Sex Differences in the Relationships Between Electrocardiographic Abnormalities and the Extent of Left Ventricular Hypertrophy by Echocardiography

Background: Several criteria have been proposed for the electrocardiographic diagnosis of left ventricular hypertrophy (LVH). However, their diagnostic accuracy is questionable. Furthermore, the diagnostic accuracy of abnormalities in ST‐T patterns for LVH is known to be uncertain, especially in women. We examined the relationship between electrocardiographic abnormalities and the extent of LVH. Methods: We studied 76 men and 48 women who satisfied electrocardiographic voltage criteria for LVH (RV₅ or RV₆≥ 2.6 mV, SV₁+ RV₅ or SV₁+ RV₆≥ 3.5 mV) . They were classified into three groups based on ST‐T pattern: normal, early strain, and strain. We defined echocardiographic evidence of LVH as an LV wall thickness ≥ 12 mm. Results: LVH was identified by echocardiography in 55.3% of men and in 47.9% of women. In strain and early strain groups, the prevalence of echocardiographic LVH was significantly higher in men than in women (strain group: 100 vs 75%, P < 0.05, early strain group: 81.8 vs 42.1%, P < 0.05), it did not differ significantly between men and women in normal group. In men, QRS voltage values were significantly correlated with echocardiographic indices. In group strain of men, significant good correlations were observed between QRS voltage values and echocardiographic indices. However, in women, there were no significant correlation between QRS voltage values and echocardiographic indices even in strain group. Conclusions: The combined criteria of both QRS voltage and ST‐T classification could provide a greater accuracy in diagnosing LVH compared to the criteria using QRS voltage alone in men rather than in women.     

Electrocardiographic criteria for the diagnosis of abnormal hypertensive cardiac phenotypes

This article compared the performance of 18 electrocardiographic (ECG) left ventricular hypertrophic (LVH) criteria and four P‐wave indices for the diagnosis of echocardiographic (ECHO) LVH and left atrial enlargement (LAE), including the deepest S‐wave amplitude added to the S‐wave amplitude of lead V₄ (S_D+SV₄) and P‐wave terminal force in lead V₁ (PTFV₁). A total of 152 middle‐aged hypertensive patients without evident cardiovascular diseases (CVDs) were enrolled. The gold standard for the diagnosis of LVH and LAE was ECHO left ventricular mass index (LVMI) and largest left atrial volume index (LAVI). For the detection of LVH, Sokolow‐Lyon voltage, Cornell voltage, Cornell product, S_D+SV₄, Manning, and R+S in any precordial lead had relatively higher sensitivity, especially S_D+SV₄ criteria. Their combination could further increase sensitivity (43% vs 29% [S_D+SV₄], P = 0.016). PTFV₁ was the only criterion that had significant diagnostic value for ECHO LAE (AUC, 0.68; 95% CI: 0.54‐0.73, P = 0.008). For middle‐aged hypertensive patients without evident cardiovascular diseases, S_D+SV₄ had the highest sensitivity for the diagnosis of LVH and the combination of several ECG LVH criteria might further increase sensitivity. PTFV₁ had significant diagnostic value for ECHO LAE.     

Relation of echocardiographic left ventricular mass and hypertrophy to persistent electrocardiographic left ventricular hypertropy in hypertensive patients: the LIFE study

Background: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) trial used left ventricular hypertrophy (LVH) on a screening ECG to identify patients at high risk for morbid events. Because of regression to the mean, not all patients who met screening criteria had persistent ECG LVH on the ECG performed at study baseline.Methods: The relationship of echocardiographic LV mass and LVH to persistence or loss of ECG LVH between screening and baseline evaluation was examined in 906 hypertensive patients in the LIFE study, who had echocardiograms and additional ECG performed at study baseline. Patients were categorized according to the presence or absence of ECG LVH by Cornell voltage-duration product criteria or Sokolow-Lyon voltage criteria; echocardiographic LVH was defined by LV mass index (LVMI) > 104 g/m² in women and > 116 g/m² in men.Results: A total of 678 patients (75%) had persistent ECG LVH at baseline evaluation. Compared with the 228 patients without ECG LVH on the second ECG by either criterion, the 106 patients with LVH by both Cornell product and Sokolow-Lyon criteria had significantly higher LVMI (140 ± 31 v 114 ± 21 g/m², P < .001) and a higher prevalence of echocardiographic LVH (86% v 55%, P < .001). Patients with ECG LVH on the baseline ECG by either Cornell product criteria (n = 410) or Sokolow-Lyon voltage criteria (n = 162) had intermediate values of LVMI (125 ± 25 and 121 ± 21 g/m²) and prevalences of echocardiographic LVH (78% and 62%). After controlling for possible effects of age, sex, ethnicity, systolic blood pressure, and body mass index, persistence of ECG LVH on the baseline ECG was associated with an increased risk of echocardiographic LVH: compared with patients with neither ECG criteria for LVH, patients with only Sokolow-Lyon voltage criteria had a 1.2-fold increased risk of echocardiographic LVH, those with only Cornell product criteria had a 2.7-fold increased risk, and patients with both ECG criteria had a 4.1-fold increased risk of echocardiographic LVH (P < .001).Conclusions: Persistent ECG LVH between screening and LIFE study baseline identified patients with greater LV mass and a higher prevalence of echocardiographic LVH, suggesting that these patients may be at higher risk for subsequent morbid and mortal events.     

