Opening of K(ATP) channel attenuates the increase in QT dispersion produced by the first balloon inflation during coronary angioplasty.

Increased QT dispersion predicts the occurrence of lethal ventricular arrhythmias complicating percutaneous transluminal coronary angioplasty (PTCA). Moreover, these arrhythmias occur more frequently at the first balloon inflation. Activation of the K(ATP) channel may influence QT dispersion and ventricular arrhythmias during coronary angioplasty, so 40 consecutive patients with stable angina were randomized to receive 3 mg/h of nicorandil infusion or placebo and QT dispersion and the incidence of ventricular ectopy were investigated before and throughout PTCA. There were no significant differences in QT dispersion at baseline between the nicorandil group (42+/-8 ms) and placebo (42+/-12ms). At the first balloon inflation, the QT dispersion in the nicorandil group (51+/-13 ms) was significantly less than that observed with placebo (76+/-16ms, p<0.001). However, the QT dispersion at the second inflation was similar in both groups (nicorandil: 45+/-12ms; placebo: 52+/-14ms). Ventricular ectopy was observed in 1 patient receiving nicorandil and 5 patients in the placebo group during the first inflation, and none in the nicorandil and 1 patient in the placebo group during the second balloon inflation. Activation of the K(ATP) channel may inhibit the development of ventricular arrhythmias during PTCA, particularly at the first balloon inflation.     

Effect of glucose--insulin--potassium solution on the exercise performance of patients with coronary artery disease.

Treadmill exercise testing was performed in double blind fashion on nine untrained nondiabetic subjects with angiographically proven coronary artery disease and stable exercise tolerance. They were exercised on three different days in randomized sequence as follows: With infusion of 30 per cent solution of glucose in water containing 50 units of regular insulin and 80 mM. of KCl per liter, 50 ml. bolus followed by 1 ml./Kg./hr. (GIK); with infusion of normal saline, (NSS), 50 ml. bolus followed by 1 ml./Kg./hr. and without infusion (control). There were no significant differences between control and saline experiments.A decrease in work capacity (9.9 ± 3.4 to 7.0 ± 2.1 METS p < 0.005) and the product of the heart rate and systolic blood pressure (20318 ± 6068 to 17597 ± 5788 mm. Hg min.^?1, p < 0.05) at the end of exercise was observed in GIK experiments. Angina occurred at lower exercise levels in GIK studies (6.4 ± 1.4 METS) than in NSS studies (9.9 ± 3.4 METS p < 0.01). When compared at the same exercise level (5 METS), more pronounced ST depression (0.21 ± 0.11 mV.) was seen in GIK than in NSS studies (0.1 ± 0.18 mV., p < .025). In two patients, the exercise test was negative in NSS and became positive in GIK.In GIK, a decrease in serum FFA compared to resting level was noted at the end of exercise (197 ± 246 μEq/L.) and during exercise at 5 METS (272 ± 400 μEq/L.) as opposed to an increase (566 ± 853 μEq/L., p < 0.025 at 5 METS and 650 ± 996 μEq/L., p < 0.05 at the end of exercise) in NSS. An increase in blood glucose (73 ± 74 mg./100 ml., p < 0.01) at the end of exercise and (116 ± 75 mg./100 ml., p < 0.005) at 5 METS was noted in GIK but not in NSS studies. A small decrease in serum potassium (by 0.11 ± 0.23 mEq./L. at 5 METS and by 0.15 ± 0.24 mEq./L. at the end of exercise) was seen in GIK but an increase in the saline group (by 0.21 ± 0.39 mEq./L., p < 0.05 at 5 METS and by 0.43 ± 0.38 mEq./L., p < 0.001 at the end of exercise). No significant differences in serum lactate were noted.The data indicate that GIK diminishes the exercise performance and hastens the onset of angina in patients with coronary artery disease. It appears that increased availability of glucose and potassium does not have a beneficial effect in the presence of depressed FFA levels during exercise.     

