Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study

The increased QRS voltage is considered to be a specific electrocardiogram (ECG) sign of left ventricular hypertrophy (LVH), and it is expected that the QRS voltage reflects the increase in left ventricular mass (LVM). However, the increased QRS voltage is only one of QRS patterns observed in patients with LVH. According to the solid angle theory, the resultant QRS voltage is influenced not only by spatial (anatomic) but also by nonspatial (electrophysiologic) determinants. In this study, we used a computer model to evaluate the effect of changes in anatomy and conduction velocity of the left ventricle on QRS complex characteristics.

Material and Methods

The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change dimensions of the ventricles, as well as the conduction velocity in the individual layers of myocardium. Three types of anatomic changes were simulated: concentric hypertrophy, eccentric hypertrophy, and dilatation. The conduction velocity was slowed in the inner layer of the left ventricle representing the Purkinje fiber mesh and in the layers representing the working myocardium. The outcomes of the model are presented as the time course of the spatial QRS vector magnitude, the vectorcardiographic QRS loops (VCGs) in horizontal, left sagittal, and frontal planes, as well as derived 12-lead ECGs. The following indicators of the 12-lead ECG were evaluated: the left axis deviation, the intrinsicoid deflection in V6, Cornell voltage, Cornell voltage-duration product, and Sokolow-Lyon index.

Results

The increase in LVM did not affect the QRS voltage proportionally, and the LVM and type of hypertrophy were not the only determinants of the QRS patterns. The conduction velocity slowing resulted in a spectrum of QRS patterns including increased QRS voltage and duration, left axis deviation, prolonged intrinsicoid deflection, VCG patterns of left bundle branch block, as well as pseudo-normal VCG/ECG patterns. The anatomic changes and conduction velocity slowing affected differently Sokolow-Lyon index and Cornell criteria.

Conclusion

We showed that the LVM is not the only determinant of the QRS complex changes in LVH, but it is rather a combination of anatomic and electric remodeling that creates the whole spectrum of the QRS complex changes seen in LVH patients. The slowed conduction velocity in the model heart produced QRS patterns consistent with changes described in LVH, even if the LVM was not changed.     

Discrepancy between increased left ventricular mass and "normal" QRS voltage is associated with decreased connexin 43 expression in early stage of left ventricular hypertrophy in spontaneously hypertensive rats

Background and Purpose

On the basis of our previous results of animal and human studies, we assume that the discrepancies between increased left ventricular mass (LVM) and electrocardiographic (ECG) findings not exceeding the upper normal limits in left ventricular hypertrophy (LVH) are conditioned by the electrical remodeling of hypertrophied myocardium. We assumed that these discrepancies observed in the early stage of LVH in spontaneously hypertensive rats (SHR) are associated with a decreased expression of connexin 43.

Methods

Standard 12-lead ECG was recorded in 20-week-old male SHR and age-matched and sex-matched normotensive Wistar rats (Institute of Experimental Pharmacology SAV, Dobra Voda, Slovakia). The approximated maximum QRS spatial vector magnitude (QRSmax) was calculated from leads V₂, aVF, and V₅. Left ventricular mass was weighed, and the specific potential (SP) of myocardium was calculated as the QRSmax-to-LVM ratio. Left ventricular protein levels of connexin 43 were analyzed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting.

Results

The LVM values were significantly higher in SHR than in normotensive controls (0.96 ± 0.03 g and 0.680 ± 0.07 g, respectively; P < .001). The QRSmax values in SHR did not follow the increase either in systolic blood pressure or in LVM. The SP values in SHR were significantly lower than those in control rats (0.92 ± 0.11 mV/g and 1.358 ± 0.06 mV/g, respectively; P < .01). A 37% decrease in connexin 43 level was observed in SHR.

Conclusions

The QRS voltage did not follow the increase in the LVM in 20-week-old SHR, and the values of connexin 43 were lower in SHR than in normotensive controls. We believe that the discrepant findings between ECG voltage and LVM can be caused by the electrical remodeling in the early stages of LVH.     

