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Background Patients with cardiac amyloidosis (CA) have increased mortality, which can be explained in part by an increased risk of arrhythmias. The burden of arrhythmias in CA, their predictors, and impact on in‐hospital outcomes remains unclear. The role of implantable cardioverter‐defibrillators (ICD) in this population is also uncertain. Methods We queried the National Inpatient Sample (NIS) using ICD‐9‐CM codes 277.39 and 425.7 to identify CA. Twelve common arrhythmias were extracted using appropriate, validated ICD‐9‐CM codes. ICD implantation was identified using procedure ICD‐9 codes 37.94 to 37.98, 00.51 and 00.54. Results There were a total of 145,920 CA hospitalizations between 1999 and 2014 in the United States and 56,199 (38.5%) of them were associated with arrhythmias. The prevalence of arrhythmias remained relatively constant from 41.5% in 1999 to 40.2% in 2014. The most common arrhythmia was atrial fibrillation (25.4%). In‐patient mortality was significantly higher in CA patients with arrhythmias (10.4% vs 6.5%, P, Arrhythmias are common in patients with Cardiac amyloidosis with most common being atrial fibrillation. These are associated with worse in‐hospital outcomes, increased length of stay, and cost of hospitalization.

Key Clinical Message Inappropriate shock due to residual air in subcutaneous implantable cardiac defibrillators is not a well-known complication. Obtaining overpenetrated X-rays, recognizing electrocardiogram findings, limiting blunt finger dissection, and switching to sense at another vector are techniques which might lead to avoidance of unnecessary wound exploration or device removal.

As Implantable Cardioverter Defibrillators (ICDs) have become more common, ethical issues have arisen regarding the deactivation of these devices. Goldstein et al., have shown that both patients and cardiologists consider ICD deactivation to be different from the discontinuation of other life-sustaining treatments. It cannot be argued ethically that ICDs raise new questions about the distinction between withholding and withdrawing treatment, and neither the fact that they are used intermittently, nor the duration of therapy, nor the mere fact that they are located inside the body can be considered unique to these devices and morally decisive. However, frequent allusions to the fact that they are located inside the body might provide a clue about what bothers patients and physicians. As technology progresses, some interventions seem to become a part of the patient as a unified whole person, completely replacing body parts and lost physiological functions rather than merely substituting for impaired structure and function. If a life-sustaining intervention can be considered a "replacement"--a part of the patient as a unified whole person--then it seems that deactivation is better classified as a case of killing rather than a case of forgoing a life-sustaining treatment. ICDs are not a "replacement" therapy in this sense. The deactivation of an ICD is best classified, under the proper conditions, as the forgoing of an extraordinary means of care. As technology becomes more sophisticated, however, and new interventions come to be best classified as "replacements" (a heart transplant would be a good example), "discontinuing" these interventions should be much more morally troubling for those clinicians who oppose euthanasia and assisted suicide.

Background:In the past 2 years, multiple implantable cardioverter-defibrillator (ICD) manufacturers have issued recalls on ICD models due to the potential for serious malfunction and even patient death. Previous studies examining the relationship between these recalls and patients' psychological well-being have been limited by small sample size and conflicting results. The purpose of this study is to examine the association between ICD recalls and patients' anxiety, depression, and quality of life. Methods:Patients were drawn from an outpatient electrophysiology clinic at a tertiary care hospital in New York City. Patients who had devices subject to a recall (cases) were identified from lists provided by device manufacturer and controls (patients with ICDs not subjected to a recall) were drawn from a convenience sample of outpatients. The survey instrument consisted of two validated questionnaires–-Hospital Anxiety and Depression Score (HADS) and MacNew heart disease health-related quality of life (QOL) instrument. In addition, a series of Likert-type scales were designed to elucidate patients' concerns related to the following domains: anger, trust, hope, concerns regarding ICD shock, fear of death (FOD), and physicians' ability to reduce their concern about the ICD recall. Data were analyzed using simple descriptive statistics and bivariate analyses (χ2 and t-test) as appropriate. Result:Sixty-one cases and 43 control patients were enrolled. Thirty-two patients (52%) with devices subject to a recall opted for a generator replacement. There were no significant differences in the mean scores on the HADS scale, or the MacNew QOL scale between these two groups of patients (cases and controls). Subgroup analysis within the group of patients whose ICDs were recalled (cases) revealed a reduced QOL among patients with a class I recall (reasonable probability that the product will cause serious adverse health consequences or death) as compared to those with a class II recall (product may cause temporary or medically reversible adverse health consequences) (P = 0.01). Both cases and control patients reported having reduced trust in the health-care system. On the whole, however, patients were satisfied with the way their physicians dealt with the recall. There was no significant change in the overall concern of ICD shocks or FOD between the two groups. Conclusion:In this study of ICD recall, we found no difference in the levels of anxiety, depression, or QOL expressed by patients with an ICD subject to a recall as compared to those without. These findings may be a reflection of good physician-patient communication, which might have reduced any anxiety associated with recalls.

