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PubMed1993

Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of left bundle branch block: an echocardiographic correlation.

Surface electrocardiographic findings of 10 cases of left bundle branch block with echocardiographically determined left ventricular hypertrophy were compared with another 10 cases of left bundle branch block without left ventricular hypertrophy. Horizontal plane QRS- and T-wave angle > or = 150 degrees was highly sensitive (70%) and specific (90%) in diagnosing left ventricular hypertrophy in the presence of left bundle branch block. This diagnosis criterion was better than any other conventional criterion described before.

Adult↗
PubMed1990

[Electrovectorcardiographic diagnosis of left ventricular hypertrophy in complete left bundle-branch block].

Diagnosis of left ventricular hypertrophy (LVH) in the presence of complete left bundle-branch block (CLBB) is difficult. The value of several electro-vectorcardiographic criteria were studied in a series of 71 patients with CLBB analyzed by echocardiography. Thirty nine of the patients (55%) had anatomical LVH defined as being a left ventricular weight (LVW) above 316 g. Twenty five of the 71 patients (35%) had dilated cardiomyopathy (dCMP). Of the hypervoltage indices, only the sum of RV6 + SV2 and the QRS spatial maximum vector (MAXQRSxyz) showed a significant difference between the group with LVH and the group without LVH. The duration of QRS and the average vector of spatial area (AQRSxyz) also differed significantly between the two groups and showed a good correlation with LVW. Of the various criteria for LVH, the best balance between sensitivity and specificity belonged to the criteria of duration of QRS greater than 150 msec and AQRSxyz greater than 140 mV.msec, with a merit ratio of 0.44 and a diagnostic accuracy of 72 per cent. In the dCMP subgroup, all the voltage and duration indices were significantly different between the two groups. The criterion AQRSxyz greater than 135 mV.msec obtained the best diagnostic score, with a sensitivity of 94 per cent, specificity of 100 per cent, and accuracy of 96 per cent. This parameter gave the best overall expression of the combination of hypervoltage and delay in ventricular depolarization produced both by hypertrophy/ventricular dilation and conduction disturbances.

Aged↗
PubMed2005

Reversal of left ventricular hypertrophy by propranolol in hypertensive rats.

BACKGROUND: Hypertension contributes significantly to the development of left ventricular hypertrophy. Left ventricular hypertrophy is associated with increased incidence of sudden cardiac death. Recognition and management of hypertension is, therefore, imperative. OBJECTIVE: To establish whether propranolol can reverse left ventricular hypertrophy in hypertensive rats. METHODS: Hypertension was induced in male albino rats by giving them 1% NaCl solution as their only drink for four weeks. Propranolol was then administered orally to one of the four groups of rats used in this study. Systolic blood pressure of each rat was measured twice a week using a modified tail-cuff method. Each rat was then sacrificed, its heart excised from the chest cavity and geometric studies carried on the left ventricle. RESULTS: Excessive intake of sodium salt by the rats caused an increase in their systolic blood pressure which was accompanied by left ventricular hypertrophy. The elevated blood pressure (139.4 +/- 0.5 mm Hg) was, however, brought back to normal (108.4 +/- 0.2 mm Hg) by propranolol. Data on weight, thickness, and volume of the left ventricle strongly indicated that propranolol can reverse ventricular hypertrophy. CONCLUSION: Propranolol reverses left ventricular hypertrophy besides lowering elevated systolic blood pressure in rats.

Adrenergic beta-Antagonists↗
PubMed1995

[Detection of left ventricular hypertrophy in arterial hypertension].

Left ventricular hypertrophy is an important risk factor in hypertension and the results of the HYCAR study confirm that it is possible to treat this risk factor independently of an action on the blood pressure. Should systematic echocardiography be performed in every hypertensive patient to diagnose left ventricular hypertrophy and follow up its outcome with treatment? This attitude seems to be premature for two reasons. Firstly, echocardiography, though much more sensitive than electrocardiography for diagnosing left ventricular hypertrophy, has a number of limitations. Good recordings cannot be obtained in all patients; even under the best conditions of reproducibility, the measurement of left ventricular mass is not excellent and does not allow reliable individual follow-up of treatment; even the criteria of left ventricular hypertrophy used at present are open to criticism. Secondly, it remains to be shown whether the reversibility of left ventricular hypertrophy, independently of lowering the blood pressure, improves the prognosis of the hypertensive patient. The intensive research into this problem, further stimulated by the encouraging results of the HYCAR study, should help define the role and value of echocardiography in the future management of hypertension.

