The prevention of Sudden Cardiac Death- Sports & Exercise The prevention of Sudden Cardiac...

The prevention of Sudden Cardiac Death- Sports & ExerciseThe prevention of Sudden Cardiac Death- Sports & Exercise

ECG Abnormalities in the AthleteCauses and Outcomes

DOMENICO CORRADO, MD, PhDDOMENICO CORRADO, MD, PhD Department of Cardiac, Thoracic and Vascular Sciences

University of Padova, Italydomenico.corrado@unipd.it

Irish Heart Foundation - Third National ConferenceIrish Heart Foundation - Third National ConferenceDublin - November 22, 2008Dublin - November 22, 2008

Athlete’s Heart

ECG changes in athletes are common and usually reflect morphofunctional remodelling of the heart as an adaptation to regular physical training (athlete’s heart).

Physiologic hypertrophy of Athlete’s Heart

Distribution of cardiac dimensions in large populations of highly trained male and female athletes

Physiologic vs malignant ECG changes

• Rarely abnormalities of athlete’s ECG may be an expression of an underlying heart disease at risk of sudden arrhythmic death during sport.

• It is imperative that ECG abnormalities resulting from intensive physical training and those potentially associated with an increased cardiovascular risk are properly defined.

Cardiovascular causes of sudden death associated with sports

Adults (age > 35 years):Atherosclerotic coronary artery disease

Young competitive athletes (age ≤35 years):Hypertrophic cardiomyopathyArrhythmogenic right ventricular cardiomyopathyCongenital anomalies of coronary arteriesMyocarditisAortic ruptureValvular diseasePreexcitation syndromes and conduction diseasesIon channel diseasesCongenital heart disease, operated or unoperated

Leading causes of sudden cardiovascular death in young competitive athletes

HCM ARVC/D

Physiologic vs malignant ECG changes

• Rarely abnormalities of athlete’s ECG may be an expression of an underlying heart disease at risk of sudden arrhythmic death during sport.

• It is imperative that ECG abnormalities resulting from intensive physical training and those potentially associated with an increased cardiovascular risk are properly defined.

Physiologic vs malignant ECG changes

ECG has been traditionally considered to be a non specific and non cost-effective screening tool in the athletic population, because of its presumed high level of false positive results. This has been the result of the misconception that physiologic ECG changes, that usually occur in trained athletes as an expression of heart adaptation to sustained physical exercise, overlap significantly with pathologic ECG abnormalities seen in the cardiovascular diseases which cause SCD.

HCM athletes?

Screening of young athletes for Cardiovascular diseases

(Center for Sports Medicine, Padua 1979-2004)

Athletes screened 42,386

Positive findingsPositive findings 3,914 (9%)3,914 (9%)

Heart diseases879 (2%)

Corrado et al JAMA 2006; 296: 1593-1601

Potentially lethal heart diseases 91 (0.2%)

False positive≈ 7%

Italian Sports Physicians

• Italian sports physicians have a specific training, scientific background and medical skill for appropriate interpretation of ECG abnormalities in the athlete

• Such physicians attend postgraduate residency training programs in sports medicine (and sports cardiology) full-time for four year and work in sports medical centres specifically devoted to periodical screening of athletes.

How to interprete 12-lead ECG in the athletePERSPECTIVE

• Appropriate interpretation of athlete’s ECG requires the distinction of two main groups of abnormalities based on:– prevalence, – relation to exercise training, – inherent cardiovascular risk, – and need for further clinical investigation to

confirm (or exclude) an underlying cardiovascular disease

How to interprete 12-lead ECG in the athlete

• The importance of distinguishing ECG abnormalities due to the normal athletic heart from heart disease has profound implications.

• Athletes may undergo expensive diagnostic work-up or may be unnecessarily disqualified from competition for abnormalities that fall within the normal range for athletes.

• Alternatively, signs of potentially lethal cardiovascular disorders may be misinterpreted as normal variants of an athlete's ECG.

