Modifiable risk factors for vascular access site complications in the IMPACT II Trial of angioplasty with versus without eptifibatide. Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis.

OBJECTIVES: This study was designed to identify potential predictors of vascular access site (VAS) complications in the large-scale Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis (IMPACT) II trial, which studied angioplasty with versus without a new glycoprotein (GP) IIb/IIIa receptor inhibitor (eptifibatide). BACKGROUND: GP IIb/IIIa receptor inhibition during coronary interventions has been associated with excess VAS complications. If other predictors of VAS complications could be identified, they might be manipulated to reduce complications. METHODS: A total of 4,010 patients undergoing percutaneous transluminal coronary revascularization (PTCR) were randomized into one of three bolus/20- to 24-h infusion arms: placebo bolus/placebo infusion; 135-microg/kg body weight eptifibatide bolus/0.5-microg/kg per min eptifibatide infusion; or 135-microg/kg eptifibatide bolus/0.75-microg/kg per min eptifibatide infusion. Heparin during the procedure was weight adjusted and stopped 4 h before sheaths were removed. Logistic regression modeling was used to identify independent predictors of VAS complications. RESULTS: VAS complications were more common in patients treated with eptifibatide (9.9% vs. 5.9% placebo-treated patients, p < 0.001). Multivariate analysis identified eptifibatide therapy (p < 0.0001), advanced age (p = 0.0001), longer time to sheath removal (p = 0.0002), stent placement (with intense post-stent anticoagulation) (p = 0.0004), female gender (p = 0.0006), PTCR within 24 h of thrombolytic therapy (p = 0.002), larger heparin doses during PTCR (p = 0.009), major coronary dissection (p = 0.03) and placement of a venous sheath (p = 0.04) as independent predictors of VAS complications. CONCLUSIONS: VAS complications may be reduced by early sheath removal, by avoiding placement of venous sheaths and by limiting heparin dosing to avoid excessive activated clotting times. Early sheath removal during inhibition of platelet aggregation by eptifibatide is feasible.

Pulmonary manifestations of chronic heart failure.

These findings underscore the importance of understanding the complex interactions of multiple-organ systems in a chronic systemic disease state like congestive heart failure. The exaggerated ventilatory response in patients with heart failure is clearly multifactorial and it remains difficult to decipher whether this response results from or contributes to the sensation of dyspnea. Pulmonary dysfunction including ventilation-perfusion mismatching, decreased lung compliance, restriction, airway obstruction, decreased diffusion capacity, and decreases in respiratory muscle strength and endurance contribute to an inefficient breathing pattern and increased work of breathing. This is further compounded by the limited ability of the failing heart to meet the metabolic demands of the respiratory muscles, leading to under-perfusion and ischemia. This imbalance contributes to perceived dyspnea and exercise limitations. Understanding these physiologic cardiopulmonary interactions may lead to therapeutic modalities, such as respiratory muscle training, aimed at disrupting this intertwined cycle of events and improving functional capacity in patients with heart failure.

Angle closure glaucoma complicating systemic atropine use in the cardiac catheterization laboratory.

Atropine may precipitate angle closure glaucoma in those predisposed to the disorder. Previously reported cases demonstrate the frequent misdiagnosis of acute glaucoma as conjunctivitis. Resultant delays in treatment can lead to vision loss. The present case describes a 66-yr-old man who developed acute angle closure glaucoma after receiving atropine during a coronary angioplasty produce. Clinicians who utilize atropine should be aware of the possibility of precipitating angle closure glaucoma and the predisposing factors, signs, and symptoms to facilitate prompt diagnosis and treatment of this disorder.

Acalculous candidal cholecystitis: a previously unrecognized complication after cardiac transplantation.

Acalculous cholecystitis is a life-threatening complication in critically ill surgical patients. Whereas Candida albicans and Torulopsis glabrata have been reported as the primary pathogens in 14 previous cases of acalculous cholecystitis, we report the first case of Candida parapsilosis as a biliary pathogen in a patient after cardiac transplantation. Although cardiac transplant recipients often have many of the risk factors for acalculous candidal cholecystitis, including major surgery, immunosuppression, antibiotic therapy, parenteral nutrition, and prolonged intensive care unit stay, this entity has not been previously reported in the cardiac transplant population. Although rare, acalculous candidal cholecystitis is associated with very high morbidity and a mortality rate of 40%. Early diagnosis necessitates an aggressive approach to the critically ill patient with abdominal complaints. Prompt drainage or cholecystectomy, if possible, represent the mainstays of therapy and offer the greatest chance for survival.

Serial assessment of exercise capacity after heart transplantation.

BACKGROUND: Exercise capacity after heart transplantation is abnormal. This reduced exercise performance may in part be due to treatment with high-dose immunosuppressive therapy, deconditioning, graft rejection, or cardiac denervation. METHODS: To investigate whether exercise capacity significantly improves over time as immunosupression is lessened or whether reinnervation occurs, we measured peak exercise oxygen consumption in 60 patients 0.5 to 60 months after transplantation (age: 52 +/- 11 years; left ventricular ejection fraction: 56% +/- 10%) and in 14 healthy subjects (age: 44 +/- 8 years; p = Not significant). Resting hemodynamic measurements, left ventricular ejection fraction, and immunosuppressive therapy were recorded at the time of each of the patients' 116 exercise tests. Exercise test results were stratified into groups according to time after transplantation. RESULTS: Exercise capacity significantly improved after transplantation (pretransplantation peak exercise oxygen consumption: 9.9 +/- 4.3; posttransplantation: 16.6 +/- 4.0 ml/kg/min; p < 0.001). Patient groups after transplantation were without significance differences with regard to age, gender, left ventricular ejection fraction, resting hemodynamic measurements, antihypertensive regimen, and number of rejection episodes. For those patients exercising at 2 months compared with the patients exercising at 12 months, a significant increase was observed in peak exercise oxygen consumption (14.0 +/- 3.8 ml/kg/min at 2 +/- 2 months to 16.2 +/- 3.8 ml/kg/min at 12 +/- 2 months) and maximum heart rate (124 +/- 24 to 137 +/- 24 beats/min). No significant changes were found in peak exercise oxygen consumption or maximum heart rate after the first year after transplantation. Patients' exercise capacities as measured by peak exercise oxygen consumption remained abnormal (N1 peak exercise oxygen consumption: 35 +/- 11 ml/kg/min) despite significant reductions in steroid, azathioprine, and cyclosporine therapy. Peak exercise oxygen consumption was significantly correlated with maximal heart rate (r = 0.42) (p < 0.0001) but not with maximal blood pressure response, change in heart rate, left ventricular ejection fraction, or resting cardiac index (all p = Not significant). CONCLUSIONS: Exercise capacity is markedly improved after heart transplantation although it remains impaired compared with healthy individuals. Patients achieve their maximal exercise capacity by 1 year after transplantation. Subsequently, exercise capacity does not improve despite significant reductions in immunosuppressive agents. The lack of alteration in the heart rate response to exercise over time suggests that no significant functional reinnervation occurs.