Pietro Delise

Recommendations for interpretation of 12-lead electrocardiogram in the athlete.

Cardiovascular remodelling in the conditioned athlete is frequently associated with physiological ECG changes. Abnormalities, however, may be detected which represent expression of an underlying heart disease that puts the athlete at risk of arrhythmic cardiac arrest during sports. It is mandatory that ECG changes resulting from intensive physical training are distinguished from abnormalities which reflect a potential cardiac pathology. The present article represents the consensus statement of an international panel of cardiologists and sports medical physicians with expertise in the fields of electrocardiography, imaging, inherited cardiovascular disease, cardiovascular pathology, and management of young competitive athletes. The document provides cardiologists and sports medical physicians with a modern approach to correct interpretation of 12-lead ECG in the athlete and emerging understanding of incomplete penetrance of inherited cardiovascular disease. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause no alarm and those that require action and/or additional testing to exclude (or confirm) the suspicion of an underlying cardiovascular condition carrying the risk of sudden death during sports. The aim of the present position paper is to provide a framework for this distinction. For every ECG abnormality, the document focuses on the ensuing clinical work-up required for differential diagnosis and clinical assessment. When appropriate the referral options for risk stratification and cardiovascular management of the athlete are briefly addressed.

Implantable Cardioverter-Defibrillator Therapy for Prevention of Sudden Death in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia

Background—Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a condition associated with the risk of sudden death (SD). Methods and Results—We conducted a multicenter study of the impact of the implantable cardioverter-defibrillator (ICD) for prevention of SD in 132 patients (93 males and 39 females, age 40±15 years) with ARVC/D. Implant indications were a history of cardiac arrest in 13 patients (10%), sustained ventricular tachycardia in 82 (62%), syncope in 21 (16%), and other in 16 (12%). During a mean follow-up of 39±25 months, 64 patients (48%) had appropriate ICD interventions, 21 (16%) had inappropriate interventions, and 19 (14%) had ICD-related complications. Fifty-three (83%) of the 64 patients with appropriate interventions received antiarrhythmic drug therapy at the time of first ICD discharge. Programmed ventricular stimulation was of limited value in identifying patients at risk of tachyarrhythmias during the follow-up (positive predictive value 49%, negative predictive value 54%). Four patients (3%) died, and 32 (24%) experienced ventricular fibrillation/flutter that in all likelihood would have been fatal in the absence of the device. At 36 months, the actual patient survival rate was 96% compared with the ventricular fibrillation/flutter-free survival rate of 72% (P <0.001). Patients who received implants because of ventricular tachycardia without hemodynamic compromise had a significantly lower incidence of ventricular fibrillation/flutter (log rank=0.01). History of cardiac arrest or ventricular tachycardia with hemodynamic compromise, younger age, and left ventricular involvement were independent predictors of ventricular fibrillation/flutter. Conclusions—In patients with ARVC/D, ICD therapy provided life-saving protection by effectively terminating life-threatening ventricular arrhythmias. Patients who were prone to ventricular fibrillation/flutter could be identified on the basis of clinical presentation, irrespective of programmed ventricular stimulation outcome.

Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study.

The vasovagal nature of syncope, which remained unexplained despite full clinical and electrophysiologic investigation, was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (17 men and 13 women, mean age 65 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5) episodes of syncope of unknown origin were studied. Head-up tilt test was considered positive if syncope developed in association with hypotension, bradycardia, or both. During baseline head-up tilt 15 patients (50%) had a positive response. Ten patients had a vasodepressor response (marked hypotension without marked bradycardia) and 5 had a mixed response (marked hypotension with marked bradycardia). None of 8 control subjects became symptomatic during the test. Baseline head-up tilt test was positively reproducible in 10 of 14 patients (71%). Nine of these 10 patients underwent serial head-up tilt tests after drug administration to determine the pathogenesis of vasovagal syncope. Atropine prevented tilt-induced syncope in 3 of 8 patients (37.5%), propranolol in 2 of 8 (25%) and etilephrine in 7 of 7 (100%). Seven patients received long-term drug treatment with drugs selected on the basis of acute drug testing. One responder to atropine received transdermal scopolamine and 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 12 months. Head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vasovagal reaction in patients with syncope of unknown origin. Withdrawal of alpha-sympathetic stimulation is a principal mechanism responsible for vasodilation and syncope during head-up tilt.(ABSTRACT TRUNCATED AT 250 WORDS)

