Devereux Formula Research Articles

Left ventricular geometric patterns and cardiac function in patients with chronic renal failure undergoing hemodialysis

The aim of this study was to estimate the impact and prevalence of left ventricular geometric alterations and systolic and diastolic dysfunction in hemodialysis patients, as well as the relationship with cardiac troponin as a marker of myocardial damage. 31 patients (pts), 19 males and 12 females, age 58.1+/-16.4 (26 on hemodialysis, 5 on peritoneal dialysis) and 31 healthy normal controls were enrolled. Echocardiography measurements were carried out according to the American Society of Echocardiography recommendations. Left ventricular mass was calculated, according to the Devereux formula and indexed to height and weight 2.7. Doppler echocardiography was performed to study diastolic function by measurements of isovolumetric relaxation period (IVRT), E wave deceleretion time (DTE) and E/A ratio. Cardiac troponin was measured by a third generation electro-chemiluminescence immunoassay. Statistical analysis was performed using the t-test for between-group comparisons and the Pearson and Spearman's tests to investigate correlations; p values of <0.05 were considered statistically significant. Eccentric hypertrophy was the most frequent pattern (n=17; 55%), followed by normal cardiac geometry (n=7; 23%), and concentric hypertrophy (n=5; 16%). Only 6% of pts (n=2) showed concentric remodelling. Systolic dysfunction was present in terms of endocardial parameters in 3 pts (9%) (fractional shortening <25%, EF<50%), but in terms of midwall myocardial shortening in 51% (n=16). Diastolic dysfunction was present in 87% (n=27) with a pattern of impaired relaxation (in 5 without left ventricular hypertrophy). E/A was negatively correlated with age (r=-0.41, p=0.02); DTE was positively correlated with posterior wall thickness (r=0.36, p=0.05) and interventricular septum thickness (r=0.45, p=0.01); cardiac troponin was positively correlated with age (r=0.50, p=0.00), left ventricular mass (r=0.41, p=0.02), posterior wall thickness (r=0.41; p=0.02) and interventricular septum thickness (r=0.39, p=0.03) but not with diastolic dysfunction parameters. No significant difference was found in terms of duration of dialysis between patients with normal left ventricular geometry and those with left ventricular hypertrophy, but a significant difference in age was found (p=0.03). Pts with diastolic dysfunction had more frequent hypotensive episodes during dialysis (p<0.01). Impaired geometry and cardiac function is frequently observed in pts undergoing hemodialysis. Diastolic dysfunction is associated to a geometric pattern of left ventricular hypertrophy, although it can be an isolated initial manifestation of myocardial damage. Depressed midwall myocardial shortening can discriminate left ventricular dysfunction better than traditional endocardial systolic indexes.

Effect of losartan and spironolactone on left ventricular mass and heart sympathetic activity in prehypertensive obese subjects: a 16-week randomized trial

Obesity has been shown to be associated with increased left ventricular mass (LVM) and heart sympathetic activity even in nonhypertensive subjects. These factors are predictors of cardiovascular morbidity and mortality independent of other traditional risk factors. We evaluated the effect of losartan and spironolactone on LVM and heart sympathetic activity in prehypertensive obese subjects. A 16-week blinded randomized trial was performed in middle-aged men selected from a Health Public program. Anthropometric and clinical variables were measured at baseline and after losartan (50 mg/day; n=25) or spironolactone (25 mg/day; n=25) treatment. Heart sympathetic activity was evaluated with 60-min electrocardiograph monitoring, and spectral analysis was carried out. LVM was measured by echocardiography according to Devereux and Reicheck's formula indexed for body height (m2.7) to account for obesity. Anthropometric variables, systolic, and diastolic blood pressure levels decreased in both groups of treatment without statisticall difference between them. Losartan increased heart rate variability (from 70.0 to 82.3 ms; P=0.01), and decreased low frequency-high frequency index (from 6.6 to 4.9; P=0.001), and LVM (from 49.2 to 45.2 g; P=0.004). In the multiple regression analysis for factors associated with reduction in LVM; treatment with losartan, and decrease in SBP were the only factors included in the model (R2=0.60; P=0.003). To conclude losartan, but not spironolactone, decreased LVM and heart sympathetic overactivity in prehypertensive obese subjects after 16 weeks of treatment. Regression on LVM was associated with reduction on SBP levels.

