Circulating natriuretic peptide concentrations in patients with end-stage renal disease: role of brain natriuretic peptide as a biomarker for ventricular remodeling.

OBJECTIVES: To determine levels of natriuretic peptides (NPs) in patients with end-stage renal disease (ESRD) and to examine the relationship of these cardiovascular peptides to left ventricular hypertrophy (LVH) and to cardiac mortality. PATIENTS AND METHODS: One hundred twelve dialysis patients without clinical evidence of congestive heart failure underwent plasma measurement of NP concentrations and echocardiographic investigation for left ventricular mass index (LVMI). RESULTS: Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations correlated positively with LVMI and inversely with left ventricular ejection fraction, whereas C-type NP and Dendroaspis NP levels did not correlate with LVMI. In dialysis patients with LVH (LVMI >125 g/m2), plasma ANP and BNP concentrations were increased compared with those in dialysis patients without LVH (both P<001). In a subset of 15 dialysis patients without LVH or other concomitant diseases, plasma BNP concentrations were not significantly increased compared with those in 35 controls (mean +/- SD, 20.1+/-13.4 vs 13.5+/-9.6 pg/mL; P=.06), demonstrating that the BNP concentration was not increased by renal dysfunction alone. Furthermore, the BNP level was significantly higher in the 16 patients who died from cardiovascular causes compared with survivors (mean +/- SD, 129+/-13 vs 57+/-7 pg/mL; P<.003) and was significantly associated with greater risk of cardiovascular death in Cox regression analysis (P<.001), as was the ANP level (P=.002). CONCLUSIONS: Elevation of the plasma BNP concentration is more specifically related to LVH compared with the other NP levels in patients with ESRD independent of congestive heart failure. Thus, BNP serves as an important plasma biomarker for ventricular hypertrophy in dialysis patients with ESRD.     

Left ventricular hypertrophy increases transepicardial dispersion of repolarisation in hypertensive patients: a differential effect on QTpeak and QTend dispersion

BACKGROUND: Ventricular arrhythmias in left ventricular hypertrophy (LVH) are related to regional electrical heterogeneity. The significance of noninvasive electrocardiographic indices of electrical heterogeneity in LVH has not been established. The aim of the study was to investigate changes in the Tpeak-Tend interval (an index of transmural dispersion of repolarisation) in addition to other traditional electrocardiographic indices of electrical dispersion in patients with hypertensive LVH. METHODS: Consecutive patients were screened for the presence of hypertensive echocardiographic LVH and compared with a control group. LVH was identified as left ventricular mass > 134 g m-2 in men and > 110 g m-2 in women. Twelve-lead ECGs were analysed in respect of various indices of electrical dispersion. RESULTS: Left ventricular mass was greater in the LVH than in the control group (174 +/- 39 vs. 101 +/- 18 g m-2, P < 0.0001). The Tpeak-Tend interval was not affected by LVH. The main effect of LVH was an increase in QTpeak dispersion (40 +/- 13 vs. 53 +/- 21 ms, P < 0.05), which resulted from an increase in the maximum QTpeak interval (337 +/- 24 vs. 358 +/- 30 ms, P < 0.04), without any change in the minimum QTpeak interval. There was a significant correlation between the left ventricular mass index and QTpeak dispersion (r = 0.40; P < 0.01). In contrast, LVH did not exert any effect on QTend dispersion (65 +/- 21 vs. 65 +/- 16 ms, ns), because LVH increased both the maximum QTend interval (430 +/- 30 vs. 449 +/- 28 ms, P < 0.05) and the minimum QTend interval (365 +/- 29 vs. 384 +/- 27 ms, P < 0.04). CONCLUSIONS: Hypertensive LVH exerts a differential effect on QTpeak and QTend interval dispersion. The most likely explanation is that these changes reflect a nonuniform prolongation of action potential duration across the epicardium, leading to an increase in transepicardial dispersion of repolarisation.     

Effect of nebivolol on QT dispersion in hypertensive patients with left ventricular hypertrophy.