OBJECTIVE--To assess immediate and long term success of "fast" pathway catheter ablation with graded use of radiofrequency energy in patients with classic atrioventricular nodal reentrant tachycardia (AVNRT) and evaluate clinical, procedure related, and electrophysiological features affecting long term results. DESIGN--31 consecutive patients with classic AVNRT at electrophysiological study, who were candidates for radiofrequency ablation. Patients were followed for an average of 24 months after ablation. SETTING--All studies and ablations were performed in an electrophysiological laboratory under fluoroscopic guidance using standard electrophysiological techniques. INTERVENTION--Radiofrequency application was performed at the site of proximal His bundle electrogram with A:V ratio of > 1. It was started at 10 W with increment of 5 W to a maximum of 25 W at 60 s. With the onset of junctional rhythm, atrial pacing was begun in order to monitor the PR interval. Application was terminated prematurely with a non-conducted P wave, continued prolongation of the PR interval beyond 50% of the baseline, or a threefold rise in impedance. RESULTS--Successful ablation was possible in 30/31 patients (97%) with an average of seven applications (range 1-10). It was associated with significant prolongation of PR interval (P < 0.001) and AV Wenckebach cycle length (P = 0.01). Ventriculo-atrial conduction was abolished in 24/30 patients (82%) with successful ablation. Two patients developed transient complete heart block (3 and 12 min) and one persistent right branch block. Four patients had late recurrence. Presence of ventriculo-atrial block was the only electrophysiological index predictive of long term success (P = 0.01). CONCLUSIONS--Graded use of radiofrequency energy and atrial pacing to monitor PR interval decreases the risk of atrioventricular block in patients undergoing fast pathway ablation for AVNRT. Ventriculo-atrial block is predictive of long term success and should be a preferred end point for fast pathway ablation.

A comparison of the efficacy of verapamil, sotalol, and flecainide to suppress right ventricular tachycardia (VT) in patients with a clinically normal heart.Patients underwent treatment serially with verapamil (360 mg daily), sotalol (240 or 320 mg daily), and flecainide (200 or 300 mg daily), (the larger dose was for patients heavier than 80 kg) to suppress tachycardia. Each drug was given orally for five half lives before testing.23 patients with right VT associated with a clinically normal heart were studied.The effects of drug treatment were examined by the number of ventricular events on 24 hour Holter monitoring, and the ability of tachycardia to be induced by treadmill exercise testing (Bruce protocol) and programmed ventricular stimulation (Wellens protocol), compared with drug free baseline tests.Patients were studied in a tertiary referral centre.All three drugs suppressed ventricular salvos (3,5 consecutive ventricular premature contractions) (p0.01) and VT (p0.05) on Holter monitoring and did not differ statistically in effect. Exercise induced VT was also suppressed by all three drugs (p0.01), and of these sotalol was the most effective although this was not statistically significant (14/23 inducible when drug free, 4/23 on flecainide, 2/23 on sotalol, 5/23 on verapamil). Sustained and non-sustained VT induced by programmed stimulation was also suppressed by the three drugs (p0.01) and again sotalol was the best of these though the differences did not achieve statistical significance (17/23 inducible when drug free, 4/17 on flecainide, 2/17 on sotalol, and 6/17 on verapamil). Proarrhythmic effects of drugs were found in a few patients. There was no difference in the efficacy of the drugs in patients with histological abnormalities of the myocardium when compared with those of normal histology.Ventricular tachycardia associated with a clinically normal heart can be suppressed by flecainide, sotalol, or verapamil. In individual patients sotalol was the most frequently effective drug (effective in89% of patients) and is a suitable choice for first line treatment.

Objective. We sought to determine whether a prolonged QRS interval duration is associated with decreased left ventricular (LV) systolic function.Background. The 12-lead electrocardiogram (ECG) is a routine test for suspected cardiac disease. Although several scoring systems have been devised to estimate LV systolic function, no studies have examined the direct relationship between QRS duration alone and LV systolic function.Methods. We analyzed the standard 12-lead surface ECG of 270 consecutive patients, referred for radionuclide ventriculography. Patients (n = 44) with bundle branch blocks, atrial flutter or fibrillation, pacemaker rhythm, recent myocardial infarction or bypass surgery, and patients on antiarrhythmic drugs were excluded. In the remaining patients (n = 226), we correlated the QRS duration on standard resting ECG, and the resting LV ejection fraction (EF), end-systolic and end-diastolic counts (ESC and EDC, respectively; LV volume indices), as obtained by radionuclide angiography. We used a multivariate analysis to identify independent predictors of reduced ventricular function entering QRS duration, the previously described R-wave score and clinical variables in our model.Results. The QRS duration in the abnormal EF group was significantly longer than in the normal EF group (0.102 vs. 0.091 s, p < 0.0001). A QRS duration >0.10 s was highly specific (83.6%), but modestly sensitive (43.8%), for the prediction of abnormal EF. Furthermore, an abnormal EF was predicted with incrementally increased specificity (83.6% to 99.3%) and a corresponding decrease in sensitivity (43.8% to 13.8%) for each 0.01-s increase in the definition of prolonged QRS (from >0.10 to >0.12 s). Accordingly, the positive likelihood ratio for the prediction of decreased LV function was increased from 2.67 to 19.7 as the definition of prolonged QRS duration was increased from >0.10 to >0.12 s. In the multivariate analysis, a prolonged QRS duration and a low R-wave score were the only independent predictors of decreased LV systolic function.Conclusions. Prolonged QRS duration (>0.10 s) obtained from a standard resting 12-lead ECG is a specific, but relatively insensitive indicator of decreased LV systolic function. Further prolongation of the QRS had a higher specificity for decreased LV EF and a higher positive likelihood ratio for predicting abnormal LV EF.

