Left Ventricular Hypertrophy by the Surface ECG.

Left ventricular hypertrophy (LVH) is defined as an increase in left ventricular mass (LVM) associated with structural changes of myocardium. The increase in LVM and associated changes are associated with changes in depolarization and repolarization, manifested as a variety of altered QRS and T patterns. Increased QRS voltage has been considered to be a specific ECG finding in LVH, and ECG criteria based on this increased QRS voltage are generally recommended. These ECG changes are also predictive of adverse cardiovascular outcomes. However, it must also be noted that the majority of patients with increased LVM do not have increased QRS voltage. While this is often considered a limitation of ECG in LVH diagnosis, the authors of this minireview consider it more likely that the electrical effects, represented in the altered ECG, and the increased LVM are independent effects, associated by virtue of their common relationship with an underlying pathologic state. This revised view challenges cardiologists and electrocardiologists to explore the interrelationships between electrical, biochemical, and mechanical alterations of myocardial remodeling seen with heart disease, to advance our understanding of this process and its effects, including the evolution of the ECG changes known as "LVH".

Electrocardiographic J Wave and Cardiovascular Outcomes in the General Population (from the Atherosclerosis Risk In Communities Study).

The association between the J wave, a key component of the early repolarization pattern, and adverse cardiovascular outcomes remains unclear. Inconsistencies have stemmed from the different methods used to measure the J wave. We examined the association between the J wave, detected by an automated method, and adverse cardiovascular outcomes in 14,592 (mean age = 54 ± 5.8 years; 56% women; 26% black) participants from the Atherosclerosis Risk In Communities (ARIC) study. The J wave was detected at baseline (1987 to 1989) and during follow-up study visits (1990 to 1992, 1993 to 1995, and 1996 to 1998) using a fully automated method. Sudden cardiac death, coronary heart disease death, and cardiovascular mortality were ascertained from hospital discharge records, death certificates, and autopsy data through December 31, 2010. A total of 278 participants (1.9%) had evidence of a J wave. Over a median follow-up of 22 years, 4,376 of the participants (30%) died. In a multivariable Cox regression analysis adjusted for demographics, cardiovascular risk factors, and potential confounders, the J wave was not associated with an increased risk of sudden cardiac death (hazard ratio [HR] 0.74, 95% CI 0.36 to 1.50), coronary heart disease death (HR 0.72, 95% CI 0.40 to 1.32), or cardiovascular mortality (HR 1.16, 95% CI 0.87 to 1.56). An interaction was detected for cardiovascular mortality by gender with men (HR 1.54, 95% CI 1.09 to 2.19) having a stronger association than women (HR 0.74, 95% CI 0.43 to 1.25; P-interaction = 0.030). In conclusion, our findings suggest that the J wave is a benign entity that is not associated with an increased risk for sudden cardiac arrest in middle-aged adults in the United States.

Individual components of the Romhilt-Estes left ventricular hypertrophy score differ in their prediction of cardiovascular events: The Atherosclerosis Risk in Communities (ARIC) study.

BACKGROUND: It has been recently reported that the Romhilt-Estes (R-E) score, originally proposed for detection of left ventricular hypertrophy from the electrocardiogram, is a strong predictor of all-cause mortality. Whether the R-E score is also predictive of cardiovascular disease (CVD) and whether its individual components differ in their ability to predict different CVD outcomes are not well established. METHODS: This analysis includes 13,261 participants from the ARIC study who were free of CVD at baseline (1987-1989). Incident CVD, coronary heart disease (CHD), heart failure (HF), and stroke were ascertained by an adjudication committee through December 2010. The R-E left ventricular hypertrophy score was measured from automatically processed baseline electrocardiogram data. Cox proportional hazard models were used to examine the association between baseline the R-E overall score (overall) and each of its 6 individual components separately, with each of the CVD outcomes. RESULTS: During a median follow-up of 21.8 years, 3,579, 2,205, 1,814, and 731 CVD, CHD, HF, and stroke events, respectively, occurred. In multivariable adjusted models, R-E score ≥4 points (compared with 0 points) was associated with increased risk of CVD, CHD, HF, and stroke (hazard ratio [95% CI] 1.66 [1.41-1.96], 1.66 [1.34-2.07], 1.97 [1.60-2.43], and 1.49 [1.07-2.07], respectively). The 6 component of the R-E score varied in their relationship to different CVD outcomes. CONCLUSIONS: The R-E score is predictive of CVD outcomes. The 6 R-E score components differ in their associations with different CVD outcomes, indicating that they may be electrical biomarkers of different physiological events within the myocardium.

