Biomedical subjects
Publications and source records attributed to M Borggrefe.
Intracranial microembolic signals, probably caused by gaseous emboli, are readily detectable in patients undergoing radiofrequency ablation in the left side of the heart only. Clinical value of the detected signals could not be equivocably assessed, because only 2 of the patients who were examined (both emboli positive) had transient neurologic symptoms.
BACKGROUND: Programmed ventricular stimulation is commonly used to guide therapy in post-myocardial infarction patients with sustained monomorphic ventricular tachycardia (VT) or ventricular fibrillation (VF). In patients with valvular heart disease presenting with spontaneous VT, VF, or syncope, the usefulness of this technique is still unclear. The aim of the study was to analyze whether programmed ventricular stimulation was helpful in guiding therapy and determining prognosis in 97 patients with valvular heart disease presenting with VT (60%), VF (18%), or syncope (22%). METHODS AND RESULTS: Patients were classified as having either predominant ventricular pressure or volume overload or no significant pressure or volume overload. Overall, sustained VT or VF was inducible in 38 (39%) and 19 (20%) patients, respectively. Forty-six (47%) patients were discharged on antiarrhythmic drugs, 29 (30%) received an implantable cardioverter-defibrillator, and 22 (23%) remained without therapy. With serial drug testing, inducibility was completely or partially suppressed in 18 (19%) and 9 (9%) patients, respectively. During a mean follow-up of 51 months (n=97), 17 patients (18%) died (sudden death, n=7; heart failure, n=4; noncardiac causes, n=6). One-, 2- and 3-year event-free survival for sudden death, sustained VT, or VF was 77%, 68%, and 61%, respectively. Only inducibility of VT during baseline study (P<.0003) and left ventricular volume overload (P<.008) were significant predictors of arrhythmic events. Recurrence of arrhythmic events occurred in 56% and 56% of patients with complete or partial suppression of inducibility during serial drug testing as well as in 10 of 19 (53%) patients without a change in inducibility. CONCLUSIONS: Although programmed ventricular stimulation seems to predict adverse outcome, serial drug testing is unreliable in guiding therapy. The type of workload imposed on the ventricles influences outcome, being worse in patients with left ventricular volume overload. Therefore, implantation of a cardioverter-defibrillator should be considered early for the management of these patients.
BACKGROUND: The ability of radiofrequency energy to extend across scar tissue is unknown. We investigated the effects of radiofrequency catheter ablation on intramural temperature in experimental chronic myocardial infarction. METHODS AND RESULTS: Myocardial infarction was induced in eight dogs by a transcatheter coronary artery occlusion-reperfusion technique. The dogs were reanesthetized after 15 to 24 days. Four additional dogs served as controls. The freshly excised preparations were cut and placed in a saline bath at 37 degrees C. Temperature-guided energy applications with a preselected catheter tip temperature of 80 degrees C were performed for 60 seconds with a 7F ablation catheter. Thermoelements were inserted into the ventricular muscle at depths of 2.5 to 3.0 mm ("subendocardial") and 5.5 to 6.0 mm ("intramural"). Surviving muscle fibers were interspersed among the transmural scar tissue. The maximal temperatures did not differ significantly between normal hearts and chronic infarctions at the subendocardial (64.5+/-6.4 degrees C versus 66.7+/-6.6 degrees C) or intramural thermo-element (51.9+/-5.7 degrees C versus 52.3+/-5.7 degrees C). The myocardial temperature rise was slow, and steady-state temperatures had not been reached after 60 seconds. The intramural temperatures in chronic infarctions measured 49.0+/-4.3 degrees C after 40 seconds of energy delivery and were still below the critical tissue temperature of 50 degrees C that is necessary to induce permanent myocardial damage. CONCLUSIONS: Temperature-guided radiofrequency ablation in a dog model of chronic myocardial infarction may induce tissue temperatures >50 degrees C at a depth of 5.5 to 6.0 mm. The intramural temperature rise was slow, indicating that long energy applications might be necessary if the arrhythmogenic substrate is subepicardial.
