The Year of 2009 in Electrocardiology

Abstract

Ann Noninvasive Electrocardiol 2010;15(4):378‐383

Due to space limitations in Annals, I have limited my selection to just 50 of several hundred outstanding publications devoted to electrocardiography that were published in 2009, representing no change from previous years. ¹ , ² , ³ , ⁴ I apologize to those investigators, who are rightly looking for, but not finding their article in the following review.

THE P WAVE AND PR INTERVAL

Changes in P‐wave morphology, indicating abnormal interatrial conduction was demonstrated in MADIT II patients, ⁵ and a substantial heritability was demonstrated for P‐wave duration and PR interval in a South Pacific isolated founder population. ⁶ Yasar and coworkers found that patients with metabolic syndrome have higher P‐wave dispersion and maximum P‐wave duration, indicating increased risk for atrial fibrillation. ⁷

THE QRS COMPLEX

A fragmented QRS, defined by the presence of single or multiple notches in the R or S wave, without a typical bundle branch block (BBB), in ≥ 2 contiguous leads was an independent predictor of mortality in patients with acute coronary syndrome. ⁸ Schinkel and coworkers ⁹ reconfirmed that QRS duration ≥ 120 ms is an independent predictor of cardiac death and nonfatal infarction in patients with suspected coronary heart disease and demonstrated that this risk is persistent after adjustment for clinical variables, left ventricular function, and myocardial ischemia.

In hypertensive patients receiving intensive medical therapy, the QRS duration predicted sudden cardiac death (SCD) (not necessarily arrhythmic) during a nearly 5‐year follow‐up, even after controlling for the presence of left BBB, the effects of hypertensive treatment, and other known risk factors for SCD. ¹⁰ QRS duration ≥ 150 ms even in class I‐II patients with an ejection fraction (EF) ≤ 30% was recommended to be an indication for cardiac resynchronization therapy. ¹¹ The baseline QRS duration was found to be an independent predictor of 30‐day mortality in patients with anterior acute myocardial infarction (AMI), even when unaccompanied by right BBB, but did not stratify mortality risk in patients with inferior AMI. ¹² The hemodynamic disadvantage of left BBB was reemphasized by finding a relative under perfusion of the septum during exercise, reversible by short‐term right ventricular pacing. ¹³

THE QT INTERVAL

For reliable QT measurement 12‐lead Holter recordings were annotated beat‐to‐beat by an automatic algorithm for global QRS onset and T offset: variances of the beat‐to‐beat QT measurements were in the range 2.5–3.4 ms over three distinct databases and application to a moxifloxacin/placebo control database showed excellent results. ¹⁴

A 30‐km cross‐country race in runners aged ≥ 50 was the model for studying with vectocardiography the effect of prolonged exercise on ventricular repolarization: postrace corrected QT (QTc) increased immediately after the excessive physical exercise and remained unchanged on day 1 (P < 0.05), mainly because of an increased peak‐end T interval. T area remained high even on postrace day 6. ¹⁵

Twenty‐four hour Holter recordings in patients with chronic heart failure demonstrated ¹⁶ that repolarization lability as reflected in measuring QT variability has a pronounced diurnal variation and increases significantly after 6 AM, the time of greatest arrhythmic risk. The authors concluded that QT variability measured for 24 hours might improve risk prediction in chronic heart failure patients and should be tested in appropriate trials. Zhou et al. ¹⁷ developed for resting diagnostic, ambulatory Holter, an in‐hospital patient monitoring QT interval algorithms that provide accurate QT interval measurements and promises to capture early signs of QT prolongation. Dimopoulos and coworkers ¹⁸ found that QTc dispersion is an independent predictor of major cardiovascular events in elderly hypertensive and normotensive patients and suggested to use in risk stratification.

J point‐T peak interval measured from a 12‐lead ECG was found to be highly specific in diagnosing short QT syndrome ¹⁹ ; although based on a small sample size, this observation suggests that the diagnosis of short QT syndrome should not be made in asymptomatic subjects without a family history of SCD or serious arrhythmias if their J point‐T peak interval is not shortened (i.e., is >150 ms).

THE T WAVE

In a general population sample four T‐wave morphology parameters (principal component analysis ratio, T‐wave morphology dispersion, total cosine R‐to‐T, and T‐wave residuum) provided independent prognostic information cardiovascular mortality: ²⁰ the authors demonstrated that T‐wave morphology parameters have gender‐related differences in their predictive value and for risk assessment, these parameters must be assessed separately in men and women.

