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Diagnostic Efficacy of Electrocardiography in Determining Left Ventricular Hypertrophy in Patients with Essential Hypertension
Abstract
A total of 37 hypertensive patients of both sexes over 18 years of age and more than four years of duration after diagnosis and only those having evidence of left ventricular hypertrophy (LVH) by echocardiography (ECHO) were enrolled to analyze the diagnostic efficacy of electrocardiography in determining left ventricular hypertrophy in patients with essential hypertension. Electrocardiograhpy (ECG) of 37 LVH diagnosed cases were analysed and 31 of them were found to have LVH on voltage criteria. Thus, the sensitivity of ECG in diagnosing LVH is 83%.Key Words: Left Ventricular Hypertrophy (LVH), Electrocardiography (ECG), Echocardiography (ECHO).
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To assess whether echocardiographic and electrocardiographic detection of left ventricular hypertrophy could predict cardiovascular morbid events in patients with uncomplicated essential hypertension, we followed 140 men for a mean of 4.8 years. Initial echocardiographic measurements of left ventricular mass were normal (< 125 g/m2 body surface area) in 111 patients and revealed hypertrophy in 29 patients. Morbid events occurred in more patients with hypertrophy on echocardiography (7 of 29,4.6/100 patient-years) than with normal ventricular mass (7 of 111,1.4/100 patient-years; p < 0.01). Electrocardiography showed hypertrophy in too few patients to be of predictive value. Multiple logistic regression analysis showed that left ventricular mass index had the highest independent relative risk for future events and that systolic and diastolic pressures and age had slightly lower relative risks. In men with mild uncomplicated hypertension, left ventricular hypertrophy detected by echocardiography identifies patients at high risk for cardiovascular morbid events and is a significant risk factor for future morbid events independent of age, blood pressure, or resting ventricular function.
The spectrum of left ventricular geometric adaptation to hypertension was investigated in 165 patients with untreated essential hypertension and 125 age- and gender-matched normal adults studied by two-dimensional and M-mode echocardiography. Among hypertensive patients, left ventricular mass index and relative wall thickness were normal in 52%, whereas 13% had increased relative wall thickness with normal ventricular mass ("concentric remodeling"), 27% had increased mass with normal relative wall thickness (eccentric hypertrophy) and only 8% had "typical" hypertensive concentric hypertrophy (increase in both variables). Systemic hemodynamics paralleled ventricular geometry, with the highest peripheral resistance in the groups with concentric remodeling and hypertrophy, whereas cardiac index was super-normal in those with eccentric hypertrophy and low normal in patients with concentric remodeling. The left ventricular short-axis/long-axis ratio was positively related to stroke volume (r = 0.45, p less than 0.001), with cavity shape most elliptic in patients with concentric remodeling and most spheric in those with eccentric hypertrophy. Normality of left ventricular mass in concentric remodeling appeared to reflect offsetting by volume "underload" of the effects of pressure overload, whereas eccentric hypertrophy was associated with concomitant pressure and volume overload. Thus, arterial hypertension is associated with a spectrum of cardiac geometric adaptation matched to systemic hemodynamics and ventricular load. Concentric left ventricular remodeling and eccentric hypertrophy are more common than the typical pattern of concentric hypertrophy in untreated hypertensive patients.
Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.
Left ventricular (LV) hypertrophy on the electrocardiogram is an ominous harbinger of cardiovascular disease in the general population markedly increasing the risk of coronary heart disease, cardiac failure, stroke and peripheral arterial disease. This contribution to risk exceeds that of the often accompanying hypertension. Once overt coronary disease occurs, electrocardiographic LV hypertrophy also further escalates risk of cardiovascular morbidity and mortality. The risk associated with electrocardiographic LV hypertrophy is particularly great when repolarization abnormality is present. Electrocardiographic LV hypertrophy and silent electrocardiographic myocardial infarction are similar in evolution and prognosis. LV hypertrophy is an important predictor of risk of cardiac failure; the electrocardiographic manifestation of LV hypertrophy predisposes to cardiac failure more than x-ray cardiac enlargement. Electrocardiographic LV hypertrophy heralds the onset of serious cardiovascular disease and premature mortality despite lack of associated symptoms. The serious prognosis of this abnormality warrants vigorous preventive management. More prospective data are needed comparing the prognosis of echocardiographic anatomical hypertrophy with that diagnosed by electrocardiography.
Quantitative echocardiography is the gold standard for the evaluation of abnormalities in left ventricular (LV) geometry and systolic function, information very important for risk stratification, and also applicable in clinical practice when some conditions are met. Few primary measures (LV diameter, septal and posterior wall thickness) provide a valuable information which fully represents the type and degree of hemodynamic alteration. These measures should be collected ideally by M-mode tracings, but often M-mode examination cannot be performed. When M-mode is suboptimal, LV mass can be computed using two-dimensional imaging and the formulas used for M-mode. LV mass is expressed as an index normalized for some measure of body size. Normalization for height in meters to the power 2.7 can identify a higher proportion of individuals at high cardiovascular risk and provides a greater attributable risk than other methods of indexation. When LV hypertrophy develops to provide sufficient strength to compensate for hemodynamic overload, the increase in LV mass is not clearly associated with increased cardiovascular risk. In contrast, individuals with LV mass inappropriately high as compared to the value sufficient to compensate for hemodynamic load at a given body size present with a phenotype characterized by high cardiovascular risk, even in the absence of arterial hypertension.
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