Jervell Lange-Nielsen syndrome (JLNS) is a recessive disorder with congenital deafness and long-QT syndrome (LQTS 1). Mutations in the potassium-channel gene KVLQT1 (LQTS 1) have been identified in JLNS and in autosomal-dominant LQTS as well. We performed haplotype analysis with microsatellite markers in a Lebanese family with JLNS, but failed to detect linkage at LQTS 1. Moreover, using this approach, we excluded two other ion-channel genes involved in autosomal-dominant LQTS, HERG (LQTS 2) and SCN5A (LQTS 3). Our findings indicate that JLNS is genetically heterogeneous and that, in this family, an unknown LQTS gene causes the disease.
OBJECTIVE: The aim of this study was to assess the antiarrhythmic efficacy and safety of d,l-sotalol in patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) and in survivors of cardiac arrest and to identify the factors that are associated with arrhythmia suppression and therefore might be helpful in predicting drug efficacy. BACKGROUND: Despite increasing use of the class III antiarrhythmic agent d,l-sotalol, data on its short- and long-term efficacy in a large patient cohort are lacking. Information on its long-term tolerability and safety is limited. METHODS: A total of 396 patients with inducible sustained VT or VF (VT/VF) underwent programmed stimulation before and after receiving oral d,l-sotalol (240 to 640 mg/day). Patients in whom VT/VF was rendered either noninducible or more difficult to induce (more extrastimuli or faster drive cycle length needed for VT/VF induction) were discharged on a regimen of oral d,l-sotalol. RESULTS: d,l-Sotalol suppressed VT/VF in 151 patients (38.1%) and rendered the arrhythmia more difficult to induce in 76 patients (19.2%). The extent of drug-induced prolongation of right ventricular refractoriness and a shorter VT cycle length at baseline were independent predictors of immediate drug efficacy. Torsade de pointes developed in seven patients (1.8%). Two hundred ten patients (53%) continued to receive d,l-sotalol and were followed up for 34 +/- 18 months (mean +/- SD). The actuarial rates for the absence of arrhythmic recurrence (either VT/VF or sudden death) at 1 and 3 years were 89% and 77%, respectively. Actuarial rates for overall survival at 1 and 3 years were 94% and 86%, respectively. VT/VF suppression by d,l-sotalol was an independent discriminant variable that separated patients with and without arrhythmia recurrence. However, noninducibility of VT/VF did not predict freedom from sudden death. CONCLUSION: Oral d,l-sotalol is effective and safe in patients with VT/VF. However, sudden cardiac death develops in a significant proportion of patients, and programmed stimulation seems to be of limited value for its prediction.
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In patients surviving acute MI, identification of those at high risk for life-threatening ventricular tachyarrhythmias and/or sudden death is of great importance. Numerous strategies based on indices such as the degree of left ventricular dysfunction, complex ventricular arrhythmias, or parameters of autonomic dysfunction have not yet led to an effective identification of the individual patient at risk. During the past decade, many investigators have recorded low amplitude, high frequency components in the terminal QRS complex (so-called late potentials) from patients prone to sustained ventricular tachycardia. The SAECG has been used to predict life-threatening tachyarrhythmias in patients after acute MI and to screen for inducible ventricular tachycardia in patients with unexplained syncope or sustained ventricular tachycardia. This review article describes the most frequently applied methodology and clinical applications of the SAECG in post-MI patients and discusses the usefulness of noninvasive recordings in various other clinical settings.