Electrocardiographic features differentiating dilated cardiomyopathy from hypertrophic cardiomyopathy

To determine the usefulness of electrocardiographic (ECG) features in differentiating between hypertrophic cardiomyopathy with features mimicking dilated cardiomyopathy (D-HCM) and true dilated cardiomyopathy (DCM), we compared ECGs of 52 consecutive patients (11 with D-HCM, 41 with DCM). Left atrial dimension, left ventricular internal dimension, and septal and posterior wall thickness were employed as echocardiographic indexes, while QRS duration, amplitude of RV₅ or V₆ + SV₁, number of abnormal Q waves, P-terminal force in V₁, and frontal plane QRS axis were used as ECG parameters. The patients with D-HCM demonstrated a larger number of abnormal Q waves (P < .0001), greater prolongation of QRS duration (P < .0001), and lower amplitude of RV₅ or V₆ + SV₁ (P < .0001). In all cases of D-HCM, atrial overload was observed and abnormal QRS axis in 9 (82%) of the 11 patients. These features were noted in 21 (51%) and 17 (41%), respectively, of the 41 DCM patients (P < .005 and P < .05, respectively). Despite significant differences in the echocardiographic parameters between D-HCM and DCM, excluding left ventricular end-diastolic dimension, ECG abnormalities were more significant between the two groups. The results indicate that ECG features are extremely useful in differentiation between DCM and D-HCM.     

ECG characteristics of dilated cardiomyopathy

To elucidate the electrocardiographic (ECG) characteristics of dilated cardiomyopathy (DCM), the authors analyzed the 12-lead ECGs and echocardiograms in 45 patients with DCM, 54 patients with left ventricular (LV) dilatation secondary to valvular heart disease (VHD), 101 hypertensive patients with LV hypertrophy, and 63 normal control subjects. In addition, serial ECG and echocardiographic changes in DCM during a mean follow-up period of 1.6 years were evaluated. Sokolow's criterion (S wave in lead V₁ [SV₁] + R wave in lead V₅ or V₆ [RV₅ or RV₆] > 35 mm) was met comparably in patients with DCM (69%), VHD (61%), and hypertension (74%) (P = NS). Notably, RV₆ in DCM was the highest among the four groups and correlated with the degree of LV dilatation. In contrast, the R waves in leads I, II, and III (RI, RII, RIII) in DCM were the lowest and were not affected by the degree of LV dilatation, although RII and RIII in VHD and RI in hypertension correlated with the degree of LV dilatation and hypertrophy, respectively. As a result, all voltage ratios of RV6/RI, RII, RIII in DCM were not only the highest, but also increased linearly as the LV dilated progressively during the follow-up period. In particular, RV₆ over the maximum R wave in leads I, II, and III (RV₆/Rmax) in DCM correlated with the degree of LV dilatation and inversely correlated with ejection fraction. Subjects with DCM had a significantly higher RV₆/Rmax than did patients with VHD, hypertension, and normal subjects (3.4 vs 1.7, 1.4, 1.2, respectively; P < .001), and this ratio of ≥3 was seen in 67% of the DCM patients versus 4% of the VHD patients, 1% of the hypertensive patients, and 0% of the normal subjects. Thus, DCM commonly shows the ECG signs of LV hypertrophy, but characteristically has the high voltage ratios of RV6/RI, RII, RIII.     

