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      Left Ventricular Hypertrophy May Be Transient in the Emergency Department

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          Abstract

          Background:

          While research has established that the bedside electrocardiogram (ECG) is an insensitive test for the presence or absence of left ventricular hypertrophy (LVH), the finding, when present, is thought to be reproducible.

          Objective:

          To assess the reproducibility of serial ECGs done in the emergency department (ED) with regard to the presence or absence of LVH.

          Method:

          A prospective study on consecutive patients admitted to an ED-run cardiac observation unit. A single reviewer collected and scored ECGs for the presence of LVH, using three established criteria (Cornell, Sokolow-Lyon and Romhilt-Estes). Demographic and medical history was also collected.

          Results:

          Over a three-year time period, 295 patients were enrolled; 132 males and 163 females with a mean age of 54.4 years (range, 19–89 years). The prevalence of LVH ranged from 11–14% and the agreement among all three criteria was fair (kappa = 0.325). Using the Cornell criteria, 33 patients had ECG#1 consistent with LVH. Of the patients meeting LVH criteria on ECG #1, only 15 retained their diagnosis of LVH on ECG#2 (i.e. 55% of the LVH identified in ECG#1 was not seen in ECG#2). Additionally, nine patients developed an ECG diagnosis of LVH between ECG#1 and ECG#2. In total, 27 (nine percent of the total) had ECG measurements that changed between ECG#1 and ECG#2. We made similar findings with the Sokolow-Lyon and Romhilt-Estes criteria. The results were not modified by gender, blood pressure or medication use.

          Conclusion:

          The finding of LVH on ECG was not very reproducible during serial measurements on the same person during a single 24-hour observation period.

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          Most cited references23

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          Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol.

          The most suitable antihypertensive drug to reduce the risk of cardiovascular disease in patients with hypertension and diabetes is unclear. In prespecified analyses, we compared the effects of losartan and atenolol on cardiovascular morbidity and mortality in diabetic patients. As part of the LIFE study, in a double-masked, randomised, parallel-group trial, we assigned a group of 1195 patients with diabetes, hypertension, and signs of left-ventricular hypertrophy (LVH) on electrocardiograms losartan-based or atenolol-based treatment. Mean age of patients was 67 years (SD 7) and mean blood pressure 177/96 mm Hg (14/10) after placebo run-in. We followed up patients for at least 4 years (mean 4.7 years [1.1]). We used Cox regression analysis with baseline Framingham risk score and electrocardiogram-LVH as covariates to compare the effects of the drugs on the primary composite endpoint of cardiovascular morbidity and mortality (cardiovascular death, stroke, or myocardial infarction). Mean blood pressure fell to 146/79 mm Hg (17/11) in losartan patients and 148/79 mm Hg (19/11) in atenolol patients. The primary endpoint occurred in 103 patients assigned losartan (n=586) and 139 assigned atenolol (n=609); relative risk 0.76 (95% CI 0.58-.98), p=0.031. 38 and 61 patients in the losartan and atenolol groups, respectively, died from cardiovascular disease; 0.63 (0.42-0.95), p=0.028. Mortality from all causes was 63 and 104 in losartan and atenolol groups, respectively; 0.61 (0.45-0.84), p=0.002. Losartan was more effective than atenolol in reducing cardiovascular morbidity and mortality as well as mortality from all causes in patients with hypertension, diabetes, and LVH. Losartan seems to have benefits beyond blood pressure reduction.
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            Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin-converting enzyme inhibitor ramipril.