Variation at the Beta-1Adrenoceptor Gene Locus is Associated with Left Ventricular Mass in Endurance Athletes

0714 Left ventricular hypertrophy in response to endurance training is a common feature in athletes. Twin studies, as well as association studies have shown that genetic factors play a role in the determination of the so called athlete's heart. In two recent studies, variants of the gene encoding the Beta-1 adrenoceptor (B1AR) has been associated with enlargement of the left ventricle in two different cohorts of sedentary subjects. PURPOSE: The aim of our study was to investigate the role of B1AR genetic polymorphisms for the development of left ventricular hypertrophy in endurance athletes. METHODS: We studied a cohort of 198 male Caucasian athletes involved in different endurance sports with a training history of at least 5 years (Tab. 1). Left ventricular mass was determined using M-mode echocardiography. Left ventricular mass index (LVMI) was calculated using Devereux's formula with correction for the body surface area. Subjects were typed for two single nucleotide polymorphisms (SNPs) that result in serine/glycine (Ser49Gly) and arginine/glycine (Arg389Gly) amino acid substitutions at residues 49 and 389 in the B1AR gene, respectively.Tab. 1: Characteristics of subjects (mean +/− std)RESULTS: Genotype distributions for both polymorphisms were in Hardy-Weinberg equilibrium. A significant association was found for Ser49Gly genotype and LVM (p = 0.036). Further analysis revealed a higher LVMI in carriers of the Gly-Allele compared to subjects homozygote for the Ser-Allele (LVMI 154g/m-2 vs. 145g/m-2, p = 0.014). No association was seen between the Arg389Gly polymorphism and LVM or LVMI (p = 0.093 and 0.232, respectively). CONCLUSION: In summary, we found evidence that the Ser49Gly polymorphism in the gene encoding for the B1AR may play a role in the development of left ventricular hypertrophy in highly trained endurance athletes.

Detection of incipient left ventricular hypertrophy in mild to moderate arterial hypertension with normal electrocardiogram and echocardiogram: a new use for signal-averaged electrocardiography.

To assess signal-averaged electrocardiogram (SAECG) for diagnosing incipient left ventricular hypertrophy (LVH). A study with 115 individuals was carried out. The individuals were divided as follows: GI - 38 healthy individuals; GII - 47 individuals with mild to moderate hypertension and normal findings on echocardiogram and ECG; and GIII - 30 individuals with hypertension and documented LVH. The magnitude vector of the SAECG was analyzed with the high-pass cutoff frequency of 40 Hz through the bidirectional four-pole Butterworth high-pass digital filter. The mean quadratic root of the total QRS voltage (RMST) and the two-dimensional integral of the QRS area of the spectro-temporal map were analyzed between 0 and 30 Hz for the frequency domain (Int FD), and between 40 and 250 Hz for the time domain (Int TD). The electrocardiographic criterion for LVH was based on the Cornell Product. Left ventricular mass was calculated with the Devereux formula. All parameters analyzed increased from GI to GIII, except for Int FD (GII vs GIII) and RMST log (GII vs GIII). Int TD showed greater accuracy for detecting LVH with an appropriate cutoff > 8 (sensitivity of 55%, specificity of 81%). Positive values (> 8) were found in 56.5% of the G II patients and in 18.4% of the GI patients (p< 0.0005). SAECG can be used in the early diagnosis of LVH in hypertensive patients with normal ECG and echocardiogram.

Left ventricular hypertrophy and body mass index in patients with diabetes mellitus type 2 and hypertension