急性心肌梗死患者介入治疗时血糖水平变化及对预后的影响

目的探讨急性心肌梗死PCI时血糖水平变化及对预后的影响。方法选择非糖尿病急性心肌梗死患者85例,检测入院即刻血糖分为无应激性高血糖组(A组)48例和应激性高血糖组(B组)37例,对比分析2组的临床资料及30 d内心力衰竭、再发心肌梗死、梗死后心绞痛、严重心律失常及心血管死亡情况。结果与A组比较,B组患者入院即刻血糖、入院后空腹血糖及餐后2 h血糖明显升高(P<0.01);且急性心肌梗死急性期心力衰竭、再发心肌梗死、梗死后心绞痛、严重心律失常及心血管死亡均明显升高(P<0.05)。B组患者LVEF(48.57±8.21)%明显低于A组[(53.25±7.34)%,P<0.05]。结论入院血糖异常升高与急性心肌梗死患者PCI术后30 d内预后差相关。     

不同类型冠心病与脂蛋白及载脂蛋白异常

对三种不同类型冠心病患者作血清脂蛋白、载脂蛋白的测定，以了解不同类型冠心病患者脂质异常情况及异常类型。急性心肌梗死组21例；不稳定型心绞痛组27例；稳定型心绞痛组35例；正常对照组50例。总胆固醇和甘油三酯测定采用酶法；高密度脂蛋白胆固醇及其亚组分以聚乙二醇沉淀后用酶法测定；载脂蛋白A1、载脂蛋白B100以免疫火箭电泳法测定：脂蛋白（a）、载脂蛋白E采用酶联免疫法测定；低密度脂蛋白胆固醇含量由Friedwald公式推算。结果发现三组的脂蛋白（a）、载脂蛋白B100和载脂蛋白E含量均高于正常对照组；高密度脂蛋白胆固醇及其亚组分和载脂蛋白A1含量均低于正常对照组。低密度脂蛋白／高密度脂蛋白胆固醇的比值在急性心肌梗死组高于稳定型心绞痛组。三组冠心病患者的血清脂质异常检出率，以载脂蛋白B100、载脂蛋白E含量增高者最多见，次之为高密度脂蛋白胆固醇含量降低者；在三组的脂质异常类型方面，以脂蛋白（a）含量增高者为最多见。以上结果提示：应重视血清脂蛋白（a）、载脂蛋白B100、载脂蛋白E含量的增高以及高密度脂蛋白胆固醇含量的下降在冠心病患者血清脂质异常中的重要性；低密度脂蛋白胆固醇／高密度脂蛋白胆固醇比值增高是冠心病的一个预告指标。     

Effect of continuous exenatide infusion on cardiac function and peri‐operative glucose control in patients undergoing cardiac surgery: A single‐blind,randomized controlled trial

We performed a randomized controlled trial with the glucagon‐like peptide‐1 (GLP‐1) receptor agonist exenatide as add‐on to standard peri‐operative insulin therapy in patients undergoing elective cardiac surgery. The aims of the study were to intensify peri‐operative glucose control while minimizing the risk of hypoglycaemia and to evaluate the suggested cardioprotective effects of GLP‐1‐based treatments. A total of 38 patients with decreased left ventricular systolic function (ejection fraction ≤50%) scheduled for elective coronary artery bypass grafting (CABG) were randomized to receive either exenatide or placebo in a continuous 72‐hour intravenous (i.v.) infusion on top of standard peri‐operative insulin therapy. While no significant difference in postoperative echocardiographic variables was found between the groups, participants receiving exenatide showed improved peri‐operative glucose control as compared with the placebo group (average glycaemia 6.4 ± 0.5 vs 7.3 ± 0.8 mmol/L; P < .001; percentage of time in target range of 4.5–6.5 mmol/L 54.8% ± 14.5% vs 38.6% ± 14.4%; P = .001; percentage of time above target range 39.7% ± 13.9% vs 52.8% ± 15.2%; P = .009) without an increased risk of hypoglycaemia (glycaemia <3.3 mmol/L: 0.10 ± 0.32 vs 0.21 ± 0.42 episodes per participant; P = .586). Continuous administration of i.v. exenatide in patients undergoing elective CABG could provide a safe option for intensifying the peri‐operative glucose management of such patients.     

