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PubMed2002

[Evaluation of pro-arrhythmic risk of drugs due to QT interval prolongation by the HERG expression system].

Recently, there has been considerable attention focused on drugs that prolong the QT interval of the electrocardiogram. This occasionally evolves to fetal, polymorphic ventricular arrhythmias, torsades de pointes. Therefore, the early detection of the risk of drug-induced QT prolongation is important for avoiding the adverse cardiovascular effect in clinical use. It has been suggested that the QT prolongation and ventricular arrhythmia caused by drugs might be secondary to their ability to interfere with cardiac potassium channels involved in action potential repolarization and in particular with rapidly activating delayed rectifier K+ current (IKr). In cardiac myocytes, IKr contributes to termination of the plateau phase of action potential. The ether-a-go-go related gene in humans expressed a K+ channel current with biophysical characteristics similar to those of IKr. Electrophysiological studies on cloned HERG channels can provide fundamental information concerning the cardiac safety profile of new developing drugs.

Animals↗
PubMed1999

Assessment of cardiac arrhythmic risk in diabetic patients using QT dispersion abnormalities.

The purpose of this study was to assess the abnormalities and prevalence of QT dispersion in 154 diabetic patients (DP) who underwent a standard 12-lead ECG. QT interval was measured from the beginning of the QRS complex until the T wave returned to baseline. Atrial fibrillation, pacemakers and the impossibility of measuring 6 QT intervals per ECG were reasons for exclusion from the study. Diabetic patients were compared with 104 sex- and age-matched controls (C): mean age 50.7 +/- 2.3 years (DP) vs 48.4 +/- 10.1 (C) (ns); diabetes duration: 11.6 +/- 7.9 years. Seventy-eight percent of DP were non-insulin-dependent. Mean QT duration was 0.383 +/- 0.031 s (DP) vs 0.381 +/- 0.026 (C) (ns); QT dispersion (difference between the longest and shortest QT interval measurement) 0.033 +/- 0.015 s (DP) vs 0.024 +/- 0.011 (C) (p < 0.001); and QT variability 3.003 +/- 1.23% (DP) vs 2.295 +/- 0.936 (C) (p < 0.001); with a standard deviation of 0.012 +/- 0.005 s (DP) vs 0.009 +/- 0.004 (C) (ns). QT dispersion indices (dispersion, variability) were significantly increased in DP, even for short diabetes duration. Future studies should focus on QT dispersion to assess the usefulness of such indices in detecting DP at high risk of sudden death and ventricular arrhythmias.

Arrhythmias, Cardiac↗
PubMed1999

QT dispersion and early arrhythmic risk during acute myocardial infarction.

BACKGROUND: QT dispersion (maximal minus minimal QT interval calculated on a standard 12-lead electrocardiogram) has been suggested to reflect regional variations of ventricular repolarization and to provide a substrate for reentry ventricular arrhythmias. In this study we evaluate QT dispersion in patients with acute myocardial infarction and assess its relation with early severe ventricular arrhythmias. METHODS AND RESULTS: We studied 101 patients with acute myocardial infarction and a control group of 97 healthy subjects. We determined QT and QTc dispersion on the electrocardiograms performed 12 hours and 3 and 10 days after the onset of symptoms in myocardial infarction patients and on the control group. The average values of QT and QTc dispersion (measured hereafter in milliseconds, ms) were as follows: 70.5 +/- 42.5-87 +/- 46.6 (after 12 hours), 66.5 +/- 37.8-76.9 +/- 43.5 (on day 3), 68.9 +/- 42-76.3 +/- 43.8 (on day 10) and 44 +/- 13.4-54.2 +/- 16.3 (in control group). We observed statistically significant differences in QT and QTc dispersion between the electrocardiogram of normal subjects and each of the three electrocardiograms performed on patients with infarction (p < 0.0005, p < 0.005). We recorded a greater QT dispersion in patients with anterior infarction with respect to those with inferior/lateral infarction (79 +/- 38.6 vs 65.2 +/- 43.16, p < 0.05) and in patients with ejection fraction < 45% (93.1 +/- 28.4 vs 68.3 +/- 34.1 p < 0.005). During the first three days, QT dispersion did not differ in patients treated with thrombolytic agents with respect to those who were untreated, while on day 10 untreated patients showed higher values (74.9 +/- 45.3 vs 60.5 +/- 37.7, p < 0.05). Creatine kinase peak level, sex and age of the patients did not influence QT dispersion. Thirteen patients (12.8%) developed severe ventricular arrhythmias within 72 hours after infarction: 8 patients (7.9%) had ventricular fibrillation and 5 patients (4.9%) had sustained ventricular tachycardia. We found higher early QT and QTc dispersion values in patients who developed severe ventricular arrhythmias (108.8 +/- 63.2 and 125.8 +/- 68.5) with respect to patients who did not (63.3 +/- 32.9 and 80.8 +/- 38.9, p < 0.0005, p < 0.0005). CONCLUSIONS: Our data suggest that QT dispersion: 1) increases during acute myocardial infarction; 2) peaks in the early hours after symptom onset; 3) drops late after infarction in patients treated with thrombolytic agents; 4) is associated with early severe ventricular arrhythmias.

