Age at onset and gender of patients with different types of supraventricular tachycardias.
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Adolescent↗
Biomedical subjects
H J Wellens
Publications and source records attributed to H J Wellens.
[Radiofrequency energy as treatment for arrhythmias in patients with accessory atrioventricular pathways].
OBJECTIVE: Evaluation of the use of radiofrequency energy to interrupt accessory atrioventricular pathways. DESIGN: Prospective study. SETTING: University Hospital Maastricht. METHOD: The outcome is presented of radiofrequency catheter ablation of accessory atrioventricular pathways in our first 50 consecutive patients, with a total of 54 accessory pathways. All but one patient suffered from symptomatic tachycardias. A catheter electrode was positioned next to the accessory pathway and 30 second pulses of 40 W radiofrequency energy were used to interrupt the connection. RESULTS: Complete block in conduction was accomplished in 44/54 (81%) of accessory pathways. No complications occurred. Success rate, procedure time and radiation dose were found to be related to the location of the accessory connection. The highest success rate was found in left free wall pathways (24/26; 92%), the lowest in right lateral pathways which seldom occur (1/4; 25%). The total procedure took 1-6 hours. The maximal duration of radiographic imaging was 2.5 hours. CONCLUSION: Although insufficient information on long-term efficacy is available, current results support the use of radiofrequency ablation of accessory pathways in institutions with expertise in the invasive management of cardiac arrhythmias. Technical improvements leading to reduction in procedure time and radiation dose will facilitate acceptance of this technique by patient and operator.
Adolescent↗
Ventricular arrhythmias in heart failure.
Heart failure is an increasingly common disorder leading to reduced quality and expectancy of life. Asymptomatic and symptomatic ventricular arrhythmias are a frequent complication and have been found to be independent prognostic predictors for sudden cardiac death in patients with heart failure. Unfortunately, the positive predictive failure for this finding is low, but in patients with sustained ventricular arrhythmias, variables indicating impaired pump function are the most important predictors of sudden and of nonsudden cardiac death. Arrhythmias in heart failure may have many different underlying mechanisms. Indications for, and mode of treatment of, arrhythmias in heart failure depend on the symptoms and prognostic significance of the arrhythmia. Primarily, pump function should be optimized and antiarrhythmic drug therapy instituted only when the arrhythmia persists. In poorly tolerated and life-threatening arrhythmias, implantable devices allowing pacing and defibrillation must be considered. No data are presently available indicating a protective role of antiarrhythmic drugs in the prevention of sudden cardiac death in heart failure. Future directions should concentrate on the development of better stratification of risk for sudden death, better delineation of mechanisms of arrhythmias in heart failure (allowing the development of mechanism-specific antiarrhythmic drugs), and research into new nonpharmacologic techniques such as cardiomyoplasty and molecular biologic techniques to rebuild the failing heart muscles.
Arrhythmias, Cardiac↗
Incidence, pathophysiology and prognosis of exercise-induced sustained ventricular tachycardia associated with healed myocardial infarction.
Of 150 consecutive patients with sustained monomorphic ventricular tachycardia (VT) (n = 116) or ventricular fibrillation (VF) (n = 34) late after acute myocardial infarction, 17 had reproduction of their sustained monomorphic VT during exercise testing. Data from these patients (group I) were compared with data from patients without exercise-induced VT (group II). No statistical difference was found between groups I and II with relation to age, sex, number of vessels with greater than 70% stenosis, left ventricular ejection fraction, number of previous myocardial infarctions, inducibility during programmed stimulation and total mortality during follow-up. In group I, only 1 patient (6%) developed ST depression during exercise compared with 47 patients (35%) in group II (p less than 0.01). After a 34-month mean follow-up, 6 patients in group I (35%) and 18 patients in group II (13%) died suddenly (p = 0.02). It is concluded that sustained monomorphic VT is reproduced during exercise in only 11% of patients with spontaneous late sustained monomorphic VT or VF. Electrocardiographic findings do not support ischemia as a triggering mechanism of exercise-induced sustained monomorphic VT. Patients with exercise-induced sustained monomorphic VT have a high incidence of sudden death.
