Heart Disease In HIV-infected Patients Research Articles

Coronary Heart Disease in HIV-Infected Patients

Currently, there are methods of drug exposure to the infection caused by the human immunodeficiency viruses (HIV), that allow to suppress the active replication of the virus in the patient's body. The era of antiretroviral therapy, which has allowed HIV-infected people to live longer, has begun. This led to an increase in their cardiovascular diseases, which occur at an earlier age and are more severe than in people without HIV. Specific or “nontraditional” risk factors damaging vascular wall occur in HIV patients along with traditional risk factors. These factors include: the negative impact of HIV on endothelium, an imbalance of inflammatory mediators, pathological immune activation, a decrease in the level of CD4 cells, a change in the number and function of platelets. The question of the effect of antiretroviral therapy on the occurrence of atherosclerotic vascular lesions remains debatable. Acute coronary syndrome (ACS) is one of the most frequent and most severe cardiovascular events in HIV-infected patients. The risk of myocardial infarction is highest in patients with a viral load of HIV-1 ribonucleic acid (RNA)≥500 copies/ml and a CD4 cell count of <200/ml. The most common form of ACS in HIV patients is ACS with ST segment elevation. Treatment of ACS in HIV patients has some difficulties: a high frequency of stent thrombosis, the frequent occurrence of thrombocytopenia, drug interactions with antiretroviral therapy. The high risk of developing cardiovascular diseases in HIV patients necessitates the introduction of active measures of primary and secondary prevention, taking into account the specific interaction of all drugs taken by the patient.

The Framingham function overestimates the risk of ischemic heart disease in HIV-infected patients from Barcelona

Background: Cardiovascular risk (CVR) assessment helps to identify patients at high CVR. The Framingham CVR score (FRS) is the most widely used methods but may overestimate risk in regions with low incidence of cardiovascular disease. The objective was to compare the 10-year performance of the original and the adapted REGICOR – Framingham CVR functions in HIV-infected individuals.Methods: We carried out a longitudinal study of HIV-infected patients with CVR evaluation in a hospital in Barcelona between 2003 and 2013. Statistics: Risk probability was calculated using the FRAMINGHAM function and REGICOR adaptation to the Spanish population, and individuals were categorized in three groups (low, 0 < 5%; moderate, 5–10%; and high, >10%). For each risk group, the number of events over 10 years was calculated using the Kaplan–Meier method, and the expected number of events was calculated by multiplying the frequency of participants in the group by the mean of the probabilities from the risk function. We used the X2 goodness-of-fit test to assess agreement between observed and expected.Results: Six hundred and forty-one patients were followed up for a median of 10.2 years, and 20 ischemic heart events (IHE) were observed. The mean (95% CI) number of IHEs per 1000 person-years was 3.7 (2.06–5.27). The estimates from the Framingham and REGICOR functions were 40 and 14 IHEs, respectively. The estimate from the original Framingham function differed significantly from the observed incidence (p < 0.001), whereas that from the REGICOR-adapted function did not (p = 0.15). In terms of the number of cardiovascular events (38 events observed), the REGICOR function significantly underestimated risk (p = 0.01), whereas the estimate from the Framingham function was similar to observed (p:0.93).Conclusions: The FRS significantly overestimates risk of IHE events in our HIV-infected patients, while the REGICOR function is a better predictor of these events. In terms of cardiovascular events, the REGICOR function significantly underestimates risk, whereas the FRS is a better estimator. We recommend using CVR scales and adjusting them to the origin of the population being studied.

HEART FAILURE ADMISSION IN HIV-INFECTED PATIENTS

With increased survival of HIV-infected patients, cardiovascular diseases have become a major cause of mortality and morbidity in this population. There is an increasing attention to ischemic heart disease in HIV-infected patients, but much less is known about heart failure (HF) and the mortality

HIV Infection and Cardiovascular Disease

HIV Infection and Cardiovascular Disease

Cholesterol, vitamin D and cardiovascular prevention in HIV patients treated with antiretroviral therapy

It is widely believed that dyslipidaemia related to the duration of highly active antiretroviral therapy (HAART) contributes most to an increased predicted risk of cardiovascular disease (CVD) among patients with HIV. Consequently, it is increasingly suggested that hypercholesterolemia should be actively managed with the use of lipid-lowering drugs. However, when studying the impact of individual antiretroviral drugs on the risk of coronary heart disease in HIV-infected patients, it has been shown that the risk of myocardial infarction is only partly mediated by an effect of HAART on lipid metabolism [ [1] Lang S. Mary-Krause M. Cotte L. Clinical Epidemiology Group of the French Hospital Database on HIV et al. Impact of individual antiretroviral drugs on the risk of myocardial infarction in human immunodeficiency virus-infected patients: a case–control study nested within the French Hospital Database on HIV ANRS cohort CO4. Arch Intern Med. 2010; 170: 1228-1238 Crossref PubMed Scopus (264) Google Scholar ]. Furthermore, in this setting, hypercholesterolemia may represent a blessing in disguise.

