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PubMed2004

[Does syncope change the results of programmed ventricular stimulation in patients with previous myocardial infarction?].

UNLABELLED: The induction of a ventricular tachycardia (VT) after myocardial infarction (MI) is associated with a high risk of VT and sudden death (SD) in asymptomatic patients; the purpose of the study was to know if syncope modifies the results of programmed ventricular stimulation (PVS) and the clinical consequences. METHODS: PVS using two and three extra stimuli delivered in two sites of right ventricle was performed in 1057 patients without spontaneous VT or resuscitated SD at least 1 month after an acute MI; 836 patients (group I) were asymptomatic and were studied for a low ejection fraction or nonsustained VT on Holter monitoring or late potentials; 228 patients (group II) were studied for unexplained syncope. The patients were followed up to 5 years of heart transplantation. RESULTS: Sustained monomorphic VT (< 280 b/min) was induced in 238 group I patients (28%) and 62 group II patients (29%); ventricular flutter (VT > 270 b/min) or ventricular fibrillation (VF) was induced in 245 group I patients (29%) and 42 group II patients (18%) (P < 0.05); PVS was negative in 353 group I patients (42%) and 124 (55%) group II patients (NS). The patients differ by their prognosis; cardiac mortality was 13% in group I patients and 34% in group II patients with inducible VT < 280 b/min (P < 0.01), 4% in group I patients and 13% in group II patients with inducible VF (P < 0.05), 5% in group I patients and 7% in group II patients with negative study (NS). In conclusion, syncope did not change the results of programmed ventricular stimulation after myocardial infarction. However, syncope increased significantly cardiac mortality of patients with inducible ventricular tachycardia, flutter or fibrillation.

Adult↗
PubMed2000

Pulmonary edema after cardioversion for paroxysmal atrial flutter: left ventricular diastolic dysfunction induced by direct current shock.

This report describes a patient with the pulmonary edema after cardioversion for paroxysmal atrial flutter without organic heart disease. A 68-year-old man was admitted to hospital for paroxysmal atrial flutter. Antiarrhythmic agents were not effective, and direct current cardioversion was performed on the 4th hospital day. Three hours after cardioversion, the patient complained of dyspnea, and a chest X-ray showed pulmonary edema. He responded to oxygen, intravenous furosemide and drip infusion of nitroglycerine. During tapering of the medication, his condition remained stable. The patient was discharged on the 7th day after admission. Echocardiographic findings indicated that transient left ventricular diastolic dysfunction due to direct current shock was the most likely cause of the lung edema.

Aged↗
PubMed2005

Significance of inducible ventricular flutter-fibrillation after myocardial infarction.

AIM: The purpose of this study was to determine the factors associated with the induction of ventricular flutter/fibrillation (VFl/VF)and its prognostic significance in post-myocardial infarction. METHODS: Programmed ventricular stimulation was performed after myocardial infarction (MI) for syncope (n = 232) or systematically (n = 755); 230 patients had an induced VFl/VF and were followed during 4 +/- 2 years. RESULTS: VFl/VF was induced in 49/232 patients (21%) with syncope versus 181/755 asymptomatic patients (24%) (NS) and 94/410 patients (23%) with left ventricular ejection fraction (LVEF) <40% versus 136/577 patients (22.5%) with LVEF >40% (NS). Cardiac mortality was 9%; LVEF was 33 +/- 15% in patients who died, 43 +/- 13% in alive patients (P < 0.004). In patients with LVEF <40%, induced VFl/VF, mortality rate was 31% in those with syncope, 10% in asymptomatic patients (P < 0.001), because of an increase of deaths by heart failure; patients with LVEF >40% with or without syncope had a low mortality (5% and 3%). After linear logistic regression, VFl/VF and LVEF were predictors of total cardiac mortality, but only LVEF <40% predicted sudden death. CONCLUSION: Syncope and the level of LVEF did not increase the incidence of VFl/VF induction after MI, but modified the cardiac mortality: induced VF increased total cardiac mortality in patients with syncope and LVEF <40%, but did not increase sudden death. In patients with LVEF >40%, induced VFl/VF has no significance neither in asymptomatic patients nor in those with syncope.

