Incidence Of Malignant Ventricular Arrhythmias Research Articles

A Territory-Wide Study of Arrhythmogenic Right Ventricular Cardiomyopathy Patients from Hong Kong

Background: Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a hereditary disease characterized by fibrofatty infiltration of the right ventricular myocardium that predisposes affected patients to malignant ventricular arrhythmias, dual-chamber cardiac failure and sudden cardiac death (SCD). The present study aims to investigate the risk of detrimental cardiovascular events in an Asian population of ARVC/D patients, including the incidence of malignant ventricular arrhythmias, new-onset heart failure with reduced ejection fraction (HFrEF), as well as long-term mortality. Methods and Results: This was a territory-wide retrospective cohort study of patients diagnosed with ARVC/D between 1997 and 2019 in Hong Kong. This study consisted of 109 ARVC/D patients (median age: 61 [46–71] years; 58% male). Of these, 51 and 24 patients developed incident VT/VF and new-onset HFrEF, respectively. Five patients underwent cardiac transplantation, and 14 died during follow-up. Multivariate Cox regression identified prolonged QRS duration as a predictor of VT/VF (p < 0.05). Female gender, prolonged QTc duration, the presence of epsilon waves and T-wave inversion (TWI) in any lead except aVR/V1 predicted new-onset HFrEF (p < 0.05). The presence of epsilon waves, in addition to the parameters of prolonged QRS duration and worsening ejection fraction predicted all-cause mortality (p < 0.05). Clinical scores were developed to predict incident VT/VF, new-onset HFrEF and all-cause mortality, and all were significantly improved by machine learning techniques. Conclusions: Clinical and electrocardiographic parameters are important for assessing prognosis in ARVC/D patients and should in turn be used in tandem to aid risk stratification in the hospital setting.

Rationale and design of the pragmatic clinical trial tREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fracTion (REBOOT).

There is a lack of evidence regarding the benefits of β-blocker treatment after invasively managed acute myocardial infarction (MI) without reduced left ventricular ejection fraction (LVEF). The tREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fracTion (REBOOT) trial is a pragmatic, controlled, prospective, randomized, open-label blinded endpoint (PROBE design) clinical trial testing the benefits of β-blocker maintenance therapy in patients discharged after MI with or without ST-segment elevation. Patients eligible for participation are those managed invasively during index hospitalization (coronary angiography), with LVEF >40%, and no history of heart failure (HF). At discharge, patients will be randomized 1:1 to β-blocker therapy (agent and dose according to treating physician) or no β-blocker therapy. The primary endpoint is a composite of all-cause death, non-fatal reinfarction, or HF hospitalization over a median follow-up period of 2.75 years (minimum 2 years, maximum 3 years). Key secondary endpoints include the incidence of the individual components of the primary composite endpoint, the incidence of cardiac death, and incidence of malignant ventricular arrhythmias or resuscitated cardiac arrest. The primary endpoint will be analysed according to the intention-to-treat principle. The REBOOT trial will provide robust evidence to guide the prescription of β-blockers to patients discharged after MI without reduced LVEF.

TLR4 participates in sympathetic hyperactivity Post-MI in the PVN by regulating NF-κB pathway and ROS production

Sympathetic nerve hyperactivity is a primary reason for fatal ventricular arrhythmias (VAs) following myocardial infarction (MI). Pro-inflammatory cytokines produced in the paraventricular nucleus (PVN) post-MI are associated with sympathetic overexcitation; however, the precise mechanism needs further investigation. Our aim was to explore the mechanism of toll-like receptor 4 (TLR4) and its downstream molecular pathway in mediating sympathetic activity post-MI within the PVN. A rat MI model was developed via left anterior descending coronary artery ligation. TLR4 was primarily localized in microglia and increased markedly within the PVN at 3 days in MI rats. Sympathoexcitation also increased, as indicated by high levels of renal sympathetic nerve activity (RSNA) and norepinephrine (NE) concentration. TLR4 knockdown via shRNA microinjection to the PVN resulted in decreased activation of Fos protein (+) neurons in the PVN and peripheral sympathetic nerve activity. TLR4 knockdown also exhibited a lower arrhythmia score following programmed electrical stimulation than those treated with MI surgery only, indicating that the knockdown of TLR4 decreased the incidence of malignant ventricular arrhythmias following MI. LPS-induced inflammatory response was analyzed to explore the underlying mechanism of TLR4 in sympathetic hyperactivity. High levels of NF-κB protein, the pro-inflammatory cytokines IL-1β and TNF-α, and ROS production were observed in the LPS group. PVN-targeted injection of the NF-κB inhibitor PDTC attenuated NF-κB expression and sympathetic activity. Taken together, the results suggested that knockdown of microglial TLR4 within the PVN decreased sympathetic hyperactivity and subsequent VAs post-MI. The downstream NF-κB pathway and ROS production participated in the process. Interventions targeting TLR4 signaling in the PVN may be a novel approach to ameliorate the incidence of VAs post-MI.