Hypertensive patients with left ventricular hypertrophy (LVH) have increased QT dispersion, which is considered an early indicator of end-organ damage and a non-invasive marker of risk for clinically important ventricular arrhythmias and cardiac mortality. The purpose of this study was to examine the effect of nebivolol antihypertensive therapy on QT dispersion in hypertensive subjects. Twenty-five subjects (15 men and 10 women, mean age 53.6 +/- 4.5 years) with essential arterial hypertension and mild-to-moderate LVH (blood pressure: 147.2 +/- 6.2/90.6 +/- 3.8 mmHg; left ventricular mass indexed: 149.1 +/- 10.7 g/m(2)) were compared with 25 age-matched healthy control subjects. All the participants underwent a complete clinical examination, including electrocardiogram for QT interval measurements. The QT dispersion was defined as the difference between the longest and the shortest QT interval occurring in the 12-lead electrocardiogram. The QT dispersion was corrected (QTc) with Bazett's formula. Hypertensive subjects were treated with 5 mg daily of nebivolol. The ECG and echocardiogram were repeated after four weeks of treatment. At baseline, hypertensive patients showed QT dispersion (56.9 +/- 6.4 vs. 31.7 +/- 8.4 ms, P < 0.001) and QTc dispersion (58.3 +/- 6.2 vs. 33.2 +/- 7.8 ms, P < 0.001) significantly higher than control subjects. Four-week nebivolol treatment reduced blood pressure from 147.2 +/- 6.2/90.6 +/- 3.6 mmHg to 136.3 +/- 3.1/83.3 +/- 2.5 mmHg (P < 0.0001), and resting heart rate from 75.3 +/- 4.7 to 64.2 +/- 3.0 bpm (P < 0.001), without significant change in left ventricular mass (LVMi: 149.1 +/- 10.7 vs. 151.4 +/- 9.8 g/m(2), ns). Nebivolol-based treatment improved QT dispersion (56.9 +/- 6.4 vs. 40.5 +/- 5.8 ms, P < 0.001) and QTc dispersion (58.3 +/- 6.2 vs. 42.2 +/- 5.6 ms, P < 0.001), which remained higher than in control subjects (P < 0.001 in both cases). The reduction of QT dispersion did not correlate with arterial BP reduction. In conclusion, nebivolol reduced increased QT dispersion in hypertensive subjects after four weeks. This effect, occurred without any change in LVM, did not seem to be related to the blood pressure lowering and could contribute to reduce arrhythmias as well as sudden cardiac death in at-risk hypertensive patients.     

Volume control associated with better cardiac function in long-term peritoneal dialysis patients.

BACKGROUND: This study was undertaken to investigate the effect of long-term blood pressure (BP) reduction, achieved with salt restriction and strict volume control, on frequency and regression of left ventricular hypertrophy (LVH) in long-term peritoneal dialysis (PD) patients. METHODS: 56 patients who had been treated for more than 2 years under our care were enrolled. After echocardiographic (Echo) evaluation, 46 patients were included in the follow-up study. In our unit, we aim to keep patients' BP below 130/85 mmHg and cardiothoracic index below 0.50. To reach these targets, moderate salt restriction is advised, and if necessary, hypertonic PD solutions are used. Echo was performed at the beginning of the study (after a mean period of 36 months on PD) and at the end of the prospective follow-up period (24 months later). RESULTS: At the time of the first Echo, LVH was detected in only 8 (21%) patients. Residual urine volume was significantly decreased compared to data taken when they first started PD (658 +/- 795 vs 236 +/- 307 mL/day). Mean left ventricular mass index (LVMI) was 107 +/- 26.5 g/m2. LVMI was significantly decreased at the end of the follow-up in patients who had LVH at baseline. No LVH developed in patients who had normal LVMI at baseline. CONCLUSION: Our results indicate that control of hypertension is possible when extracellular fluid volume is kept under control using hypertonic PD solutions in case of recruitment in addition to salt restriction in long-term PD patients. Sustained normovolemia is associated with low incidence and regression of LVH.     

Contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy and diastolic dysfunction in hypertensive subjects

Matrix metalloproteinases (MMPs) are involved in the regulation of the extracellular matrix (ECM) of the myocardium and thus the pathogenesis of vascular and cardiac hypertrophy. In this study, we investigated contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy (LVH) and diastolic dysfunction in hypertensive subjects. Hypertensive patients with (n = 27) and without LVH (n = 23) were included. All participants underwent a complete transthoracic echocardiographic examination, including recordings of the mitral annular early, late, systolic and diastolic velocities by Doppler imaging. Plasma concentrations of MMP-3 and MMP-9 were determined by the one-step sandwich enzyme immunoassay method. Plasma MMP-3 and MMP-9 concentrations were significantly higher in patients with LVH than those without LVH (2.4 +/- 1.2 vs 1.5 +/- 0.7 ng/ml, p = 0.006 and 5.2 +/- 2.8 vs 3.3 +/- 1.7 ng/ml, p = 0.003, respectively). MMP-3 and MMP-9 levels were also correlated with left ventricular posterior wall thickness and Doppler indices of diastolic dysfunction. Our findings have suggested that increased MMP levels may contribute to LVH and left ventricular diastolic dysfunction. Therefore, treatment of hypertension with MMP lowering drugs, such as angiotensin converting enzyme inhibitors and angiotensin receptor blockers, may have favorable effects on LVH and left ventricular diastolic dysfunction.     

