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Background: Pulmonary embolism (PE) is an uncommon, life-threatening complication after living donor nephrectomy (LDN), and is considered among the most common causes for donor mortality. Most cases of postoperative PEs are thought to originate in deep venous thrombosis (DVT) of the lower extremities., Case Report: A 56-year-old, healthy woman underwent laparoscopic left LDN. Her postoperative course was complicated by PE, presenting at postoperative day 7. Doppler ultrasonography of her lower extremities did not demonstrate DVT. Both transthoracic echocardiogram and contrast-enhanced computed tomography demonstrated a floating thrombus within the inferior vena cava (IVC) originating from a thrombus in the left renal vein stump. Symptoms resolved with systemic anticoagulation. Repeat transesophageal echocardiography demonstrated resolution of the IVC thrombus., Conclusions: Thrombus originating in left renal vein stump should be considered in patients who develop PE after LDN, especially when lower extremity DVT is not demonstrated., (Copyright © 2014. Published by Elsevier Inc.)

The utility of programmed ventricular stimulation to predict future arrhythmic events in patients with cardiac sarcoidosis is unknown. Similarly, the long-term benefit of implantable cardioverter-defibrillators (ICDs) in cardiac sarcoidosis has not been established. Thirty-two consecutive patients with cardiac sarcoidosis underwent programmed ventricular stimulation. Patients with spontaneous or inducible sustained ventricular arrhythmias (n = 12) underwent ICD insertion. All study patients were followed for the combined arrhythmic event end point of appropriate ICD therapies or sudden death. Mean length of follow-up to sustained ventricular arrhythmia or sudden death was 32 +/- 30 months. Five of 6 patients (83%) with spontaneous sustained ventricular arrhythmias and 4 of 6 patients (67%) without spontaneous but with inducible sustained ventricular arrhythmias received appropriate ICD therapy. Two of 20 patients (10%) with neither spontaneous nor inducible sustained ventricular arrhythmias experienced sustained ventricular arrhythmias or sudden death. Programmed ventricular stimulation predicted subsequent arrhythmic events in the entire population (relative hazard 4.47, 95% confidence interval [CI] 1.30 to 15.39) and in patients who presented without spontaneous sustained ventricular arrhythmias (relative hazard 6.97, 95% CI 1.27 to 38.27). No patient with an ICD died of a primary arrhythmic event. In patients with spontaneous or inducible sustained ventricular arrhythmias, mean survival from first appropriate ICD therapy to death or cardiac transplant was 60 +/- 46 months, with only 2 patients dying or reaching transplant at study end. In conclusion, programmed ventricular stimulation identifies patients with cardiac sarcoidosis at high risk for future arrhythmic events. ICDs effectively terminate life-threatening arrhythmias in high-risk patients, with significant survival after first appropriate therapy.

Maintenance of adequate serum blood levels is crucial to successful antiarrhythmic therapy. Serum levels of four antiarrhythmic agents (long-acting procainamide, quinidine sulfate, quinidine gluconate, and disopyramide) were determined in 98 consecutive ambulatory patients receiving long-term oral therapy. Medication dosages, dosing intervals, and time elapsed from last dosage until blood sampling were determined. Seventy-five patients (76.5 percent) had subtherapeutic blood levels (with mean levels less than 50 percent of the suggested minimum), and only 22 patients (22.5 percent) had therapeutic levels. Even among the 61 patients who claimed to have taken their medications within the six hours prior to blood sampling, 43 (70 percent) had subtherapeutic levels. These ratios held among all subgroups studied. Physicians should be aware of the high proportion of patients receiving long-term oral antiarrhythmic therapy with inadequate serum blood levels when planning therapeutic regimens.

