Asian Cardiovasc Thorac Ann 2008;16:103-106
© 2008 Asia Publishing EXchange Ltd
Differentiation of Ischemic and Dilated Cardiomyopathy on Electrocardiograms
Kamran Aghasadeghi, MD,
Amir Aslani, MD
Department of Cardiology, Shiraz University of Medical Sciences, Shiraz, Iran
For reprint information contact: Amir Aslani, MD, Tel: 98 711 843 3095, Fax: 98 711 227 7182, Email: aslanidr{at}yahoo.com, Namazee Hospital, PO Box 71935 1334, Shiraz, Iran.
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ABSTRACT
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Differentiating coronary artery disease with left ventricular dysfunction from dilated cardiomyopathy is important prognostically and therapeutically. To provide a diagnostic algorithm to distinguish these conditions using a standard 12-lead electrocardiogram, all 105 patients with left ventricular ejection fraction < 50% who underwent angiography between January 2004 and December 2006 were studied prospectively. Coronary artery disease was defined as 
50% stenosis of the left main coronary artery or 70% stenosis of 1 or more of the 3 major epicardial arteries. Normal coronary angiography findings with left ventricular ejection fraction < 50% was defined as dilated cardiomyopathy. The most specific finding for differentiation of these diseases was pathologic Q waves in lead II, aVF, V3 or V4. The most sensitive parameter was a ratio 5 of R-wave amplitudes in lead V6 and lead III (94% sensitive). The 12-lead electrocardiogram provides a useful noninvasive method for differentiation of dilated cardiomyopathy from coronary artery disease with left ventricular systolic dysfunction.
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INTRODUCTION
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Coronary artery disease (CAD) and dilated cardiomyopathy (DCM) are the most common causes of left ventricular (LV) dysfunction which imposes a significant burden on healthcare systems because of high morbidity and mortality.1–5 Differentiating CAD with LV dysfunction from DCM is important prognostically and therapeutically.6–8 The standard 12-lead electrocardiogram (EKG) is the primary clinical method used to identify many cardiac abnormalities. The aim of this study was to evaluate EKG differences between DCM and CAD with LV dysfunction.
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PATIENTS AND METHODS
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Between January 2004 and December 2006, patients with LV ejection fraction < 50% who were referred to our catheterization laboratory for coronary angiography were studied prospectively. Medical histories, 12-lead EKGs and echocardiograms were reviewed. The 105 patients with LV systolic dysfunction (LV ejection fraction < 50%) were divided into 2 groups: the DCM group had angiographic documentation of normal coronary arteries, the CAD group had stenosis 50% of the left main coronary artery or 70% in 1 or more of the 3 major epicardial arteries or their main branches. A reference group of 100 patients with LV systolic dysfunction referred for coronary angiography was also established. The sensitivity, specificity, positive and negative predictive values of our results were calculated in the reference group. Electrocardiogram evaluation was performed without knowledge of the angiographic results. A junior and senior investigator examined each EKG and recorded the results separately. Any discrepancies between the investigators were resolved by joint review of the findings. R-wave, Q-wave and S-wave amplitudes in all EKG leads were determined in each subject. Patients were excluded from the study if they had congenital heart disease, bundle branch block, LV aneurysm detected by echocardiography or LV hypertrophy (defined as the sum of R waves in leads V5 or V6 plus S waves in lead V1 > 3.5 mV).
Data are expressed as mean ± standard deviation. Comparisons of data in the 2 groups were performed with an unpaired 2-tailed t test for continuous variables and chi-squared statistics with the Fisher correction when appropriate for categorical variables. Sensitivity, specificity, positive and negative predictive values were plotted against the range of cut-off values. A p value < 0.05 was considered significant.
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RESULTS
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Baseline characteristics of the patients are listed in Table 1
. R-wave amplitude in lead V5 was greater in the DCM group compared to the CAD group (1.51 ± 0.3 vs 0.72 ± 0.2 mV, p < 0.05). R-wave amplitude in lead V6 was also greater in the DCM group (1.50 ± 0.4 vs 0.73 ± 0.3 mV, p < 0.05). Except for lead aVR, lead III had the lowest voltage among limb leads in the DCM group. Therefore, the ratio of R-wave amplitudes in lead V6 and lead III was evaluated in both groups; it was significantly greater in the DCM group (7.90 ± 0.8 vs 3.59 ± 0.9, p < 0.05). The sum of the Q wave amplitudes in the precordial leads ( QV1-V6) in both groups was higher in the CAD group (1.23 ± 0.2 mV vs 0.46 ± 0.09 mV, p < 0.05). Careful evaluation of all leads revealed that pathologic Q waves (width > 40 msec and voltage > 0.1 mV) in leads II, aVF, V3 and V4 were more common in the CAD group.
