[Vectorcardiographic system of Frank. II. Left ventricular hypertrophy & left branch block].
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Cardiomegaly↗
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Influence of hypertension, left ventricular hypertrophy, and left ventricular systolic dysfunction on plasma N terminal proBNP.
OBJECTIVES: To examine the relation between plasma concentration of the N terminal of the precursor of brain natriuretic peptide (NT proBNP), left ventricular hypertrophy (LVH), and left ventricular systolic dysfunction (LVSD) in patients with a history of hypertension. DESIGN: Prospective study. SETTING: Teaching hospital based study. PATIENTS: NT proBNP concentrations were determined in five groups of individuals. Group 1: 15 echocardiographic normal controls; group 2: 22 patients with hypertension, normal left ventricular systolic function, and no LVH; group 3: 24 patients with hypertension, normal left ventricular systolic function, and LVH; group 4: 13 patients with history of hypertension, no history of ischaemic heart disease, and left ventricular wall motion index (WMI) between 1.9-1.3; and group 5:17 patients with a history of hypertension, no history of ischaemic heart disease, and WMI < 1.2. RESULTS: Median (range) NT proBNP concentrations (in fmol/ml) for groups 1-5, respectively, were: 129.4 (53.6-159.7), 147.4 (54.3-730. 5), 137.1 (35.8-403.9), 356.7 (124.4-934.4), and 493.5 (248.9-909). Mean log NT proBNP differed among all five groups (p < 0.0001), and between groups 4 and 5 versus groups 1-3 (p < 0.0001), and group 4 versus group 5 (p = 0.02) only. CONCLUSIONS: The results suggest that the presence of hypertension with or without LVH (and normal left ventricular systolic function) does not affect NT proBNP concentrations. Moreover, there is a significant rise in NT proBNP only when LVSD develops in hypertension. Thus, NT proBNP remains a useful diagnostic aid for LVSD, even in hypertensive patients.
Adult↗
[Correlations between blood pressure, left ventricular hypertrophy, and left ventricular diastolic function in hypertensive patients].
We examined the relationship of hypertension to left ventricular hypertrophy (LVH) and left ventricular diastolic function by ambulatory blood pressure monitoring device and echocardiography. We studied 36 untreated hypertensive non-diabetic patients (16 males and 20 females) whose casual systolic blood pressure (CSBP) and/or diastolic blood pressure (CDBP) were higher than 140 mmHg and 90 mmHg, respectively. All patients were less than 65 years of age without organic heart disease. Resting systolic and diastolic blood pressures (RSBP, RDBP) were measured after lying in a supine position for 30 min by the auscultatory method. Ambulatory blood pressure was measured every 30 or 60 min for 24 hours by Colin ABPM 630, and the mean 24-hour ambulatory systolic and diastolic blood pressures (ASBP, ADBP) and the systolic and diastolic hyperbaric indices (SHI, DHI) were obtained. The left ventricular mass index (LVMI) was obtained as an indicator of LVH by M-mode echocardiography. The ratio of peak velocity of mitral inflow caused by atrial contraction to that of rapid inflow (A/R) was obtained as an indicator of the LV diastolic function by Doppler echocardiography. The coefficients of correlation between BP and the LVMI, and the A/R were determined. There were significant positive correlations between the LVMI and ASBP (r = 0.51, p < 0.005), the SHI (r = 0.49, p < 0.005), CSBP (r = 0.47, p < 0.01) and RSBP (r = 0.41, p < 0.05), however, there were no significant correlations between the LVMI and ADBP, the DHI, CDBP, RDBP and age. There were significant positive correlations between the A/R and ADBP (r = 0.44, p < 0.01), age (r = 0.40, p < 0.02), CSBP (r = 0.38, p < 0.05) and RDBP (r = 0.38, p < 0.05), however, no significant correlations between the A/R and ASBP, the SHI, DHI, RSBP and CDBP. Only a weak correlation was observed in all subjects between the LVMI and A/R, which was slightly improved by use of > 90 mmHg CSBP readings (r = 0.32). It was concluded that LVH is related mainly to continuous systolic hypertension, and that LV diastolic dysfunction is related mainly to continuous diastolic hypertension. Therefore, it was suggested that LVH and LV diastolic dysfunction in hypertensive patients are caused by different mechanisms.
