BackgroundWe investigated whether right ventricular dysfunction (RVD) as assessed by echocardiogram can be used as a prognostic factor in hemodynamically stable patients with acute pulmonary embolism (PE). Short-term mortality has been investigated only in small studies and the results have been controversial.MethodsA PubMed search was conducted using two keywords, “pulmonary embolism” and “echocardiogram”, for articles published between January 1st 1998 and December 31st 2011. Out of 991 articles, after careful review, we found 12 articles that investigated the implications of RVD as assessed by echocardiogram in predicting short-term mortality for hemodynamically stable patients with acute PE. We conducted a meta-analysis of these data to identify whether the presence of RVD increased short-term mortality.ResultsAmong 3283 hemodynamically stable patients with acute PE, 1223 patients (37.3%) had RVD, as assessed by echocardiogram, while 2060 patients (62.7%) had normal right ventricular function. Short-term mortality was reported in 167 (13.7%) out of 1223 patients with RVD and in 134 (6.5%) out of 2060 patients without RVD. Hemodynamically stable patients with acute PE who had RVD as assessed by echocardiogram had a 2.29-fold increase in short-term mortality (odds ratio 2.29, 95% confidence interval 1.61-3.26) compared with patients without RVD.ConclusionsIn hemodynamically stable patients with acute PE, RVD as assessed by echocardiogram increases short-term mortality by 2.29 times. Consideration should be given to obtaining echocardiogram to identify high-risk patients even if they are hemodynamically stable.

Three patients with human immunodeficiency virus (HIV) infection presented with QT, prolongation (> 440 ms) and torsades de pointes. We sought to evaluate the etiology of the long QT syndrome in these patients without previously identified causes for QT, prolongation, and determine the prevalence among patients with HIV infection. The three index patients underwent: (1) left stellate ganglion block; (2) beta-blocker challenge; and (3) electrocardiographic stress testing. QTc interval was measured before and after intervention. We undertook a retrospective analysis of prevalence of QTC prolongation among all patients with computerized ECGs over a 6-month period at one institution and compared it to the prevalence in hospitalized patients with HIV disease. Thirty-four thousand one hundred eighty-one patients with computerized ECGs were screened for QTc prolongation. Forty-two hospitalized patients with HI disease had computerized ECG during the same 6-month period. In the three index patients, the QTc failed to shorten with left stellate ganglion blockade, beta-blocker challenge, or stress testing, suggesting an acquired form of the long QT syndrome in these patients with HIV disease. None had previously recognized acquired causes of QT, prolongation. Mexiletine hydrochloride was useful in preventing recurrences of torsades de pointes. We observed a 7.0% prevalence of QT, prolongation among all patients screened. Hospitalized patients with HIV disease (n = 42) during this same period, demonstrated an increased prevalence of QT, prolongation (28.6%, P = 0.002). Patients with HIV disease have a significantly higher prevalence of QTc prolongation than a general hospital-based population, may have an unrecognized acquired form of the long QT syndrome, and are at risk for torsades de pointes.

Sudden unexpected death in epilepsy (SUDEP) is a major clinical problem in epilepsy patients in the United States, especially those with chronic, uncontrolled epilepsy. Several pathophysiological events contributing to SUDEP include cardiac arrhythmias, respiratory dysfunction, and dysregulation of systemic or cerebral circulation. There is a significant body of literature suggesting the prominent role of cardiac arrhythmias in the pathogenesis of SUDEP. There is evidence to say that long-standing epilepsy can cause physiological and anatomical autonomic instability resulting in life-threatening arrhythmias. Tachyarrhythmias, bradyarrhythmias, and asystole are commonly seen during ictal, interictal, and postictal phase in epilepsy patients. It is unclear if these rhythm disturbances need attention as some of them may be just benign findings. Evidence regarding prolonged cardiovascular monitoring or the benefit of pacemaker/defibrillator implantation for primary or secondary prevention in epilepsy patients is limited. Awareness regarding pathophysiology, cardiac effects, and management options of SUDEP will become useful in guiding more individualized treatment in the near future. (PACE 2011; 1-8).