The Effects of Amlodipine on Left Ventricular Mass and Diastolic Function in Concentric and Eccentric Left Ventricular Hypertrophy

BACKGROUND: The effects of the antihypertensive therapy with amlodipine (5-10 mg/day) on left ventricular mass and diastolic function were examined in 30 mild to moderate essential hypertensive patients who have left ventricular hypertrophy (LVH) and diastolic dysfunction. METHODS AND RESULTS: Each patient's left ventricular mass was measured, and left ventricular diastolic function was assessed by echocardiographic Doppler examination at entry, and at 3 and 6 months after the initiation of the treatment. Amlodipine reduced both blood pressure (from 164 +/- 14/104 +/- 6 mmHg to 134 +/- 9/83 +/- 4 mmHg) and left ventricular mass index (from 160 +/- 30 g/m(2) to 137 +/- 26 g/m(2)) significantly at 3 months and both parameters maintained at these levels for 6 months. When the patients were classified according to the type of the LVH, a significant regression in left ventricular mass index was seen only in the patients who had concentric LVH was a relative wall thickness >/=0.44 (n = 16), but not in the eccentric LVH group (n = 14), although both groups were not significantly different from each other regarding the basal hemodynamic parameters, baseline left ventricular mass index and the decrease in blood pressure in response to amlodipine treatment. The mitral inflow E/A ratio did not show any significant change in either group. CONCLUSIONS: Amlodipine produced significant regression in LVH only in the patients with concentric LVH, but not those with eccentric LVH, while it did not change the diastolic dysfunction. Therefore, the type of LVH seems to be an important feature in determining the effects of antihypertensive treatment on left ventricular mass index.     

Polymorphisms of the peroxisome proliferator-activated receptor-gamma coactivator-1alpha gene are associated with hypertrophic cardiomyopathy and not with hypertension hypertrophy.

BACKGROUND: The clinical phenotype of both hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) induced by hypertension is heterogeneous. Genetic factors may contribute to this heterogeneity. Evidence is accumulating that the peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) gene plays a role in cardiac hypertrophy. The aim of our study was to identify the association between PGC-1alpha gene polymorphisms and cardiac hypertrophy. METHODS: A total of 270 consecutive HCM patients and 2486 hypertensive patients, comprising 1180 with LVH and 1306 without LVH, as well as 894 healthy controls, were successfully investigated. Polymorphisms of the PGC-1alpha gene were genotyped by PCR-restriction fragment length polymorphism and confirmed by sequencing. RESULTS: The Ser482 allele (rs8192678 G>A and A>A) and CC genotype of Thr394Thr (rs2970847) conferred increased risk for HCM [odds ratio (OR) 1.52, 95% confidence interval (CI) 1.11-2.11; OR 1.49, 95% CI 1.15-1.98, respectively]. The maximum ventricular thickness was greater in HCM patients carrying the Ser482 risk allele than in carriers of the non-risk allele (20.7+/-4.1 vs. 19.1+/-4.3 mm, p<0.05) and for the CC Thr394Thr genotype (20.9+/-4.6 vs. 19.0+/-4.2 mm, p<0.05). No association was found between PGC-1alpha polymorphism and hypertension with or without LVH. Conclusions: Our data indicate that variants of the PGC-1alpha gene are correlated with increased risk for HCM.     

