慢性肾衰规律血透患者QT间期离散度与室性心律失常的相关性研究

目的 研究65例慢性肾衰竭行规律血液透析的患者透析前后QT间期离散度(QTd)的变化以及QTd与室性心律失常的关系.方法 65例血透患者分为有室性心律失常组及无室性心律失常组,记录患者透析前及透析后心电图并计算QTd值,同时记录临床参数并检测相关实验室指标,最后进行统计学分析处理.结果 存在室性心律失常的血透患者较无室性心律失常患者透析前QTd显著增高(P＜0.01);透析后QTd较透析前明显增加(P＜0.01);透析后QTd的增加程度与透析前后钾离子浓度及二氧化碳结合率(CO2CP)的变化程度呈显著正相关.结论 血透患者室性心律失常的发生与QTd的增加有关;血透中QTd进一步增大,可能与钾离子浓度快速变化以及酸中毒的快速纠正有关.     

Carbon monoxide poisoning - a cause of increased QT dispersion

BACKGROUND: Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. QT dispersion (QTd) of the ECG is an indirect measure of heterogeneity of ventricular repolarization, which may contribute to ventricular arrhythmias. Our aim was to study QTd in patients with acute CO poisoning. METHODS: CO intoxication was confirmed by arterial blood gas analysis. A control group consisted of age- and sex-matched individuals admitted to the hospital for unrelated clinical conditions. 12-lead ECG's were recorded on admission and repeated 1 week after discharge from the hospital. QT dispersion was defined as the difference between the greatest and the least QT intervals in any of the 12 leads. RESULTS: Seventeen intoxicated patients, aged 5-46 years, had mean carboxyhemoglobin levels of 22.5 +/- 11.1%. On admission, corrected QT intervals of the intoxicated patients were significantly increased compared to the control group (431 +/- 18 ms vs. 404 +/- 28 ms, P = 0.008), but not the QT interval (358 +/- 25 ms vs. 345 +/- 20 ms, P = 0.17). Mean QTd and cQTd values (46 +/- 15 ms and 62 +/- 13 ms) of the intoxicated patients were significantly increased compared to the control group (17 +/- 4 ms and 33 +/- 15 ms, P < 0.0001 for both). Both QTd and cQTd decreased significantly after discharge from the hospital (P = 0.0001). CONCLUSION: Although QT dispersion increased in patients with CO poisoning, none of ECG's showed ventricular arrhythmia. Increased QTd in the absence of QT interval prolongation may have a lowered arrhythmogenic potential of CO poisoning.     

Effects of halothane and sevoflurane on QT dispersion in paediatric patients

BACKGROUND: The QT dispersion (QTd) of the ECG is an indirect measure of heterogeneity of ventricular repolarization which may contribute to complex ventricular arrhythmias. We compared the effects of halothane and sevoflurane on QTd, and heart-rate corrected QT dispersion (QTcd). METHODS: Fifty ASA physical status I patients, aged 5-15 years, undergoing general anaesthesia were studied. A control ECG recording was printed before induction of anaesthesia. In the halothane group, anaesthesia was induced with halothane 4% in 2 : 1 ratio of air : O2 mixture and in the sevoflurane group with sevoflurane 8% in 2 : 1 ratio of air : O2 mixture. The ECG was recorded 1 and 3 min after induction of anaesthesia, 1 and 3 min after the administration of vecuronium 0.08 m.kg(-1) intravenous and 1 and 3 min after the tracheal intubation. All ECGs were analysed by two cardiologists blinded to the anaesthetic. RESULTS: Although QTd increased in both groups following intubation, this difference was not statistically significant when compared with control values. Following intubation five patients in the halothane group had ventricular arrhythmias of short duration, whereas no arrhythmias were recorded in the sevoflurane group (P = 0.052). Following intubation, QTd (45 +/- 15 ms vs 40 +/- 14 ms) and QTcd (60 +/- 17 ms vs 55 +/- 16 ms) values in the halothane group were significantly greater than the sevoflurane group (P < 0.05). CONCLUSION: Neither sevoflurane nor halothane caused a significant increase in QTd compared with control values before induction. Only QTd following intubation was significantly greater in the halothane group than the sevoflurane group.     

