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.     

Relation of QT interval and QT dispersion to echocardiographic left ventricular hypertrophy and geometric pattern in hypertensive patients. The LIFE study. The Losartan Intervention For Endpoint Reduction

OBJECTIVE: In hypertensive patients, left ventricular hypertrophy (LVH) predicts increased mortality, in part due to an increased incidence of sudden death. Repolarization-related arrhythmogenesis may be an important mechanism of sudden death in hypertensive patients with LVH. Increased QT interval and QT dispersion are electrocardiographic (ECG) measures of ventricular repolarization, and also risk markers for ventricular tachyarrhythmias. We assessed the relation of QT intervals and QT dispersion to echocardiographically determined left ventricular (LV) mass and geometry in a large population of hypertensive patients with ECG evidence of LVH. METHODS: QT intervals and QT dispersion were determined from baseline 12-lead ECGs in 577 (57% male; mean age 65 +/- 7 years) participants in the LIFE study. LV mass index (LVMI) and geometric pattern were determined by echocardiography and QT interval duration and QT dispersion were assessed in relation to gender-specific LVMI quartiles. RESULTS: In both genders, increasing LVMI was associated with longer rate-adjusted QT intervals. QT dispersion measures showed a weaker association with LVMI quartiles. Both concentric and eccentric LVH were associated with increased QT interval duration and QT dispersion. These relations remained significant after controlling for relevant clinical variables. CONCLUSIONS: In hypertensive patients with ECG evidence of LVH, increased LVMI and LVH are associated with a prolonged QT interval and increased QT dispersion. These findings suggest that an increased vulnerability to repolarization-related ventricular arrhythmias might in part explain the increased risk of sudden death in hypertensive patients with increased LV mass.     

高血压伴左心室肥厚与T波顶峰后宽度的关系

目的探讨高血压左心室肥厚(LVH)患者T波顶峰后宽度(TpTe间期)的改变及其临床意义。方法随机抽取2010-10-2011-06桂林医学院附属医院心内科住院的原发性高血压(EH)患者313例,根据超声心动图(UCG)测定的左心室质量指数(LVMI)分为LVH组和非LVH(NLVH)组。比较两组TpTe间期、校正TpTe间期(TpTec)、QT间期、校正QT间期(QTc)、QRS时限、LVMI、左心室舒张末期内径(LVEDD)、室间隔厚度(IVST)、左心室后壁厚度(LVPWT)的改变及其相互关系;比较不同血压水平对TpTe间期的影响;EH患者左心室不同构型TpTe间期改变的特点。结果与NLVH组比较,LVH组TpTe间期[(100.0±23.3)比(85.3±14.1)ms]、TpTec[(108.6±26.7)比(91.4±15.4)ms]、QTc[(435.0±23.6)比(420.0±23.5)ms]、QRS时限[(105.3±22.3)比(95.6±16.1)ms]均延长(均P<0.01),LVMI[(142.8±29.3)比(82.5±19.0)g/m2],LVEDD[(58.9±7.5)比(47.6±6.5)cm],IVST[(9.7±1.0)比(8.8±1.2)cm],LVPWT[(9.4±1.1)比(8.5±1.1)cm]明显增大(均P<0.01),QT间期延长,但差异无统计学意义。TpTe间期在不同左心室构型间的改变为:离心型肥厚>向心性肥厚>左心室游离壁肥厚>正常心室形态。Pearson相关分析表明,TpTe间期、TpTec与LVMI(r=0.43,0.44)、LVEDD(r=0.41,0.43)呈正相关(P<0.05)。多元线性回归分析显示,LVMI、LVEDD是TpTe间期重要的影响因素(β=0.026、0.280)。结论 TpTe间期可作为评价高血压伴左心室肥厚靶器官损害程度的心电学指标之一。     

Ventricular repolarization is prolonged in nondipper hypertensive patients: role of left ventricular hypertrophy and autonomic dysfunction

