Atrial fibrillation in myocardial infarction complicated by heart failure: cause or consequence?
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Atrial Fibrillation↗
Biomedical subjects
B Waldecker
Publications and source records attributed to B Waldecker.
[Disorders of microcirculation in coronary heart disease].
Disturbances of microcirculation in coronary artery disease can be seen in the presence of critical stenosis of epicardial coronary arteries, as a result of endothelial dysfunction in the absence of significant stenosis or during recovery of ischaemic myocardium after successful angioplasty of stenosed or occluded coronary arteries. Diagnostic methods are morphologic/morphometric analyses, measurement of the global coronary reserve, measurement of the regional coronary microcirculation (scintigraphy, positron emission tomography) and laboratory analysis of haemorheological alterations (plasma, erythrocytes, leucocytes). After successful angioplasty, normalisation of glutamate extraction rate takes three to six months. In patients with unstable angina, changes in plasma viscosity, erythrocyte aggregation and neutrophil activation occur. Neutrophils are activated after successful angioplasty in acute myocardial infarction and even after elective angioplasty (when measured in the coronary sinus). Therapeutic improvements of disturbed microvascular flow can be obtained by increasing perfusion pressure (by revascularisation, nitrates, calcium antagonists, physical training), by improving the fluidity of the blood and by reducing the extravascular component of coronary vascular resistance (by antihypertensive treatment).
Angina Pectoris↗
Mechanisms for spontaneous termination of monomorphic, sustained ventricular tachycardia: results of activation mapping of reentrant circuits in the epicardial border zone of subacute canine infarcts.
OBJECTIVES: The objective of this study was to determine why sustained ventricular tachycardias (VT) sometimes stop without outside intervention. BACKGROUND: Sustained, monomorphic VT in patients with ischemic heart disease is often caused by reentrant excitation. These tachycardias can degenerate into rapid polymorphic rhythms or occasionally terminate spontaneously. METHODS: Sustained VT was induced by programmed stimulation in dog hearts 4 to 5 days after ligation of the left anterior descending coronary artery. Activation in reentrant circuits in the epicardial border zone of the infarct was mapped using 192 to 312 bipolar electrodes. RESULTS: Spontaneous termination of sustained VT always occurred when the reentrant wave front blocked in the central common pathway in reentrant circuits with a figure-of-eight configuration. Two major patterns of termination were identified from activation maps of the circuits that were not distinguishable from each other on the surface electrocardiogram: 1) Abrupt termination was not preceded by any change in the pattern of activation or cycle length. It could occur at different locations within the central common pathway, was not related to the directions of the muscle fiber orientation and was not caused by a short excitable gap. 2) Termination caused by premature activation (after a short cycle) either resulted from shortening of the functional lines of block around which the reentrant impulse circulated or was caused by wave fronts originating outside the reentrant circuit. In only one episode were oscillations of cycle length associated with termination. CONCLUSIONS: The mechanisms for termination of reentry in functional circuits causing VT are different from those in anatomic circuits where oscillatory behavior precedes termination.
Animals↗
Long-term follow-up after direct percutaneous transluminal coronary angioplasty for acute myocardial infarction.
OBJECTIVES: The purpose of this study was to analyze long-term follow-up information over several years from consecutive, unselected patients treated with direct percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (MI). BACKGROUND: Direct PTCA is often used in patients with acute MI. Short-term results are favorable. However, there is less information available on long-term observations over several years in these patients. METHODS: A total of 416 consecutive and unselected patients with acute MI underwent direct PTCA. Survival of the acute infarct phase was 94.2%; the remaining 392 patients--the study population-were discharged and followed for 3.3+/-1.4 years. Mortality as well as cardiac events and reinterventions are reported. Clinical variables assessed at the time of discharge are submitted to statistical analysis to detect potential risk factors. RESULTS: Total cumulative mortality in the first year was 10% for the entire group and 6% for patients not presenting in cardiogenic shock. Mortality after discharge was 4.6% in the first year and dropped to <4% per year thereafter. Reinterventions after discharge were required in 16% in the first year and in <4% per year in years 2 to 4. Poor left ventricular ejection fraction (<35%), three-vessel disease and advanced age (> or =75 years) were long-term risk factors for total mortality after direct PTCA. CONCLUSIONS: The clinical benefit of direct PTCA for acute MI is maintained during follow-up with respect to mortality. However, reinterventions for restenosis or de novo stenosis are often required (10% to 20%). Although few in number (<10%), patients with severely impaired left ventricular function continue to have a poor prognosis.