Effect of sitagliptin on glucose control in type 2 diabetes mellitus after Roux‐en‐Y gastric bypass surgery

The present study was a 4‐week randomized trial to assess the efficacy and safety of sitagliptin, a dipeptidyl‐peptidase‐4 inhibitor, in persistent or recurring type 2 diabetes after Roux‐en‐Y gastric bypass surgery (RYGB). Participants (n = 32) completed a mixed meal test (MMT) and self‐monitoring of plasma glucose (SMPG) before and 4 weeks after randomization to either sitagliptin 100 mg daily or placebo daily. Questionnaires were administered to assess gastrointestinal discomfort. Outcome variables were glucose, active glucagon‐like peptide‐1 and β‐cell function during the MMT, and glucose levels during SMPG. Age (56.3 ± 8.2 years), body mass index (34.4 ± 6.7 kg/m²), glycated haemoglobin (7.21 ± 0.77%), diabetes duration (12.9 ± 10.0 years), years since RYGB (5.6 ± 3.3 years) and β‐cell function did not differ between the placebo and sitagliptin groups at pre‐intervention. Sitagliptin was well tolerated, decreased postprandial glucose levels during the MMT (from 8.31 ± 1.92 mmol/L to 7.67 ± 1.59 mmol/L, P = 0.03) and mean SMPG levels, but had no effect on β‐cell function. In patients with diabetes and mild hyperglycemia after RYGB, a short course of sitagliptin provided a small but significant glucose‐lowering effect, with no identified improvement in β‐cell function.     

完全性房室传导阻滞患者发生尖端扭转型室性心动过速的危险因素分析

目的　分析完全性房室传导阻滞患者发生尖端扭转型室性心动过速 (Td P)的危险因素。方法　用 logistic回归法分析 116例完全性房室传导阻滞住院患者 Td P的发生率与年龄、性别、治疗前血钾浓度、QT间期、校正的 QT间期 (QTc)、心率 (HR)的相关性。结果　 12例患者 (10 .3% )发生 Td P,其中女性 9例。Td P组血钾浓度为 (3.5 4±0 .5 5 ) m mol/ L ,明显低于未发生 Td P组血钾浓度 (4 .0 1± 0 .5 7) mm ol/ L (P<0 .0 1)。 Td P组 QT间期为 (0 .5 7±0 .0 75 ) s,明显大于未发生 Td P组 QT间期 (0 .4 6 5± 0 .0 93) s,(P<0 .0 1)。 Td P组年龄、HR、QTc与未发生 Td P组无显著差异。女性、血钾浓度和 QT的风险比值 (OR)分别为 5 .6 39、6 .773和 5 .90 5 ;而年龄、HR、QTc的 OR分别为 1.0 12、0 .92 5、1.0 30。结论　完全性房室传导阻滞患者发生 Td P的独立危险因素是低血钾浓度、长 QT间期和女性。对女性完全性房室传导阻滞患者应给予更积极的治疗 ,以免发生 Td P。     

Long‐Term Improvement of QT Dispersion is Unaffected by Short‐Term Changes in Blood Pressure During Treatment of Systemic Hypertension with Enalapril

