Coronary revascularization in patients with HIV.

With combined antiretroviral therapy, people living with HIV (PLWH) survive longer and are now more likely to die from cardiovascular diseases. PLWH presenting with a ST-segment elevation myocardial infarction are likely to have a high thrombus burden and are at high risk for in-hospital and long-term adverse events. An increasing number of PLWH are presenting with stable coronary artery disease related to atherosclerosis. Revascularization in these patients is associated with higher in-hospital and long-term major adverse cardiovascular events, including stent thrombosis and in-stent restenosis. However, data in this expanding population concerning optimal revascularization strategy are still lacking. In particular, data comparing percutaneous versus surgical revascularization in PLWH are needed. In this review we highlight the currently available data related to coronary revascularization in PLWH.

Inferior ST-elevation myocardial infarction managed with a pharmacoinvasive strategy and conservative management of delayed atrioventricular block: classical case report.

BACKGROUND: The 2017 ESC guideline on patients with ST-segment elevation myocardial infarction (STEMI) provides guidance regarding the optimal management of these patients. Transient atrioventricular (AV) block is a relatively common complication of inferior STEMI and its management is also addressed in the guidelines. CASE SUMMARY: A 64-year-old gentleman with multiple cardiovascular risk factors presented to the emergency department with a history of ischaemic type chest pain and evidence of inferior ST-segment elevation on his electrocardiogram (ECG). First-degree AV block was noted on his initial ECG. He was given thrombolytic therapy as part of a pharmacoinvasive strategy of reperfusion. He, however, failed fibrinolytic therapy, and emergency angiography revealed critical disease of the right coronary artery which was successfully stented. Subsequent to reperfusion, he developed complete AV block without evidence of re-infarction, which was managed conservatively with successful resolution of the block after 7 days of expectant management with temporary transvenous pacing. DISCUSSION: We highlight some of the important management principles from the ESC guideline of STEMI including timing and the management of AV block in these patients. In addition, we highlight the role of a pharmacoinvasive strategy for reperfusion where timeous primary percutaneous coronary intervention cannot be performed. The usefulness of such a strategy within the COVID-19 era is also emphasized.

Dynamic Changes in the Molecular Signature of Adverse Left Ventricular Remodeling in Patients With Compensated and Decompensated Chronic Primary Mitral Regurgitation.

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.

Atherosclerotic plaque in HIV-positive patients presenting with acute coronary syndromes.

AIM: This study aimed to characterise the atherosclerotic plaque and plaque burden in HIV-positive patients presenting with acute coronary syndromes (ACS), using intravascular ultrasound (IVUS) and virtual histology (VH). METHODS: This was a prospective study of 20 HIV-positive patients who presented with ACS. IVUS and VH were used to assess plaque burden and plaque characteristics in the culprit and non-culprit coronary arteries. RESULTS: HIV-positive patients with ACS had a mean age of 51.1 ± 8.1 years. There were 13 (65%) male patients. ST-segment elevation myocardial infarction was the most common presentation of ACS (75%) with the left anterior descending artery being the most common culprit artery (60%). In 60% of patients, the total plaque burden was of moderate degree (40-70% stenosis) while it was of mild degree (< 40% stenosis) in 35%, and in 5% of patients it was severe (> 70% stenosis). A severe degree of total plaque burden was more commonly found in the culprit vessel (30%) than in the non-culprit vessels (5%). Furthermore, the plaque burden was found to be located predominantly in the proximal portion of the coronary arteries. The predominant plaque morphology consisted of fibrous plaque (55.4%) and fibro-fatty plaque (26.6%), while necrotic core was present in 13.3%. Dense calcium was present in only 4.7% of the cohort. CONCLUSIONS: IVUS and VH demonstrated a high burden of atherosclerosis in the left anterior descending artery and proximal vasculature of HIV-positive patients. The atherosclerotic plaque predominantly comprised non-calcified fibrous and fibro-fatty plaque.

A New Face of Cardiac Emergencies: Human Immunodeficiency Virus-Related Cardiac Disease.

The human immunodeficiency virus epidemic is a major health challenge of the twenty-first century as the transition from infectious complications to noncommunicable disease becomes more evident. These patients may present to the emergency department with a variety of cardiovascular diseases, such as acute coronary syndromes, heart failure, pericardial disease, infective endocarditis, venothromboembolism, and other conditions. Increased awareness is needed among health care professionals to enhance adequate identification and promote prompt management of these patients.

HIV and Nonischemic Heart Disease.

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.

HIV and Ischemic Heart Disease.

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.