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The Electrocardiogram Is an Unreliable Method of Identifying Left Ventricular Hypertrophy in Stable, Treated Angina Patients

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The Electrocardiogram Is an Unreliable Method of Identifying Left Ventricular Hypertrophy in Stable, Treated Angina Patients Journal of Human Hypertension (2008) 22, 394–400 & 2008 Nature Publishing Group All rights reserved 0950-9240/08 $30.00 www.nature.com/jhh ORIGINAL ARTICLE The electrocardiogram is an unreliable method of identifying left ventricular hypertrophy in stable, treated angina patients DSC Ang, LL Ti and AD Struthers Division of Medicine and Therapeutics, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK In coronary artery disease (CAD), a potentially reversible sensitivity, specificity, positive predictive value and factor leading to cardiac death is left ventricular negative predictive value were calculated for each ECG hypertrophy (LVH). While the electrocardiogram (ECG) LVH criteria. The prevalence of echo LVH in the entire is a widely available way to diagnose LVH, its sensitivity CAD population was 43%. All the proposed ECG criteria and specificity has never been assessed in this were poor at identifying echo LVH. The Cornell product particular patient group where added ischaemic yielded the highest rate of change value but still missed changes on ECG might complicate things. Furthermore, up to 80% of the echo LVH cases. We conclude that in there are at least 11 different ECG criteria proposed to a group of stable, treated angina patients, ECG is an identify LVH. We sought to determine how many cases unreliable method of identifying LVH. As LVH is very of echocardiography (echo) LVH would be missed if all common in this patient population, screening by means of these different ECG criteria were applied in a group of of echo might be indicated. This will enable intensified stable, treated angina patients. A total of 241 consecu- efforts to ensure LVH regression, which is associated tive patients with angiographically confirmed CAD with reduction in both cardiovascular morbidity and were prospectively recruited and 11 ECG criteria were mortality. assessed on each subject and compared with the Journal of Human Hypertension (2008) 22, 394–400; presence or absence of LVH on echo. Individual doi:10.1038/jhh.2008.18; published online 20 March 2008 Keywords: electrocardiogram; echocardiogram; left ventricular hypertrophy; sensitivity; specificity; coronary artery disease Introduction valence would be around 30–35% in controls. Secondly, in a comparative study in CAD patients, Left ventricular hypertrophy (LVH) is associated Liao et al.4 showed that the independent relative with increased risk of cardiovascular morbidity, all 1 risk of cardiac death conferred by LVH was higher cause mortality and sudden cardiac death. This has (2.4) and accounted for more deaths than multi- been shown to be independent of conventional vessel coronary disease (relative risk ¼ 1.6) or LV cardiovascular risk factors. Recent evidence shows systolic dysfunction (relative risk ¼ 2.0). Therefore, that LVH is an important cause of cardiac death even it appears that LVH is a strong, if not the strongest, in patients with overt coronary artery disease (CAD). risk factor in CAD. In addition, recent studies have This is based on two main observations. Firstly, LVH also demonstrated that LVH regression is associated is more prevalent in this patient population than in with improved clinical outcome. In the hyperten- the general population. In a study carried out in a sive population, ECG and echo LVH regression has predominantly black population with established been associated with a significant reduction in both CAD, the prevalence of echocardiography (echo) 5,6 2 fatal and non-fatal cardiovascular events. In a LVH was as high as 50%. We recently found similar 7 3 recent review, Mancini et al. emphasized, ‘We now figures, while according to Framingham, the pre- have the ultimate documentation for both ECG LVH and echo LVH that reversal has an independent Correspondence: Dr DSC Ang, Division of Medicine and Thera- prognostic value, independent of therapy and blood peutics, University of Dundee, Clinical Pharmacology, Ninewells pressure’.7 This view was endorsed again by Hospital and Medical School, Dundee DD1 9SY, UK. Schillaci et al.8 E-mail: [email protected] Received 11 December 2007; revised 15 February 2008; accepted Nevertheless, detection of LVH in CAD remains a 16 February 2008; published online 20 March 2008 challenge. While echo is a reliable method for ECG LVH in stable angina patients DSC Ang et al 395 detecting anatomic LVH, it is less widely available Table 1 Demographic characteristics of the CAD population especially in the non US countries and obviously studied (n ¼ 241) requires technical expertize. Conversely, the 12-lead Variable Mean (s.d.) ECG is universally available, technically easy to perform and highly specific. The major limitation of Male subjects (%) 76 the ECG in other populations is its low sensitivity in Age (years) 64 (8) detecting LVH. Previous