OBJECTIVE: The aim of this study was to investigate the influence of circadian behavior of blood pressure, left ventricular hypertrophy, and autonomic function on QTc interval duration in untreated hypertensive patients. DESIGN: Hypertensive patients underwent simultaneous blood pressure and ECG 24-h ambulatory monitoring. Patients were classified into two groups on the basis of a lack of nocturnal fall in blood pressure, as dippers and nondippers. A group of normotensive healthy subjects was studied as controls. METHODS: QT and QTc intervals were automatically computed and spectral analysis was applied to RR interval time series from the same electrocardiogram (ECG) recordings. Left ventricular mass index (LVMI) was computed by echocardiogram. RESULTS: No difference among the three groups was found concerning mean values and circadian pattern of heart rate; by contrast, QTc was significantly longer in nondippers compared to dippers or to normotensive subjects, particularly at night-time, whereas all groups exhibited similar circadian variations in heart rate. Compared to dippers, nondippers showed significantly higher LVMI, which positively correlated with QTc, and parasympathetic withdrawal, which negatively correlated with QTc. CONCLUSIONS: Nondippers show a prolonged ventricular repolarization throughout the 24-h period, absent either in dippers or normotensives. The association of left ventricular hypertrophy and vagal deactivation may lead to prolongation of QTc, potentially facilitating ventricular arrhythmias in nondipper hypertensive patients.     

QTc dispersion and complex ventricular arrhythmias in untreated newly presenting hypertensive patients.

Increased dispersion of ventricular repolarisation (increased QT dispersion) is believed to predispose to arrhythmias associated with sudden death in certain cardiac diseases. Hypertension is also associated with increased risk of sudden death, particularly in those with left ventricular hypertrophy (LVH). Therefore, the first aim of this study is to look into the possible pathogenic role of QT dispersion on the ventricular arrhythmias occurring in a group of never-treated hypertensive patients. The second aim is to look at other possible determinants of QT dispersion (ie, level of blood pressure, hypokalaemia, electrocardiographic LVH and presence or absence of strain pattern) in hypertensive patients, and their relevance to complex ventricular arrhythmias. QTc (corrected QT) was measured in 70 newly presenting (never-treated) hypertensive patients (47 male, 23 female, mean age 51.9 +/- 12.5 years) from a standard 12-lead surface electrocardiogram (ECG). Blood pressure measurements and 24-h ECG holter recordings were performed in all patients. Serum potassium level was measured in 51 of the patients. Ventricular arrhythmias were classified using a modified Lown's scoring system. Maximum QTc, minimum QTc and QTc dispersion for all patients were 442 +/- 30.3 ms, 380 +/- 26.7 ms and 61.5 +/- 21.6 ms respectively. High grade ventricular arrhythmias (Lown's score >/=3) were found in 43% of the patients. The QTc dispersion was strongly correlated with the Lown's classification of arrhythmia and the age of the patients. Patients with more severe ectopy (Lown's score >/=3) were significantly older (57.4 +/- 10.3 years) compared to those with score /=3 Lown's score compared to 39% in the group with LVH but without strain. In the presence of relative hypokalaemia, hypertensive patients with LVH showed more QTc dispersion (85.7 +/- 15.5 ms) and a greater tendency for complex ventricular arrhythmias (100% grade >/=3 Lown's score) compared to those with LVH and normal serum potassium levels (64.1 +/- 22.6 ms and 35%, QTc dispersion and Lown's score >/=3, respectively P = 0. 05). The level of blood pressure had no effect on either the QTc dispersion or the prevalence of complex ventricular arrhythmias. Prevalence of complex ventricular arrhythmias in hypertensive patients is strongly correlated with QTc dispersion and age. When hypertensive patients with LVH have low potassium levels the risk of developing complex ventricular arrhythmias is significantly increased.     

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.     

伴左心室肥厚高血压病人的QT离散度变化

目的观察高血压左心室肥厚者的ＱＴ离散度变化及与左心室肥厚程度的关系。方法１０５例高血压病人和４５例正常人均进行体表心电图和超声心动图检查,测量ＱＴ离散度（ＱＴｄ）和改良法校正的ＱＴ离散度（ＱＴｌｃｄ）。结果高血压左室肥厚组（ｎ＝４２）的ＱＴｄ和ＱＴｌｃｄ明显大于正常对照组（ｎ＝４５）和高血压无左室肥厚组（ｎ＝６３）。高血压病人的ＱＴｄ和ＱＴｌｃｄ与左室心肌重量指数（ＬＶＭＩ）呈正相关（ｒ＝０．４６７,Ｐ＜０．００１;ｒ＝０．４６９,Ｐ＜０．００１）。结论高血压左室肥厚者的ＱＴ离散度增加且与左室肥厚的程度正相关     

