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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus (HIV) infection is associated with accelerated atherosclerosis and vasculopathy, although the mechanisms underlying these findings have not been determined. Hypotheses for these observations include: 1) an increase in the prevalence of established cardiac risk factors observed in HIV-infected individuals who are currently experiencing longer life expectancies; 2) the dyslipidemia reported with certain HIV anti-retroviral therapies; and/or 3) the proinflammatory effects of infiltrating HIV-infected monocytes/macrophages. An unexplored possibility is whether HIV itself can infect vascular smooth muscle cells (SMCs) and, by doing so, whether SMCs can accelerate vascular disease. Our studies demonstrate that human SMCs can be infected with HIV both in vivo and in vitro. The HIV protein p24 was detected by fluorescence confocal microscopy in SMCs from tissue sections of human atherosclerotic plaques obtained from HIV-infected individuals. Human SMCs could also be infected in vitro with HIV by a mechanism dependent on CD4, the chemokine receptors CXCR4 or CCR5, and endocytosis, resulting in a marked increase in SMC secretion of the chemokine CCL2/MCP-1, which has been previously shown to be a critical mediator of atherosclerosis. In addition, SMC proliferation appeared concentric to the vessel lumen, and minimal inflammation was detected, unlike typical atherosclerosis. Our data suggest that direct infection of human arterial SMCs by HIV represents a potential mechanism in a multifactorial paradigm to explain the exacerbated atherosclerosis and vasculopathy reported in individuals infected with HIV.
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PMID:Human immunodeficiency virus (HIV) infects human arterial smooth muscle cells in vivo and in vitro: implications for the pathogenesis of HIV-mediated vascular disease. 1831 May 3

Human immunodeficiency virus (HIV) infection causes stroke through several mechanisms. Stroke results from opportunistic infection and neoplasia, HIV induced cardiac disease, HIV associated cerebral vasculopathy, and perhaps of HIV induced facilitation of some forms of systemic vasculitis and prothrombotic haematological conditions. HIV causes more ischaemic stroke than cerebral haemorrhage. Although stroke is currently a relatively infrequent manifestation of HIV infection, the incidence of stroke in HIV infected individuals is likely to increase with current combination antiretroviral therapy. HIV infection per se induces endothelial activation and dyslipidaemia, predisposing to accelerated atherosclerosis. Antiretroviral therapy, which increases life expectancy and therefore inherently increases ischaemic stroke risk with advancing age and length of exposure to traditional risk factors, also causes pro-atherosclerotic metabolic and endothelial dysfunction. Antiretroviral induced vascular dysfunction together with pre-existing HIV induced vascular disease has the potential to increase atherosclerotic causes of ischaemic stroke. New antiretroviral agents should ideally eradicate the human immunodeficiency virus thereby reducing vascular risk and HIV related causes of stroke without inducing metabolic or endothelial dysfunction. Future studies of vascular disease in HIV infected individuals, particularly studies investigating the impact of current and future antiretroviral agents, should ideally assess stroke as a specific outcome, and provide data by pathological stroke type and ischaemic stroke subtype, to clarify the mechanisms of stroke and guide the approach to treatment and prevention of stroke.
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PMID:Human immunodeficiency virus (HIV) and stroke: targets for intervention. 2016 74

HIV/AIDS (Human immunodeficiency virus/ Acquired immuno deficiency syndrome) is a growing global problem, in terms of its incidence and mortality. Patients with HIV/AIDS are living much longer with HAART (Highly active antiretroviral therapy) therapy so much so that HIV/AIDS has now become a part of the chronic disease burden, like hypertension and diabetes. Patients with HIV/AIDS and symptoms suggestive of cardiac disease represent a diagnostic and therapeutic challenge in clinical practice; Cardiologists are more frequently encountering this problem. An algorithmic, anatomic approach to diagnosis, localizing disease to the endocardium, myocardium and pericardium can be useful. An intimate knowledge of opportunistic infections affecting the heart, effects of HAART therapy and therapy for opportunistic infections on the heart is needed to be able to formulate a differential diagnosis. Effects of HAART therapy, especially protease inhibitors on lipid and glucose metabolism, and their influence on progression to premature vascular disease require consideration. Treatment of cardiac disease, in HIV/AIDS patients can vary from non-HIV patients, based on drug interactions, differences in responsiveness, and other factors; and this area requires further research.
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PMID:Heart Disease in Patients with HIV/AIDS-An Emerging Clinical Problem. 2043 55