Comparison of infarct size changes with delayed contrast-enhanced magnetic resonance imaging and electrocardiogram QRS scoring during the 6 months after acutely reperfused myocardial infarction

Introduction

Magnetic resonance imaging using the delayed contrast-enhanced (DE-MRI) method can be used for characterizing and quantifying myocardial infarction (MI). Electrocardiogram (ECG) score after the acute phase of MI can be used to estimate the portion of left ventricular myocardium that has infracted. There are no comparison of serial changes on ECG and DE-MRI measuring infarct size.

Aim

The general aim of this study was to describe the acute, healing, and chronic phases of the changes in infarct size estimated by the ECG and DE-MRI. The specific aim was to compare estimates of the Selvester QRS scoring system and DE-MRI to identify the difference between the extent of left ventricle occupied by infarction in the acute and chronic phases.

Methods

In 31 patients (26 men, age 56 ± 9) with reperfused ST-elevation MI (11 anterior, 20 inferior), standard 12-lead ECG and DE-MRI were taken from 1 to 2 days (acute), 1 month (healing), and 6 months (chronic) after the MI. Selvester QRS scoring was used to estimate the infarct size from the ECG.

Results

The correlation values between infarct size measured by DE-MRI and QRS scoring range from 0.33 to 0.43 higher for anterior than inferior infarcts. The infarct size estimated by QRS scoring was larger (about 5% of the left ventricle) than infarct size by DE-MRI acute and 1 month, but at 6 months, there was no difference. In about half of the patients, the QRS score agreed with DE-MRI in change of infarct size from acute to 6 months.

Conclusion

In conclusion, the Selvester QRS scoring system is in half of the patients with reperfused first time MI in good accordance with DE-MRI in identifying a decrease or no change in the extent of left ventricle occupied by infarction in the acute and chronic phases.     

New precordial bipolar electrocardiographic leads for detecting left ventricular hypertrophy

Background

Novel small and wearable electrocardiogram (ECG) devices offer new means of recording cardiac activity in different applications. Our objective was to evaluate the performance of closely separated (6 cm) bipolar leads in differentiating subjects with left ventricular hypertrophy (LVH) from healthy subjects.

Methods

The material contained body surface ECG of 236 healthy and 116 LVH subjects. A total of 36 vertical, 30 horizontal, and 66 diagonal bipolar leads located on the anterior thorax were analyzed. The QRS amplitudes were calculated, and the leads' overall diagnostic performance was assessed by receiver operating characteristic (ROC) analysis.

Results

The best overall diagnostic performances were obtained from 2 areas: one near the precordial electrodes of standard leads V₁ to V₃ and the other on lower anterior thorax. Vertical and diagonal bipolar leads located at lower anterior thorax provided the highest ROC areas (≥0.79). These bipolar leads also provided similar sensitivities than the traditional Sokolow-Lyon method.

Conclusion

The new short distance vertical and diagonal bipolar leads are efficient in discriminating subjects with LVH from healthy subjects based on QRS amplitude.     

Electrocardiogram voltage discordance: interpretation of low QRS voltage only in the limb leads

Introduction

Low voltage on the surface electrocardiogram (ECG) is defined as QRS voltage less than 5 mm in all limb leads and less than 10 mm in all precordial leads. The clinical correlate of an ECG with low voltage in the limb leads but normal precordial QRS amplitudes is unclear.

Methods

Twelve-lead ECGs with QRS voltage less than 5 mm in all limb leads and more than 10 mm in at least 2 contiguous precordial leads were collected. Presence of clinical conditions associated with low voltage was determined from clinical data and chest imaging.

Results

Fifty-one of 100 patients had voltage discordant ECGs that correlated with conditions known to cause diffuse low voltage. Among those without associated conditions, 63% had dilated ventricles, with an average ejection fraction of 33%.

Conclusions

Low voltage isolated to the limb leads is associated with the same conditions that cause diffuse low voltage in only half of patients. In the remainder, more than 60% have dilated cardiomyopathies.     