A novel T‐wave morphology analysis showed that increased lead dispersion or decreased normalized T‐loop area on standard 12‐lead ECG identified heart failure patients at high risk for life‐threatening ventricular tachycardia/ventricullar fibrillation (VT/VF). ²¹

The Tpeak‐Tend interval (TpTe), linked to an increased arrhythmic risk was investigated before and after primary percutaneous coronary intervention in patients with ST‐segment elevation myocardial infarction; a prolonged preprocedural TpTe predicted subsequent all‐cause mortality. ²² TpTe, T‐wave flatness, T‐wave symmetry, and T‐wave notch were included in a cell‐to‐ECG model for studying relationship between multiple ion‐channel factors with ECG morphology‐related changes. These parameters were highly correlated with transmural dispersion and are heart rate independent. ²³

T‐wave alternans (TWA), evaluated by modified moving average‐based method, was found to be a good predictor for the incidence of life‐threatening ventricular arrhythmias during a mean follow‐up of 72 months in patients with old myocardial infarction. ²⁴ In patients with ischemic and nonischemic left ventricular dysfunction time domain TWA measured from 24‐hour Holter ECGs predicted cardiac mortality, ²⁵ with a hazard ratio over that of functional class, diabetes, renal dysfunction, or nonsustained ventricular tachycardia.

THE U WAVE

The “100‐year‐old enigma” of the U wave was challenged by Postema and coworkers ²⁶ in their meticulous investigation of the relationship between the U wave and the inward rectifier repolarizing current I _K1; they concluded that the U wave is modulated by either an increase or a decrease of this current, with a corresponding decrease or increase of its amplitude, supporting the notion that the U wave is caused by intrinsic potential differences in the terminal part of the action potential.

ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA (ARVD)

A comprehensive reevaluation of the diagnostic ECG features revealed that in the absence of a complete or incomplete right BBB, T‐wave inversion through lead V₃ was the single ECG parameter that demonstrated optimal sensitivity and specificity; in incomplete right BBB (15% of patients) T‐wave inversion through V₃ and in complete right BBB (17% of patients) an r’/s ratio in V₁ < 1 was provided optimal sensitivity and specificity. ²⁷ The authors concluded that ECG can be relied on with confidence as a screening tool for ARVD.

LONG QT SYNDROME (LQTS)

In LQTS patients, giant T‐U waves separated Torsades de Pointes (TdP) initiation from premature ventricular complexes (PVCs) in other heart diseases and from other PVCs in LQTS patients, suggesting that early after depolarizations initiate TdP. ²⁸ Manually measured short‐term variability of the QT interval on surface ECG was found to be increased in patients with congenital LQTS and this effect is increased in patients with symptoms before therapy; hence, this parameter could prove to be a useful noninvasive additive marker for diagnostic screening. ²⁹

CARDIOMYOPATHIES

In patients even with echocardiographic evidence of hypertrophic cardiomyopathy (HCM), a normal ECG appears to exhibit a less severe phenotype with better cardiovascular outcomes ² , ³⁰ in a retrospective cohort study of HCM patients followed for a mean period of 5.3 years. A “hump” at the ST segment during exercise testing appears to be a risk factor for SCD. ³¹

Using extended‐length ECG, the differential diagnosis between physiologic left ventricular hypertrophy (LVH) and HCM could be improved by using QTc interval, QT dispersion, mean resting heart rate, and low‐amplitude signal duration at 25 Hz at the end of filtered QRS. ³²

In patients with dilated cardiomyopathy (DM) QRS duration > 110 ms from conventional surface ECG had prognostic impact for cardiac and SCD in univariate and multivariable analyses, similarly to diabetes mellitus and magnetic resonance imaging parameters. ³³

Papadakis and coworkers ³⁴ suggested, based on an evaluation of 1710 Caucasian adolescent athletes and 400 controls that T‐wave inversions in any lead are unusual, warranting further investigations for underlying cardiomyopathy.

HYPERTENSION

The development of a new ECG strain pattern of lateral ST depression and T‐wave inversion in lead V₅ or V₆ between baseline and year 1 identified, in the LIFE study, patients at increased risk of cardiovascular morbidity and mortality, SCD, and all‐cause mortality. ³⁵ The authors suggested that the development of new strain on the ECG may be used to identify hypertensive patients with electrocardiographic LVH who require more aggressive antihypertensive therapy aimed at further risk reduction. Okin advocated ³⁶ serial evaluation of ECG LVH for prediction of risk in hypertensive patients, suggesting that antihypertensive therapy targeted at regression or prevention of ECG LVH may improve prognosis.

HEART RATE VARIABILITY (HRV) AND TURBULENCE (HRT)

A Holter‐based methodology showed that enhanced HRV and R‐wave amplitude analysis were an easily accessible and reliable method for suspicion of sleep apnea or hypopnea in a general population. ³⁷

HRT parameters like turbulence onset and turbulence slope correlated significantly on Holter monitoring correlated significantly with C‐reactive protein and was helpful for risk stratification of patients with unstable angina. ³⁸ 24‐hour Holter derived HRT pathologies were independent predictors of cardiovascular death in high‐risk post‐MI patients with left ventricular dysfunction; the optimal cutpoint for HRT slope was found to be higher in this study than previously reported. ³⁹

Abnormal HRT on 24‐hour Holter in the presence of abnormal deceleration capacity, a sign of severe autonomic failure, identified in postinfarction patients with preserved left ventricular function a subgroup with increased mortality risk equivalent to patients with left ventricular ejection fraction (LVEF) of ≤ 30%. ⁴⁰

EXERCISE ECG

In a population‐based sample of 1769 men without evident coronary heart disease, ⁴¹ the authors used the accepted criteria for ischemia during exercise and recovery of horizontal or down‐sloping ST depression 1.0 mm at 80 ms after J point or any ST depression of > 1.0 mm at 80 ms J point, even if painless. These findings were strong predictors of SCD, especially in smokers, as well as in hyperchlolesterolemic, and hypertensive men.

