Renal insufficiency and the risk of infection from pacemaker or defibrillator surgery.

BACKGROUND: Pacemakers and implanted cardioverter defibrillator (ICD) infection rates are rising. Renal insufficiency impairs immune function and is known to increase the risk of infection following implantation of orthopedic hardware. The purpose of the current study is to characterize the risk factors for pacemaker and ICD infection and to evaluate the role of renal insufficiency in this complication. METHODS AND RESULTS: A large (n = 4,856) single center experience with pacemaker and ICD procedures was reviewed. Of these, 141 were extractions of infected devices and 76 of these patients had been implanted in the Emory system and had preimplant creatinine information available for analysis. These cases were compared to 76 control patients undergoing device implantation matched by date of implant who had no infective complications. Demographic and clinical data from both groups were compared using both univariate and multivariate analysis. The overall rate of infection was 1.5%. Patients with device infection were more likely to have congestive heart failure (CHF), be diabetic, have generator exchanges, and to take warfarin than controls. There was no difference in the prevalence of coronary disease, atrial fibrillation, steroid use, or malignancy between the two groups. Elevated creatinine (Cr > or = 1.5 mg/dL) was much more frequent in patients with infection than in controls (38% vs 12%, odds ratio 4.6, P < 0.001). Moderate to severe renal disease (GFR < or = 60 cc/min/1.73 m2) was the most potent risk factor for infection, with a prevalence of 42% in infected patients versus 13% in controls (odds ratio of 4.8). CONCLUSIONS: Renal insufficiency dramatically increases the risk of infection complicating pacemaker or ICD surgery. This association should be part of the risk-benefit consideration prior to device implantation. Additional study of more extensive perioperative antibiotic therapy in this subset of patients is warranted.

The impact of cardiac resynchronization therapy on ventricular tachycardia/fibrillation: an analysis from the combined Contak-CD and InSync-ICD studies.

OBJECTIVES: To determine the potential influence of cardiac resynchronization therapy (CRT) on the frequency and types of ventricular arrhythmia (VA) in patients with an indication for the implantable cardioverter-defibrillator (ICD), we performed a retrospective electrogram (EGM) analysis of stored VA events from the two largest CRT-ICD trials. BACKGROUND: Previous reports suggest that CRT might promote polymorphic VT (PVT), while a beneficial effect of CRT on ventricular function might reduce the frequency of monomorphic VT (MVT). Theoretically, a balanced effect produces no change in overall VA. METHODS: We analyzed stored EGMs from patients in the Contak-CD and Insync-ICD studies receiving appropriate therapy for VA. EGM inspection distinguishes MVT and PVT using morphologic criteria rather than cycle length classification alone. RESULTS: Of 1,041 subjects entering the two trials, 880 were randomized CRT (N = 439) or control (N = 441). We were able to analyze 840 EGMs in 150 patients with VA, including 678 MVT episodes and 162 PVT episodes. These events were distributed among 68 patients with active CRT (390 MVT vs 111 PVT) and 82 patients assigned to control (288 MVT compared to 51 PVT). The apparent increase in PVT episodes in the CRT group is not significant and can be explained by a disproportionate number of episodes in a few patients. We were unable to identify clinical variables predictive of PVT during CRT. CONCLUSIONS: CRT is not associated with a measurable increase in the incidence of PVT, or in a reduction in MVT in the combined InSync-ICD and Contak-CD populations.

Downregulation of endocardial nitric oxide synthase expression and nitric oxide production in atrial fibrillation: potential mechanisms for atrial thrombosis and stroke.

BACKGROUND: In the arterial endothelium, laminar flow and cyclical stretch induce expression of NO synthase (NOS). We hypothesized that atrial fibrillation (AF) causes a downregulation of atrial endocardial NOS expression and NO* production. Because NO* has antithrombotic properties, this may contribute to thromboembolism in AF. METHODS AND RESULTS: In pigs, AF was produced with rapid atrial pacing at 600 bpm for 1 week, whereas controls had atrial pacing at 100 bpm. All animals production from freshly isolated tissue was measured by a NO*-specific microelectrode. Left atrial basal and stimulated NO* production was decreased in AF by 73% and 71% (P<0.01). Endocardial NOS expression, determined by Western analysis, was also significantly decreased by 46%. Expression of the prothombotic protein plasminogen activator inhibitor 1 (PAI-1) is known to be regulated by NO* and was increased in the left atrium by 1.8-fold in AF (P<0.05). NO* concentration was decreased in the left atrial appendage, although NOS expression was not affected. Neither NOS concentration, NO* levels, nor PAI-1 expression were altered in the aortas or right atria of animals with AF. CONCLUSIONS: AF is associated with a marked decrease in endocardial NOS expression and NO* bioavailability and an increase in PAI-1 expression in the left atrium. These data suggest that organized atrial contraction is needed to maintain normal endocardial expression of NOS. It is likely that loss of this antithrombotic enzyme contributes to the thromboembolic phenomena commonly observed in AF.

Cardiac resynchronization in patients with congestive heart failure and chronic atrial fibrillation: effect of upgrading to biventricular pacing after chronic right ventricular pacing.

OBJECTIVES: This study assessed the effects of biventricular pacing (BVP) on ventricular function, functional status, quality of life and hospitalization in patients with congestive heart failure (CHF), prior atrioventricular (AV) junction ablation and right ventricular (RV) pacing performed for chronic atrial fibrillation (AF). BACKGROUND: Although the benefit of BVP in CHF should theoretically extend to the patient with chronic RV pacing and AF, to our knowledge, no study has determined the effects of BVP on symptoms and ventricular function in these patients. This patient population allows for the evaluation of ventricular resynchronization independent of any BVP-induced changes on the AV interval. METHODS: Twenty consecutive patients with severe CHF (ejection fraction < or = 0.35, New York Heart Association [NYHA] functional class III or IV), prior AV junction ablation and RV pacing performed for permanent AF of at least six months' duration were studied. Electrocardiograms, echocardiograms, functional status evaluations and quality of life surveys were completed before and at three to six months after implant. RESULTS: The NYHA functional classification improved 29% (p < 0.001). The left ventricular (LV) ejection fraction increased 44% (p < 0.001), the LV diastolic diameter decreased 6.5% (p <0.003) and the end-systolic diameter decreased 8.5% (p < 0.01). The number of hospitalizations decreased by 81% (p < 0.001). The scores on the Minnesota Living with Heart Failure survey improved by 33% (p < 0.01). CONCLUSIONS: We conclude that BVP improves the LV function and the symptoms of CHF in patients with permanent AF and chronic RV pacing. These benefits are comparable to those described for patients in sinus rhythm suggesting that BVP acts through ventricular resynchronization rather than optimization of the AV delay.