Adult↗
Mechanisms causing sustained ventricular tachycardia with multiple QRS morphologies: results of mapping studies in the infarcted canine heart.
BACKGROUND: Sustained reentrant ventricular tachycardias (VTs) with different QRS morphologies have been observed to occur spontaneously and during programmed stimulation in human hearts. We determined mechanisms that can cause tachycardias with multiple morphologies in a canine model of myocardial infarction by mapping reentrant circuits. METHODS AND RESULTS: Reentrant VT with multiple QRS morphologies was induced in 11 canine hearts with 4-day-old infarcts. Comparison of activation maps of the reentrant circuits in the epicardial border zone associated with each morphology indicated two basic mechanisms. Less frequently, VTs of different morphologies in the same heart were caused by reentrant circuits in different regions of the infarct. Most commonly, the reentrant circuits associated with different morphologies were in the same region. Three different factors caused different exit routes from circuits in the same region, leading to the multiple morphologies. (1) The reentrant wave front for each morphology rotated around the same line of block but in different directions. (2) Reentrant circuits associated with each morphology were similar, but there were small changes in the extent of the central line of block. (3) Reentrant circuits with completely different sizes and shapes caused different morphologies. CONCLUSIONS: In this canine model, tachycardias with multiple morphologies most commonly arise from reentrant circuits in the same region of the infarct, suggesting that most often only one area has electrophysiological properties necessary to sustain reentry.
Animals↗
[New studies, new trends: directional coronary atherectomy].
Despite theoretical advantages of Directional Coronary Atherectomy (DCA) vs. PTCA, the first two controlled studies comparing both methods, the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT), and the Canadian Coronary Atherectomy Trial (CCAT), showed no clinical benefit of DCA, A second generation of trials, the Optimal Atherectomy Restenosis Study (OARS) and the Balloon versus Optimal Atherectomy Trial (BOAT), designed to optimize DCA with the use of 7F devices and adjunctive PTCA revealed lower angiographic restenosis rates compared to CAVEAT. In addition, the preliminary follow-up results of BOAT, presented by Donald S. Baim in Birmingham in August 1996, showed a 20% reduction of angiographic restenosis after DCA compared to PTCA. There was no association between post-procedure CK-MB elevation in the DCA group and late mortality. These results may further expand the application of DCA to clinical routine, whereas this procedure still has specific indications like treatment of ostial and bifurcation lesions and atherectomy in future may be the treatment of choice for restenosis in coronary stents.
Angioplasty, Balloon, Coronary↗
[Early and long-term results of direct PTCA in patients with acute myocardial infarct].
A review of the literature suggests that direct PTCA for acute myocardial infarction is indicated and feasible in 90-95% of unselected, consecutive patients; direct PTCA is reported to be successful in > 90% of procedures. This results in a hospital mortality of 3-7% for unselected patients and a 4% re-infarction rate. A recent meta-analysis of direct PTCA vs i.v. thrombolysis in patients with acute infarction demonstrates a lower mortality after PTCA (4.4% vs 6.5%, p = 0.02) as well as lower mortality/re-infarction rate (7.2% vs 11.9%, p < 0.001). Mortality in the 1st year after discharge is < 5% with about half of the fatalities being due to cardiac causes. Patients presenting with or developing cardiogenic shock in the acute infarct phase experience a 20-50% acute mortality. Mortality rests at < 10% in these patients in the first year after discharge. In conclusion, (1) direct PTCA is feasible without additional risks in patients with acute myocardial infarction, (2) angiographic and clinical success rates of direct PTCA are favorable and superior to i.v. thrombolysis in the hands of expert operators, and (3) referral to an institution providing the option of immediate, direct PTCA must be considered in the patient with acute infarction but contraindication(s) to i.v. thrombolysis.
Angioplasty, Balloon, Coronary↗
Inappropriate management of self-terminating ventricular arrhythmias by implantable cardioverter defibrillators despite a specific reconfirmation algorithm: a report of two cases.
Algorithms that attempt to reconfirm the presence of an arrhythmia prior to definite treatment have been implemented in ICDs to prevent inappropriate shock therapy due to self-terminating ventricular arrhythmias. Nevertheless, in two patients, clinically inappropriate shocks were delivered after spontaneous conversion of the arrhythmia despite the use of a specific reconfirmation algorithm. Reconfirmation criteria were met due to a premature ventricular complex causing a short cycle in the first patient and a long postextrasystolic pause in the second patient. To avoid inappropriate shock therapy due to self-terminating ventricular arrhythmias, further improvement of detection algorithms is required.