Renin-angiotensin polymorphisms and QTc interval prolongation in end-stage renal disease

BACKGROUND: Polymorphisms of renin-angiotensin system (RAS) genes in patients with end-stage renal disease (ESRD) on chronic hemodialysis may be associated with QTc interval prolongation, leading to fatal arrhythmias. The objective of this study was to determine (1) the prevalence of QTc prolongation in hemodialysis patients, and (2) the association of a prolonged QTc in these patients with RAS polymorphisms [angiotensin-converting enzyme-insertion/deletion (ACE-I/D), angiotensin type 1 receptor-A1166C (AT1R-A1166C), and angiotensinogen-M235T (AGT-M235T)]. METHODS: Twelve-lead electrocardiograms (ECGs), serum electrolytes (sodium, potassium, and calcium), and ACE and angiotensin II levels were obtained 10 to 12 hours after a hemodialysis session in 43 patients with ESRD on chronic hemodialysis [mean age (+/-SD), 55 +/- 14 years]. Using polymerase chain reaction (PCR), the presence of polymorphisms of the ACE-I/D, AT1R-A1166C, and AGT-M235T genes was determined from the buccal cells. A maximum QT interval in patients with sinus rhythm and normal QRS duration was corrected for heart rate using Hodges' formula. RESULTS: Fifty-eight percent of the patients had QTc interval prolongation (>440 msec). The ACE-DD genotype (P = 0.002) and the C allele of the AT1R-A1166C gene (P = 0.004), but not the AGT-M235T gene, contributed to QTc prolongation. CONCLUSION: Polymorphisms of ACE and AT1R genes additively contribute to QTc prolongation found in a great majority of ESRD patients. Therefore, ESRD patients with both or one of these polymorphisms may be at a higher risk for sudden cardiac death.     

Droperidol for perioperative sedation causes a transient prolongation of the QTc time in children under volatile anesthesia

BACKGROUND: Droperidol is useful for postoperative sedation in infants and children after cardiac surgery because it provides sedation and akinesia with minimal respiratory depression. However, droperidol has been associated with QT prolongation and ventricular arrhythmias. We investigated, if neuroleptanalgesic doses of droperidol led to QT prolongation and cardiac arrhythmias in children undergoing cardiac surgery. METHODS: We retrospectively analysed electrocardiogram rhythm strips that were obtained before and in time increments after a 100 microg x kg(-1) intravenous bolus of droperidol in 20 children undergoing cardiac surgery. The longest QT interval was determined in each ECG and corrected for heart rate (QTc). All arrhythmias were recorded. RESULTS: Droperidol led to a significant increase in QTc time that was still present at 15 min but had resolved within 30 min after the bolus. No associated arrhythmias were observed. CONCLUSIONS: The statistically significant prolongation of QTc time after a sedative dose of droperidol is of concern because it may increase the risk for malignant cardiac arrhythmias. A large, prospective study is necessary to identify the true risk for arrhythmias after droperidol in this patient population, but our study suggests that any arrhythmogenic risk, if present, will be very transient, since the increase in QTc time was limited to a period of less than 30 min after the bolus.     

Correlation between iron stores and QTc dispersion in chronic ambulatory peritoneal dialysis patients