Left ventricular hypertrophy in patients with autonomic failure

BACKGROUND: In autonomic failure (AF), supine hypertension may predispose patients to end-organ damage. The pathophysiology of hypertensive heart disease in AF is not known. The aim of the present study was to evaluate the prevalence and predisposing factors of left ventricular hypertrophy (LVH) in patients with AF. METHODS: We studied 25 patients with AF (67 +/- 8 years); 80% were being treated for orthostatic hypotension. Twenty patients with essential hypertension (68 +/- 6 years) were considered as the control group. All subjects underwent echocardiography for measurement of left ventricular mass (LVM). The patients with AF underwent a 24-h BP monitoring and long-term blood pressure (BP) variability was calculated as standard deviation (SD) of the average of the half-hour mean values. RESULTS: The LVM is comparable in patients with AF and hypertensive controls (145 +/- 35 g/m2 v 127 +/- 32 g/m2, P = .07). The proportion of patients with LVH is similar in both populations (AF 80%, hypertensive 70%). The patients with AF were divided into two groups, with and without LVH. The SDs are significantly higher in AF patients with LVH than in those with normal LVM (SD 24-h systolic BP: 22 +/- 4 v 14 +/- 1 mm Hg, P = .001). CONCLUSIONS: A high proportion of patients with AF show LVH. The LVM values are comparable with those of patients with essential hypertension. The development of LVH seems to depend on high BP variability, characteristic of AF patients. Detection of LVH may help in the choice of treatment for orthostatic hypotension and in the prevention of heart failure.     

Predictors of sudden cardiac death in never previously treated patients with essential hypertension: long-term follow-up

Increased QT dispersion has been associated with ventricular arrhythmia and sudden death in a variety of cardiac disorders. Left ventricular hypertrophy (LVH) has also been associated with increased incidence of sudden cardiac death in patients with essential hypertension. Furthermore, patients with essential hypertension, particularly those with LVH, are more likely to develop ventricular arrhythmias than are the normal population. The relationship between LVH, QT dispersion, complex ventricular arrhythmia and sudden cardiac death in previously untreated patients over long-term follow-up in hypertension has not been reported before and is the purpose of this study. Fifty-nine adult subjects with essential hypertension, who had never been previously on antihypertensive treatment were followed up for a total of 119.2 +/- 26.2 months. QTc (corrected QT), blood pressure, electrocardiograms, and 24-h Holter ECG recordings were performed in all patients at the time of entry to the study. Ventricular arrhythmias were classified using a modified Lown's scoring system. During the follow-up period death occurred in 12 cases (20%) of which only six (10%) deaths were sudden. The findings of this study indicate that LVH and complex ventricular arrhythmias (Lown's score > or =3) are the only significant predictors of sudden death. Although patients who died suddenly had higher systolic and diastolic blood pressures and greater QTc dispersion compared to surviving patients, this difference was statistically not significant. Similarly, when those who died suddenly were compared to those non-cardiac deaths, LVH and complex ventricular arrhythmias were the only significant predictors of sudden death. In spite of increased QTc dispersion in hypertensive patients, this finding was not associated with increased risk of sudden death and only LVH and high grade ventricular arrhythmias identified hypertensive patients at risk of sudden cardiac death over a 10-year follow-up period.     

QT dispersion intervals in hypertensives with left ventricular hypertrophy

Left ventricular hypertrophy is an important risk factor of cardiovascular complications during the course of hypertension. Increased QT dispersion is associated with sudden cardiac death in congestive heart failure and in other cardiovascular diseases. Our aim was to compare QT dispersion from routine ECG in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Authors examined 71 hypertensives treated in our medical department. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. QT dispersion was defined from routine ECG (QTmax - QTmin). Presence of LVH was found in 26 patients (mean age 59.3 years), absence of LVH in 45 patients (mean age 57.8 years). Hypertensives with secondary hypertension, hypertrophic cardiomyopathy, sings of ischemia in ECG, arrhythmias, myocardial infarction, heart failure, diabetes mellitus and patients treated by antiarrhythmic drugs of the Ic and III groups were excluded. Both groups of hypertensives were matched by demographic parameters, and by the presence of hypertension, obesity, hyperlipidemia and smoking habites. There were statistically significant longer QT dispersion and QTc dispersion (59.0 +/- 20.1 ms, 64.0 +/- 23.7 ms) in LVH-positive patients than in LVH-negative once (43.2 +/- 9.5 ms, 48.4 +/- 11.1 ms). Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease. Authors recommend to look after left ventricular hypertrophy presence in hypertensives as it carries much more complicated course of the disease. Measurment of QT dispersion adds farther stratificational information to these patients.     

Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular Hypertrophy

Objective: The objective of this article is to assess whether left ventricular hypertrophy (LVH) due to physical training or of hypertensive patients shows similarities in QT length and QT dispersion. Methods: A total of 51 subjects were studied: 17 essential hypertensive patients (27.7 ± 5.6 years), 17 athletes involved in agonistic activity (canoeing) (24.8 ± 6.1 years), and 17 normotensive healthy subjects as control group (24.8 ± 3.6 years). The testing protocol consisted of (1) clinic BP measurement, (2) echocardiography, (3) 12‐lead electrocardiographic examination (QT max, QTc max, QT min, QTc min, ΔQT, ΔQTc). Results: There were no significant differences between the body surface area, height, and age of the three groups. Clinic blood pressure was higher in hypertensives (146.5 ± 45.2/93.5 ± 4.9 mmHg) versus athletes (120.9 ± 10.8/77.1 ± 6.0 mmHg) and controls (123.5 ± 4.8/78.8 ± 2.9 mmHg) by definition. Indexed left ventricular mass (LVM/BSA) was significantly greater in both athletes (148.9 ± 21.1 g/m²) and hypertensives (117.1 ± 15.2 g/m²) versus controls (81.1 ± 14.5 g/m²; P < 0.01), there being no statistical difference among them. LVH (LVMI > 125 g/m²) was observed in all athletes, while the prevalence in hypertensives was 50%. In spite of this large difference in cardiac structure there were no significant differences in QT parameters between athletes and the control group, while hypertensive patients showed a significant increase in QT dispersion versus the two other groups (ΔQT 82 ± 2.1, 48 ± 1.3, 49 ± 2.3 ms; P < 0.01; ΔQTc 88 ± 2.0, 47 ± 1.4, 54 ± 2.7; P < 0.01). Conclusions: LVH induced by physical training activity is not associated with an increase in QT dispersion, whereas pathological increase in LVM secondary to hypertension is accompanied by an increased QT dispersion.     

Relationship between left ventricular mass index and 24-h urinary free cortisol and cortisone in essential arterial hypertension

OBJECTIVE: Besides arterial blood pressure, nonhemodynamic factors are known to induce cardiac hypertrophy. In Cushing's syndrome, severe ventricular hypertrophy has been linked not only to increased aortic pressure, but also to elevated plasma cortisol. The aim of this study was to examine the relationship between the cortisol/cortisone levels and left ventricular mass index (LVMI) in essential arterial hypertension with and without echocardiographic left ventricular hypertrophy (LVH). DESIGN: Eighteen untreated Caucasian patients (nine men, nine women, mean age 48+/-6 years) with essential hypertension (163+/-26/100+/-14 mm Hg) were enrolled. An age-matched control group of 13 subjects (seven men, six women) with normotension (121+/-9/79+/-7 mm Hg) were enrolled also. Left ventricular dimensions were echocardiographically assessed and cortisol production evaluated by 24-h urinary free cortisol and cortisone concentrations. RESULTS: LVMI averaged 115+/-31 g/m2 and 24-h urinary free cortisol and cortisone were 23+/-14 microg per 24 h and 31+/-18 microg per 24 h. Prevalence of echocardiographic LVH was 56%. LVMI correlated significantly with 24-h urinary free cortisol (r = 0.61, P = 0.007) and cortisone (r = 0.60, P = 0.009). Patients with echocardiographic LVH were characterized by higher daytime ambulatory blood pressure, LVMI (particularly the posterior wall), and 24-h urinary cortisol, while office blood pressure, septal: posterior wall ratio and 24-h urinary cortisone were comparable in all patients. In control individuals, LVMI averaged 91+/-18 g/m2 and 24-h urinary free cortisol and cortisone, respectively, were 34.7+/-6.6 microg per 24 h and 64.3+/-10.8 microg per 24 h (P<0.05 versus patients). Neither LVMI nor the contributing ventricular dimensions showed significant correlation with 24-h urinary free cortisol or cortisone in the control group. CONCLUSIONS: Our data provide evidence for a significant relationship between LVMI and cortisol production independently of arterial blood pressure in untreated mild to moderate hypertension.     