Extract: Pulmonary hypertension (PH) was previously termed primary (idiopathic or of unknown origin, i.e., spontaneous) or secondary (as a result of another disorder) pulmonary hypertension. It is now clear, however, that many of the entities labeled as secondary pulmonary hypertension resemble primary pulmonary hypertension in both their histopathological features and their response to treatment. For this reason, the World Health Organization (WHO) has recently classified PH into five groups on the basis of their proposed underlying mechanism. Group I in this classification, designated pulmonary arterial hypertension, is the focus of this overview. Pulmonary arterial hypertension (PAH) is defined as a sustained elevation of the pulmonary arterial pressure to greater than 25 mmHg at rest or greater than 30 mmHg following exercise, with a mean pulmonary-capillary wedge pressure (an indirect measure of left atrial pressure) of less than 15 mmHg. The entities within the category of PAH include idiopathic pulmonary arterial hypertension (IPAH; formerly, primary pulmonary hypertension), PAH associated with collagen vascular disease (e.g., in limited systemic sclerosis), portal hypertension (high pressure in the vessel that carries blood from the intestines to the liver), congenital left-to-right intra-cardiac shunts, infection with the human immunodeficiency virus (HIV), and persistent pulmonary hypertension of the newborn. The histological appearance of lung vessels in each of these conditions is similar: intimal fibrosis (formation of fibrous material in the inner lining of the blood vessel), increased medial thickness, pulmonary arteriolar occlusion (block of arterioles [the vessels that join the arteries and capillaries] in the lung), and plexiform (web-like) lesions predominate.
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PMID:Mechanism of disease: Pulmonary hypertension. 2070 29

Thrombophilias, an inherited and/or acquired predisposition to vascular thrombosis beyond hemostatic needs are common in cardiovascular medicine and include systemic disorders such as coronary atherosclerosis, atrial fibrillation, exogenous obesity, metabolic syndrome, collagen vascular disease, human immunodeficiency virus, blood replacement therapy and several commonly used medications. A contemporary approach to patients with suspected thrombophilias, in addition to a very selective investigation for gain-of-function and loss-of-function gene mutations affecting thromboresistance, must consider prevalent diseases and management decisions encountered regularly by cardiologists in clinical practice. An appropriate recognition of common disease states as thrombophilias will also stimulate platforms for much needed scientific investigation.
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PMID:A clinical cardiology perspective of thrombophilias. 2071 34

Cardiovascular abnormalities were appreciated early in the epidemic of the acquired immunodeficiency syndrome (AIDS), even before the aetiological agent, human immunodeficiency virus (HIV) was isolated and characterised. The aetiology and pathogenesis of cardiovascular disease in HIV infection is still the subject of intense speculation, and is likely multi-factorial. HIV affects every aspect of the cardiac axis, causing pericarditis, myocarditis, cardiomyopathy, coronary artery disease and microvascular dysfunction, valvular heart disease, pulmonary vascular disease and pulmonary hypertension, stroke and peripheral vascular disease. HIV-associated vasculopathy is an increasingly recognised clinical entity, causing high morbidity and increasing mortality in southern Africa, particularly from stroke and cardiovascular disease. HIV causes disease of the vascular tree, either by a direct effect on vascular or perivascular tissue, or indirectly via immune complex-mediated mechanisms, associated opportunistic infections and malignancies. As a result, highly active antiretroviral therapy (HAART) may have an important role in controlling disease progression. We report a case of histologically defined primary HIV vasculopathy in which the chance to start HAART was initially missed and in which the patient progressed to require bilateral amputations, but obtained disease quiescence upon commencement of HAART.
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PMID:Progressive human immunodeficiency virus-associated vasculopathy: time to revise antiretroviral therapy guidelines? 2188 85