Background: We report the reduction of QT and QT_c dispersion in patients treated for 7 years with enalapril for systemic hypertension with left ventricular (LV) hypertrophy. We assess the correlation between QT dispersion and LV mass during this period and at the end of an 8‐week period of suspension of enalapril treatment after 5 years. Methods: Twenty‐four previously untreated patients with this condition took enalapril (20 mg twice daily) for 7 years, except during an 8‐week period following 5‐year follow‐up. Cardiovascular parameters were determined by two‐dimensional guided M‐mode echocardiography, and QT interval was measured, in a pretreatment placebo phase, 8 weeks and 1, 3, 5, and 7 years after the start of the therapy, at the end of the 8‐week suspension effected after 5 years, and 8 weeks after the end of the suspension. Results: Therapy rapidly reduced blood pressure (BP) from 156/105 mmHg to normal values: 134/84 mmHg after 8 weeks’ treatment, 130–84 mmHg at 7‐year follow‐up (P < 0.001 with respect to the placebo phase). LV mass index decreased progressively until at 5‐year follow‐up the reduction had reached 39% (P < 0.001), after which neither LV mass nor any other structural parameter underwent any further significant change. During this time, QT dispersion (ΔQT) and the dispersion of “corrected” QT (ΔQT_c) decreased significantly: ΔQT (from 61 ± 21 to 37 ± 13 ms ) and ΔQT_c (from 67 ± 27 to 41 ± 16 ms ). After suspension of treatment for 8 weeks following 5‐year follow‐up, ΔQT was 40 ± 14 ms and ΔQT_c was 44 ± 17 ms ; there were no significant changes either in ΔQT and ΔQT_c or LV hypertrophy although BP had returned to pretreatment values (BP: 150 ± 16; 101 ± 10 mmHg ). Conclusions: Long‐term enalapril treatment of hypertensive patients with LV hypertrophy induces marked regression of LV mass and improvement of QT dispersion. These improvements occur on a longer timescale than improvement in BP, and are not affected by transient changes in BP values.     

冠状动脉粥样硬化性心脏病患者QT离散度与血浆内皮素和胰岛素敏感性的关系

为探讨冠状动脉粥样硬化性心脏病患者QT离散度与血浆内皮素水平、胰岛素敏感性及严重室性心律失常的关系 ,对 47例冠状动脉粥样硬化性心脏病患者和 2 0例健康对照者进行口服葡萄糖耐量试验、胰岛素和C肽释放试验 ,并测定血浆内皮素水平。急性心肌梗死患者糖耐量试验在梗死后第四周进行 ,第一天血样本也检测内皮素水平。所有对象在抽血当天同步记录常规 12导联心电图测算QT离散度。以QT离散度为因变量 ,以 9个胰岛素敏感性指标和血浆内皮素水平为自变量 ,进行逐步回归和 /或简单相关分析。结果发现 ,冠状动脉粥样硬化性心脏病各亚组内皮素被有效选入回归方程 ,QT离散度与内皮素呈显著正相关 ;急性心肌梗死组空腹血糖也被有效选入回归方程 ,但QT离散度与空腹血糖呈负相关 ;其它自变量均未被选入方程。急性心肌梗死早期发生严重室性心律失常者第一天内皮素水平 (16 0 .5± 2 3.0ng/L)和QT离散度 (86± 19ms)高于未发生严重室性心律失常者 (119.7± 15 .2ng/L ,6± 13ms) ,也高于正常对照组 (45 .0± 14.7ng/L ,P <0 .0 5 ) ;此两组QT离散度与内皮素呈正相关 (r分别为 0 .94和 0 .84,P均 <0 .0 1)。提示冠状动脉粥样硬化性心脏病患者尤其是急性心肌梗死患者血浆内皮素水平增高是QT离散度增大的独立相关因素     

Intravenous nicorandil can reduce the occurrence of ventricular fibrillation and QT dispersion in patients with successful coronary angioplasty in acute myocardial infarction