Our aim was to examine the association between body mass index (BMI) and left ventricular hypertrophy (LVH) in patients with diabetes mellitus (DM) type 2 and hypertension. There were observed 40 patients with DM type 2 and hypertension (mean age was 52,2 ± 2,16 year) by echocardiography. The traces were read according to the Penn convention and the left ventricular internal diameter (LVID), interventricular septum thickness (IVST) and posterior wall thickness (PWT) were measured at the end of the diastole. Left ventricular mass (LVM) was calculated according to the Devereux formula: LVM (g) = 1.04*[(IVSTd + PWTd +LVIDd )3 – (LVIDd)3] –13.6. LVM index (LVMI) was obtained by dividing the LVM by body surface area. LVH was defined as LVMI >134 g/m2 for men and >110 g/m2 for women. Relative wall thickness (RWT) was calculated by the formula 100*(IVST+PWT)/LVID. Concentric hypertrophy was estimated when RWT was above 45% and eccentric hypertrophy was estimated when RWT was below 45%. All patients were divided for 3 groups dependence on BMI. The first group (n=12) consisted of patients with BMI 18.5-24.9 kg/ m2, the second one (n=13) consisted of patients with BMI 25-29.9 kg/ m2, and the third one (n=15) consisted of patients with BMI >30 kg/ m2. It was found the positive association between BMI and BP, as patients with obesity have had greater level SBP 163.5 ± 2.5 mm.Hg and DBP 99.1 ± 1.4 mm.Hg in comparison with those with preobesity (SBP 157.8 ± 1.95 mm.Hg and DBP 94.2 ± 1.3 mm.Hg, p<0.01) and with normal weight (SBP 152.5 ± 1.73 mm.Hg and DBP 90.0 ± 2.3 mm.Hg, p<0.001). Moreover, it was estimated the dependence of LVH on BMI, as LVM was significantly higher in obese patients than in those with normal weight (334.13 ± 19.91g vs 273.82 ± 18.86g, p<0.01). LVMI also was significantly greater in obese patients in comparison with those with normal weight (159.32 ± 1.47g/ m2 vs 129.43 ± 9.65 g/ m2, p<0.05). The evaluation of the values RWT has shown that concentric hypertrophy was characteristic for patients with preobesity and obesity (RWT 46.99 ± 2.5% and 50.37 ± 1.9%), but patients with normal weight have had eccentric hypertrophy (RWT 44.0 ± 3.7%). This study demonstrates that obesity is strong risk factor for development of LVH and concentric remodeling in patients DM type 2 and hypertension.

ANGIOTENSIN-CONVERTING ENZYME I/D POLYMORPHISM AND LEFT VENTRICULAR HYPERTROPHY IN ENDURANCE ATHLETES

Adaptive left ventricular hypertrophy is a common feature in endurance trained athletes. However, several studies have reported that the extend of adaptation to endurance exercise can be extremely different between individuals, suggesting that genetic factors play a role in the determination of the so called athlete's heart. The genes encoding for the renin-angiotensin-system (RAS) are potential candidates in that context. PURPOSE: The aim of our study was to investigate whether the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism is associated with left ventricular mass (LVM) in endurance athletes. METHODS: We studied a cohort of 161 highly trained male Caucasianthletes (VO2max 79,6 ± 3,7 ml/kg, LVM 272,0 ± 56, 0ml/kg), involved in different endurance sports with a training history of at least 5 years. LVM was determined using M-mode echocardiography. Left ventricular mass index (LVMI) was calculated using Devereux's formula with correction for the body surface area. The ACE I/D polymorphism in intron 16 was typed with the three-primer polymerase chain reaction method. RESULTS: No association was found between ACE I/D genotypes and LVMI (Tab. 1, p = 0.073). A significant association was found for carriers of the I-allele and LVMI (I-allele p = 0.047). Further analysis revealed an excess of I-allele carriers within the highest tertile (> 153g/m−2) of LVMI compared to the subjects in the other two tertiles (p = 0.026). CONCLUSION: In summary, we found weak evidence that the ACE I/D polymorphism might play a role in the development of left ventricular hypertrophy in highly trained endurance athletes.Table: No Caption Available

Left Ventricular Mass Measurement Using Tc-99m MIBI Myocardial Perfusion SPECT: Comparison with Echocardiographic Method

Background and Objectives:A left ventricular mass (LVM can be used as a prognostic factor in patients with cardiovascular disease, and echocardiographic LVM measurements are most commonly used. We have measured LVM using quantitativel gated myocardial perfusion SPECT (QGS, and compared these results with LVM measured by echocardiography. Subjects and Methods:One hundred and sixteen subjects (M/F=66/50, mean age:58 yrs underwent both rest QGS with Tc-99m MIBI and echocardiography. On visual interpretation, thirty-six subjects (31% showed perfusion defects. The myocardial volume was obtained using the AutoQU- ANT program, and the LVM (LVMSPECT was calculated by multiplying the volume by the specific gravity of the myocardium. We also measured the echocardiographic LVM (LVMEcho by the Devereux formula, within one month of the LVMSPECT. Results:The LVMSPECT and LVMEcho were well correlated (r= 0.717, p<0.001, but a significant difference was noted between the two values. The mean difference between the LVMSPECT and LVMEcho was 24 g. The LVMEcho was smaller than the LVMSPECT in those subjects with a small LVMEcho, and greater than the LVMSPECT in the subjects with a large LVMEcho. The difference between the LVMEcho and LVMSPECT (LVMEcho-LVMSPECT was positively correlated with the LVMEcho (r=0.893, p<0.001. Conclusion:The LVMs measured by gated myocardial perfusion SPECT and echocar- diography were well correlated. But they were significantly different, especially in subjects with large LVMs. ( ( ( (Korean Circulation J 2002;32(12 :1072-1077