Cardiovascular complications are more common in human immunodeficiency virus-infected individuals than in age-matched uninfected individuals. Antiretroviral therapy reduces the risk of cardiovascular complications, suggesting that viral replication directly or indirectly causes vascular disease. Long-term effective antiretroviral therapy does not fully restore vascular health, and treated adults continue to have higher-than-expected rates of disease progression. Although this excess risk during therapy is likely due to multiple factors, a growing body of evidence suggests that chronic inflammation, which persists during effective antiretroviral therapy, is directly and causally associated with vascular dysfunction and the accelerated development of atherosclerosis.
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PMID:Immunologic basis of cardiovascular disease in HIV-infected adults. 2257 11

Pathogenesis of atherosclerosis involves multiple mechanisms, including imbalanced lipid metabolism, disturbed equilibrium of the immune response, and chronic inflammation of the artery wall. Several reports have shown a relationship between the development of atherosclerosis and the presence of infectious diseases, widely occurring in the general population, often chronic and/or asymptomatic. Beyond Chlamydia pneumoniae, a large number of infectious agents have been linked with an increased risk of vascular disease, with variable strength of supporting data: Porphyromonas gingivalis, Helicobacter pylori, influenza A virus, herpes virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. Infections may contribute to atherosclerosis either via direct infection of vascular cells or via the indirect effects of cytokines or acute phase proteins induced by infection at "nonvascular" sites. More recently, investigators reported that the aggregate burden ("infectious burden") of these chronic infections, rather than the effects of a single organism, might contribute to atherosclerosis and its thrombotic complications. However, the role of infection, as a proinflammatory cause of atherosclerosis, is still debated in the literature. This article will review available data suggesting a relationship between different infective pathogens and atherothrombosis, the hypothesized mechanisms, and the potential role for antimicrobial treatment.
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PMID:The infectious burden in atherothrombosis. 2266 Sep 18

Pulmonary arterial hypertension (PAH) is a disease that leads to characteristic vascular wall remodeling and hemodynamic alterations. Consequently, this pulmonary vascular disease contributes to substantial morbidity and mortality in afflicted patients. PAH may be idiopathic in nature or associated with connective tissue disease, chronic liver disease, human immunodeficiency virus, congenital heart disease, and a growing list of other conditions. There are currently nine Food and Drug Administration-approved therapies for specific PAH treatment. Therapeutic targets include prostacyclin replacement, endothelin-1 antagonism, and phosphodiesterase-5 inhibition. This article focuses on the prostanoid treprostinil and explores its role in the management of patients with PAH.
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PMID:Clinical utility of treprostinil and its overall place in the treatment of pulmonary arterial hypertension. 2287 90

Human immunodeficiency virus (HIV) induces acquired immunodeficiency syndrome (AIDS) in humans. Neurological complications occur frequently in patients with AIDS. About 20 to 40% of all these patients develop neurological symptoms, and in about 10% of AIDS patients, the onset of the disease is characterized by neurological symptoms. These may be related to primary HIV infection or to any of a large number of opportunistic viral and non-viral infections. HIV itself induces acute HIV aseptic meningitis, HIV-1-associated neurocognitive disorder (HAND), HIV distal sensory polyneuropathy, and HIV vacuolar myelopathy. The opportunistic neurological infections are cytomegalovirus encephalitis and polyradiculomyelitis, toxoplasmosis encephalitis, cryptococcal meningitis, and progressive multifocal leukoencephalopathy. Other neurological complications are primary central nervous system lymphoma, cerebral vascular disease (CVD), and nucleoside neuropathy (NN). Among these complications, HAND, CVD, and NN are expected to have an increased incidence in the future, they may be more important complications in HIV infection.
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PMID:[Neurological complications with HIV infection]. 2347 19


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