HIV Infection: An Independent Risk Factor of Peripheral Arterial Disease

HIV Infection: An Independent Risk Factor of Peripheral Arterial Disease

Prevention Strategies for Cardiovascular Disease in HIV-Infected Patients

Effective antiretroviral therapy (ART) improves the survival of patients with human immunodeficiency virus (HIV) infection.1 With increased life expectancy, HIV-infected patients increasingly are experiencing complications of illnesses that are not directly related to HIV infection.2 Cardiovascular disease (CVD), the leading cause of death in the United States,3 recently has been recognized as an important cause of morbidity and mortality among patients with HIV (see Working Group 2, Epidemiological Evidence for Cardiovascular Disease in HIV-Infected Patients and Relationship to Highly Active Antiretroviral Therapy).2,4–6 Among these patients, traditional CVD risk factors predict CVD events; however, certain components of ART appear to be associated with increased CVD risk.5 Much of the increased CVD risk observed in patients undergoing ART is related primarily to the effects of ART on traditional CVD risk factors; however, direct effects of ART on the vasculature and other inflammatory, immune, and viral factors associated with HIV infection may also contribute to increased CVD risk.5,7,8 A central tenet of preventing CVD is that the intensity of risk-reducing interventions should be based on the level of CVD risk.9 Patients with established CVD are at the highest risk and qualify for the most aggressive risk factor management, with special focus on interventions that have been proven to prevent cardiovascular death, myocardial infarction, and stroke. For patients without established CVD, management is based on the presence of risk factors for developing complications of CVD, such as death, myocardial infarction, and stroke9–12 (see Working Group 4, Screening and Assessment of Coronary Heart Disease in HIV-Infected Patients). The intensity of CVD risk-reducing therapy, however, must be modified by the context of the patient’s overall health. This is an especially important consideration in patients with HIV infection, who often have competing morbidities that may be as likely to …

Screening and Assessment of Coronary Heart Disease in HIV-Infected Patients

Human immunodeficiency virus (HIV)–infected individuals are living longer in the era of antiretroviral therapy. As a result, they are increasingly prone to the development of concomitant chronic disease. Coronary heart disease (CHD) is the leading cause of death in the United States and Europe. Recent studies suggest that CHD rates may be increasing among HIV-infected patients (see Epidemiological Evidence for Cardiovascular Disease in HIV-Infected Patients and Relationship to Highly Active Antiretroviral Therapy, Working Group 2), and thus appropriate screening strategies for CHD in this population are needed. Recently, approaches to screening and assessment of cardiovascular disease (CVD) in HIV-infected individuals were discussed at a State of the Science Conference. Although insufficient evidence now exists to recommend a screening strategy for CHD in HIV that differs from that recommended in the non-HIV population, emerging risk factors and surrogate markers for atherosclerosis unique to the HIV population suggest specific strategies that may be useful in this population. Two broad screening categories are discussed here. The first screening strategy seeks to define the pretest likelihood of disease by identifying the presence of predisposing risk factors such as hypertension, elevated serum cholesterol, cigarette smoking, and physical inactivity. The second screening strategy aims at the detection of established CHD, even in its earliest stages. The currently available recommendations and guidelines for screening for the presence of cardiovascular risk factors in the general, non–HIV-infected population are detailed in Table 1.1–7 View this table: Table 1. Recommendations and Guidelines for Screening for Cardiovascular Risk Factors in the General Population The currently available recommendations and guidelines for screening for the presence of CVD risk factors in persons with HIV infection are detailed in Table 2. These recommendations take into account the evidence for dyslipidemia, insulin resistance, and changes in body fat distribution that have been shown to occur …

Coronary heart disease in HIV-infected patients

Increased risk of coronary heart disease has emerged as a long-term concern among HIV-infected patients receiving antiretroviral therapy. HIV-infected patients may have modifiable risk factors for heart disease that are associated with HIV itself, antiretroviral therapy, or factors unrelated to HIV. Dyslipidemia, insulin resistance, and diabetes mellitus are often multifactorial in origin. Patients with lipodystrophy frequently have a constellation of metabolic changes that may predispose them to accelerated atherosclerosis. There is also concern about contributions of chronic inflammation and prothrombotic tendencies in the pathogenesis of coronary heart disease in the HIV-infected population. Several epidemiological studies support an increased relative risk of myocardial infarction in HIV-infected patients on highly active antiretroviral therapy. Although absolute risk appears low in the short term, patients may accrue significant risk over time. Clinicians are advised to assess coronary heart disease risk in HIV-infected patients and to intervene to reduce the impact of modifiable risk factors.

