Asian Cardiovasc Thorac Ann 1998;6:129-131
© 1998 Asia Publishing EXchange Pte Ltd
Discordant Limb-Lead and Precordial-Lead QRS Voltages in Inferior Myocardial Infarction
James Yip Wei Luen, MBBS, MRCP,
Lim Yean Teng, MBBS, MRCP,
Tan Huay Cheem, MBBS, M MED,
Chia Boon Lock, MBBS, FRACP
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Cardiac Department National University Hospital
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For reprint information contact: Chia Boon Lock, MBBS, FRACP Cardiac Department National University Hospital 5 Lower Kent Ridge Road Singapore 119074 Republic of Singapore Tel: 65 772 5213 Fax: 65 872 2998
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ABSTRACT
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A 70-year-old man with acute inferolateral and posterior myocardial infarction presented with congestive heart failure. The 12-lead electrocardiogram showed a discordant pattern consisting of very low limb-lead QRS voltages and tall R waves in leads V2 and V3.
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INTRODUCTION
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In 1982, Goldberger1 described a specific triad of electrocardiographic features consisting of: (1) prominent precordial QRS voltage such that [SV1 or SV2] + [RV5 or RV6] is greater than or equal to 3.5 mV, (2) a relatively low limb-lead QRS voltage such that the total QRS amplitude in each of the 6 limb leads equals 0.8 mV or less, and (3) poor R wave progression defined as R less than the S wave amplitude in lead V4. In a subsequent study in 1985, Goldberger and colleagues2 confirmed that this electrocardiographic triad was a specific indicator of congestive heart failure and left ventricular dysfunction. We describe a patient who presented with severe congestive heart failure due to acute inferolateral and posterior myocardial infarction of the left ventricle. The patient's 12-lead electrocardiogram (ECG) showed a variant of the Goldberger electrocardiographic triad; the limb-lead QRS voltages were markedly decreased, whereas 2 of the precordial-lead QRS voltages were considerably increased as reflected by very tall R waves in leads V2 and V3. To our knowledge, these unique ECG abnormalities have not been reported previously.
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CASE REPORT
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A 70-year-old man was admitted with severe chest pain. Clinical examination revealed a dual heart rhythm and a blood pressure of 160/90 mm Hg. There were no cardiac murmurs. The 12-lead ECG recorded soon after this admission showed acute Q wave inferolateral and posterior myocardial infarction. The right-sided chest leads V4R to V6R showed no evidence of myocardial infarction. Figure 1
was recorded 9 hours after admission and showed the fully evolved pattern of inferolateral and posterior infarction as reflected by: deep Q waves, mildly elevated ST segment, and T wave inversion in leads II, III, and AVF; very tall R waves in leads V2 and V3; a slight reduction in the amplitude of the R wave in lead V6. The diagnosis of acute myocardial infarction was confirmed by an elevated serum creatine kinase MB level of 131 ng•mL. The two-dimensional echocardiogram showed akinesia of the inferior wall and hypokinesia of the posterolateral wall of the left ventricle. The ejection fraction was estimated to be around 45%. The hospital stay was uncomplicated and he was discharged 8 days after admission.
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Figure 1. 12-lead electrocardiogram showing the fully evolved pattern of inferolateral and posterior myocardial infarction during the patient's first hospital admission. The tall R waves in leads V2 and V3 are a reflection of the posterior infarction. The arrow indicates the nadir of the S wave in lead V2 and the arrowhead shows the peak of the R wave in lead V3.