The ACE/DD genotype is associated with the extent of exercise-induced left ventricular growth in endurance athletes

OBJECTIVES: We studied the impact of the angiotensin-converting enzyme (ACE)/DD genotype on morphologic and functional cardiac changes in adult endurance athletes. BACKGROUND: Trained athletes usually develop adaptive left ventricular hypertrophy (LVH), and ACE gene polymorphisms may regulate myocardial growth. However, little is known about the impact of the ACE/DD genotype and D allele dose on the cardiac changes in adult endurance athletes. METHODS; Echocardiographic studies (including tissue Doppler) were performed in 61 male endurance athletes ranging in age from 25 to 40 years, with a similar period of training (15.6 +/- 4 h/week for 12.6 +/- 5.7 years). The ACE genotype (insertion [I] or deletion [D] alleles) was ascertained by polymerase chain reaction (DD = 27, ID = 31, and II = 3). Athletes with the DD genotype were compared with their ID counterparts. RESULTS: The DD genotype was associated with a higher left ventricular mass index (LVMI) than the ID genotype (162.6 +/- 36.5 g/m(2) vs. 141.6 +/- 34 g/m(2), p = 0.031), regardless of other confounder variables. As a result, 70.4% of DD athletes and only 42% of ID athletes met the criteria for LVH (p = 0.037). Although systolic and early diastolic myocardial velocities were similar in DD and ID subjects, a more prolonged E-wave deceleration time (DT) was observed in DD as compared with ID athletes, after adjusting for other biologic variables (210 +/- 48 ms vs. 174 +/- 36 ms, respectively; p = 0.008). Finally, a positive association between DT and myocardial systolic peak velocity (medial and lateral peak S(m)) was only observed in DD athletes (p = 0.013, r = 0.481). CONCLUSIONS: The ACE/DD genotype is associated with the extent of exercise-induced LVH in endurance athletes, regardless of other known biologic factors.     

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.     

依那普利对高血压病左心室肥厚患者QT离散度的影响

目的　研究长期使用依那普利治疗高血压病合并左心室肥厚时对QT离散度的影响。方法　 2 4例高血压病 (EH)合并左心室肥厚 (LVH)者 ,服用依那普利 (10mg 1次 /d) 3年 ,用标准 12导联心电图测量QT间期、校正的QT间期 (QTc)、QT间期离散度 (QTd)及校正的QT间期离散度 (QTcd) ;用二维及M型超声心动测定有关心血管参数。结果　依那普利不仅能迅速降压 ,而且能逐渐降低左心室重量指数 (LVMI)达 3 9% (P <0 .0 0 1) ,显著提高左心室泵血功能 ;同时明显缩短QTd[从 (61± 2 1)到 (41± 15 )ms、QTcd从 (67± 2 7)到 (46± 18)ms] ,QT及QTc也同样明显缩短。结论　长期用依那普利治疗EH合并LVH ,能明显使患者左心室肥厚回缩 ,提高其左心室收缩功能 ,并通过降低QTd及QTcd ,进一步降低室性心律失常发生率 ,从而改善预后。     

Left ventricular hypertrophy and QT interval in obesity and in hypertension: effects of weight loss and of normalisation of blood pressure

BACKGROUND: Left ventricular hypertrophy (LVH) and prolonged QT interval at ECG (QTc) are common in both obesity and arterial hypertension (AH), and are risk factors for cardiovascular disease and sudden death. METHODS: We compared the frequencies of LVH (ECG criteria) and QTc in obese-AH (n=41), in normotensive obese (n=75), in lean-AH (n=30), and in lean controls (n=68) comparable for age and sex; in obese patients, LVH and QTc were evaluated under basal conditions and 1 y later, that is, after a significant weight loss induced by bariatric surgery. RESULTS: LVH was more frequent, and QTc was longer, in obese-AH, in normotensive obese, and in lean-AH than in lean controls; after weight loss, frequency of LVH decreased in obese subjects becoming normotensive (n=87), not in obese subjects remaining hypertensive (n=29), while QTc decreased in all obese subjects. CONCLUSION: Weight loss can effectively reduce QTc; when concomitant AH disappears, weight loss can also reduce the prevalence of LVH. In obese patients remaining hypertensive, aggressive pharmacological treatment is therefore indicated to correct LVH.     

原发性高血压病人QT间期离散度与左室肥厚关系研究

目的：探讨原发性高血压病人左室重量与QT间期离散度的关系。方法：测定82例原发性高血压病人血压,计算QT间期离散度（QTcd)及QTcd%变化与左室重量指数（LVMI）的关系,结果：高血压伴左室肥厚（LVH）组的QTcd及QTcd^均明显高于无LVH组的;QTcd及QTcd%随LVMI增高而增高（r=0.7718,r=0.6798),但与血压无明显相关性,结论：高血压病人QTcd的增加不是血压变化结果,而是左室肥厚所致。     

Ethnic and gender differences in electrocardiographic QT length and QT dispersion in hypertensive subjects

