QT间期离散度与左心室肥厚的关系及依那普利对其影响

目的：探讨ＱＴ间期离散度（ＱＴｄ）与左心室肥厚的关系及依那普利治疗对其的影响。方法：选择高血压病（ＥＨ）患者５７例，其中合并左心室肥厚（ＬＶＨ）者（ＥＨ＋ＬＶＨ组）３０例，无合并左心室肥厚者（ＥＨ－ＬＶＨ组）２７例；正常对照者（正常对照组）２４例。用超声心动图仪检测法求得左心室重量，同时从心电图上测得ＱＴｄ与校正后ＱＴｄ（ＱＴｃｄ）。ＥＨ＋ＬＶＨ组患者用依那普利治疗６个月。结果：①ＥＨ＋ＬＶＨ组患者ＱＴｄ与ＱＴｃｄ明显大于ＥＨ－ＬＶＨ组和正常对照组，而ＥＨ－ＬＶＨ组和正常对照组间无显著性差异；②ＱＴｄ和ＱＴｃｄ与左心室重量呈显著正相关（ｒ＝０．７５，Ｐ＜０．０５及ｒ＝０．６１，Ｐ＜０．０５）；③治疗６个月后，ＱＴｄ和ＱＴｃｄ、左心室重量均降低，且ＱＴｄ缩小程度（ΔＱＴｄ）、ＱＴｃｄ缩小程度（ΔＱＴｃｄ）与左心室重量减轻程度（ΔＬＶＭ）亦呈显著正相关。结论：左心室肥厚是高血压病患者ＱＴｄ增大的主要原因；ＱＴｄ可作为左心室肥厚程度的评估指标；依那普利能有效逆转左心室肥厚，减小ＱＴｄ。     

苯那普利对高血压左室肥厚与QTc离散度的影响

目的:探讨苯那普利对高血压左室肥厚（ＬＶＨ）与ＱＴｃ离散度（ＱＴｃｄ）的影响。方法原发性高血压６０例用苯那普利治疗６个月,测定治疗前后左室重量指数（ＬＶＭＩ）和ＱＴｃｄ。结果ＬＶＨ组患者治疗后ＬＶＭＩ明显减少（Ｐ＜０．００１）,ＬＶＨ逆转率７２％。ＬＶＨ组ＱＴｃｄ治疗前显著高于无ＬＶＨ组（６９．１±１７．３比４０．６±１１．６ｍＳ,Ｐ＜０．００１）,治疗后明显降低（６９．１(１７．３比４３．９(１２．６ｍｓ,Ｐ＜０．００１）,而无ＬＶＨ组治疗前后ＱＴｃｄ无明显变化（Ｐ＞０．０５）。ＬＶＨ组中ＬＶＨ逆转者ＱＴｃｄ明显小于未逆转者（３８．２±１０．４比６０．０±１６．１ｍｓ,Ｐ＜０．００１）。ＬＶＭＩ与ＱＴｃｄ之间呈正相关（ｒ＝０．６７８,Ｐ＜０．００１）。结论高血压ＬＶＨ时ＱＴｃｄ增大,苯那普利长期治疗使ＬＶＭＩ减少的同时ＱＴｃｄ也明显降低。     

老年冠心病患者QT离散度变化及其临床意义

目的探讨老年冠心病患者ＱＴ离散度（ＱＴｄ）和心率校正的ＱＴ离散度（ＱＴｃｄ）与致命性室性心律失常（ＦＶＡ）及心衰（ＨＦ）之间的关系。方法测定了８４例老年冠心病患者的ＱＴｄ及ＱＴｃｄ，其中心原性猝死（ＣＳＤ）９例，ＦＶＡ２３例，非ＦＶＡ６１例。有ＨＦ４７例，无ＨＦ３７例。结果ＣＳＤ组ＱＴｄ、ＱＴｃｄ显著大于ＦＶＡ及非ＦＶＡ组（Ｐ＜０．０５；Ｐ＜０．０１），ＦＶＡ组ＱＴｄ、ＱＴｃｄ大于非ＦＶＡ组（Ｐ＜０．０１），ＨＦ组ＱＴｄ、ＱＴｃｄ显著长于无ＨＦ组（Ｐ＜０．０１）。本文ＱＴｄ和ＱＴｃｄ呈显著正相关（ｒ＝０．９７２０，Ｐ＜０．０１）。结论作者认为ＱＴｄ和（或）ＱＴｃｄ可作为评估老年冠心病患者发生ＦＶＡ和（或）ＨＦ预后的重要参考指标。     