Radiofrequency catheter ablation has been established as a first-line curative treatment modality in patients with symptomatic AV nodal reentrant tachycardia (AVNRT). The successful sites of stepwise catheter ablation approaches of the so-called fast and slow pathways strongly suggest that AVNRT involves the atrial approaches to the AV node. The typical fast pathway ablation sites are located anterosuperior toward the apex of the triangle of Koch, which also contains the compact AV node, whereas the usual slow pathway ablation sites are located posteroinferior toward the base of the triangle of Koch at a greater distance to the compact AV node and bundle of His. Accordingly, ablation studies with large patient cohorts have demonstrated that fast pathway ablation carries a higher risk of inadvertent complete AV block. Thus, the slow pathway is clearly the primary target site, and fast pathway ablation is rarely necessary. Different approaches for slow pathway ablation have been elaborated: anatomically oriented stepwise techniques, ablation guided by double potentials recorded within the area of the slow pathway insertion, and combined techniques. The modern concept of AVNRT suggests that this arrhythmia involves the highly complex three-dimensional nonuniform anisotropic AV junctional area. Accordingly, mapping and ablation studies demonstrated that the anterior approach is not identical with fast pathway ablation, and the posterior approach is not identical with slow pathway ablation. Therefore, it is essential for interventional electrophysiologists to familiarize themselves with the anatomic and electrophysiologic details of this complex and variable specialized AV junctional region. In this review, the anatomic and pathophysiologic aspects of the AV junctional area as they relate to interventional therapy are summarized briefly, and the catheter techniques for ablation of the so-called fast and slow AV nodal pathways for the treatment of AVNRT are described.
INTRODUCTION: The difficult catheter orientation and navigation associated with conventional technology and mono-/multiplane fluoroscopy may complicate ablation procedures of atrial tachycardias. A new three-dimensional catheter technology for electroanatomical mapping of the right atrium and ablation of ectopic atrial tachycardia is described. METHODS AND RESULTS: A novel electromagnetic catheter-based mapping system was investigated for electroanatomical mapping of the entire right atrium in 12 patients. The system reconstructed three-dimensional maps from the multitude of endocardial sites that were sequentially mapped and color coded the individual activation times. The electrophysiologic information was superimposed on the geometry of the mapped area. The anatomical landmarks of the right atrium, i.e., the tricuspid annulus, mouth of the coronary sinus, ostia of the superior and inferior venae cavae, and right atrial appendage, could be depicted in all cases. The sinus node area and the preferential conduction along the crista terminalis could be delineated. In four patients with ectopic atrial tachycardia, the earliest endocardial activation could be identified with high spatial resolution as a "hot spot." After completion of the mapping procedure, the ablation catheter could be reliably renavigated to the site of origin, and ablation was successful with one or two impulses. In one patient with previous atrial septal repair, the activation map allowed the reconstruction of a long line of conduction block induced by the atriotomy. CONCLUSION: Three-dimensional electroanatomical mapping of the right atrium allowed detailed reconstruction of the chamber geometry and activation sequence. The sites of origin of ectopic atrial tachycardias could be identified precisely. The system allowed accurate renavigation to the site of earliest activation, thereby guiding successful ablation of the foci.
BACKGROUND AND PURPOSE: We undertook this study to evaluate the prevalence and clinical correlations of Doppler microembolic signals (MES) in stroke-prone patients. METHODS: Patients with potential cardiac (n = 300) or carotid (n = 100) embolic source and control subjects (n = 100) were monitored with transcranial Doppler sonography for MES. Transthoracic (n = 192) and/or transesophageal (n = 134) echocardiography and carotid studies (continuous-wave Doppler, n = 181; color-coded duplex, n = 47) were performed in all patients with potential native cardioembolic source. Carotid disease was evaluated by means of continuous-wave Doppler (n = 87), color-coded duplex (n = 70), or intra-arterial angiography (n = 24) in patients with potential carotid embolic source. RESULTS: Overall MES prevalence was 23% in patients with potential native cardioembolic source (infective endocarditis [n = 7] 43%, left ventricular aneurysm [n = 38] 34%, intracardiac thrombus [n = 23] 26%, dilative cardiomyopathy [n = 39] 26%, nonvalvular atrial fibrillation [n = 24] 21%, valvular disease [n = 80] 15%), 55% in patients with prosthetic cardiac valves (mechanical [n = 77] 58%, porcine [n = 7] 43%, homografts [n = 5] 20%), 28% in patients with carotid disease (symptomatic [n = 46] 52%, asymptomatic [n = 54] 7%; P < .01), and 5% in control subjects. No relationship between MES counts and patients' age, sex, or actual medication was noted. The sensitivity and specificity of MES detection in identifying patients with potential embolic sources were 31% and 95%, respectively. CONCLUSIONS: Our study confirmed the reported clinical significance of MES in patients with carotid disease and the high specificity of this technique. The demonstrated low sensitivity of MES detection could be due to short monitoring duration or application of antihemostatic treatment. Prospective large-scale studies are needed to determine the definitive value of MES detection as a diagnostic method in patients with potential cardioembolic source.