Signal-averaged electrocardiography (ECG) was performed in 38 patients (mean age 38 years, range 15 to 70) with ventricular tachycardia who had no clinical evidence of structural heart disease. Spontaneous ventricular tachycardia was nonsustained in 23 patients and sustained in 15. None of the patients had symptoms of heart failure or ischemic heart disease, and at cardiac catheterization none had significant coronary artery disease or left ventricular wall motion abnormalities. In addition, all patients underwent left and right ventricular endomyocardial biopsy and ventricular stimulation studies. Signal-averaged ECG was performed and late QRS potentials were defined with use of Simson's method.Late QRS potentials were detected in a minority (18%) of patients including 2 of 23 with nonsustained and 5 of 15 with sustained (p = NS) ventricular tachycardia. Fifteen patients (40%) had abnormal endomyocardial biopsy results and these findings were more common in patients with s sustained than in those with nonsustained ventricular tachycardia (9 of 15 versus 6 of 23, p < 0.05). Late potentials were associated with abnormal endomyocardial biopsy findings (6 of 15 versus 1 of 23, p < 0.01). An increase in fibrous tissue was the most frequent histopatho logic abnormality; this increase was quantified by morphometric methods and compared with biopsy findings in normal control subjects. In the control group the proportion of collagen in relation to myocytes was 15% ratio of collagen to myocytes in at least one specimen and the biopsies revealed marked interstitial fibrosis. At programmed electrical stimulation clinical tachycardia was more commonly induced in patients with sustained than in those with nonsustained ventricular tachycardia (12 of 15 versus 7 of 23, p < 0.01).The presence of late QRS potentials in patients with ventricular tachycardia without clinically apparent structural heart disease was not a sensitive marker for abnormal myocardial histologic findings (63%) or inducible ventricular arrhythmia (37%), but was very specific for these variables (84% and 100%, respectively). The majority of patients with normal findings on endomyocardial histologic study and signal-averaged ECG have a tachycardia with a left bundle branch block configuration and a right frontal plane axis.

OBJECTIVES The purpose of this prospective, randomized, double-blind, placebo-controlled study was to assess the efficacy of preoperatively and postoperatively administered oral d,lsotalol in preventing the occurrence of postoperative atrial fibrillation (AF). BACKGROUND Atrial fibrillation is the most common arrhythmia following coronary artery bypass surgery (CABG). Its etiology, prevention and treatment remain highly controversial. Furthermore, its associated morbidity results in a prolongation of the length of hospital stay post-CABG. METHODS A total of 85 patients, of which 73 were to undergo CABG and 12 CABG plus valvular surgery (ejection fraction ≥28% and absence of clinical heart failure), were randomized to receive either sotalol (40 patients; mean dose = 190 ± 43 mg/day) started 24 to 48 h before open heart surgery and continued for four days postoperatively, or placebo (45 patients, mean dose = 176 ± 32 mg/day). RESULTS Atrial fibrillation occurred in a total of 22/85 (26%) patients. The incidence of postoperative AF was significantly (p = 0.008) lower in patients on sotalol (12.5%) as compared with placebo (38%). Significant bradycardia/hypotension, necessitating drug withdrawal, occurred in 2 of 40 (5%) patients on sotalol and none in the placebo group (p = 0.2). None of the patients on sotalol developed Torsade de pointes or sustained ventricular arrhythmias. Postoperative mortality was not significantly different in sotalol versus placebo (0% vs. 2%, p = 1.0). Patients in the sotalol group had a nonsignificantly shorter length of hospital stay as compared with placebo (7 ± 2 days vs. 8 ± 4 days; p = 0.24). CONCLUSIONS The administration of sotalol, in dosages ranging from 80 to 120 mg, was associated with a significant decrease (67%) in postoperative AF in patients undergoing CABG without appreciable side effects. Sotalol should be considered for the prevention of postoperative AF in patients undergoing CABG in the absence of heart failure and significant left ventricular dysfunction.

Tall T waves and pronounced prolongation of the QT interval developed 24 hours after an apparently complete recovery from an acute anaphylactic reaction to oral ampicillin in a previously healthy woman of 29. These electrocardiographic abnormalities gradually subsided over five days. The prolongation of the QT interval has not previously been reported after anaphylaxis.