高血压病左房、室构型与心律失常

目的 探讨高血压病患者左房、室构型情况及其与心律失常的关系。方法 95例高血压病患者（EH组）依年龄分为＜60岁和≥60岁两亚组。全组经彩色超声心动图检测左房内径（LAD）,左室重量指数（LVMI）;经动态心电图（Holter）判定心律失常,并将相关指标进行对比分析。结果 EH组中检出左房扩大（LAE）63例（66.3％）,左室肥顾（LVH）45例（47.4%),两者比较有差异（P＜0.05）;其中单纯左房扩大37例,单纯左室肥厚19例,左房扩大并左室肥厚（LEH）26例,与对照组比较P＜0.01。EH组中≥60岁单纯左房扩大、左室肥厚及左房扩大并左室肥厚发生率与＜60岁亚组比较P＜0.05。EH组检出室性心率失常（VA）54例（56.8%）,房性心律失常（AA）71例（74.7％）,两才有显著性差异（P＜0.05）。EH组年龄≥60岁各种房、室性心律失常发生率与＜60岁比较P＜0。05。结论 高血压病除存在LVH外,还存在左房扩大并左室肥厚,其发生率高于左室肥厚。高血压病左房、室构型与心律失常有关,房性心律失常高于室性心律失常;老年高血压病者比中年人更易发生左房、室内型改变及各种心律失常。     

Heart rate variability in arrhythmogenic right ventricular cardiomyopathy correlation with clinical and prognostic features

The identification of subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC) at higher risk for sudden death is an unresolved issue. An influence of the autonomic activity on the genesis of ventricular arrhythmias was postulated. Heart rate variability (HRV) analysis provides a useful method to measure autonomic activity, and is a predictor of increased risk of death after myocardial infarction. For these reasons, the aim of the study was to evaluate HRV and its correlations with ventricular arrhythmias, heart function, and prognostic outcome in patients with ARVC. The study included 46 patients with ARVC who were not taking antiarrhythmic medications. The diagnosis was made by ECG, echocardiography, angiography, and endomyocardial biopsy. Exercise stress test and Holter monitoring were obtained in all patients. Time-domain analysis of HRV was expressed as the standard deviation of all normal to normal NN intervals (SDNN) detected during 24-hour Holter monitoring. Thirty healthy subjects represented a control group for HRV analysis. The mean follow-up was 10.8 +/- 1.86 years. SDNN was reduced in patients with ARVC in comparison with the control group (151 +/- 36 vs 176 +/- 34, P = 0.00042). Moreover, there was a significant correlation of this index with the age of the patients (r = - 0.59, P < 0.001), with the left (r = 0.44, P = 0.002) and right (r = 0.47, P = 0.001) ventricle ejection fraction, with the right ventricular end diastolic volume (r = - 0.62, P < 0.001), and with the ventricular arrhythmias, detected during the same Holter record used for HRV analysis (patients with isolated ventricular ectopic beats < 1,000/24 hours, 184 +/- 34; patients with isolated ventricular ectopic beats > 1,000/24 hours and/or couplets, 156 +/- 25; patients with repetitive ventricular ectopic beats (> or = 3) and/or ventricular tachycardia, 129 +/- 25; P < 0.001). During follow-up two patients showed a transient but significant reduction of SDNN and a concomitant increase of the arrhythmic events. In eight patients an episode of sustained ventricular tachycardia occurred, but the mean SDNN of this subgroup did not differ from the mean value of the remaining patients (152 +/- 15 vs 150 +/- 39; P = NS). Only one subject died after heart transplantation during follow-up (case censored). Time-domain analysis of HRV seems to be a useful method to assess the autonomic influences in ARVC. A reduction of vagal influences correlates with the extent of the disease. The significant correlation between SDNN and ventricular arrhythmias confirmed the influences of autonomic activity in the modulation of the electrical instability in ARVC patients. However, SDNN was not predictive of spontaneous episodes of sustained ventricular tachycardia.     

Regression of left ventricular hypertrophy with moexipril, an angiotensin-converting enzyme inhibitor, in hypertensive patients

