Ventricular arrhythmias are associated with increased QT interval and QRS dispersion in patients with ST-elevation myocardial infarction

Introduction and ObjectivesThe electrocardiogram continues to be essential in the diagnosis of acute myocardial infarction, and a useful tool in arrhythmic risk stratification. We aimed to determine which electrocardiographic variables can successfully predict the occurrence of ventricular arrhythmias (VA) in patients following ST-segment elevation myocardial infarction (STEMI).MethodsWe performed an observational study including 667 patients with STEMI admitted to the University Hospital in Sancti Spíritus, Cuba. Demographic variables, cardiovascular risk factors, and clinical variables were recorded. Electrocardiographic variables included QT interval duration (measured and corrected) and QT dispersion, QRS duration and dispersion, JT interval duration and ST-segment elevation magnitude. We also determined left ventricular ejection fraction and glomerular filtration rate. A binary statistical regression model and a regression tree were used to determine the variables that successfully predicted VA.ResultsVA occurred in 92 (13.8%) patients, within the first 48 hours in 68 (73.9%) and after this period in 24 (26.1%) patients. The variables associated with VA were QT interval duration >529 ms and QT dispersion >66 ms, QRS dispersion >50 ms, and the presence of ST-segment elevation in six or more leads.ConclusionsThe main predictor of VA occurring during the initial 48 hours was QT interval duration, while, after this period, it was QRS dispersion.     

QT dispersion in patients with chronic heart failure: beta blockers are associated with a reduction in QT dispersion

OBJECTIVE: To compare QT dispersion in patients with impaired left ventricular systolic function and in matched control patients with normal left ventricular systolic function. DESIGN: A retrospective, case-control study with controls matched 4:1 for age, sex, previous myocardial infarction, and diuretic and beta blocker treatment. SETTING: A regional cardiology centre and a university teaching hospital. PATIENTS: 25 patients with impaired left ventricular systolic function and 100 patients with normal left ventricular systolic function. MAIN OUTCOME MEASURES: QT and QTc dispersion measured by three methods: the difference between maximum and minimum QT and QTc intervals, the standard deviation of QT and QTc intervals, and the "lead adjusted" QT and QTc dispersion. RESULTS: All measures of QT/QTc dispersion were closely interrelated (r values 0.86 to 0.99; all p < 0.001). All measures of QT and QTc dispersion were significantly increased in the patients with impaired left ventricular systolic function v controls (p < 0.001): 71.9 (6.5) (mean (SEM)) v 46.9 (1.7) ms for QT dispersion, and 83.6 (7.6) v 54.3 (2.1) ms(-1-2) for QTc dispersion. All six dispersion parameters were reduced in patients taking beta blockers (p < 0.05), regardless of whether left ventricular function was normal or impaired-by 9.4 (4.6) ms for QT dispersion (p < 0.05) and by 13.8 (6. 5) ms(-1-2) for QTc dispersion (p = 0.01). CONCLUSIONS: QT and QTc dispersion are increased in patients with systolic heart failure in comparison with matched controls, regardless of the method of measurement and independently of possible confounding factors. beta Blockers are associated with a reduction in both QT and QTc dispersion, raising the possibility that a reduction in dispersion of ventricular repolarisation may be an important antiarrhythmic mechanism of beta blockade.     

胺碘酮对室性心律失常患者QT离散度的影响

要：目的观察胺碘酮对室性心律失常患叩离散度的影响。方at400例室性心律失常患应用口服或静脉注射胺碘酮治疗,其中18例持续性室性心动过速患静脉应用胺碘酮治疗,负荷量为24h总量900～1500mg,同时口服胺碘酮600mg/d。382例频发室早伴或不伴短阵室速的患口服胺碘酮治疗,负荷量为第1周600mg/d,并根据病情逐渐减量。结果400例室性心律失常患应用胺碘酮治疗均有效,并发现该药能减少叽离散度,未见严重毒副作用．结论胺碘酮治疗室性心律失常安全有效．能影响患的QT离散度．且能减少室颤的发生。     

Ventricular arrhythmias and QT/QS2 index in patients with ischemic heart disease

This multicenter study comprised a group of 900 patients (207 females and 693 males, aged 23-68 years, mean 53) with ischaemic heart disease. Go medications other than nitrates, nifedipine and diuretics were administered at the time of study. In all patients a simultaneous standard 12-lead ecg and a phonocardiogram was registered. QT and QS2 intervals were then measured, and the QT/QS2 index calculated. QT/QS2 ratio 1.0 was considered as a normal one. A 24-h Holter ecg monitoring was performed in each patients, and ectopic ventricular activity was graded according to the Lown's classification. For patients with each class of arrhythmia the mean value of QT/QS2 was calculated. All means were similar, with values 1.0. Proportion of patients with abnormal values of QT/QS2 index was similar in patients showing different Lown classes of arrhythmia. Since a 24-hour monitoring does not give a full information about the arrhythmic events, patients with the history of VT/VF were analyzed separately. In this group an increase of QT/QS2 index was observed significantly more frequently than in other patients (37% vs 19%, p = 0.016). It is concluded that no close relationship exists between QT/QS2 index and the type of ventricular arrhythmia found on the Holter monitoring. However, pathologic QT/QS2 values seem to characterize the patients with increase risk of VT/VF.     