Late Gadolinium Enhancement and Extracellular Volume Fraction Between Sarcomeric Mutation Positive and Negative Hypertrophic Cardiomyopathy

Introduction Hypertrophic cardiomyopathy (HCM) is a genetic disorder with an autosomal dominant pattern of inheritance and variable expression and penetrance. Traditional genetic testing has a yield of approximately 60%, due in part to a lack of identified causal genes. Patients with an identified sarcomeric mutation have worse outcomes with a higher incidence of sudden cardiac death though the underlying mechanism behind this is incompletely understood. Cardiac MRI has emerged as a modality to detect fibrosis, and HCM patients with focal/replacement fibrosis measured by late gadolinium enhancement (LGE) have a higher incidence of malignant ventricular arrhythmias and may develop systolic heart failure. Few studies exist investigating patterns of LGE between gene mutation positive (G+) and gene mutation negative HCM patients (G−). And to date, no study has compared diffuse fibrosis measured by extracellular volume (ECV) between these two groups in HCM. Hypothesis HCM patients with an identified gene mutation will have more focal/replacement fibrosis (measured by LGE) and diffuse fibrosis (measured by ECV) than HCM patients without an identified mutation. Methods and Results A total of 336 patients with a diagnosis of HCM underwent a cardiac MRI at our institution between 4/2012 and 2/2017. Genetic testing was performed on 73 (mean age 49.6, 66% male) of these patients (29 G+, 39 G−, 5 variant of unknown significance or VUS). LGE was more commonly seen in G+ compared to G− patients (86 vs. 56%, OR 4.3, p = 0.01) and LGE measured as percentage of LV mass was significantly higher in G+ patients (7.5 ± 5.5 vs. 3.0 ± 3.0%, p Figure 1 ]. ECV from myocardial segments excluding LGE was similar among all groups (26.9 ± 2.9, 25.6 ± 3.0, and 25.9 ± 1.2%, p = 0.28) for G+, G-, and VUS cases respectively [ Figure 2 ]. Conclusion Genotyped HCM patients with an identified sarcomeric mutation have more focal/replacement fibrosis, but not diffuse fibrosis measured by ECV when compared to HCM patients without an identified mutation.

Effects of propofol on ventricular repolarization and incidence of malignant arrhythmias in adults

BackgroundPropofol is commonly used for procedural sedation in interventional electrophysiology. However, ventricular arrhythmias under Propofol have been reported. Our aim was to investigate ventricular repolarization and incidence of ventricular arrhythmias under Propofol infusion in adults with cardiac arrhythmias. MethodsQRS, QTcB (Bazett), QTcFri (Fridericia), JTc, measurement of T peak to Tend time (Tp-e) at baseline and under Propofol infusion was performed in 235 patients. Screening for unexpected ventricular arrhythmias was performed in 1165 patients undergoing EP procedures under Propofol. ResultsA significant prolongation of Tp-e under Propofol infusion (79.7±17.3 vs. 86.4±22.5ms, p<0.001) and of QTcFri (429.3±35.8 vs. 435.5±36.5, p=0.033) was detected. No significant change of the QTcB interval, JTc interval or QRS duration was observed. One case (0.09%) of ventricular fibrillation during rapid ventricular pacing under Propofol occurred. ConclusionAlthough transmural dispersion of ventricular repolarisation is increased under Propofol, incidence of malignant ventricular arrhythmias is low. For evaluation of QT interval under Propofol, Fridericia's correction formula should be used rather than Bazett's formula.