Incidence of high-risk acute coronary syndromes and eligibility for glycoprotein IIb/IIIa inhibitors among patients admitted for possible myocardial ischemia

Objective Recent studies have demonstrated that glycoprotein (GP) IIb/IIIa inhibitors can reduce cardiac events in patients with acute coronary syndromes (ACS). However, little is known about how many patients are actually eligible for treatment. Our purpose was to determine how many patients admitted for possible myocardial infarction (MI) meet GP IIb/IIIa inhibitor treatment criteria. Methods Patients admitted for possible MI who underwent a standard protocol that included serial sampling of total creatine kinase (CK), CK-MB, and troponin I (TnI) were retrospectively assigned to different treatment algorithms on the basis of criteria from GP IIb/IIIa inhibitor trials: an electrocardiogram (ECG) consistent with acute MI or ischemia, and myocardial marker elevations. Elevated CK-MB was considered diagnostic of MI. High-risk ACS was defined as ischemic ECG changes or troponin elevations without CK-MB elevations. Results A total of 2179 patients were admitted for MI exclusion. MI was identified in 304 patients (14.0%) (123 ST-elevation, 49 ischemic ECG, 132 nonischemic ECG). Another 273 patients (12.5%) without CK-MB criteria for MI met high-risk ACS criteria (172 ischemic ECG, 120 TnI elevations). Ischemic ECGs or elevated myocardial markers identified 454 (21%) patients as eligible for treatment. Inclusion of patients with ST elevation increased eligibility to 26.5%. Of the 454 non-ST-elevation ACS patients, 340 (74%) were identified early by the ECG or the initial markers. Conclusions A large proportion of patients admitted for possible MI met criteria for treatment with GP IIb/IIIa inhibitors. The non-ST-elevation ACS group was >3 times larger than the ST-elevation MI group. These findings have important implications for treatment of patients with ACS. (Am Heart J 2002;143:70-5.)     

ECG Abnormalities and Arterial Stiffness by HIV Status among High-Risk Populations in Rakai,Uganda: A Pilot Study

Background:People living with HIV are at increased risk for cardiovascular disease (CVD). In sub-Saharan Africa, population-based data on major CVD events such as stroke and myocardial infarction are difficult to collect. The use of proxy measures could be a feasible way to better study CVD in such settings. This study aimed to determine the acceptance of incorporating ECG and arterial function measurements into a population-based cohort study and to assess the prevalence of ECG abnormalities and arterial stiffness.Methods:A pilot study was conducted within the Rakai Community Cohort Study in Uganda on two high-risk CVD populations; one determined by age (35–49) and Framingham CVD risk scores and the other by age alone (50+). Data on ECG, arterial function, blood pressure, and HIV status were collected. The acceptability of incorporating ECG and arterial function measurements was established as an acceptance rate difference of no more than 5% to blood pressure measurements.Results:A total of 118 participants were enrolled, 57 participants living with HIV and 61 HIV-negative participants. Both ECG measurements and arterial function were well accepted (2% difference). Left ventricular hypertrophy (LVH) and arterial stiffness (>10 m/s) were common in both participants living with HIV and HIV-negative participants across the two high-risk populations. Prevalence rates ranged from 30% to 53% for LVH and 25% to 58% for arterial stiffness. Arterial stiffness at the 11 m/s cutoff (p = 0.03) was found to be more common among participants living with HIV in the 35–49 population.Conclusions:The incorporation of ECG and arterial function measurements into routine activities of a population-based cohort was acceptable and incorporating these proxy measures into cohort studies should be explored further. LVH and arterial stiffness were both common irrespective of HIV status with arterial stiffness potentially more common among people living with HIV.     

Relationships between reduced heart rate variability and pre-clinical cardiovascular disease in patients with type 2 diabetes

Aims

Reduced heart rate variability (HRV), an early sign of diabetic cardiovascular autonomic neuropathy (CAN), is associated with worse cardiovascular outcomes. The objective was to evaluate relationships between HRV parameters and three pre-clinical cardiovascular disease markers (left ventricular hypertrophy [LVH], aortic stiffness and carotid atherosclerosis) in type 2 diabetes.

Methods

In a cross-sectional study, 313 patients with type 2 diabetes performed 24-h Holter monitoring, carotid ultrasonography (intima-media thickness and plaques measurements), aortic pulse wave velocity measurement and echocardiography (left ventricular mass index [LVMI] measurement). Time-domain HRV parameters were the standard deviation of all normal RR intervals (SDNN), the standard deviation of the averaged normal RR intervals for all 5 min segments (SDANN), the root mean square of differences between adjacent R-R intervals (rMSSD), and the percentage of adjacent R-R intervals that varied by >50 ms (pNN50). Multivariate linear and logistic regressions assessed associations between HRV parameters and the three markers of pre-clinical cardiovascular disease.