Gorodeski and coworkers ⁴² scrutinized 11 quantative ECG measures relating to heart rate, conduction, left ventricular mass, and repolarization, in patients without known cardiovascular disease who had a clinically normal resting ECG and who underwent treadmill exercise testing; subtle ECG findings relating to these variables provided modest but definite prognostic information during a median follow‐up of over 10 years, additional to clinical and exercise measures. Reduced heart rate recovery and heightened TWA during routine exercise testing predicted risk for cardiovascular and all‐cause death in a low‐risk population. ⁴³ Perez and coworkers ⁴⁴ described an artificial resting ECG neural network (RENN) that uses the resting ECG and demographic variables to predict cardiovascular mortality; this RENN score could further risk stratify patients deemed at moderate risk on exercise treadmill testing.

THE BRUGADA SYNDROME (BS)

In a prospective study, ⁴⁵ late potentials (LPs) detected by signal‐averaged ECG had the most significant hazard ratio for the occurrence of arrhythmic events during a follow‐up period of 33 ± 9 months in patients with BS. Somewhat similar results were reported by Mizobuchi and coworkers ⁴⁶ who found that LPs in apparently normal ECGs can predict the alterations to a drug‐induced type‐1 Brugada ECG and unmask the patients at risk.

OCCURRENCE OF J WAVES: THE EARLY REPOLARIZATION SYNDROME

While for several decades, J‐wave deflection occurring at the QRS‐ST junction was looked upon as a benign condition, Tikkanen and coworkers ⁴⁷ found in a community‐based general population of over 10,000 middle‐aged subjects a 5.8% frequency of this pattern. During a mean follow‐up of 30 ± 11 years early repolarization of ≥ mV in inferior leads was associated with an increased risk of cardiac death (P = 0.03), while of > 0.2 mV had a markedly elevated risk of cardiac deaths (P < 0.001) and from arrhythmia (P = 0.01), observations in line with last year's two reports.

The ability of terminal QRS notching in leads V₄ and V₅ to distinguish benign from malignant electrocardiographic forms of early repolarization, based on over 1200 consecutive implantable cardioverter‐defibrillator (ICD) implants, was demonstrated by Merchant and coworkers. ⁴⁸

Haissaguerre and coworkers, ⁴⁹ who earlier reported findings similar to Tikkanen et al., reported that prior to the arrhythmic episode 12‐lead ECGs showed a consistent increase in the amplitude of early repolarization, compared with that seen in baseline; the authors stressed that isoproterenol in acute cases or the oral administration of quinidine are effective in correcting the ECG pattern and suppressing recurrence of arrhythmias. Dr.Viskin in his Editorial Comment ^a stressed the overlap between VF patients and control subjects in terms of J‐wave amplitude, J‐wave location, and QT‐intervals. Based on a meticulous study of seven patients, Jastrzebski and Kukla ⁵⁰ entertained the possibility that the J‐wave‐like terminal QRS notch and/or J‐wave‐like ST‐segment elevation in the patients with VF episodes may be ischemia induced, representing acquired ion‐channel dysfunctions.

RHYTHM DISORDERS

In examinees without any structural heart disease, ruled out by echocardiography and cardiac magnetic resonance imaging, frequent PVCs originating from the ventricular outflow tract, during a follow‐up period of at least 4 years there was a significant negative correlation between the PVC prevalence and ΔLV ejection fraction and positive correlation between the PVC prevalence and ΔLV diastolic dimension. As the patients with highly frequent PVCs (> 20,000 beats/day) exhibited a significant decrease in the LVEF at the 4 and 5.8 (2.3) year follow‐ups, the authors call for attention to the progression of left ventricular dysfunction in such persons. ⁵¹

ECG IN VARIOUS DISORDERS

In patients with unexplained syncope, an abnormal 12‐lead ECG together with pathologic findings on 24‐hour Holter monitoring and these predicted the results of subsequent electrophysiology testing. ⁵² In the author's experience, if resting ECG and Holter were negative, electrophysiological testing was only rarely abnormal. In patients with sarcoidosis, a fragmented QRS complexes on 12‐lead ECG was associated with cardiac involvement, proved by gadolinium cardiac magnetic resonance imaging. ⁵³

Following two reported cases about the disappearance of Brugada‐like ECG after surgical castration for prostate cancer, Haruta and coworkers ⁵⁴ found a higher risk of prostate cancer in men with Brugada‐like ECG, independent of age, smoking habit, and radiation exposure; the authors recommend regular prostate examinations for elderly men with BS.