Malignant ventricular arrhythmias in alcoholic cardiomyopathy

BackgroundExcessive alcohol consumption is a well-known aetiology of atrial arrhythmias but there is little information concerning the prevalence or incidence of malignant ventricular arrhythmias in alcoholic cardiomyopathy (ACM). This study sought to investigate incidence and predictive factors of ventricular arrhythmias in ACM. MethodsRetrospective observational study of the clinical characteristics and long-term arrhythmic events in 282 consecutive patients with ACM (94 individuals) and idiopathic dilated cardiomyopathy (IDCM) (188 individuals) evaluated between 1993 and 2011. ResultsDuring a median follow-up of 38months (IQR:12–77), 42 patients died and 79 underwent heart transplantation [31 (33%) with ACM vs 90 (48%) with IDCM; p=0.017]. A total of 37 (13%) patients [18 (19%) ACM vs 20 (11%) IDCM; p=0.048] suffered malignant ventricular arrhythmias. On multivariate analysis, left bundle branch block (LBBB) (OR 2.4; CI95%: 1.2–5; p=0.015) and alcoholic aetiology (OR 2.3; CI95%: 1.1–4.5; p=0.026) were the only independent predictors of malignant ventricular arrhythmic events.A total of 18 (19%) ACM patients experienced 20 malignant ventricular arrhythmic events (4 aborted SCD, 8 SCD and 8 appropriate ICD therapies). At baseline evaluation, the only independent predictor of malignant ventricular arrhythmias in ACM patients was LBBB (OR 11.2; CI95%: 2.6–50; p=0.001). No malignant ventricular arrhythmias were recorded during follow-up in ACM patients if left ventricular ejection fraction (LVEF) had increased or remained ≥40%. ConclusionsMalignant ventricular arrhythmias are more frequent in ACM than in IDCM. LBBB identifies ACM patients with increased risk of SCD. No malignant ventricular arrhythmias were found during follow-up in ACM patients when LVEF was ≥40%.

Effects of ramipril on ventricular arrhythmia after myocardial infarction in rabbits.

Ventricular arrhythmia (VA) is one of the most common complications of myocardial infarction (MI), and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits. Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups: sham-operated (SHAM) group (n=8), MI group (n=8) and MI with ramipril (RAM) group (n=8). Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and III. After MI, rabbits in the RAM group were fed with intragastric ramipril (1 mg/kg per day) for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation (VT/VF) episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student's t test and ANOVA were used for statistical analysis. VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks (2.6±0.8 vs. 12.4±2.9, P<0.05). Twelve weeks after MI, the duration of repolarization for 90% (APD90) of three-tier ventricular myocytes in the MI group was longer than that before MI (258.2±21.1 vs. 230.1±23.2, 278.0±23.8 vs. 245.8±25.4, 242.6±22.7 vs. 227.0±21.7, P<0.05). However, the APD90 was not significantly different at 12 weeks before and after MI in the RAM group (P>0.05). Moreover, the transmural dispersion of repolarization (TDR) was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups (36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P<0.05). But the TDR was not significantly different between the RAM and SHAM groups (18.7±6.2 vs. 24.9±8.7, P>0.05). Ramipril may reduce the incidence of malignant ventricular arrhythmia via improvement of transmembrance repolarization heterogeneity after MI.

GW24-e3970 Study of prevalence and predictors of malignant ventricular arrhythmias after ST-segment elevation myocardial infarction

ObjectivesWe hypothesised that primary percutaneous coronary intervention (PCI) and contemporary medical treatment will result in a lower incidence of malignant ventricular arrhythmias (VA) and shorten the time frame of their...