Adult↗
Hypertensive left ventricular hypertrophy with left ventricular outflow tract obstructive physiology: a case of successful treatment with dual-chamber pacing.
Controversy exists over the use of atrioventricular synchronous pacing for patients with hypertrophic obstructive cardiomyopathy who are refractory to medical treatment. We present the case of an elderly man with severe-effort dyspnea attributable to hypertensive left ventricular hypertrophy with dynamic aortic outflow obstruction. We were able to achieve dramatic subjective and objective improvement in the exercise capacity of this patient with dual-chamber pacing after attempts at medical management had failed. This patient's response to therapy and his impressive response to minor pacemaker adjustments suggest that atrioventricular synchronous pacing should be considered for patients with secondary left ventricular hypertrophy as well as patients with hypertrophic obstructive cardiomyopathy.
Cardiac Pacing, Artificial↗
Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.
Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 +/- 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a,a') derived from P-V and normalized P-V relations, respectively, for end-diastolic myocardial elastic stiffness (ES or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (KS or KE) of the circumferential stress-strain relation. Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 +/- 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV,dP/dV/V,ES and EE and a tendency for increase in the chamber stiffness constants (a,a') and myocardial stiffness constants (KS, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid- and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.
Adult↗
Left ventricular papillary muscle morphology and function in left ventricular hypertrophy and left ventricular dysfunction.
BACKGROUND: This study was prospectively performed to evaluate the anatomy and contractile performance of LV papillary muscles (PM) in humans using transesophageal echocardiography (TEE), and to determine the relationship between PM anatomy and contractile function in normal left ventricle (LV), left ventricular hypertrophy (LVH) and systolic dysfunction. MATERIAL AND METHODS: TEE examinations were prospectively performed in 153 patients. End-diastolic (ED) and end-systolic (ES) cross sectional areas of both PMs were obtained at the transgastric mid papillary short axis views. ED and ES lengths of PMs were obtained from the transgastric long axis views, and fractional systolic shortening (FS) was calculated. PM shape description was derived from the formula Area/L2. LV EF, wall thickness and mass were determined from transthoracic echocardiographic measurements. RESULTS: The % FS in patients with normal EF (>55%) was 21.1 +/- 9.1% for anterior PM (APM) and 17.1 +/- 6.2% for posterior PM (PPM). The values for hypertrophic LV were as follows; 25.2 +/- 8.1 (APM) and 15.8 +/- 5.6 (PPM), for dilated cardiomyopathy, 15.0 +/- 6.8 (APM) and 13.4 +/- 4.2 while values for non-dilated cardiomyopathy were 15.6 +/- 8.0 and 11.3 +/- 6.0 respectively. In dilated cardiomyopathy patients, both PM lengths were significantly longer (p<0.05) and thinner (p<0.05) than in patients with normal EF. In the hypertrophied LV, the PMs were thicker (p<0.05) and had larger cross sectional areas p<0.05. CONCLUSIONS: TEE is a safe and useful method for detailed study of PM morphology and contractile performance in living humans with normal or impaired LV systolic function. Quantitative TEE data on PM geometry, size, and contractile function are presented here for the first time.
Cardiomegaly↗
Grading, staging and scoring of left-ventricular hypertrophy, left-ventricular dilatation, asymptomatic left-ventricular dysfunction and chronic heart failure.
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Adaptation, Physiological↗
Effect of electrocardiographic left ventricular hypertrophy on left ventricular systolic function in systemic hypertension (The LIFE Study). Losartan Intervention For Endpoint.