Recommendations for participation in leisure-time physical activity and competitive sports of patients with arrhythmias and potentially arrhythmogenic conditions Part II: Ventricular arrhythmias, channelopathies and implantable defibrillators

This consensus paper on behalf of the Study Group on Sports Cardiology of the European Society of Cardiology follows a previous one on guidelines for sports participation in competitive and recreational athletes with supraventricular arrhythmias and pacemakers. The question of imminent life-threatening arrhythmias is especially relevant when some form of ventricular rhythm disorder is documented, or when the patient is diagnosed to have inherited a pro-arrhythmogenic disorder. Frequent ventricular premature beats or nonsustained ventricular tachycardia may be a hallmark of underlying pathology and increased risk. Their finding should prompt a thorough cardiac evaluation, including both imaging modalities and electrophysiological techniques. This should allow distinguishing idiopathic rhythm disorders from underlying disease that carries a more ominous prognosis. Recommendations on sports participation in inherited arrhythmogenic conditions and asymptomatic gene carriers are also discussed: congenital and acquired long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular cardiomyopathy and other familial electrical disease of unknown origin. If an implantable cardioverter defibrillator is indicated, it is no substitute for the guidelines relating to the underlying pathology. Moreover, some particular recommendations for patients/athletes with an implantable cardioverter defibrillator are to be observed.

Risk stratification in individuals with the Brugada type 1 ECG pattern without previous cardiac arrest: usefulness of a combined clinical and electrophysiologic approach

Aims Risk stratification in individuals with type 1 Brugada electrocardiogram (ECG) pattern (type 1 ECG) for primary prevention of sudden death (SD). Methods and results Three hundred and twenty patients (258 males, median age 43 years) with type 1 ECG were enrolled. No patient had previous cardiac arrest. Fifty-four per cent of patients had a spontaneous and 46% a drug-induced type 1 ECG. One-third had syncope, two-thirds were asymptomatic. Two hundred and forty-five patients underwent electrophysiologic study (EPS) and 110 patients received an implantable cardiac defibrillator (ICD). During follow-up [median length 40 months (IQ20-67)], 17 patients had major arrhythmic events (MAE) (14 resuscitated ventricular fibrillation (VF) and three SD). Both a spontaneous type 1 ECG and syncope significantly increased the risk (2.6 and 3.0% event rate per year vs. 0.4 and 0.8%). Major arrhythmic events occurred in 14% of subjects with positive EPS, in no subjects with negative EPS and in 5.3% of subjects without EPS. All MAE occurred in subjects who had at least two potential risk factors (syncope, family history of SD, and positive EPS). Among these patients, those with spontaneous type 1 ECG had a 30% event rate. Conclusion (1) In subjects with the Brugada type 1 ECG, no single clinical risk factor, nor EPS alone, is able to identify subjects at highest risk; (2) a multiparametric approach (including syncope, family history of SD, and positive EPS) helps to identify populations at highest risk; (3) subjects at highest risk are those with a spontaneous type 1 ECG and at least two risk factors; (4) the remainder are at low risk.

Recommendations for participation in leisure-time physical activity and competitive sports in patients with arrhythmias and potentially arrhythmogenic conditions Part I: Supraventricular arrhythmias and pacemakers.