Results

Patients with reduced HRV had longer diabetes duration, greater prevalences of microvascular complications, lower physical fitness, and higher heart rate, glycated hemoglobin, albuminuria and LVMI than patients with normal HRV. On multivariate regressions, after adjustments for several confounders, reduced SDNN and SDANN were independently associated with LVH and aortic stiffness. No HRV parameter was associated with carotid atherosclerosis.

Conclusions

Two reduced HRV parameters, SDNN and SDANN, which reflect cardiovascular autonomic imbalance, were associated with LVH and aortic stiffness, markers of pre-clinical cardiovascular disease. These findings may offer insights into physiopathological mechanisms linking CAN to worse cardiovascular prognosis.     

R2CHADS2 Score and Thromboembolic Events After Catheter Ablation of Atrial Fibrillation in Comparison With the CHA2DS2-VASc Score

Background

A new risk model, the R₂CHADS₂ (Renal Dysfunction, Congestive Heart Failure, Hypertension, Age, Diabetes, Stroke/Transient Ischemic Attack) score, was proposed to be a powerful scoring scheme in predicting stroke or systemic embolism in atrial fibrillation (AF). The goal of the present study is to validate the usefulness of the R₂CHADS₂ score among patients with AF after catheter ablation. We also aimed to compare the accuracy of the CHA₂DS₂-VASc (Congestive Heart Failure, Hypertension, Age [≥ 75 y], Diabetes, Stroke/Transient Ischemic Attack, Vascular Disease, Age [65-74 y], Sex [Female]) and R₂CHADS₂ scores for risk stratification of thromboembolic (TE) events after ablation procedures.

Methods

We enrolled a total of 526 patients with AF who underwent catheter ablation. The clinical end point was the occurrence of TE events (ischemic stroke, transient ischemic attack, or other systemic embolisms) during the postablation follow-up.

Results

During a follow-up of 37.5 ± 21.3 months, 14 patients (2.7%) experienced TE events. The R₂CHADS₂ score was an independent predictor of TE events in the multivariate analysis. Patients with an R₂CHADS₂ score of > 2 had a higher event rate compared with those with a score of 0 or 1 (0.5% vs 7.7%). The areas under the receiver operating characteristic (ROC) curves of CHA₂DS₂-VASc and R₂CHADS₂ scores in predicting TE events were 0.832 and 0.872, respectively. The difference between these 2 curves did not reach statistical significance (P = 0.338). In addition, the R₂CHADS₂ score did not improve net stroke risk reclassification over the CHA₂DS₂-VASc score (net reclassification improvement, −0.9%; P = 0.948).

Conclusions

The R₂CHADS₂ and CHA₂DS₂-VASc scores could be used to predict TE events for patients with AF undergoing catheter ablation. The predictive accuracy of both scores were similar in this relatively small cohort undergoing ablation.     

Endogenous nitric oxide prevents myocardial ischemia in patients with hypertension and left ventricular hypertrophy

Background Left ventricular hypertrophy (LVH) caused by chronic pressure overload is associated with increased risk of myocardial ischemia without epicardial coronary artery disease. We aimed to test the hypothesis that endogenous nitric oxide (NO) prevents myocardial ischemia in patients with LVH. Methods Epicardial coronary blood flow (Doppler wire and quantitative coronary arteriography) and myocardial lactate metabolism (paired arterial and coronary sinus blood sampling) were measured in 12 patients with hypertension, LVH, and angiographically normal epicardial coronary arteries and in 7 control subjects. Measurements were done under 3 pacing protocols: with no treatment (control), with intracoronary N^G-monomethyl-L-arginine (L-NMMA; NO synthesis inhibitor), and with intracoronary L-arginine (NO substrate). Results In control subjects the myocardial lactate extraction ratio was normal and stable during the 3 pacing protocols. In contrast, lactate uptake was significantly decreased from 0.21 ± 0.05 to 0.10 ± 0.06 (P <.05) during L-NMMA pacing in patients with LVH; in 6 of them, lactate production was demonstrated. After L-arginine administration, the lactate extraction ratio during pacing was normalized (0.18 ± 0.04) and lactate production was not observed in any patient. The level of myocardial lactate uptake at peak pacing after L-NMMA was correlated with that under untreated condition (P <.0001). Conclusions In patients with hypertension, LVH, and angiographically normal coronary arteries, inhibition of endogenous NO synthesis in the coronary circulation unmasked myocardial ischemia during tachycardia, and L-arginine reversed the adverse effects of L-NMMA. Although the precise mechanism remains to be determined, our results suggest that constitutive NO in the coronary circulation plays an anti-ischemic role in this population. (Am Heart J 2002;143:684-9.)     