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The aim of this study was to extract and combine non-invasive risk parameters from the signal-averaged electrocardiogram (SAECG) and heart rate variability (HRV) based on 24-hour ambulatory electrocardiography to optimize the prognostic value for arrhythmic events after acute myocardial infarction. A prospective series of 553 men < 66 years of age enrolled in the Post-Infarction Late Potential study were analyzed. Within 2 to 4 weeks after acute myocardial infarction, all patients underwent SAECG and 24-hour ambulatory electrocardiography before hospital discharge. During 6 months of followup, 25 patients (4.5%) experienced arrhythmic events (sustained ventricular tachycardia, n = 11; ventricular fibrillation, n = 7; sudden cardiac death, n = 7). The predictive power of SAECG and HRV parameters was assessed using a Cox proportional-hazards model. In HRV analysis, the most significant differences between patients with and without arrhythmic events were observed for the beat-to-beat parameter root-meansquare of successive RR differences [RMSSD]): 25.7 +/- 16.9 ms in patients with arrhythmic events versus 34.1 +/- 18.6 ms in patients free of arrhythmic events (p = 0.004). Time domain analysis of the SAECG showed the QRS duration to be most significantly different in both patient groups: 106.4 +/- 18.7 ms (arrhythmic events) versus 95.3 +/- 18.7 ms (no arrhythmic events) (p = 0.001). Based on the Cox regression model, RMSSD and QRS duration were demonstrated to be independent significant risk factors (regression coefficient for QRS duration: cq = 0.014 +/- 0.006 ms(-1), p = 0.014; for RMSSD: cr = -0.041 +/- 0.016 ms(-1), p = 0.009). Based on the regression coefficients, an analytic risk model was developed describing the arrhythmic risk as a function of QRS duration, RMSSD, and time after infarction. We conclude that the combination of beat-to-beat changes of heart rate measured by RMSSD and QRS duration from the SAECG enhances noninvasive risk stratification after myocardial infarction.
Poor left ventricular function is a predictor of sudden death. Both antiarrhythmic drugs and implantable cardioverter-defibrillators (ICDs) promise to reduce the sudden death rate in these patients and consequently improve survival. In patients without spontaneous ventricular tachyarrhythmias, only beta-blocking agents and amiodarone have been shown to reduce sudden death and improve survival in some studies, whereas class I antiarrhythmic drugs increased mortality. For patients with documented ventricular tachyarrhythmias, protection against sudden death by serially tested class I antiarrhythmic drugs is at best moderate. There is some evidence suggesting that therapy with class III antiarrhythmic drugs, either amiodarone or dl-sotalol, may reduce sudden death rates and improve overall mortality in comparison to therapy with class I antiarrhythmic drugs. ICDs have been shown to prevent sudden death reliably. In published patient cohorts in which only patients who were not inducible off antiarrhythmic drugs or still inducible on antiarrhythmic drugs received an ICD, the ICD seemed to improve overall survival in comparison to class I antiarrhythmic drugs. A small prospective randomized study that compared a conventional therapy strategy to primary ICD implantations showed an improved outcome with ICDs as therapy of first choice. However, these studies included many patients treated with class I antiarrhythmic drugs considered to be less effective. In matched control studies comparing the ICD to amiodarone or dl-sotalol, less sudden deaths and an improved overall survival could be shown for the ICD in general without stratification for left ventricular function. Thus, in patients with hemodynamically nontolerated ventricular tachyarrhythmias, the ICD seems to improve survival in comparison to class I antiarrhythmic drugs, dl-sotalol, or amiodarone. However, in patients with poor left ventricular function, therapy with ICDs seems to be less cost-effective than in patients with preserved left ventricular function. In patients with very poor left ventricular function who are evaluated for cardiac transplantation, the ICD seems to change only the mode of death from sudden to a nonsudden cardiac death if transplantation cannot be performed soon.
