Progression of coronary artery disease in a HIV-infected patient previously treated for ascending aorta aneurysm

The pathophysiology of increased cardiovascular risk in HIV infection is complex and multifactorial but chronic inflammation and immune activation seem to play a crucial role. Direct effects of HIV, leakage of bacteria from the gut, damage of lymphoid tissues as well as co-infections are responsible for the activation of the immune system [1], resulting in pro-inflammatory and pro-thrombotic status [2]. Pro-inflammatory high density lipoprotein (HDL) is dysfunctional with high redox activity and easy non-calcified coronary atherosclerotic plaque rupture [3]. Endothelial and macrophage cell function is significantly impaired. Some antiretroviral agents (either directly or via associated dyslipidemia and insulin resistance) may also contribute to the increased rate of cardiovascular disease in HIV and therefore require careful selection according to the underlying cardiovascular risk factors.
A 35-year-old man was diagnosed (02.09.2009) with syphilis and HIV infection classified as stage A3. The patient was a cigarette smoker and had arterial hypertension and a family history of coronary artery disease (CAD). Combined antiretroviral therapy (cART) was composed of lamivudine, abacavir atazanavir and ritonavir. One year later atazanavir was replaced with darunavir due to potential drug-to-drug interaction with protein pump inhibitor (PPI). The patient remained asymptomatic and HIV RNA was undetectable. The CD4 T lymphocyte count was 386 cells/l.
Due to exercise capacity impairment control transthoracic echocardiography (TTE) was performed and revealed: aneurysm of the ascending aorta with maximal diameter 60 mm, aortic bulb 50 mm, aortic annulus 26 mm with good left ventricular ejection fraction (LVEF) – 66%. The aortic valve function was preserved. Preoperative coronarography revealed no significant atherosclerosis in coronary vessels. Initial lipid profile revealed hypertriglyceridemia (LDL 130 mg/dl, HDL 41 mg/dl, TG 240 mg/dl). Lipid-lowering therapy was initiated (atorvastatin 40 mg, fenofibrate 267 mg).
Supracoronary ascending aorta replacement with a vascular prosthesis (Vascutek 28) and aortic commissure suspension were performed (25.03.2011) without complications. The patient was discharged on the 5th day after the surgery. The patient had outpatient check-ups regularly.
Eighteen months later (22.08.2012) the patient had lateral ST elevation myocardial infarction (STEMI). Coronary angiography revealed narrowing of the...


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