Risk Factors for Sudden cardiac Death

Transcription

1 Risk Factors for Sudden cardiac Death A. Arenal Arrhythmias in competitive sports

2 Disclosure Conflict of interest Advisory board: Medtronic, Boston Scientific Research grants: Medtronic, Boston Scientific, Biosense-Webter

3 Exercise and Eletrophysiology Exercise is associated with increased sympathetic tone and parasympathetic withdrawal Shortening of VERP Refractoriness dispersion

4 Exercise EP changes Kannankeril et al. Am J Physiol Heart Circ Physiol 282: H2091 H2098, 2002.

5 Exercise EP changes

6 Sudden death and exercise THE RISK OF SUDDEN DEATH is increased nearly 17-fold during and immediately after exercise Albert C. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med 343: , 2000.

7 Questions Are competing athletes at higher SCD risk? What are the risk factors?

8 Incidence of Sudden Cardiac Death Study Patients Age group Collection y Country SCD Inc. Atkins et al Non-Ath US-CA 6.37 Eckart et al Non-Ath US 13 Maron et al HS-Ath Min, US 0.46 Maron et al HS-Ath Min, US 0.93 Maron et al HS-Ath Min, US 0.97 Winkel et al All SD Denmark 2.8 Holst et al Ath Denmark 1.21 Corrado et al Non-Ath Veneto, I 0.9 Corrado et al Ath Veneto, I 2.3 Corrado et al Non-Ath Veneto, I 0.79 Corrado et al Ath Veneto, I 1.9

9 Exercise related SCD in nonathletes SCD among 6 million military recruits (age 17-35) over a 25-year period ( ) ACO Myocarditis CAD HCM Unknown Eckart et al. Ann Intern Med 2004; 141:829.

10 Sudden Cardiac Death in Athletes ARVC 10% 8% 2% 23% Atherosclerotic Coronary disease Anomalous Coronary origin Mitral Valve prolpase 12% 19% ATHLETS < 35 AÑOS Other Myocarditis 12% Conduction Disease 14% HCM * Athlets < 35 years, Veneto , Corrado et al. J Am Coll 2003

11 Sudden Cardiac Death in Athletes HCM 36% Normal heart 3% Other 3% Aortic rupture 2% Lon channelopathies 3% Other Congenital Sarcoidosis HD 2% 1% Tunneled LAD 3% AS 3% CAD 3% Indeterminate LVH Possible HCM 8% Coronary artery Anomalies 16% Maron BJ, et al. Circulation 2007; 115:1643.

12 Hypertrophic Myocardiopathy In the general population, it is diagnosed in about 1 in 500 people, although it seems to be somewhat lower in athletes, slightly less than 0.1%, as a consequence of selection bias;

13 Hypertrophic Myocardiopathy Patched fibrosis possibilities reentrant ventricular arrhythmias Adrenergic predominance during exercise can enhance risk or reentrant ventricular tachycardia. In addition, exercise-induced ischemia in severe hypertrophic myocardium might lead to ventricular arrhythmias.

14 Hypertrophy Cardiomyopathy When mild to moderate hypertrophy is determined, a dilated LV and preserved diastolic function suggests physiological adaptation to intense exercise. On the contrary, nondilated LV with impaired LV function is suggestive of HCM.

15 Arrhythmogenic Right Ventricle Dysplasia ARVC is histologically defined by cardiomyocite death that are replaced by fibrofatty tissue. It causes free RV wall thinning, enlargement and dysfunction, and formation of aneurisms. ARVC patients might be especially sensible to adrenergic states because of denervation that develops in some ARVD areas.

16 Exercise and ARVD Right ventricle dilatation and RV arrhythmias, are related to age and intensity of exercise training, Increases in RV preload and afterload as a consequence of exercise could accelerate loss of intercellular junctions and accelerating ventricular dilatation and arrhythmogenesis

17 ARVD However, less than 10% of sudden deaths in ARVC happen during exercise. ARVC patients who regularly practice sport have 5.4 times more risk of SD compared to sedentary population. Tabib A, et al Circulation. 2003;108(24): Corrado D, J Am Coll Cardiol. 2003;42(11):

18 Channelopathies and primary electrical diseases Because studies are mainly based on necropsies, and previous EKG are lacking, channelopathies or WPW syndrome are probably underestimated as a cause of sudden death. They are usually reported to account for about 1 2% of SD causes. However, they might be responsible for, at least, part of patients without heart disease at necropsy who make about 2 4% of patients with sudden death.