Arrhythmias, Cardiac↗
PubMed1999

[Evaluation of arrhythmic risk in coronary insufficiency].

Half of all deaths occurring in patients with heart failure are sudden deaths probably related to a malignant ventricular arrhythmia. The pathophysiological mechanisms of these arrhythmias are unclear, but left ventricular function, hypokalaemia accentuated by diuretics and treatments altering inotropism play a definite role. Because of the diversity of aetiologies generating heart failure, the multiplicity of fatal arrhythmias and the multifactorial origin of these arrhythmias, there is no formal marker for the risk of sudden death in patients with heart failure, at the present time. In addition to the NYHA classification and detection of episodes of syncope, assessment of these patients must be as complete as possible, at least including repeated evaluation of the ejection fraction, Holter ECG monitoring and detection of delayed ventricular potentials.

Arrhythmias, Cardiac↗
PubMed2004

[Arrhythmic risk in essential hypertension: late potentials].

AIM: A higher incidence of cardiac death exists in patients with essential hypertension, and it is higher still in those with ventricular arrhythmia. The purpose of noninvasive diagnostic imaging in hypertensive patients is to determine those with a greater risk for arrhythmia. In previous studies on hypertension, one of the inclusion criteria is diastolic blood pressure <95 mmHg, which, however, is a low selectivity criterion. Instead, our study emphasizes the need to evaluate the incidence of ventricular arrhythmia in hypertensive patients not yet receiving drug therapy and to formulate the diagnosis based on 24-h ambulatory arterial blood pressure monitoring, which represents a more selective criterion than the diastolic pressure value proposed by the World Health Organization (WHO). METHODS: A total of 128 consecutive patients with essential hypertension classified according to WHO criteria underwent 24-h monitoring, 85 (66.4%) of which presented with a mean 24-h arterial pressure >135/85 mmHg. These patients were then evaluated using mono- and two-dimensional echocardiography and 24-h dynamic Holter monitoring to detect arrhythmias and the presence of left ventricular later potentials. RESULTS: Left ventricular hypertrophy was present in 60 (70.6%) patients and absent in 25 (29.4%). Based on the Lown classification of ventricular arrhythmia, 20 (23.5%) patients had Grade I arrhythmia, 5 (5.9%) Grade II, 4 (4.7%) Grade III, 9 (10.6%) Grade IVA, 20 (23.5%) Grade IVB, 12 (14.1%) Grade V, 15 (17.6%) clinically unremarkable arrhythmia, and 17 (20%) had late potentials because they tested positive to at least 2 out of three criteria, and 2 patients were positive to all 3 criteria. CONCLUSION: Our study findings demonstrated a significant correlation between left ventricular hypertrophy and grade of arrhythmia (r=0.552; p<0.0001) and late potentials (r=0.405; p<0.001). The presence of late potentials was also found to correlate significantly with grade of arrhythmia (r=0.593; p<0.001). These patients present with a more severe stage of the disease and should therefore receive more aggressive treatment to prevent sudden cardiac death resulting from arrhythmia.