高血压左室肥厚的室性心律失常与QT间期离散度的关系

目的 探讨高血压左室肥厚（ＬＶＨ）与非左室肥厚（ＮＬＶＨ）患者的室性心律失常与ＱＴｃｄ的关系。方法 对１００例有或无左室肥厚高血压患者行ＱＴｃｄ与２４小时动态心电图监测,结果 ＬＶＨ组ＱＴｃｄ室性心律失常,复杂室性心律失常明显高于ＮＬＶＨ组（Ｐ〈０．０１）,并发现ＬＶＨ组有ＱＴｃｄ〉６０ｍｓ者室性心律失常检出率明显高于ＬＶＨ而ＱＴｃｄ〈６０ｍｓ者（０．０５≥Ｐ〉０．０１）。结论 高血压ＬＶＨ组ＱＴ     

冠心病患者的心室晚电位、室性早搏与心肌复极离散度的关系

对７０例冠心病患者和２１例健康人的心电图数值进行测量，并对心室晚电位、室性早搏与心电图各测值的关系进行研究。结果：①心绞痛和陈旧性心肌梗塞患者ＱＴｃ、ＱＴｄ、ＪＴ、ＪＴｃ、ＪＴｄ及ＪＴｃｄ明显高于健康对照组（Ｐ＜０．０５或＜０．０１）。陈旧性心肌梗塞组患者ＱＴｃ、ＱＴｄ、ＱＴｃｄ及ＪＴｄ、ＪＴｃｄ高于心绞痛组（Ｐ＜０．０５或＜０．０１）。②心室晚电位阳性的冠心病患者的ＱＴｄ、ＱＴｃｄ、ＪＴｄ、ＪＴｃｄ明显高于心室晚电位阴性的冠心病组（Ｐ＜０．０５或＜０．０１）。③冠心病伴室性早搏者ＱＴｃ、ＱＴｄ、ＱＴｃｄ、ＪＴ、ＪＴｃ、ＪＴｄ、ＪＴｃｄ明显增加（Ｐ＜０．０５或＜０．０１）。提示冠心病存在明显心肌复极不均匀，心室晚电位和室性早搏与心肌复极离散度有关。     

老年高血压左室肥厚与心率变异性,QT离散度及心室晚电位关系

老年高血压左室肥厚与心率变异性、ＱＴ离散度及心室晚电位关系任斌江苏省老年医学研究所心功能室（２１００２４）表１２组ＬＶＭＩ、ＬＶＤＤ、ＬＶＥＦ、ＳＤＮＮ、ＰＮＮ５０、ＱＴｄ比较（ｘ±ｓ）对照组（ｎ＝３０）ＬＶＨ组（ｎ＝４５）ＬＶＭＩ８１．８０±１６．...     

高血压左室肥厚与外周血淋巴细胞β受体密度的关系

目的观察高血压左室肥厚与外周血淋巴细胞β受体密度的关系。方法４１例高血压患者和２３例正常人进行超声心动图检查，并采用放射配体结合法测定外周血β受体密度。结果高血压左室肥厚组（ｎ＝２１）βｍａｘ高于正常对照组，高血压无左室肥厚组（ｎ＝２０）βｍａｘ低于正常对照组。高血压左室肥厚组βｍａｘ与左室肌重指数呈正相关（ｒ＝０．７６５，Ｐ＜０．０１）。结论在高血压肥厚发展期，外周血淋巴细胞β受体密度降低，心室肥厚一旦形成，淋巴细胞β受体密度反而增高。     

老年急性心肌梗死患者的QT离散度变化及其与泵衰竭的关系

测定７１例老年急性心肌梗死（ＡＭＩ）患者的ＱＴ离散度（ＱＴｄ）、ＱＴｃ离散度（ＱＴｃｄ），以探讨其与泵衰竭的关系。结果显示泵衰竭室颤组（ｎ＝１０）的最大ＱＴｃ间期、ＱＴｄ、ＱＴｃｄ显著大于泵衰竭无室颤组（ｎ＝２１）和对照组（ｎ＝４０），泵衰竭无室颤组的ＱＴｄ、ＱＴｃｄ显著大于对照组。提示最大ＱＴｃ间期延长和ＱＴｄ、ＱＴｃｄ增大与ＡＭＩ泵衰竭患者室颤的发生密切相关，观察ＱＴｄ和ＱＴｃｄ对判断老年人ＡＭＩ早期泵功能和预后有一定价值。     