Biochemical and clinical predictors of long-term outcome in patients with nonspecific chest pain and nondiagnostic electrocardiograms

Background There are few data assessing the relative value of clinical factors and sensitive cardiac markers in determining the long-term prognosis of patients with chest pain. Likewise, little information exists about the long-term outcome of patients with chest pain who have negative markers of myocardial cell necrosis. This study addresses these issues in a cohort of patients with nonspecific chest pain and nondiagnostic electrocardiograms (ECGs).Methods Eligible subjects (n = 501) had experienced >15 minutes chest pain at rest during the previous 24 hours, but were found to be at low-risk for acute myocardial infarction (AMI) by means of a well-validated clinical algorithm. Cardiac troponin I, creatine kinase MB_mass, myoglobin, and myosin light chain-1 were collected at presentation and 3, 6, and 12 hours later. Patients were observed for a median of 31 months. The composite end point was death or AMI subsequent to the index admission.Results Cardiac troponin I was the best single biochemical predictor of outcome (risk ratio 2.34, 95% CI 1.31-4.17, P = .004), but was of less independent prognostic value than age and an abnormal presenting ECG. It was also inferior to a combination strategy, using all 4 markers tested (risk ratio 2.37, 95% CI 1.44-3.91, P < .001). Fifty of 428 patients (12%) with a cardiac troponin I level ≤0.2 ng/mL and 25 of 287 patients (9%) without elevation of any marker tested sustained an adverse event during follow-up.Conclusions Cardiac troponin I is the most useful single biochemical predictor of long-term outcome, but the best determinants are age, an abnormal presenting ECG, and an “any marker positive” strategy. Patients without elevated cardiac markers have an adverse event rate of approximately 10% in the subsequent 31 months. (Am Heart J 2003;145:88-94.)     

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.     

Validity of the reduced-sample insulin modified frequently-sampled intravenous glucose tolerance test using the nonlinear regression approach

The disposition index, the product of the insulin sensitivity index (S_I) and the acute insulin response to glucose, is linked in African Americans to chromosome 11q. This link was determined with S_I calculated with the nonlinear regression approach to the minimal model and data from the reduced-sample insulin-modified frequently-sampled intravenous glucose tolerance test (Reduced-Sample-IM-FSIGT). However, the application of the nonlinear regression approach to calculate S_I using data from the Reduced-Sample-IM-FSIGT has been challenged as being not only inaccurate but also having a high failure rate in insulin-resistant subjects. Our goal was to determine the accuracy and failure rate of the Reduced-Sample-IM-FSIGT using the nonlinear regression approach to the minimal model. With S_I from the Full-Sample-IM-FSIGT considered the standard and using the nonlinear regression approach to the minimal model, we compared the agreement between S_I from the Full- and Reduced-Sample-IM-FSIGT protocols. One hundred African Americans (body mass index, 31.3 ± 7.6 kg/m² [mean ± SD]; range, 19.0-56.9 kg/m²) had FSIGTs. Glucose (0.3 g/kg) was given at baseline. Insulin was infused from 20 to 25 minutes (total insulin dose, 0.02 U/kg). For the Full-Sample-IM-FSIGT, S_I was calculated based on the glucose and insulin samples taken at −1, 1, 2, 3, 4, 5, 6, 7, 8,10, 12, 14, 16, 19, 22, 23, 24, 25, 27, 30, 40, 50, 60, 70, 80, 90, 100, 120, 150, and 180 minutes. For the Reduced-Sample-FSIGT, S_I was calculated based on the time points that appear in bold. Agreement was determined by Spearman correlation, concordance, and the Bland-Altman method. In addition, for both protocols, the population was divided into tertiles of S_I. Insulin resistance was defined by the lowest tertile of S_I from the Full-Sample-IM-FSIGT. The distribution of subjects across tertiles was compared by rank order and κ statistic. We found that the rate of failure of resolution of S_I by the Reduced-Sample-IM-FSIGT was 3% (3/100). For the remaining 97 subjects, S_I for the Full- and Reduced-Sample-IM-FSIGTs were as follows: 3.76 ± 2.41 L mU⁻¹ min⁻¹ (range, 0.58-14.50) and 4.29 ± 2.89 L mU⁻¹ min⁻¹ (range, 0.52-14.42); relative error, 21% ± 18%; Spearman r = 0.97; and concordance, 0.94 (both P < .001). After log transformation, the Bland-Altman limits of agreement were −0.29 and 0.53. The exact agreement for distribution of the population in the insulin-resistant tertile vs the insulin-sensitive tertiles was 92%, κ of 0.82 ± 0.06. Using the nonlinear regression approach and data from the Reduced-Sample-IM-FSIGT in subjects with a wide range of insulin sensitivity, failure to resolve S_I occurred in only 3% of subjects. The agreement and maintenance of rank order of S_I between protocols support the use of the nonlinear regression approach to the minimal model and the Reduced-Sample-IM-FSIGT in clinical studies.     