Adult↗
PubMed2005

Temporal trends on the risk of arrhythmic vs. non-arrhythmic deaths in high-risk patients after myocardial infarction: a combined analysis from multicentre trials.

AIMS: An understanding of the temporal trends on the risks of arrhythmic death (AD) vs. non-arrhythmic deaths (NAD) after myocardial infarction (MI) is crucial in deciding the optimal timing for risk stratification and treatment window for prophylactic antiarrhythmic treatment. However, contemporary data on such information is lacking. METHODS AND RESULTS: Individual patient data were pooled from the placebo arms of EMIAT, CAMIAT, SWORD, TRACE, and DIAMOND-MI who had a recent MI and left ventricular ejection fraction (LVEF) <40% or frequent ventricular premature beats (VPBs). Temporal trends were investigated for all studies from day 45 after acute myocardial infarction (AMI) to account for different recruitment periods between trials, and then from the onset of MI for TRACE and DIAMOND-MI that recruited patients within 2 weeks after MI. In total, 3104 patients (median age 65, range: 23-92; 2471 males) were pooled from all five studies, with a total of 487 deaths at 2-year follow-up; 220 deaths were ADs and 172 were NADs. The risks of both AD and NAD were highest in the first 6 months but the risk of AD was consistently higher than that of NAD throughout the 2-year period [rate of death/100 person-year at risk (AD/NAD): 8.09/6.07 (45 days to 6 months), 4.07/3.35 (>6-12 months), 4.34/3.60 (>12-18 months), 3.76/2.77 (>18-24 months)]. There were significant interactions between the temporal trends of mortalities and gender (P=0.03) and history of hypertension (P=0.04). A similar trend was observed when mortality was measured from time of onset of MI from the combined TRACE and DIAMOND-MI dataset. CONCLUSION: Our study provided the first contemporary evidence that in high-risk post-MI patients with LVEF <40% or frequent VPBs, the risk of AD was higher than that of NAD for up to 2 years although in female patients, they became increasingly more likely to die from NAD after 6 months. Therefore, risk stratification of post-MI patient at high risk of AD remains a worthwhile exercise. However, the risks of AD (and NAD) were highest in the first 6 months after AMI and level-off thereafter, suggesting that the optimal window period for risk stratification for implantable cardioverter defibrillator after AMI is in the first 6 months.

Adult↗
PubMed1992

[Evaluation of the risk of arrhythmia after infarction].

Evaluation of the risk of arrhythmias after myocardial infarction involves identification of those patients at a high risk of arrhythmic events, i.e. those who fall victim to ventricular tachycardia or sudden death. Such identification is an essential first stage before any treatment can be proposed. It has been clearly shown that the existence of premature ventricular contractions following infarction is an indicator of poor prognosis. In addition to evaluation of premature ventricular contractions, a Holter record can identify sinus variability, a parameter which the prognostic importance is currently being increasingly emphasized. Electrocardiography with averaging and high amplification has now been shown to be of value in the evaluation of arrhythmic risk after infarction. The negative predictive value of this investigation is very high, of the order of 90 percent. In addition to Holter and electrocardiography with averaging, two other non-invasive investigations can be used to determine arrhythmic risks after infarction. Stress testing can seek the presence of premature ventricular contractions related to exercise, while isotope ventriculography measures the value of ejection fraction which, in itself, has a high predictive value in terms of arrhythmic events. Mortality after infarction is proportional to the lowering of ejection fraction and among deaths approximately half are probably due to arrhythmias. Programmed ventricular pacing also has a role to play in evaluation of arrhythmic risk after infarction, but should not be routine. It may be indicated in those patients showing all of the signs of risk, i.e. repetitious forms by Holter, late potentials and low ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed2003

Risk stratification for arrhythmic events in patients with idiopathic dilated cardiomyopathy: a review of the literature and current perspectives.