Calculating Cornell voltage from nonstandard chest electrode recording site in the Reasons for Geographic And Racial Differences in Stroke study

Background

To minimize participants' burden and the need for disrobing, a 7-lead electrocardiogram (ECG) recording using a single mid-sternal chest lead was recorded at the initial stages of The REasons for Geographic And Racial Differences in Stroke (REGARDS) study. Electrocardiogram-detected left ventricular hypertrophy (ECG-LVH) by Cornell voltage (RaVL + S-wave amplitude in V₃ [SV₃]) cannot be assessed from this method because of the absence of V₃. We examined the possibility that the S-wave amplitude in the mid-sternal lead (SV) could be used as a surrogate for SV₃.

Methods

The REGARDS study is a US national study where 7-lead ECGs were performed in 8,330 (29%) participants and standard 12-lead EGCs were performed in 20?811 (71%). Cornell voltage was calculated as the sum of aVL amplitude + SV (in the 7-lead group) or SV₃ (in the 12-lead group). Logistic regression analysis was used to examine and compare the magnitude of the association between the LVH risk factors with ECG-LVH in both groups, and Cox proportional hazards analysis was used to examine and compare the hazard ratios of overall mortality and cardiovascular mortality associated with ECG-LVH in both groups.

Results

Regardless of the Cornell voltage calculation method, ECG-LVH was significantly associated with LVH risk factors; and with the exception of sex, there was no evidence of a difference in the magnitude of the association. ECG-LVH from both approaches were significantly and similarly associated with both all-cause and cardiovascular mortality.

Conclusion

ECG-LVH by Cornell voltage calculated from a 7-lead ECG (using SV in the formula) has demographic and clinical associations that are similar to that calculated from a standard 12-lead ECG (using SV₃). In epidemiologic studies recording 7-lead ECG, SV could be used as an alternative to SV₃ in the Cornell voltage formula.     

Serial evaluation of electrocardiographic left ventricular hypertrophy for prediction of risk in hypertensive patients

Background

Although the presence and severity of electrocardiographic (ECG) left ventricular hypertrophy (LVH) have been associated with an increased risk of cardiovascular (CV) morbidity and mortality, the relationship of regression of ECG LVH during antihypertensive therapy to CV risk has only recently been examined.

Methods

Electrocardiographic LVH was evaluated over time in 9193 hypertensive patients enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension study. Patients were treated with losartan- or atenolol-based regimens and followed with serial ECGs at 6 months and then yearly until death or study end. Electrocardiographic LVH was measured using gender-adjusted Cornell product (RaVL + SV3 [+6 mm in women]) ? QRS duration) and Sokolow-Lyon voltage (SV1 + RV5/6).

Results

After mean (SD) follow-up of 4.8 (0.9) years, the Losartan Intervention for Endpoint Reduction in Hypertension study composite end point of CV death, nonfatal myocardial infarction, or stroke occurred in 1096 patients. In Cox regression models controlling for treatment type, baseline Framingham risk score, baseline, and in-treatment blood pressure and for severity of baseline ECG LVH by Cornell product and Sokolow-Lyon voltage, lower in-treatment ECG LVH by Cornell product and Sokolow-Lyon voltage were associated with 14% and 17% lower rates, respectively, of the composite CV end point: adjusted hazard ratios (HRs) of 0.86 (95% confidence interval [CI], 0.82-0.90; P < .001) for every 1050 mm · ms (1 SD) decrease in Cornell product and 0.83 (95% CI, 0.78-0.88; P < .001) for every 10.5 mm (1 SD) decrease in Sokolow-Lyon voltage. In parallel analyses, lower Cornell product and Sokolow- Lyon voltage were each independently associated with lower risks of CV mortality (HR, 0.78; 95% CI, 0.73-0.83; P < .001; HR, 0.80; 95% CI, 0.73-0.87; P < .001), of myocardial infarction (HR, 0.90; 95% CI, 0.82-0.98; P = .011; HR, 0.90; 95% CI, 0.81-1.00; P = .043), and of stroke (HR, 0.90; 95% CI, 0.84-0.96; P = .002; HR, 0.81; 95% CI, 0.75-0.89; P < .001). Regression of ECG LVH was also associated with significantly reduced risks of sudden cardiac death, new-onset atrial fibrillation, hospitalization for heart failure, and new-onset diabetes mellitus.