高血压对靶器官细胞凋亡影响的实验研究

本研究采用自发性高血压大鼠（ Ｓ Ｈ Ｒ）、服用依那普利的 Ｓ Ｈ Ｒ大鼠（ Ｓ Ｈ Ｒ ｄ）及正常血压大鼠（ Ｗ Ｋ Ｙ）三组作对照研究,应用原位标记检测技术观察高血压左室肥厚及心脏左室逆转后心肌平滑肌细胞凋亡现象。并检测凋亡相关基因ｂｃｌ ２,ｃ ｍ ｙｃ 的表达。结果显示: Ｓ Ｈ Ｒ ｄ 左室肥厚逆转,其左室壁细胞凋亡数比 Ｓ Ｈ Ｒ 组明显增多（ Ｐ＜ ０．０１）。 Ｓ Ｈ Ｒ 组左心室肥厚,其左室壁细胞凋亡数则比 Ｗ Ｋ Ｙ,即无高血压及左室肥厚组明显增多（ Ｐ＜ ０．０１）。各组ｂｃｌ ２,ｃ ｍ ｙｃ 均有表达,依据辉度检测表达强度,则ｂｃｌ ２ 表达的强度为 Ｓ Ｈ Ｒ明显高于 Ｓ Ｈ Ｒ ｄ 及 Ｗ Ｋ Ｙ（ Ｐ＜ ０．０１）; Ｓ Ｈ Ｒ ｄ 和 Ｗ Ｋ Ｙ 辉度接近（ Ｐ＞ ０．０５）;ｃ ｍ ｙｃ 表达的强度为 Ｓ Ｈ Ｒ ｄ＞ Ｓ Ｈ Ｒ＞ Ｗ Ｋ Ｙ,各组比较,差别有非常显著意义（ Ｐ＜ ０．０１）或显著意义（ Ｐ＜ ０．０５）。     

高血压性左室肥厚与肥厚型心肌病的QT离散度对比观察

本研究目的在于评估肥厚型心肌病（ＨＣＭ）和高血压性左室心肌肥厚（ＬＶＨ）患者的ＱＴ离散度,研究组共１０７人,３８位正常对照,３３位有左室肥大和３６位肥厚型心肌病,与对照组相比,ＬＶＨ组和ＨＣＭ组的ＱＴ离散度均增大（Ｐ＜００１）,ＱＴｓｄ亦增大（Ｐ＜...     

QT dispersion in patients with different etiologies of left ventricular hypertrophy: the significance of QT dispersion in endurance athletes

Left ventricular hypertrophy (LVH) increases the risk of ventricular arrhythmias and sudden death and has a significant effect on total cardiovascular mortality. QT dispersion (QTd) is a measure of inhomogeneous repolarization and is used as an indicator of arrhythmogenicity. In this study we detected QTd in patients with different etiologies of left ventricular hypertrophy and the effect of LVH in QTd on endurance athletes. The study group consisted of 147 white male subjects with 3 different etiologies of LVH and 30 healthy male individuals. The underlying etiologies of LVH were essential hypertension, valvular aortic stenosis and long-term training (athletic heart). QTd was measured by surface electrocardiogram and Bazett's formula was used to correct QTd for heart rate (QTcd). Left ventricular mass was determined by transthoracic echocardiography and left ventricular mass index was calculated in relation to body surface area. The QTcd was significantly higher in patients with pathological LVH (due to hypertension and aortic stenosis) than in the athletes' group (physiological LVH) and healthy subjects (P<0.05). The magnitude of QTcd was similar between athletes and the control group (P=0.6). The difference of QTcd between the groups with pathological LVH was not statistically significant (P=0.1). In conclusion; the increasing of QT dispersion is associated with only pathological conditions of LVH. The left ventricular hypertrophy has not a negative effect in QT dispersion on endurance athletes. The measurement of QT dispersion may be a non-invasive useful method for screening additional pathological conditions in endurance athletes.     

Clinical determinants of increased QT dispersion in patients with diabetes mellitus.