Prognostic impact of electrocardiographic left ventricular hypertrophy following transcatheter aortic valve replacement

BackgroundLeft ventricular hypertrophy (LVH) develops with both structural and electrical remodeling in response to elevated afterload due to aortic stenosis (AS). This study evaluated the prognostic value of electrocardiographic LVH (ECG LVH) after transcatheter aortic valve replacement (TAVR).MethodsA retrospective study including 157 consecutive patients who underwent TAVR was conducted. ECG LVH was defined as Sokolow–Lyon voltage (S in V₁ + R in V_5/6) before TAVR was ≥3.5mV. We investigated the association between ECG LVH and the 1-year composite outcome comprising all-cause death and rehospitalization related to heart failure. ECG and echocardiographic measurements at 1, 6, and 12 months after TAVR were assessed.ResultsThe baseline characteristics were comparable between the ECG LVH (n = 74) and non-ECG LVH groups (n = 83). The ECG LVH was associated with a significantly greater reduction of Sokolow–Lyon voltage and LV mass index than the non-ECG LVH after TAVR. The absence of ECG LVH was an independent predictor of the 1-year composite outcome [adjusted hazard ratio (HR), 2.27; 95% confidence interval (CI), 1.01 – 5.60; p = 0.04]. Furthermore, a reduction of Sokolow–Lyon voltage from baseline to 1-month follow-up, but not a reduction of LV mass index, was associated with a lower cumulative composite outcome from 1 month to 1 year (adjusted HR, 0.36; 95% CI, 0.15 – 0.86; p = 0.02).ConclusionsECG LVH was associated with a low incidence of adverse clinical outcomes and greater reverse LV remodeling after TAVR. Preprocedural and serial LVH assessment by ECG might be useful in AS patients undergoing TAVR.     

Prevalence of premature ventricular contractions in a population of African American and white men and women: the Atherosclerosis Risk in Communities (ARIC) study

Background The distribution or the causes of premature ventricular contractions (PVCs) in diverse populations are not fully known. We describe the prevalence of PVCs on a 2-minute electrocardiogram (ECG) in adults to determine whether hypertension has an important association with such PVCs. Methods A cross-sectional analysis of the 15,792 individuals (aged 45-65 years) from the four US communities participating at visit 1 of the Atherosclerosis Risk In Communities (ARIC) study was performed. Multiple logistic regression was used to determine the association of PVCs with potential causal predictors of PVCs. Results Based on a 2-minute ECG, PVCs are present in >6% of middle-aged adults. Increasing age, the presence of heart disease, faster sinus rates, African American ethnicity, male sex, lower educational attainment, and lower serum magnesium or potassium levels are directly related to PVC prevalence. Independently of these factors, hypertension is associated with a 23% increase in the prevalence of PVCs. Conclusions The prevalence of PVCs on a 2-minute ECG differs by age, ethnicity, and sex and is associated with hypertension, heart disease, faster sinus rates, electrolyte abnormalities, and lower educational attainment. Hypertension is likely to be a major cause of PVCs in adults. (Am Heart J 2002;143:535-40.)     