Left ventricular hypertrophy (LVH) is a common complication of essential hypertension and an independent risk factor for the development of cardiovascular disease. Therefore, antihypertensive treatment should decrease blood pressure (BP) and reverse LVH. However, antihypertensive drugs have been shown to have different effects on LVH despite similar effects on BP reduction. Although lowering BP produces a beneficial effect on LVH per se, meta-analyses of clinical trials have indicated that angiotensin-converting enzyme (ACE) inhibitors decrease left ventricular mass (LVM) to a greater extent than do some other antihypertensives. The aim of this study was to evaluate the effect of a 24-week treatment with the ACE inhibitor moexipril (15 mg once daily) on the regression of LVH in hypertensive patients. This was a multicenter, international, single-blind, single-group, nonrandomized study. After a wash-out placebo period of 2 weeks, 15 mg moexipril once daily was administered for 24 weeks followed by a 2-week follow-up placebo period. Subjects with mild to moderate essential hypertension were screened; those with LVH [defined as an LVM indexed for body surface area (LVMIs) >111 g/m in men and LVMIs >106 g/m in women] were eligible to participate in this study. Echocardiograms were recorded on videotape and sent to a centralized laboratory for reading by 2 independent experts blinded for treatment, center, and visit; the mean values of these readings were calculated and used for analysis. Valid echocardiographic data were obtained from 72 patients (50 males, 22 females) with a mean age of 49 +/- 11 years. Analysis showed significant decrease of LVMIs (121 +/- 20 versus 103 +/- 17 g/m; P < 0.001) and BP (152 +/- 12/96 +/- 9 versus 140 +/- 13/86 +/- 9 mm Hg; P < 0.001) with moexipril. For patients who met LVMI inclusion criteria after centralized, blinded readings, the decrease from baseline in LVMIs was 23.4 g/m. The decrease in LVMIs was independent from the regression to the mean phenomenon as observed from the follow-up placebo period. Moexipril 15 mg once daily administered for 24 weeks resulted in a significant reversal of LVH in patients with essential hypertension. The result compares favorably with results previously obtained in trials of similar duration with other ACE inhibitors.     

Left ventricular hypertrophy in normoalbuminuric type 2 diabetic patients not taking antihypertensive treatment

BACKGROUND: Left ventricular hypertrophy (LVH) is an independent risk factor for myocardial ischaemia, cardiac arrhythmia, sudden death, and heart failure, all common findings in patients with type 2 diabetes. AIM: To determine the prevalence of, and risk factors for, LVH in normoalbuminuric type 2 diabetic patients not taking antihypertensive treatment. DESIGN: Cross-sectional study. METHODS: From 1994 to 1998, M-mode echocardiography was performed by one experienced examiner in 262 consecutive, normoalbuminuric Caucasian type 2 diabetic patients, all with blood pressure <160/95 mmHg and not taking antihypertensive medication. Mean +/- SD age was 54 +/- 10 years, 109 were women, and median known duration of diabetes was 4 (range 1-28) years. Body mass index (BMI) was 28 +/- 5 kg/m(2), and blood pressure 134 +/- 13/79 +/- 8 mmHg, all means +/- SD. Median urinary albumin excretion rate was 9 (range 2-30) mg/24 h. RESULTS: The prevalence of LVH indexed to height(2.7) was 43% (95%CI 38-50%), and was similar in men and women. BMI, HbA(1c) and log urinary albumin excretion were significantly associated with left ventricular hypertrophy in a logistic regression model, whereas sex, age, known duration of diabetes and blood pressure were not. Similar results were obtained for left ventricular mass index. DISCUSSION: LVH was frequent in our normoalbuminuric type 2 diabetic patients not taking antihypertensive treatment. Several potentially modifiable risk factors, such as raised BMI, poor glycaemic control and elevated urinary albumin excretion rate, were associated with LVH.     

The association of peritoneal transport properties with 24-hour blood pressure levels in CAPD patients.

OBJECTIVES: We aimed to investigate the effects of peritoneal transport characteristics on blood pressure (BP) parameters, measured by 24-hour ambulatory blood pressure monitoring (ABPM), and on the development of left ventricular hypertrophy (LVH) in continuous ambulatory peritoneal dialysis (CAPD) patients. DESIGN: Cross-sectional and prospective design. SETTING: Tertiary-care center. PATIENTS: 25 CAPD patients (11 male, 14 female; mean age 47 +/- 14 years) were included. Mean time on CAPD was 22.9 +/- 18 months and all patients had been dialyzed for more than 6 months. The patients were divided into high, high-average, low-average, and low transport groups according to peritoneal equilibration test results. MAIN OUTCOME MEASURES: Daytime and nighttime systolic and diastolic BP and left ventricular mass index among the different peritoneal transport groups; changes in BP parameters before and after increase in ultrafiltration. RESULTS: On 24-hour ABPM records, 13 patients (52%) were found to be hypertensive. Both mean systolic and diastolic BP were significantly increased in high-transporter groups compared to low transporters in both daytime and nighttime BP parameters. Left ventricular mass index was higher in high transporters compared to low transporters, without reaching statistical significance: 160 +/- 23 vs 119 +/- 41 g/m2, p > 0.05. Following increase in ultrafiltration, mean systolic (145 +/- 13 vs 128 +/- 5 mmHg, p < 0.001) and diastolic (96 +/- 10 vs 81 +/- 3 mmHg, p < 0.001) BP decreased, and BP levels returned to normotensive levels in 6 (46%) of the 13 hypertensive patients, requiring discontinuation of antihypertensive drugs. CONCLUSION: Improvement in volume status resulted in a decrease in both daytime and nighttime BP. Differences in peritoneal transport properties were associated with the development of hypertension and LVH.     