AIMS: To compare QT dispersion measurements in diabetic patients to control subjects and assess any associations between QT dispersion and diabetic clinical characteristics. METHODS: A total of 512 diabetics and 50 age and gender matched controls were studied. QT interval was measured manually in 12-lead conventional electrocardiograms, and QT dispersion (QTd), heart rate-corrected QT dispersion (QTcd), number of leads-adjusted QT dispersion (adjuQTd) and adjacent QT dispersion (adjaQTd) were calculated. Demographic, clinical, laboratory and electrocardiographic data were recorded. RESULTS: Diabetics showed increased QT dispersion compared to controls (QTd: P<0.001, QTcd: P<0.001, adjuQTd: P<0.001), even those with recent diagnosis (less than 2 years) and without arterial hypertension, ECG abnormalities or chronic degenerative complications (QTd: P=0.01, QTcd: P<0.001, adjuQTd: P=0.04). Left ventricular hypertrophy (QTd: P<0.001, QTcd: P<0.001, adjuQTd: P<0.001, adjaQTd: P<0.001) and conduction disturbances (QTd: P=0.002, QTcd: P=0.003, adjuQTd: P=0.003) were the electrocardiographic findings associated with increased QT dispersion in bivariate analysis. Clinical variables were the presence of arterial hypertension (QTd: P=0.004, QTcd: P=0.01, adjuQTd: P<0.001), even without left ventricular hypertrophy (QTd: P=0.01, QTcd: P=0.03, adjuQTd: P=0.003), and the presence of diabetic cardiovascular complications (QTd: P=0.02, QTcd: P=0.01, adjuQTd: P=0.008, adjaQTd: P=0.03). No association between QT dispersion and the presence of diabetic microvascular complications, glycaemic control, age and gender, or cardiovascular drugs was observed. Multivariate regressive statistical analysis confirmed the associations noted in bivariate analysis. CONCLUSIONS: Diabetic patients have increased QT dispersion compared to non-diabetics even those without arterial hypertension and cardiovascular complications and with recent diagnosis. The presence of arterial hypertension, diabetic cardiovascular complications and electrocardiographic abnormalities of left ventricular hypertrophy and conduction disturbances were associated to increased QT dispersion in diabetes mellitus.     

Multivariate associates of QT interval parameters in diabetic patients with arterial hypertension: importance of left ventricular mass and geometric patterns

The aim of the study was to assess the determinants of increased QT interval parameters in diabetic patients with arterial hypertension and, in particular, the strength of their relationships to echocardiographically derived left ventricular mass (LVM) and geometric patterns. In a cross-sectional study with 289 hypertensive type 2 diabetic outpatients, maximal QT and QTc (heart rate-corrected) intervals, and QT, QTc, and number-of-leads-adjusted QT interval dispersions were manually measured from standard baseline 12-lead ECGs. Electrocardiographic criteria for left ventricular hypertrophy (LVH) were either Sokolow-Lyon or Cornell sex-specific voltages. LVM and geometric patterns were determined by 2D echocardiography. Statistical analyses involved bivariate tests (Mann-Whitney, chi2, Spearman's correlation coefficients, ANOVA and receiver-operating-characteristic (ROC) curve analyses) and multivariate tests (multiple linear and logistic regressions). QT dispersion measurements showed significant correlations with echocardiographic LVM (r=0.26-0.27). ROC curves demonstrated a poor isolated predictive performance of all QT parameters for detection of LVH (areas under curve: 0.58-0.59), comparable to that of electrocardiographic voltage criteria. Only patients with concentric hypertrophy had significantly increased QT dispersion (QTd) when compared to those with normal geometries (64.24+/-21.09 vs 53.20+/-15.35, P<0.05). In multivariate analyses, both electrocardiographic and echocardiographic LVH were independent predictors of increased QTd, as well as only QTd and gender were determinants of LVM. In conclusion, increased QT interval dispersion is associated with LVM and concentric hypertrophy geometric pattern in diabetic hypertensive patients, although in isolation neither QTd nor any QT parameter presents enough predictive performance to be recommended as screening procedures for detection of LVH.     

氯沙坦对老年高血压病患者心室肥大和QTd的影响

目的　评价氯沙坦对老年原发性高血压病患者左心室肥大及 QT离散度 (QTd)的影响。方法　依据是否伴有左心室肥大 ,将 5 7例轻、中度高血压病患者分为两组 ,分别给予氯沙坦 5 0 mg/d,或氯沙坦 5 0 m g/d加双氢克尿噻12 .5 mg/d治疗 ,共 16～ 18周 ,比较两组治疗前后左心室大小 ,及 QTd改变 ,并分析 L VMI与 QTd的相关性。结果　治疗后高血压伴左心室肥大组 L VDd,IVST,PWT,L VMI比治疗前下降 (P<0 .0 5或 P<0 .0 1)。高血压伴左心室肥大组 QTd比不伴左心室肥大组大 (P<0 .0 1) ,治疗后则明显减小 (P<0 .0 1)。高血压伴左心室肥大组 L VMI与 QTd有较好的相关性。结论　氯沙坦或氯沙坦加双氢克尿噻能逆转老年高血压病患者的左心室肥大 ,并使 QTd相应减小。     

