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Obstructive sleep apnea (OSA) is associated with an increase in high-sensitivity C-reactive protein (hs-CRP). Studies suggested that the degree of severity of OSA in obese patients with no known coronary artery disease correlates with higher levels of hs-CRP and that continuous positive airway pressure (CPAP) could reduce this inflammation marker. In this study we tested the hypothesis that CPAP therapy could also reduce hs-CRP in cardiac patients with multiple comorbidities and known OSA. Sixty-two consecutive patients were included in this study. All patients were referred for a sleep test because of clinical suspicion of OSA. Clinical variables, body mass index (BMI), hs-CRP, and lipid profile were obtained at the time of their referral and at 126.2 ± 33.7 days followup. Thirty-four patients (group A) underwent CPAP therapy and 28 patients did not (group B). The linear regression of hs-CRP level on the severity of the apnea–hypopnea index (AHI) was significant (p = 0.05), but this significance is lost when ln(hs-CRP) was used (p = 0.263). Through analysis of covariance, ln(hs-CRP) was predicted by BMI (p = 0.000) (R-Sq = 46.2%). In group A, and despite a significant drop in the AHI with CPAP [median difference = −29.7 (−41.8, −22.2)], there were no significant differences in patients’ BMI, lipid profile, or hs-CRP [median difference = −0.15 (−0.83, 0.64)] (p = 0.53) on followup. When both groups A and B were compared, they had matched BMI, lipids, ejection fraction, blood pressure, age, creatinine, awake O2 saturations, alcohol consumption, coronary artery disease, and baseline and followup hs-CRP despite significant differences in baseline AHI (37.65 vs 14.30, respectively, p = 0.000). We conclude that the degree of OSA or CPAP treatment does not independently predict levels of ln(hs-CRP) in cardiac outpatients when other clinical variables, BMI, and lipids are adjusted for. BMI remains the strongest independent predictor of hs-CRP in this patient population.

Severe graft disease occurs in patients at a rate of approximately 15% within the first year of coronary artery bypass grafting (CABG). In this study, the authors examined predictors of the combined end point of death, nonfatal myocardial infarction (MI), and bypass graft disease at 2-year follow-up after CABG. One hundred twenty-one consecutive patients were included in this study after informed consent was obtained. In univariate analysis, there was a significantly (P

An acute inflammatory response occurs following percutaneous coronary and peripheral vascular interventions (PVI), partly mediated by platelet activation. Glycoprotein (GP) IIb-IIIa inhibitors might partially attenuate this inflammation rise in the coronary patient, but data in patients undergoing PVI are lacking. In the Integrilin Reduces Inflammation in Peripheral Vascular Interventions trial (INFLAME), we hypothesized that eptifibatide reduces the acute inflammatory responses following PVI. This is a single-center, randomized, open-label study of intravenous eptifibatide (180 micro/kg bolus x 2, 10 minutes apart, then 2 micro/kg/min infusion over 18 hours) and low-dose unfractionated heparin (60 Units per kg, target activated clotting time (ACT) 200-250 sec) [LDH+I group; n = 21] versus high-dose unfractionated heparin alone (100 Units per kg, target ACT 300-400 sec) [HDH group; n = 21] in patients undergoing iliac and infrainguinal interventions. The primary endpoints of the study were markers of inflammation (soluble CD-40L [sCD-40L], high-sensitivity C-reactive protein [hs-CRP] and interleukin-6 [IL-6]), thrombin generation (Fragment 1.2 [F1.2]), and fibrinogen measured at baseline and postrandomization. Markers were assayed at baseline, postdilatation at 30 minutes, 2 hours, 18 hours, 48 hours and 7 days. Mean platelet inhibition with eptifibatide was 98% (range 92-100%) using the Accumetrics Rapid Platelet Function Assay at 10 minutes after final bolus. After adjusting for baseline values, the mean +/- SE difference in sCD-40L (loge scale), hs-CRP and F1.2 between the LDH+I group and the HDH was not significant. Fibrinogen had significantly higher mean levels at 7 days for the LDH+I group (541.19 mg/dL versus 472.26 mg/dL; p-value = 0.024). IL-6 was more detectable in the LDH+I group compared to the HDH following intervention. We conclude that LDH+I combination did not reduce acute inflammatory responses as compared to HDH in patients undergoing peripheral vascular interventions.

The left internal mammary (LIMA) is an ideal conduit for bypassing the left anterior descending artery (LAD) during coronary artery bypass surgery (CABG). In this study, we evaluate the frequency of significant disease in the LIMA prior to CABG and describe associated significant lateral costal branches (1.5 mm), subclavian disease and vertebral disease. In 115 consecutive patients referred to CABG, 101 patients met the inclusion criteria. All patients who underwent routine visualization of the LIMA vessels were reviewed and quantitatively analyzed by an independent reader. Disease in the LIMA, left subclavian and vertebral arteries were graded and considered significant if lesions were50%. Lateral costal branches of the LIMA were also noted for their presence and size. Of the 101 patients, 87.1% of the LIMAs prior to surgery were without any disease. One LIMA had a 25-50% narrowing and the remaining LIMAs showed 0-25% disease. Of the LIMAs, 48.5% had lateral costal branches with diameters1.5 mm. The incidence of significant left vertebral disease and proximal subclavian disease was 37.6% and 5%, respectively. Cardiolite stress imaging post-CABG (n = 75) showed that when ischemia persisted in the anterior wall in patients with a LIMA to the LAD, this was not associated with the presence of significant LIMA disease, lateral costal branches, or subclavian disease identified pre-operatively. We conclude that the LIMA rarely shows significant disease on routine visualization prior to CABG. Asymptomatic subclavian artery disease and the presence of lateral costal branches pre-operatively did not correlate with post-CABG ischemia in the LAD territory.

Percutaneous stenting has become the procedure of choice for treatment of obstructive atherosclerotic renal artery (RA) disease. Restenosis, however, continues to be in the range of 15-25% of treated vessels. In this study, clinical and angiographic predictors of restenosis were assessed. Of 132 vessels included, fifty-eight were followed for restenosis using duplex Doppler (n=15), conventional angiogram (n=33) or multislice computed tomography (CT) angiogram (n=10). Fifteen vessels (26%) met the criteria for restenosis (lesionor =50% by conventional or CT angiography or60% by Doppler) at a follow-up range of 2-20 months (5%2 months; 68% 3-12 months; 27% 13-20 months). Cox Regression analyses were performed for selected variables. A p-value0.05 was considered statistically significant. History of smoking [odds ratio (OR), 6.6:1; p=0.005] and time to evaluate for restenosis were independent predictors of the occurrence of restenosis. Also, a high restenosis rate (40%) was seen in vesselsor =4 mm in diameter (n=20) in contrast to larger vessels (n=38)4 mm (18.4%). Although statistical significance was not reached (possibly because of the small sample size), clinically this is a significant finding. A significant drop in systolic (-15.6 mmHg) and diastolic (-6.2 mmHg) blood pressures was seen following RA stenting with no significant change in the total number of antihypertensives used (2.4 versus 2.5 for pre- and post-renal stenting, respectively).Restenosis occurred in 26% of successfully stented RAs. History of smoking, time to evaluate for restenosis and small vessels (or =4 mm) were predictors of its occurrence. Clinically, a significant drop in blood pressure was seen with RA stenting without a change in the total number of antihypertensives on follow-up.