This document by the Study Group on Sports Cardiology of the European Society of Cardiology extends on previous recommendations for sports participation for competitive athletes by also incorporating guidelines for those who want to perform recreational physical activity. For different supraventricular arrhythmias and arrhythmogenic conditions, a description of the relationship between the condition and physical activity is given, stressing how arrhythmias can be influenced by exertion or can be a reflection of the (patho)physiological cardiac adaptation to sports participation itself. The following topics are covered in this text: sinus bradycardia; atrioventricular nodal condition disturbances; pacemakers; atrial premature beats; paroxysmal supraventricular tachycardia without pre-excitation; pre-excitation, asymptomatic or with associated arrhythmias (i.e. Wolff-Parkinson-White syndrome); atrial fibrillation; and atrial flutter. A related document discusses ventricular arrhythmias, channelopathies and implantable cardioverter defibrillators.

Management of syncope referred urgently to general hospitals with and without syncope units

OBJECTIVE We tested the hypothesis that management of patients with syncope admitted urgently to a general hospital may be influenced by the presence of an in-hospital structured syncope unit. BACKGROUND The management of syncope is not standardized. Methods We compared six hospitals equipped with a syncope unit organized inside the department of cardiology with six matched hospitals without such facilities. The study enroled all consecutive patients referred to the emergency room from 5 November 2001 to 7 December 2001 who were affected by transient loss of consciousness as their principal symptom. RESULTS There were 279 patients in the syncope unit hospitals and 274 in the control hospitals. In the study group, 30 (11%) patients were referred to the syncope unit for evaluation. In the study group, 12% fewer patients were hospitalized (43 vs 49%, not significant) and 8% fewer tests were performed (3.3+/-2.2 vs 3.6+/-2.2 per patient, not significant). In particular, the study group patients underwent fewer basic laboratory tests (75 vs 86%, P=0.002), fewer brain-imaging examinations (17 vs 24%, P=0.05), fewer echocardiograms (11 vs 16%, P=0.04), more carotid sinus massage (13 vs 8%, P=0.03) and more tilt testing (8 vs 1%, P=0.000). In the study group, there was a +56% rate of final diagnosis of neurally mediated syncope (56 vs 36%, P=0.000). CONCLUSION Although only a minority of patients admitted as an emergency are referred to the syncope unit, overall management is substantially affected. It is speculated that the use of a standardized approach, such as that typically adopted in the syncope unit, is able to influence overall practice in the hospital.

Programmed ventricular stimulation for risk stratification in the Brugada syndrome: A pooled analysis

Background— The role of programmed ventricular stimulation in identifying patients with Brugada syndrome at the highest risk for sudden death is uncertain. Methods and Results— We performed a systematic review and pooled analysis of prospective, observational studies of patients with Brugada syndrome without a history of sudden cardiac arrest who underwent programmed ventricular stimulation. We estimated incidence rates and relative hazards of cardiac arrest or implantable cardioverter-defibrillator shock. We analyzed individual-level data from 8 studies comprising 1312 patients who experienced 65 cardiac events (median follow-up, 38.3 months). A total of 527 patients were induced into arrhythmias with up to triple extrastimuli. Induction was associated with cardiac events during follow-up (hazard ratio, 2.66; 95% confidence interval [CI], 1.44–4.92, P<0.001), with the greatest risk observed among those induced with single or double extrastimuli. Annual event rates varied substantially by syncope history, presence of spontaneous type 1 ECG pattern, and arrhythmia induction. The lowest risk occurred in individuals without syncope and with drug-induced type 1 patterns (0.23%, 95% CI, 0.05–0.68 for no induced arrhythmia with up to double extrastimuli; 0.45%, 95% CI, 0.01–2.49 for induced arrhythmia), and the highest risk occurred in individuals with syncope and spontaneous type 1 patterns (2.55%, 95% CI, 1.58–3.89 for no induced arrhythmia; 5.60%, 95% CI, 2.98–9.58 for induced arrhythmia). Conclusions— In patients with Brugada syndrome, arrhythmias induced with programmed ventricular stimulation are associated with future ventricular arrhythmia risk. Induction with fewer extrastimuli is associated with higher risk. However, clinical risk factors are important determinants of arrhythmia risk, and lack of induction does not necessarily portend low ventricular arrhythmia risk, particularly in patients with high-risk clinical features.