            Electrocardiographic markers of left ventricular hypertrophy (LVH) predict poor prognosis. We determined whether the ACE inhibitor ramipril prevents the development and causes regression of ECG-LVH and whether these changes are associated with improved prognosis independent of blood pressure reduction. In the Heart Outcomes Prevention Evaluation (HOPE) study, patients at high risk were randomly assigned to ramipril or placebo and followed for 4.5years. ECGs were recorded at baseline and at study end. We compared prevention/regression and development/persistence of ECG-LVH in the two groups and related these changes to outcomes. At baseline, 676 patients had LVH (321 in the ramipril group and 355 in the placebo group) and 7605 patients did not have LVH (3814 in the ramipril group and 3791 in the placebo group). By study end, 336 patients in the ramipril group (8.1%) compared with 406 in the placebo group (9.8%) had development/persistence of LVH; in contrast, 3799 patients in the ramipril group (91.9%) compared with 3740 in the placebo group (90.2%) had regression/prevention of LVH (P=0.007). The effect of ramipril on LVH was independent of blood pressure changes. Patients who had regression/prevention of LVH had a lower risk of the predefined primary outcome (cardiovascular death, myocardial infarction, or stroke) compared with those who had development/persistence of LVH (12.3% versus 15.8%, P=0.006) and of congestive heart failure (9.3% versus 15.4%, P<0.0001). The ACE inhibitor ramipril decreases the development and causes regression of ECG-LVH independent of blood pressure reduction, and these changes are associated with reduced risk of death, myocardial infarction, stroke, and congestive heart failure.
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              Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy.

              Numerous electrocardiographic criteria, which are largely dependent on fixed voltage thresholds, have been proposed for the diagnosis of left ventricular hypertrophy (LVH). Electrocardiographic criteria for LVH were examined in 4,684 subjects of the Framingham Heart Study who underwent echocardiographic study for LVH. Echocardiographic LVH was detected in 290 men (14.2%) and 465 women (17.6%). Electrocardiographic features of LVH were present in 2.9% of men (60/2,042) and 1.5% of women (39/2,642). The overall sensitivity of the electrocardiographic diagnosis of LVH was 6.9%, whereas specificity was 98.8%. Sensitivity of the electrocardiogram (ECG) for LVH was marginally lower in women than in men (5.6% vs. 9.0%, p = 0.075). Obesity was inversely associated with sensitivity (p less than 0.05, both sexes combined, sex-adjusted). Smoking was also inversely related to sensitivity (p = 0.001, both sexes combined, sex-adjusted). In contrast, sensitivity of the ECG increased with age (p less than 0.001, both sexes combined, sex-adjusted). These findings suggest that electrocardiographic detection of LVH can be improved by incorporating information about noncardiac factors that impact on electrocardiographic sensitivity for LVH, presumably by attenuating QRS voltage. New strategies that take into consideration sex, age, smoking status, and obesity might improve the sensitivity of the ECG without diminishing specificity.
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                Author and article information

                Journal
                West J Emerg Med
                WestJEM
                Western Journal of Emergency Medicine
                Department of Emergency Medicine, University of California, Irvine School of Medicine
                1936-900X
                1936-9018
                August 2009
                : 10
                : 3
                : 140-143
                Affiliations
                [* ]Keck School of Medicine of the University of Southern California, Department of Emergency Medicine, Los Angeles, CA
                []Keck School of Medicine of the University of Southern California, Los Angeles, CA
                []Keck School of Medicine of the University of Southern California, Department of Preventive Medicine, Los Angeles, CA
                Author notes
                Address for Correspondence: Jan M. Shoenberger, MD, Department of Emergency Medicine, LAC + USC Medical Center, 1200 N. State Street Room 1011, Los Angeles, CA 90033. Email: sohender@ 123456usc.edu
                Article
                wjem-10-140
                2729211
                19718372
                9832d29b-8a71-47c6-a22a-6975ffb32f27
                Copyright © 2009 the authors.

                This is an Open Access article distributed under the terms of the Creative Commons Non-Commercial Attribution License, which permits its use in any digital medium, provided the original work is properly cited and not altered. For details, please refer to http://creativecommons.org/licenses/by-nc/3.0/. Authors grant Western Journal of Emergency Medicine a nonexclusive license to publish the manuscript.

                History
                : 09 August 2007
                : 08 November 2008
                : 03 December 2008
                Categories
                Trauma / Critical Care
                Original Research

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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