Left ventricular (LV) ejection fraction is normal in most patients with uncomplicated hypertension, but the prevalence and correlates of decreased LV systolic chamber and myocardial function, as assessed by midwall mechanics, in hypertensive patients identified as being at high risk by the presence of LV hypertrophy on the electrocardiogram has not been established. Therefore echocardiograms were obtained in 913 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiographic (Cornell voltage duration or Sokolow-Lyon voltage) criteria after 14 days' placebo treatment. The 913 patients' mean age was 66 years, and 42% were women. Fourteen percent had subnormal LV endocardial shortening, 24% had subnormal midwall shortening, and 13% had reduced stress-corrected midwall shortening. Nineteen percent had normal LV geometry, 11% had concentric remodeling, 47% had eccentric hypertrophy, and 23% had concentric hypertrophy. LV systolic performance evaluated by LV endocardial shortening and midwall shortening was impaired in 10% of patients with normal geometry, 20% with concentric remodeling, 27% with eccentric hypertrophy, and 42% with concentric hypertrophy. Relative wall thickness, an important independent correlate of LV chamber function, was related directly to endocardial shortening and negatively to midwall shortening and stress-corrected midwall shortening. LV mass was the strongest independent correlate of impaired endocardial shortening, midwall shortening, or both. In hypertensive patients with electrocardiographic LV hypertrophy, indexes of systolic performance are subnormal in 10% to 42% with different LV geometric patterns. Depressed endocardial shortening is most common in patients with eccentric LV hypertrophy, whereas impaired midwall shortening is most prevalent in patients with concentric remodeling or hypertrophy. Thus, in hypertensive patients with electrocardiographic LV hypertrophy, impaired LV performance occurs most often, and is associated with greater LV mass and relative wall thickness and may contribute to the high rate of cardiovascular events.
Aged↗
[Effect of enalapril on left ventricular hypertrophy and left ventricular function in patients with hypertension].
The aim of this study was to study the effect of enalapril (E) on left ventricular (LV) mass, LV function and blood renin-angiotensin (RA) in patients with hypertension. Sixteen hypertensives were included in this study (WHO I 8, WHO II 8, 49.5 +/- 10.5 yrs). They were examined for blood pressure and heart rate. Chest X-ray film, echocardiography (echo), X-ray computed tomography (CT) and RA before and after about 6 months of E administration were studied. The LV mass was calculated by CT. The LV function was measured by echo. RAS was unchanged during this study. LV mass was significantly reduced after E (121.4 +/- 25.6 vs 104.6 +/- 13.7 g/cm2). The LV systolic function was unchanged after E, but LV diastolic function improved. It was shown that the long-term administration of E improves LV hypertrophy and LV diastolic function without any change of RAS.
Adult↗
Relation of obesity, high sodium intake, and eccentric left ventricular hypertrophy to left ventricular exercise dysfunction in essential hypertension.
PURPOSE: To elucidate determinants of abnormal left ventricular functional responses to exercise in hypertensive patients. PATIENTS AND METHODS: One hundred twenty-seven patients with uncomplicated essential hypertension were studied by rest and exercise radionuclide angiography and by echocardiography at rest. RESULTS: The 24 patients with subnormal left ventricular ejection fraction at peak exercise (less than 54%) were similar in age and rest and exercise blood pressures to the 103 with normal exercise ejection fraction, but were more obese (p less than 0.005) and had greater left ventricular mass (p less than 0.03) and internal dimensions (p less than 0.001). The parallel increase in left ventricular chamber size and mass (eccentric hypertrophy) in the group of patients with exercise dysfunction was associated with higher resting end-systolic wall stress (p less than 0.001) and abnormal increases of end-systolic left ventricular volume from rest to peak exercise (p less than 0.001). Multivariate analysis revealed that exercise left ventricular dysfunction was independently associated with higher left ventricular mass (p less than 0.0005), end-systolic wall stress (p less than 0.001), dietary sodium intake (p less than 0.01), and body mass index (p less than 0.03). CONCLUSION: Among patients with uncomplicated essential hypertension, abnormal functional responses to exercise are strongly associated with eccentric ventricular hypertrophy, obesity, and high sodium intake.
Cardiomegaly↗
[The heart in hypertension. III. Determinants of left ventricular hypertrophy and diastolic left ventricular compliance (author's transl)].