19 Channelopathies and primary electrical diseases Type 1 and 2 LQTS are are associated with sudden cardiac death during exercise and stress. But type 3 LQTS is strongly related to ventricular arrhythmias at rest SD in patients with Brugada syndrome is usually related to rest and sleeping, increased vagal tone is capable of unmasking typicalmekg. Thus, increased vagal tone in athletes could enhance propensity to suffer ventricular arrhythmias. Also hyperthermia can unmask Brugada EKG. Catecholaminergic ventricular tachycardia.

20 SYNCOPE

21 Colivicchi F. Epidemiology and prognostic implications of syncope in young competing athletes. Eur Heart J 2004; 25:1749.

22 Syncope in young competing athletes the 472 athletes with syncope before the first pre-participation screening and without any cardiac abnormality continued their training during the follow-up period and did not experience any major cardiac event. Colivicchi F. Epidemiology and prognostic implications of syncope in young competing athletes. Eur Heart J 2004; 25:1749.

23 Syncope in young competing athletes Colivicchi F. Epidemiology and prognostic implications of syncope in young competing athletes. Eur Heart J 2004; 25:1749.

24 Syncope in young competing athletes Br J Sports Med 2007;41:

25 Syncope in young competing athletes A 30-year-old male endurance cyclist with right bundle branch block Since he had started on heavy training in the year before admission, he experienced around ten short episodes of light-headedness and one episode of syncope. These symptoms always occurred in a seated position in the initial minutes after aerobic endurance training.

26 Syncope in young competing athletes Br J Sports Med 2007;41:

27 Syncope in young competing athletes Br J Sports Med 2007;41:

28 J Am Coll Cardiol 2002;40:446 52

29 J Am Coll Cardiol 2002;40:446 52

30 Ventricular Arrhythmias J Am Coll Cardiol 2002;40:446 52

31 EP Study In only one of the 24 athletes with EP study (a 32-year-old cyclist with ARVC and 12,000 PVDs and 5 NSVT bursts on Holter ECG) was sustained VT provoked by programmed ventricular stimulation. J Am Coll Cardiol 2002;40:446 52

32 Follow-up Over the follow-up only a 24-year-old man with ARVC, died suddenly while participating in a competition six months after official disqualification. J Am Coll Cardiol 2002;40:446 52

33 Conclusions In a highly trained athletic population presenting with frequent and complex ventricular tachyarrhythmias only about one-third harbored structural cardiovascular abnormalities. These arrhythmias are particularly common in the absence of underlying disease and compatible with survival without cardiovascular events in an eight year follow-up period. J Am Coll Cardiol 2002;40:446 52

34 EARLY REPOLARIZATION

35 Circ Arrhythm Electrophysiol. 2011;4:

36 Training cause early repolarization Circ Arrhythm Electrophysiol. 2011;4:

37 Training cause early repolarization Circ Arrhythm Electrophysiol. 2011;4:

38 Early Repolarization Circulation. 2011;123:

39 Early Repolarization Circulation. 2011;123:

40 Early Repolarization Circulation. 2011;123:

41 Early Repolarization in Athletes Circulation. 2011;123:

42 Conclusions Athletes have an increased risk of sudden death, as compared to an age-matched sedentary population, with a relative risk of 2.1. This increase in SD does not seem to be related to unfavorable effects of sport, but to enhance risk of SD in athletes with underlying heart disease, in whom exercise acts as a trigger for ventricular arrhythmias. This increase in SD risk is particularly high in patients who has abnormal coronary arteries or ARVD; thus, a patient with coronary disease or ARVC has, respectively, 79-fold and 5.6-fold, increase in risk of death when they are regular sport practitioners.