Aim: We aimed to investigate the QT dispersion and corrected QT (QTc) dispersion which are suggested as the signals of ventricular arrhythmias, in patients on maintenance CAPD and to evaluate the correlation between iron stores and these electrocardiographic parameters. Materials and method: Fifty-eight patients on maintenance CAPD and 19 healthy age- and sex-matched adults without cardiac disease were included. The PD patients were divided into two groups according to whether their computerized measurements of QTc dispersion were longer than 65?ms. Results: Although QT interval was statistically significantly shorter in control group (34?±?28 vs. 43?±?34?ms; p?<?0.05), there was no significant difference in regards to the QTc, QT dispersion and QTc dispersion between two groups. PD patients with QTc dispersion longer than 65?ms had higher levels of serum ferritin (p?=?0.038) and transferrin saturation (TSAT; p?=?0.022) than the others. QTc dispersion were positively correlated with ferritin (r?=?0.469, p?<?0.01) and TSAT (r?=?0.430, p?<?0.01) in CAPD patients. Conclusion: Although prolonged QTc, QT dispersion and QTc dispersion were suggested as the markers of ventricular arrhythmias we did not find any significant difference in regards to these parameters between control patients and CAPD patients. But the high body iron stores in these patients increase the risk of increased QT dispersion. The concern over iron overload in dialysis patients is not only because of its oxidative toxicity, but also its precipitation of arrhythmias, which may be measured by the surrogate marker of QTc dispersion.     

Effects of halothane and quinidine on intracardiac conduction and QTc interval in pentobarbital-anesthetized dogs.

To confirm in vitro data that halothane and quinidine depressed cardiac conduction and prolonged action potential (AP) duration, the electrocardiogram and His bundle electrogram were recorded in dogs during basal pentobarbital anesthesia, after 1% halothane or quinidine (2.38 +/- 0.22 micrograms/mL serum concentration [mean +/- SEM]), or both. Purkinje fibers from a second dog were superfused with blood from the intact (support) dog, and APs were recorded. In the intact dogs, 1% halothane caused no changes in the electrocardiogram or His bundle electrogram. Quinidine prolonged QRS duration, QT interval, and rate-corrected QT (P < 0.05). Ventricular conduction (HS interval) slowed, and atrial effective refractory period increased (P < 0.05). Quinidine combined with halothane widened QRS, QT, and rate-corrected QT, prolonged the HS interval, and increased the vulnerability of the atrioventricular node to conduction block. Three of 20 dogs developed torsades de pointes-type ventricular tachycardia during simultaneous quinidine and halothane administration. In cross-superfused Purkinje fibers, the AP duration to 50% repolarization was shortened, and conduction time was prolonged by 1% halothane (both P < 0.05). Quinidine decreased AP amplitude, prolonged AP duration to 90% repolarization, and slowed conduction (P < 0.05). Quinidine combined with halothane decreased AP amplitude, and prolonged both AP duration to 90% repolarization and conduction (P < 0.05). When 1% halothane and therapeutic concentrations of quinidine are administered in dogs, depressed conduction and an acquired long QT syndrome with malignant ventricular arrhythmias may develop.     

QT dispersion in renal transplant recipients

An increased QT dispersion (QTd) is associated with a variety of cardiac diseases and predicts sudden death. Although chronic renal failure patients and patients on hemodialysis are shown to have an increased QTd, evidence of increased QTd in renal transplant patients is scarce. In this study, renal transplant patients were evaluated to find out if they had an increased QTd. Thirty-four renal transplant recipients aged 35 +/- 8 years and 34 healthy control subjects aged 34 +/- 8 years were included in the study. The mean time after transplantation was 51.8 +/- 40.4 (range 5-154) months. The QT interval was measured by 12-lead electrocardiogram, and the QTd was defined as the difference between the maximum and minimum QT interval. Bazett's formula was used to correct for the heart rate (QTc). Both QTd and QTc dispersion (QTcd) in renal transplant patients were compared with those of control subjects. All patients underwent transthoracic echocardiographic assessment and 24-hour ambulatory blood pressure monitoring. Renal transplant recipients had similar QTd (37 +/- 15 vs. 39 +/- 17 ms) and QTcd (50 +/- 18 vs. 55 +/- 20 ms) compared to control subjects. QTd and QTcd were similar in patients with and without left ventricular hypertrophy (QTd 37 +/- 14 vs. 36 +/- 17 ms and QTcd 50 +/- 14 vs. 49 +/- 21 ms, respectively). No association was found between QTd and left ventricular mass index or blood pressure measurements. The QTd was not found to be increased in renal transplant recipients as compared with that of healthy controls in this study. Normalization of the QTd after renal transplantation may be through the correction of several factors responsible for increased QTd in uremic patients.     