Intracoronary Injection of Drugs to Treat No – Reflow Phenomenon and Microcirculatory Dysfunction

In a variant proportion of patients presenting with chest pain and electrocardiographic changes characteristic for ST - elevation myocardial infarction, percutaneous coronary intervention achieves epicardial coronary artery reperfusion but not the myocardial reperfusion (ranging from 5% to 50%). Furthermore, prolonged myocardial ischemia often breaks down the coronary microvasculature and the flow to the infarct myocardium may seem to be markedly reduced. This condition is known as no reflow - phenomenon. The no reflow - phenomenon is associated with an increased incidence of malignant ventricular arrhythmias, heart failure and 30-days mortality. In the recent years in literature, several articles (subsequently discussed in the present review) have been published and made relevant to the study of the pathophysiology regarding no reflow - phenomenon. This knowledge has assisted in the development of new treatment strategies, such as prophylactic use of vasodilators, mechanical devices and drugs inhibiting platelet. The review has focused on the current literature about intra - coronary injection of drugs to treat no - reflow and microvascular dysfunction.

E0456 Relationship between hypokalaemia at the early stage of acute myocardial infarction and malignant ventricular arrhythmia

ObjectiveTo investigate the relationship between hypokalaemia at the early stage of acute myocardial infarction (AMI) and malignant ventricular arrhythmia (MVA) as well as the features of hypokalaemia.MethodsTotal of 302 patients...

E0634 The relationship between hypokalaemia at the early stage of acute myocardial infarction and malignant ventricular arrhythmia

ObjectiveTo investigate the relationship between hypokalaemia at the early stage of acute myocardial infarction (AMI) and malignant ventricular arrhythmia (MVA) as well as the features of hypokalaemia.MethodsTotal of 302 patients...

An impaired renal function and advanced heart failure represent independent predictors of the incidence of malignant ventricular arrhythmias in patients with an implantable cardioverter/defibrillator for primary prevention

Malignant ventricular arrhythmias and inappropriate therapies represent unsolved problems in patients with implantable cardioverter/defibrillator (ICD) for primary prevention. This study focuses on the incidence of such therapies and thereby seeks to identify new predictors of adverse events to enhance risk stratification. Ninety-four consecutive patients with mild-to-moderate heart failure (NYHA II-III) and depressed left ventricular function (≤35%) were followed for 34 ± 20 months. Two hundred and ninety-one malignant ventricular arrhythmias were documented in 51 patients (54%). Eighteen patients (19%) received inappropriate ICD therapies (e.g. atrial fibrillation, sinus tachycardia, etc.). Patients with malignant arrhythmia (1.34 ± 0.44 vs. 1.16 ± 0.4 mg/dL, P = 0.017) and patients suffering from inappropriate ICD therapies (1.54 ± 0.48 vs. 1.2 ± 0.38 mg/dL; P = 0.007) revealed a significantly worse renal function before ICD implantation than participants without any therapy. An increased serum creatinine at baseline (2 vs. 1 mg/dL; odds ratio (OR) 3.96; P = 0.02; 95% CI: 1.2-13.04) and NHYA class III compared with II (OR: 2.96; P = 0.02; 95% CI: 1.16-7.48) represent strong and independent predictors for the occurrence of ventricular arrhythmias. Moreover, an impaired renal function is identified as an independent risk factor for inappropriate therapies (OR: 5.6; P = 0.004; 95% CI: 1.72-18.22). An impaired renal function and advanced heart failure before ICD implantation for primary prevention are identified as independent predictors for the incidence of appropriate ICD interventions. With regard to current guidelines and economical aspects, patients suffering from an impaired renal function or advanced heart failure seem to benefit most from ICD therapy.

Effect of bisoprolol on heart rate turbulence in patients with unstable angina pectoris

Objective To observe the effect of bisoprulol on malignant ventricular arrhythmia (MVA) and heart rate turbulence (HRT) in ambulatory electrocardiogram monitoring for twenty-four hours in patients with unsta-ble angina pectoris (UAP). Methods 40 UAP patients with premature ventricu]ar beats were observed. All patients were examined with ambulatory electrocardiogram monitoring for twenty-four hours before and after bisoprolol (5mg, Qd) was administered for 7 days. The number of patients with MVA、turbulence onset (TO) and turbulence slope (TS) were analyzed. Results After bisoprolol was administered for 7 days in patients with UAP,the number of pa-tients with MVA decreased by 14.2%. TO decreased and TS increased, and HRT was improved. Conclusions HRT had clinical prognostic value for malignant ventricular arrhythmia and sudden death in patients with UPA. Bisoprolol can improve HRT and reduce the incidence of MVA. Key words: Bisoprolol; Angina, unstable; Heart rate; Arrhythmia

