Abstract
Highly active antiretroviral therapy has greatly reduced AIDS-related morbidity and mortality; however, its widespread use has been associated with a marked rise in the frequency of cardiovascular diseases in patients with HIV. Moreover, HIV infection is associated with accelerated coronary atherosclerosis and vasculopathy, although the mechanisms underlying these findings have not been determined. We describe the case of a 45-year-old woman with HIV/HCV coinfection, irritable bowel syndrome, and accelerated progression of coronary atherosclerosis after execution of percutaneous coronary intervention (PCI). In this case, the rapidity of progression of atherosclerosis seems linked principally to chronic inflammation and excess immune activation that can depend by a concourse of factors (chronic C hepatitis, irritable bowel syndrome, PCI execution) not directly associated with traditional risk factors. Caregivers following HIV-infected patients should be aware of the increased risk of accelerated atherogenesis in these subjects, principally in case of presence of causes of intense immune activation.
1
Introduction
Widespread use of antiretroviral therapy has caused a remarkable decline in rates of morbidity and death related to AIDS and has effectively made HIV infection a manageable, although not yet curable, chronic condition. Anyway, HIV-infected patients receiving combination antiretroviral therapy may experience metabolic complications (i.e., dyslipidemia, impaired glucose metabolism, and abnormal body fat distribution), potentially increasing their risk of coronary heart disease . Both traditional and nontraditional risk factors, including HIV exposure, immune activation, and inflammation appear to contribute to the high rate of major cardiovascular events . Furthermore, the cardiovascular risk assessment based on conventional risk prediction models (Framingham, PROCAM, SCORE) does not offer a good predictive value for the HIV-positive population . In fact it has been reported in the literature that in an asymptomatic population of HIV-positive subjects, coronary computed tomography revealed an unexpectedly overall prevalence of coronary plaques . HIV infection is associated with a marked rise in the frequency of cardiovascular diseases and with accelerated coronary atherosclerosis and vasculopathy.
On these basis, recently, an increasing number of HIV patients undergo invasive cardiovascular procedures. Although percutaneous coronary intervention (PCI) is frequently used to treat coronary artery disease in HIV, little is known regarding PCI outcomes.
2
Case report
We describe the case of a 45-year-old woman with HIV/HCV coinfection, irritable bowel syndrome and accelerated progression of coronary atherosclerosis after execution of PCI. The patient was an ex-drug abuser and was affected by irritable bowel syndrome. From 2005 her antiretroviral regimen consisted of abacavir+lamivudine+lopinavir/r with a persistent undetectable HIV-RNA and a good recover of CD4+ (647 cells/mmc). The risk of presenting a fatal cardiovascular event according to the Framingham risk score was 8%, almost similar to the expected risk for the general population. Metabolic and anthropometric parameters were normal but blood tests revealed high-sensitivity C-reactive protein (hs-CRP), high haematic leptin, and low adiponectin levels; moreover, elevated plasma levels of lipopolysaccharide (LPS) were also found. In December 2007, due to atypical chest pain, the patient underwent cardiologic examination: electrocardiogram (ECG) and myocardiospecific enzyme monitoring were within normal ranges. A coronary computed tomographic (CT) scan with spiral multilayer technique revealed severe stenosis (73%) of the medium third of the circumflex artery due to a concentric atheromatous plaque of mixed density, but no significant alterations were found on other tract of other coronary vassals ( Fig. 1 ). In January 2008, coronarography confirmed the CT scan report and percutaneous revascularization using coronary stent was performed. The lesion was treated with drug-eluting stents (Biosensors, Biomatrix DES).
Following cardiologic evaluation, the patient was started on antiagregants, beta-blockers, and nitrates; moreover, antiretroviral therapy was changed to a cardiovascular safe antiretroviral drug combination of atazanavir+tenofovir/emtricitabine. At 3 months of follow-up, no significant abnormalities were found on ECG and echocardiography monitoring. The immunological and virological responses to antiretroviral therapy were good (CD4+ 684 cells/mmc, undetectable HIV-RNA) and metabolic values were normal. In June 2008, the patient complained of symptoms which were suggestive of exertion angina; coronary CT scan revealed an unexpected presence of new lesions that were not present before. There was a right dominant coronary artery with a long concentric atheromatous plaque of soft density that determined a lumen stenosis of 65%. The first branch of the obtuse margin had a mixed density plaque that determined a lumen stenosis of 70%. This clinical situation was confirmed by a subsequent coronarographic exam that gave indications for the execution of a new coronary stent procedure ( Fig. 2 ).
2
Case report
We describe the case of a 45-year-old woman with HIV/HCV coinfection, irritable bowel syndrome and accelerated progression of coronary atherosclerosis after execution of PCI. The patient was an ex-drug abuser and was affected by irritable bowel syndrome. From 2005 her antiretroviral regimen consisted of abacavir+lamivudine+lopinavir/r with a persistent undetectable HIV-RNA and a good recover of CD4+ (647 cells/mmc). The risk of presenting a fatal cardiovascular event according to the Framingham risk score was 8%, almost similar to the expected risk for the general population. Metabolic and anthropometric parameters were normal but blood tests revealed high-sensitivity C-reactive protein (hs-CRP), high haematic leptin, and low adiponectin levels; moreover, elevated plasma levels of lipopolysaccharide (LPS) were also found. In December 2007, due to atypical chest pain, the patient underwent cardiologic examination: electrocardiogram (ECG) and myocardiospecific enzyme monitoring were within normal ranges. A coronary computed tomographic (CT) scan with spiral multilayer technique revealed severe stenosis (73%) of the medium third of the circumflex artery due to a concentric atheromatous plaque of mixed density, but no significant alterations were found on other tract of other coronary vassals ( Fig. 1 ). In January 2008, coronarography confirmed the CT scan report and percutaneous revascularization using coronary stent was performed. The lesion was treated with drug-eluting stents (Biosensors, Biomatrix DES).
Following cardiologic evaluation, the patient was started on antiagregants, beta-blockers, and nitrates; moreover, antiretroviral therapy was changed to a cardiovascular safe antiretroviral drug combination of atazanavir+tenofovir/emtricitabine. At 3 months of follow-up, no significant abnormalities were found on ECG and echocardiography monitoring. The immunological and virological responses to antiretroviral therapy were good (CD4+ 684 cells/mmc, undetectable HIV-RNA) and metabolic values were normal. In June 2008, the patient complained of symptoms which were suggestive of exertion angina; coronary CT scan revealed an unexpected presence of new lesions that were not present before. There was a right dominant coronary artery with a long concentric atheromatous plaque of soft density that determined a lumen stenosis of 65%. The first branch of the obtuse margin had a mixed density plaque that determined a lumen stenosis of 70%. This clinical situation was confirmed by a subsequent coronarographic exam that gave indications for the execution of a new coronary stent procedure ( Fig. 2 ).