BACKGROUND: Because nicorandil, a potassium channel opener, has a cardioprotective effect and attenuates reperfusion injury in patients with acute myocardial infarction (AMI), intravenous nicorandil should reduce arrhythmic mortality and QT dispersion in patients with AMI. OBJECTIVES: The purpose of this study was to evaluate whether intravenous nicorandil reduces the occurrence of ventricular fibrillation and QT dispersion in patients with successful coronary angioplasty in AMI. METHODS: A historical cohort study on the effect of nicorandil on ventricular fibrillation and QT dispersion was conducted. Eighty-three patients with AMI who underwent successful percutaneous transluminal coronary angioplasty (PTCA) were enrolled. The patients were divided into two groups: nicorandil (n=46) and control group (n=37). Nicorandil was injected at 4 mg/h continuously from admission to 48 h after PTCA in the nicorandil group. QT dispersion was measured before, immediately after, 24 h after and 48 h after PTCA. RESULTS: Ventricular fibrillation was observed in three patients in the control group, but none was observed in the nicorandil group. QT dispersion in the nicorandil group was shorter than that in the control group 48 h after PTCA (QT dispersion was 23.2+/-16.1 ms and 33.4+/-24.0 ms, respectively, P<0.05). There was a significant difference between the two groups in time course after the onset of AMI (P<0.05). CONCLUSIONS: Because intravenous nicorandil reduces the occurrence of ventricular fibrillation and QT dispersion in patients with successful coronary angioplasty in AMI, it would prevent the occurrence of cardiac events after successful PTCA for AMI.     

Effects of Epinephrine and Phenylephrine on QT Interval Dispersion in Congenital Long QT Syndrome

Objectives. Measurement of QT interval dispersion during pharmacologic adrenergic stimulation was used to assess the effect of alpha- and beta-adrenergic stimulation on arrhythmic vulnerability in familial long QT syndrome (LQTS).Background. Nonhomogeneity in the ventricular action potential duration causes electrical instability leading to life-threatening ventricular arrhythmias and is markedly increased in LQTS. QT interval dispersion measured from the electrocardiogram (ECG) can be used as an index of nonhomogeneous ventricular repolarization.Methods. Sixteen symptomatic patients with LQTS and nine healthy control subjects were examined at baseline and during epinephrine (mainly beta-adrenergic agonist, 0.05 μg/kg body weight per min) and phenylephrine infusions (alpha-adrenergic agonist, mean 1.4 μg/kg per min). QT interval dispersion was determined from a 12-lead ECG as interlead range and coefficient of variation measured to the end (QT_end) and apex (QT_apex) of the T wave.Results. At baseline QT_enddispersion was greater in patients with LQTS compared with control subjects (mean [±SD] 68 ± 34 vs. 36 ± 7 ms, p = 0.001). QT_enddispersion was markedly increased in patients with LQTS by use of epinephrine (from 68 ± 34 to 90 ± 36 ms, p = 0.002), but remained unchanged in control subjects. Phenylephrine did not affect QT dispersion in either group (all p = NS). Atrial pacing to achieve comparable heart rates during baseline and epinephrine and phenylephrine infusions did not influence the magnitude of QT dispersion in either group. QT_apexdispersion analysis gave congruent results.Conclusions. Epinephrine but not phenylephrine increased QT dispersion, suggesting that beta-adrenergic stimulation provokes arrhythmias in patients with LQTS by aggravating nonhomogeneity of ventricular repolarization, whereas alpha-adrenergic stimulation is less important for arrhythmic vulnerability. The results also suggest that rapid pacing may not reduce vulnerability to arrhythmias in congenital LQTS.     