QT离散度与原发性高血压患者的相关性研究

目的探讨OT离散度（QTd）的变化对原发性高血压（EH）患者的临床意义。方法126例EH患者,其中72例伴左室肥厚（LVH）,54例左室正常;健康对照组40名。所有患者均进行体表心电图QT离散度测定及二维超声心动图检查。结果原发性高血压伴左室肥厚组QT离散度与左室正常组、对照组比较明显升高,差异有统计学意义（P〈0．01）,而原发性高血压左室正常组QT离散度与对照组比较差异无统计学意义（P〉0．05）。结论原发性高血压伴左室肥厚时QT离散度增大,表明QT离散度与原发性高血压左室肥厚密切相关。早期检测及时逆转左室肥厚,降低QT离散度对预防严重心律失常事件发生及改善患者预后具有重要的临床价值。     

Relationship between the elastic properties of aorta and QT dispersion in newly diagnosed arterial adult hypertensives.

OBJECTIVE: Afterload is increased in hypertensive patients and increased afterload associated with both ventricular repolarization inhomogeneity and impaired elastic properties of aorta. Thus, we investigated whether QT dispersion (QTd), which is a reflection of ventricular repolarization inhomogeneity, is related to aortic elastic properties in patients with hypertension. METHODS: Overall 113 patients with newly diagnosed hypertension and 25 normal control subjects were included in this cross-sectional case-controlled study. Aortic strain (AS) and aortic distensibility (AD) were calculated echocardiographically from the derived ascending aorta diameters. Electrocardiograms were recorded in all subjects, and QTd and corrected QTd (cQTd) were then calculated. RESULTS: Patients as compared with control subjects had lower mean AS and AD (p<0.001, for both). The QT interval maximum and corrected QT interval maximum durations, QTd and cQTd were increased in patients compared with control subjects. Multiple linear regression analysis showed that corrected QTd was independently related to age, left ventricular mass index (LVMI), AS and AD (b=0.204, p=0.030, b=0.219, p=0.026, b=-0.238, p=0.021 and b=-0.208, p=0.032 respectively) in hypertensive patients. The QTd was independently related to AS (p=0.043) and AD (p=0.037), as well as age (p=0.003) and LVMI (p=0.008). CONCLUSION: The QTd and cQTd were increased in hypertensives. Aortic elastic properties may play a role in increased dispersion of QT and cQT intervals.     

QT dispersion and left ventricular hypertrophy in athletes: relationship with angiotensin-converting enzyme I/D polymorphism

BACKGROUND: QT dispersion (QTd) is a measure of inhomogeneous repolarization of myocardium and is used as an indicator of arrhythmogenicity. QTd is increased in myocardial hypertrophy secondary to systemic hypertension. The relation between left ventricular (LV) enlargement in endurance trained subjects and QTd is unknown. The cloning of the angiotensin-converting enzyme (ACE) gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of this study was to assess whether physiologic left ventricular hypertrophy as a result of physical training is associated with an increased QT length or dispersion depending on ACE I/D polymorphism. METHODS: 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic and electrocardiographic examination, the QT interval was measured manually as an average based on a 12-lead ECG. We also analysed ACE I and D allele frequencies in all patients. RESULTS: Athletes had a significantly increased LV mass (235.1 +/- 68.5 g vs. 144.9 +/- 44.5 g, p < 0.001) and corrected QTd (QTcd) (55.5 +/- 18.1 ms vs. 42.9 +/- 17.2 ms, p < 0.001) in comparison to control subjects. There was a positive correlation between left ventricular mass index and QTcd in athletes (r = 0.3, p = 0.024). Left ventricular mass and mass index in ACE DD, DI and II genotypes were significantly different (p < 0.001). QTcd was significantly different between ACE DD (63.2 +/- 12.8 ms) and ACE II (44.9 +/- 17.6 ms) genotypes in athletes (p < 0.05). CONCLUSION: These data show that myocardial hypertrophy induced by exercise training might be associated with increased QTd as observed in systemic hypertension and might be affected by ACE I/D polymorphism.     