Echocardiography↗
PubMed2002

Electrocardiographic measures of left ventricular hypertrophy show greater heritability than echocardiographic left ventricular mass.

AIMS: To assess the heritability (i.e. relative contribution of genetic factors to the variability) of continuous measures of left ventricular hypertrophy determined by electrocardiography and echocardiography. METHODS AND RESULTS: We studied 955 members of 229 Caucasian families, ascertained through a hypertensive proband. Electrocardiographic measurements were performed manually on resting 12-lead electrocardiograms, and echocardiographic measurements were made on M-mode images. Sex-specific residuals for the left ventricular phenotypes were calculated, adjusted for age, systolic blood pressure, weight, height, waist-hip ratio, and presence of diabetes. Heritability was estimated in two ways: firstly, from familial correlations with adjustment for spouse resemblance; and secondly by using variance components methods with ascertainment correction for proband status. The heritability estimates (given as a range derived from the two methods) were higher for Sokolow-Lyon voltage (39-41%) than for echocardiographic left ventricular mass (23-29%). Electrocardiographic left ventricular mass, Cornell voltage, and Cornell product had heritability estimates of 12-18%, 19-25%, and 28-32%, respectively. CONCLUSIONS: Genetic factors may explain a substantial proportion of variability in quantitative electrocardiographic and echocardiographic measures of left ventricular hypertrophy. The greater heritability of Sokolow-Lyon voltage suggests that electrocardiographic phenotypes may be particularly important for the molecular investigation of the genetic susceptibility to cardiac hypertrophy.

Echocardiography↗
PubMed1994

Prolonged QT interval in hypertrophic and dilated cardiomyopathy in children.

When the QT interval is prolonged in a patient with structural heart disease, there is a question of whether the QT interval prolongation is the result of coexistent long QT interval syndrome or ventricular hypertrophy. The purpose of this study was to assess whether QT interval prolongation can be attributed to ventricular hypertrophy/dilation alone. Electrocardiograms (ECGs) of 25 children in each of six echocardiographically proven groups (right ventricular hypertrophy, left ventricular hypertrophy, biventricular hypertrophy, hypertrophic cardiomyopathy, dilated cardiomyopathy, and normals) were analyzed. All patients had QRS interval durations < 100 msec, and patients with ventriculotomies were excluded. No patients in the normal group had a QTc interval > or = 0.45 sec. Eight (32%) of 25 patients with dilated cardiomyopathy had a QTc interval > or = 0.45 sec (p = 0.007 vs normal), 6 (24%) of 25 patients with hypertrophic cardiomyopathy had a QTc interval > or = 0.45 sec (p = 0.03 vs normal), and 2 of 25 patients each with right ventricular hypertrophy, left ventricular hypertrophy, and biventricular hypertrophy had a QTc interval > or = 0.45 sec (p = NS vs normal). There was no relation of the QTc interval to age, QRS duration, T-wave axis, or heart rate in any group. In the dilated cardiomyopathy group, there was no relationship of QTc interval to age, shortening fraction, or left ventricular end diastolic dimension. In conclusion, (1) a significant number of patients (24% to 32%) with dilated or hypertrophic cardiomyopathy may have a long QTc interval on the surface ECG, and (2) ventricular hypertrophy/dilation may be additional rare causes of acquired prolongation of the QT interval.

Adolescent↗
PubMed2002

Microalbuminuria in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study.

