Cytomegalovirus reactivation and colitis after left ventricular assist device placement.

We describe two patients who developed gastrointestinal bleeding due to cytomegalovirus (CMV) colitis after placement of a HeartMate II left ventricular assist device (LVAD). We aim to raise awareness of CMV colitis as a possible cause of gastrointestinal bleeding after LVAD placement and discuss potential mechanisms for CMV reactivation and areas for future research.

Elevated levels of homocysteine predict cardiovascular death, nonfatal myocardial infarction, and symptomatic bypass graft disease at 2-year follow-up following coronary artery bypass surgery.

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<.05) higher homocysteine level (11.0 ng/mol vs 9.7 ng/mol, P=.04) in patients who met the combined end point vs those who did not. There were no statistically significant differences in the following: low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and lipoprotein(a) values; age; body mass index; smoking and diabetes status; statin or aspirin use; creatinine level; hematologic markers; left ventricular ejection fraction; number of bypass grafts; and distribution of coronary artery disease. Logistic regression analysis modeling for low-density lipoprotein cholesterol, lipoprotein(a), fibrinogen, and homocysteine showed that homocysteine value (P=.016) was an independent predictor of the primary combined end point.

Eptifibatide in peripheral vascular interventions: results of the Integrilin Reduces Inflammation in Peripheral Vascular Interventions (INFLAME) trial.

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.

Routine visualization of the left internal mammary artery before bypass surgery: is it necessary?

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 were > 50%. 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 diameters > 1.5 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.

Clinical and angiographic predictors of restenosis following renal artery stenting.

UNLABELLED: 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 (lesion > or =50% by conventional or CT angiography or >60% 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-value <0.05 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 vessels < or =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). CONCLUSION: 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.

Effectiveness of statin-gemfibrozil combination therapy in patients with mixed hyperlipidemia: experience of a community lipid clinic and safety review from the literature.

This retrospective study was carried out to assess the effectiveness of statin-gemfibrozil combination therapy in a community practice lipid clinic and to review safety data from published literature. Forty-six consecutive patients received a statin and gemfibrozil combination for resistant hyperlipidemia to either agent therapy. Fasting total cholesterol (mg/dL), high-density lipoprotein cholesterol (mg/dL), and triglycerides (mg/dL) were measured. Low-density lipoprotein cholesterol (mg/dL) was calculated using the Friedewald formula if triglycerides were <400 mg/dL. Combination therapy reduced total cholesterol, low-density lipoprotein cholesterol, and triglycerides by 11% (p=0.02), 22% (p=0.049), and 39% (p=0.0002), respectively, and raised high-density lipoprotein cholesterol by 5% (p=0.3). A pooled analysis of 838 patients from the literature on statin-gemfibrozil combination therapy revealed an incidence of myositis and severe myopathy of 0.7% and 0.6%, respectively (excluding cerivastatin). We conclude that statin-gemfibrozil combination therapy is effective in significantly reducing total cholesterol, low-density lipoprotein cholesterol, and triglycerides with a trend toward raising high-density lipoprotein cholesterol in patients with hyperlipidemia resistant to either agent alone. Myositis and severe myopathy are infrequent, but not rare side effects which may be statin-specific regarding the incidence of occurrence.

In-hospital complications of peripheral vascular interventions using unfractionated heparin as the primary anticoagulant.

Unfractionated heparin is the current antithrombotic of choice in peripheral vascular interventions. The rate of in-hospital major complications during peripheral angioplasty procedures (PTA) using heparin as the primary anticoagulant has not been well defined. In this single-center study, the charts of 213 consecutive PTA procedures in a 1-year period were reviewed. Of unstaged procedures, a total of 131 patients (57.3% males; mean age, 66.4 12.1 years) met inclusion criteria. Forty-five patients (34.4%) had recent onset of claudication and 15 (11.5%) had ulceration. Thrombus was angiographically visualized in 16.7% of patients. Unfractionated heparin was administered at a mean of 4,672 1,238 U (59.1 20.0 U/kg) during the procedure. The highest activated clotting time (ACT) during the procedure was recorded in 114 patients. ACTs were < 300, 300 400 and > 400 seconds in 29.0%, 29.0% and 42.1%, respectively. In-hospital clinical events occurred in 12 patients (9.2%) who met any one of the following endpoints: death (0.8%), limb loss (1.5%), major bleeding (4.6%), emergent need for repeat revascularization of the same vessel (7.6%), embolic stroke (0.0%) and vascular complications (1.5%). The best model associated with salvage revascularization included cigarette smoking within the past year, recent onset of claudication and PTA treatment below the knee. Increased dosages of heparin (U/kg) were associated with a trend toward higher rates of complications. A significant number of patients have in-hospital major complications following PTA procedures using unfractionated heparin as the primary anticoagulant. Current ongoing registries are evaluating the feasibility of direct thrombin inhibitors bivalirudin instead of heparin as a primary anticoagulant during PTA.