Effects of Head‐Up Tilt‐Table Test on the QT Interval

Background. The QT interval shortens in response to sympathetic stimulation and its response to epinephrine infusion (in healthy individuals and patients with long QT syndrome) has been thoroughly studied. Head‐up tilt‐table (HUT) testing is an easy way to achieve brisk sympathetic stimulation. Yet, little is known about the response of the QT interval to HUT. Methods. We reviewed the electrocardiograms of HUT tests performed at our institution and compare the heart rate, QT, and QTc obtained immediately after HUT with the rest values. Results. The study group consisted of 41 patients (27 females and 14 males) aged 23.9 ± 8.4 years. Head‐up tilting led to a significant shortening of the RR interval (from 825 ± 128 msec at rest phase to 712 ± 130 msec in the upward tilt phase, P < 0.001) but only to a moderate shortening of the QT interval (from 363.7 ± 27.9 msec during rest to 355 ± 30.3 msec during upward tilt, P = 0.001). Since the RR interval shortened more than the QT interval, the QTc actually increased (from 403 ± 21.5 msec during rest phase to 423.2 ± 27.4 msec during upward tilt, P < 0.001). The QTc value measured for the upward tilt position was longer than the resting QTc value in 33 of 41 patients. Of those, 4 male patients and 2 female patients developed upward‐tilt QTc values above what would be considered abnormal at rest. Conclusions. During HUT the QT shortens less than the RR interval. Consequently, the QTc increases during head‐up tilt. Ann Noninvasive Electrocardiol 2010;15(3):245–249     

The Relation of QT Dispersion to Spontaneous Ventricular Arrhythmias During the Acute Phase of Myocardial Infarction

Background: QT dispersion is associated with ventricular arrhythmias and sudden death among patients with a previous myocardial infarction (Ml). The relationship between QT dispersion and ventricular arrhythmias during the acute phase of Ml is uncertain. Methods: Patients enrolled in the Multicenter Study of Silent Myocardial Ischemia who had first Q wave myocardial infarctions (n = 363) were screened for the presence of ventricular arrhythmias during the initial hospitalization. Twelve patients had ventricular fibrillation, and 18 patients had an episode of monomorphic ventricular tachycardia. Each patient who had ventricular arrhythmias was matched with four controls on the basis of age, peak creatine kinase, thrombolysis, and the presence of congestive heart failure. The final study population consisted of 150 patients: 12 patients with ventricular fibrillation (VF+) who were compared to 48 controls (VF—), and 18 patients with ventricular tachycardia (VT+) who were compared to 72 controls (VT–). The RR, QRS, and QT intervals were measured manually using standard 12-lead ECGs (25 mm/s) obtained after hospital admission. The maximal QT dispersion (maximum — minimum value) was calculated. Multivariate logistic regression analysis was performed to determine if QT dispersion was independently associated with ventricular arrhythmias during the acute phase of Ml. Results: QT dispersion was significantly greater in VF+ patients compared to VF— patients (89 ± 18 ms vs 66 ± 22 ms, P > 0.01). QT dispersion was similar in VT+ and VT— patients (68 ± 25 ms vs 68 ± 26 ms, P = NS). QT dispersion was the only variable that was independently associated with ventricular fibrillation (OR 1.7 for each 10-ms increment in QT dispersion; 95% Cl 1.2–2.6; P = 0.008). QT dispersion was not associated with monomorphic ventricular tachycardia (OR 1.0; 95% Cl 0.8–1.2; P = NS). Conclusion: QT dispersion is independently associated with ventricular fibrillation, but not monomorphic ventricular tachycardia, during the acute phase of Ml.     

Dapagliflozin for prednisone‐induced hyperglycaemia in acute exacerbation of chronic obstructive pulmonary disease

The aim of the present study was to compare the effectiveness and safety of add‐on treatment with dapagliflozin to placebo in patients with prednisone‐induced hyperglycaemia during treatment for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). We enrolled 46 patients hospitalized for an AECOPD in a multicentre double‐blind randomized controlled study in which add‐on treatment with dapagliflozin 10 mg was compared with placebo. Glycaemic control and incidence of hypoglycaemia were measured through a blinded subcutaneous continuous glucose monitoring device. Participants in the dapagliflozin group spent 54 ± 27.7% of the time in target range (3.9–10 mmol/L) and participants in the placebo group spent 53.6 ± 23.4% of the time in target range (P = .96). The mean glucose concentration was 10.1 mmol/L in the dapagliflozin group and 10.4 mmol/L in the placebo group (P = .66). One participant using dapagliflozin and 2 participants using placebo experienced symptomatic hypoglycaemia. Treatment with dapagliflozin was safe and there was no difference in risk of hypoglycaemia compared with placebo. Dapagliflozin did not result in better glycaemic control compared with placebo in participants with prednisone‐induced hyperglycaemia during AECOPD.     