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The patient was readmitted to hospital approximately one year later with severe chest pain. Clinical examination revealed a blood pressure of 120/60 mm Hg. The 12-lead ECG showed evidence of reinfarction of the inferolateral and posterior wall of the left ventricle as reflected by ST-segment elevation in the inferior leads and leads V5 and V6, marked ST-segment depression in leads V1 to V4 and tall R waves in leads V2 and V3. The QRS voltages in all the limb leads as well as those in the precordial leads were essentially similar to those seen in the ECG in Figure 1
. Soon after admission, he developed ventricular tachycardia that was successfully electrocardioverted and this was followed by an intravenous infusion of lidocaine. Five hours after admission, the patient developed severe congestive cardiac failure and was treated with intravenous frusemide and oral captopril. At this time, the two-dimensional echocardiogram showed that the left ventricular systolic function was globally impaired with akinesia of the inferior and posterolateral left ventricular wall. The ejection fraction was estimated to be approximately 20%. Figure 2 was recorded 16 hours after this admission when the patient was in severe congestive heart failure. The hyperacute changes of inferior and posterior infarction were all absent. The amplitudes of the QRS voltages in all the limb leads and lead V6 had all become extremely small (0.5 mV or less). The tall R waves that were seen previously in leads V2 and V3 remained essentially unchanged and measured 2.0 mV and 2.9 mV, respectively.
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Figure 2. 12-lead electrocardiogram recorded about one year after that in Figure 1 during the patient's second hospital admission. It shows the fully evolved pattern of inferolateral and posterior myocardial infarction. The QRS voltages in all the limb leads are extremely small (0.5 mV or less). Tall R waves are seen in leads V2 and V3. The arrow indicates the nadir of the S wave in lead V2 and the arrowhead indicates the peak of the R wave in lead V3.
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Over the next few days, the patient's general condition improved with the treatment given. However, on the 12th day of admission, he suddenly collapsed and was noted to be in asystole. Resuscitative measures were unsuccessful. No postmortem was carried out.
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DISCUSSION
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Our patient showed two of the three criteria of Goldberger's electrocardiographic triad. These were low QRS voltages in all the limb leads and increased precordial-lead QRS voltages that were seen only in leads V2 and V3. The tall R waves in leads V2 and V3 were a reflection of an old posterior infarction.3
The most important aspect of the ECGs in this patient is that in the fully-evolved phase of inferolateral and posterior myocardial infarction during the first hospital admission, the QRS voltages in all the limb leads were not decreased (Figure 1). At that time, the left ventricular ejection fraction as determined by two-dimensional echocardiography was approximately 45%. However, during the second attack of inferolateral and posterior infarction, the patient developed severe congestive cardiac failure and the echocardiographic estimation of the left ventricular ejection fraction had dropped to a very low level of about 20%. The 12-lead ECG at that time showed that the QRS voltages in all the limb leads had decreased markedly to 0.5 mV or less in every lead, thus fulfilling the second of the three criteria of Goldberger's electrocardiographic triad.2 On the other hand, since the amplitudes of the R waves in the precordial leads V2 and V3 in the earlier ECGs did not change, these very tall R waves fulfilled part of the first criterion of Goldberger's triad of prominent QRS voltage in the precordial leads. The only major difference was that in our patient, the prominent precordial QRS voltages were reflected by tall R waves in leads V2 and V3, whereas in Goldberger's patients this was reflected by an increased QRS voltage in lead V1 or V2 and also in lead V5 or V6 such that [S V1/V2 + R V5/V6
3.5 mV]. In our patient, since tall R waves were seen in leads V2 and V3 and not rS complexes in leads V1 to V4, the third criterion of the Goldberger's ECG triad of poor r wave progression such that the r/S ratio in lead V4 is less than 1, obviously cannot apply.
This case illustrates that in patients with inferolateral and posterior Q wave myocardial infarction, the discordant pattern of low limb-lead QRS voltages and tall R waves in leads V2 and V3 may be an important indicator of poor left ventricular function. However, the sensitivity and specificity of this ECG abnormality must await future studies involving large numbers of patients.
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REFERENCES
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Goldberger AL. A specific ECG triad associated with congestive heart failure. PACE
1982;5:593–9.
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Goldberger AL, Dresselhaus T, Bhargava V. Dilated cardiomyopathy: utility of the transverse: frontal plane QRS voltage ratio. J Electrocardiol
1985;18:35–40.[Medline]
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Schamroth L. The 12-lead electrocardiogram. Oxford: Blackwell Scientific Publications, 1989:176–80.
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ABSTRACT
INTRODUCTION