ECG IN ELITE ATHLETES

AHA Scientific Sessions 2007

Male, 22 years oldSport: middle- distance running

Pelliccia et al. Circulation. 2000;102:278-84

Clinical significance of abnormal ECGpatterns in trained athletes

Physiologic vs pathologic LVH

• In order to differentiate physiologic from pathologic LV hypertrophy, it is important to know whether differences exist between: – the ECG pattern associated with physiologic

remodelling in the context of “athlete’s heart” and– the ECG abnormalities occurring in structural

heart diseases manifesting with an increased LV wall thickened, including hypertrophic cardiomyopathy (HCM), aortic valve diseases, or hypertensive heart disease.

AHA Scientific Sessions 2007

Objectives

• The purpose of the study is to assess whether ECG abnormalities of pathologic hypertrophy (HCM) overlaps with those of physiologic hypertrophy (athlete’s heart).

AHA Scientific Sessions 2007

• The ECG analysis was focused on what proportion of both groups presented with the ECG pattern of isolated voltage criteria for LVH.

HCM athletes?

AHA Scientific Sessions 2007

Study populations & DemographicsHCM

(n. 260)

• Age: 42 years (3 – 82 ys)• Sex: 184 male (71%)• DNA analysis: 48 pts (18%)• Max LV WT: 22 mm 6

(range 16 – 46 mm)• LV EDD: 43 mm 10• Obstruction: 22% (57 pts)

ATHLETES(n. 1005)

• Age: 23 years (9 - 55 ys)• Sex: 745 male (74%)• Race: 1003 Europeans, 2

Africans• Sport discipline: 38• Training program: median of 7

years (2-30 ys)• Max LV WT: 10.74• LV EDD: 54 mm 6

RESULTS: ECG IN HCM AND IN ELITE ATHLETES

P< 0.0001

%

5,4

94,6

18,7

81,3

0

10

20

30

40

50

60

70

80

90

100

normal abnormal

HCM elite athletes

AHA Scientific Sessions 2007

P <0.0001

%

P <0.0001

ECG pattern

Athletesn=1005

(%)

HCM

n=260 (%)

p value

Isolated increase of QRS voltages

403

(40)

5

(1.9) <0.0001

Nonvoltage criteria of LVH

13

( 1.3)

155

(59.6)<0.0001

ST/T repolarization abnormalities

27

(2.7)

209

(80)<0.0001

Pathologic Q waves17

(1.7)

103

(39.6)<0.0001

ECG patterns Elite athletes vs HCM pts

AHA Scientific Sessions 2007

ECG IN HCM

Female, 16 years old

Max Wall Thickness: 27 mm

25 mm/s 10 mm/mV ~0.15 Hz-40 Hz AHA Scientific Sessions 2007

ECG IN HCM

25 mm/s 10 mm/mV ~0.15 Hz-40 Hz AHA Scientific Sessions 2007

Male, 23 years oldMax Wall Thickness: 25 mm

ECG IN HCM

Male, 25 years old

Max Wall Thickness: 29 mm

25 mm/s 10 mm/mV ~0.15 Hz-40 Hz AHA Scientific Sessions 2007

ECG patterns

Athletesn=1005

(%)

HCM

n=87 (%)

p value

Isolated increase of QRS voltages

403

(40)

2

(2.3) <0.0001

Nonvoltage criteria of LVH

13

(1.3)

17

(19.5)<0.0001

ST/T repolarization abnormalities

27

(2.7)

29

(33.3)<0.0001

Pathologic Q waves17

(1.7)

39

(44.8)<0.0001

ECG abnormalities in HCM ptsand elite athletes matched for age

• The vast majority of patients with confirmed diagnosis of HCM presents an abnormal ECG

•The ECG of HCM overlaps marginally with ECG of trained athletes.

•In HCM isolated electrocardiographic voltage criteria (Sokolow-Lyon) for LVH are an uncommon pattern, whereas physiological hypertrophy of trained athletes presents characteristically with pure increased of QRS voltages

•Systematic echocardiographic evaluation of athletes fullfilling isolated voltage criteria for LVH at preparticipation screening is not justified, resulting in a considerable cost saving.

Remarks

AHA Scientific Sessions 2007