Randomized,Double‐Blind,Placebo‐Controlled Trial of Spironolactone for Hypokalemia in Continuous Ambulatory Peritoneal Dialysis Patients

The incidence of hypokalemia in continuous ambulatory peritoneal dialysis (CAPD) patients is about 15–60%, leading to significant complications. There is no standard treatment other than potassium supplement in this setting. The aim of this study was to evaluate effect of spironolactone 25 mg/day in CAPD patients who have a history of hypokalemia. This is a randomized, double‐blind, placebo‐controlled, cross‐over study in CAPD patients who had a history of hypokalemia. Study intervention is 4 weeks of oral spironolactone 25 mg/day or placebo, cross‐over after a 2‐week wash‐out period. The primary outcome was the difference of serum potassium before and after 4 weeks of spironolactone treatment. Serum potassium was measured every 2 weeks, serum magnesium, urine and peritoneal fluid potassium measured before and after each treatment period. We enrolled 24 patients, and 20 completed the cross‐over study. Ten patients were anuric. The total doses of potassium supplement were the same during the study period. Serum potassium levels before and after study intervention were not significantly different in both groups (4.23 ± 0.64 vs. 3.90 ± 0.59 mEq/L for spironolactone P = 0.077 and 3.84 ± 0.62 vs. 3.91 ± 0.52 for placebo P = 0.551). Total 24‐h potassium, magnesium, sodium excretion, urine volume and ultrafiltration volume were not affected by spironolactone or placebo. There was one episode of hyperkalemia (5.6 mEq/L) during the spironolactone treatment period. Spironolactone 25 mg/day does not have a significant effect on serum potassium or urine and peritoneal excretion rate in CAPD patients who have a history of hypokalemia.     

The effect of glucose-insulin-potassium solution on ventricular late potentials and heart rate variability in acute myocardial infarction.

BACKGROUND: Blunted heart rate variability (HRV) and presence of ventricular late potentials (VLPs) are known to correlate with an increased risk of ventricular tachycardia and sudden cardiac death in acute myocardial infarction (AMI). In the present study, we investigated the effect of glucose-insulin-potassium (GIK) solution on the VLPs and HRV in AMI. METHODS: Seventy-two consecutive patients with first Q wave AMI were randomized to GIK solution and placebo. HRV analysis and ambulatory electrocardiographic recordings were taken in all patients between 24 and 48 h. Sub-maximal exercise testing and echocardiography were performed and signal-averaged electrocardiography (SAECG) was recorded before discharge. RESULTS: Total filtered QRS duration (FQRS: 102 +/- 7 versus 108 +/- 11 ms; P < 0.05), low-amplitude signal (LAS: 25 +/- 8 versus 32 +/- 11 ms; P < 0.01) and frequency of VLPs (21 versus 45%; P < 0.05) were found to be significantly lower while root-mean-square voltage of the terminal 40 ms of QRS (RMS-40: 45 +/- 18 versus 36 +/- 20 microV; P < 0.05), and left ventricular ejection fraction (EF: 55 +/- 6 versus 48 +/- 7; P < 0.05) were significantly higher in the GIK group when compared to placebo. During the hospital period, the presence and frequency of post-myocardial infarction angina were significantly lower in the GIK group (15 versus 29%, P < 0.05), whereas an insignificant decrease in frequency of ventricular arrhythmias was observed in these patients. On HRV analysis, there was no significant difference between two groups in either time domain (SD, SDNN, RMS-SD) or frequency domain (HF, LF, LF/HF ratio) parameters. CONCLUSION: GIK solution may be beneficial to VLPs, ischaemic events, and left ventricular systolic performance in the early period of AMI. This therapy has no significant effect on HRV in AMI patients.     