Conclusions

Regression of ECG LVH by Cornell product and/or Sokolow-Lyon voltage criteria during antihypertensive therapy is associated with lower likelihoods of CV morbidity and mortality, all-cause mortality, and new-onset diabetes, independent of blood pressure lowering and treatment modality in essential hypertension. These findings suggest that antihypertensive therapy targeted at regression or prevention of ECG LVH may improve prognosis.     

Relation of QT interval and QT dispersion to regression of echocardiographic and electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan Intervention For Endpoint Reduction (LIFE) study

Background

In hypertensive patients, both echocardiographic and electrocardiographic left ventricular hypertrophy (LVH) increase the risk of sudden death, possibly in part because of LVH-induced proarrhythmic repolarization changes. Experimentally, regression of LVH normalizes ventricular electrophysiology.

Methods

To assess the relation of regression of LVH to changes in electrocardiographic measures of ventricular repolarization, we studied 317 hypertensive (61.2% men, mean age 65 ± 7 years) participants in the Losartan Intervention For Endpoint Reduction (LIFE) study with electrocardiographic evidence of LVH, at study baseline, and after 1 year of blood pressure-lowering treatment with losartan or atenolol and hydrochlorothiatzide as the first adjunct therapy if needed to reach target blood pressure of 140/90 mm Hg. As indexes of LVH, we used echocardiographically determined LV mass as well as the Sokolow-Lyon and Cornell voltages from the electrocardiogram. QT interval duration and QT dispersion from the 12-lead electrocardiogram were used as ventricular repolarization measures.

Results

By using tertiles of LV mass change and adjusting for the difference in treatment (losartan or atenolol), shortening of the rate-adjusted QT intervals as well as reduction in QT_apex dispersion were observed in the tertile showing the greatest decrease in LV mass but not in the tertile without substantial changes in LV mass despite a significant reduction in blood pressure. Similar results were obtained with the use of Sokolow-Lyon and Cornell voltage change tertiles.

Conclusions

In hypertensive patients with electrocardiographic evidence of LVH, regression of echocardiographically determined LV mass and electrocardiographic indexes of LVH may partially reverse the LVH-induced proarrhythmic repolarization changes. This may have a beneficial impact on the increased incidence of sudden death in these patients.     

Validity of electrocardiographic classification of left ventricular hypertrophy across adult ethnic groups with echocardiography as a standard

Aims

To assess the validity of the electrocardiogram (ECG) as a diagnostic tool for left ventricular hypertrophy (LVH) for different ethnic groups with echocardiography as a standard.

Methods

Systematic review of the literature using the Cornell and Sokolow-Lyon voltage criteria for LVH.

Results

Five studies were identified. Pooled data from these studies demonstrated low sensitivity using both types of ECG criteria for white and African-origin groups, but with slightly higher sensitivity values for the African-origin group (Cornell, 31.2%; 95% confidence interval [CI], 28%-34.8%; Sokolow-Lyon, 32.9%; 95% CI, 29.5%-36.4%) compared with the white group (Cornell, 26.5%; 95% CI, 25.2%-27.8%; Sokolow-Lyon, 18.2%; 95% CI, 17.2%-19.3%). Specificity was high using both types of criteria in the white group (Cornell, 87.4%; 95% CI, 86.4%-88.4%; Sokolow-Lyon, 88.9%; 95% CI, 88%-90%) but was much lower in the African-origin group using the Sokolow-Lyon criteria (72.1%; 95% CI, 68.7%-75.3%). Specificity was high however for the African-origin group using the Cornell criteria (86.2%, 95% CI, 83.4%-88.5%).

Conclusions

Both types of criteria are more sensitive in African-origin populations. The Sokolow-Lyon criteria are less specific for LVH in people of African origin. The evidence favors the Cornell criteria in research and service contexts involving African-origin and white populations. Further research is needed to adapt ECG criteria to take into account ethnicity to a greater degree. The issue needs to be studied in a broader range of ethnic groups.     