The prognosis for patients with idiopathic dilated cardiomyopathy (DCM) has markedly improved during the last decade, mainly because of advancements in therapeutic strategies. However, sudden death still accounts for a significant part of the total mortality in patients with moderate disease. Recent primary prophylactic trials failed to demonstrate any benefit of cardioverter-defibrillator implantation in an unselected group of idiopathic DCM patients and thus the identification of the subgroup of patients at high arrhythmic risk is crucial. Although different risk stratification methods have been evaluated in risk assessment, the reported clinical value differs in studies, mainly because of differences in either methodology and/or patient selection. The present review focuses on arrhythmic events in idiopathic DCM and on the value of noninvasive methods and electrophysiological study in the risk stratification of this group of patients.

Arrhythmias, Cardiac↗
PubMed1999

Diuretics and risk of arrhythmic death in patients with left ventricular dysfunction.

Background-Treatment with diuretics has been reported to increase the risk of arrhythmic death in patients with hypertension. The effect of diuretic therapy on arrhythmic death in patients with left ventricular dysfunction is unknown. Methods and Results-We conducted a retrospective analysis of 6797 patients with an ejection fraction <0.36 enrolled in the Studies Of Left Ventricular Dysfunction (SOLVD) to assess the relation between diuretic use at baseline and the subsequent risk of arrhythmic death. Participants receiving a diuretic at baseline were more likely to have an arrhythmic death than those not receiving a diuretic (3.1 vs 1.7 arrhythmic deaths per 100 person-years, P=0.001). On univariate analysis, diuretic use was associated with an increased risk of arrhythmic death (relative risk [RR] 1.85, P=0.0001). After controlling for important covariates, diuretic use remained significantly associated with an increased risk of arrhythmic death (RR 1.37, P=0.009). Only non-potassium-sparing diuretic use was independently associated with arrhythmic death (RR 1.33, P=0.02). Use of a potassium-sparing diuretic, alone or in combination with a non-potassium-sparing diuretic, was not independently associated with an increased risk of arrhythmic death (RR 0.90, P=0.6). Conclusions-In SOLVD, baseline use of a non-potassium-sparing diuretic was associated with an increased risk of arrhythmic death, whereas baseline use of a potassium-sparing diuretic was not. These data suggest that diuretic-induced electrolyte disturbances may result in fatal arrhythmias in patients with systolic left ventricular dysfunction.

Analysis of Variance↗
PubMed2005

Effect of epirubicin-based chemotherapy and dexrazoxane supplementation on QT dispersion in non-Hodgkin lymphoma patients.

BACKGROUND AND OBJECTIVE: Aim of the present study was to assess the effect of epirubicin-based chemotherapy on QT interval dispersion in patients with aggressive non-Hodgkin lymphoma (NHL), and the effect of dexrazoxane supplementation. Prolongation of QT dispersion may not only represent a sensitive tool in identifying the first sign of anthracycline-induced cardiotoxicity, but it may serve also in identifying patients who are at risk of arrhythmic events. METHODS: Twenty untreated patients, <or=60 years of age with newly-diagnosed aggressive NHL, eligible for a treatment with epirubicin-based chemotherapy were selected for the study. The patients were randomly allocated in two subgroups (N=10) to receive or not dexrazoxane hydrochloride (400 mg/m(2)) after epirubicin infusion. The patients underwent 12-lead electrocardiogram (ECG) before and after epirubicin infusion and after dexrazoxane supplementation. QT dispersion was defined as the difference between the maximum and the minimum QT interval occurring in any of the 12 ECG leads, corrected (QTc) for heart rate. RESULTS: All the 20 patients showed increased QT dispersion (44.3 +/- 8.4 vs. 68.4+/-11.4 ms, P<0.001) and QTc dispersion (46.2 +/- 6.2 vs. 72.2 +/- 8.4, P<0.001) after chemotherapy infusion. The 10 patients who underwent supplementation with dexrazoxane exhibited a significant reduction of QT dispersion (67.4 +/- 8.1 vs. 49.5 +/- 4.2 ms, P<0.001) and QTc dispersion (71.2 +/- .7 vs. 51.4 +/- 4.3 ms, P<0.001), while the 10 patients not supplemented with dexrazoxane did not (QT dispersion: 69.3 +/- 7.6 vs. 64.2 +/- 6.9 ms; QTc dispersion: 72.8 +/- 8.1 vs. 67.3 +/- 7.2 ms, ns). CONCLUSIONS: Epirubicin-based chemotherapy causes an early increase of the QT and QTc dispersion, which is attenuated by dexrazoxane supplementation. Therefore, dexrazoxane can reduce the arrhythmic risk in patients treated with epirubicin.