体外循环先天性心脏病纠治术对QT离散度的影响及意义

目的 研究体外循环心脏不停姚心内直视术纠治先天性心脏病对ＱＴ离散度（ＱＴｄ）的影响及其意义。方法 记录２０例先天性心脏病纠治术患者术前、术终和术后７天内同步１２导联心电图,测定各时间点ＱＴｄ值和ＱＴ离散校正值（ＱＴｃｄ）。结果 术终及术后ＱＴｄ、ＱＴｃｄ明显升高（Ｐ〈０．０５）。术后第２天达最高值,虽然术后第７天仍未能恢复至术前水平,但总体表现为一个缓慢回落的趋势。１例术后频发室性早搏患者及１例术     

Mechanisms of abnormal cardiac repolarization during insulin-induced hypoglycemia

Prolonged cardiac repolarization causes fatal cardiac arrhythmias. There is evidence that these contribute to sudden death associated with nocturnal hypoglycemia in young people with diabetes. We measured cardiac repolarization (QT interval [QTc] and QT dispersion [QTd]) during experimental hypoglycemia with and without beta-blockade and potassium infusion to establish possible mechanisms. Two groups of 10 nondiabetic men (study 1 and study 2) each underwent four hyperinsulinemic clamps: two euglycemic (5 mmol/l) and two hypoglycemic (5 mmol/l and 2.5 mmol/l for 60 min each). Study 1 was performed with and without potassium infusion to maintain normal concentrations and study 2 with and without beta-blockade (atenolol, 100 mg/day for 7 days). QTd was unchanged during euglycemia but increased during hypoglycemia (55 ms, P < 0.0001 vs. baseline), which was prevented by potassium (6 ms, P = 0.78). QTc increased significantly during hypoglycemia alone (67 ms, P < 0.0001) and during potassium replacement (46 ms, P = 0.02). In study 2, the increase in QTd during hypoglycemia (68 ms, P < 0.0001) was prevented by beta-blockade (3 ms, P = 0.88). The increase in QTc during hypoglycemia (55 ms, P < 0.0001) was prevented by beta-blockade (1 ms, P = 0.98). Our data indicate that hypoglycemia causes an acquired long QT syndrome. Sympathoadrenal stimulation is the main cause, through mechanisms that involve but are not limited to catecholamine-mediated hypokalemia. These abnormalities are prevented by selective beta-blockade.     

Relationships between brain natriuretic peptide, troponin I and QT dispersion in asymptomatic dialysis patients

OBJECTIVES: The relationships between increased wall stress, myocyte death, and ventricular repolarization instability in patients with heart failure were reported. DESIGN AND METHODS: The relationships between brain natriuretic peptide (BNP), a predictor of increased wall stress of hearth; troponin I (cTnI), a predictor of myocyte death; and QT dispersion (QTd), a reflection of ventricular repolarization instability were evaluated in age- and sex-matched asymptomatic 29 hemodialysis (HD) patients and 26 peritoneal dialysis (PD) patients, and the finding were compared. RESULTS: Serum BNP and cTnI levels in HD patients (722.9 +/- 907.9 pg/mL, 0.05 +/- 0.07 microg/L, respectively), just before HD, were significantly higher than those of PD patients (255.4 +/- 463.7 pg/mL, 0.02 +/- 0.02 microg/L, respectively; p < 0.05). There was no significant difference between groups with regard to corrected QTd and maximum and minimum QT intervals (p > 0.05). Serum cTnI levels were significantly and positively correlated with serum BNP levels in both dialysis groups (r = 0.447, p = 0.048). No relationship was found between plasma BNP and ECG parameters studied in both groups (p > 0.05). CONCLUSION: Increased serum cTnI levels were associated with elevated BNP levels in both dialysis groups. The increases in BNP and troponin I are more likely to reflect hypervolemia. Although CAPD patients were receiving dialysis daily and HD patients were more hypervolemic, CAPD patients have similar QTdc and accordingly a similar tendency toward arrhythmias. This suggests that factors other than electromechanical interaction may be important in determining the QT interval length in patients on dialysis.     

