risk and treatment of HIV-positive patients presenting with CHD.
Human immunodeficiency virus (HIV)-associated heart disease encompasses a broad spectrum of diseases. HIV infection may involve the pericardium, myocardium, coronary arteries, pulmonary vasculature, and valves, as well as the systemic vasculature. Access to combination antiretroviral therapy, as well as health resources, has had a significant influence on the prevalence and severity of the effects on each cardiac structure. Investigations over the recent past have improved our understanding of the epidemiology and pathophysiology of HIV-associated cardiovascular disease. This review will focus on our current understanding of pathogenesis and risk factors associated with HIV infection and heart disease, and it will discuss relevant advances in diagnosis and management of these conditions.
Background Mental health illnesses are associated with frequent hospitalisation and an increased risk of all-cause mortality. Despite the high prevalence of depression in patients with chronic heart failure (CHF), there is a paucity of data on this subject from low and middle-income countries (LMIC). The aim of this study was to determine the prevalence of depression, anxiety, and stress symptoms in patients attending a dedicated CHF clinic. Methods A prospective study was conducted at an outpatient heart failure clinic in a tertiary academic centre. The study participants completed a Depression, Anxiety and Stress (DASS-21) questionnaire to screen for the presence and severity of depression, anxiety and stress symptoms. Furthermore, the Minnesota Living with Heart Failure Questionnaire (MLHFQ) was completed and used to evaluate the impact of CHF on health-related quality of life (QoL). Descriptive statistics were used to describe patients' characteristics and logistic regression analysis to identify predictors of symptoms of depression. Results The study population comprised of 103 patients, predominantly female (62.1%) with a median age of 53 (interquartile range 38–61) years. Symptoms of depression were reported by 52.4%, with 11.6% reporting symptoms suggestive of extremely severe depression. Anxiety was diagnosed in 53.4% of patients and extremely severe anxiety was reported by 18.4% of patients. Fifty patients were classified as stressed, and only 7.7% had extremely severe stress. More than half of the patients (54.4%) were in New York Heart Association functional class I. The mean left ventricular ejection fraction in the entire cohort was 30% (SD = ± 11.1%). In the multivariable logistic regression model, the MLHFQ score [odds ratio (OR) 1.04, 95% CI:1.02–1.06, p = 0.001] and the six-minute walk test [OR 0.99, 95% CI: 0.98–0.99, p = 0.014] were identified as independent predictors of depression. Conclusion Depression and anxiety symptoms were found in over half of patients attending the CHF clinic. We recommend that mental health screening should be routinely performed in patients with CHF. Prospective, adequately powered, multicentre studies from LMIC investigating the impact of depression, anxiety and stress on CHF outcomes such as health-related QoL, hospitalisation and mortality are required.
Background: There is no proven medical therapy that attenuates adverse left ventricular remodeling in patients with chronic primary mitral regurgitation (CPMR). Identification of molecular pathways important in the progression of left ventricular remodeling in patients with CPMR may lead to development of new therapeutic strategies. Methods and Results: We performed baseline echocardiographic, cardiac catheterization, and serum NT-pro-BNP analysis in patients with severe CPMR awaiting mitral valve surgery and stratified the study population into compensated or decompensated CPMR. We obtained left ventricular endomyocardial biopsies (n=12) for mRNA expression analysis, and compared baseline transcript levels of 109 genes important in volume-overload left ventricular remodeling with levels in normal hearts (n=5) and between patients with compensated (n=6) versus decompensated (n=6) CPMR. Patients were then randomized to treatment with and without carvedilol and followed until the time of surgery (mean follow-up 8.3 months) when repeat endomyocardial biopsies were obtained to correlate transcriptional dynamics with indices of adverse remodeling. CPMR was associated with increased NPPA expression levels (21.6-fold, P =0.004), decreased transcripts of genes important in cell survival, and enrichment of extracellular matrix genes. Decompensated CPMR was associated with downregulation of SERCA2 (0.77-fold, P =0.009) and mitochondrial gene expression levels and upregulation of genes related to inflammation, the extracellular matrix, and apoptosis, which were refractory to carvedilol therapy. Conclusions: Transition to decompensated CPMR is associated with calcium dysregulation, increased expression of inflammatory, extracellular matrix and apoptotic genes, and downregulation of genes important in bioenergetics. These changes are not attenuated by carvedilol therapy and highlight the need for development of specific combinatorial therapies, targeting myocardial inflammation and apoptosis, together with urgent surgical or percutaneous valve interventions.
Objectives: The management of heart failure (HF) is most effective when established treatment guidelines and recommendations are followed. We aimed to develop a “Toolbox” of resources to facilitate the care of patients with acute HF and chronic HF with reduced ejection fraction delivered by healthcare professionals across Asia-Pacific, the Middle East and Africa (henceforth referred to as the “Region”). Methods: We convened a group of cardiologists from across the Region to develop a set of checklists, algorithms, and other practical resources. These resources are based on our experiences, current evidence, and international guidelines. Results: The HF Toolbox comprises three simplified sets of resources for use in the Emergency Room (ER), hospital and outpatient settings. Resources include admission and discharge checklists, treatment algorithms, recommendations for forming a multidisciplinary team, patient education, and self-management materials, and key performance indicators to monitor whether standards of care are met or maintained, or should be improved. Conclusions: The HF Toolbox provides practical resources to simplify the management of patients with HF and to support the formation of HF programs in the Region. The Toolbox is aligned with current guideline recommendations and can support the management of patients from presentation in the ER, through hospital admission to outpatient care.
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