QT intervals and QT dispersion as measures of left ventricular hypertrophy in an unselected hypertensive population

Electrocardiographic (ECG) QT intervals and dispersion correlate with echocardiographic left ventricular mass index (LVMI) in groups of selected essential hypertensives. We tested the strength of this relationship in a large group of unselected hypertensives to assess whether QT measurements may be a simple screening test for LVH in clinical practice. In a cross-sectional study of 386 unselected hypertensive subjects, maximal QT intervals (QT_max), QT dispersion (QT_disp), and ECG voltages (Sokolow-Lyon and Cornell sex-specific voltages) were measured from 12-lead ECG. The LVMI correlated most strongly with Cornell voltage (linear regression r = 0.44, P < .001). The strongest relationship between LVMI and QT parameters was with QT_max, (r = 0.25, P < .001). This relationship weakened using heart rate-corrected QT_max. Correlations between LVMI and QT_disp were weak, whether or not they were corrected for heart rate. Sokolow-Lyon voltages, Cornell voltage and QT_max, but not QT_disp, were independently predictive of LVMI after adjustment for age, sex, race, and the other ECG parameters. Receiver operating characteristic (ROC) curve analyses demonstrated that no QT parameter performed better than simple ECG voltage criteria in the detection of LVH. In conclusion, QT_max, the QT parameter most strongly associated with LVMI, was independently associated with LVMI after adjustment for standard ECG voltage criteria. However, as an isolated measure it was no better than simple ECG voltage criteria as a screening test for LVH in clinical practice.     

High triglycerides/low high-density lipoprotein cholesterol,ischemic electrocardiogram changes,and risk of ischemic heart disease

Background High triglycerides (TG)/low high-density lipoprotein cholesterol (HDL-C)(TG ≥1.60 and HDL-C ≤1.18 mmol/L) and ischemic ST-T changes in the resting electrocardiogram (ECG) are both strong risk factors of ischemic heart disease (IHD) in men without clinical cardiovascular diseases. This study tested the hypothesis that men free of clinical IHD with high TG/low HDL-C and resting ischemic ECG changes would have a particularly poor prognosis with respect to IHD.Methods We conducted a cohort study of 2906 men, aged 53 to 74 years, without overt IHD at baseline.Results During 8 years, IHD developed in 229 men; 61 cases were fatal. Of the risk factors recorded, ischemic ECG changes and high TG/low HDL-C were the strongest risk factors of IHD. Compared with men without high TG/low HDL-C and without ischemic ECG changes, age-adjusted relative risk of total IHD (95% CI) was 3.5 (1.7-7.2) in men with both high TG/low HDL-C and ischemic ECG changes; the corresponding value for fatal IHD was 11.2 (4.9-25.8). Adjusted for conventional risk factors, the interaction term high TG/low HDL-C × ischemic ECG changes was a significant predictor of IHD death, with a relative risk of 2.6 (1.0-6.9).Conclusions In men free of clinical IHD, ischemic ECG changes were significantly more predictive of fatal IHD in men with high TG/low HDL-C, indicating an adverse synergistic effect of these 2 risk factors. (Am Heart J 2003;145:103-8.)     

Prognostic Value of Standard Electrocardiographic Parameters for Predicting Major Adverse Cardiac Events after Acute Myocardial Infarction

Background: The prognostic value of electrocardiographic (ECG) variables in predicting major adverse cardiac events (MACEs) after acute myocardial infarction (AMI) in the era of modern therapy is unclear. This study was conducted to evaluate the prognostic significance of ECG parameters in predicting 1‐year MACEs for AMI patients. Methods: Between January 2006 and January 2008, 529 AMI patients were included. ECG variables were analyzed from the ECG taken on discharge day. The 1‐year MACEs were defined as death, nonfatal MI, and revascularization including repeat percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Mean follow‐up duration was 360 ± 119 days. Results: Of these patients, 497 (94%) patients provided complete follow‐up data (355 males; 67 ± 12 years old). The rate of 1‐year MACEs was 16%. In univariate analysis, heart rate, corrected QT interval, left ventricular (LV) hypertrophy, voltage (SV₁+ RV₅), lateral ST‐depression (V_5–6 or I, aVL), pathologic Q wave (V_1–4, V_5–6), ST‐elevation (V_1–4, V_5–6 or I, aVL), and T‐wave inversion (V_1–4, V_5–6, or I, aVL) had a significant association with 1‐year MACEs. In the Cox regression hazard model, lateral ST‐depression (hazard ratio [HR] 2.260, 95% confidence interval [CI] 1.204 to 4.241, P = 0.011) and corrected QT interval (HR 1.007, 95% CI 1.002 to 1.011, P = 0.004) were independent predictors of 1‐year MACEs. After adjustment for all risk variables, lateral ST‐depression (HR 3.781, 95% CI 1.047 to 13.656, P = 0.042) was the only ECG variable that independently predicted 1‐year MACEs. Conclusion: Lateral ST‐depression on discharge day ECG is an independent predictor of 1‐year MACEs after AMI. Ann Noninvasive Electrocardiol 2011;16(1):56–63     

