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(Hypertension. 1996;28:3-7.)
© 1996 American Heart Association, Inc.
Articles |
Association of Carotid Atherosclerosis With Electrocardiographic Myocardial Ischemia and Left Ventricular Hypertrophy
The Division of Cardiology, Department of Medicine, The New York Hospital–Cornell Medical Center, New York.
Correspondence to Peter M. Okin, MD, The New York Hospital–Cornell Medical Center, 525 E 68th St, New York, NY 10021. E-mail pokin@mail.med.cornell.edu.
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Abstract |
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Patients with carotid atherosclerosis have an increased risk of coronary events and an increased prevalence of echocardiographic left ventricular hypertrophy. However, little is known regarding the association between electrocardiographic abnormalities and carotid atherosclerosis. The relationship of electrocardiographic evidence of myocardial ischemia and left ventricular hypertrophy to the presence of carotid atherosclerosis was prospectively studied in 349 asymptomatic subjects who underwent echocardiography and carotid ultrasonography. Myocardial ischemia on the electrocardiogram was defined by the presence of localized T-wave inversions, and electrocardiographic hypertrophy was defined by the product of Cornell voltage and QRS duration. Carotid atherosclerosis was present in 21% (72/349) of subjects and was associated with older age, higher systolic and pulse pressures, and greater left ventricular mass. Both ischemia and hypertrophy on the electrocardiogram were strongly associated with carotid plaque. Carotid atherosclerosis was more than three times more prevalent in subjects with electrocardiographic ischemia (69% [11/16] versus 18% [61/333], P<.0001) or electrocardiographic left ventricular hypertrophy (78% [7/9] versus 19% [65/340], P=.0003) than in subjects without these findings. Logistic regression analysis, including standard risk factors, revealed that both ischemia and hypertrophy on the electrocardiogram remained significant independent predictors of the presence of carotid atherosclerosis, along with age and echocardiographic left ventricular mass. These findings suggest that the associations of ischemia and left ventricular hypertrophy with carotid atherosclerosis may contribute to the increased incidence of coronary events in patients with carotid atherosclerosis.
Key Words: electrocardiography • atherosclerosis • hypertrophy • ischemia
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Introduction |
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Previous studies have demonstrated that a strong association exists between carotid and coronary atherosclerosis1 2 3 4 5 6 7 and that coronary disease is a major cause of morbidity and mortality in patients with cerebrovascular disease.3 4 7 Although the predictive value of electrocardiographic (ECG) repolarization abnormalities8 9 10 11 12 13 14 and left ventricular hypertrophy (LVH)15 16 for cardiac events is firmly established, recent studies have demonstrated a higher sensitivity of echocardiographic LVH for the prediction of cardiovascular morbidity and mortality17 18 19 20 21 22 23 and identified relations between echocardiographic LVH and the risk of stroke24 and presence of carotid atherosclerosis.25 Additional observations have documented relations of unspecified ECG manifestations of LVH to carotid atherosclerosis1 and subsequent risk of stroke26 and between nonspecific ECG repolarization abnormalities and both increased mortality in asymptomatic patients with carotid disease27 and greater likelihood of carotid atherosclerosis in the elderly.1 However, the relation of specific ECG criteria for LVH or localized repolarization abnormalities to the presence of carotid atherosclerosis has not been examined.
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Methods |
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Study Population
The study included 217 normotensive subjects and 132 untreated hypertensive subjects who underwent resting ECG, transthoracic echocardiography, and carotid ultrasonography as part of several ongoing, longitudinal studies.25 28 29 All 349 subjects were asymptomatic, had no clinical evidence of coronary artery or cerebrovascular disease, and were without Q-wave myocardial infarction or bundle branch block on their ECG. The study was performed in accordance with protocols approved by the Committee on Human Rights in Research of Cornell University Medical College.
Electrocardiography
Standard 12-lead ECGs were recorded at 25 mm/s and 1 mV/cm standardization with equipment (Marquette Electronics, Inc) whose frequency response characteristics met American Heart Association recommendations.30 ECGs were digitized at 250 or 500 Hz, and all measurements were performed by computer from median complexes; QRS duration was measured to the nearest 2 milliseconds and QRS amplitudes to the nearest microvolt.
Criteria for ischemia on the ECG were based on a modification of Minnesota codes 5-1 and 5-231 for isolated T-wave abnormalities. To minimize overdiagnosis of ischemia, we considered ischemic repolarization abnormalities present only when codes 5-1 and/or 5-2 were present in two anatomically adjacent ECG leads. ECG criteria for the detection of LVH included QRS duration, Sokolow-Lyon voltage,32 sex-specific Cornell voltage (sum of the amplitude of the R wave in lead aVL and the amplitude of the S wave in lead V3 adjusted by the addition of 800 µV in women),33 34 35 and the sum of QRS voltage in all 12 leads.36 Because the product of QRS duration and voltage improves the sensitivity of the ECG for LVH,34 35 a voltage-duration product was calculated for each voltage criterion.34 35 A Cornell product partition with 98% specificity for LVH in a previously published cohort35 was used for the identification of LVH.
