高血压病左室肥厚与QTc离散度关系的研究

目的 探讨高血压病病左室肥厚（ＬＶＨ）与非在室肥厚（ＮＬＶＨ）患者ＱＴｃｄ的关系及临床意义。方法 用分层抽样法测定１０３例原发性高血压病患者住院首次１２导联心电图ＱＴｃ离散度（ＱＴｃｄ）其中合并ＬＶＨ患者５７例，合并ＮＬＶＨ患者４６例，并与２０例健康人作对照，结果 ＱＴｃｄＬＶＨ组分别与ＮＬＶＨ组，对照组比较均有非常显著性差异（Ｐ〈０．０１）ＮＬＶＨ组与对照组比较无显著性差异（Ｐ〉０．０５）。结论     

围绝经期及其前后妇女QTcd离散度的研究

目的探讨绝经后妇女冠心病及心血管事件发生率升高的相关机制.方法分别测量42例围绝经期前健康妇女(Ⅰ组,平均年龄41.40±0.92岁)、43例围绝经期健康妇女(Ⅱ组,平均年龄45.5±4.32岁)、40例绝经后健康妇女(Ⅲ组,平均年龄51.45±7.26岁)的校正QT离散度(QTcd)和性激素(SH)水平,研究其变化规律和相互关系.结果绝经后妇女的QTcd与围绝经期前妇女的QTcd相比略有延长,尚无显著性差异;而围绝经期妇女的QTcd与围绝经期前妇女的QTcd相比延长明显,有显著性差异.结论围绝经期妇女SH紊乱导致心肌电不稳定性增高,是除了脂代谢异常之外的导致冠心病发病率升高及心血管事件发生率升高的机制之一.     

QT and RR intervals in conscious and anesthetized guinea pigs with highly varying RR intervals and given QTc-lengthening test articles.

A facile system for obtaining electrocardiograms from conscious animals was used to conduct studies on 12 animals studied both conscious and anesthetized, on 4 conscious animals given vehicle (0.5% methylcellulose) and QT-lengthening test articles, and on 6 animals given test articles thought to not lengthen QTc. In 12 animals whose ECGs were monitored via a bipolar transthoracic ECG, heart rates were slowed with 1.0 mg/kg zatebradine, while they were conscious in their slings, and after being anesthetized with ketamine/xylazine. The following regression equations were obtained relating QT to RR: QT = 44.7 ln RR - 132.9, r2 = 0.7, for conscious animals; QT = 79.4 ln RR - 287.4, r2 = 0.8 for anesthetized animals, with RR intervals varying between 150 and 550 ms. The anesthetic increases QT at all RR intervals (p < 0.001), but does not change the slope of the relationship between QT and RR when compared with the conscious guinea pig. The Fridericia method was best for correcting QT for RR interval in conscious guinea pigs, but the Bazett method was best for correcting in anesthetized animals. QTc lengthened significantly in all conscious guinea pigs given, orally, cisapride, ketoconazole, and sotalol (positive test articles) and did not change with methylcellulose (the vehicle) or with propranolol, verapamil, or enalapril (negative controls). These techniques and relationships demonstrate that this methodology may be useful in exploring torsadogenic effects of novel pharmacological entities.     

Prevalence and Risk Factors of Prolonged QTc Interval in HIV-Infected Patients: Results of the HIV-HEART Study

Abstract

Background: Corrected QT (QTc) prolongation is predictive of cardiovascular mortality in both the general and human immunodeficiency virus (HIV) populations. Objective: As part of the HIV-HEART study, we assessed the prevalence and risk factors of a prolonged QTc interval in patients with HIV infection. Methods: In this cross-sectional cohort study, 802 unselected HIV-infected patients were included. Data were analyzed by the use of gender-specific QTc categories (men abnormal at > 440 ms and women abnormal at >460 ms). Multiple variables related to infection and treatment were collected. Results were analyzed with a multivariable model. Results: The QTc interval was found to be prolonged in 154 patients (19.8%; 95% CI 17–23). The mean (±SD) QTc in men (n = 142) presenting with a prolonged QTc interval was 456 ± 16.3 ms (range 441–548 ms).The mean (±SD) QTc in women (n = 12) presenting with a prolonged QTc interval was 479 ± 9 ms (range 465–498 ms). In the multivariable model, female gender, diabetes mellitus, and arterial hypertension were associated with prolonged QTc. There were no parameters related to HIV independently associated with QT interval prolongation. In particular, no anti-HIV drug was associated with QTc prolongation. Conclusions: Our study demonstrated that in an HIV-infected population, QTc prolongation had a high prevalence of nearly 20% compared to the general population and was possibly influenced by common factors like gender, diabetes, and arterial hypertension.     

Clinical and therapeutic aspects of congenital and acquired long QT syndrome.