Urine albumin/creatinine ratio and echocardiographic left ventricular structure and function in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. Losartan Intervention for Endpoint Reduction

Background Albuminuria, reflecting systemic microvascular damage, and left ventricular (LV) geometric abnormalities have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiovascular damage has not been evaluated in a large hypertensive population. Methods The urine albumin/creatinine ratio (UACR) and echocardiographic measures of LV structure and function were obtained in 833 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiogram (ECG) (Cornell voltage-duration or Sokolow-Lyon voltage criteria) after 14 days of placebo treatment. Results Patients' mean ages were 66 years, 42% were women, 23% had microalbuminuria, and 5% had macroalbuminuria. Patients with eccentric or concentric LV hypertrophy had higher prevalences of microalbuminuria (average 26%-30% vs 9%, P < .001) and macroalbuminuria (6%-7% vs <1%, P < .001). Furthermore, patients with microalbuminuria and macroalbuminuria had a significantly higher LV mass and lower endocardial and midwall fractional shortening. Patients with abnormal diastolic LV filling parameters had a significantly increased prevalence of microalbuminuria. In univariate analyses, UACR correlated positively to LV mass, systolic blood pressure, age (all P < .001) and pulse pressure/stroke volume and negatively to relative wall thickness (both P < .01) and endocardial (P < .05) and midwall shortening (P < .001) but not to diastolic filling parameters. In multiple regression analysis higher UACR was associated with higher LV mass (β = .169, P < .001) independently of older age (β = .095, P < .01), higher systolic pressure (β = .163), black race (β = .186), and diabetes (β = .241, all P < .001). Conclusions In hypertensive patients with ECG LV hypertrophy, abnormal LV geometry and high LV mass are associated with high UACR independent of age, systolic blood pressure, diabetes, and race, suggesting parallel cardiac and microvascular damage. (Am Heart J 2002;143:319-26.)     

Evaluation of the electrocardiogram RV5/V6 criteria in the diagnosis of left ventricular hypertrophy in marathon runners

To assess the value of electrocardiogram (ECG) RV5/V6 criteria for diagnosing left ventricular hypertrophy (LVH) in marathons. A total of 112 marathon runners who met the requirements for “Class A1” events certified by the Chinese Athletics Association in Changzhou City were selected, and their general clinical information was collected. ECG examinations were performed using a Fukuda FX7402 Cardimax Comprehensive Electrocardiograph Automatic Analyser, whereas routine cardiac ultrasound examinations were performed using a Philips EPIQ 7C echocardiography system. Real-time 3-dimensional echocardiography (RT-3DE) was performed to acquire 3-dimensional images of the left ventricle and to calculate the left ventricular mass index (LVMI). According to the LVMI criteria of the American Society of Echocardiography for the diagnosis of LVH, the participants were divided into an LVMI normal group (n = 96) and an LVH group (n = 16). The correlation between the ECG RV5/V6 criteria and LVH in marathon runners was analysed using multiple linear regression stratified by sex and compared with the Cornell (SV3 + RaVL), modified Cornell (SD + RaVL), Sokolow–Lyon (SV1 + RV5/V6), Peguero–Lo Presti (SD + SV4), SV1, SV3, SV4, and SD criteria. In marathon runners, the ECG parameters SV3 + RaVL, SD + RaVL, SV1 + RV5/V6, SD + SV4, SV3, SD, and RV5/V6 were able to identify LVH (all p < .05). When stratified by sex, linear regression analysis revealed that a significantly higher number of ECG RV5/V6 criteria were evident in the LVH group than in the LVMI normal group (p < .05), both with no adjustment and after initial adjustment (including age and body mass index), as well as after full adjustment (including age, body mass index, interventricular septal thickness, left ventricular end-diastolic diameter, left ventricular posterior wall thickness, and history of hypertension). Additionally, curve fitting showed that the ECG RV5/V6 values increased with increasing LVMI in marathon runners, exhibiting a nearly linear positive correlation. In conclusions, the ECG RV5/V6 criteria were correlated with LVH in marathon runners.