Antibiotics, Antineoplastic↗
PubMed2005

Reduced ejection fraction after myocardial infarction: is it sufficient to justify implantation of a defibrillator?

BACKGROUND: Improved survival after prophylactic implantation of a defibrillator in patients with reduced left ventricular ejection fraction (EF) after myocardial infarction (MI) has been demonstrated in patients who experienced remote MIs in the 1990s. The absolute survival benefit conferred by this recommended strategy must be related to the current risk of arrhythmic death, which is evolving. This study evaluates the mortality rate in survivors of MI with impaired left ventricular function and its relation to pre-hospital discharge baseline characteristics. METHODS: The clinical records of patients who had sustained an acute MI between 1999 and 2000 and had been discharged from the hospital with an EF of < or = 40% were included. Baseline characteristics, drug prescriptions, and invasive procedures were recorded. Bivariate and multivariate analyses were performed using a primary end point of total mortality. RESULTS: One hundred sixty-five patients were included. During a median follow-up period of 30 months (interquartile range, 22 to 36 months) 18 patients died. The 1-year and 2-year mortality rates were 6.7% and 8.6%, respectively. Variables reflecting coronary artery disease and its management (ie, prior MI, acute reperfusion, and complete revascularization) had a greater impact on mortality than variables reflecting mechanical dysfunction (ie, EF and Killip class). CONCLUSIONS: The mortality rate among survivors of MIs with reduced EF was substantially lower than that reported in the 1990s. The strong decrease in the arrhythmic risk implies a proportional increase in the number of patients needed to treat with a prophylactic defibrillator to prevent one adverse event. The risk of an event may even be sufficiently low to limit the detectable benefit of defibrillators in patients with the prognostic features identified in our study. This argues for additional risk stratification prior to the prophylactic implantation of a defibrillator.

Aged↗
PubMed1995

[Outcome of arrhythmogenic right ventricular dysplasia. Apropos of 4 cases].

The authors propose a classification of the outcome of arrhythmogenic right ventricular dysplasia with reference to 4 selected cases with a follow-up period of over 9 years. In type I, the left ventricular ejection fraction is normal (EF > 50%) and the risk, exclusively arrhythmic, can be controlled by appropriate antiarrhythmic therapy. This is the commonest form of arrhythmogenic right ventricular dysplasia with different varieties according to the degree of dilatation of the right ventricle. In type II, there is a variable degree of left ventricular involvement (30 < EF < 50%) either by extension of a comparable disease process as observed in the right ventricle or by an isolated or superimposed phenomenon of myocarditis. This form is stable and may remain stable for many years providing the arrhythmias are correctly treated. In type III, progressive degradation of the myocardium is observed over a period of about 10 years with a clinical presentation comparable to that of certain arrhythmogenic dilated cardiomyopathies which are often hereditary. In this case, the patients have an arrhythmic risk associated with that of cardiac failure which becomes progressively irreversible. The histology shows interstitial fibrosis with biventricular lymphocytic infiltration suggesting an autoimmune phenomenon. Therefore, the classification of cases of arrhythmogenic right ventricular dysplasia depends on the potential evolutivity of the lesions. When the patient is seen in the early stages of the disease, the prognosis should be garded, especially in a hereditary form.