Cardiovascular magnetic resonance in the diagnosis of acute heart transplant rejection: a review

Background

Left ventricular hypertrophy (LVH) is a hallmark of chronic pressure or volume overload of the left ventricle and is associated with risk of cardiovascular morbidity and mortality. The purpose was to evaluate different electrocardiographic criteria for LVH as determined by cardiovascular magnetic resonance (CMR). Additionally, the effects of concentric and eccentric LVH on depolarization and repolarization were assessed.

Methods

120 patients with aortic valve disease and 30 healthy volunteers were analysed. As ECG criteria for LVH, we assessed the Sokolow-Lyon voltage/product, Gubner-Ungerleider voltage, Cornell voltage/product, Perugia-score and Romhilt-Estes score.

Results

All ECG criteria demonstrated a significant correlation with LV mass and chamber size. The highest predictive values were achieved by the Romhilt-Estes score 4 points with a sensitivity of 86% and specificity of 81%. There was no difference in all ECG criteria between concentric and eccentric LVH. However, the intrinsicoid deflection (V6 37 ± 1.0 ms vs. 43 ± 1.6 ms, p < 0.05) was shorter in concentric LVH than in eccentric LVH and amplitudes of ST-segment (V5 -0.06 ± 0.01 vs. -0.02 ± 0.01) and T-wave (V5 -0.03 ± 0.04 vs. 0.18 ± 0.05) in the anterolateral leads (p < 0.05) were deeper.

Conclusion

By calibration with CMR, a wide range of predictive values was found for the various ECG criteria for LVH with the most favourable results for the Romhilt-Estes score. As electrocardiographic correlate for concentric LVH as compared with eccentric LVH, a shorter intrinsicoid deflection and a significant ST-segment and T-wave depression in the anterolateral leads was noted.     

Comparison of myocardial tissue Doppler with transmitral flow Doppler in left ventricular hypertrophy

We sought to determine the most useful echocardiographic measurements for assessment of diastolic function in patients with left ventricular hypertrophy (LVH) and normal systolic function. We compared myocardial Doppler velocities of the basal inferoposterior wall with mitral inflow pulsed wave Doppler velocities in 11 healthy volunteers (age, 36 +/- 6 years), 25 patients (age, 64 +/- 14 years) without LVH, and 37 patients (age, 67 +/- 14 years) with LVH and otherwise normal echocardiograms. The discriminatory measurements were myocardial A-wave duration (120 +/- 18 versus 98 +/- 20 and 92 +/- 12 ms, P <.0001), myocardial isovolumetric relaxation time (124 +/- 45 versus 95 +/- 48 and 78 +/- 25 ms, P =.0035), mitral A-wave velocity (0.98 +/- 0.37 versus 0.73 +/- 0.28 m/s and 0.61 +/- 0.22 m/s, P =.009), and mitral E-wave deceleration time (257 +/- 93 versus 201 +/- 85 ms and 184 +/- 83 ms, P =.015), which were significantly increased, and myocardial E-wave velocity (0.84 +/- 0.04 m/s versus 0.13 +/- 0.03 m/s and 0.14 +/- 0.03 m/s, P <.0001), which was significantly decreased, in patients with LVH compared with patients without LVH and normal volunteers, respectively. Left ventricular posterior wall thickness correlated with myocardial isovolumetric relaxation time (r = 0.52, P <.0001) and myocardial A-wave duration (r = 0.59, P <.0001), negatively with myocardial E wave (r = -0.43, P <.0001), and showed no correlation with mitral inflow parameters except mitral inflow A wave (r = 0.43, P =.002). On multivariate analysis using these variables, myocardial isovolumetric relaxation time (P =.0014) and A-wave duration (P =.001) were the only 2 variables that correlated with posterior wall thickness (multiple R = 0.71). In the presence of LVH and preserved left ventricular systolic function, myocardial relaxation time and velocities are more sensitive than mitral Doppler inflow parameters in detecting abnormal left ventricular relaxation.     

