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      Comparison of electrocardiographic versus echocardiographic detection of left ventricular mass changes over time and evaluation of new onset left ventricular hypertrophy

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          Abstract

          We assessed the value of 3 electrocardiographic (EKG) voltage criteria in detecting variations of left ventricular mass (LVM) over time, taking echocardiographic (ECHO) LVM as reference, in the Pressioni Arteriose Monitorate E Loro Associazioni study. In 927 subjects (age 47 ± 13 years on entry, 49.9% men) an ECHO evaluation of LVM and EKG suitable for measurement of EKG‐LVH criteria (Sokolow‐Lyon voltage, Cornell voltage and R‐wave voltage in aVL) were available at baseline and at a 2 nd evaluation performed 10 years later. Δ (delta) LVM, Δ LVMI, and Δ EKG parameters values were calculated from 2 nd evaluation to baseline. The sensitivity of the EKG criteria in the diagnosis of LVH, poor at baseline, becomes even worse after 10 years, reaching very low values. Only the sensitivity of R‐wave amplitude exhibited slight increase over time but with unsatisfactory absolute values. Despite the prevalence of ECHO‐LVH at the 2 nd evaluation was threefold increased compared to baseline (29.3% and 33.7% for LVM indexed to BSA and height 2.7, respectively), the prevalence of EKG‐LVH was unchanged when evaluated by Sokolow‐Lyon criteria, significantly reduced when assessed by Cornell voltage index, while significantly increased using R‐wave voltage in aVL criteria. Despite an ECHO‐LVM increase over the time, mean EKG changes were of opposite sign, except for R‐wave amplitude in aVL. Our study highlights the discrepancy between ECHO and EKG in monitoring LVM changes over the time, especially for Sokolow‐Lyon and Cornell voltage. Thus, EKG is an unsuitable method for the longitudinal evaluation of LVM variations.

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          Most cited references23

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          The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads.

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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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              Quantification of diffuse myocardial fibrosis and its association with myocardial dysfunction in congenital heart disease.

              the etiology of ventricular dysfunction in adult congenital heart disease (ACHD) is not well understood. Diffuse fibrosis is a likely common final pathway and is quantifiable using MRI. patients with ACHD (n=50) were studied with cardiac MRI to quantify systemic ventricular volume and function and diffuse fibrosis. The fibrosis index for a single midventricular plane of the systemic ventricle was quantified by measuring T1 values for blood pool and myocardium before and after administration of gadolinium (0.15 mmol/kg) and then adjusted for hematocrit. Results were compared to healthy volunteers (normal controls, n=14) and patients with acquired heart failure (positive controls, n=4). Patients studied (age, 37±12 years; female sex, 40%) included 11 with a systemic right ventricle (RV), 17 with tetralogy of Fallot, 10 with cyanosis, and 12 with other lesions. The fibrosis index was significantly elevated in patients with ACHD compared to normal controls (31.9±4.9% versus 24.8±2.0%; P=0.001). Values were highest in patients with a systemic RV (35.0±5.8%; P<0.001) and those who were cyanotic (33.7±5.6%; P<0.001). The fibrosis index correlated with end-diastolic volume index (r=0.60; P<0.001) and ventricular ejection fraction (r=-0.53; P<0.001) but not with age or oxygen saturation in patients who were cyanotic. Late gadolinium enhancement did not account for the differences seen. patients with ACHD have evidence of diffuse, extracellular matrix remodeling similar to patients with acquired heart failure. The fibrosis index may facilitate studies on the mechanisms and treatment of myocardial fibrosis and heart failure in these patients.
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                Author and article information

                Contributors
                guido.grassi@unimib.it
                Journal
                J Clin Hypertens (Greenwich)
                J Clin Hypertens (Greenwich)
                10.1111/(ISSN)1751-7176
                JCH
                The Journal of Clinical Hypertension
                John Wiley and Sons Inc. (Hoboken )
                1524-6175
                1751-7176
                23 February 2023
                April 2023
                : 25
                : 4 ( doiID: 10.1111/jch.v25.4 )
                : 343-349
                Affiliations
                [ 1 ] University of Milano‐Bicocca Pio XI Hospital Internal Medicine, Desio Milan Italy
                [ 2 ] Clinica Medica University of Milano‐Bicocca Milan Italy
                Author notes
                [*] [* ] Correspondence

                Guido Grassi, Clinica Medica, University Milano‐Bicocca, Via Pergolesi 33, 20052 Monza, Italy.

                Email: guido.grassi@ 123456unimib.it

                Author information
                https://orcid.org/0000-0002-7689-478X
                https://orcid.org/0000-0003-1922-6547
                Article
                JCH14631
                10.1111/jch.14631
                10085814
                36824023
                326e04ff-7659-49c0-9db9-ca39f8857432
                © 2023 The Authors. The Journal of Clinical Hypertension published by Wiley Periodicals LLC.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 14 December 2022
                : 22 November 2022
                : 20 December 2022
                Page count
                Figures: 1, Tables: 4, Pages: 7, Words: 4420
                Categories
                Original Article
                Left Ventricular Hypertrophy
                Custom metadata
                2.0
                April 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.7 mode:remove_FC converted:10.04.2023

                echocardiography,electrocardiography,left ventricular hypertrophy,left ventricular mass

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