Chi-Square Distribution↗
PubMed1988

Torsade de pointes and ventricular flutter-fibrillation following spontaneous cerebral subarachnoid hemorrhage.

Five cases (3.8%) in a series of 132 patients with spontaneous subarachnoid hemorrhage, studied by 24-hour Holter monitoring, presented with ventricular tachycardia of torsade de pointes variety. In all cases, the arrhythmias were observed within 24 hours after the bleeding. The QTc interval was prolonged more than 0.55 sec, and hypokalemia of less than 3.5 mEq/liter was present in all patients. The clinical status was not significant. Torsade de pointes occurred in comatose patients (3 cases) as well as in alert patients (2 cases). The arrhythmia was reversed by therapy in 3 patients, one of whom survived while 2 died due to cerebral damage. Our observations confirm the presence of life-threatening ventricular arrhythmias in the acute phase of subarachnoid hemorrhage. Continuous electrocardiographic monitoring is therefore advisable in view of its potential role in alerting to the need for treatment.

Adult↗
PubMed1989

Ventricular fibrillation in six adults without overt heart disease.

Findings are described in six patients with no clinical evidence of heart disease who had documented ventricular fibrillation (five patients) or ventricular flutter (one patient). The mean age of the six patients, all men, was 34 years (range 26 to 43). Cardiovascular collapse occurred in all and was followed by successful cardioversion. No patient had electrolyte or QT abnormalities. One patient had slight right ventricular enlargement on M-mode echocardiography, and another had a left ventricular pressure gradient at rest of 30 mm Hg with a normal two-dimensional echocardiogram. Holter electrocardiographic monitoring revealed incessant ventricular tachycardia in one patient and nonsustained ventricular tachycardia in three others. Exercise testing revealed nonsustained ventricular tachycardia in one patient. Ventricular fibrillation was induced at the time of programmed electrical stimulation in four of the six patients. Documented recurrence of ventricular fibrillation or ventricular flutter occurred in three patients, but in only one patient receiving antiarrhythmic drugs. Four patients were treated with amiodarone and one received an automatic implantable cardioverter-defibrillator. All patients are alive after a mean follow-up period of 78 months after the first documentation of their arrhythmia and 37 months after programmed electrical stimulation. Ventricular fibrillation can occur in the apparently structurally normal human heart. Antiarrhythmic treatment can provide effective control of this malignant arrhythmia.

Adult↗
PubMed1993

[Results of systematic programmed ventricular stimulation after myocardial infarction. Which protocol should be recommended?].

The authors report the prognostic value of ventricular arrhythmias induced by routine programmed ventricular stimulation after the acute phase of myocardial infarction. The protocol consisted of two extrastimuli in the first 185 patients and 3 extrastimuli in 308 patients. The use of 3 extrastimuli increased the incidence of inducible sustained monomorphic ventricular tachycardia (VT) < 270/mn, from 17 to 22% and, more importantly, that of ventricular fibrillation from 4 to 17%. Induction of ventricular flutter (monomorphic VT > 270/mn) was not increased. A long follow-up period (average 4 +/- 2 years) showed that the risk of VT was increased during the first months after infarction (n = 14), and that, 4 years later, other patients develop VT (n = 6). The risk of serious arrhythmias (VT and sudden death) was significantly higher in patients with inducible VT < 270/mn (20%) than in patients without inducible VT, but it was also higher in patients with inducible ventricular flutter (12.5%). The use of a third extrastimulus has a low positive predictive value for arrhythmic events (10%). This study confirms that the induction of sustained monomorphic VT after myocardial infarction is associated with an increased risk of arrhythmic events but the positive predictive value is relatively low (17%). In view of the risk of inducing non-specific ventricular fibrillation, the authors recommended using a stimulation protocol with only 2 ventricular extrastimuli.

