More than two-thirds of the burden of HIV-associated heart disease was found in sub-Saharan Africa and Asia Pacific regions, the study found. In some parts of the world, HIV ranks alongside better-known risk factors -- such as diet and lifestyle -- as a major cause of heart disease. There are more than 35 million people infected with HIV worldwide, a figure that is steadily increasing.
HIV infection doubles risk of heart disease -- ScienceDaily
Those infected are now more likely to die from chronic diseases, such as cancer or cardiovascular disease, because life-saving medications can keep the virus in check. The link between HIV and heart disease is poorly understood. Scientists think the virus may cause inflammation of blood vessels, which puts pressure on the cardiovascular system.
The virus is also thought to raise fat levels in the blood and affect the body's ability to regulate sugar levels, which may also contribute to heart disease. Dr Anoop Shah, Clinical Lecturer in Cardiology at the University of Edinburgh, said: "This study has important implications when planning cardiovascular preventative policies in low resource countries where the burden of HIV remains high and that of cardiovascular disease is growing. This news will have major public health implications globally, but particularly in developing countries in Africa where the burden of HIV is higher.
But, with an ageing population, the number of people living with more than one disease will continue to rise. It's essential we build our understanding of the interplay between conditions so we can give patients the best treatments and advice. Materials provided by University of Edinburgh. Note: Content may be edited for style and length.
Science News. Story Source: Materials provided by University of Edinburgh. Journal Reference : Anoop S. Longenecker, Fiona E. Newby, David A. McAllister, Nicholas L. CMR balanced steady state free precession images showing A 4-chamber view, B 2-chamber view, and C a mid-ventricular short-axis image; and D late gadolinium enhancement image showing linear mid-wall enhancement in a patient diagnosed with HIV-associated cardiomyopathy.
Coronary Heart Disease in HIV/AIDS: Confronting 2 Major Health Issues
A phenotype of HIV-associated heart muscle disease with normal chamber size and mildly impaired systolic function increases risk of heart failure, even in the absence of coronary artery disease [ 48 ]. Left ventricular dysfunction associated with HIV is often clinically silent but may progress to symptomatic heart failure. In addition, diastolic dysfunction is considered an early marker of coronary artery disease in HIV uninfected patients without cardiac symptoms and preserved systolic function [ 51 ]. Diastolic dysfunction in HIV is associated with longer duration of HIV infection, higher body mass index and exposure to zidovudine [ 52 , 53 ].
In these studies, diastolic dysfunction has been associated with elevated body mass, total cholesterol, hypertension, smoking and viral load. CMR cine tagging using spatial modulation of magnetisation in a short axis image through the mid left ventricle at end-diastole a and at end-systole B in a patient infected with HIV. Tagging for strain and strain rate imaging in circumferential, longitudinal and radial directions is one of the main techniques for assessment of diastolic dysfunction with CMR.
Myocardial fibrosis an important reason of development and progression systolic and diastolic cardiac failure [ 55 ]. Diffuse myocardial fibrosis estimated by extracellular volume ECV calculation was also found to be elevated in HIV infected individuals [ 56 ]. Late post gadolinium images showing mid-wall focal fibrosis in the basal inferolateral wall in a 3-chamber view and in the lateral wall in B short-axis white arrows depict the fibrosis. Cardiovascular magnetic resonance spectroscopy studies have reported increased incidence of myocardial lipidosis in HIV infected patients receiving ART, even in the absence of cardiovascular symptoms [ 22 , 25 ].
In these studies, steatosis was associated with elevated serum lipid levels, duration of ART use and impaired strain. Primary pulmonary arterial hypertension is rare in HIV infected persons, with a prevalence of 0. The pathogenesis of HIV-associated pulmonary arterial hypertension is poorly understood, with inflammatory and genetic factors both implicated [ 59 ].
Pulmonary hypertension in HIV occurs without documented thromboembolic disease, intravenous drug use or pulmonary infections [ 57 , 58 ]. In a study of 47 patients in the Swiss Cohort Study, patients receiving ART had a significantly decreased median right ventricular systolic pressure over right atrial pressure gradient compared to patients who did not receive ART [ 60 ]. Histologically, HIV-associated pulmonary arterial hypertension manifests most commonly as a plexogenic pulmonary arteriopathy, but thrombotic pulmonary arteriopathy and pulmonary veno-occlusive disease also described [ 62 ].