Thirty-year electrocardiographic follow-up after repair of tetralogy of Fallot or atrial septal defect

Background and Purpose

Knowledge about long-term electrocardiographic changes after surgery for congenital heart disease is limited.

Methods

Eleven patients with corrected tetralogy of Fallot (ToF) and 14 with corrected atrial septal defect (ASD) were followed up at 20 and 30 years after surgery.

Results

Approximately 50% of the ASD group developed prolonged QRS duration. In the ToF group, 7 increased QRS duration by more than 20 milliseconds. Nearly all had right bundle-branch block, and 30% of them also had bifascicular block. Two in the ASD group developed first grade atrioventricular block. Five ASD and 6 ToF had prolonged corrected QT duration in the late postoperative phase.

Conclusions

Even after primarily good results of surgery in congenital heart disease, unknown late effects may occur not only in complex lesions such as ToF but also after ASD correction. Regular medical checkups are important after surgical correction in congenital heart disease.     

Effects of ischemic preconditioning and arterial collateral flow on ST-segment elevation and QRS complex prolongation in a canine model of acute coronary occlusion

Background

During acute myocardial infarction, both ST elevation and QRS distortion on the initial electrocardiogram (ECG) have been correlated with poorer prognosis. Studies in dogs and humans suggest that these ECG markers provide information about myocardial protection from both collateral blood flow and ischemic preconditioning.

Methods

In a protocol designed to precondition the heart with ischemia, we examined both ST-segment elevation and QRS complex prolongation in lead II of the ECG in 23 mongrel dogs during the first and fourth episode of 5 minutes of left circumflex artery occlusion. Myocardial collateral flow was measured during each of these episodes by injection of radioactive microspheres 2.5 minutes into the episode of ischemia.

Results

During ischemia, the degree of elevation of the ST segments was reduced markedly in hearts preconditioned with ischemia and/or in hearts with the greatest amounts of collateral arterial flow. During the first episode of ischemia, the ST segments increased to a similar extent in severe and moderate ischemia, but less in hearts in which the ischemia was mild. However, marked QRS prolongation was present only in hearts with severe ischemia, and decreased when the hearts were preconditioned. In addition, large ischemic beds exhibited the most marked QRS prolongation, whereas small but even severely ischemic beds showed little or no change in QRS duration.

Conclusion

Both ST elevation and QRS prolongation are reduced by the presence of collateral flow and ischemic preconditioning. The QRS complex merits further study as an important marker of the degree of myocardial protection during human acute myocardial ischemia/infarction.     

Does modifying electrode placement of the 12 lead ECG matter in healthy subjects?

Background

Limb electrodes for the 12 lead ECG are routinely placed on the torso during exercise stress testing or when limbs are clinically inaccessible. It is unclear whether such electrode modification produces ECG changes in healthy male or female subjects that are clinically important according to the 2009 AHA, ACCF, HRS guidelines. We therefore measured whether ECG modification produced clinically important or false positive ECG changes e.g., appearance of Q waves in leads V_1-3, ST changes greater than 0.1 mV, T wave changes greater than 0.5 mV (frontal plane) or 1 mV (transverse plane), QRS axis shifts or alterations to QTc/P-R/QRS intervals.

Methods

The 12 lead ECG was measured in 18 healthy and semi-recumbent subjects using the standard and Takuma modified limb placements.

Results

In the frontal plane we demonstrate that the modification of limb electrode placement produces small Q, R and T wave amplitude and QRS axis changes that are statistically but not clinically significant. In the transverse plane it produces no statistically or clinically significant changes in the ECG or in ST segment morphology, P-R, QRS or QTc intervals.

Conclusions

We provide better and more robust evidence that routine modification of limb electrode placement produces only minor changes to the ECG waveform in healthy subjects. These are not clinically significant according to the 2009 guidelines and thus have no effect on the clinical specificity of the 12 lead ECG.     

