CardioStim Sports Cardiology Report

Seattle ECG Criteria: What's Normal in an Athlete?

John Mandrola

Disclosures

June 25, 2014

At an electrophysiology meeting one would expect a lot of interest in the high-tech and cutting edge. Yet one constant I find at European meetings is the popularity of sports cardiology, a decidedly low-tech judgment-intensive area. A late-afternoon session at CardioStim 2014 was no exception. The room was jammed. This, in Nice, France, in June?

What Is a Normal ECG in Athletes?

Dr Matthias Antz (Oldenburg Clinic, Germany) gave a session on using the Seattle ECG criteria to help define a normal ECG in an athlete. The Seattle ECG criteria were first published in the British Journal of Sports Medicine in 2013 in a series of three papers[1]. Perhaps the most important result of the international effort is this free online ECG training course[2].

This session interested me because the patterns of an ECG, especially in an athlete, are challenging. I find ECG reading to be beautiful because it is qualitative—it is about patterns. Truly "seeing" an ECG is like seeing a face. You remember it as a sum of everything, not just the components.

ECGs pose major issues for the modern-day practitioner. First, we are evolving into a binary protocol-driven way of practicing medicine. The quantitative is  favored over the qualitative, and hence, expertise in ECG reading is waning. Second, caregivers are growing increasingly risk averse. And finally, the cardiac adaptation of athletics—the training effect—creates special patterns on an ECG. Antz remarked that up to 60% of athletes show ECG changes, and some of these changes are striking to look at. Combine all these issues and you get trouble.

The purpose of this lecture, therefore, was to review the criteria used to separate the normal from the abnormal ECG in an athlete. This is important, as was pointed out by a European specialist during the question-and-answer session, when he told the audience he has seen normal athletes undergo cardiac angiography and even pacemaker surgery. And this is far from hyperbole, as I have seen it myself in the real world. You probably have, too.

Antz started by reviewing the specifics of the Seattle ECG criteria, adding his own (useful) commentary on points of emphasis. I recorded the session and will list some of the notables here:

  • Bradycardia: A low heart rate in an athlete should be self-evident—but it is not in the real world. Common normal athletic ECG patterns he chose to highlight included the inverted P-wave and junctional rhythm, Mobitz type I Wenckebach block, and sinus arrhythmia.

  • Incomplete right bundle branch block (IRBBB): While only 10% of the general population has IRBBB, up to 40% of athletes have it as a normal pattern. Antz speculated that this might be due to remodeling of the athletic right ventricle.

  • Left ventricular hypertrophy (LVH): It is normal for athletes to have voltage criteria for LVH. It is abnormal when voltage criteria comes with other LVH patterns, such as left atrial abnormality, ST-segment strain patterns, left axis deviation, etc.

  • Early repolarization: It is common and normal for athletes to have early repolarization, including terminal QRS notching. The pattern is especially common in black athletes.

  • T-wave changes: Antz spent extra time on this confusing area. "T-wave inversions can be normal, or they can be abnormal," he said. Up to one in three black athletes have terminal T-wave inversions in leads V1–V4. He showed pictures of these remarkable patterns and noted they can be mistaken for anterior-wall ischemia. The details here are outside the scope of this post, but the take-home involves paying attention to the location of the inversions and the company they keep. Namely, it is normal to have T-wave inversions in leads V1–V4 but not in V5 or V6 and not with accompanying QRS abnormalities or frequent premature ventricular contractions (PVCs).

  • Notable abnormal findings in athletes: Some of the abnormal ECG findings mentioned in his talk included any complete left bundle branch block, intraventricular conduction delay (IVCD) greater than 140 ms, left atrial abnormality, right ventricular hypertrophy, Wolff-Parkinson-White (WPW) syndrome, QT prolongation (greater than 470 ms in males and 480 ms in females), high-degree AV block, atrial fibrillation/flutter, and high-density PVCs. The matter of PVCs was discussed in the Q & A after the session. A commenter from the audience opined that most PVCs in athletes are benign. Antz agreed there was some gray area with PVCs—well, sort of.

  • Making accurate QT measurements: Antz stressed the importance of excluding the U-wave when measuring the QT interval. I added this issue because computer ECG readings often fail in this regard.

Validation of Seattle Criteria

The final few minutes of the talk dealt with the clinical utility of the Seattle criteria. Antz noted that up to15% of cardiologists surveyed made mistakes interpreting ECGs in athletes; the percentage was worse with noncardiologists. When these same physicians applied the Seattle criteria to the same ECGs, accuracy improved. The false-negative rate improved the most—an important fact for the athlete/patient.

Far From Perfect

Antz emphasized the Seattle criteria were developed in Europe using a white cohort. This fact might limit its accuracy in black athletes. He noted work is ongoing to improve the increased false-positive rate in black athletes.

What's more, he added, the main impediment to ECG accuracy is the clinician's fear of overlooking something. He assured the audience that this was unfounded, saying, "You will not overlook much pathologic abnormality if you use these criteria." For the US clinician, the key modifier in that bold statement is much—as in overlooking any pathology in a young athlete has been deemed unacceptable.

Antz's conclusions were simple: The Seattle criteria define normal and abnormal ECG findings in athletes. Every physician should know these criteria.

My Thoughts

I see four reasons why this is an important and timely message.

The first reason centers on the specific matter of the athlete. Participation in endurance sport is on the rise. This means doctors can expect to see more of these athletic (yet normal) patterns on the ECG. In a later talk, Dr Luis Mont (University of Barcelona, Spain) mentioned that athletes have a discordant view of what is normal. As a lifelong endurance exerciser, I would say this is an understatement.

The second reason this topic is important centers on the quantified-self movement. There is a perplexing notion that health needs to be quantified. No longer are one's belt size, weight, ambulation speed, and percentage of time spent smiling good-enough measures of health. Now we have to have data—the more the better. You can expect more (not fewer) ECGs to be done on healthy athletic people.

The third reason is fear. We are an increasingly fearful, risk-averse society, which, as behavioral psychologists have noted, leads to disordered decision making. Although many thousands more teens and young adults die from texting and driving, substance abuse, and suicide, the death of an athlete stimulates our (collective) action centers. The do-something urge calls many to consider widespread ECG screening—as if data from a small homogenous area in Italy could be extrapolated to the US. The irony of sudden-death prevention in athletes is that perhaps the best way to prevent death in athletes is the same as preventing sudden death in anyone: increased (societal) CPR awareness and AED availability.

Finally, one of the most difficult tasks of a modern-day heart specialist is defining normal. I would say it is courageous to diagnose nothing. And the concept of normal extends past what is normal on an ECG; it goes to what is normal for life, for aging.

To diagnose nothing is to do a lot.

JMM

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