Coronary Angiography↗
Incidence and timing of recurrences of sudden death and ventricular tachycardia during antiarrhythmic drug treatment after myocardial infarction.
Incidence and timing of recurrences of sustained ventricular tachycardia (VT) or sudden death were studied in 206 patients who survived their first episode of ventricular fibrillation (VF; n = 52) or sustained VT (n = 154) after myocardial infarction. All patients were treated with (empirically selected) antiarrhythmic drugs; 49% received amiodarone. After a mean follow-up of 36 months, 64 patients (41%) in the VT group and 10 (19%) in the VF group had nonfatal VT recurrences. Sudden death occurred in 22 (14%) and 9 (17%) patients in the VT and VF groups, respectively. Incidence of sudden death had 2 peaks at approximately 3 and 12 months. Nonfatal VT recurrences were more frequent (most often occurring in first 6 months) in the VT than in the VF group. Sudden death occurred during the following 3 years in only 10% of patients who survived 1 year. There was a much higher incidence of sudden death in patients with left ventricular ejection fraction (LVEF) less than or equal to 40% than in those with LVEF greater than 40% (28 of 65 vs 3 of 141; p less than 0.0001), but no relation between LVEF and nonfatal VT recurrences.
Aged↗
Identification of patients at high risk for recurrence of sustained ventricular tachycardia after healing of acute myocardial infarction.
A prognostic index for nonfatal recurrences of ventricular tachycardia (VT) was developed using a retrospective analysis of a group of 206 patients with sustained monomorphic VT or ventricular fibrillation (VF) after healing of acute myocardial infarction. 74 patients (36%) (64 with VT and 10 with VF) had recurrences of sustained monomorphic VT during 3.4 +/- 9 years of follow-up. Three clinical variables were selected and weighted by stepwise logistic discriminant analysis of the study group. They were coded as follows: interval of myocardial infarction to arrhythmia (less than 2 months = 1; 2 to 6 months = 2; greater than 6 months = 3), drug therapy with or without sotalol (with = 1, without = 2), and VT or VF as the presenting arrhythmia (VT = 1, VF = 2). The prognostic index was: 3.41 - (0.56 x interval) - (1.94 x therapy) + (0.86 x arrhythmia). This index was validated prospectively in a test group of 158 consecutive patients with VT or VF after healing of acute myocardial infarction. Patients were allocated into different classes with decreasing prognostic index values associated with increasing risk for recurrences of VT. In the test group, 27 of 158 (17%) patients (22 with VT and 5 with VF) had recurrences of VT (follow-up of 2 +/- 2 years). Two risk classes of patients were identified: high risk for recurrences of VT (61%) corresponding to patients with a negative index; and low risk (4%) consisting of those with a positive index. Thus, using O as the cutoff point, the sensitivity, specificity, and positive and negative predictive values were 81, 89, 62 and 96%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Adaptation of energy metabolism of canine latissimus dorsi muscle in response to chronic electrical stimulation.
Transformation of the latissimus dorsi (LD) muscle from a fast-twitch, fatigue-prone to a fatigue-resistant ("heart-like") muscle, necessary to allow its application in cardiac assist devices, can be induced by chronic electrical stimulation. In adult dogs we studied the nature and time course of myofibrillar and metabolic adaptations in the LD muscle when exposed in situ to 24 weeks of continuous electrical stimulation. In addition, the metabolic properties of the stimulated muscle were compared with those of canine cardiac muscle. The proportion of immunohistochemically identified type I fibres increased on stimulation from 28% to 80%, while that of type II fibres decreased from 69% to 16%. Fibres of intermediate type (IIC and IC) appeared transiently; the highest levels were found between 4 and 8 weeks of stimulation. The activities of fructose-6-phosphate kinase and lactate dehydrogenase (LDH), which before stimulation were similar to those in heart, decreased to 18% and 34% of their initial values respectively. However, the LDH isozyme pattern changed towards that typical for cardiac muscle. These changes indicate a markedly decreased flux capacity through the glycolytic pathway which, however, is directed more towards the oxidative conversion of substrates. The mitochondrial capacity (maximal palmitate oxidation and pyruvate dehydrogenase complex activities) of the muscle did not change and remained at a level less than half of that of cardiac ventricular muscle. Contents of adenine nucleotides and endogenous substrates were maintained during stimulation. No further changes in the observed adaptations occurred after week 12 of stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adaptation, Physiological↗
The electrocardiographic, clinical, and electrophysiologic spectrum of idiopathic monomorphic ventricular tachycardia.