High-frequency electrocardiogram as a supplement to standard 12-lead ischemia monitoring during reperfusion therapy of acute inferior myocardial infarction

Background

Resolution of ST-segment elevation in the electrocardiogram (ECG) is used as a reperfusion sign during thrombolytic therapy in acute myocardial infarction. Analysis of high-frequency QRS components (HF-QRS) might provide additional information. The study compares changes in HF-QRS (150-250 Hz) to ST-segment changes in the standard ECG during thrombolytic therapy.

Methods

Twelve patients receiving intravenous thrombolytic therapy were included. A continuous 12-lead ECG recording was acquired for 4 hours.

Results

After 1 hour of therapy, 3 patients showed ST-elevation resolution as well as an increase in HF-QRS. These changes in ST and HF-QRS occurred simultaneously. No other patient showed significant changes in ST or HF-QRS after 1 hour. After 2 and 4 hours, there was less concordance between the standard and high-frequency ECGs.

Conclusions

In patients with early ST-elevation resolution, the standard and high-frequency ECGs show similar results. Later changes are more disparate and may provide different clinical information.     

Diagnosis and characterization of left ventricular hypertrophy by computerized acoustic cardiography, brain natriuretic peptide, and electrocardiography

Background

Using echocardiography as the gold standard to diagnose and classify subtypes of left ventricular hypertrophy (LVH), we compared the diagnostic accuracy of computerized acoustic cardiography, brain natriuretic peptide (BNP), and the Cornell voltage criteria.

Methods

Three hundred fifty-two patients with suspected heart failure had contemporaneous BNP sampling, 12-lead electrocardiography, computerized acoustic cardiography, and echocardiography. Left ventricular hypertrophy was classified as eccentric vs concentric based on echocardiographic relative wall thickness. Computerized acoustic cardiography was used to measure acoustic and automated electrical parameters.

Results

Of all models, BNP combined with either computerized acoustic cardiography (c-statistic, 0.78; 95% confidence interval [CI], 0.74-0.78) or Cornell voltage (c-statistic, 0.76; 95% CI, 0.71-0.81) had the best diagnostic performance for LVH detection. For LVH characterization, the computerized acoustic cardiography model outperformed other models (c-statistic, 0.73; 95% CI, 0.66-0.80).

Conclusions

Brain natriuretic peptide combined with either computerized acoustic cardiography or Cornell voltage had the highest diagnostic accuracy for the detection of LVH, compared to Cornell voltage, BNP, or computerized acoustic cardiography alone. Computerized acoustic cardiography outperformed other models for the characterization of LVH subtypes.     

Correlation of electrocardiographic left ventricular hypertrophy criteria with left ventricular mass by echocardiogram in obese hypertensive patients

Introduction

Left ventricular hypertrophy (LVH) and obesity are important cardiovascular risk factors. This study evaluates the influence of obesity on the diagnostic performance of the most used electrocardiographic criteria for LVH in hypertensive patients.

Methods

One thousand two hundred four outpatients from the Hypertensive Unit of the Hospital São Paulo, São Paulo, SP, Brazil, were studied. All underwent 12-lead electrocardiogram and echocardiogram. The most known electrocardiographic criteria for LVH were assessed and compared with the left ventricular mass index obtained by echocardiogram in obese and nonobese groups of hypertensive patients.

Results

The population's mean age was 57.4 ± 4.7 years; 351 were men (29.1%) and 853 women (70.8%). Cornell voltage, Cornell duration, Sokolow-Lyon voltage, Romhilt-Estes criteria, and R wave in aVL 11 mm or higher showed a positive correlation with left ventricular mass index (P < .05). Notwithstanding, there were no changes regarding specificity for obese or nonobese characteristics. However, sensitivity had a statistically significant decrease in obese patients in regard to Sokolow-Lyon voltage and Romhilt-Estes criteria and strain pattern (P < .05).

Conclusion

Cornell voltage and Cornell duration criteria, Perugia score, R wave in aVL, and QTc variable had no significant changes in diagnostic sensitivity in the obese patients.     