The effect of sotalol on the rate and the RR interval variability of induced ventricular tachycardia was studied in 26 patients. Sotalol increased the mean cycle length and irregularity of RR intervals, which may affect detection of ventricular tachycardia by implantable cardioverter-defibrillator devices.
BACKGROUND: Implantable cardioverter-defibrillators (ICDs) and d,l-sotalol are widely used to treat ventricular tachyarrhythmia and ventricular fibrillation (VT/VF). The purpose of this study was to compare the long-term efficacy of d,l-sotalol and ICDs in patients with coronary artery disease. METHODS AND RESULTS: In a case-control study, 50 patients treated with oral d,l-sotalol were matched to 50 patients treated with ICDs. Both groups were matched for sex (82 men), age (58 +/- 10 years), ejection fraction (40 +/- 12%), extent of coronary artery disease, presenting arrhythmia, and year that treatment began. In all patients in the sotalol group, VT/VF was inducible in the drug-free electrophysiological study. Induction of sustained VT/VF was suppressed by d,l-sotalol (438 +/- 95 mg/d). In the ICD group, either VT/VF was not inducible (n = 5) or inducible sustained VT/VF was refractory to antiarrhythmic drug treatment (n = 45). Sotalol treatment led to a marked reduction in arrhythmic events. Whereas 83% of the patients in the sotalol group were free of sudden death and nonfatal VT at 3 years, only 33% of the ICD patients did not receive appropriate ICD therapies (P < .005). Actuarial rates for absence of sudden death at 3 years were 85% in the sotalol group and 100% in the ICD group (P < .005). Actuarial rates for overall survival at 3 years were 75% in the sotalol group and 85% in the ICD group (P = .02). CONCLUSIONS: In this case-control study, ICD therapy was more effective tha electrophysiologically guided antiar-rhythmic treatment with d,l-sotalol in prevention of sudden death and reduction of total morality in patients with coronary artery disease. Prospective studies are needed to confirm these results.
BACKGROUND: Algorithms to reject irregular tachyarrhythmias are available in implantable cardioverter-defibrillator devices to discriminate ventricular tachycardia (VT) from atrial fibrillation (AF). The hazard of underdetection of irregular monomorphic VTs using these algorithms has not yet been fully evaluated. The purpose of this study was to determine the ability of a commonly used stability algorithm to reject AF and to correctly detect VT with a high RR interval variability. METHODS AND RESULTS: The electrophysiological studies from 232 patients with induced monomorphic VT (cycle length > 250 ms) and 21 with AF were reviewed. A preliminary analysis was performed to classify the VT episodes in irregular (successive RR differences > 20 ms after 4 seconds from onset) or regular (otherwise). Three study groups were defined: group 1 (27 patients with irregular VT), group 2 (22 randomly selected patients with regular VT), and group 3 (21 patients with AF). A computer program analyzed the first 50 RR intervals of the induced VT (AF), resetting a VT counter if the interval was greater than a tachycardia detection interval (TDI) or if its absolute difference with the preceding three beats exceeded a programmed stability value (STAB). The VT was detected when the VT counter reached a preset number of intervals (NIDs). Different combinations of TDI, STAB, and NID were analyzed. All VTs in group 2 were correctly detected. In contrast, up to 10 VTs from group 1 were not detected when high NIDs and low STAB parameters were programmed. With usual values (10 to 16 beats and 50 to 60 ms, respectively), only 1 to 2 VTs remained undetected, but 20% to 50% had a detection delay > 8 seconds. Undetected VTs were significantly slower than early detected VTs for most STAB and NID combinations. With usual stability and NID values, 10% to 20% of episodes of AF were inappropriately detected. Changes in TDI had a small impact on sensitivity and specificity when currently used values for stability were programmed. CONCLUSIONS: Animplantable cardioverter-defibrillator tachycardia detection algorithm with a stability criterion of 50 to 60 ms and 12 to 14 RR intervals is able to detect over 90% of monomorphic irregular VTs. Nevertheless, significant VT detection delays may arise, and inappropriate detection of AF cannot be totally prevented.