Clinical, ECG, and electrophysiologic data from 47 patients who had episodes of sustained or nonsustained monomorphic VT with no evidence of structural heart disease were reviewed. According to the QRS configuration during tachycardia, four groups were distinguished. Nine patients had a right bundle branch block configuration and superior frontal plane QRS axis (group 1). Nine patients had a right bundle branch block configuration but an intermediate or right QRS axis (group 2). Group 3 consisted of five patients with a left bundle branch block configuration and a left axis deviation, and in group 4 there were 24 patients who had a left bundle branch block configuration with an intermediate or right frontal axis. Patients in group 1 had dizziness during tachycardia less frequently, but they needed cardioversion to terminate their arrhythmias more often. They experienced tachycardia during exercise less often, and tachycardia was not initiated during exercise testing. They had fewer ventricular premature beats according to the Holter recording. During the electrophysiologic study, VT was induced and terminated by pacing more often in this group. Patients with idiopathic VT with a right bundle branch block configuration and a superior axis seem to be a unique group of patients with idiopathic VT, and reentry seems to be the most likely arrhythmia mechanism in this group. The other ECG configurations share the same clinical and electrophysiologic characteristics, which suggest that the underlying arrhythmia mechanism is the same.
Adult↗
Clinical characteristics and electrophysiologic properties of atrioventricular accessory pathways: importance of the accessory pathway location.
OBJECTIVES: This study was designed to assess the influence of accessory atrioventricular (AV) pathway location on the clinical and electrophysiologic characteristics of 384 consecutive symptomatic patients having a single accessory pathway. METHODS: Four locations were studied: left free wall (n = 270), posteroseptal (n = 52), anteroseptal (n = 29) and right free wall (n = 33). Ten clinical variables and 12 electrophysiologic variables were analyzed, including the effective refractory period of the accessory pathway and the different clinically occurring and inducible arrhythmias. RESULTS: Only two clinical findings were associated with accessory pathway location: 1) later age at onset of symptoms in the left free wall versus other accessory pathway locations (24 +/- 12 vs. 20 +/- 11 years, p = 0.02), and 2) later age at the time of electrophysiologic study in the left free wall accessory pathway location (36 +/- 13 vs. 32 +/- 11 years, p = 0.01). Six electrophysiologic variables showed a correlation with the accessory pathway location: 1) retrograde conduction only was found less frequently in right free wall (9%) and anteroseptal (10%) than in left free wall (26%) and posteroseptal (29%) accessory pathway locations (p = 0.05); 2) the retrograde effective refractory period of the accessory pathway was shorter in anteroseptal (253 +/- 52 ms) and left free wall (270 +/- 72 ms) as compared with right free wall (296 +/- 101 ms) and posteroseptal (301 +/- 76 ms) locations (p = 0.05); 3) retrograde decremental conduction over the accessory pathway was present in the posteroseptal (17%) and left free wall (3%) but absent in the other locations (p less than 0.001); 4) anterograde decremental conduction was only seen in the right free wall location (12%) (p less than 0.001); 5) orthodromic reentrant tachycardia was induced less frequently in the right free wall than in other locations (70% vs. 93%, p less than 0.001); and 6) inducibility of atrial fibrillation was greater in anteroseptal (62%) than in right free wall (21%), left free wall (44%) and posteroseptal (36%) locations (p = 0.01). CONCLUSIONS: The location of the accessory AV pathway is associated with specific electrophysiologic characteristics.
Adolescent↗
Imipramine induced heart failure in the dog: a model to study the effect of cardiac assist devices.
