Time dependent variability of QT dispersion after acute myocardial infarction and its relation to ventricular fibrillation: a prospective study

OBJECTIVE—To show whether increased QT dispersion on admission predicts ventricular fibrillation after acute myocardial infarction, and to determine the nature of time related changes in QT dispersion.
DESIGN—Prospective cohort study.
SETTING—Coronary care units of three teaching hospitals in Newcastle-upon-Tyne over an eight month period.
PATIENTS—All had acute myocardial infarction according to World Health Organization criteria.
INTERVENTIONS—For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded on admission at a paper speed of 50 mm/s. In a subset, serial ECGs were recorded regularly to show time related changes in QTcd following acute myocardial infarction.
MAIN OUTCOME MEASURES—Occurrence of ventricular fibrillation within the first 24 hours after myocardial infarction.
RESULTS—Data collected from 201 patients, 12 of whom (6%) developed ventricular fibrillation within 24 hours. Neither QTd nor QTcd differed between those developing ventricular fibrillation and those who did not: QTd mean (SD), 74 (24) ms (95% confidence interval (CI) 59 to 89) v 66 (24) ms (95% CI 62 to 70), respectively; QTcd, 86 (26) ms^0.5 (95% CI 70 to 102) v 77 (29) ms^0.5 (95% CI 72 to 82), respectively. Significant QTcd changes occurred early after myocardial infarction.
CONCLUSIONS—Admission QTd and QTcd do not predict ventricular fibrillation after acute myocardial infarction. There are significant changes in QTcd with time, which may account for this measured lack of correlation.


Keywords: acute myocardial infarction; arrhythmia; ventricular fibrillation; QT dispersion     

Incidence of nonsustained and sustained ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator

INTRODUCTION: Nonsustained ventricular tachycardia (NSVT) is a frequent phenomenon in some patients with heart disease, but its association with sustained ventricular tachycardias (ventricular tachycardia [VT]/ventricular fibrillation [VF]) is still not clear. The aim of this study was to determine whether NSVT incidence was associated with sustained VT/VF in patients with an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Retrospective data analysis was conducted in 923 ICD patients with a mean follow-up of 4 months. NSVT and sustained VT/VF were defined as device-detected tachycardias. The incidence rates of NSVT and sustained VT/VF as well as ICD therapies were determined as episodes per patient. The NSVT index was defined as the product of NSVT episodes/day times the mean number of beats per episode, i.e., total beats/day. The NSVT index peak was defined as the highest value on or prior to the day with sustained VT/VF episodes. Patients (n = 393) with NSVT experienced a higher incidence of sustained VT/VF (17.2 +/- 63.0 episodes/patient) and ICD therapies (15.2 +/- 61.4 episodes/patient) than patients (n = 530) without NSVT (sustained VT/VF: 0.5 +/- 6.6 and therapies: 0.5 +/- 5.6; P < 0.0001). Approximately 74% of NSVT index peaks occurred on the same day or <3 days prior to sustained VT/VF episodes. The index was higher for peaks < or =3 days prior to the day with sustained VT/VF (94.3 +/- 140.1 total beats/day) than for peaks >3 days prior to the day with sustained VT/VF (32.7 +/- 55.9 total beats/day; P < 0.0001). CONCLUSION: ICD patients with NSVT represent a population more likely to experience sustained VT/VF episodes with a temporal association between an NSVT surge and sustained VT/VF occurrence.     

Reduction of exercise-induced regional contractile dysfunction in dogs using a novel calcium channel blocker (Ro 40-5967)

Summary Ro 40-5967 is a calcium channel blocker with a novel chemical structure. The purpose of this study was to evaluate the effects of Ro 40-5967 on systemic hemodynamics and regional contractile function in a canine model of chronic coronary artery stenosis in which no contractile dysfunction is observed at rest, but dynamic exercise elicits regional myocardial ischemia and contractile dysfunction. Thirteen dogs were chronically instrumented with sonomicrometers for the measurement of wall thickness in the anterior and posterior left ventricular walls, a micromanometer for measuring left ventricular pressure (LVP) and its first derivative (dP/dt), and a catheter in the aorta for measuring systemic arterial pressure. An ameroid constrictor on the left circumflex coronary artery produced gradual constriction of the vessel such that treadmill exercise elicited regional contractile dysfunction. Runs were repeated 3 hours later after the administration of Ro 40-5967 (0.3 mg/kg, IV). During the control run, regional systolic wall thickening in the posterior wall fell from 25.5 ± 6.3% (SD) to 15.9 ± 5.1% (p<0.05). Ro 40-5967 did not change resting function in the poststenotic myocardium (26.9 ± 8.4%) but improved regional function during the run to 18.2 ± 6.2% (p<0.05). This improvement was associated with a slight decrease in the exercise heart rate (213 ± 18 vs. 200 ± 16 bpm, NS), no change in peak ventricular pressure (156 ± 22 vs. 157 ± 20 mmHg), mean aortic pressure (123 ± 19 vs. 118 ± 20 mmHg), dP/dt (5129 ± 1143 vs. 5288 ± 1120 mm Hg/sec), or systolic wall thickening in a distant control region. Thus, in the exercising dog with fixed coronary stenosis, Ro 40-5967 had an antiischemic effect with no detectable negative inotropic effect.Studies were performed at the Seaweed Canyon Laboratory, Division of Cardiology, Department of Medicine, University of California, San Diego     