Time course of left ventricular remodeling after stentless aortic valve replacement

Background Stentless aortic valves are associated with a significant decrease in left ventricular hypertrophy. This study examined the time course and factors affecting left ventricular mass regression (LVMR) after aortic valve replacement (AVR) with Cryolife O’Brien (CLOB) (Cryolife International, Atlanta, Ga) stentless valves. Methods Between 1993 and 2000, 130 consecutive patients underwent AVR with CLOB. Mean age was 71.3 ± 6.3 years. Sixty-four (49.2%) were male. Mean body surface area (BSA) was 1.7 ± 0.2 m2. Mean valve size implanted was 23.6 ± 2.0 mm. All patients were monitored with serial echocardiograms; the first study was performed preoperatively, and subsequent controls were at 6 months, 1, 2, 3, 4, 5, 6, and 7 years, respectively. Left ventricular mass was calculated by the Devereux formula and indexed by BSA. Results Analysis of variance showed a significant reduction in the left ventricular mass index (LVMI) over time (P <.001). Most LVMRs occurred within the first 6 months, and after 1 year LVMI had decreased by 37.5% with further, but not statistically significant, reductions at later examinations. We found that baseline BSA >1.75 m2, male sex, arterial blood pressure ≥150 mm Hg, left ventricular ejection fraction ≤35%, New York Heart Association functional class ≥III, non–sinus rhythm, and prevalent aortic incompetence to be factors influencing LVMR. LVMR was not related to postoperative effective orifice area ≤0.85 cm/m2 and prosthetic size. Conclusions AVR with a CLOB valve is followed by a significant LVMR that occurs soon after surgery. It is influenced by several patient-related factors: most of them can be predicted preoperatively. (Am Heart J 2001;142:556-62.)

The importance of age and obesity on the relation between diabetes and left ventricular mass

OBJECTIVESThe study investigated the relation of age with diabetes, obesity and hypertension on left ventricular mass (LVM).BACKGROUNDEpidemiological studies demonstrate a general rise of LVM with aging, but whether this phenomenon is independent or a function of coexisting diseases that accompany the aging process is unclear. Although obesity, hypertension and diabetes often coexist and increase in prevalence with age, studies of LVM in diabetics have been reported in mostly nonobese populations, and with little regard to the age-hypertension-obesity interactions and effects on LVM.METHODSWe prospectively measured LVM in 875 consecutive, mostly obese individuals (673 men, 202 women). Clinical data were obtained by chart review and clinical history. Echocardiographic measurements of LVM (American Society of Echocardiography criteria) were calculated using the Devereux formula and corrected for height2.7(LVM/Ht).RESULTSMean age was 49.3 ± 12.3 years, body mass index 33.3 ± 8.0 kg/m2, and LVM/Ht2.741.7 ± 13.4 g/m2.7. Of the total cohort, 673 patients were men, 519 obese, 228 hypertensive, and 52 diabetic. Of the 519 obese, 183 were hypertensive and 44 were diabetic (22 of those were hypertensive). Of the 228 hypertensives, 183 were obese and 26 were diabetic. On multivariate analysis, obesity (p = 0.0001), age (p = 0.0001), hypertension (p = 0.0003) and diabetes (p = 0.02) were all independently associated with LVM/Ht2.7. Obesity was the most potent independent predictor of LVM/Ht2.7, associated with an increase of 8.1 g/m2.7in LVM/Ht2.7. In diabetics, obesity had a synergistic effect on LVM/Ht2.7(p = 0.006), which was further amplified by age (p = 0.03).CONCLUSIONSAge, obesity, hypertension and diabetes are all independent determinants of LVM. The magnitude of the effect of diabetes on LVM is mainly consequent to a significant interaction of diabetes with obesity and age.

Left ventricular mass and function in young obese women.