Arrhythmias, Cardiac↗
PubMed2004

Differences in mechanisms and outcomes of syncope in patients with coronary disease or idiopathic left ventricular dysfunction as assessed by electrophysiologic testing.

OBJECTIVES: This study evaluated the causes of syncope and the significance and differences in left ventricular (LV) dysfunction, coronary disease, and idiopathic dilated cardiomyopathy (DCM). BACKGROUND: Risk stratification of and indications for an automated defibrillator could differ according to the cause of LV dysfunction. METHODS: Electrophysiologic study, including atrial and ventricular programmed stimulation, was performed in 119 patients with coronary disease (group I) and 61 patients with DCM (group II) with an left ventricular ejection fraction (LVEF) <40% and syncope. Patients were followed from one to six years (mean 4 +/- 2 years). RESULTS: Sustained monomorphic ventricular tachycardia (VT) was induced in 44 group I patients (37%) and 13 group II patients (21%); ventricular flutter (>270 beats/min) or ventricular fibrillation (VF) was induced in 24 group I patients (19%) and 9 group II patients (15%); and various other arrhythmias were identified. Syncope remained unexplained in 34 group I patients (30%) and 16 group II patients (27%). Prognosis depended on the heart disease: VT or VF induction was a predictive factor of mortality in coronary disease and identified a group with high cardiac mortality (46%), compared with patients with a negative study, who had a lower mortality (6%; p < 0.001) than in other studies. Cardiac mortality was only correlated with LVEF in DCM. CONCLUSIONS: Various causes could explain syncope in 70% of patients with coronary disease and DCM, but differences were noted: VT was frequent in coronary disease with a bad prognosis, and ischemia could explain syncope; in DCM, different causes such as atrial tachycardia could be responsible for syncope, but the prognosis only depended on LVEF.

Aged↗
PubMed1995

Computer-assisted instruction of arrhythmia for MS-windows.

1. INTRODUCTION. Training in the diagnosis of arrhythmias is an important part of the curriculum for medical students, postgraduates, and paramedical staff. Although several CAI for arrhythmia have been developed [1-3], we could not get CAI software for arrhythmia for the MS-Windows environment. In this report, we present a newly-developed computer-assisted reference system for arrhythmia that functions in the Windows environment. 2. DESCRIPTION OF THE SYSTEM. The system consists of a program and two data files. An MS-Windows program (ECG9405.EXE, 180kB) was compiled using Borland's C++ v.3.1. A binary file (ECPAT.BAS 33kB) includes data of normal and abnormal wave segments of ECG: P wave, PQ interval segment, and QRs complex with/without T wave. A mother file (ECG9405.sys, 57kB) includes 85 data sets to generate ECG waveforms of arrhythmia. Each data set contains a sequence of wave form numbers, the text for questions and answers, and the commands strings. There are five major commands: 1) to create a new window as "wave window"; 2) to make electrocardiogram data; 3) to plot the data on the window; 4) to create a "dialog box" for questions and explanations; and 5) to check the answers. he program gets a data set from the data according to the user's choice. The program then interprets the data set and executes the commands. The wave segment data are plotted in a "wave window" at every 10 milliseconds; this is controlled by the MS-Windows' timer. The timer interval can be changed by selecting the speed button. The ECG waveforms are displayed on a window just like an ordinary ECG monitor with beat sound. Many windows can be created by the user and many ECG waves simultaneously plotted on CRT. 3. USAGE OF THE SYSTEM. The "main window" has a menu that has three items corresponding to the training course: BASIC, TRY, and TEST. Thirty-five types of arrythmias are listed in the "list box" of the windows in BASIC course e.g., sinus arrhythmia, atrial flutter, atrial premature contraction, ventricular extrasystole, ventricular flutter, etc. If the user selects one of them on the list by double clicking, some textual explanations of the wave are described in a dialog box. Ten multiple choice questions are displayed in the dialog box in course of learning TRY and TEST; the answers to these are requested. In the TEST course, the system offers random access to each arrhythmia. he user can send the pictorial ECG data in the window to other graphics programs through a clip board. 4. DISCUSSION. It was successfully used in a lecture of electrocardiogram for medical students. They seem to be interested in this system because of its simple usage and the dynamic drawing of ECG waves on CRT. Multiple computer-based medical resources can be run on MS-Windows. The system is able to run simultaneously with other programs, such as an electronic reference system [4]. The system may be obtained from the authors upon request.