高血压病左室肥大Q-T离散度异常与室性心律失常的关系

观察180例高血压病患者的Q-T离散度(Q-Td),左室肥大组及左室正常组Q-Td分别为67.31±13.57和38.8±8.55ms(P<0.001),左室肥大组室性心律失常检出率为92.5%,其中复杂性者为64.2%,室速为23.9%,该组中Q-Td>60ms 3项检出率均高于<60ms及左室正常组中Q-Td>60ms者,复杂性室性心律失常及室速有显著性差异(P<0.001).提示高血压左室肥大Q-Td增加与室性心律失常尤其是复杂性室性心律失常及室速有一定关系,结合左室重量指数(LVMI)和Q-Td可作为评估高血压病患者预后的参考指标.     

胺碘酮对冠心病合并室性心律失常患者QT离散度影响的临床观察

目的观察胺碘酮对冠心病合并室性心律失常患者的QT离散度(QTd)及预后影响。方法选择的患者予以可达龙治疗8周,并比较治疗前后室性心律失常疗效及QTd的变化。结果治疗后室性心律失常均明显减少,有效率85.2%,QTd由(65.06±11.24)ms减至(33.9±16.2)ms(P<0.01=)。结论胺碘酮能有效减少冠心病伴室性心律失常而且使患者QTd明显减少,改善患者的预后。     

Influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and clinical outcome

Increased QT dispersion, defined as the difference between the maximum and minimum QT interval on the standard 12-lead electrocardiogram, is assumed to reflect regional inhomogeneity of ventricular repolarization and has been shown to be associated with an increased risk of arrhythmic events. The purpose of the present study is to examine the influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and to evaluate the predictive value of QT dispersion after amiodarone therapy for further arrhythmic events. ECG's were obtained in 47 patients 1–2 days before and 6–8 weeks after amiodarone was started. All patients had coronary artery disease with a mean EF of 34±14%. The QT interval was measured in each lead of a digitized ECG displayed on a high resolution monitor (250 mm s⁻¹). Amiodarone therapy resulted in a significant increase in the maximal QT_c interval (476±44 to 505±44 ms, p<0.001). However, measurement of QT dispersion (70±34 vs 73±29 ms) and Qtc dispersion (78±37 vs 77±31 ms) revealed no significant difference before and after amiodarone. During a one year follow-up period 26 patients were free of arrhythmic events and 7 patients developed further arrhythmic events. The remaining 14 patients were excluded from the one year follow-up analysis because of drug discontinuation (n=8), death due to heart failure (n=1), medical intervention (n=3) and incomplete follow-up (n=2). No measure of QT dispersion was predictive of recurrent arrhythmic events during treatment with amiodarone.

Conclusion: Treatment with amiodarone results in significant QT prolongation without altering QT dispersion. Measurements of QT dispersion were not predictive of amiodarone efficacy in this patient population.     

QT dispersion as a predictor for arrhythmias in patients with acute ST elevation myocardial infarction

Aims and Objectives

To study the effect of Heart Rate Variability (HRV) and QT dispersion (QTd) in patients presenting with Acute ST elevation myocardial infarction (STEMI).

Methods

This is a retrospective study conducted on patients admitted with the diagnosis of acute ST elevation myocardial infarction. In all 100 patients with acute myocardial infarction in one year were subjected to a complete evaluation in terms of history and examination. Besides routine investigations standard 12 lead ECG was evaluated in all cases on admission, after 4 hrs, 24 hrs, 48 hrs and on discharge.

Results

The most common presenting symptoms were chest pain (88%) and dyspnea (50%). Tachycardia was seen in 56% while congestive heart failure was present in 29% patients. Patients who died had a higher QTd in comparison to patients who survived.

Conclusions

Markers of autonomic regulation of heart like QTd provides valuable information about the future course of events in a patient following acute STEMI which can be utilized to plan the future course of management in patients especially predisposed to adverse and catastrophic outcomes.     

Decreases by magnesium of QT dispersion and ventricular arrhythmias in patients with acute myocardial infarction.