Associations of Left Ventricular Hypertrophy and Geometry with Adverse Outcomes in Patients with CKD and Hypertension

Background and objectives

Left ventricular hypertrophy (LVH) and abnormal left ventricular (LV) geometry predict adverse outcomes in the general and hypertensive populations, but findings in CKD are still inconclusive.

Design, setting, participants, & measurements

We enrolled 445 patients with hypertension and CKD stages 2–5 in two academic nephrology clinics in 1999–2003 who underwent both echocardiography and ambulatory BP monitoring. LVH (LV mass >100 g/m² [women] and >131 g/m² [men]) and relative wall thickness (RWT) were used to define LV geometry: no LVH and RWT≤0.45 (normal), no LVH and RWT>0.45 (remodeling), LVH and RWT≤0.45 (eccentric), and LVH and RWT>0.45 (concentric). We evaluated the prognostic role of LVH and LV geometry on cardiovascular (CV; composite of fatal and nonfatal events) and renal outcomes (composite of ESRD and all-cause death).

Results

Age was 64.1±13.8 years old; 19% had diabetes, and 22% had CV disease. eGFR was 39.9±20.2 ml/min per 1.73 m². LVH was detected in 249 patients (56.0%); of these, 125 had concentric LVH, and 124 had eccentric pattern, whereas 71 patients had concentric remodeling. Age, women, anemia, and nocturnal hypertension were independently associated with both concentric and eccentric LVH, whereas diabetes and history of CV disease associated with eccentric LVH only, and CKD stages 4 and 5 associated with concentric LVH only. During follow-up (median, 5.9 years; range, 0.04–15.3), 188 renal deaths (112 ESRD) and 103 CV events (61 fatal) occurred. Using multivariable Cox analysis, concentric and eccentric LVH was associated with higher risk of CV outcomes (hazard ratio [HR], 2.59; 95% confidence interval [95% CI], 1.39 to 4.84 and HR, 2.79; 95% CI, 1.47 to 5.26, respectively). Similarly, greater risk of renal end point was detected in concentric (HR, 2.33; 95% CI, 1.44 to 3.80) and eccentric (HR, 2.30; 95% CI, 1.42 to 3.74) LVH. Sensitivity analysis using LVH and RWT separately showed that LVH but not RWT was associated with higher cardiorenal risk.

Conclusions

In patients with CKD, LVH is a strong predictor of the risk of poor CV and renal outcomes independent from LV geometry.     

Regression of Left Ventricular Mass After Transcatheter Aortic Valve Replacement: The PARTNER Trials and Registries

BackgroundGreater early left ventricular mass index (LVMi) regression is associated with fewer hospitalizations 1 year after transcatheter aortic valve replacement (TAVR). The association between LVMi regression and longer-term post-TAVR outcomes is unclear.ObjectivesThe purpose of this study was to determine the association between LVMi regression at 1-year post-TAVR and clinical outcomes between 1 and 5 years.MethodsAmong intermediate- and high-risk patients who received TAVR in the PARTNER (Placement of Aortic Transcatheter Valves) I, II, and S3 trials or registries and were alive at 1 year, we included patients with baseline moderate or severe left ventricular hypertrophy (LVH) and paired measurements of LVMi at baseline and 1 year. The associations between LVMi regression (percent change between baseline and 1 year) and death or rehospitalization from 1 to 5 years were examined.ResultsAmong 1,434 patients, LVMi was 146 g/m² (interquartile range [IQR]: 133 to 168 g/m²) at baseline and decreased 14.5% (IQR: 4.2% to 26.1%) to 126 g/m² (IQR: 106 to 148 g/m²) at 1 year. After adjustment, greater LVMi regression at 1 year was associated with lower all-cause death (adjusted hazard ratio [aHR]: 0.95 per 10% decrease in LVMi; 95% confidence interval [CI]: 0.91 to 0.98; p = 0.004; aHR of the quartile with greatest vs. least LVMi regression: 0.61; 95% CI: 0.43 to 0.86; p = 0.005). Severe LVH at 1 year was observed in 39%, which was independently associated with increased all-cause death (aHR of severe LVH vs. no LVH: 1.71; 95% CI: 1.20 to 2.44; p = 0.003). Similar associations were found for rates of cardiovascular mortality and rehospitalization.ConclusionsAmong patients with moderate or severe LVH treated with TAVR who are alive at 1 year, greater LVMi regression at 1 year is associated with lower death and hospitalization rates to 5 years. These findings may have implications for the timing of valve replacement and the role of adjunctive medical therapy after TAVR.     