Arrhythmias, Cardiac↗
PubMed2003

Frequent ventricular ectopy after exercise as a predictor of death.

BACKGROUND: Exercise-induced ventricular ectopy predicts an increased risk of death in population-based cohorts. We sought to examine in a clinical cohort the prognostic importance of ventricular ectopy immediately after exercise, when reactivation of parasympathetic activity occurs. We hypothesized that ventricular ectopy after exercise (i.e., during the recovery phase) would predict an increased risk of death better than ventricular ectopy during exercise. METHODS: We studied 29,244 patients (mean [+/-SD] age, 56+/-11 years; 70 percent men) who had been referred for symptom-limited exercise testing without a history of heart failure, valve disease, or arrhythmia. Frequent ventricular ectopy was defined by the presence of seven or more ventricular premature beats per minute, ventricular bigeminy or trigeminy, ventricular couplets or triplets, ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation. RESULTS: Frequent ventricular ectopy occurred only during exercise in 945 patients (3 percent), only during recovery in 589 (2 percent), and during both exercise and recovery in 491 (2 percent). There were 1862 deaths during a mean of 5.3 years of follow-up. Frequent ventricular ectopy during exercise predicted an increased risk of death (five-year death rate, 9 percent, vs. 5 percent among patients without frequent ventricular ectopy during exercise; hazard ratio, 1.8; 95 percent confidence interval, 1.5 to 2.1; P<0.001), but frequent ventricular ectopy during recovery was a stronger predictor (11 percent vs. 5 percent; hazard ratio, 2.4; 95 percent confidence interval, 2.0 to 2.9; P<0.001). After propensity matching for confounding variables, frequent ventricular ectopy during recovery predicted an increased risk of death (adjusted hazard ratio, 1.5; 95 percent confidence interval, 1.1 to 1.9; P=0.003), but frequent ventricular ectopy during exercise did not (adjusted hazard ratio, 1.1; 95 percent confidence interval, 0.9 to 1.3; P=0.53). CONCLUSIONS: Frequent ventricular ectopy during recovery after exercise is a better predictor of an increased risk of death than ventricular ectopy occurring only during exercise.

Aged↗
PubMed1999

[Electric programmed ventricular stimulation using a permanent cardiac pacing system--a noninvasive method in arrhythmia].

BACKGROUND: Complex forms of ventricular arrhythmias often occur in patients with an implanted permanent cardiac pacing system. Some of the pacemakers are provided with software which allows electrophysiological testing of the cardiac conduction system by coupling with an external diagnostic pacemaker via their programmer. This method is non-invasive. METHODS AND RESULTS: In a group of 26 patients (19 males, 7 females) with an implanted pacemaker (Paragon III, Synchrony III, Sensorithm--all Pacesetter) complex ventricular arrhythmias were observed (class Lown IVa and higher). In these patients the electrical stability of the myocardium was tested by the described method (protocol: incremental pacing 90-220 bpm, pacing drives 110 bpm and 140 bpm with 1-3 extrastimuli). Complex ventricular arrhythmias were induced in 42% patients (n = 11), in this subgroup 55% (n = 6) was non-sustained ventricular tachycardia, 36% (n = 4) sustained ventricular flutter, 9% (n = 1) sustained ventricular tachycardia. Patients with non-sustained ventricular tachycardia were treated with beta-blockers, in the others the effective therapy was selected according to electrophysiological testing (amiodarone in 4 patients, ICD in 1 patient). During a 24-month follow-up the overall mortality was 7.7% (n = 2), sudden death mortality was 3.8% (n = 1). CONCLUSIONS: Programmed ventricular stimulation performed by a permanent cardiac pacing system is a simple and above all non-invasive method with no need for fluoroscopy. It can be repeated several times. It is not possible to pace from the right ventricle outflow tract. This is the main disadvantage. Nevertheless, by using non-invasive risk stratification methods (echocardiography, signal averaged ECG, heart rate variability, baroreflex sensitivity, dispersion of QT interval) the patients in need of an invasive study can be identified. This method can be considered an alternative screening method and a standard part of the investigation of the algorithm in patients with a previously implanted pacemaker.