Coronary heart disease in HIV-infected patients in the highly active antiretroviral treatment era.

To assess the incidence and the clinical features of coronary heart disease in HIV-infected patients. To assess atherosclerosis risk factors in this population. A review of our experience consisting of 16 patients with acute myocardial infarction (AMI) was the basis of our retrospective analysis of two cohorts in France. Incidence was compared with the national database on the incidence of AMI in the general population. Incidence appears to be between 5 and 5.5 per 1000 person-years among HIV-infected patients. This accounts for at least a threefold increase in incidence (1.52 per 1000 person-years reported in the Monica database registry in France). Age of onset of AMI in HIV-infected patients (younger than 50 years in most cases) is a point of major concern and is an indirect way to confirm the increased incidence. AMI was typically of sudden onset without prior history of angina pectoris. Treatment and prognosis of AMI in this population has no specificity. Patients with coronary heart disease present several risk factors such as tobacco smoking, hypertension, diabetes mellitus and low high-density lipoprotein level. The links between AMI and protease inhibitor exposure is still a matter of debate, and longer duration of follow-up is needed in order to reach any conclusion. Coronary heart disease is of a higher than expected incidence in HIV-infected patients. The limitation of risk factors (mainly tobacco smoking) is a new challenge. An adaptation of the Framingham score is necessary to state the individual risk. Prospective, controlled studies are necessary to assess new strategies such as the role of statins and switching therapeutic regimens.

Thiazolidinediones could improve endothelial dysfunction and risk of premature coronary heart disease in HIV-infected patients.

The use of Human Immunodeficiency Virus (HIV) protease inhibitors as part of the Highly Active Antiretroviral Therapy (HAART) is associated with atherogenic dyslipoproteinemia, insulin resistance, hypertension and endothelial dysfunction, all of which contribute to premature coronary heart disease. These abnormalities appear to be associated with an increase in cardiovascular events in HIV-infected patients. Beneficial metabolic effects of anti-diabetic agents used in HIV-infected patients have been reported. The thiazolidinediones (TZDs), a new group of antidiabetic drugs, may modulate the proliferative and inflammatory cascades involved in atherosclerosis. Thus, an increasing totality of evidence suggests that TZDs may represent a unique and powerful research tool to find a common denominator underlying the pathophysiology and treatment of the metabolic cardiovascular risk factors associated with HIV infection.

Drugs and cardiotoxicity in HIV and AIDS.

The advent of potent antiretroviral drugs in recent years has had an impressive impact on mortality and disease progression in HIV-infected patients, so that issues related to long-term effects of drugs are of growing importance. Hyperlipidemia, hyperglycemia, and lipodystrophy are increasingly described adverse effects of highly active antiretroviral therapy (HAART), in particular when protease inhibitors are used. Hyperlipidemia is strikingly associated with the use of most available protease inhibitors, with an estimated prevalence of up to 50%. Because of the short observation period and the small number of cardiovascular events, epidemiological evidence for an increased risk of coronary heart disease in HIV-infected patients treated with HAART is not adequate at present; however, it is likely that shortly more data will accumulate to quantify this risk. Before starting HAART and during treatment it is reasonable to evaluate all patients for traditional coronary risk factors, including lipid profile. Among the drugs that are currently used in HIV+ patients, antibacterials, antifungals, psychotropic drugs and anti-histamines have been associated with QT prolongation or torsade de pointe, a life-threatening ventricular arrhythmia. Among the risk factors that may precipitate an asymptomatic electrocardiographic abnormality into a dangerous arrhythmia is the concomitant use of drugs that share the CYP3A metabolic pathway. Since most protease inhibitors are potent inhibitors of CYP3A, clinicians should be aware of this potentially dangerous effect of HAART. Anthracyclines are potent cytotoxic antibiotics that have been widely used for the treatment of HIV-related neoplasms. Their cardiotoxicity is well known, ranging from benign and reversible arrhythmias to progressive severe cardiomyopathy. The increased survival and quality of life of HIV+ patients emphasize the importance of a high awareness of adverse drug-related cardiac effects.