Obesity is associated with a high mortality rate due to cardiovascular disease. Left ventricular (LV) hypertrophy has been described in relation to obesity. The aim of this study was to evaluate echocardiographically the LV mass and function in young obese women as compared to lean women with similar characteristics. Prospective study. Eighty-two young women (< or =40 y), with obesity degree varying from I to III (BMI from 30 to 50 kg/m2) were compared to eighty young lean women. All of them were normotensive, none had cardiovascular complaints or any previous history of pulmonary disease, and none were taking any medication. The LV mass was calculated by the Devereux and Reichek formula. The LV mass was strongly increased in all obese groups (P<0.00003 to 0.000005) compared to lean subjects. LV mass adjusted indexes for height, BMI or volume were also increased compared to lean subjects and when adjusted for weight it was decreased. However when comparing LV mass/body surface area index this difference was not statistically significant. The linear regression analysis showed a strong association between the degree of obesity and LV mass, (r=0.52, P<0.001). Systolic and diastolic function in obese patients were similar to lean subjects, except for a lower E/A ratio in the obese group (P=0.005). In asymptomatic young obese women, there are some echocardiographic findings suggesting early cardiac involvement that seems to be related to the degree of obesity.

Is ventricular repolarization heterogeneity a cause of serious ventricular tachyarrhythmias in aortic valve stenosis?

It is well known that there is a close relation between sudden cardiac death and serious ventricular tachyarrhythmias in patients with aortic valve stenosis (AS). QT dispersion (QTd) reflects the ventricular repolarization heterogeneity and has been proposed as an indicator for ventricular arrhythmias. This study investigated the QTd and its relevance to the clinical and echocardiographic variables. In all, 51 patients (33 men, 18 women, mean age 56 +/- 12) with isolated AS and 51 age- and gender-matched healthy controls comprised the study group. Left ventricular mass index (LVMI) was calculated by the Devereux formula, and we used continuous-wave Doppler (n = 15) and cardiac catheterization (n = 36) for the determination of the maximum aortic valve pressure gradient (PG). Corrected QTd (QTcd) (89 +/- 39 vs. 49 +/- 15 ms, p < 0.001) and LVMI (176 +/- 69 g/m2 vs. 101 +/- 28 g/m2, p < 0.001) in patients with AS were significantly different from those in the control group. The group of 21 patients had a significantly greater number of 24-h mean ventricular premature beats (VPB) and mean number of couplet VT episodes than did the control group (p < 0.05). QTcd also correlated significantly well with LVMI (r = 0.58, p < 0.001), PG (r = 0.41, p = 0.003), and number of 24-h VPB (r = 0.56, p = 0.008). With respect to symptoms (e.g., angina, syncope, and dyspnea) patients without symptoms (n = 19) displayed less QTcd (71 +/- 31 vs. 100 +/- 39 ms, p = 0.007) and less LVMI (144 +/- 80 g/m2 vs. 195 +/- 57 g/m2, p = 0.01) than patients with symptoms. Statistical analysis was similar for all variables with uncorrected QTd values. We found that ventricular repolarization heterogeneity was greater in patients with AS than in controls. Our findings also showed that QTd in the patient group correlates well with LVMI, severity of AS, and PG. The present results suggest that serious ventricular arrhythmias in patients with AS may be due to spatial ventricular repolarization abnormality.

Left ventricular function and mass after orthotopic heart transplantation: a comparison of cardiovascular magnetic resonance with echocardiography

Objective: We compared the assessment of left ventricular function and mass by M-mode echocardiography (echo) with fast breath-hold cardiovascular magnetic resonance (CMR) in patients who received orthotopic heart transplantation. We also sought to establish the reproducibility of breath-hold CMR in this patient population. Method We prospectively acquired 51 sets of echo and CMR data in 21 patients who had undergone orthotopic heart transplantation. We examined the intraobserver and interobserver reproducibility of breath-hold CMR in this group and compared it with published data. We compared the left ventricular ejection fraction (EF) and mass determined by echo with the CMR data. Results The average time between CMR and echo was 0 ± 7 days (mean ± SD), the time between each set of CMR–echo data acquisition was 5.1 ± 4.1 months. Cardiovascular magnetic resonance showed good reproducibility in this population, with intraobserver percentage variability of 2.2% ± 2.4% for EF and 3.2% ± 2.7% for mass, and interobserver percentage variability of 2.4% ± 1.9% for EF and 2.2% ± 1.9% for mass. The Bland-Altman limits of agreement between echo and CMR were wide for both EF (−9.6% to 15%) and mass, irrespective of the formula used (−61.3 to 198 g for the Bennett and Evans formula, −65.4 to 196.8 g for the American Society of Echocardiography (ASE) formula, −65.3 to 181 g for the Devereux formula, and −95.2 to 64.6 g for the Teichholz formula). Conclusion Fast-acquisition CMR is reproducible in recipients of transplanted hearts. We found poor agreement with the results of echo. The choice of technique will depend on local resources as well as the clinical importance of the result. Echo remains readily available and gives rapid assessment of volumes, EF, and mass. However, the good reproducibility of CMR may make it a more suitable technique for long-term follow-up of an individual or of a study population.