Arrhythmias, Cardiac↗
PubMed1989

[Adams-stokes syndrome due to neuroleptic agents].

Data on an investigation and analysis of 8 cases taken neuroleptics followed by Adams-Stokes syndrome were reported. All patients were diagnosed as schizophrenia without cardiovascular diseases previously. In the process of treatment with 1 or 2 kinds of neuroleptics, Adams-Stokes syndrome appeared, while the potassium was in a range of 1.1--3.8 mEq/L. EKG profile varied, such as showed hypokalemia, ventricular flutter or fibrillation, frequent multifocal ventricular premature beat including bigeminy, and complained with second or third A-V block. The authors deem that neuroleptics may give rise to hypokalemia and then result in cardiac arrhythmias. Damage to heart tends to happen when more than one kind of neuroleptics were medicated. The treatment measures depend above all upon the active and effective attendance to hypokalemia. The patients may die from ventricular fibrillation without proper treatment.

Adams-Stokes Syndrome↗
PubMed2006

Equivalent arrhythmic risk in patients recently diagnosed with dilated cardiomyopathy compared with patients diagnosed for 9 months or more.

BACKGROUND: The Centers for Medicare and Medicaid Services (CMS) recently expanded coverage for implantable cardioverter-defibrillators (ICDs) in patients with left ventricular ejection fraction < or =35% and nonischemic dilated cardiomyopathy for > or =9 months. To investigate the ramifications of these criteria, the ICD registry from Tufts-New England Medical Center was analyzed for arrhythmic events and death in patients with newly diagnosed (<9 months) vs late-diagnosed (> or =9 months) nonischemic dilated cardiomyopathy. OBJECTIVES: The purpose of this study was to analyze the arrhythmic risk in patients with recent vs late diagnosis of nonischemic dilated cardiomyopathy. METHODS: One hundred thirty-one patients with nonischemic dilated cardiomyopathy were divided into two cohorts (<9 or > or =9 months of symptoms) and analyzed for any occurrence of treated ventricular arrhythmia, potentially lethal arrhythmias defined as ventricular flutter rates > or =230 bpm, and ventricular fibrillation. Patients with documented sustained ventricular tachycardias (included in prior CMS coverage) were excluded. RESULTS: In the study group, the mean age was 58.1 +/- 15 years and ejection fraction 20.6% +/- 8%. In a follow-up period of 25.3 +/- 24 months, the 52 patients with a recent diagnosis (1.4 +/- 2 months) had no difference in the occurrence of ventricular arrhythmias (P = .49) and malignant ventricular arrhythmias (P = .16) compared with the 79 patients diagnosed > or =9 months (mean 58.1 +/- 39 months). CONCLUSION: Patients with nonischemic dilated cardiomyopathy experienced equivalent occurrences of treated and potentially lethal arrhythmias irrespective of diagnosis duration. These findings suggest that the 9-month time qualifier used in the CMS guidelines for ICD reimbursement may not reliably discriminate patients at high risk for sudden cardiac death in this selected population.

Adult↗