John U. Doherty

ACCF/AHA/ASE/ASNC/HFSA/HRS/SCAI/SCCT/SCMR/STS 2013 multimodality appropriate use criteria for the detection and risk assessment of stable ischemic heart disease

The American College of Cardiology Foundation along with key specialty and subspecialty societies, conducted an appropriate use review of common clinical presentations for stable ischemic heart disease (SIHD) to consider use of stress testing and anatomic diagnostic procedures. This document reflects an updating of the prior Appropriate Use Criteria (AUC) published for radionuclide imaging (RNI), stress echocardiography (Echo), calcium scoring, coronary computed tomography angiography (CCTA), stress cardiac magnetic resonance (CMR), and invasive coronary angiography for SIHD. This is in keeping with the commitment to revise and refine the AUC on a frequent basis. A major innovation in this document is the rating of tests side by side for the same indication. The side-by-side rating removes any concerns about differences in indication or interpretation stemming from prior use of separate documents for each test. However, the ratings were explicitly not competitive rankings due to the limited availability of comparative evidence, patient variability, and range of capabilities available in any given local setting. The indications for this review are limited to the detection and risk assessment of SIHD and were drawn from common applications or anticipated uses, as well as from current clinical practice guidelines. Eighty clinical scenarios were developed by a writing committee and scored by a separate rating panel on a scale of 1 to 9, to designate Appropriate, May Be Appropriate, or Rarely Appropriate use following a modified Delphi process following the recently updated AUC development methodology. The use of some modalities of testing in the initial evaluation of patients with symptoms representing ischemic equivalents, newly diagnosed heart failure, arrhythmias, and syncope was generally found to be Appropriate or May Be Appropriate, except in cases where low pre-test probability or low risk limited the benefit of most testing except exercise electrocardiogram (ECG). Testing for the evaluation of new or worsening symptoms following a prior test or procedure was found to be Appropriate. In addition, testing was found to be Appropriate or May Be Appropriate for patients within 90 days of an abnormal or uncertain prior result. Pre-operative testing was rated Appropriate or May Be Appropriate only for patients who had poor functional capacity and were undergoing vascular or intermediate risk surgery with 1 or more clinical risk factors or an organ transplant. The exercise ECG was suggested as an Appropriate test for cardiac rehabilitation clearance or for exercise prescription purposes. Testing in asymptomatic patients was generally found to be Rarely Appropriate, except for calcium scoring and exercise testing in intermediate and high-risk individuals and either stress or anatomic imaging in higher-risk individuals, which were all rated as May Be Appropriate. All modalities of follow-up testing after a prior test or percutaneous coronary intervention (PCI) within 2 years and within 5 years after coronary artery bypass graft (CABG) in the absence of new symptoms were rated Rarely Appropriate. Pre-operative testing for patients with good functional capacity, prior normal testing within 1 year, or prior to low-risk surgery also were found to be Rarely Appropriate. Imaging for an exercise prescription or prior to the initiation of cardiac rehabilitation was Rarely Appropriate except for cardiac rehabilitation clearance for heart failure patients.

The Automatic Implantable Cardioverter-Defibrillator: Efficacy, Complications, and Device Failures

Twenty-six patients with refractory ventricular arrhythmias received the automatic implantable cardioverter-defibrillator. A patch lead only was placed during arrhythmia surgery in 7 other patients. During 13 +/- 6 (SD) months, the device discharged in 10 patients because of a sustained ventricular arrhythmia. No sudden deaths occurred. There were 31 complications in 17 patients, including postoperative refractory heart failure, coronary artery erosion, subclavian vein thrombosis, postoperative stroke after conversion of atrial fibrillation, atelectasis with pneumonia, symptomatic pleural effusions, and infection at the generator site. The cardioverter-defibrillator discharged in 9 asymptomatic patients, failed to terminate ventricular fibrillation during postoperative testing in 3 patients, and had premature battery failure in 4 patients. Tachycardia slowing during chronic amiodarone therapy and unipolar ventricular pacing during ventricular fibrillation precluded or delayed arrhythmia sensing. Thus, the cardioverter-defibrillator can be life saving, but its potential complications and interactions with antiarrhythmic drugs and pacemakers must be considered at patient selection.

ACCF/HRS/AHA/ASE/HFSA/SCAI/SCCT/SCMR 2013 appropriate use criteria for implantable cardioverter-defibrillators and cardiac resynchronization therapy

Steven R. Bailey, MD, FACC, FSCAI, FAHA, Moderator Andrea M. Russo, MD, FACC, FHRS, Writing Group Liaison [⁎][1] Suraj Kapa, MD, Writing Group Liaison Michael B. Alexander, MD, FACC[§][2] Steven R. Bailey, MD, FACC, FSCAI, FAHA[∥][3] Ulrika Birgersdotter-Green, MD, FHRS[∥][3] Alan S.

Endocardial activation of left bundle branch block.