Diastolic wall stress and compliance were determined in 74 patients with essential hypertension during diagnostic cardiac catheterization. Ventricular compliance was normal in compensated essential hypertension without coronary artery disease even at severe left ventricular hypertrophy. In contrast, additional coronary stenosis and ventricular dilatation due to cardiac decompensation was asscociated with considerable decrease in ventricular compliance. Thus, left ventricular hypertrophy in essential hypertension does not imply per se a change in ventricular compliance. A decrease in ventricular compliance was followed by a decrease of forward pump function of the left ventricle. whereas ventricular work index (as estimated as the product out of systolic wall stress and the stroke volume) increased. This disproportion between external and internal ventricular work increased with increasing ventricular dilatation and was greatest in decompensated essential hypertension. Accordingly, decompensated essential hypertension had largest ventricular work load and lowest forward pump function in comparison to all other patient groups with essential hypertension. The mass to volume ratio may be considered an important determinant of the degree of left ventricular hypertrophy in essential hypertension. The relationship between the mass to volume ratio and the systolic wall stress may provide a diagnostic and prognostic evaluation of the left ventricle in essential hypertension on the basis of dynamic ventricular geometry.
Adult↗
[Left ventricular hypertrophy and left atrial morphology in untreated hypertensive patients].
The level of arterial pressure is not the sole determinant of cardiac and vascular adaptation to hypertension. In order to identify other factors (such as preload) we categorized by echocardiography, 55 never treated hypertensive patients and 39 age and gender-matched normal subjects, according to values of relative wall thickness and left ventricular mass index. Normal left ventricular anatomy was found in 63% hypertensives, whereas among hypertensives 7% had "concentric left ventricular remodeling", 16% concentric left ventricular hypertrophy and 14% had eccentric left ventricular hypertrophy. Systolic left atrial area (LA) was obtained from the four-chamber views. Mitral peak early diastolic (E) and late diastolic (A) flow velocity was assessed by Doppler. Because clinical characteristics such age and sex differed among the 5 groups only results of ANCOVA were reported (means +/- SD). [table: see text] We conclude that eccentric left ventricular hypertrophy may be associated with a parallel increase of left atrial area. Thus the association of an increase of cardiac volume in hypertensive patients with normal diastolic function suggest that volume overload may modulate the effect of arterial pressure on cardiac morphology.
Adult↗
Electrocardiographic diagnosis of left ventricular hypertrophy: the effect of left ventricular wall thickness, size, and mass on the specific criteria for left ventricular hypertrophy.
BACKGROUND: The purpose of our study was to determine the relative importance and effect of an increased left ventricle wall thickness, left ventricular diastolic diameter, and left ventricular mass (LVM) on the performance of the 4 major electrocardiogram (ECG) criteria of left ventricular hypertrophy (LVH) and to determine how these findings could be incorporated into the routine ECG interpretation of LVH. METHODS: The ECG criteria of LVH that we chose to examine were voltage, repolarization abnormalities, left atrial abnormality, and ventricular conduction time. We analyzed data from 608 consecutive patients with left ventricular wall thickness of >13 mm on the echocardiogram and with a concurrent ECG. We arbitrarily divided patients into 3 groups (groups I-III) according to the calculated LVM. Group I had an LVM of <400 g; group II had an LVM from 400 to 600 g, and group III had an LVM of >600 g. We evaluated the effect of increasing LVM, wall thickness, and ventricular diameter on the performance of the 4 ECG criteria at different severity of thickness, diameter, and mass. RESULTS: An increase in the echocardiogram-derived LVM had significant effect on all 4 ECG criteria. As LVM progressively increased from groups I to III, the frequency of voltage criteria for LVH increased from 52% to 83%; left atrial abnormality rose from 46% to 68%; ST-T wave changes increases from 55% to 95%, and QRS prolongation significantly increased from 42% to 70%. CONCLUSION: Increased wall thickness and ventricular diameter failed to correlate with the overall ECG score or significantly influence the frequency of any of the 4 ECG criteria for LVH in patients when LVM was held relatively constant. We also demonstrated that an increasing number of criteria on the ECG are associated with a greater mean LVM.
Cohort Studies↗
Effects of eplerenone, enalapril, and eplerenone/enalapril in patients with essential hypertension and left ventricular hypertrophy: the 4E-left ventricular hypertrophy study.