AIMS: Magnesium treatment suppresses ventricular arrhythmias in acute myocardial infarction and possibly mortality after infarction, but the underlying mechanisms are inadequately understood. We tested whether the effect of magnesium could be attributed to an influence on the autonomic control of the heart, changes in disturbed repolarization, relief of ischaemia or limitation of myocardial injury. METHODS AND RESULTS: Fifty-nine consecutive patients with acute myocardial infarction were randomized to receive 70 mmol of magnesium (n = 31) infused over 24 h or placebo (n = 26). Occurrence of ventricular arrhythmias and heart rate variability (SD of 5-min mean sinus beat intervals over a 24 h period, SDANN; low frequency/high frequency amplitude ratio, LF/HF ratio), and the number of ischaemic episodes on vectorcardiography were measured from the first day of treatment. QT dispersion corrected for heart rate was measured from the 12-lead ECG. Magnesium decreased the number of hourly ventricular premature beats (P < 0.001) and the number of ventricular tachycardias (P < 0.05). QT dispersion corrected for heart rate was decreased in both measurements at 24 h and 1 week (P < 0.001). SDANN and LF/HF ratio were unchanged. The number of ischaemic episodes on vectorcardiography were equal, and peak creatine kinase MB release did not differ between the groups. In testing the pathophysiological mechanisms, serum magnesium levels after infusion correlated with hourly ventricular premature beats (rs = -0.47; P < 0.01), ventricular tachycardias (rs = -0.26; P < 0.05), and QT dispersion corrected for heart rate (rs = -0.75; P < 0.001), but not with SDANN, LF/HF ratio or peak creatine kinase MB. QT dispersion corrected for heart rate correlated with hourly ventricular premature beats (rs = 0.48; P < 0.001) and ventricular tachycardias (rs = 0.27; P < 0.05). CONCLUSIONS: Magnesium suppresses early ventricular arrhythmias in acute myocardial infarction. The decreased arrhythmicity is related to enhancement of homogeneity in repolarization, but not to attenuation of prevailing ischaemia, improvement of autonomic nervous derangements or myocardial salvage.     

QT dispersion in patients with Takayasu arteritis

This study was designed to test the hypothesis that myocardial involvement exists in patients with Takayasu arteritis and is associated with increased QT dispersion, which is a marker of repolarization inhomogeneity. Twenty-one consecutive patients with Takayasu arteritis and no significant coronary artery disease were included. Twelve-lead electrocardiogram and exercise-induced thallium-201 myocardial scintigraphy were performed in all patients. Ten of 21 patients (48%) had abnormal findings on scintigraphy. Patients were divided into two groups by the presence (group P, n = 10) or absence (group N, n = 11) of exercise-induced thallium-201 myocardial scintigraphic perfusion abnormalities, including permanent defects in three, reversible defects in four, and slow washout in three. The QT dispersion at rest was significantly greater in group P than that in group N (54 +/- 12 vs 40 +/- 8 msec, p < 0.005). The QTc dispersion at rest was also significantly greater in group P than in group N (59 +/- 15 vs 43 +/- 11 msec, p < 0.01). In patients with Takayasu arteritis, myocardial involvement suggested by exercise-induced thallium-201 myocardial scintigraphic perfusion abnormalities is not rare, even when no significant coronary stenosis is present on angiography. Increased baseline QT dispersion was associated with scintigraphic abnormalities and may be a useful marker of myocardial involvement in patients with Takayasu arteritis.     

无器质性心脏病者QT离散度与室性心律失常的关系

目的 评价无器质性心脏病者ＱＴ离散度（ＱＴＤ）与室性心律失常的关系。方法 于ＤＣＧ检查前进行常规１２导ＥＣＧ检查，测量ＱＴ间期，计算ＱＴＤ，ＱＴｃｄ（校正的ＱＴＤ）根据２４小时ＥＣＧ检出的室性心律失常情况，分为无室早组，室早〈１００次，室早≥１００次组，成对室早组及无成对室早组，比较各组病人之ＱＴＤ，ＱＴｃＤ。结果 无室早组，室早〈１００次，室早≥１００次组，成室早组及无成对室早组之ＱＴＤ分别为２     

QT dispersion in patients with polycystic ovary syndrome

Cardiac risk factors are observed more frequently in patients with polycystic ovary syndrome (PCOS). On the other hand, increased QT dispersion, which is a risk factor for cardiac arrhythmias and sudden death, has not been investigated in this syndrome. In this study, we evaluated QT dispersion in PCOS patients without overt heart disease. Thirty-six consecutive women with PCOS (mean age 24+/-5 years) and 36 healthy women of similar ages (mean age 24+/-4 years) participated in this study. PCOS was diagnosed if there were polycystic ovaries by ultrasound (enlarged ovaries with > or =8 cysts 2-8 mm in diameter), oligoamenorrhea (intermenstrual interval >35 days), hirsutism (Ferriman-Gallwey score, > or =7) and elevated serum levels of testosterone (> or =2.7 nmol/L). Electrocardiograms were recorded at a paper speed of 50 mm/s. QT intervals were manually measured by a cardiologist. All intervals were corrected for heart rate according to Bazett's formula: QTc interval=QT interval/square root of the RR interval. Mean values of body mass index, heart rate, and blood pressure were not significantly different between the two groups (P>0.05). No significant differences in QT intervals (maximum QT, minimum QT, QT dispersion, minimum corrected QT, maximum corrected QT, and corrected QT dispersion) were observed between the two groups (P>0.05). Our results suggest that the risk of ventricular arrhythmias or sudden cardiac death is not increased in PCOS patients.     