The Romhilt-Estes left ventricular hypertrophy score and its components predict all-cause mortality in the general population.

BACKGROUND: The same electrocardiographic (ECG) criteria that have been used for detection of left ventricular hypertrophy (LVH) have recently been recognized as predictors of adverse clinical outcomes, but this predictive ability is inadequately explored and understood. METHODS: A total of 14,984 participants from the ARIC study were included in this analysis. Romhilt-Estes (R-E) LVH score was measured from the automatically processed baseline (1987-1989) ECG data. All-cause mortality was ascertained up to December 2010. Cox proportional hazard models were used to examine the association between baseline R-E score, overall and each of its 6 individual components separately, with all-cause mortality. The associations between change in R-E score between baseline and first follow-up visit with mortality were also examined. RESULTS: During a median follow-up of 21.7 years, 4,549 all-cause mortality events occurred during follow-up. In multivariable-adjusted models, increasing levels of the R-E score was associated with increasing risk of mortality both as a baseline finding and as a change between the baseline and the first follow-up visit. Of the 6 ECG components of the score, 4 were predictive of all-cause mortality (P-terminal force, QRS amplitude, LV strain, and intrinsicoid deflection), whereas 2 of the components were not (left axis deviation and prolonged QRS duration). Differences in the strengths of the associations between the individual components of the score and mortality were observed. CONCLUSIONS: The R-E score, traditionally used for detection of LVH, could be used as a useful tool for predication of adverse outcomes.

Automated J wave detection from digital 12-lead electrocardiogram.

In this report we provide a method for automated detection of J wave, defined as a notch or slur in the descending slope of the terminal positive wave of the QRS complex, using signal processing and functional data analysis techniques. Two different sets of ECG tracings were selected from the EPICARE ECG core laboratory, Wake Forest School of Medicine, Winston Salem, NC. The first set was a training set comprised of 100 ECGs of which 50 ECGs had J-wave and the other 50 did not. The second set was a test set (n=116 ECGs) in which the J-wave status (present/absent) was only known by the ECG Center staff. All ECGs were recorded using GE MAC 1200 (GE Marquette, Milwaukee, Wisconsin) at 10mm/mV calibration, speed of 25mm/s and 500HZ sampling rate. All ECGs were initially inspected visually for technical errors and inadequate quality, and then automatically processed with the GE Marquette 12-SL program 2001 version (GE Marquette, Milwaukee, WI). We excluded ECG tracings with major abnormalities or rhythm disorder. Confirmation of the presence or absence of a J wave was done visually by the ECG Center staff and verified once again by three of the coauthors. There was no disagreement in the identification of the J wave state. The signal processing and functional data analysis techniques applied to the ECGs were conducted at Duke University and the University of Toronto. In the training set, the automated detection had sensitivity of 100% and specificity of 94%. For the test set, sensitivity was 89% and specificity was 86%. In conclusion, test results of the automated method we developed show a good J wave detection accuracy, suggesting possible utility of this approach for defining and detection of other complex ECG waveforms.

Determinants of discrepancies in detection and comparison of the prognostic significance of left ventricular hypertrophy by electrocardiogram and cardiac magnetic resonance imaging.