Left ventricular geometry in pregnancy-induced hypertension

The changes induced by transient hypertension upon cardiac geometry (G) are unclear. Pregnancy-induced hypertension (PIH) offers a natural and spontaneous model of this condition. To assess geometric changes according to two-dimensionally guided M-mode echocardiography, we compared patients with PIH with normal pregnant women (NPW). Fifty-five women, aged 28.5 ± 7.5 years, with PIH (defined as blood pressure >140/90 mm Hg in the third trimester of pregnancy and without a history of hypertension) were compared with 57 NPW aged 30.7 ± 7.5 years. Left ventricular mass index (LVMI) (Devereux formula) and relative wall thickness (RWT) (Ganau formula) were calculated by means of echocardiography done in the left lateral decubitus 2 to 4 days postpartum. Subjects were considered to have: normal geometry (NG) if both LVMI and RWT fell below the mean ± 1 SD or 2 SD; concentric hypertrophy (CH) if both were elevated; eccentric hypertrophy (EH) if LVMI was elevated and RWT was normal; and concentric remodeling (CR) if LVMI was normal and RWT was elevated. Comparisons were performed by the Student t test. Patients with PIH had higher LVMI (106 ± 29.4 v 90.6 ± 19.8 g/m 2; P < .05) and RWT (0.41 ± 0.07 v 0.38 ± 0.05; P < .05). Considering the mean ± 1 SD of NPW as the limit of normality the G pattern was NG in 26 (47%) and abnormal in 29 (53%), of which 14 (25.5%) had EH, 11 (20%) had CR, and four (7%) had CH. If we considered the mean ± 2 SD, the G pattern was NG in 46 (84%) and abnormal G in nine (16%), EH in four (7%), CR in three (5%), and CH in 2 (4%). According to these data, women with PIH had higher LVMI and RWT compared with NPW. The most frequent abnormal G patterns were EH and CR.

Relationship between left ventricular mass and endothelium-dependent vasodilation in never-treated hypertensive patients.

Hypertensive patients are characterized by development of both left ventricular hypertrophy (LVH) and endothelial dysfunction We enrolled 65 never-treated hypertensive patients (36 men and 29 women aged 45.6+/-6.0 years) to assess the possible relationship between echocardiographic left ventricular mass (LVM) and endothelium-dependent vasodilation. Left ventricular measurements were performed at end diastole and end systole according to the recommendations of the American Society of Echocardiography and the Penn Convention. LVM was calculated with the Devereux formula and indexed by body surface area and height raised to the 2.7th power. The endothelial function was tested as responses of forearm vasculature to acetylcholine (ACh), an endothelium-dependent vasodilator (7.5, 15, and 30 microg. mL-1. min-1, each for 5 minutes), and sodium nitroprusside (SNP), an endothelium-independent vasodilator (0.8, 1.6, and 3.2 microg. mL-1. min-1, each for 5 minutes). Drugs were infused into the brachial artery, and forearm blood flow (FBF) was measured by strain-gauge plethysmography. A negative significant relationship between indexed LVM and peak of increase in FBF was found during ACh infusions (r=-0. 554; P<0.0001). In addition, hypertrophic patients had a significantly lower responsive to ACh than patients without LVH (the peak increase in FBF was 9.9+/-3.7 versus 16.1+/-8.1 mL per 100 mL of tissue per minute; P<0.0001). No significant correlation was observed between LVM and FBF during SNP infusion. Our data provide the first evidence that echocardiographic LVM in hypertensive patients is inversely related to FBF responses to the endothelium-dependent vasodilating agent ACh, but it is likely that both endothelium and LVM are damaged by hypertension.