Cardiac and Carotid Ultrasound
All subjects underwent standard M-mode and two-dimensional echocardiography,25 35 with left ventricular (LV) dimensions determined according to recommendations of the American Society of Echocardiography.37 38 LV mass was calculated according to an anatomically validated formula,39 and LVH was considered present if the LV mass index was greater than 110 g/m2 in women and greater than 125 g/m2 in men.17 19 40
Imaging of both carotid arteries was performed with a Biosound Genesis II system (OTE Biomedica).25 41 Carotid atherosclerosis was defined as the presence of discrete plaque at least 50% thicker than the surrounding wall within any segment of either carotid artery.42 Intimal-medial thickness of the far wall was measured with electronic calipers on several cycles and averaged. The accuracy and reproducibility of ultrasound measurements of the carotid artery have been previously demonstrated.41 43 44 45
Data Analysis and Statistical Methods
Comparisons of mean values between subjects with and without carotid plaque were performed with Student's t test and further compared after adjustment for the presence or absence of clinical hypertension by two-way ANOVA. Differences in prevalences between groups were compared with 
2 analysis or Fisher's exact test. The relation between carotid wall thickness and clinical, echocardiographic, and ECG variables was evaluated by linear regression, and independence of association was assessed by stepwise multiple regression. The independent predictive power of risk factors and ECG variables for the presence of carotid plaque was determined by logistic regression analysis. For all tests, a value of P<.05 was required for rejection of the null hypothesis.
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Results |
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Relation of Clinical and Echocardiographic Variables to Carotid Plaque
Table 1
shows clinical and echocardiographic characteristics of subjects with and without carotid atherosclerosis. The 72 (21%) subjects who had plaques were older, had lower serum high-density lipoprotein levels, had higher systolic and pulse pressures, were slightly more likely to have clinical hypertension, had higher LV mass, and were more likely to have LVH. There was a trend toward an increased proportion of women among the subjects with carotid plaque, but this primarily reflected the significantly older mean age of women than men with carotid atherosclerosis (63±13 versus 54±8 years, P=.03). Differences between groups in both clinical and echocardiographic variables persisted after adjusting for the presence or absence of clinical hypertension.
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Relation of ECG Variables to Carotid Atherosclerosis
Mean values of ECG criteria for LVH and the prevalence of localized T-wave abnormalities on the ECG in subjects with and without discrete carotid plaques are given in Table 2. Subjects with plaques had a greater frequency of ECG ischemia, greater Cornell voltage, slightly longer QRS duration, and significantly greater Cornell products than subjects without plaque. In contrast, there were no significant differences between groups in Sokolow-Lyon voltage, the 12-lead sum of voltage, or their voltage-duration products. Differences in mean values of ECG variables also persisted after adjustment for the presence or absence of clinical hypertension.
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Both ischemia and LVH on the ECG were strongly associated with carotid plaque (Figure). The prevalence of carotid atherosclerosis was more than three times higher in subjects with than without localized repolarization abnormalities on the ECG (69% [11/16] versus 18% [61/333], P<.0001) or with ECG LVH as defined by an abnormal Cornell product (78% [7/9] versus 19% [65/340], P=.0003). Logistic regression analysis (Table 3), including standard risk factors, revealed that both ECG ischemia and an abnormal Cornell product remained significant predictors of the presence of carotid atherosclerosis, along with age and echocardiographic LV mass, but not sex. Of note, echocardiographic and ECG LVH had identical sensitivity (10% [7/72]) and nearly identical specificity (99% [273/277] versus 99% [275/277], P=NS) for the identification of carotid plaque.
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Because carotid intimal-medial thickening may reflect both smooth muscle hypertrophy and atherosclerotic changes, we also examined the relations of ECG evidence of myocardial ischemia and LVH to carotid hypertrophy. When subjects were divided into tertiles of carotid wall thickness, those in the upper tertile were more than three times as likely to have ECG ischemia than those in the lower two tertiles (9.5% [11/116] versus 1.7% [2/116] versus 2.6% [3/117], P=.008). ECG LVH was also significantly more likely to be present among subjects in the upper tertile of carotid wall thickness (5.2% [6/116] versus 2.6% [3/116] versus 0% [0/117], P=.045). Multivariate linear regression analysis (Table 4) revealed that ECG ischemia remained a significant correlate of carotid wall thickness (P=.04) along with age, systolic pressure, and body surface area.
