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.

CKD patients typically presented with significant endotoxemia and overt volume overload, which may contribute significantly to chronic low-grade inflammation and left ventricular dysfunction. An additive contribution from hemodialysis treatment may strongly enhance the severity of endotoxemia in HD patients.

BackgroundKidney disease is a major complication of HIV infection, with both acute kidney injury (AKI) and chronic kidney disease (CKD) contributing to morbidity and mortality. Incidence of AKI was reported as 5.9 per 100 patient years in ambulatory patients and ∼18% in hospitalized HIV-infected patients, an almost 3-fold higher risk compared with HIV uninfected patients in developed countries. CKD was reported in 6–48.5% of HIV-infected patients in Africa. There is a paucity of data regarding the prevalence and outcomes of AKI in HIV-infected patients in sub-Saharan Africa, the region most affected by HIV.MethodsA retrospective review of 101 HIV-positive anti-retroviral therapy (ART)-naïve patients presenting with renal failure from 1 October 2005 to 30 September 2006 was undertaken.ResultsA total of 684 patients presented with renal failure, 101 (14.8%) of whom were HIV positive. Ninety-nine (98%) of HIV-positive patients were black and 56 (55%) were male, with mean age 38 ± 9.9 years (range 21–61 years). HIV-positive patients demonstrated severe immunosuppression, with mean CD4 count of 135 cells/µL (range 1–579 cells/µL). Fifty-seven (56%) HIV-positive patients presented with AKI, 21 (21%) with acute-on-chronic kidney disease and 23 (23%) with CKD; seven patients with AKI were excluded due to lack of records. The causes of AKI in the HIV-positive group included sepsis (60%), volume depletion and haemodynamic instability (19%), toxins (9%), urological obstruction (7%) and miscellaneous (14%). Forty-four per cent of HIV-positive and 47% of HIV-negative patients with AKI demised; P = 0.45. Hyponatraemia (P = 0.018), acidosis (P = 0.018), anaemia (P = 0.019) and hyperphosphataemia (P = 0.003) were predictors of mortality in HIV-positive patients with AKI. In comparison, predictors of mortality in the HIV-negative group were age (P = 0.023) and black ethnicity (P = 0.04).ConclusionHIV-positive patients, compared with the HIV-negative group, presented with AKI at a younger age and at an advanced stage of immunosuppression. Appropriate support, including dialysis, resulted in similar outcomes in both groups.

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Background Transforming growth factor-β (TGF-β) may inhibit the development of atherosclerosis. We evaluated serum levels of TGF-β isoforms concurrently with serum levels of endotoxin and various inflammatory markers. In addition, we determined if any association exists between polymorphisms in the TGF-β1 gene and atherosclerosis in South African CKD patients. Methods We studied 120 CKD patients and 40 healthy controls. Serum TGF-β1, TGF-β2, TGF-β3, endotoxin, and inflammatory markers were measured. Functional polymorphisms in the TGF-β1 genes were genotyped using a polymerase chain reaction-sequence specific primer method and carotid intima media thickness (CIMT) was assessed by B-mode ultrasonography. Results TGF-β isoforms levels were significantly lower in the patients with atherosclerosis compared to patients without atherosclerosis (p<0.001). Overall, TGF-β isoforms had inverse relationships with CIMT. TGF-β1 and TGF-β2 levels were significantly lower in patients with carotid plaque compared to those without carotid plaque [TGF-β1: 31.9 (17.2 – 42.2) versus 45.9 (35.4 – 58.1) ng/ml, p=0.016; and TGF-β2: 1.46 (1.30 – 1.57) versus 1.70 (1.50 – 1.87) ng/ml, p=0.013]. In multiple logistic regression, age, TGF-β2, and TGF-β3 were the only independent predictors of subclinical atherosclerosis in CKD patients [age: odds ratio (OR), 1.054; 95% confidence interval (CI): 1.003 – 1.109, p=0.039; TGF-β2: OR, 0.996; 95% CI: 0.994–0.999, p=0.018; TGF-β3: OR, 0.992; 95% CI: 0.985–0.999, p=0.029). TGF-β1 genotypes did not influence serum levels of TGF-β1 and no association was found between the TGF-β1 gene polymorphisms and atherosclerosis risk. Conclusion TGF-β isoforms seem to offer protection against the development of atherosclerosis among South African CKD patients.

A patient with end-stage liver disease developed stressinduced Takotsubo cardiomyopathy post liver transplantation, with haemodynamic instability requiring a left ventricular assist device. We discuss the diagnosis and management of this condition.