Algorithms↗
Specific cardiological evaluation after focal cerebral ischemia.
Purpose of this study was to define a subgroup of TIA/stroke patients who should be examined by transthoracal and transesophageal echocardiography or Holter-electrocardiography to identify those with cardiogenic brain embolism reliably; 300 consecutive patients with acute focal brain ischemia underwent a standardized diagnostic protocol for the evaluation of the etiology including, clinical examination by a cardiologist and routine electrocardiography, Holter-electrocardiography, transthoracal and transesophageal echocardiography. 188 patients had a potential cardiac source of embolism. In particular echocardiography was diagnostic in 163 patients, and Holter-electrocardiography 10; 159 of these 188 patients (84.6%) had competitive etiologies, predominantly large vessel atherosclerosis. In 136 patients cardiogenic brain embolism was assumed as quite definite or possible. To identify these patients reliably, transthoracal and transesophageal echocardiography would have been necessary in 89% of the entire group of patients (all with clinically cardiological abnormalities, pathological routine ECG, without vascular risk factors, or no atherosclerosis in duplex sonography), and Holter-electrocardiography in 54%.
Cerebral Infarction↗
Electrophysiological effects of flecainide on anisotropic conduction and reentry in infarcted canine hearts.
BACKGROUND: The class IC antiarrhythmic drug flecainide has been shown to be ineffective for the treatment of ventricular arrhythmias in some patients who have had a prior myocardial infarction and sometimes even provoke arrhythmias (proarrhythmic effect). Since some ventricular tachycardias may be caused by anisotropic reentry, we determined the effects of flecainide on this mechanism for reentry in infarcted canine hearts in order to determine possible causes for its clinical effects. METHODS AND RESULTS: The effects of flecainide were determined on ventricular tachycardia induced by programmed electrical stimulation in dogs with healing myocardial infarction 4 days after coronary artery occlusion. Activation in the reentrant circuits causing tachycardia was mapped with a 196-channel computerized mapping system. We found that flecainide converted inducible unsustained ventricular tachycardia to inducible sustained ventricular tachycardia by modifying conduction in the reentrant circuit. In general, by slowing conduction, the reentrant wave front did not block after flecainide, leading to perpetuation of reentrant excitation. When sustained ventricular tachycardia could be induced before the drug, flecainide prolonged the coupling interval of premature impulses necessary to induce tachycardia by lengthening the line of block and slowing conduction around it. Flecainide also slowed the rate of the tachycardia but did not terminate it. The anisotropic reentrant circuits were modified so that the central common pathway of "figure-of-eight" circuits was narrowed and lengthened due to extension of the lines of block that bounded the pathways. Extension of the lines of block resulted from depression of conduction in the direction transverse to the long axis of the myocardial fiber bundles caused by flecainide. Flecainide also slowed conduction in the longitudinal direction in part of the circuits. The depressant effects of flecainide on both longitudinal and transverse anisotropic conduction were quantified by pacing from the center of the electrode array and it was found, contrary to predictions, that transverse conduction was depressed as much as longitudinal conduction. CONCLUSIONS: Flecainide slows conduction in both the longitudinal and transverse direction relative to the orientation of the myocardial fibers. This enables sustained reentry to occur more easily. Flecainide does not cause conduction block in crucial regions of reentrant circuits (central common pathway) and therefore does not prevent reentrant tachycardia in healing infarcts.
Animals↗
[Heart rhythm after conversion of ventricular tachyarrhythmia by internal shock delivery].
The purpose of this retrospective study is the analysis of dysrhythmias following internal cardioversion/defibrillation of ventricular tachycardia (VT) or fibrillation (VF) and to discuss their relevance to the therapy with automatic implantable devices. Therefore, 304 internal conversions of VT/VF during and/or after implantation of automatic defibrillators were evaluated in 51 patients. Significant post-shock arrhythmias (bradycardia, atrial fibrillation, non-sustained VT of > or = 10 cycles) were absent after 89% of internal shocks. Pauses of > 2 s were observed in 2/9 patients without VVI-back-up pacing. The heart rate was > or = 50 bpm in 10/51 patients. Atrial fibrillation occurred in 7 patients. Non-sustained, mostly polymorphic VT consisting of > or = 10 cycles followed 18/304 (6%) internal shocks in 13 patients. The VT rate was > or = 200/min in 17/18 episodes and triggered an inadequate shock once. The incidence of non-sustained VT post-shock was unrelated to shock energy, type, and duration of the converted arrhythmia. In conclusion, automatic implantable devices should provide back-up pacing. Tachycardic rhythms can mislead automatic interpretation of the effect of internal shocks.