The long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram. It is associated with precipitation of a polymorphic ventricular tachycardia, torsade de pointes, which may cause sudden death. The syndrome is a disorder of cardiac repolarization caused by the alterations in the transmembrane potassium and sodium currents. Six genetic loci for the congenital forms of the syndrome have been identified; sporadic cases occur because of spontaneous mutations. Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. Clinical symptoms are the result of the precipitation of torsade de pointes and range from such minor symptoms as dizziness to syncope and sudden death. Short-term treatment is aimed at preventing the recurrences of torsade de pointes and includes intravenous magnesium and potassium administration, temporary cardiac pacing, and correction of electrolyte imbalance; rarely, intravenous isoproterenol is indicated. Long-term management includes use of beta-blockers, permanent pacemaker placement, and cardioverter-defibrillator implantation. Asymptomatic patients are treated if under the age of 40 years at the time of diagnosis.     

多巴酚丁胺负荷试验QTcd对冠心病的诊断价值

目的探讨多巴酚丁胺负荷试验前、后冠心病与非冠心病患者QTc散离度(QTcd)的变化,评估多巴酚丁胺负荷试验QTcd对冠心病的诊断价值。方法测量选择性冠脉造影证实的30例冠心病与20例非冠心病患者试验前、后QTcd值,并比较分析。结果冠心病组多巴酚丁胺负荷试验终点QTcd明显高于试验前QTcd(P<0.01),非冠心病组无明显差异(P>0.05)。多巴酚丁胺负荷试验终点QTcd≥55ms诊断冠心病的敏感性、特异性、准确性分别为83.3%、85%、84%,QTcd≥10ms(86.7%、85%、86%)高于传统试验ST段压低诊断冠心病的价值(56.7%、50%、54%)(P<0.05)。结论多巴酚丁胺负荷试验QTcd、QTcd可提高冠心病的诊断价值,是一种安全、简便、有效的无创检查方法。     

Prolongation of QTc interval: relationship with etiology and severity of liver disease,mortality and liver transplantation

Background: A prolonged QTc interval has been reported in patients with liver disease. The objectives of our study were to determine whether a prolonged QTc interval was an independent predictor of mortality in patients with cirrhosis and to examine the effect of liver transplantation (LT) on QTc interval. Patients and methods: We retrospectively studied two cohorts of patients – QTc interval was measured in 409 patients (pre‐transplant group), and in 162 patients (transplant group) before and 6 months after LT. QT interval (mean) corrected (QTc) for ventricular rate was read from a 12‐lead EKG. Patients with known cardiovascular disease or other risk factors that are known to cause a prolonged QTc interval were excluded. Results: Pre‐transplant group. One hundred and sixty‐two patients (40%) had a prolonged QTc interval (>440 ms). By binary logistic regression, age (P=0.005), alcoholic cirrhosis (P=0.007) and Child–Pugh scores (P=0.007) were independent predictors of prolonged QTc interval. Sixty‐six patients died during a mean follow‐up of 8.9 years. Although the Kaplan–Meier survival curve showed a lower survival in patients with a prolonged QTc interval (P=0.03 by log rank test), when survival was adjusted for the Child–Pugh score by Cox regression survival analysis, there were no survival differences in patients with and without prolonged QTc interval. Cox regression analysis showed that the Child–Pugh score (hazard ratio 1.5, CI 1.3–1.6, s<0.001) was the only independent predictor of survival. Transplant group. In this cohort, 91 patients (56%) had prolonged QTc (>440 ms) before LT. Mean QTc improved significantly after LT (429 ± 29 ms vs. 450 ± 39 ms P<0.002). Of the 91 patients with prolonged QTc, 50 (55%) normalized, three (3.3%) remained unchanged, 12 (13.3%) showed further prolongation, and 26 (28%) showed improvement but remained above normal limits. An additional nine patients who had normal QTc before LT developed prolonged QTc (>440 ms) after LT. Conclusion: A prolonged QTc interval was common in patients with cirrhosis, but its presence had no independent effect on mortality. Prolonged QTc returns to normal values in about half of the patients after LT, suggesting that liver disease plays a role, but may not be the only factor in the pathogenesis of prolonged QTc.     

Long QT syndrome

The hereditary long QT syndrome (LQTS) is a genetic channelopathy with variable penetrance that is associated with increased propensity to syncope, polymorphous ventricular tachycardia (torsades de pointes), and sudden arrhythmic death. This inherited cardiac disorder constitutes an important cause of malignant ventricular arrhythmias and sudden cardiac death in young individuals with normal cardiac morphology. Risk assessment in affected LQTS patients relies upon a constellation of electrocardiographic, clinical, and genetic factors. Administration of beta-blockers is the mainstay therapy in affected patients, and primary prevention with an implantable cardioverter defibrillator or left cervicothoracic sympathetic denervation are therapeutic options in patients who remain symptomatic despite beta-blocker therapy. Accumulating data from the International LQTS Registry have recently facilitated a comprehensive analysis of risk factors for aborted cardiac arrest or sudden cardiac death in pre-specified age groups, including the childhood, adolescence, adulthood, and post-40 periods. These analyses have consistently indicated that the phenotypic expression of LQTS is time dependent and age specific, warranting continuous risk assessment in affected patients. Furthermore, the biophysical function, type, and location of the ion-channel mutation are currently emerging as important determinants of outcome in genotyped patients. These new data may be used to improve risk stratification and for the development of gene-specific therapies that may reduce the risk of life-threatening cardiac events in patients with this inherited cardiac disorder.