QT dispersion and hypertensive heart disease in the elderly

AIM: To determine the predictors and risk of increased QT dispersion in the elderly hypertensive patients. METHODS: A 12-lead electrocardiogram (ECG), M-mode echocardiography and ambulatory blood pressure as well as Holter monitoring were performed for 67 patients over 60 years of age with essential hypertension (I and II(o) WHO). The presence of ischaemic changes on ECG was evaluated based on the Minnesota Code. QT intervals were corrected with Bazett's formulae and QT dispersion was determined as the difference between maximal and minimal QTc intervals. Interventricular septal thickness (IVSTd), left ventricular internal diameter (LVDd) and posterior wall thickness (PWTd) were measured and left ventricular mass index (LVMI) was calculated. Subjects were divided according to the median of QTc dispersion (0.10 s). The differences between groups were assessed using chi-squared and Student's t-test. RESULTS: Subjects with increased QTc dispersion did not differ from those with low QTc dispersion when age, gender and body mass index were analysed. Similarly, the average systolic blood pressure, diastolic blood pressure and blood pressure variability were comparable in both groups. The mean QTc interval was similar in both groups. In patients with increased QT dispersion, left ventricular hypertrophy (LVH) and ischaemic changes on ECG were more frequently recognized (respectively 41.2 versus 18.2%, P < 0.001; 47.1 versus 21.2%, P < 0.05). Moreover, these subjects presented a significantly greater number of premature ventricular beats (317.1 +/- 665.6 versus 64.88 +/- 188.6, P < 0.05) and higher classes of Lown's arrhythmia scale (classes III-IV, 23.35% versus 9.1%). LVMI was insignificantly higher in the group with greater QTc dispersion (165.82 +/- 54.5 versus 145.07 +/- 36.47 g/ m2). Other echocardiographic indices of LVH were similar in both groups. On the other hand, the analysis of regression indicated positive correlation between the dispersion of QTc interval and thickness of left ventricle walls (for IVSd - r = 0.37; for PWd - r = 0.31), relative wall thickness (r = 0.28) and LVMI (r = 0.28). CONCLUSIONS: QTc dispersion is increased in the elderly hypertensive individuals, with the presence of LVH and myocardial ischaemia on ECG. These patients are more likely to demonstrate severe ventricular dysrhythmias.     

QT dispersion and characteristics of left ventricular hypertrophy in primary hypertension

The aim of the study was to evaluate the QT dispersion and the severity of arrhythmias in hypertensive patients according to the asymmetry of the left ventricular hypertrophy. The study group consisted of 47 hypertensive patients. In 24 of them the left ventricular hypertrophy was symmetrical (group I) and in 23--asymmetrical (group II). For the evaluation of the left ventricular hypertrophy its thickness was analyzed in 13 segments. The ratio between the maximum and minimum thickness from any location was determined as the asymmetry index (AI). The value of this index 1,3 distinguished between patients with the symmetrical and asymmetrical left ventricular hypertrophy. 20 healthy subjects were examined as a control group (group III). All subjects underwent physical examination, the standard 12-lead electrocardiogram (ECG), twenty-four hour Holter recording and echocardiography. All the results for the QT dispersion (QTd, QTdc, QTdR) were highest in group II, lower in patients from group I and the lowest were observed in the control group. The differences in all parameters between group I and II were statistically significant: for QTd--V p < 0.01, QTdc--p < 0.05, QTdR--p < 0.05. The differences between groups II and III as well as I and III were statistically significant for all QT dispersion parameters: for QTd--p < 0.001 and p < 0.01 respectively, QTdc--p < 0.001, QTdR--p < 0.001 for both groups. We have observed a very distinct positive correlation between the asymmetry index and QTd, QTdc, QTdR (p < 0.001). These values correlated also, but less distinctly with the left ventricular mass index--LVMI (p < 0.05). The frequency and severity of ventricular ectopic beats did not differ significantly between group I and II. The results obtained indicate the lack of connection between the frequency of ventricular premature complexes and (1) all QT dispersion parameters, (2) LVMI, (3) AI. Supraventricular premature complexes occurred significantly more frequently in patients with the asymmetrical left ventricular hypertrophy compared to the group with the regular left ventricular hypertrophy (p < 0.05) and control group (p < 0.01). CONCLUSIONS: The left ventricular hypertrophy in primary hypertension may increase the QT dispersion. It seems that asymmetry of the left ventricular hypertrophy reinforces this increase. The increased QT dispersion in primary hypertension does not influence significantly the occurrence of ventricular arrhythmias.