The most specific EKG parameter for diagnosis of DCM was R-wave amplitude 1.5 mV in V6 and V5 (Table 2). There was a highly positive predictive value of R-wave amplitude in V6 and V5 1.5 mV. R-wave amplitude ratio V6/III 5 had a low specificity but was useful in differentiating DCM from CAD with LV systolic dysfunction because of high sensitivity (Table 2, Figure 1). The most specific EKG parameter for diagnosis of CAD with LV systolic dysfunction was pathologic Q waves in leads II, V3, V4 and aVF (Table 3), but the sensitivity of this parameter was very low. The positive predictive value of pathologic Q waves in leads II, V3, V4 and aVF was high (Table 3). The specificity of QV1-V6 1.5 mV was 90% for diagnosis of CAD with LV systolic dysfunction, but the sensitivity of this parameter was relatively low (Table 3). Results of the S-wave voltages in different leads, QRS axis, QT intervals and QT dispersions showed no significant differences between groups. On combining specificity, sensitivity and positive predictive value of the data, an algorithm was produced for differentiation between DCM and CAD (Figure 1).
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Figure 1. Differentiation between dilated cardiomyopathy (DCM) and coronary artery disease (CAD) with left ventricular (LV) systolic dysfunction by 12-lead electrocardiogram (EKG); pathologic Q waves in lead II, aVF, V3 or V4 is highly specific for diagnosis of CAD; ratio of R-wave amplitudes in lead V6 and lead III (RV6/RIII) 5 has a high sensitivity for diagnosis of DCM.
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DISCUSSION
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The treatment of patients with LV systolic dysfunction is determined in part by identification of the underlying disease process (DCM or CAD). In many centers, coronary angiography is routinely performed for this task. In patients with unobstructed coronary arteries and no other etiological factor, a diagnosis of DCM is usually made. This differentiation is important clinically in patients with CAD because they have a worse prognosis and they may benefit from revascularization and secondary preventive pharmacotherapy with statins and aspirin.6,7 Conversely, in patients with DCM, secondary causes such as excess alcohol ingestion or myocardial iron overload need to be excluded, and as genetic studies of DCM begin to identify inherited abnormalities, accurate phenotyping and family screening will become more important for early diagnosis.9–11
McCrohon and colleagues12 suggested that cardiovascular magnetic resonance imaging distinguishes LV dysfunction related to DCM or CAD on the basis of gadolinium enhancement and patterns within the myocardium. Their findings also suggest a potential to reduce the costs and inherent risks associated with invasive cardiac catheterization on which the diagnosis of DCM has depended until now. Right ventricular function was used as a criterion to differentiate DCM from CAD by de Groote and colleagues13 who found a significantly higher prevalence of reduced right ventricular ejection fraction ( 39%) in DCM. Analysis of clinical data shows that patients with DCM are younger than those with CAD. This difference may be related to the etiology of each condition. The most common cause of CAD is atherosclerosis which is more common in older age.8 In contrast, DCM is related to myocarditis, genetics and familial factors which are more common among the younger age group.6
In this study, the specificity, sensitivity and positive predictive values of the EKG findings provided a simple algorithm for differentiation of DCM and CAD with LV dysfunction. Before using this algorithm, one has to keep a few points in mind. Firstly, the finding of pathologic Q waves in lead II, aVF, V3 or V4 has a high specificity which favors a diagnosis of CAD. Therefore, a diagnosis of CAD with pathologic Q waves in lead II, aVF, V3 or V4 is fairly definite. Secondly, a ratio 5 of R-wave amplitudes in leads V6/III has a high sensitivity for diagnosis of DCM. Therefore, when the V6/III R-wave amplitude ratio is less than 5, DCM is unlikely. It was concluded that the 12-lead EKG provides a useful noninvasive method for differentiation of DCM from CAD in patients with LV systolic dysfunction.
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ABSTRACT
INTRODUCTION