Prognostic value of predischarge electrocardiographic measurement of infarct size after thrombolysis: insights from GUSTO I Economics and Quality of Life substudy

Background

Current methods for risk stratification after acute myocardial infarction (MI) include several noninvasive studies. In this cost-containment era, the development of low-cost means should be encouraged. We assessed the ability of an electrocardiogram (ECG) MI-sizing score to predict outcomes in patients enrolled in the Economics and Quality of Life (EQOL) sub study of the Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries -I (GUSTO-I) trial.

Methods

We classified patients by electrocardiographic Selvester QRS score at hospital discharge: those with a score 0-9 versus ≥10. Endpoints were 30-day and 1-year mortality, resource use, and quality-of-life measures.

Results

Patients with a QRS score <10 were well-matched with those with QRS score ≥10 with the exception of a trend to more anterior MI in the higher scored group. Patients with QRS score ≥10 had increased risk of death at 30-days (8.9% vs. 2.9% P < .001), and this difference persisted at 1 year (12.6% vs. 5.4%, P = .001). Recurrent chest pain, use of angiography, and angioplasty were similar during follow-up. However, there was a trend toward less coronary bypass surgery in patients with a QRS score ≥10. Readmission rates were higher at 30 days but similar at 1 year.

Conclusions

Stratification of patients after acute MI by a simple measure of MI size identifies populations with different long-term prognoses; patients with a QRS score ≥10 (approximately 30% of the left ventricle infarcted) at discharge have poorer outcomes in both the short- and long-term. The standard 12-lead ECG provides a simple, economical means of risk stratification at discharge.     

Simulation of the QRS complex using papillary muscle positions as the site of early activation in human subjects

Background

Simulation of the electrical activation of the heart and its comparison with real in vivo activation is a promising method in testing potential determinants of excitation. Simulation of the electrical activity of the human heart is now emerging as a step forward for understanding and predicting electrophysiologic patterns in humans. Initial points of excitation and the manner in which the activation spreads from these points are important variables determining QRS complex characteristics. It has been suggested that in humans, the initial excitation of the left ventricle is a primary determinant of QRS complex characteristics, and that excitation begins at the papillary muscles and septum, where the fascicles of the left bundle branch insert. The aim of this study is to test the hypothesis that QRS duration and direction of QRS axis in the frontal plane have excellent agreement between real QRS and simulated QRS using papillary muscle position to indicate the border of the origin of early ventricular activation.

Methods

Fourteen healthy adult volunteers were included in the study. Magnetic resonance imaging data were obtained to assess the papillary muscle positions. Twelve-lead electrocardiographic (ECG) recordings were used to obtain real ECG data for assessment of QRS duration and QRS axis in each subject. Simulation software developed by ECG-TECH Corp (Huntington, NY) was used to simulate the ECG of each subject to determine simulated QRS duration and QRS frontal plane axis. QRS duration and QRS axis data were compared between simulated and real ECG and agreement between these variables was calculated.

Results

Seventy-nine percent of subjects had a difference of the QRS duration between real and simulated ECG of less than 10 milliseconds. The calculated strength of agreement between simulated and real QRS duration was 71% and considered as “good” (κ statistics). In 70% of subjects, the difference in the QRS axis was less than 10°. The calculated strength of agreement between simulated and real QRS axis was 80% and considered as “excellent” (κ statistics).

Conclusions

The results of this study suggest that the sites of the initiation of electrical activity in the left ventricle, as assessed by the positions of papillary muscles, may be considered as primary determinants of the QRS duration and QRS axis in humans. This knowledge may help in predicting normal QRS characteristic on a patient-specific basis. In this study, simulation of the QRS complex was based on papillary muscles from human hearts.     

Additional impact of electrocardiographic over echocardiographic diagnosis of left ventricular hypertrophy for predicting the risk of ischemic stroke

Background

Patients with left ventricular hypertrophy (LVH) have an increased risk of ischemic stroke. Although echocardiography is commonly used for the diagnosis of LVH, there is little information about the potential role of electrocardiography in providing additional prognostic information. The purpose of this study is to determine if electrocardiographically derived criteria for LVH provide additional prognostic value over echocardiography for predicting ischemic stroke in a multiethnic population.