Efficacy of mexiletine in ventricular arrhythmias among patients in Taiwan: assessment by 24-hour Holter electrocardiography

The effects of mexiletine in 30 patients with symptomatic recurrent ventricular arrhythmias were assessed by 24-hour Holter electrocardiography and M-mode echocardiography. The mean daily dose of mexiletine was 534 mg (range, 300 to 900 mg) and the interval of Holter follow-up was 16.9 days (range, 10 to 25 days). Total ventricular premature beats were reduced by 85% or more in 21 patients; in 19 of these patients there was a reduction of one or more modified Lown grades of ventricular arrhythmias. The overall reduction in Lown grades in the 30 patients was from 3.3 +/- 0.8 to 1.5 +/- 1.4 (P less than 0.0001). No significant changes in heart rate before or after mexiletine therapy were noted. Left ventricular echocardiography showed no significant changes in percentage fractional shortening after treatment. Adverse effects included gastrointestinal intolerance in seven patients and neurogenic symptoms in three. During the follow-up period of 1 to 11 (mean, 3.2) months, ventricular arrhythmias recurred in three patients. It is concluded that oral mexiletine is moderately effective and safe in controlling symptomatic recurrent ventricular arrhythmias.     

Abnormal heart rate turbulence predicts the initiation of ventricular arrhythmias

BACKGROUND: Abnormal heart rate turbulence (HRT) reflects autonomic derangements predicting all-cause mortality, yet has not been shown to predict ventricular arrhythmias in at-risk patients. We hypothesized that HRT at programmed ventricular stimulation (PVS) would predict arrhythmia initiation in patients with left ventricular dysfunction. METHODS: We studied 27 patients with coronary disease, left ventricular ejection fraction (LVEF) 26.7 +/- 9.1%, and plasma B-type natriuretic peptide (BNP) 461 +/- 561 pg/mL. Prior to arrhythmia induction at PVS, we measured sinus cycles after spontaneous or paced premature ventricular contractions (PVCs) for turbulence onset (TO; % cycle length change following PVC) and slope (TS; greatest slope of return to baseline cycle). T-wave alternans (TWA) was also measured during atrial pacing. RESULTS: At PVS, abnormal TO (> or =0%) predicted inducible ventricular tachycardia (VT; n = 10 patients; P < 0.05). TO was greater in inducible than in noninducible patients (2.3 +/- 3.1% vs -0.02 +/- 2.8%, P < 0.05) and correlated with LVEF (P < 0.05) but not with BNP. TS did not differ between groups. Conversely, ambulatory HRT differed significantly from HRT at PVS (TO -0.55 +/- 1.08% vs 0.85 +/- 3.02%, P < 0.05; TS 2.63 +/- 2.09 ms/RR vs 8.70 +/- 6.56 ms/RR, P < 0.01), and did not predict inducible VT but trended (P = 0.05) to predict sustained VT on 739 +/- 179 days follow-up. TWA predicted inducible (P < 0.05) and spontaneous (P = 0.0001) VT but did not co-migrate with HRT. CONCLUSIONS: Abnormal HRT measured at PVS predicted the induction of sustained ventricular arrhythmias in patients with ischemic cardiomyopathy. However, HRT at PVS did not correlate with ambulatory HRT, nor with TWA, both of which predicted spontaneous ventricular arrhythmias. Thus, HRT may reflect the influence of autonomic milieu on arrhythmic susceptibility and is likely complementary to traditional arrhythmic indices.     

Hypertensive left ventricular hypertrophy is linked to an enhanced catecholamine response to submaximal exercise.