Endocardial catheter mapping was performed in 18 patients with left bundle branch block (LBBB). Four patients had no organic heart disease (group I), six had cardiomyopathy (group II), and eight had coronary artery disease and previous infarction (group III). Twelve patients had one septal site of left ventricular endocardial breakthrough, while six had two left ventricular endocardial breakthrough sites, with one site always being septal. There was no significant difference among the groups with respect to time of left ventricular breakthrough (group I, 44 msec after the onset of the QRS complex; group II, 58 msec; and group III, 51 msec). Total left ventricular endocardial activation time was significantly longer in group III (119 msec) than group I (81 msec; p less than .05) and group II (61 msec; p less than .001). Duration of total right ventricular endocardial activation was 36 msec (seven patients). The final site of right ventricular activation was at 44 msec after the onset of the QRS complex. We conclude that (1) right ventricular activation occurs before initiation of left ventricular activation in patients with LBBB, (2) left ventricular endocardial activation in patients with LBBB most likely occurs as a result of right-to-left transseptal activation, (3) left ventricular endocardial activation sequence in patients with LBBB is heterogeneous, and (4) patients with coronary artery disease and LBBB have significantly longer total left ventricular endocardial activation times than patients with no organic heart disease or those with cardiomyopathies.

The value of catheter mapping during sinus rhythm to localize site of origin of ventricular tachycardia.

We assessed the value of endocardial catheter mapping in 52 patients in sinus rhythm and with 102 morphologically distinct ventricular tachycardias. The local bipolar electrograms from various regions of the left ventricle were assessed and quantitatively classified with respect to the characteristics of amplitude and duration. With the use of this assessment we found that electrograms from the site of origin were of significantly lower amplitude and longer duration; however, because such an overlap occurred with electrograms that were not from sites of origin, this does not serve as a useful clinical marker. Various types of electrograms, including normal, abnormal, fractionated, abnormal late, fractionated late, and longest, were evaluated with respect to sensitivity, specificity, and positive predictive value. None of these types possessed the ability to reliably localize the site of origin of ventricular tachycardia. We therefore conclude that endocardial catheter mapping during sinus rhythm is not useful as a guide in localized surgical therapy of ventricular tachycardia. Surgery guided only by the results of mapping during sinus rhythm would result in a more extensive excision than that directed by maps obtained during ventricular tachycardia and in some cases would result in the exclusion of the area considered to be the site of origin of the tachycardia.

Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy.

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.

Electrophysiologic evaluation and follow-up characteristics of patients with recurrent unexplained syncope and presyncope

One hundred nineteen patients with unexplained syncope (82%) or presyncope (18%) underwent complete electrophysiologic study (EPS). Symptoms were recurrent in 72% of the patients. Fifty-two percent of the patients had structural heart disease. Forty-one patients had normal EPS results and 78 had electrophysiologic abnormalities (ventricular tachycardia in 31, induced atrial flutter/fibrillation in 17, vasovagal syncope in 8, hypersensitive carotid sinus syndrome in 7, supraventricular tachycardia in 6, heart block in 5 and sick sinus syndrome in 4). The presence of structural heart disease (p = 0.0033) and previous myocardial infarction (p = 0.05) were the only clinical or electrocardiographic predictors of a positive EPS response. Therapy was guided by EPS and patients were followed for 27 +/- 20 months (mean +/- standard deviation). In the patients with negative EPS results, 76 +/- 11% (mean +/- standard error) were symptom-free at follow-up, compared to 68 +/- 10% in the group with positive EPS responses. No clinical variables helped to predict remission in the absence of therapy. One patient in the negative EPS response group and 2 patients in the EPS positive group died suddenly (cumulative survival 94 +/- 4%). Total cardiovascular mortality was 13% in the positive EPS response group, and 4% in the negative EPS response group. Thus, certain clinical characteristics are helpful in selecting patients for study. Electrophysiologically guided therapy is associated with a recurrence and sudden death rate similar to an untreated control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study.

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)

Repetitive, monomorphic ventricular tachycardia: Clinical and electrophysiologic characteristics in patients with and patients without organic heart disease

The clinical and electrophysiologic characteristics of 6 patients who had repetitive monomorphic ventricular tachycardia (VT) after a remote myocardial infarction (group A) were compared with those of 22 patients who had this arrhythmia without structural heart disease (group B). VT had a right bundle branch block morphologic pattern in 5 of 6 group A patients and a left bundle branch block morphologic pattern in all group B patients. Endocardial catheter activation mapping was performed in 4 group A patients and in 9 group B patients during VT. In all group A patients, the site of VT origin was on the border of the previous infarction; in all group B patients VT originated at the right ventricular outflow tract. Pacing and programmed stimulation induced VT in 5 of 6 group A patients and 7 of 22 group B patients (p = 0.03). Isoproterenol infusion provoked VT in 4 group A patients and 9 group B patients. Type I antiarrhythmic agents suppressed VT in 4 group A patients and in 14 group B patients, whereas propranolol suppressed VT in 3 of 3 group A patients tested and in 12 of 20 group B patients. Verapamil suppressed spontaneous VT in 1 group A patient and in 4 group B patients. During a mean follow-up of 19 months for group A and 40 months for group B, no patient had died suddenly or had cardiac arrest.

Hazards of intravenous verapamil for sustained ventricular tachycardia

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction. VT terminated after verapamil infusion in 6 patients. No single electrocardiographic morphologic pattern characterized these patients. A control group of 25 patients presenting with hemodynamically stable VT who received other antiarrhythmic agents was examined. Hypotension developed in only 1 patient during acute therapy and did not require emergency cardioversion. Thus, although verapamil may terminate VT, severe adverse effects occur much more often. Use of verapamil to differentiate supraventricular tachycardia with aberrant conduction from ventricular tachycardia is hazardous.