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Discussion |
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These data indicate that both ischemia and LVH on the ECG are associated with the presence of carotid atherosclerosis, independent of age, echocardiographic LV mass, and other cardiac risk factors. These findings provide further support for the parallel nature of cardiac and vascular hypertrophy and atherosclerosis25 41 and provide additional evidence that the relations among ischemia, LVH, and carotid atherosclerosis may contribute to the increased incidence of coronary events in individuals with carotid atherosclerosis.
Relation of Electrocardiographic Ischemia to Carotid Atherosclerosis
In a population-based prospective study of more than 5000 men and women aged 65 years or older, the Cardiovascular Health Study1 found a strong relation between three different measures of carotid atherosclerosis and the presence of any major abnormality, including T-wave inversions, on the resting ECG. Unfortunately, this study did not examine the prevalence of isolated T-wave abnormalities in relation to carotid disease separately from other major ECG abnormalities and included subjects with angina, myocardial infarction, and coronary revascularization.1 The strong association between nonspecific repolarization abnormalities, which included localized T-wave inversions, and subsequent coronary morbidity and mortality found in large population studies8 9 10 11 12 13 14 and the increased mortality in asymptomatic patients with carotid disease and similar nonspecific ECG abnormalities27 suggest that asymptomatic individuals with carotid hypertrophy and localized T-wave inversions on the resting ECG may be at particularly high risk of future coronary events.
Possible overlap of ECG repolarization abnormalities due to ischemia with those secondary to LVH in the current study could potentially affect the interpretation of our findings concerning the association of isolated T-wave abnormalities with carotid disease. However, although there is no certain method of separating ischemic T-wave findings from those due to hypertrophy, the fact that only 3 (19%) of the 16 patients with localized T-wave abnormalities had ECG evidence of LVH makes it unlikely that LVH played a major role in the localized repolarization abnormalities found in this study. Importantly, repolarization abnormalities were not included in the ECG criteria used for the diagnosis of LVH; only the product of QRS duration and Cornell voltage was used for this purpose.
Relation of ECG LVH to Carotid Atherosclerosis
The current study demonstrates an increased risk of carotid atherosclerosis in subjects with an abnormal Cornell product, independent of and additive to the increased risk of carotid disease associated with increasing LV mass, increasing age, and a localized repolarization abnormality on the ECG and independent of sex and other known risk factors associated with carotid disease (Table 3
). These data add to previous findings of the relation between unspecified ECG LVH criteria and carotid atherosclerosis1 and support the finding of a similar association between echocardiographic LVH and carotid plaque.25 These associations and the known predictive power of both ECG and echocardiographic LVH for cardiovascular morbidity and mortality15 16 17 18 19 20 21 22 23 further suggest that individuals with ECG LVH and carotid atherosclerosis may also be at high risk of future events.
ECG Findings and Carotid Hypertrophy
Previous studies suggest that the relative contribution of hypertrophy and atherosclerosis to increased carotid wall thickness may vary depending on individual and population characteristics.42 45 The parallel increases in ventricular and carotid wall thicknesses in hypertensive patients,41 the increasing prevalence of ECG LVH with increasing carotid wall thickness, and the independent association of intimal-medial thickness with systolic pressure in the current study support the concept that increased carotid wall thickness is in part due to hypertrophy. The association of increased carotid intimal-medial thickness with subsequent myocardial infarction in Finnish men46 and with localized repolarization abnormalities consistent with myocardial ischemia in the current study suggest that increased intimal-medial thickness also reflects a more generalized atherosclerotic process. The similar prevalence of carotid plaque in the presence of isolated LVH (67%) or isolated repolarization abnormalities (62%) on the ECG and the similar carotid wall thickness in these subjects (0.82±0.07 versus 0.87±0.17 mm, P=NS) suggest that a comparable degree of atherosclerosis and hypertrophy are present in this cross-sectional analysis of subjects with either LVH or ischemia on the resting ECG.
Summary
In conclusion, the current study documents a high prevalence of carotid atherosclerosis in asymptomatic subjects with no clinical evidence of either coronary or cerebrovascular disease who have resting ECG evidence of myocardial ischemia or LVH. Longitudinal studies of the relationship of resting ECG evidence of myocardial ischemia or LVH to clinical outcome in subjects with carotid atherosclerosis will be necessary to determine whether these findings additively heighten risk or whether they represent parallel windows into a common adverse pathophysiology.
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Acknowledgments |
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This work was supported in part by a grant from The Michael Wolk Heart Foundation, Inc, New York, NY, and by grant HL-18323 from the National Heart, Lung, and Blood Institute.
Received January 10, 1996;
first decision February 16, 1996; first decision March 11, 1996;
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