OBJECTIVES: Left ventricular hypertrophy and albuminuria have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiac and renal glomerular damage has not been evaluated in a large hypertensive population with target organ damage. The present study was undertaken to determine whether albuminuria is associated with persistent electrocardiographic (ECG) left ventricular hypertrophy, independent of established risk factors for cardiac hypertrophy, in a large hypertensive population with left ventricular hypertrophy who were free of overt renal failure. METHODS: Patients with stage II-III hypertension were enrolled in the study if they had left ventricular hypertrophy on a screening ECG by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria, and clinic blood pressures between 160 and 200/95-115 mmHg and plasma creatinine < 160 mmol/l. A second ECG and morning spot urine were obtained after 14 days of placebo treatment. Renal glomerular permeability was evaluated by urine albumin/creatinine (UACR, mg/mmol). Microalbuminuria was present if UACR > 3.5 mg/mmol and macroalbuminuria if UACR > 35 mg/mmol. RESULTS: The mean age of the 8029 patients was 66 years, 54% were women. Microalbuminuria was found in 23% and macroalbuminuria in 4% of patients. Microalbuminuria was more prevalent in patients of African American (35%), Hispanic (37%) and Asian (36%) ethnicity, heavy smokers (32%), diabetics (36%) and in patients with ECG left ventricular hypertrophy by both ECG-criteria (29%). Urine albumin/creatinine was positively related to Sokolow-Lyon voltage criteria and Cornell voltage-duration product criteria. In multiple regression analysis, higher UACR was independently associated with older age, diabetes, higher blood pressure, serum creatinine, smoking and left ventricular hypertrophy. Patients smoking > 20 cigarettes/day had a 1.6-fold higher prevalence of microalbuminuria and a 3.7-fold higher prevalence of macroalbuminuria than never-smokers. ECG left ventricular hypertrophy by Cornell voltage-duration product or Sokolow-Lyon criteria was associated with a 1.6-fold increased prevalence of microalbuminuria and a 2.6-fold increase risk of macroalbuminuria compared to no left ventricular hypertrophy on the second ECG. CONCLUSIONS: In patients with moderately severe hypertension, left ventricular hypertrophy on two consecutive ECGs is associated with increased prevalences of micro- and macroalbuminuria compared to patients without persistent ECG left ventricular hypertrophy. High albumin excretion was related to left ventricular hypertrophy independent of age, blood pressure, diabetes, race, serum creatinine or smoking, suggesting parallel cardiac damage and albuminuria.

Aged↗
PubMed1994

Left ventricular mass and cardiac function in patients with essential hypertension.

Two-dimensional guided M-mode echocardiography was used to estimate left ventricular mass and left ventricular performance in 140 untreated hypertensive patients, 38 (27%) of whom had left ventricular hypertrophy. Left ventricular contractility as reflected by ratio of end-systolic wall stress to end-systolic volume index and normalised early left ventricular peak filling rate were decreased in the patients with left ventricular hypertrophy compared with those without hypertrophy and correlated inversely with the left ventricular mass (r = -0.44; P < 0.0001 and r = -0.31; P = 0.0004, respectively). Positive correlations were found between the peak filling rate and either the ejection fraction or the contractility index (r = 0.44; P < 0.0001 and r = 0.24; P = 0.004, respectively). Left ventricular mass also correlated with mean arterial pressure in the whole study population (r = 0.43; P < 0.0001). The data suggest that with the development of left ventricular hypertrophy both contractility and filling of the left ventricle become progressively impaired in hypertensive patients. The decline in cardiac function with progressive left ventricular hypertrophy may represent a pathophysiological correlate of the epidemiological observation identifying left ventricular hypertrophy as one of the most powerful risk factors for future cardiovascular morbidity and mortality. The present study shows that with development of left ventricular hypertrophy in essential hypertension both contractility and filling of the left ventricle become progressively impaired.

Adolescent↗
PubMed1997

Comparison of therapeutic studies on regression of left ventricular hypertrophy.