Adult↗
In-hospital experience with multiprogrammable implantable antitachycardia/antifibrillation devices.
Multiprogrammable, automatic internal defibrillators with (n = 45) and without (n = 15) antitachycardia pacing features were implanted in 60 consecutive patients with refractory, malignant ventricular tachycardia (VT) (n = 42) or fibrillation (VF) (n = 18). Left ventricular (LV) ejection fraction was reduced to 39% +/- 12% as a result of structural heart disease in 56 patients. The complexity of the systems caused no additional risks to the surgical procedure or postoperative management. VT/VF detection parameters were individually adjusted to the arrhythmia type (detection cycle length 323 +/- 40 ms in patients with VF vs 405 +/- 40 ms for VT patients, P < 0.05) and incidence (longer detection periods if frequent nonsustained VT was also present). Shock energy was reduced in patients with VT as compared to VF (11J vs 24J, P < 0.05). Antitachycardia pacing was activated in 19/28 (68%) patients with well tolerated VT. Signal, telemetry, as detected by the device, combined with programmability allowed the device to be checked for correct decisions (these were inappropriate in four patients in three of whom corrections were non-invasive) prior to discharge. In conclusion, in the automatic tachyarrhythmia control devices we studied, programmability and flexibility appeared to be clinically safe and useful. Prolonged observation periods are required, however, to evaluate the true clinical safety and persistent efficacy of device programmability and flexibility.
Algorithms↗
Effects of overdrive stimulation on functional reentrant circuits causing ventricular tachycardia in the canine heart: mechanisms for resumption or alteration of tachycardia.
INTRODUCTION: The purpose of the experiments described in this article was to investigate the effects of overdrive stimulation on functional anisotropic reentrant circuits causing ventricular tachycardia in infarcted canine ventricles. We determined how overdrive stimuli affect reentrant circuits to alter characteristics of the tachycardia. METHODS AND RESULTS: Activation patterns were determined by mapping excitation with a 192 bipolar electrode array. We found that overdrive stimuli could activate the circuits with the same pattern as the reentrant wavefront and that after overdrive stopped either the last or the next to last stimulated wavefront continued propagating through the circuit as a new reentrant impulse and tachycardia continued. When the circuit was not altered after overdrive, the exit route that the stimulated wavefront took from the circuit to activate the rest of the ventricles was also not altered and the tachycardia after overdrive had the same cycle length and QRS morphology as prior to overdrive. In some experiments, however, the overdrive stimuli did not follow the original reentrant pathway but led to the formation of a different circuit with a different exit route to the ventricles. As a result, after overdrive stimulation tachycardia had a different QRS morphology and cycle length than prior to stimulation. When the new circuit after overdrive was small and the revolution time of the reentrant impulse around the circuit was short, fibrillation occurred. CONCLUSION: Functional reentrant circuits can either be maintained or altered after a period of overdrive stimulation. The results explain many of the effects that have been seen during overdrive stimulation of clinical ventricular tachycardia.
Animals↗
Overdrive stimulation of functional reentrant circuits causing ventricular tachycardia in the infarcted canine heart. Resetting and entrainment.
BACKGROUND: Clinical electrophysiology studies have used, for the most part, models of anatomic reentrant circuits to explain entrainment of ventricular tachycardia. Our studies use activation maps to directly determine mechanisms of entrainment of functional circuits that cause tachycardia. METHODS AND RESULTS: Electrograms were recorded from 192 sites on reentrant circuits in the epicardial border zone of canine myocardial infarcts during sustained ventricular tachycardia. Overdrive stimulation from different sites and at different cycle lengths was investigated. The reentrant circuits were shown to be functional, yet stimulated impulses could enter and repetitively reset the circuits (entrainment), demonstrating the presence of an excitable gap. Entrainment could occur from different stimulation sites with the stimulated impulses from each site activating the circuit with a different pattern. Entrainment, however, did not occur when the stimulated wave fronts obliterated the lines of functional block in the circuit. Fusion on the ECG occurred during entrainment when the stimulated impulses activated the ventricles concurrently with a previous stimulated impulse leaving the reentrant circuit at a different site. The first postpacing QRS was captured but not fused because it was caused by the last stimulated impulse emerging from the circuit. The first postpacing cycle length on the ECG was either equal to or longer than the overdrive cycle length depending on whether there was a fusion QRS during overdrive. The first postpacing cycle length at sites in the reentrant circuit equaled the pacing cycle length. At an appropriately short overdrive cycle length, stimulated impulses blocked in the circuit to terminate reentry. CONCLUSIONS: Functional reentrant circuits causing ventricular tachycardia can be reset and entrained. Activation maps directly show the mechanisms.