Despite the low sensitivity of the electrocardiogram (ECG) in detecting left ventricular hypertrophy (LVH), ECG-LVH is known to be a strong predictor of cardiovascular risk. Understanding reasons for the discrepancies in detection of LVH by ECG versus imaging could help improve the diagnostic ability of ECG. We examined factors associated with false-positive and false-negative ECG-LVH, using cardiac magnetic resonance imaging (MRI) as the gold standard. We also compared the prognostic significance of ECG-LVH and MRI-LVH as predictors of cardiovascular events. This analysis included 4,748 participants (mean age 61.9 years, 53.5% females, 61.7% nonwhites). Logistic regression with stepwise selection was used to identify factors associated with false-positive (n = 208) and false-negative (n = 387), compared with true-positive (n = 208) and true-negative (n = 4,041) ECG-LVH, respectively. A false-negative ECG-LVH status was associated with increased odds of Hispanic race/ethnicity, current smoking, hypertension, increased systolic blood pressure, prolongation of QRS duration, and higher body mass index and with lower odds of increased ejection fraction (model-generalized R(2) = 0.20). A false-positive ECG-LVH status was associated with lower odds of black race, Hispanic race/ethnicity, minor ST-T abnormalities, increased systolic blood pressure, and presence of any major electrocardiographic abnormalities (model-generalized R(2) = 0.29). Both ECG-LVH and MRI-LVH were associated with an increased risk of cardiovascular disease events (hazard ratio 1.51, 95% confidence interval 1.03 to 2.20 and hazard ratio 1.81, 95% confidence interval 1.33 to 2.46, respectively). In conclusion, discrepancy in LVH detection by ECG and MRI can be relatively improved by considering certain participant characteristics. Discrepancy in diagnostic performance, yet agreement on predictive ability, suggests that LVH by ECG and LVH by imaging are likely to be two distinct but somehow related phenotypes.

An archaeologic dig: a rice-fruit diet reverses ECG changes in hypertension.

In 1940, a young German refugee physician scientist at Duke University in Durham, North Carolina began to treat patients with accelerated or "malignant" hypertension with a radical diet consisting of only white rice and fruit, with strikingly favorable results. He reported rapid reduction in blood pressure, rapid improvement in renal failure, papilledema, congestive heart failure and other manifestations of this previously fatal illness. This treatment was based on his theory that the kidney had both an excretory and a metabolic function, and that removing most of the sodium and protein burden from this organ enabled it to regain its normal ability to perform its more important metabolic functions. It was also effective in "ordinary" hypertension, in the absence of the dramatic vasculopathy of the accelerated form. The results were so dramatic that many experienced physicians suspected him of falsifying data. Among these results was the normalization of the ECG changes seen with hypertension. This paper reviews his published experience with this radical therapy, its controversial rise to fame, and its decline in popularity with the advent of effective antihypertensive drugs. It features the ECG changes seen in this then fatal disease, and the reversal of these changes by the rice diet. This treatment, though very difficult for the patient, produced effects which make it equal or superior to current multi-drug treatment of hypertension. A poorly known but important observation was that patients who were able to follow the regime, and who were slowly guided through a gradual modification of the diet over many months, were able to transition into a very tolerable low fat, largely vegetarian diet, while leading a normal, active life, without medications, indicating that the disease state had been permanently modified.

Olson method for locating and calculating the extent of transmural ischemic areas at risk of infarction.

