Objectives: HIV-infected population may have increased risk of cardiovascular disease. The prevalence of traditional cardiovascular disease risk factors such as hypertension, diabetes and dyslipidemia in HIV-infected individuals has made it difficult to assess the direct effects of HIV and immune factors on endothelial dysfunction and associated increased risk of atherosclerosis. The purpose of this study was to investigate indicators of endothelial dysfunction in an HIV cohort without hypertension and diabetes. Methods: We studied 19 HIV-infected patients between the ages of 25–76 years old with effectively suppressed viral load and without diagnosis of hypertension or diabetes. Endothelial function was measured by digital thermal monitoring of vascular reactivity using the VENDYS technique. Endothelial function was reported as vascular reactivity index. Systolic blood pressure and diastolic blood pressure at the time of VENDYS test were measured and latest lipid panels were recorded. The association between vascular reactivity index and CD4-T cells count, different antiretroviral therapy types (non-nucleoside reverse transcriptase, nucleoside reverse transcriptase, protease inhibitors, integrase inhibitors), vitamins use, systolic blood pressure, diastolic blood pressure, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol was investigated. Results: Mean vascular reactivity index was 1.87 ± 0.53. Vascular reactivity index, marker of endothelial dysfunction, showed a significant correlation with lower nadir CD4 count (p = 0.003) as well as low-density lipoprotein cholesterol (p = 0.02). No additional significant correlation between vascular reactivity index and the rest of the investigated variables was found. Conclusion: Vascular reactivity index, a clinical predictor of endothelial dysfunction, is associated with lower nadir CD4-T cell and low-density lipoprotein cholesterol in HIV-infected men with no history of hypertension or diabetes and before clinical evidence of cardiovascular disease.

Several factors contribute to the risk of percutaneous coronary intervention (PCI) related major entry site complications (MES). We sought to examine the trends in MES among unselected patients during the stent era. Data from the Dynamic Registry including five distinct recruitment waves from 1997 to 2006 (N=10,932) were used to assess baseline characteristics and MES among consecutive patients undergoing PCI. MES was defined as bleeding requiring transfusion, pseudoaneurysm, arterial thrombosis or dissection, vascular complication requiring surgery, or retroperitoneal bleed. Uncomplicated hematomas were not included. Several trends were observed in baseline characteristics including an increase from wave 1 to wave 5 in BMI >30 kg/m2 (30.2% to 40.4%), renal disease (3.5% to 9.1%), diabetes (28.0% to 34.1%), and hypertension (59.4% to 78%) (ptrend <0.001 for all). Use of a thienopyridine increased significantly from wave 1 (49.7%) to wave 5 (84%) whereas glycoprotein (GP) IIbIIIa inhibitor use peaked in wave 3 (53.1%) and then decreased (p<0.001). Access site was predominately femoral but radial access increased over time (0.3% wave 1, 6.6% wave 5) (p=<.0001). The rates of MES (2.8% to 2.2%, ptrend =0.01) and MES requiring transfusion (2.0% to 0.74%, ptrend <0.001) were low and decreased with time. The trend in lower risk for MES in later time periods remained after adjustment. In conclusion, MES has decreased over time however opportunity for bleeding avoidance strategies still exists.

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Background: Nadir CD4 T-cell count is a predictor of negative outcomes in HIV -infected patients and strongly correlates with WHO disease staging. There is lack of data pertaining the relationship between vascular function and nadir CD4 in patients without risk factors of hypertension and diabetes. Therefore we investigated the association between low nadir CD4 T-cells and endothelial function in these otherwise cardiovascular healthy patients. Methods: We conducted a study of 19 HIV-infected men on antiretroviral therapy with undetectable plasma RNA levels without hypertension or diabetes. Vascular reactivity index (VRI), a marker for vascular endothelial function, was measured via VENDYS technique using temperature rebound in response to hyperemic blood flow and vasodilation to the forearm following a 5-minute cuff occlusion of the brachial artery. Results: VRI showed a significant correlation with low nadir CD4 count (p = 0.019) (Figure 1). Lower CD4 counts were associated with significant endothelial dysfunction. We examined the effect of potential mediators on such association. No significant correlation was found with LDL-C (p=0.60), HDL-C (p=0.59), systolic and diastolic blood pressures (p=0.12 and 0.13) or history of smoking (p=0.55) with VRI in the studied HIV cohort. Conclusion: Low nadir CD4 count remained independently associated with vascular reactivity index and thus a significant clinical predictor of endothelial dysfunction in HIV infected patients with no history of hypertension or diabetes even before clinical evidence of cardiovascular disease. Vascular Reactivity Index vs CD4 Nadir(Figure1).