Increased myocardial ultrasonic reflectivity is associated with extreme hypertensive left ventricular hypertrophy: A tissue characterization study in humans

We assessed myocardial reflectivity pattern in a large spectrum of left ventricular mass values, covering the extremes from absent to severe myocardial hypertensive hypertrophy. Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to the morphometrically evaluated collagen content in humans. We enrolled 88 essential hypertensives. With an echo prototype implemented in our Institute, integrated values of the radiofrequency signal of myocardial walls were obtained and normalized for those of the pericardium (Integrated Backscatter Index, IBI, %). Left ventricular mass index (LVMI) was measured by Devereux formula. There was a weak correlation between septal IBI and LVMI (r = 0.35; P < .001). On the basis of LVMI values, three groups of hypertensives were identified, with absent (Group I, n = 23; LVMI < 125 g/m 2), mild to moderate (Group II, n = 44; LVMI from 125 to 174 g/m 2), or severe (Group III, n = 21; LVMI > 175 g/m 2) left ventricular hypertrophy. The Integrated Backscatter Index in the septum was lower in patients of Group I (IBI = 23.3% ± 3.6%) and II (IBI = 26.5 ± 7.6; P = NS v Group I), in comparison with patients of Group III (IBI = 31.1 ± 5.9; P < .02 v II; P < .0001 v I). An increased myocardial wall reflectivity is detectable only in the presence of extreme forms of hypertensive left ventricular hypertrophy.

Regression of left ventricular hypertrophy results in improvement of QT dispersion in patients with hypertension

Objectives Increased QT dispersion has been considered as predisposing to ventricular arrhythmias in hypertrophic cardiomyopathy, congestive heart failure, and coronary artery disease. An increased QT dispersion has also been found in hypertensive patients with left ventricular hypertrophy (LVH). The data on the effect of LVH regression on QT dispersion are limited. Methods and Results To assess the relation of LVH regression and QT dispersion decrease, 68 patients (42 men and 26 women, mean age 56.3 ± 9.5 years) with uncomplicated essential hypertension were studied. All underwent full electrocardiographic and echocardiographic studies at baseline and after 6 months of monotherapy, 29 with angiotensin-converting enzyme inhibitors and 39 with calcium antagonists. QT dispersion was calculated by subtracting the shortest QT from the longest QT, in absolute value (QTmax – QTmin). It was also corrected with Bazett’s formula (QTc dispersion). Left ventricular mass index was assessed according to the Devereux formula. After treatment, LVH decreased with both angiotensin-converting enzyme inhibitors (from 155 to 130 g/m 2 , P < .001) and calcium antagonists (156 to 133/92/m 2 , P < .001). QT dispersion decreased both after angiotensin-converting enzyme inhibitor treatment (from 82 to 63 ms) and calcium antagonist treatment (from 77 to 63 ms, both P < .001). There was a significant correlation of QT dispersion and left ventricular mass after therapy ( r = 0.36, P < .005). There was a correlation of the degree of LVH and QT dispersion decrease ( r = 0.27, P < .05). Conclusions It is concluded that LVH regression influences ΔQT favorably. Its prognostic value has yet to be determined. (Am Heart J 1998;136:765-8.)

Increased myocardial echo density in left ventricular pressure and volume overload in human aortic valvular disease: an ultrasonic tissue characterization study

Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to morphometrically evaluated collagen content in human beings. Our objective was to assess myocardial reflectivity pattern in patients with severe left ventricular hypertrophy caused by either aortic stenosis (AS) or aortic regurgitation (AR). Ten patients with AS, 10 patients with AR, and 10 closely age- and gender-matched healthy controls were studied by two-dimensional Doppler echocardiography. By using an echocardiographic prototype, we performed a radiofrequency analysis to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall (integrated backscatter index: IBI, expressed in percentage). All patients with stenosis or aortic insufficiency showed a normal regional and global resting systolic function (fractional shortening: AS = 36.0 ± 6.6 versus AR = 40.3 ± 6.2 versus control = 40.2 ± 8.7; p = not significant [NS]). Left ventricular mass index (Devereux's formula) was markedly increased in patients with stenosis or aortic insufficiency (AS = 199.3 ± 18 versus AR = 208.8 ± 60 versus control = 97.3 ± 11 g/m 2; p < 0.0001). Myocardial echo density was increased in patients with stenosis or aortic insufficiency in comparison with controls, both in the septum (IBI%: AR = 40.7 ± 7.9 versus AS = 33.4 ± 4.2 versus control = 23.0 ± 6.2; p < 0.0001) and in the posterior wall (IBI%: AR = 27.1 ± 4.3 versus AS = 23.0 ± 2.6 versus control = 15.0 ± 4.2; p < 0.0001). No significant correlations were found between septal and posterior wall IBI and their thickness. Abnormally increased myocardial echo density—possibly related to disproportionate collagen deposition—can be detected in patients with pressure or volume overload caused by aortic valve disease and without overt systolic dysfunction. (J Am Soc Echocardiogr 1997;10:320-9.)