BACKGROUND: The serial plasma catecholamine response to exercise has not been studied fully in relation to left ventricular hypertrophy (LVH) in patients with hypertension (HT). This study determined whether plasma catecholamine responses to exercise are altered in essential HT in the presence or absence of LVH. MATERIALS AND METHODS: Plasma noradrenaline (NA) and plasma adrenaline (A) were measured at rest, during and after treadmill exercise in 59 hypertensive subjects and 22 age-matched control subjects. Patients were divided into LVH(-) (n = 20) and LVH(+) (n = 39) stratified by left ventricular mass index [LVMI: control subjects, LVH(-), LVH(+): 114 +/- 4, 105 +/- 3, 151 +/- 3 g m-2]. RESULTS: Exercise time (9.9 +/- 0.6, 7.6 +/- 0.7, 7.3 +/- 0.6 min) was shorter in patients with HT. Both systolic and diastolic blood pressures were higher in patients with HT, and no difference was observed between LVH(-) and LVH(+) patients. Resting plasma NA was not different (157 +/- 16, 173 +/- 17, 167 +/- 14 pg mL-1), but plasma NA at stage I (300 +/- 30, 342 +/- 40, 469 +/- 40 pg mL-1) was higher in LVH(+) patients than in LVH(-) patients or control subjects. Plasma A response to exercise was similar among the three groups. There was a positive correlation (r = 0.38, P < 0.001) between LVMI and Deltaplasma NA at stage I in all subjects. CONCLUSIONS: Patients with essential HT with LVH had augmented plasma NA response during submaximal exercise, whereas patients without LVH did not exhibit this augmentation. The positive correlation between LVMI and Deltaplasma NA suggested a possible association between the degree of cardiac hypertrophy and sympathetic activation during exercise.     

Platelet size and left ventricular hypertrophy in hypertensive patients over 50 years of age

Abstract. Both mean platelet volume (MPV) and left ventricular hypertrophy have been described as associated with increased risk for vascular events. Seventy-six hypertensive patients (37 M and 39 F) over 50 years of age were studied. They were divided into subgroups according to the presence of left ventricular hypertrophy (LVH = LV mass index >125 gm^-2, when LV mass was assessed by M-mode echocardiography according to Penn's Convention). MPV was 3% higher in hypertensive patients with LVH compared with those without LVH ( P >0.05) and it was associated with the occurrence of LVH (chi-square = 8.44, P = 0.042). MPV significantly correlated with left ventricular mass index ( r = 0.298, P = 0.004) and interventricular septum thickness ( r = 0.231, P = 0.022). Both correlations remained significant after adjustment for age, blood pressure and glycaemia. MPV seemed to be associated with increased left ventricular mass and interventricular septum thickness in middle-aged to elderly hypertensive patients.     

Effects of arterial compliance on geometry of the left ventricle in patients with pre-dialysis chronic renal failure]

AIM: To examine relationships between left ventricular geometry and general arterial compliance (GAC) in patients with predialysis chronic renal failure (CRF). 102 patients with predialysis CRF unrelated to diabetes mellitus (males 46, females 56, mean age 49.1 +/- 18.3 years). CRF was caused by chronic glomerulonephritis and essential hypertension (77.4%). 92 (90.2%) patients were hypertensive. Serum creatinin was 432.1 +/- 165.3 mcmol/l. GAC was defined as stroke volume/pulse arterial pressure. Echocardiography determined the index of the left ventricular myocardial mass (ILVMM), relative thickness of the left ventricular wall (RTW). Left ventricular hypertrophy (LVH) was diagnosed in 86 (84.3%) patients. In 64 patients it was concentric and in 22 patients--excentric). Multivariance regression analysis showed that systolic arterial pressure and anemia have a direct independent effect on ILVMM (p = 0.004). Independent inverse relationship was between GAC and RTW. Patients with concentric LVH had GAC lower than those with excentric LVH (p = 0.003). Reduction of GAC is an independent factor influencing the development of concentric LVH in patients with predialysis CRF.     

Cardiovascular effects of doxepin in cardiac patients with ventricular arrhythmias

The effect of doxepin on ventricular arrhythmias, the ECG, and left ventricular function was evaluated in 10 cardiac patients with symptoms with frequent ventricular premature depolarizations in a dose-ranging protocol. Four patients (40%) had greater than or equal to 80% ventricular premature depolarization suppression; four of eight with pairs and four of six with ventricular tachycardia had greater than or equal to 90% suppression. The mean maximal doxepin dose was 115 +/- 41 mg/day; mean nadir total doxepin concentration was 61 +/- 48 ng/ml and mean nadir total desmethyldoxepin concentration was 51 +/- 42 ng/ml. Doxepin increased the heart rate and the PR, QRS, and QTc intervals of the surface ECG (P not significant). There was no significant change in resting mean left ventricular ejection fraction with doxepin: 41% +/- 15% vs. 43% +/- 19% (P not significant). Complaints of sedation (eight patients) limited dose ranging and tolerance to the drug. Although doxepin suppressed ventricular premature depolarizations in four patients, marked sedation limits its usefulness for primary treatment of arrhythmias in this population.