Methods

A population-based, case-control study was conducted in 177 patients who had had a first ischemic stroke and in 246 control patients matched for age, gender, and race or ethnicity. Left ventricular mass was measured by using 2-dimensional transthoracic echocardiography. Logistic regression analysis was performed to assess the risk of stroke associated with the presence of LVH diagnosed by electrocardiography (defined by 4 established criteria) after adjustment for the presence of other stroke risk factors and for echocardiographically determined LVH.

Results

After adjustment for the presence of other established stroke risk factors, ECG-LVH was associated with ischemic stroke, using Sokolow-Lyon (odds ratio [OR] 2.12, 95% CI 1.05-4.30), Cornell voltage (OR 2.06, 95% CI, 1.26-3.35), and Cornell product criteria (OR 2.12, 95% CI, 1.13-3.97). Cornell voltage criterion (men, >2.8mV; women, >2.0mV) was associated with ischemic stroke even after adjustment for echocardiographically determined LVH (OR 1.73, 95% CI, 1.04-2.88). The combination of echo-LVH and a positive Cornell voltage criterion was associated with a 3.5-fold increase in stroke risk.

Conclusions

Our study indicates that the presence of ECG-LVH is associated with an increased risk of ischemic stroke after adjustment for other stroke risk factors. For Cornell voltage criteria, this relationship persisted even after adjustment for echocardiographic LVH. Electrocardiographic results can provide independent information for left ventricular myocardial changes and should be considered together with echocardiographic results to fully assess the risk of ischemic stroke.     

Elevated blood pressure and electrocardiographic frontal T axis and spatial QRS-T angle changes in postmenopausal women

Introduction

Frontal T axis and spatial QRS-T angle are both measures of disturbances in ventricular repolarization and depolarization. We determined whether increased blood pressure is a risk factor for changes in these parameters in postmenopausal women free of left ventricular hypertrophy.

Materials and Methods

This cross-sectional study included 969 women. A standard 12-lead electrocardiogram (ECG) was recorded, and frontal T axes and spatial QRS-T angles were computed from vectorcardiography. Logistic regression analysis was used to assess the relationship between systolic and diastolic blood pressures on the one hand and both ECG parameters on the other.

Results

Odds ratios were 1.08 (95% confidence interval [CI], 0.99-1.18) and 1.12 (95% CI, 1.03-1.23) per 10 mm Hg systolic blood pressure for frontal T axis and QRS-T angle, respectively. These values were 1.05 (95% CI, 0.95-1.16) and 1.12 (95% CI, 1.02-1.23) per 5 mm Hg diastolic blood pressure for frontal T-axis and QRS-T angle, respectively.

Conclusion

Elevated blood pressure may lead to ventricular depolarization and repolarization disturbances before overt ECG left ventricular hypertrophy has developed.     

The decrease in QRS amplitude after aortic valve replacement in patients with aortic valve stenosis

Purpose

The purpose of this study was to evaluate the effect of aortic valve replacement on electrocardiogram (ECG) in patients with aortic valve stenosis.

Methods

Serial 12-lead ECGs were obtained in 15 patients with aortic valve stenosis who underwent aortic valve replacement. Three ECG indexes for left ventricular hypertrophy were manually measured in each ECG: Sokolow-Lyon index (sum of S wave in V₁ and R wave in V₅), Cornell voltage index (sum of R wave in aVL and S wave in V₃), and Gubner index (sum of R wave in I and S wave in III).

Results

After aortic valve replacement, Sokolow-Lyon index gradually decreased during 2 years (51.1 ± 17.9 to 34.8 ± 12.5 mm, P < .01). Cornell voltage index (25.6 ± 7.0 to 15.0 ± 4.8 mm, P < .01) and Gubner index (15.8 ± 7.6 to 10.3 ± 5.5 mm, P < .01) also gradually decreased during 2 years. ST depression in V₆ was found in 14 patients (93%) before aortic valve replacement. It resolved in 9 of 14 patients during 2 years.

Conclusions

Electrocardiographic evidence of left ventricular hypertrophy gradually resolved after aortic valve replacement in patients with aortic valve stenosis.