We evaluated the effectiveness of oral verapamil therapy for control of ventricular rate in digitalized patients with atrial fibrillation (AF) with three clinical problems: chronic AF with rapid rate at rest (four patients), chronic AF with accelerated rate during modest exercise (five patients), and rapid rates during paroxysmal AF (four patients). Patients in the first two categories were evaluated both by open-label dosage titration and by a randomized, double-blind, cross-over protocol. In chronic AF with rapid rate of rest, there was a significant reduction in resting heart rate (from 125 +/- 7 to 87 +/- 14, P less than 0.01) and in peak exercise heart rate (from 162 +/- 33 to 126 +/- 25, P less than 0.01). In chronic AF with rapid rate during exercise, there was also a significant decrease in resting heart rate (from 90 +/- 7 to 66 +/- 4, P less than 0.01) and in peak exercise heart rate (from 126 +/- 19 to 101 +/- 15, P less than 0.01). These effects continued during longterm follow-up of one to 12 months (mean seven months). In patients with paroxysmal AF, verapamil slowed the ventricular response from 16- +/- 24 to 72 +/- 4 P less than 0.01) with only some amelioration of symptoms. Therapy was well tolerated despite a high prevalence (seven of 13 patients) of radiographic cardiomegaly (cardiothoracic ratio greater than 0.55). We conclude that verapamil is a safe and useful drug for control of ventricular rate in digitalized patients with chronic and paroxysmal AF.

A 66 year old black man was examined because of fatigue and progressive right heart failure. A striking finding on his echocardiogram was intense and slow-moving contrast in the inferior vena cava. Cardiac catheterization revealed constrictive pericarditis, and pericardiectomy was performed. Postoperatively, spontaneous contrast was no longer present. This case helps explain the origin of spontaneous inferior vena cava contrast.

Aortic root abscess occurs frequently in aortic prosthetic valve infective endocarditis. The present echocardiographic report documents a ruptured abscess that led to a direct communication between the left ventricular outflow tract and the left atrium confirmed by real-time (color flow) Doppler imaging.

Skeletal myopotentials may inhibit the output of unipolar demand ventricular pacemakers, resulting in protracted episodes of asystole in susceptible patients. The new DDD-mode pacemakers have, in addition to a unipolar ventricular lead, a unipolar atrial lead to enable atrioventricular sequential or atrial synchronous function. During clinical investigation of a new dual-unipolar cardiac pacing system programmed to operate in the DDD mode (Pacesetter AFP models 281 and 283), 6 patients were noted (5 men and 1 woman, aged 22 to 68 years) who manifested paroxysmal acceleration of ventricular pacing rate approaching the maximal tracking rate. Two patients also had abrupt slowing or cessation of ventricular output. With the use of atrial electrographic recordings (obtained with telemetry), the following mechanisms of rate change were found: myopotential tracking, myopotential inhibition, interference-mode asynchronous operation, sudden increases in sinus rate, and pacemaker-mediated reentrant tachycardia. In all patients, reprogramming of the implanted devices, based on telemetered atrial electrography, resulted in disappearance of the arrhythmias and loss of symptoms while maintaining the DDD pacing mode. Thus, several mechanisms of rhythm disturbances are peculiar to dual-chamber cardiac pacing systems that use unipolar electrodes. Endocardial telemetry combined with extensive programming capability offers the best opportunity for proper diagnosis and management of these problems.

A patient with atrial premature beats (APBs) with variable return cycle lengths is reported. Two rare responses of the sinus node were observed: APBs in which the return and sinus cycle lengths were equal and APBs which were interpolated. Several possible mechanisms for these unusual effects of APBs on the sinus node are discussed. One mechanism which can explain both of these observations is sinus node re-entry. This possibility is indirectly supported by documentation of sinus node re-entry during electrophysiologic studies.

In this report we describe a case of a 68-year-old man with atrioventricular junctional parasystole in whom atrial pacing caused marked changes in the arrhythmic pattern. During atrial pacing at a cycle length of 960 ms, the duration of the ectopic cycle length was influenced by the interval between the parasystolic and nonparasystolic beat. A shorter interval from nonparasystolic to ectopic beat prolonged the ectopic cycle length and a longer one shortened it. Pacing at a cycle length of 900 ms completely suppressed the parasystole. Both of these changes are most likely due to modulation and entrainment of the parasystolic rhythm. During spontaneous variation of the sinus cycle length over 24 hours of ambulatory ECG recording, modulation could not be confirmed; however, there was parallel variation of the ectopic and sinus cycle lengths which suggests that both pacemakers were under the influence of the autonomic nervous system.