Abrupt Termination of an Ethanol Regimen Provokes Ventricular Arrhythmia and Enhances Susceptibility to the Arrhythmogenic Effects of Epinephrine in Rats

Pathologists examining victims of sudden unexpected death encounter alcoholics more often than expected; alcohol may play a role in sudden arrhythmic death. Here we determine whether a pattern of alcohol consumption, chronic ethanol intake, and withdrawal increases the incidence of malignant ventricular arrhythmia and modulates susceptibility to the arrhythmogenic potential of sympathetic stimulation from an epinephrine test in rats. Male Wistar rats were treated with a continuous ethanol liquid diet for 7 weeks, and then subjected to 1-day withdrawal or 21-day abstinence. Ventricular ectopy was evaluated by 24-hour electrocardiographic telemetry recording; whole-body sympathetic activation, cardiac sympathovagal balance, and susceptibility to ventricular arrhythmia induced by sympathetic stimulation were evaluated based on blood noradrenalin metabolite concentrations, heart rate variability, and a 3-step epinephrine test. Ventricular arrhythmia and related death were observed only in rats at 1 day of withdrawal, but not in nonalcoholic, continuous ethanol intake or 21-day abstinence rats. One-day withdrawal after a 7-week continuous ethanol regimen elevated circulating noradrenalin metabolite levels and induced cardiac sympathovagal imbalance. Deaths related to the epinephrine test and ventricular arrhythmia induced by low doses of epinephrine were observed only in 1-day withdrawal rats. However, all anomalies were normalized by 21-day abstinence. Abrupt termination of a 7-week continuous ethanol regimen is sufficient to enhance the whole-body sympathetic activation and cardiac sympathovagal imbalance that contribute to ventricular arrhythmia and sudden death in alcoholic rats. Those providing medical care for alcoholics, including in cases of legal imprisonment, should be aware of the possibility of enhanced susceptibility to sudden arrhythmic death due to the abrupt termination of a chronic ethanol regimen.

ICD Implantation in Noncompaction of the Left Ventricular Myocardium: A Case Report

Isolated noncompaction of the ventricular myocardium (INVM) is an uncommon cardiomyopathy characterized by the persistence of fetal myocardium with prominent trabecular meshwork and deep intertrabecular recesses, often associated with systolic dysfunction and ventricular dilatation. A 23-year-old man from Burkina Faso was referred to our operative unit with a diagnosis of INVM, made with echocardiogram and magnetic resonance imaging and nonsustained ventricular tachycardia. The literature reports the incidence of malignant ventricular arrhythmias in as many as 47% of the patients and sudden cardiac death in almost 50% of them and this supported our decision to perform implantable cardioverter-defibrillators implantation.

In Vivo Effects of Myocardial Creatine Depletion on Left Ventricular Function, Morphology, and Energy Metabolism—Consequences in Acute Myocardial Infarction