Adult↗
PubMed2001

Prolonged QRS duration increases QT dispersion but does not relate to arrhythmias in survivors of acute myocardial infarction.

QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2-3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%-15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 +/- 7 vs 78 +/- 1 ms, JT disp 80 +/- 6 vs 79 +/- 2 ms, mean +/- SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction.

Aged↗
PubMed2005

Association of myocardial ischemia with mortality and implantable cardioverter-defibrillator therapy in patients with coronary artery disease at risk of arrhythmic death.

OBJECTIVES: We sought to assess the relation between myocardial ischemia during stress echocardiography and major events in patients with implantable cardioverter-defibrillator (ICD). BACKGROUND: The association of myocardial ischemia with subsequent ICD therapy and mortality is unknown. METHODS: We studied 90 patients (age 65 +/- 13 years, 27 women) with history of coronary heart disease who received ICD for primary (53 patients) or secondary (37 patients) prevention of sudden cardiac death. Sixty-five (72%) patients had a previous coronary artery bypass surgery. Patients underwent exercise treadmill or dobutamine stress echocardiography. Ischemia was defined as new or worsening wall motion abnormalities. End points were death and appropriate ICD therapy. RESULTS: Mean ejection fraction was 34 +/- 12%. During a mean follow-up of 2.8 +/- 1.5 years, 5 patients died and 19 patients had ICD therapy. Ischemia was detected in 20 of 24 patients with subsequent events and in 24 of 66 patients without (83% vs. 36%, p < 0.001). Events occurred in 17 of the 32 patients (53%) with both ischemia and inducible ventricular tachycardia (VT) on electrophysiologic (EP) studies. None of the 16 patients without ischemia or inducible VT on EP studies had events. In a Cox multivariate analysis model, independent predictors of events were a history of spontaneous sustained VT (hazard ratio [HR] 1.9, 95% confidence interval [CI] 1.3 to 3.8), inducible VT on EP studies (HR 1.7, 95% CI 1.2 to 4.5), and ischemia (HR 2.1, 95% CI 1.2 to 3.5). CONCLUSIONS: Ischemia during stress echocardiography is an independent predictor of death and ICD therapy in patients with coronary heart disease at high risk of arrhythmic death. Patients without inducible ischemia or VT on a previous EP study have a very low risk of events. A combination of ischemia and a positive EP study is associated with a very high risk of events.

Aged↗
PubMed2002

[Stratification of arrhythmia risk in infarction: reflexions in the light of large trials].

The identification of patients at higher risk of life-threatening ventricular arrhythmias after myocardial infarction still represents a clinically relevant problem, particularly after results of recent studies which support the efficacy of implantable cardioverter defibrillator (ICD) in reducing total mortality in patients with a previous myocardial infarction and left ventricular dysfunction, with and without additional risk markers. However, owing to the high cost of ICD therapy, an effective arrhythmic risk stratification may be desirable. The low diagnostic accuracy reported by various studies using single risk stratifiers (either invasive and non invasive) suggested a combined use of multiple parameters in order to improve the predictive power of the risk stratification algorithms. This approach, that takes into account the multifactorial genesis of malignant ventricular arrhythmias, has been demonstrated to be able to identify subgroups of patients at very high arrhythmic risk. In particular, a two-level algorithm based upon the selection of candidates to electrophysiologic study among patients with abnormal non-invasive testing, showed itself as a particularly effective tool for identification of such patients. In this paper the Authors summarize most recent results on the risk stratification protocols and the use of ICDs and provide an operative algorithm that keeps into account either aggressive and moderate approaches to patients surviving a myocardial infarction.

Arrhythmias, Cardiac↗