Epidemiologic aspects of abnormal ankle brachial index in the HIV infected population.

AIM: HIV infection is strongly associated with accelerated vascular atherosclerosis and increased cardiovascular events. The prevalence of peripheral arterial disease (PAD) in HIV infected patients is not clearly defined and the results of different reports are contradicting. OBJECTIVE: To determine the prevalence of abnormal Ankle Brachial Index (ABI) and associated risk factors in HIV infected population. METHODS: The ABI was measured manually using 5.0 MHz handheld Doppler probe in 173 HIV infected patients. The cohort was categorized according to the ABI measurements as; normal group (ABI 0.9 to 1.3), peripheral arterial disease (PAD) group (ABI<0.9), and High ABI group (ABI>1.3). Several demographic, atherosclerosis risk factors and HIV infection parameters have been evaluated as potential risk factors. RESULTS: Median age of the cohort was 49 years (inter-quartile ranges [IQR]: 42.5 to 54); 63.4% were males. Abnormal ABI was found in 47(27.2%) patients; twenty four (13.9%) had PAD and 23(13.3%) had high ABI. Among the risk factors evaluated, we observed that PAD group is associated with diabetes (Relative risk [RR]: 4.19; 95% confidence interval [CL]: 2.13 to 8.27; P=0.0002) and age above 49 (Relative risk [RR]: 3.96; 95% confidence interval [CL]: 1.56 to 10.0; P=0.002). However, the High ABI group was significantly associated with male gender (RR: 3.94; 95% CI: 1.23 to 12.70; P=0.009). CONCLUSION: HIV infection is associated with increased prevalence of abnormal resting ABI.

Comparison of platelet activation in unstable and stable angina pectoris and correlation with coronary angiographic findings.

We sought to investigate the relation between platelet activation and the angiographic evidence of ruptured plaque in patients presenting with unstable and stable angina pectoris. We prospectively enrolled 25 consecutive patients (5 women and 20 men, mean age 62 +/- 3 years), 17 with unstable angina and 8 with stable angina. Systemic venous blood samples were collected within 4 to 6 hours of admission for flow cytometry analysis. Activation-dependent epitope CD63 and glycoprotein IIb/IIIa on the platelet membrane were assayed. Fibrinogen levels were also measured. All patients with unstable angina underwent cardiac catheterization and had angiographic evidence of ruptured plaque. Of the patients with stable angina, 5 underwent coronary angiography with smooth noncomplex lesions and 3 had negative technetium-99m sestamibi stress tests. Patients with unstable angina were characterized by 39% higher levels of fibrinogen than patients with stable angina (423 +/- 304 vs 304 +/- 51 mg/dl, p = 0.004). The percentage of platelets positive for the activation-dependent epitope CD63 was 5 times higher in patients with unstable than stable angina (14.6 +/- 5.6% vs 2.75 +/- 1.6%, p = 0.0026). They also had a 15% higher expression of their glycoprotein IIb/IIIa (517 +/- 79 vs 449 +/- 50 mean fluorescence intensity, p = 0.038). Thus, this study establishes a direct relation between the morphology of ruptured plaque and platelet activation in patients with unstable angina. This may allow for further risk stratification. Patients with unstable complex lesions had a fivefold higher expression of the platelet activation epitope CD63 than patients with stable angina. Furthermore, they had 15% more glycoprotein IIb/IIIa aggregation sites expressed on their platelet membrane, thus indicating an intense thrombogenic potential.

Restoration of patency of left internal mammary artery graft with progression of the underlying left anterior descending coronary artery disease.

The use of the left internal mammary artery (LIMA) to graft a borderline lesion in the left anterior descending coronary artery (LAD) has been associated with distal narrowing and occlusion of the LIMA. We present a patient in whom the LIMA occluded 1 year after coronary artery bypass, but was found to be fully patent 4 years later, after progression of the native LAD disease.