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Pericardial effusion and pericarditis are encountered frequently in patients with HIV infection. However, in the ART era, the incidence of pericardial effusions in HIV is much less: in a multicentre cohort study of treated HIV patients, only 2 of HIV infected patients had pericardial effusions, neither clinically important [ 64 ].
Using CMR with greater resolution, our group has demonstrated the prevalence of small, asymptomatic pericardial effusions to be much higher [ 23 ]. While generally nonspecific, pericardial effusions may indicate active inflammation and may be associated with subclinical myocarditis or disseminated tuberculosis, particularly in patients with low CD4 cell counts. In patients with large pericardial effusions, Mycobacterium tuberculosis is likely pathogen, especially in tuberculosis endemic regions [ 65 ].
In HIV, tuberculous pericarditis is commonly associated with heart failure [ 67 ]. HIV is associated with reduced incidence of pericardial constriction [ 68 ]. Mortality of pericardial effusions in HIV-infected patients is based on the severity and aetiology of the disease, especially if associated with tuberculosis [ 69 ]. We have demonstrated more frequent myocardial fibrosis in HIV-associated pericardial constriction when compared to those without HIV infection [ 35 ].
Prednisone does not reduce mortality in tuberculous pericarditis, but has been shown to be associated with reduced hospitalisation and constriction, but with increased risk of malignancies in those with HIV infection [ 70 ]. The epidemiology and clinical profile of infective endocarditis in HIV infection are the same as in uninfected individuals [ 73 ]. The one setting where HIV is associated with increased risk of infective endocarditis is intravenous drug abuse. Staphylococcus aureus, Streptococcus viridans and Salmonella species are the most common organisms and the tricuspid valve is most involved in intravenous drug users developing infective endocarditis [ 74 , 75 ].
Nonbacterial marantic endocarditis has been described in HIV, usually clinically silent and manifests with large, friable, sterile vegetations on the cardiac valves, which can lead to pulmonary embolization [ 75 ].
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Patients with low CD4 counts have a poorer prognosis when they develop infective endocarditis [ 76 ]. Rates of infective endocarditis have decreased with the advent of ARV therapy [ 76 ]. When intravenous drug use is excluded, HIV infection has not been shown to be a risk factor for infective endocarditis [ 77 ].
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Different factors related to HIV can lead to development atherosclerosis, including immune dysfunction, proliferation of T-cells, inflammation, endothelial dysfunction, and lipid abnormalities [ 79 , 80 ]. During atherogenesis, HIV promotes monocyte penetration of the vascular intima to promote secretion of cytokines and expression of endothelial cell adhesion molecules [ 81 ].
Higher number of activated CD8 T-cells is observed in relation to increased rates of coronary artery plaque and carotid artery stiffness [ 84 ]. In the early stage of HIV infection both total cholesterol and high-density lipoprotein cholesterol are decreased [ 85 ]. Lower levels of apolipoprotein B and smaller low-density lipoprotein cholesterol have been reported in more advanced stages of HIV infection [ 86 ].
In addition, deleterious metabolic effects such as dyslipidaemia and insulin resistance after exposure to certain ART treatments have been reported [ 79 ]. Recent studies observed that HIV infected patients presented with large thrombus burden than atherosclerotic plaques suggesting de novo arteriothrombosis and thrombophilia as possible causes of CAD events [ 87 , 88 ]. Cardiac malignancy usually manifests late in HIV disease. Non-Hodgkin lymphoma occurs 25—60 times more in HIV infected patients [ 90 ].
Cardiac lymphoma can infiltrate the myocardium, the subendocardial layer or be located within pericardial effusion [ 90 ].
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Clinical features include dyspnoea, right-sided heart failure, heart failure, chest pain and arrhythmia. Presentations range from asymptomatic to cardiac tamponade, myocardial infarction, heart failure or conduction abnormalities [ 91 ]. The incidence of non-Hodgkin lymphoma is not related to the level of immunosuppression and has not changed with ART use [ 92 ]. HIV-associated CVD encompasses heterogeneous disorders and has the propensity to involve every segment of the cardiovascular axis. We have described important recent developments and perspectives based on a systematic analysis of the important advances in this field.
This manuscript is not funded. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers.
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