Background-The Intracardiac Echocardiography Guided Cardioversion Helps Interventional Procedures study evaluatedthe concordance of intracardiac echocardiography (ICE) with transesophageal echocardiography (TEE) in patients with atrial fibrillation (AF). Methods and Results-Patients with AF undergoing right heart catheterization underwent left atrium (LA) and interatrial septal (IAS) imaging by TEE and ICE. A blinded comparison of the 2 modalities was performed at a core laboratory. Ninety-five patients aged 58Ϯ12 years completed the study. The LA was profiled in all patients with both techniques, and concordance for image quality was 96%. LA appendage (LAA) imaging was achieved in 85% with ICE and 96% with TEE. There was no difference in the presence of spontaneous echo contrast between ICE and TEE during LA imaging, but there was a trend toward a greater incidence in the LAA with TEE (Pϭ0.109). Intracardiac thrombus was uncommonly seen (TEE, 6.9%; ICE, 5.2%). The concordance for the presence or absence of thrombus was 97% in the LA and 92% in the LAA, but the latter was detected more frequently with TEE. IAS imaging was achieved in 91% with ICE and in 97% with TEE (Pϭ0.177). Concordance for patent foramen ovale and atrial septal aneurysms was 100% and 96%, respectively. A negative ICE examination was associated with absence of dense echo contrast or thrombus on TEE in 86%. Conclusions-This

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To date, the precise mechanism of atrial fibrillation (AF) as a possible cause of reflux disease remains uncertain, although some possibilities can be postulated. Inflammation and vagal stimulation may have a key role linking these 2 common diseases. There is some evidence in the form of case reports and limited observational studies reporting that reflux disease, and more specifically esophagitis, can cause paroxysmal AF, and various mechanisms have been proposed. Some studies have demonstrated that acid suppressive therapy by proton pump inhibitors (PPIs) may help ameliorate symptoms associated with AF and also facilitate conversion to normal sinus rhythm in a subset of patients. Further prospective studies are needed to determine if a true causal mechanism exists between the two and assess whether the mechanism is dependent on a specific subtype of AF. In addition, the response of AF‐related symptoms to PPI therapy and the potential for PPI therapy to reduce the development of AF merits further investigation. Clin. Cardiol. 2011 DOI: 10.1002/clc.21969The authors have no funding, financial relationships, or conflicts of interest to disclose.

Patients with heart failure (HF) are often instructed to temporarily adjust their diuretic dose. This approach has become routine in some HF management programs; however, no study has specifically examined the effects of a patient-directed flexible diuretic protocol. For the purposes of this study, patients were randomized into a usual care (UC) group (n = 31) or a flexible diuretic titration (DT) group (n = 35). The DT group completed a 6-item diuretic titration protocol once a day, for 3 months. The 6-minute walk distance, plasma B-type natriuretic peptide (NT-BNP), plasma norepinephrine (NE), and quality of life (QOL) were measured at baseline and at 3 months. Hospitalizations, emergency department (ED) visits, and mortality rates were measured at 3 months. Compared to baseline, at 3 months, there was a significant increase in the DT group's 6-minute walk distance (646 +/- 60 ft vs 761 +/- 61 ft, P = .01) and total QOL score (53 +/- 5 vs 38 +/- 5, P = .001), whereas these parameters remained unchanged within the UC group. There were significantly less ED visits in the DT group compared with those in the UC group (3% vs 23%, P = .015). No differences were found between the groups in HF-related hospitalizations or mortality. Within both groups, no differences were found between baseline and 3-month NE or NT-BNP plasma values. Patients with heart failure who used a sliding scale diuretic titration protocol had significant improvements in their exercise tolerance and QOL, had fewer ED visits, and had no change in plasma NE or NT-BNP levels.

Atrial fibrillation (AF), especially persistent and long-standing persistent AF, may result in electro-anatomical changes in the left atrium, resulting in remodeling and deposition of fibrous tissue. There are emerging data that atrial substrate modification may increase the risk of thromboembolic complications, including stroke. Several studies have reported that atrial fibrosis is due to complex interactions among several cellular and neurohumoral mediators. Late gadolinium enhancement MRI has been reported to allow quantitative assessment of myocardial fibrosis in patients at risk of developing a stroke. Current stroke risk stratification criteria for AF do not utilize atrial fibrosis as an independent risk factor despite its association with AF and stroke. Further research is required in developing adequate risk stratification tools for predicting the stroke risk and catheter ablation outcomes in AF.