The failing heart is characterized by disturbed myocardial energy metabolism and creatine (Cr) depletion. The aims of this study were to in vivo evaluate the effects of Cr depletion on: a) left ventricular (LV) function and morphology during rest and stress, b) LV energy metabolism, c) catecholamine in LV and plasma content, and d) incidence of malignant ventricular arrhythmias (MVA) during acute myocardial infarction (MI). Male rats weighing approximately 200 g were used. Two groups were studied: the rats treated with Cr analogue beta-guanidinopropionic acid (BGP) (n = 25) and controls (n = 23). BGP (1 M) was administered by subcutaneously implanted osmotic minipumps over 4 weeks. The rats (BGP n = 9, control n = 12) were than examined with transthoracic echocardiography at basal and at stress conditions induced by transesophageal pacing. In vivo (31)P magnetic resonance spectroscopy (MRS) was used for evaluation of myocardial energy status (BGP n = 7, control n = 12). (31)P MRS, echocardiography and high-performance liquid chromatography analysis of myocardial Cr, total adenine nucleotides and catecholamines in myocardium and plasma were performed on noninfarcted hearts. Myocardial infarction was induced in a subgroup of animals (BGP n = 15, control n = 15) by ligation of the left coronary artery resulting in a large ( approximately 50%) anterolateral MI and acute HF. A computerized electrocardiogram tracing was obtained continuously before induction of MI and up to 60 minutes postinfarction. Qualitative and quantitative variables of ventricular arrhythmias were analyzed using arrhythmia score. Body weight (BW) was lower (P < .01), whereas LV/BW was higher (P < .01) in the BGP group. Total myocardial Cr pool was decreased for at least 50% (P < .01) compared with the controls. There was no difference in total nucleotide pool. Phosphocreatine/adenosine-3-phosphate ratio was lower in the BGP group (P < .01). LV systolic function was disturbed during rest and stress (P < .05). Similarly, LV dimensions were increased in the BGP group (P < .05). Induction of acute MI resulted in markedly increased incidence of MVA and higher mortality in the BGP group (P < .01). Myocardial Cr depletion results in functional and structural LV alterations associated with lower myocardial energy reserve. Intact myocardial Cr metabolism is important for normal LV function during basal and stress conditions. Acute MI in the setting of myocardial Cr depletion leads to excessive mortality from ventricular arrhythmias and progressive heart failure.

Long‐Term Incidence of Malignant Ventricular Arrhythmia and Shock Therapy in Patients with Primary Defibrillator Implantation Does Not Differ from Event Rates in Patients Treated for Survived Cardiac Arrest

Recent trials have demonstrated benefit of prophylactic defibrillator (ICD) implantation compared to conventional treatment in high-risk patients. However, many patients have rare or no sustained arrhythmias following implantation. Our study addresses the question, whether patients with prophylactic defibrillator implantation have a lower risk for life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF) compared to sudden cardiac death (SCD) survivors. Over 7 years we enrolled 245 patients. Occurrence of spontaneous sustained VT/VF resulting in adequate ICD treatment was the endpoint. Incidence, type, and treatment of sustained arrhythmia in 43 previously asymptomatic ICD recipients (group B) were compared to data of 202 survivors of imminent SCD (group A). All patients had severely impaired left ventricular ejection fraction (<45%). Group B patients had long runs (>6 cycles, <30 s) of VT during Holter monitoring and inducible sustained arrhythmia. Incidence of rapid VT and VF (cycle length <240 ms/heart rate >250 bpm) after 4 years (35% in both groups, P = ns) and adequate defibrillator therapies (57% vs 55%, P = ns) were similar in both groups after univariate and multivariate analysis. Cumulative mortality tended to be lower in group B compared to group A, but the difference was not statistically significant. During long-term follow-up, incidence of sustained rapid ventricular arrhythmia in prophylactically treated patients is as high as that of SCD survivors. Benefit from defibrillator implantation for primary prevention (group B) appears to be comparable to that for survived cardiac arrest (group A).

Effects of Aerobic Exercise Training on Indices of Ventricular Repolarization in Patients With Chronic Heart Failure

Patients with chronic heart failure (CHF) have a markedly increased incidence of malignant ventricular arrhythmias. QT dispersion (QTd), defined as the difference between maximal and minimal QT intervals, reflects the regional inhomogeneity of ventricular repolarization dispersion and may mark the presence of malignant ventricular arrhythmias. To determine the effects of exercise training on QTd in patients with CHF. Fifteen patients with CHF and ejection fractions < 40% (mean, 28+/-9%) who were on a stable medical regimen. Standardized 12-lead surface ECGs were obtained at the beginning and end of the exercise training program, and QT and JT intervals were measured manually and corrected for heart rate by using Bazett's formula. QTd, heart rate-corrected QTd (QTc-d), JT dispersion (JTd), and heart rate-corrected JTd (JTc-d) were measured in at least eight ECG leads in each patient. Following the cardiac rehabilitation and exercise training programs, patients with CHF had only slight improvements in exercise capacity (results were not significant). However, these patients had marked improvements in QTd (71+/-11 to 59+/-17 ms; p < 0.02), QTc-d (82+/-28 to 63+/-17 ms; p < 0.01), JTd (76+/-19 to 57+/-18 ms; p < 0.002), and JTc-d (84+/-23 to 61+/-18 ms; p < 0.001) following the exercise training programs. These data indicate that aerobic exercise training significantly reduces the indices of ventricular repolarization dispersion in patients with CHF. Further studies are needed to evaluate how effectively this reduction in ventricular repolarization dispersion decreases the risk of malignant ventricular arrhythmias and sudden death in patients with CHF.

