In-stent stenosis: potential role of increased oxidative stress and glutathione-linked detoxification mechanisms.

This study was designed to determine whether red-cell oxidative stress status and antioxidant enzyme levels can serve as markers in patients predisposed to in-stent stenosis. Blood was collected from patient groups undergoing coronary angiography for chest pain evaluation, namely, group A (without coronary artery disease), group B (previous coronary stents without in-stent stenosis), and group C (previous coronary stents with in-stent stenosis). Thiobarbituric acid reactive substances (measure of lipid peroxidation), glutathione-linked detoxification enzymes, catalase, and superoxide dismutase were determined. Compared with group A, patients in group C showed increased lipid peroxidation products and glutathione-S-transferase but decreased glutathione peroxidase and glutathione reductase activities. Results in group B patients were intermediate between those of groups A and C with significant decreases in glutathione peroxidase versus controls. In-stent stenosis is associated with significant increase in lipid peroxidation and attenuated glutathione-linked detoxification enzymes, consistent with oxidative stress.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy: clinical profile of four patients and review.

Four patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) are described. Two patients presented with sustained ventricular tachycardia and two with cardiac arrest from which they were successfully resuscitated. All four patients had typical electrocardiographic and echocardiographic features and fulfilled the task force criteria for diagnosis of ARVD/C. All four patients had T wave inversion in chest leads V1 to V4, and two had epsilon waves, and all four had premature ventricular complexes of left bundle branch block and left axis deviation pattern. All patients showed a markedly enlarged, thin and hypokinetic right ventricle. Three patients had implantable cardioverter defibrillator (ICD) implanted and are doing well. One patient who refused an ICD died suddenly 6 months after his initial presentation. Three surviving patients are on sotalol for suppression of ventricular tachycardia episodes triggering ICD shocks. A review of the existing literature on diagnosis of ARVD/C, its clinical presentation and natural history, its genetic basis, risk stratification, treatment, and prognosis is presented.

Effects of electromagnetic interference on implanted cardiac devices and their management.

Potential interference between implanted cardiac devices such as pacemakers and implantable cardioverter-defibrillators and electromagnetic fields is an important concern for physicians taking care of patients with pacemakers and implantable cardioverter-defibrillators. There are many sources of electromagnetic interference (EMI); however, only a small number of these cause significant problems that need attention. Regardless of its source, EMI is of greater concern for a patient who is dependent on paced rhythm because inhibition of the pacemaker by EMI may produce ventricular standstill. It is important that cardiologists, internists, emergency medicine, critical care physicians, and anesthesiologists be aware of how EMI can affect the function of implanted cardiac devices so that appropriate treatment can be rendered and preventive measures instituted.

Association of QRS duration and outcomes after myocardial infarction: the VALIANT trial.

BACKGROUND: Prolongation of the QRS duration has been shown to be associated with adverse outcomes among heart failure (HF) patients. The association of QRS duration with clinical outcomes in the post-myocardial infarction (MI) setting is less well defined. OBJECTIVES: To assess the prognostic significance of QRS duration prolongation on initial electrocardiogram after acute MI. METHODS: QRS duration was measured in 403 patients with MI complicated by left ventricular dysfunction, signs or symptoms of HF, or both, who were enrolled in the Valsartan in Acute Myocardial Infarction (VALIANT) echo study. The cohort was divided into quartiles of QRS duration (<75 ms, 75-88 ms, 89-108 ms, >108 ms). The number of clinical events were determined and compared across the groups. RESULTS: Increasing QRS duration is associated with a higher incidence of HF, sudden death (SD), and cardiovascular (CV) death (P-trend <0.05) but not with stroke or recurrent MI. The univariate relative risks for HF, SD, and CV death with increasing QRS duration quartiles were 1.31 (95% CI, 1.06-1.64), 1.57 (95% CI, 1.03-2.40), and 1.31 (95% CI, 1.03-1.66), respectively, but QRS duration did not remain independently predictive of adverse outcome after adjusting for the 10 most predictive baseline covariates. Baseline end-diastolic and end-systolic volumes were larger and ejection fraction was lower in the higher QRS quartile groups. CONCLUSIONS: Prolonged QRS duration, even within the normal range, is associated with larger ventricular volumes, reduced systolic function, and an increased risk for development of HF, SD, and CV death after MI but appears to be a marker, rather than an independent predictor, for increased risk.

The renal patient with cardiovascular disease--no longer a simple plumbing problem.

The clinical syndrome of chronic kidney disease (CKD) with coronary artery disease (CAD) is a clinical challenge. The risk of cardiovascular disease in patients with renal impairment appears to be far greater than in the general population. Despite the high prevalence of CKD related to cardiovascular disease (CVD), it remains understudied. Most of the current research comes from small community-based studies and retrospective reviews, assuming that patients with CKD will similarly benefit from treatments as patients with normal renal function. Most of the current clinical trials have excluded patients with CKD even though they represent a group of people at high risk for cardiovascular (CV) complications. CKD is associated with adverse CV outcomes and higher mortality even after adjustment for conventional risk factors. Declining renal function portends increasing CV risk and may be explained by several other factors that are being investigated, including inflammation, decreased vascular compliance, homocysteine, albuminuria and dyslipidemia. In addition, there is a lack of appropriate intervention in patients with CKD, despite established awareness of their high cardiovascular risk.