QTc dispersion increases during hemodialysis with low-calcium dialysate

BACKGROUND: The risk of ventricular arrhythmias is known to increase during hemodialysis (HD) treatment, but the cause of this phenomenon has remained unidentified. QT dispersion (= QTmax - QTmin) reflects heterogeneity of cardiac repolarization, and increased dispersion is known to predispose the heart to ventricular arrhythmias and sudden cardiac death. METHODS: We studied the effect of dialysate calcium concentration on cardiac electrical stability during HD treatment in 23 end-stage renal disease patients. Three HD treatments were applied with dialysate Ca++ concentrations of 1.25 mmol/L (dCa++1.25), 1.5 mmol/L (dCa++1.5), and 1.75 mmol/L (dCa++1.75). The QTc interval and QTc dispersion were measured before and after the three sessions. RESULTS: With the dCa++1.5 and dCa++1.75 dialyses, serum Ca++ increased and the QTc interval remained stable (dCa++1.5) or decreased (dCa++1.75), but no significant change was noted in QTc dispersion. With dCa++1.25 HD, serum Ca++ decreased (1.24 +/- 0.11 vs. 1.20 +/- 0.09 mmol/L, P < 0. 05), and both the QTc interval (403 +/- 27 vs. 419 +/- 33 ms, P < 0. 05) and QTc dispersion increased (38 +/- 19 vs. 49 +/- 18 ms, P < 0. 05). The change in the QTc interval correlated inversely with the change in serum Ca++ (r = -0.68, P < 0.0001). Except for serum Ca++ and plasma intact parathyroid hormone, predialysis and postdialysis values in other blood chemistry, blood pressure, heart rate, body weight, and total ultrafiltration were equal in the three dialysis sessions. CONCLUSION: This study is the first, to our knowledge, to demonstrate that HD increases QTc dispersion if a low-calcium (dCa++1.25) dialysate is used. This indicates that the use of low-calcium dialysate may predispose HD patients to ventricular arrhythmias and that perhaps it should be avoided, at least when treating patients with pre-existing cardiac disease.     

QT dispersion predicts ventricular arrhythmia in pediatric cardiomyopathy patients referred for heart transplantation.

BACKGROUND: QT dispersion has been used in stratifying risk for sudden death in adults with dilated cardiomyopathy, but its role in the pediatric population has not been delineated. METHODS: We reviewed electrocardiograms in pediatric patients with dilated cardiomyopathy referred for heart transplantation, to evaluate the role of QT dispersion in predicting malignant arrhythmias in these patients. Three groups were defined: Group I (n = 13) had dilated cardiomyopathy and malignant ventricular arrhythmias, Group II (n = 13) had dilated cardiomyopathy with no ventricular arrhythmias and Group III (n = 30) consisted of normals. QT dispersion was defined as the duration of the shortest QT subtracted from that of the longest. In addition, the standard deviation of the QT intervals was calculated for each ECG, using 12 leads. RESULTS: QT dispersion was significantly prolonged in Group I (97 +/- 33 msec) compared to Group II (74 +/- 19 msec) and Group III (42 +/- 17 msec). QT standard deviation was also prolonged in Group I (30 +/- 11 msec) vs Group II (22 +/- 5 msec) and Group III (13 +/- 4 msec). Using a threshold value of 90 msec for QT dispersion or 25 msec for QT standard deviation, a sensitivity of 78% and a specificity of 70% was obtained for identifying patients who would subsequently develop ventricular arrhythmias. CONCLUSIONS: In pediatric heart transplant candidates with dilated cardiomyopathy, QT dispersion and QT standard deviation identify patients at higher risk for the development of malignant ventricular arrhythmia. This simple test can be helpful in the evaluation and management of these patients awaiting transplantation.     