Animals↗
Reverse use-dependent effects of sotalol demonstrated by recording monophasic action potentials of the right ventricle.
In 22 patients referred for electrophysiologic study, monophasic action potentials (MAP) were recorded from the right ventricular aspect of the ventricular septum. The duration of MAP at 90% (MAP90) and 30% (MAP30) repolarization was measured in sinus rhythm, at a constant atrial paced cycle length of 600 ms for 3 minutes and at constant ventricular paced cycle lengths of 600, 500, 400 and 300 ms for 20 beats. Programmed ventricular stimulation from the apex of the right ventricle was performed at a basic drive cycle length of 400 ms and MAP90 and MAP30 of premature beats was determined. Changes of MAP duration were assessed 20 minutes after administration of intravenous sotalol 1.5 mg/kg. Sotalol significantly increased MAP90 and MAP30 in sinus rhythm. This was independent from sinus cycle length prolongation as evidenced by a significant prolongation of MAP90 and MAP30 with constant atrial pacing after sotalol. With slow ventricular stimulation frequencies and with long coupling intervals at programmed ventricular stimulation, sotalol significantly prolonged MAP90 and MAP30; with high stimulation frequencies and at short coupling intervals the action potential-prolonging effect of sotalol was diminished, indicating a reverse use-dependent effect of sotalol on repolarization of the right ventricle in humans.
Action Potentials↗
Implantable cardioverter defibrillator: possible hazards of electromagnetic interference.
We report on three patients with an automatic, implantable cardioverter defibrillator (AICD, CPI) in whom the device had been deactivated due to electromagnetic interference. In all cases, the source of the electromagnetic disturbances could be identified.
Adult↗
[Combined anti-bradycardia/anti-tachycardia pacemaker-cardioverter-defibrillator systems in patients with recurrent ventricular tachyarrhythmias].
In 41 patients with recurrent sustained ventricular tachycardia and/or ventricular fibrillation an integrated pacemaker-defibrillator-system (PCD, Medtronic, model 7216 A or 7217 B) was implanted. In 21 out of 24 (88%) patients a new transvenous implantation technique in combination with a subcutaneous patch electrode was used. The implanted devices comprise antibradycardiac pacemaker functions, two different forms of antitachycardiac pacemaker functions (ramp and burst pacing), and internal cardioversion or defibrillation capabilities. During a mean follow-up of 8 months 147 episodes of ventricular tachycardia were detected, 131 of them were terminated successfully by antitachycardiac pacing; in 13 episodes internal cardioversion was applied to revert ventricular tachycardia. Twenty-seven episodes of ventricular fibrillation or rapid ventricular tachycardia (greater than 200/min) were detected and successfully terminated by internal defibrillation. In six patients with intermittent rapid atrial fibrillation, change of antiarrhythmic therapy was required to avoid activation of the device. The new integrated pacemaker-defibrillator systems improve therapy in patients with life-threatening tachyarrhythmias by reducing the number of internal cardioversions/defibrillations; the non-thoracotomy approach reduces the post operative risk.
Adult↗
Electrophysiologic effects of bepridil in patients with refractory ventricular tachycardia assessed by programmed electrical stimulation.
The effect of intravenous bepridil, a new calcium antagonist with class I and III properties, was tested in 21 patients with sustained ventricular tachyarrhythmias refractory to a mean of five antiarrhythmic agents as assessed by programmed right ventricular stimulation. At control electrophysiologic study without antiarrhythmic agents, sustained monomorphic ventricular tachycardia (VT) was initiated in 20 patients and ventricular fibrillation (VF) was initiated in one patient. After 3 mg/kg of bepridil was administered, VT was still inducible in 19 patients (3 patients had self-terminating VT); the other 2 patients had no inducible VT after bepridil. Bepridil prolonged significantly the QTc interval, the effective refractory period, and the cycle length of induced ventricular tachycardia. Two patients with no inducible VT after intravenous bepridil were placed on oral bepridil (300 mg/day). One patient died suddenly and one patient died of progressive heart failure. The results seem to indicate that the efficacy of bepridil in patients with refractory ventricular tachycardia is limited.
Aged↗