In numerous studies left ventricular hypertrophy has been clearly established to be a strong, blood-pressure independent risk factor for cardiovascular morbidity and mortality. In fact, increased echocardiographic left ventricular mass has been shown to predict cardiovascular complications not only in patients with hypertension, but also in the general population. Preliminary data revealed that regression of left ventricular hypertrophy indeed reduces cardiovascular complications. As a consequence, regression of left ventricular hypertrophy by drug treatment has emerged as a desirable goal in patients with echocardiographically determined left ventricular hypertrophy. These findings raised the question, whether certain antihypertensive drugs differ in their ability to reduce left ventricular mass. To resolve this issue several comparative studies and some meta-analyses have been carried out. In a meta-analysis by Dahlöf et al., comprising 109 treatment studies published until december 1990 with a total of 2357 patients, ACE-inhibitors (-15%) were most effective in reducing left ventricular mass followed by diuretics (-11.3%), calcium channel blockers (-8.5%) and beta-blockers (-8%). Reduction in left ventricular mass was mainly due to a decrease in wall thickness except for diuretics which predominantly reduced ventricular diameter. Although reduction in blood pressure was similar for all antihypertensive agents, the correlation between changes in mean arterial pressure and effect on left ventricular mass was only significant for beta-blockers with a modest correlation for ACE-inhibitors and no clearcut relation for diuretics and calcium channel blockers.

Adrenergic beta-Antagonists↗
PubMed2001

[Can pathological left ventricular hypertrophy in arterial hypertension be distinguished from physiological hypertrophy caused by sports?].

BACKGROUND AND OBJECTIVE: Patients with hypertensive heart disease and left ventricular hypertrophy demonstrate impaired left ventricular diastolic filling. Aim of this study was to find out if physiological left ventricular hypertrophy induced by endurance training causes abnormal left ventricular systolic and diastolic filling. METHODS: We examined 42 athletes with left ventricular hypertrophy due to endurance training (aged 25 +/- 7 years), 31 patients with left ventricular hypertrophy due to hypertensive heart disease (aged 28 +/- 6 years) and 20 untrained, healthy subjects (controls, aged 26 +/- 8 years) by conventional echocardiography and calculated left ventricular muscle mass and fractional shortening. In addition the following Doppler-echocardiographic parameters were measured: maximal early and late velocity of diastolic filling, ratio of maximal early and late velocity of diastolic filling, acceleration and deceleration time and isovolumetric relaxation time. RESULTS: All three study groups showed normal fractional shortening. Conventional echocardiography revealed a higher left ventricular muscle mass in the two study groups as compared to the controls (controls: 119 +/- 12 g, athletes: 225 +/- 18 g*; hypertensive patients: 216 +/- 16 g*; * p < 0.01 versus controls). In the athletes with physiological left ventricular hypertrophy a normal left ventricular diastolic filling pattern was documented (VE: 0.64 +/- 0.1 m/s; VA: 0.51 +/- 0.2 m/s). In hypertensive heart disease a diastolic dysfunction in terms of a delayed relaxation pattern with a decrease of maximal early velocity of diastolic filling (VE: 0.45 +/- 0.09 m/s) and a compensatory increase of the maximal late velocity of diastolic filling (VA: 0.54 +/- 0.1 m/s) was demonstrated. CONCLUSION: In pathological left ventricular hypertrophy due to hypertensive heart disease a pathological diastolic filling pattern was documented. In athletes with physiological left ventricular hypertrophy a normal left ventricular diastolic filling pattern was revealed. Thus Doppler-echocardiographic parameters of left ventricular diastolic function can be of diagnostic importance for discriminating between pathological and physiological left ventricular hypertrophy.

Adolescent↗
PubMed1991

Effect of left ventricular hypertrophy secondary to systemic hypertension on left coronary artery flow dynamics.