术中静脉输注艾司洛尔对非心脏手术老年冠心病患者QT离散度的影响

目的 评价术中静脉输注艾司洛尔对非心脏手术老年冠心病患者QT离散度的影响.方法 择期行中危非心脏手术的老年冠心病患者50例,ASA Ⅱ或Ⅲ级,年龄65～80岁,性别不限,随机分为2组(n=25):对照组和试验组.两组患者麻醉诱导和维持用药及其剂量相同.试验组切皮开始前2 min静脉注射艾司洛尔负荷量0.5 rag/kg,随后以25μg·kg-1·min-1速率输注至术毕.分别于术前、切皮后30 min、术毕、术后1、2 d时描记12导联心电图,计算QT离散度(最长QT间期与最短QT间期之差),并记录QT离散度异常的发生情况.记录术中及术后3 d内室性心律失常的发生情况.结果 与对照组比较,试验组QT离散度、QT离散度异常发生率及室性心律失常发生率降低(P<0.05).结论 术中静脉输注艾司洛尔(静脉注射负荷量0.5 mg/kg后以25μg·kg-1·min-1的速率静脉输注)可降低非心脏手术老年冠心病患者围术期QT离散度,有助于预防室性心律失常的发生.     

Effect of Weight Loss following Bariatric Surgery on Myocardial Dispersion of Repolarization in Morbidly Obese Patients

Background Weight-stable obese subjects have an increased risk of arrhythmias and sudden death, even in the absence of cardiac dysfunction, and the risk of sudden cardiac death (SCD) with increasing weight is seen in both genders. The mechanism of unexplained deaths in obese patients is still unclear and may be related to ventricular repolarization abnormalities. The aim of this study is to determine the effect of severe obesity on spatial and transmural ventricular repolarization and to clarify the influence of bariatric surgery with a consequent substantial weight loss on arrhythmogenic substrate in the morbidly obese population. Methods For the study, we enrolled 100 severely obese patients; 50 age-matched non-obese healthy subjects were also recruited as controls. All subjects underwent conventional 12-lead electrocardiography for analysis of spatial and transmural ventricular repolarization assessed by corrected QT dispersion (QTcd), corrected JT dispersion (JTc-d) and transmural dispersion of repolarization, (TDR). All subjects underwent bariatric surgery and were resubmitted to electrocardiographic, biochemical and anthropometric examination 12 months postoperatively. Results Severely obese patients had greater values in QTc-d, JTc-d and TDR than the normal-weight controls. Bariatric surgery reduced significantly the QTcd value, JTc-d value and TDR value. There was a significant correlation between decrease of heterogeneity of repolarization indexes (QTd, JTd and TDR) and bariatric surgery-induced weight loss. Conclusions In severely obese patients, surgicallyinduced weight loss is associated with significant decrease in the heterogeneity of ventricular repolarization. The reduction of spatial (QTc-d, JTc-d) and transmural dispersion of repolarization (TDR) may be of clinical significance, by reducing the risk of potentially fatal arrhythmias in morbidly obese subjects.     

Gender differences in QTc interval in young, trained individuals with lower spinal cord injury

STUDY DESIGN: Cross-sectional comparison. OBJECTIVE: To examine gender differences in rate-corrected QT interval (QTc), an index of ventricular depolarization/repolarization, in young, trained men and women with lower spinal cord injury (SCI) and able-bodied (AB) controls. SETTING: University of Illinois at Urbana-Champaign, Exercise and Cardiovascular Research Lab, USA. METHODS: Subjects consisted of 16 athletes with SCI (eight men and eight women) and 16 age-matched AB active controls (eight men and eight women). QT interval dynamics was derived from ECG recordings and rate corrected using the Bazett formula. RESULTS: Men with SCI had QTc similar to that of AB men (369.3+/-7.5 versus 357.9+/-3.0 ms, P>0.05). Women with SCI had QTc similar to that of AB women (400.0+/-4.6 versus 385.2+/-6.5 ms, P>0.05). AB women had longer QTc interval than AB men, and SCI women had longer QTc than SCI men (P<0.05). CONCLUSIONS: Gender differences in ventricular depolarization/repolarization are present in trained individuals with SCI. Thus, similar to their AB gender-matched peers, women with SCI have longer QTc intervals and may be at greater risk for the development of untoward cardiac arrhythmias than men with SCI.     