QT interval dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?

OBJECTIVE--To assess QT interval dispersion on the surface electrocardiogram in patients with sustained ventricular arrhythmias. DESIGN--A retrospective and prospective blinded controlled study of patients referred for investigation of ventricular arrhythmias at a tertiary cardiac centre. PATIENTS AND METHODS--89 consecutive patients with sustained ventricular arrhythmias due to chronic ischaemic heart disease, cardiomyopathy, or ventricular tachycardia (VT) in a normal heart. 32 patients did not meet the inclusion criteria; therefore 57 patients were compared with a control group of 40 patients with myocardial disease but no history of arrhythmias and 12 normal controls with no myocardial disease. Standard 12 lead electrocardiograms were enlarged, the QT intervals for each lead measured, and QT dispersion calculated. RESULTS--There was a significantly greater mean QT dispersion (77 ms) in patients with sustained ventricular arrhythmias compared with the control group (38 ms, p < 0.01). This held for all groups; after myocardial infarction VT (82 (22) ms v control 38 (10) ms; p < 0.01), dilated cardiomyopathy VT (76 (18) ms v control 40 (11) ms, p < 0.01), and normal heart VT (65 (7) ms v control 32 (8), p < 0.05). There was also a greater QT dispersion in patients with impaired left ventricular function and VT, with a correlation between left ventricular function and QT dispersion in patients with VT (r = 0.56, p < 0.01). CONCLUSION--QT interval dispersion may be a further non-invasive marker of susceptibility to ventricular arrhythmias.     

Increased dispersion of refractoriness in the absence of QT prolongation in patients with mitral valve prolapse and ventricular arrhythmias

BACKGROUND--The mechanism responsible for the reported high incidence of ventricular arrhythmias in mitral valve prolapse is not clear. Electrocardiographic studies show an increased occurrence of repolarisation abnormalities on the 12 lead surface electrocardiogram, indicating regional differences in ventricular recovery. The purpose of this study was to investigate whether dispersion of refractoriness was an arrhythmogenic mechanism. METHODS--QT dispersion was measured in 32 patients with echocardiographically documented mitral valve prolapse and ventricular arrhythmias on 24 hour Holter recordings. QT dispersion was defined as the difference between the maximum and minimum average QT interval in any of the 12 leads of the surface electrocardiogram. QT dispersion corrected for heart rate was calculated by Bazett's formula. The results were compared with the data from 32 matched controls without a history of cardiac disease. Patients taking drugs that influence the QT interval and patients with a QRS duration > 120 ms were excluded. RESULTS--QT dispersion was greater in patients with mitral valve prolapse than in matched controls (60 (20) v 39 (11 ms) respectively, P < or = 0.001) as was corrected QT (64 (20 ms) v 43 (12 ms) respectively, P < or = 0.001). There was no significant difference in minimum or maximum QT intervals between the two groups. CONCLUSIONS--QT dispersion on the 12 lead surface electrocardiogram was greater in patients with mitral valve prolapse with ventricular arrhythmias than in normal controls, but the maximum QT interval was not increased. The results accord with the hypothesis that regional shortening and lengthening of repolarisation times in patients with mitral valve prolapse may account for the increased dispersion of refractoriness.     

Ventricular arrhythmias in heart failure patients

Ventricular arrhythmia represents a significant cause of mortality and morbidity. Its pathophysiologic mechanisms and electroanatomic substrates are slowly being elucidated. Clinical management in patients with heart failure has progressed from antiarrhythmic drugs to device therapy. Catheter ablation is an effective adjunct in the management of ventricular arrhythmia but remains a significant challenge. Advances in robotic and magnetic catheter manipulation may shorten procedural time and increase safety. Incorporation of imaging technologies such as CT, MRI, or ultrasound with electroanatomic mapping can enhance the ability to map and ablate ventricular arrhythmia. Novel imaging modalities may provide rapid characterization of the substrate for ventricular dysfunction and arrhythmia development and the capacity for serial assessment of the disease progression, improving risk stratification for ventricular dysfunction and arrhythmia development and the capacity for serial assessment of the disease progression, improving risk stratification.