Beat-to-beat QT interval variability: novel evidence for repolarization lability in ischemic and nonischemic dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is associated with a high incidence of malignant ventricular arrhythmias and sudden death. Abnormalities in repolarization of ventricular myocardium have been implicated in the development of these arrhythmias. Spatial heterogeneity in repolarization has been studied in DCM, but temporal fluctuations in repolarization in this setting have been largely ignored. We sought to test the hypothesis that beat-to-beat QT interval variability is increased in DCM patients compared with control subjects. Eighty-three patients with ischemic and nonischemic DCM and 60 control subjects served as the study population. Beat-to-beat QT interval variability was measured by automated analysis on the basis of 256-second records of the surface ECG. A QT variability index (QTVI) was calculated for each subject as the logarithm of the ratio of normalized QT variance to heart rate variance. The coherence between heart rate and QT interval fluctuations was determined by spectral analysis. In patients, ejection fractions were assessed by echocardiography or ventriculography, and spatial QT dispersion was determined from the standard 12-lead ECG. DCM patients had greater QT variance than control subjects (60.4+/-63.1 versus 25.7+/-24.8 ms2, P<.0001) despite reduced heart rate variance (6.7+/-7.8 versus 10.5+/-10.4 bpm2, P=.01). The QTVI was higher in DCM patients than in control subjects, with a high degree of significance (-0.43+/-0.71 versus -1.29+/-0.51, P<10[-12]). QTVI did not correlate with ejection fraction or spatial QT dispersion but did depend on New York Heart Association functional class. QTVI did not differ between DCM patients with ischemic and those with nonischemic origin. Coherence between heart rate and QT interval fluctuations at physiological frequencies was lower in DCM patients compared with control subjects (0.28+/-0.14 versus 0.39+/-0.18, P<.0001). DCM is associated with beat-to-beat fluctuations in QT interval that are larger than normal and uncoupled from variations in heart rate. QT interval variability increases with worsening functional class but is independent of ejection fraction. These data indicate that DCM leads to temporal lability in ventricular repolarization.

Electrophysiologic effects of ischemic preconditioning on QT dispersion during coronary angioplasty

Objectives. The aim of this study was to examine the effect of ischemic preconditioning on the manner of ventricular repolarization by assessing the change in QT dispersion during coronary angioplasty.Background. QT interval dispersion regional variations in ventricular repolarization and cardiac electrical instability. Previous studies have suggested that increased QT dispersion is associated with an increased incidence of malignant ventricular arrhythmias, whereas brief episodes of myocardial ischemia can render the heart more resistant to subsequent ischemic episodes, a phenomenon called ischemic preconditioning.Methods. To assess the effects of ischemic preconditioning on myocardial repolarization by examining the change in QT dispersion during coronary angioplasty, we studied 47 consecutive patients (39 men and 8 women; mean age 57 ± 16 years). QT dispersion was measured after each balloon inflation during coronary angioplasty. Statistical analysis was performed by using repeated measurement of analysis of variance.Results. There were significant differences in QT dispersion as the number of balloon inflations increased (mean ± SD 52 ± 14, 42 ± 11, 36 ± 9, 31 ± 10 and 29 ± 11 ms, respectively [p < 0.01], for the first, second, third, fourth and fifth balloon inflations). The magnitude of decrease in QT dispersion was significant in the first and second balloon inflations, then became insignificant with later inflations.Conclusions. These data indicate that the gradual decrease in OT dispersion provoked by coronary artery occlusion and reperfusion during coronary angioplasty may be associated with electrophysiologic effects of ischemic preconditioning on myocardium in the human heart.