QT and JT Dispersion in Children with Long QT Syndrome

QT and JT Dispersion in Long QT Syndrome. Introduction: Abnormalities of ventricular repolarization leading to ventricular arrhythmias place children with long QT syndrome at high risk for sudden death. Dispersion of the QT (QTd) and JT (JTd) intervals, as markers of cardiac electrical heterogeneity, may be helpful in evaluating children with long QT syndrome and identifying a subset of patients at high risk for development of critical ventricular arrhythmias (ventricular tachycardia, torsades de pointes, and/or cardiac arrest). Methods and Results: The QTd and JTd intervals in 39 children with long QT syndrome were compared to those of 50 normal age-matched children. In the long QT syndrome group, QTd measured 81 ± 70 msec compared to 28 ± 14 msec in the control group (P < 0.05), and JTd in the long QT syndrome group was 80 ± 69 msec compared to 25 ± 15 msec in the control group (P < 0.05). Conclusion: Children with long QT syndrome have an increased QTd and JTd when compared to normal controls. A QTd or JTd ≥ 55 msec correlates with the presence of critical ventricular arrhythmias. These ECG measures of dispersion can be useful in stratifying children with the long QT syndrome who are at higher risk for developing critical ventricular arrhythmias.     

QT dispersion ratio in patients with unstable angina pectoris (A new risk factor?)

Background: QT dispersion has been shown to be associated with fatal arrhythmias and sudden death in coronary artery disease. A recent study indicated that marked QT dispersion in electrocardiograms (ECGs) obtained during acute ischemia demonstrated a significant correlation with ventricular fibrillation. Hypothesis: This study investigated the ECG parameters for repolarization (QT dispersion, corrected QT, corrected QT dispersion, and QT dispersion ratio) and their interrelation with acute ischemia. Methods: QT parameters as well as a newly developed repolarization index, QT dispersion ratio l(QT dispersion/RR interval) × 100] were calculated digitally during rest and ischemia in 32 patients with coronary artery disease (rest angina, Braunwald class III). Results were correlated with clinical consequences, mainly arrhythmias, within a follow-up period of 5±2days. Results: While most patients had an increase in all four parameters, only the QT dispersion ratio showed a significant difference when correlated with ventricular arrhythmias (p < 0.001, F ratio = 38). Conclusion: QT dispersion ratio appears to be a new and promising parameter in predicting ventricular arrhythmias in patients with acute ischemia.     

The effect of intravenous magnesium therapy on serum and urine levels of potassium, calcium, and sodium in patients with ischemic heart disease, with and without acute myocardial infarction

Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effect of obesity and weight loss on ventricular repolarization: a systematic review and meta‐analysis

We performed a systematic review and meta‐analysis of the effects of obesity ± overweight and weight loss on the corrected QT interval (QTc) and QT or QTc dispersion (indices of ventricular repolarization). Mean difference for both QTc and QT or QTc dispersion with 95% confidence intervals (CIs) was calculated comparing obese ± overweight subjects and normal weight controls and QTc and QT or QTc dispersion before and after weight loss from diet ± exercise or bariatric surgery. A total of 22 studies fulfilled the selection criteria. Compared with normal weight controls, there was a significantly longer QTc in obese ± overweight subjects (mean difference of 21.74 msec, 95% CI: 18.76 to 22.32) and significantly longer QT or QTc dispersion (mean difference of 15.17 msec, 95% CI: 13.59 to 16.74). Weight loss was associated with a significant decrease in QTc (mean difference ?25.77 msec, 95% CI: ?28.33–23.21) and QT or QTc dispersion (mean difference of ?13.46 msec, 95% CI: ?15.60 to ?11.32 in obese ± overweight subjects. Thus, obesity ± overweight is associated with significant prolongation of QTc and QT or QTC dispersion. Weight loss in obese ± overweight subjects produces significant decreases in these variables. © 2016 World Obesity