OBJECTIVE: The value of intravenous imipramine in creating a reversible model of short term heart failure was evaluated in anaesthetised dogs. METHODS: Acute effects of imipramine were studied in 11 dogs using invasive haemodynamic pressure measurements and two dimensional echo evaluation. RESULTS: After a 30 min imipramine infusion (7.5 mg.kg-1.h-1), positive left ventricular dP/dtmax decreased from 1368(SEM 108) to 909(119) mm Hg.s-1 (p < 0.05), left ventricular end diastolic pressure increased from 8(1) to 12(2) mm Hg (p < 0.05), while left ventricular pressure decreased from 106(4) to 87(6) mm Hg (p < 0.05). Cessation of imipramine administration resulted within 60 min in partial restoration of cardiac function. This deterioration and subsequent recovery was also demonstrated with echocardiographic measurements, which showed a decrease in ejection fraction from 54(3)% to 28(2)% (p < 0.05). During administration of imipramine neither significant electrophysiological changes nor supraventricular/ventricular arrhythmias were seen. Repeated infusions of imipramine in three anaesthetised dogs with a two week interval showed the reproducibility of the haemodynamic effects and the recovery of ventricular function. Since the model was developed to evaluate the use of cardiomyoplasty in heart failure, the effect of imipramine was also evaluated on latissimus dorsi muscle contraction. Administration of imipramine did not affect skeletal muscle force development at the dosage used to create heart failure. CONCLUSIONS: This model can be used to produce short term reversible heart failure in anaesthetised animals to test the efficacy of supportive interventions like dynamic cardiomyoplasty, intra-aortic balloon pumping, and mechanical cardiac assist devices.
Animals↗
Aviation and antiarrhythmic medication.
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Aerospace Medicine↗
Unexplained cardiac arrest. The need for a prospective registry.
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Databases, Factual↗
The importance of muscle relaxation in dynamic cardiomyoplasty.
During the last decade dynamic cardiomyoplasty has been introduced as a new method to treat patients with severe heart failure. This procedure consists of the wrapping of the latissimus dorsi (LD) muscle around the heart with electrical stimulation of the muscle synchronous to cardiac contraction. The optimal pacing mode of the muscle, during the conditioning and working period of the LD muscle, is still unclear. The pace protocol, currently used worldwide, has a maximal number of muscle tetanic contractions of 100 per minute. Data are presented on the LD muscle contraction characteristics using that protocol. Both force measurements from six in situ stimulated goat LD muscles and x-ray evaluation of the movement of metallic clips on wrapped LD muscles in two patients were used. Results demonstrate that LD muscle force is well maintained at the maximal rate of 100 contractions per minute but relaxation is severely hampered. This may lead to diminished support of the failing heart and damage of the wrapped muscle. A pacing protocol is proposed using a lower maximal stimulation rate.
Animals↗
Antiarrhythmic drug treatment: need for continuous vigilance.
Any physician treating cardiac arrhythmias should be aware of a possible worsening of the arrhythmia (so-called arrhythmogenesis) after the start of antiarrhythmic drug treatment. To facilitate the recognition of that complication the type and possible mechanisms of arrhythmogenesis are reviewed. Recognition also requires an understanding of (a) the time of appearance of arrhythmogenic effects after different drugs, (b) the value of non-invasive and invasive tests, and (c) the profile of the patient most likely to develop this problem. Guidelines are given to reduce the incidence of the arrhythmogenic effects of antiarrhythmic drugs and a plea is made that the physician should be always on the alert for this complication.
Anti-Arrhythmia Agents↗
Changes in canine latissimus dorsi muscle during 24 wk of continuous electrical stimulation.