STUDY OBJECTIVE: The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. DESIGN: Measurements of blood velocities in the left anterior descending coronary artery were made with a 20 MHz Doppler catheter with a top mounted annular crystal. All patients had normal coronary arteriograms. PATIENTS: 23 hypertensive patients [systolic/diastolic pressure: 181(SD 15)/100(4) mm Hg)] with left ventricular hypertrophy, and 13 atypical chest pain patients without left ventricular hypertrophy or any abnormal haemodynamic findings (normal controls) entered the study. MEASUREMENTS AND MAIN RESULTS: The left anterior descending coronary artery blood velocity waveform in pressure overloaded left ventricular hypertrophy was characterised by delayed early diastolic inflow. The diastolic rise time of coronary flow (TDR), ie, the time from the beginning of diastole to peak velocity, was higher in patients with hypertensive left ventricular hypertrophy than in normal controls, at 145(56) v 66(15) ms, p less than 0.001. In patients with hypertensive left ventricular hypertrophy, TDR correlated well with the degree of hypertrophy (r = 0.83, p less than 0.01) and also with peak left ventricular systolic pressure (r = 0.62, p less than 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity, decreased with prolongation of TDR (r = 0.58, p less than 0.02). CONCLUSIONS: (1) Impairment of early diastolic coronary arterial inflow is the most remarkable characteristic in pressure overloaded left ventricular hypertrophy; (2) preceding systolic vascular compression and impaired left ventricular relaxation correlate with the delayed early diastolic inflow; (3) the delayed inflow is an important possible cause of the decreased coronary flow reserve in the hypertensive left ventricular hypertrophy.

Adult↗
PubMed1999

A novel method for indexing echocardiographic left ventricular mass in infants, children and adolescents: evaluation of obesity-induced left ventricular hypertrophy.

BACKGROUND: Measurement of left ventricular mass (LVM) is important to the diagnosis of left ventricular hypertrophy in children with various cardiovascular diseases. The purpose of this study was to determine the most appropriate method for standardization of LVM and to evaluate obesity-induced left ventricular hypertrophy in children across the entire age range, from infancy through adolescence. METHODS: We studied 928 children and adolescents (527 males, 401 females), aged 0-17 years, who were classified into two groups by degree of obesity. Left ventricular mass was calculated by M-mode echocardiography using the formula of Devereux et al. and was indexed using body size (body length, bodyweight or body surface area) raised to a non-integer power using logarithmic transformation of measurements in children without obesity. RESULTS: The body length, bodyweight and body surface area exponents were 1.85, 0.88 and 1.15, respectively, in males, and 1.72, 0.82 and 1.08, respectively, in females. Whereas indexing of left ventricular mass by body length both in males and in females revealed significant differences between the two groups, indexing using bodyweight or body surface area exponents did not manifest left ventricular hypertrophy induced by obesity. CONCLUSION: It is suggested that applying body length exponents 1.85 in males and 1.72 in females is an appropriate method for indexation of LVM in children and adolescents. This method is particularly useful for the evaluation of left ventricular hypertrophy in children.

Adolescent↗
PubMed1996

Influence of isradipine and spirapril on left ventricular hypertrophy and resistance arteries.

Left ventricular hypertrophy is a common clinical feature in hypertensive patients and may be associated with structural changes in vessel morphology. In an open prospective trial, we evaluated 14 patients with previously untreated hypertension (163 +/- 2/104 +/- 2 mm Hg) and an echocardiographically determined left ventricular mass index of 141.6 +/- 5.2 g/m2, indicating left ventricular hypertrophy. We obtained a gluteal skin biopsy sample before starting treatment to investigate subcutaneous small-artery (approximately 200 to 400 microns diameter) morphology and function. Patients then received antihypertensive treatment with a combination of spirapril (3 or 6 mg) and isradipine (2.5 or 5 mg). Echocardiographic recordings were made after 6 months and 1 year, and a final biopsy was taken after 1 year. After 1 year, blood pressure was significantly reduced to 142 +/- 3/ 90 +/- 1 mm Hg (P < .001), and left ventricular mass index decreased significantly to 105.3 +/- 5.8 g/m2 (P < .001). Baseline media-lumen ratio (7.64 +/- 0.48%) was not markedly reduced (7.21 +/- 0.55%), although a decrease occurred in 7 of 12 evaluable patients. Norepinephrine-induced vasoconstriction was markedly reduced after 1 year. In conclusion, a significant regression of left ventricular hypertrophy was obtained after 1 year of treatment with spirapril and isradipine, whereas a similar reduction in medial thickness relative to lumen diameter of subcutaneous small arteries could not be observed in all patients. Reversal of structural changes in resistance vessels may require a longer treatment period in patients with proven left ventricular hypertrophy.

Angiotensin-Converting Enzyme Inhibitors↗