BACKGROUND: Elevated renin-angiotensin-aldosterone system activity correlates with left ventricular hypertrophy (LVH) and cardiovascular risk, but the relative contributions of angiotensin II and aldosterone remain unclear. This study compared LVH regression during treatment with the selective aldosterone blocker eplerenone, enalapril, and their combination in patients with hypertension. METHODS AND RESULTS: A 9-month, double-blind, randomized study was performed in 202 patients with LVH and hypertension who received eplerenone 200 mg daily, enalapril 40 mg daily, or eplerenone 200 mg and enalapril 10 mg daily. At week 8, hydrochlorothiazide 12.5 to 25 mg and/or amlodipine 10 mg was added if diastolic blood pressure was >90 mm Hg. Change in left ventricular (LV) mass as assessed by MRI was the primary end point. Change in blood pressure, renin-angiotensin-aldosterone system hormones, albuminuria, and safety were also assessed. Eplerenone significantly reduced LV mass from baseline (-14.5+/-3.36 g; n=50) similarly to enalapril (-19.7+/-3.20 g; n=54; P=0.258), but eplerenone/enalapril (-27.2+/-3.39 g; n=49) was more effective than eplerenone alone (P=0.007). All treatments reduced systolic blood pressure and diastolic blood pressure from baseline (eplerenone, -23.8 and -11.9 mm Hg; enalapril, -24.7 and -13.4 mm Hg; and eplerenone/enalapril, -28.7 and -14.4 mm Hg, P=0.048, in systolic blood pressure compared with eplerenone alone). Cough was more common with enalapril than with eplerenone (P=0.033), and elevated potassium was more common with eplerenone. CONCLUSIONS: Eplerenone was as effective as enalapril in LVH regression and blood pressure control. The combination of eplerenone and enalapril was more effective in reducing LV mass and systolic blood pressure than eplerenone alone.
Adult↗
The effect of enalapril and verapamil on the left ventricular hypertrophy and the left ventricular cardiomyocyte numerical density in rats submitted to nitric oxide inhibition.
Forty male Wistar rats were separated into four groups of ten rats each (control and other three groups that have received nitric oxide (NO) synthesis inhibitor L-NAME) but the last two groups have concomitantly received antihypertensive drugs (Enalapril and Verapamil). After 40 days of experimentation, the heart and the ventricles were measured. The optical disector was used for the calculation of numerical density of the cardiomyocytes (Nv[c]). The left ventricular myocytes number (N[c]) was calculated as the product of Nv[c] and the left ventricular myocardium volume (LVMV) that was determined by using the Scherle's method. In the L-NAME group the blood pressure (BP) had a significant weekly increment. In the enalapril and the verapamil groups, BP increased in the first two weeks, but decreased in the following weeks. The LVMV increased in the L-NAME rats and decreased in the enalapril and verapamil animals. The Nv[c] and N[c] decreased in the L-NAME rats but the verapamil and enalapril treatments maintained the Nv[c] close to the control group. In conclusion, the left ventricular hypertrophy and the significant decrease of the left ventricular cardiomyocyte number caused by the NO synthesis inhibition are efficiently prevented with the use of enalapril and verapamil.
Analysis of Variance↗
Coronary haemodynamics in left ventricular hypertrophy.
BACKGROUND: Left ventricular hypertrophy is associated with an increased risk of cardiovascular morbidity and mortality. Previous studies have shown that patients with left ventricular hypertrophy develop electrocardiographic changes and left ventricular dysfunction during acute hypotension, and suggest that the lower end of autoregulation may be shifted upwards. AIM: To measure coronary blood flow (velocity) and flow reserve during acute hypotension in patients with left ventricular hypertrophy. PATIENTS: Eight patients with atypical chest pain and seven with hypertensive left ventricular hypertrophy; all with angiographically normal epicardial vessels. SETTING: Tertiary referral centre. METHODS: The physiological range of blood pressure was determined by previous ambulatory monitoring. Left ventricular mass was determined by echocardiography. At cardiac catheterisation, left coronary blood flow velocity was measured using a Judkins style Doppler tipped catheter. During acute hypotension with sodium nitroprusside, coronary blood flow velocity was recorded at rest and during maximal hyperaemia induced by intracoronary injection of adenosine. Quantitative coronary angiography was performed manually. RESULTS: For both groups coronary blood flow velocity remained relatively constant over a range of physiological diastolic blood pressures and showed a steep relation with diastolic blood pressure during maximal hyperaemia with intracoronary adenosine. Absolute coronary blood flow (calculated from quantitative angiographic data), standardised for left ventricular mass, showed reduced flow in the hypertensive group at rest and during maximal vasodilatation. CONCLUSION: The results are consistent with an inadequate blood supply to the hypertrophied heart, but no upward shift of the lower end of the autoregulatory range was observed.