To study functional, structural, and biochemical adaptations to electrical stimulation of striated muscle in a large animal, the canine latissimus dorsi (LD) muscle was conditioned continuously for 24 wk with an increasing number of pulse bursts (burst duration 250 ms, burst frequency 30 Hz). Force measurements in vivo after 12 wk showed a significant decrease in the ripple, the ratio of interstimulus to peak force amplitude, from 0.94 +/- 0.03 to 0.13 +/- 0.08 (SE; n = 8, P less than 0.05), indicating reduction in contractile speed. Also the steep part of the force-frequency relation shifted to lower frequencies. A significant change in fiber-type composition was seen with both enzyme- and immunohistochemistry, manifested by an increase of type I fibers from 29.5 +/- 2.9 to 83 +/- 8% (SE; n = 8, P less than 0.05). During this period a transient rise in the number of type IIc/Ic fibers (from 3 to 10%) was seen. In the stimulated muscle, capillary-to-fiber ratio increased from 1.9 +/- 0.4 to 2.7 +/- 0.1 (P less than 0.05). A significant increase in mitochondrial volume was also seen, especially in the peripheral part of the fiber. Both creatine kinase and lactate dehydrogenase revealed a significant decline in activity within 12 wk. At the same time a shift in lactate dehydrogenase-isozyme pattern was observed toward the cardiac composition. No additional changes occurred after 12 wk of stimulation, indicating that conversion of the canine LD muscle was complete within this period.
Adaptation, Physiological↗
Complications after intracoronary stent implantation: three cases.
Complications after implantation of articulated Palmaz-Schatz stents in coronary arteries of 3 patients are reported. In 1 patient, embolization of the stent occurred during the acute phase, and in the other 2 patients, we observed restenosis after 4 and 5 months, respectively. Late restenosis was located in the midportion and the distal end of the stent in 1 patient. In the other patient a severe subtotal occlusion was found 1 cm proximal to the stent. These findings suggest that adaptation of the stent delivery system is needed to prevent loss of the stent and scraping of the vessel wall.
Aged↗
Programmed electrical stimulation and drugs identify two subgroups of ventricular tachycardias occurring 16-24 hours after occlusion of the left anterior descending artery.
BACKGROUND: Spontaneous sustained ventricular tachycardia (VT) occurring 16-24 hours after left anterior descending (LAD) coronary artery occlusion in the canine heart is most likely based on abnormal automaticity. In vitro, it has been demonstrated that the rate of the arrhythmia and the effect of overdrive pacing depends on the maximal diastolic potential (MDP). The MDP is also of importance in understanding the effect of antiarrhythmic drugs. To study 1) the possible presence of different responses to overdrive pacing and 2) the relation between the response to overdrive pacing and the effect of different antiarrhythmic drugs in the intact heart, we investigated the effect of 1) (prolonged) pacing and 2) lidocaine (3 mg/kg), verapamil (0.4-1.0 mg/kg), or flunarizine (2 mg/kg) during VT. METHODS AND RESULTS: In 21 conscious dogs with chronic atrioventricular block, 60 sustained VTs were observed 1 day after LAD occlusion. During VT, pacing with interstimulus intervals of 400, 300, and 200 msec for 15, 60, and 120 seconds was done on 40 VTs. Based on their response to pacing, VTs were divided into a pacing-suppressible (PS group) and a pacing-nonsuppressible group (PNS group). The mean cycle length in the PS group was significantly longer (410 +/- 50 msec) than in the PNS group (360 +/- 35 msec, p less than or equal to 0.01). Suppression was directly related to the rate and duration of pacing. Spontaneous recurrence of VTs was observed after 26 +/- 45 seconds. Lidocaine and verapamil increased cycle length of the suppressible VTs and terminated them, whereas flunarizine had no effect. Except for verapamil, which increased cycle length of the VTs, no effects were seen in the PNS group. CONCLUSIONS: In conscious dogs showing sustained VTs 16-24 hours after LAD occlusion, 1) the slower VTs can be suppressed by pacing, verapamil, and lidocaine but not by flunarizine, and 2) the faster VTs are not affected by pacing, lidocaine, and flunarizine, and are only slowed by verapamil. These findings are compatible with in vitro findings of abnormal automaticity, with the slower VTs originating from a higher MDP than the faster VTs.
Animals↗
[The localization of accessory atrioventricular pathways by the surface electrocardiogram].
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Atrioventricular Node↗