心脏交感神经重构与心律失常:新兴领域的当前认识

心脏内交感神经纤维分布十分广泛,近年发现许多心脏疾病伴有交感神经分布、密度改变的现象,并与心律失常发生、疾病预后都有密切的关联。交感神经重构与心肌组织重构、电重构相互影响,可能是心律失常发生的基础。对交感神经重构进行干预可能成为将来新的一个治疗方向。     

急性前壁心肌梗死后梗死相关血管延迟开通对晚期左室重构的影响

目的探讨急性前壁心肌梗死后,延迟经皮冠状动脉血运重建术(PCI)使梗死相关血管(IRA)开通,对心梗晚期左室重构的影响.方法选择64例急性前壁、前间壁及广泛前壁Q波性心梗后病情稳定,发病10～21天冠脉造影证实左前降支完全闭塞者,依据是否接受成功PCI,分为成功PCI组和对照组,分别于急性期、术后2个月和6个月应用超声心动图随访左室腔大小、左室功能和室壁活动异常,并观察6个月期间心力衰竭事件的发生情况.结果心梗后2个月两组左室射血分数(LVEF)、左室收缩末期容积指数(LVESVI)、左室舒张末期容积指数(LVEDVI)和室壁活动异常(VWMA)积分与急性期相比无明显差异(P＞0.05),急性期和2个月时两组上述各指标之间相比差异也无显著性(均P＞0.05).6个月时两组LVEF和VWMA积分与急性期和2个月相比无明显差异(P＞0.05),但对照组LVEDVI和LVESVI较急性期明显增大(P＜0.01,P＜0.05),且与成功PCI组相比差异具有显著性(P＜0.01,P＜0.05).6个月随访期间心力衰竭事件发生率对照组为19%,成功PCI组2%,但差异缺乏统计学意义(P＞0.05).结论急性前壁心梗后IRA延迟开通能明显减少心梗后晚期的左室重构,而对心梗后早期左室重构的影响不大.延迟PCI可能有利于减少心梗后远期心力衰竭事件的发生.     

A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill

Mutations in the cardiac Na+ channel gene SCN5A are responsible for multiple lethal ventricular arrhythmias including Brugada syndrome and congenital long QT syndrome. Here we report a case of Brugada syndrome with ST elevation in the right precordial and inferior leads accompanied by atrial standstill and spontaneous ventricular fibrillation. Atrial standstill and J wave elevation were provoked by procainamide. Genetic analysis revealed a missense mutation (R367H) in SCN5A. The resultant mutant Na+ channel was nonfunctional when expressed heterologously in Xenopus oocytes. Our study suggests that genetic defects in SCN5A may be associated with atrial standstill in combination with ventricular arrhythmias.     

Prognostic implications of ventricular fibrillation in acute myocardial infarction: new strategies required for further mortality reduction

OBJECTIVE—To determine the changing risk of ventricular fibrillation, the prognostic implications, and the potential long term prognostic benefit of earlier hospital admission, after acute myocardial infarction.
DESIGN—Prospective observational study.
SETTING—A district general hospital in east London.
PATIENTS—1225 consecutive patients admitted to a coronary care unit with acute myocardial infarction.
MAIN OUTCOME MEASURES—Time of onset of pain and ventricular fibrillation, and long term survival of patients admitted with acute myocardial infarction.
RESULTS—The rate of ventricular fibrillation in these hospital inpatients was high in the first hour from onset of pain (118 events/1000 persons/h; 95% confidence interval (CI) 50.7 to 231) and fell rapidly to an almost constant low level by six hours; 27.4% of patients with early ventricular fibrillation died in hospital, compared with 11.6% of those without (p < 0.0001), but mortality in patients who survived to hospital discharge was not altered by early ventricular fibrillation (five year survival: 75.0% (95% CI 60.0% to 84.8%) with ventricular fibrillation v 73.3% (95% CI 69.6% to 76.6%) without ventricular fibrillation).
CONCLUSIONS—Patients successfully resuscitated from early ventricular fibrillation have the same prognosis as those without ventricular fibrillation after acute myocardial infarction. Faster access to facilities for resuscitation must be achieved if major improvements in the persistently high case fatality of patients after acute myocardial infarction are to be made.


Keywords: ventricular fibrillation; acute myocardial infarction; prognosis     

Provocation of ventricular tachycardia by antimalarial drug halofantrine in congenital long QT syndrome

This report deals with two patients who suffered sustained episodes of torsade de pointes ventricular tachycardia while using the novel antimalarial drug halofantrine. Both patients had congenital long QT syndrome, and their QT interval was further prolonged at the time of the event. This first electrocardiographic documentation of ventricular arrhythmias together with halofantrine's known prolonging effect on the QT interval demonstrates that the drug has the potential to induce life-threatening arrhythmias.