BACKGROUND: Prolonged QT intervals and/or increased QT dispersion (QTd) are associated with various pathological conditions and predict death in healthy individuals. Among hypertensives, QTd correlates with blood pressure (BP) and left ventricular mass index (LVMI) and QT intervals are prolonged in those with left ventricular hypertrophy (LVH). In normotensives, heart-rate corrected QT length (QTc) is longer in females than males, but QTd is greater in males than females. There are few data comparing QT parameters between different ethnic groups and none specifically in hypertensives. Among normotensives, compared with whites, QTc is reported to be shorter in African-Americans and longer in Chinese. We looked for ethnic and gender differences in QT parameters in hypertensive subjects. METHODS: Untreated hypertensives were selected from a Hypertension Clinic database. Black and white subjects were matched for age, sex, BP and LVMI. Male and female subjects were matched for age, race, BP and the presence or absence of echocardiographic LVH. Maximum QT intervals (QTm), rate-corrected maximum QT intervals (QTc) and QT dispersion (QTd) were measured or calculated from ECGs. Data are presented as mean +/- s.d. Differences in QT parameters were sought between groups using Student's t-tests. RESULTS: No ethnic or gender differences in QT parameters achieved statistical significance. However there was a tendency for QTm and QTc to be prolonged in blacks compared with whites (443 +/- 52 vs 421 +/- 47; P = 0.08 and 480 +/- 65 vs 463 +/- 40: P = 0.24 respectively), and for QTc to be prolonged in females compared with males (479 +/- 52 vs 461 +/- 45 ms; P= 0.13). CONCLUSION: In small groups of matched hypertensives, no ethnic or gender differences in QT parameters achieved statistical significance. However, similar to findings in normotensives, QTc tended to be longer in hypertensive females than males. In hypertensives, we failed to confirm the finding that QTc is shorter in blacks than whites, as seen in US normotensives. Whether this represents a difference between hypertensives and normotensives, or between US and UK blacks requires further investigation. Whether the prognostic significance of QT parameters in hypertensives differs between different gender and ethnic groups needs to be established from prospective studies. Journal of Human Hypertension (2000) 14, 403-405     

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.     

Relation between stage of left ventricular diastolic dysfunction and QT dispersion

OBJECTIVE: In 30-40% of patients with clinical heart failure diastolic dysfunction is present although systolic function is normal. Evaluation of diastolic functions are important for the patient's early diagnosis, treatment and prognosis. QT dispersion is an important parameter that reflects heterogeneity of ventricular repolarization and predicts ventricular arrhythmia and sudden death. According to several studies, QT dispersion is significantly increased in patients with diastolic dysfunction due to ischemic heart disease and left ventricular hypertrophy compared to the patients without diastolic dysfunction. However, a study about the relation between the stage of left ventricular diastolic dysfunction and QT dispersion is not present. The aim of this study was to investigate the correlation between the stage of left ventricular diastolic function determined by transthoracic echocardiography and QT dispersion. METHODS AND RESULTS: In our study the left ventricular diastolic functions of 80 patients were evaluated by transthoracic echocardiography. Eighty patients were divided to four stages each containing 20 patients. Stage 0 was defined as normal, stage 1 as prolonged relaxation pattern, stage 2 as pseudonormal pattern and stage 3 as restrictive pattern. We measured QT dispersion (QT D) and corrected QT dispersion (QTc D) values according to Bazzet's formula in their ECGs. QT D and QTc D were found 20+/-8 ms vs. 26+/-1 ms in normal patients, 25+/-8 ms vs. 37+/-9 ms in the patients with prolonged relaxation pattern, 28+/-10 ms vs. 38+/-11 ms in the patients with pseudonormal pattern and 38+/-13 ms vs. 41+/-14 ms in the patients with restrictive pattern. A significant direct relation was found between the stage of left ventricular diastolic function and QT, QTc dispersion (p<0.01). Furthermore, when classified according to the aetiology of the left ventricular diastolic dysfunction (stage 1, 2, 3) QT D and QTc D were 24+/-6 ms vs. 32+/-9 ms in the patients with left ventricular hypertrophy (LVH), and 32+/-9 ms vs. 41+/-12 ms in the patients with ischaemic heart disease (IHD). The differences between the two groups were statistically significant (p<0.01). CONCLUSIONS: These findings show that QT D and QTc dispersion values increase in relation to increasing left ventricular diastolic functional stage that is determined by echocardiography and that the patients with ischaemic heart disease have much more increased QT values than the patients with left ventricular hypertrophy.