Adenosine↗
Influence of regression of left ventricular hypertrophy on left atrial size and function in patients with moderate hypertension.
OBJECTIVES: The aim of the study was to evaluate the effect of regression of left ventricular (LV) hypertrophy on left atrial (LA) size and function in patients treated with telmisartan, an angiotensin II receptor blocker. METHODS: Patients population included 80 patients with mild-moderate LV hypertrophy treated with telmisartan. Patients were followed over a period of 12 months from the start of telmisartan treatment. LA size was measured during systole from the parasternal long-axis view from M-mode. Atrial function was assessed by Doppler-echocardiography and the following parameters were measured: transmitral peak A velocity, atrial filling fraction, atrial ejection force (AEF), peak E velocity, deceleration time and isovolumic relaxation time, LA maximal and minimal volume, and LV cardiac mass index (LVMI). RESULTS: All patients had an increased LVMI and decrease during follow-up. LA dimensions were greater at baseline and reduced after 1 year of treatment. LA volume indexes maximal volume, minimal volume and P volume were reduced compared with baseline value (maximal volume from 35+/-5 to 32+/-5, p<0.05; minimal volumes from 14+/-2 to 10+/-4, p<0.05). AEF, a parameter of atrial systolic function, increased from 12+/-3 to 15+/-2.4 (p<0.01). The reduction of LA volumes correlate with reduction of LVMI (LA maximal volume and LVMI r = 0.45; p<0.01; LA minimal volume and LVMI r = 0.34; p<0.05). A positive correlation was also found between LV mass index and P volume (r = 0.41; p<0.01), LV mass index and LA active emptying volume (r = 0.39; p<0.01), and LV mass index and LA total emptying volume (r = 0.38; p<0.05). CONCLUSIONS: The present study suggests that regression of LV hypertrophy due to telmisartan is associated with reduction of LA volumes that expresses variation of LV end-diastolic pressure. The reduction of LV end-diastolic pressure is associated with an increase in diastolic filling and with a significant reduction of active and passive emptying contribution of left atrium to LV stroke volume.
Adult↗
A quantitative relationship of electrocardiographic criteria of left ventricular hypertrophy with echocardiographic left ventricular mass: a multivariate approach.
The purpose of this study was to evaluate the sensitivity of various electrocardiographic (EKG) criteria of left ventricular hypertrophy (LVH) in relation to echocardiographic left ventricular mass (LVME) and to assess the relative strength of various EKG variables used in the diagnosis of LVH by multivariate analysis. An attempt was also made to determine if a new combination of precordial and T-wave voltage could improve the sensitivity of EKG. In 89 patients, M-mode echocardiograms and standard EKGs were studied. Correlation of Romhilt-Estes point-score system with LVME was r = 0.621, sensitivity and specificity was 57 and 81%, respectively. Other voltage criteria had lower sensitivity. Various combinations of precordial and T-wave voltage were not superior. The quantitative relationship of individual EKG variable, QRS duration, S V1-3, R V4-6, strain T wave, left atrial abnormality, intrinsicoid deflection and axis, with LVM was, r = 0.661, 0.595, 0.429, 0.42, 0.347, and 0.225, respectively. By multivariate analysis, QRS duration, S V1-3, T-wave and R V4-6 voltage had F-value (relative strength) of 27.95, 27.15, 22.02, and 4.03, respectively, other variables were statistically insignificant. In conclusion, the most important EKG variables predictive of LVH are QRS duration, S V1-3, strain T-wave and lateral voltage in decreasing value. Rescoring these variables in accordance to their correlation to LVM may improve EKG sensitivity for the diagnosis of LVH.
Cardiomegaly↗