Manifestation of Long QT syndrome with normal QTc interval under anesthesia: a case report

Patients with congenital Long QT are known to have normal QT interval in symptom-free period and in the early years of life. Precipitating factors like surgical stress, interactions with anesthetic agents prolonging QT interval, and electrolyte imbalances can manifest with life threatening arrhythmias in congenital or acquired Long QT syndrome. We report a case of concealed LQTS manifesting under anesthesia and its subsequent perioperative course.     

Effect of different intra-abdominal pressure levels on QT dispersion in patients undergoing laparoscopic cholecystectomy

Background

Hemodynamic changes caused by carbon dioxide (CO₂) insufflation occur frequently in patients who undergo laparoscopic surgery. One indicator of these changes is corrected QT dispersion (QTcd), an index of myocardial function. Prolongation of QTcd has been associated with cardiovascular morbidity and mortality. We compared the effects of high-pressure (15 mmHg) and low-pressure (7 mmHg) CO₂ pneumoperitoneums on the QT interval, the rate-corrected QT interval (QTc), the QT dispersion (QTd), and the corrected QT dispersion (QTcd) during laparoscopic cholecystectomy.

Methods

Twenty consecutive patients were in a low-pressure pneumoperitoneum group and 32 were in a high-pressure pneumoperitoneum group. A 12-lead electrocardiogram was used to monitor cardiac variables. In all patients, serial electrocardiograms were recorded before anesthesia induction (baseline), immediately after the pneumoperitoneum had been created, every 15 minutes during CO₂ insufflation, and 5 minutes after deflation. Two observers measured the QT intervals independently, and the QTcd was calculated using Bazett’s formula.

Results

The QT interval and the QTc interval did not change significantly during the study in either group. The QTd and QTcd in the high-pressure pneumoperitoneum group increased significantly during CO₂ insufflation and were significantly higher in the high-pressure pneumoperitoneum group compared with the low-pressure pneumoperitoneum group. Changes caused by CO₂ insufflation were reversible.

Conclusions

Statistically significant increases of QTd and QTcd, which are associated with an increased risk of arrhythmias and cardiac events, occur during CO₂ insufflation in both high-pressure and low-pressure pneumoperitoneums. QTd and QTcd were significantly higher in the high-pressure pneumoperitoneum group than they were in the low-pressure pneumoperitoneum group. QT interval changes were not related to anesthetic agents, surgical stress, hypercapnia, or duration of CO₂ insufflation. Increased intra-abdominal pressure may have caused these changes.     

Effect of Intensive Glycemic and Blood Pressure Control on QT Prolongation in Diabetes: The ACCORD Trial

Compared with standard glycemic control, intensive glycemic control caused increased mortality in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. Preliminary data from several studies suggest that intensive glycemic control is associated with QT prolongation, which may lead to ventricular arrhythmias as a possible explanation of this increased mortality. We sought to assess the effects of intensive glycemic control and intensive blood pressure control on the risk of incident QT prolongation. Cox proportional hazards models were used to compare the risk of incident QT prolongation (>460 ms in women or >450 ms in men) in the intensive versus standard glycemic control arms. Over a combined 48,634 person-years of follow-up (mean 4.9), 634 participants (6.4%) developed a prolonged QTc. Participants in the intensive glycemic control arm did not have an increased risk of QT prolongation. Similarly, a strategy of intensive blood pressure control did not result in a significant change in risk of prolonged QTc. Sensitivity analyses using alternative QT correction formulas (Hodges and Bazett) yielded overall similar findings. In conclusion, the increased mortality observed in the intensive glycemic control arm in the ACCORD trial is not likely to be explained by QT prolongation leading to lethal ventricular arrhythmias.