epidemiology studies have Body mass index (kg mÀ2) 29 (4) examined the sensitivity and specificity of various Office systolic BP (mm Hg) 136 (2) ECG criteria in picking up echo LVH in the general Office diastolic (mm Hg) 74 (10) 9,10 Haemoglobin (g per 100 ml) 13.6 (1.5) population and in hypertensives. Despite the Creatinine (umol lÀ1) 100 (21) importance of detecting LVH in CAD, the ability of Total Cholesterol (mmol lÀ1) 3.87 (0.76) different ECG criteria to detect echo LVH in this History of hypertension (%) 53 specific population has never been addressed. In History of type II diabetes (%) 14 History of hypercholesterolaemia (%) 51 addition, ischaemic related ST segment changes in Current smokers (%) 5 CAD might complicate ECG interpretation. Our Ex-smokers (%) 56 study aims to answer this question and in this Previous CABG (%) 33 analysis, we used a larger number of ECG criteria Previous percutanoues coronary intervention (%) 39 (11) than in previous studies. The main aim of our Previous myocardial infarction (%) 25 study is to see how many cases of echo LVH would LVMI (BSA) be missed in a prospective cohort of 241 stable, Male subjects 127.3 (25.7) treated angina patients by applying each of these Female subjects 109.9 (21.8) many ECG criteria. Left ventricular ejection fraction (%) 58 (6) Treated with Aspirin 89% Statin 96% Methods b blockers 74% ACE inhibitors 56% A total of 351 white patients with the diagnosis of ARB 14% stable angina who had all undergone diagnostic Clopidogrel 15% coronary angiography (between 2002 and 2005) Calcium antagonist 27% Nicorandil 16% were consecutively recruited from the Cardiology Nitrate 32% Department, Ninewells Hospital, Dundee. The in- Bendrofluazide 15% clusion criteria were a history of ischaemic chest Loop diuretic 14% pain and the presence of angiographically proven CAD (greater than 50% reduction in the cross Abbreviations: ARB, angiotensin receptor blocker; BP, blood pressure; BSA, body surface area; CAD, coronary artery disease; LVMI, left sectional diameter of a major coronary artery). ventricular mass index. Majority of them had been treated with stable antianginal medication for approximately 1 year Definition of a normal clinic blood pressure (Table 1 shows the breakdown of antianginal A ‘normal’ clinic BP was defined as 140/90 mm Hg treatment of the entire study population at the p as previously described in the British Hypertension time of study) and the majority had no ongoing Society (BHS) IV guidelines.12 In contrast, the symptoms of angina pectoris. The exclusion criteria ‘target’ BP for treating CAD was 130/80 mm Hg. include: p (1) Recent hospital admission with troponin-T 40.01 ng mlÀ1 in the last year. ECG assessment of LVH (2) Valvular, pericardial or congenital heart disease Simultaneous 12-lead electrocardiograms were ob- À1 (3) An impaired LV function (characterized by tained for analysis, calibrated to 20 mm mV and À1 regional wall motion abnormality or LV ejection 25 mm s . ECG analysis was performed manually fractiono45%) on ventriculography or echo. with an ECG image digitizer board, by a second researcher (IT) blinded to patient details and the echo results. Three QRS complexes’ per lead were All subjects attended a single clinic visit and analysed and the mean value used. We applied two underwent the following: history, past medical ECG criteria for LVH used in the Losartan Interven- history, clinic blood pressure (BP) measurement, tion for Endpoint Reduction (LIFE) study as well as electrocardiography, routine blood tests and trans- an additional nine previously reported ECG criteria thoracic echo. Ethical approval was obtained from for LVH, all of which are sufficiently straightforward the Tayside Committee of Medical Research Ethics to be used in routine clinical practice. The ECG and all participating subjects gave written informed criteria are as follows: consent. Other details of this study are already published, especially data on the relationship (1) Sokolow–Lyon voltage, SV1 þ (RV5 or RV6) between BP and LVH.11 X38 mm Journal of Human Hypertension ECG LVH in stable angina patients DSC Ang et al 396 (2) Gender-specific Cornell voltage, SV3 þ RaVL constructed. We also separately analysed the 11 420 mm in women, 428 mm in men proposed ECG criteria for LVH in the hypertensive (3) Gubner–Ungerleider voltage, RI þ SIII subgroup of the CAD population. X25 mm (4) Lewis voltage, (RI þ SIII)À(SI þ RIII) X17 mm (5) RaVL 411 mm Results (6) Cornell product, Cornell voltage  QRS dura- tion 42440 in men, with addition of six to the Of the 351 consecutive patients recruited, 29 Cornell voltage in women patients were excluded due to the presence of (7) Sum of 12-lead voltage, 12-lead QRS sum impaired LV systolic function or valvular heart 4175 mm disease on echo. Of the remaining 322 patients, an (8) 12-lead QRS product, 12-lead QRS sum  QRS LVM was obtainable in 267 patients (83%). Those in duration 417 472 whom LVM could not be assessed did not differ significantly in any parameters from those in whom (9) RV5 or RV6 426 mm an adequate M-mode measurement was obtained.
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