Rationale and design of the GISSI-Atrial Fibrillation Trial: a randomized, prospective, multicentre study on the use of valsartan, an angiotensin II AT1-receptor blocker, in the prevention of atrial fibrillation recurrence.

Background The possibility of preventing atrial fibrillation recurrence with anti-arrhythmic agents is very limited, given the discouraging results obtained with current drugs in many patients. Data from experimental studies suggest that angiotensin II AT1-receptor blockers can influence atrial remodelling, a key factor in atrial fibrillation initiation and maintenance. Moreover, some preliminary clinical data show that angiotensin II AT1-receptor blockers can prevent atrial fibrillation episodes. The GISSI-Atrial Fibrillation (AF) trial is a randomized, prospective, parallel group, placebo-controlled, multicentre study designed to test whether angiotensin II AT1-receptor blockers can reduce atrial fibrillation recurrence. Objectives and Methods The primary objective of the study is to demonstrate that, in patients with a history of recent atrial fibrillation who are treated with the best recommended therapies, the addition of the angiotensin II AT1-receptor blocker valsartan (titrated up to 320 mg) is superior to placebo in reducing atrial fibrillation recurrence. A substudy will analyse the effect of valsartan on left atrial dimensions and on neurohormones. The study population consists of patients with symptomatic atrial fibrillation (at least two electrocardiogram documented atrial fibrillation episodes in the previous 6 months or successful cardioversion in the last 2 weeks) with underlying cardiovascular diseases or comorbidities. With approximately 100 centres participating in Italy, a total of 1402 patients are randomized in a 1: 1 ratio to receive valsartan or placebo. The enrolment period will last 12 months and the patients will be followed for 12 months from study entry. Conclusions The GISSI-AF is the largest trial aimed at assessing the role of angiotensin receptor blockade in reducing the recurrence of atrial fibrillation and its possible mechanisms of action in terms of its effects on atrium remodelling and neurohormones.

Patterns of ventricular tachyarrhythmias associated with training, deconditioning and retraining in elite athletes without cardiovascular abnormalities.

Ventricular tachyarrhythmias commonly occur in trained athletes during ambulatory Holter electrocardiography and are usually associated with a benign course. Such arrhythmias have been demonstrated to be sensitive to short periods of athletic deconditioning; however, their response to retraining is not known. Twenty-four hour Holter electrocardiographic monitoring was performed at peak training and after 3 to 6 months of deconditioning and was repeated in the present study after 2, 6, and 12 months of retraining in 37 athletes with frequent and complex ventricular tachyarrhythmias and without cardiovascular abnormalities. These subjects showed partial (101 to 500 ventricular premature complexes [VPCs]/24 hours) or marked (<100 VPCs) reversibility of arrhythmias after deconditioning. Retraining initially resulted in a significant increase in arrhythmia frequency compared with deconditioning (from 280 ± 475 to 1,542 ± 2,186 VPCs; p = 0.005), couplets (0.14 ± 0.42 to 4.4 ± 8.2; p = 0.005), and nonsustained ventricular tachycardia (from 0 to 0.8 ± 1.8; p = 0.02). Subsequently, a progressive reduction was seen in the frequency of all ventricular arrhythmias during the 1 year of training to well below that at the peak training levels (VPCs 917 ± 1,630, couplets 1.8 ± 4.2, and nonsustained ventricular tachycardia 0.4 ± 1.2). Such annual arrhythmia reduction was significantly greater statistically in those athletes with marked reversibility after deconditioning than in the athletes with partial reversibility (69 ± 139 vs 1,496 ± 1,917 VPCs/24 hours, respectively; p = 0.007). No cardiac events or symptoms occurred during 1 year of follow-up. In conclusion, in elite athletes without cardiovascular disease, a resumption in intense training after deconditioning was associated with variable, but prolonged, suppression of ventricular ectopy. The absence of adverse clinical events or symptoms associated with the resumption of training supports the continued eligibility in competitive sports for such athletes and is also consistent with the benign nature of physiologic athletes heart syndrome.