OBJECTIVES: The purpose of this study is to present a new and improved method for translating the electrocardiographic changes of acute myocardial ischemia into a display which reflects the location and extent of the ischemic area and the associated culprit coronary artery. This method could be automated to present a graphic image of the ischemic area in a manner understandable by all levels of caregivers; from emergency transport personnel to the consulting cardiologist. BACKGROUND: Current methods for the ECG diagnosis of ST elevated myocardial infarction (STEMI) are criteria driven, and complex, and beyond the interpretive capability of many caregivers. New methods are needed to accurately diagnose the presence of acute transmural myocardial ischemia in order to accelerate a patient's clinical "door to balloon time." The proposed new method could potentially provide the information needed to accomplish this objective. METHODS: The new method improves the precision of diagnosis and quantification of ischemia by normalizing the ST segment inputs from the standard 12 lead ECG, transforming these into a three dimensional vector representation of the ischemia at the electrical center of the heart. The myocardial areas likely to be involved in this ischemia are separately analyzed to assess the probability that they contributed to this event. The source of the ischemia is revealed as a specific region of the heart, and the likely location of the associated culprit coronary artery. Seventy 12 lead ECGs from subjects with known single artery occlusion in one of the three main coronary arteries were selected to test this new method. Graphic plots of the distribution of ischemia as indicated by the method are consistent with the known occlusion. The analysis of the distribution of ischemic areas in the myocardium reveals that the relationships between leads with either ST elevation or ST depression, provide critical information improving the current method.

ECG manifestations of left ventricular electrical remodeling.

Research and thinking about the electrocardiographic manifestations of left ventricular hypertrophy has been constrained by a limited conceptual model of the process: heart disease produces chamber enlargement (increased mass), which in turn produces an altered electrocardiogram. The process is much more complex than can be represented in this simple model. A more robust and intricate model is proposed, in which heart (and vascular) disease causes structural changes, electrical changes, biochemical changes, and others, all of which interact to produce electrical remodeling of ventricular myocardium. This electrical remodeling results in a variety of ECG changes. All of these changes interact, leading to an altered clinical course, and to premature death. It is suggested that research, based on this model, can provide new clues to the processes involved, and improve the prediction of clinical outcomes. New directions in research, in recording equipment, and in organizational activities are suggested to test this new model, and to improve the usefulness of the electrocardiogram as a research and diagnostic tool.

Second statement of the working group on electrocardiographic diagnosis of left ventricular hypertrophy.

The Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy, appointed by the Editor of the Journal of Electrocardiology, presents the alternative conceptual model for the ECG diagnosis of left ventricular hypertrophy (LVH). It is stressed that ECG is a record of electrical events, not of mechanical events and/ or anatomical characteristics. Considering the electrical characteristics of pathologically changed myocardium should lead to better understanding and improved clinical usefulness of the ECH in the clinical diagnosis of LVH.

The electrocardiogram in left ventricular hypertrophy: past and future.

The electrocardiographic diagnosis of left ventricular hypertrophy (LVH) has been centered on improving the diagnostic sensitivity and specificity of the method, using criteria whose precise relationship to increased left ventricular mass are not established. Although the electrocardiogram (ECG) has been displaced to a secondary role in the prediction of left ventricular mass, ECG/LVH has been shown to be a strong predictor of morbidity and early mortality. There are strong clues that each of the parameters in ECG/LVH is related to cardiac contractility and ejection. It is suggested that research be redirected to an exploration of these relationships and predicted that this will lead to both a better understanding of this venerable tool and an improvement in its usefulness to the clinician and patient.

Electrocardiographic diagnosis of left ventricular hypertrophy: depolarization changes.

Electrocardiographic signs of left ventricular hypertrophy (LVH) are on one hand accepted as independent cardiovascular risk factors and indicators of target organ damage in hypertensive patients, but, on the other hand they are strongly criticized for their low sensitivity. In this paper, a historic perspective on the ECG diagnosis of LVH is presented, showing the development of current views on the role of ECG in LVH detection. Based on the fact that ECG provides information on the electrical properties of myocardium and on new knowledge about electrical remodeling in LVH, a shift of paradigm in our consideration of the diagnosis of left ventricular hypertrophy is proposed, based on changes in the electrical properties of hypertrophied myocardium. This new paradigm could explain the broad spectrum of QRS patterns seen in LVH, including increased QRS voltage, prolonged duration of QRS complex, left axis deviation, prolonged intrinsicoid deflection, LBBB and LAFB patterns, as well as pseudo-normal ECG findings.