Deletion Polymorphism of Angiotensin-Converting Enzyme Gene and Left Ventricular Hypertrophy in Southern Italian Patients

Objectives. This study sought to evaluate the possible association of polymorphism of the angiotensin-converting enzyme (ACE) gene with blood pressure and left ventricular mass index (LVMI).Background. The renin–angiotensin system seems to be involved in the pathogenesis of essential hypertension. Moreover, recent epidemiologic observations demonstrate that many subjects with left ventricular hypertrophy have normal blood pressure levels, suggesting that factors other than hemodynamic overload may contribute to the hypertrophy.Methods. The study included 140 untreated hypertensive outpatients who underwent ambulatory blood pressure monitoring, echocardiographic evaluation and analysis for insertion (I)/deletion (D) polymorphism in intron 16 of the ACE gene by polymerase chain reaction. Blood pressure was measured at 24 h, and LVMI was calculated by the Devereux formula, in each patient.Results. Left ventricular mass index values (mean ± SD) were 137 ± 28 g/m2in patients with the DD genotype, 125 ± 27 g/m2in those with the ID genotype and 115 ± 27 g/m2in those with II genotype. The frequencies of the DD, ID and II genotypes were 45.71% (n = 64), 46.42% (n = 65) and 7.85% (n = 11), respectively, and were in Hardy-Weinberg equilibrium. The strongest association between left ventricular mass and DD genotype in our cohort appeared to be an independent cardiovascular risk factor (DD vs. ID: odds ratio [OR] 2.497, 95% confidence interval [CI] interval 1.158 to 5.412, p < 0.05; DD vs. II: OR 6.577, 95% CI 1.169 to 28.580, p < 0.02).Conclusions. Our data show that the LVMI was significantly enhanced in patients with the DD genotype.(J Am Coll Cardiol 1997;29:365–9)

Influence of measurement inaccuracies on determination of left ventricular mass by M mode echocardiography.

To determine to what extent inaccuracies in measuring the end diastolic diameter of the left ventricle, the interventricular septum, and the posterior wall, by M mode echocardiography influence the left ventricular mass calculated by the Devereux's formula. Mathematical model. Relatively small measurement inaccuracies such as 5%, which are known to be inherent in the echocardiographic method, will result in "changes" of left ventricular mass in the range of 8% to 15%. This is equivalent to expected changes in left ventricular mass seen during treatment. The use of Devereux's formula to calculate left ventricular mass is limited by measurement inaccuracies in individual patients.

Aldosterone Levels and Cardiac Hypertrophy in Professional Cyclists

Aldosterone has been associated with the development of cardiac hypertrophy and a correlation has been found between levels of aldosterone and the degree of cardiac hypertrophy in hypertensive patients. Our study aimed to test the relation between physiologic cardiac hypertrophy and serum aldosterone in a group of highly trained cyclists. Determination of the left ventricular mass index (LVMI) was performed in a group of 40 professional cyclists by using Devereux's formula with correction for body surface area. After an overnight fast, blood samples were collected and serum aldosterone levels were measured using RIA. LVMI and serum aldosterone were intercorrelated using linear regression analysis. Twenty-three of the 40 cyclists (58%) presented an LVMI > 130 g.m-1 and the other 17 subjects (42%) presented an LVMI < 130 g.m-1. Serum aldosterone levels did not correlate with LVMI in either of the groups (LVMI > 130 g.m-1, r = -0.089; LVMI < 130 g.m-1, r = 0.146). The lack of correlation of this hypertrophy with serum aldosterone levels suggests that physiologic hypertrophy of the athlete's heart could be caused by a different stimulus to that seen in pathologic hypertrophy of hypertensives.