Identification and management of the high risk patient with dilated cardiomyopathy.
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Anti-Arrhythmia Agents↗
Biomedical subjects
G Breithardt
Publications and source records attributed to G Breithardt.
Plasma Lp(a) levels correlate with number, severity, and length-extension of coronary lesions in male patients undergoing coronary arteriography for clinically suspected coronary atherosclerosis.
The relation between lipoprotein(a) [Lp(a)] as an independent risk factor for coronary atherosclerosis and the severity and extension of angiographically detectable coronary atherosclerotic lesions has not been systematically evaluated. In 118 male patients (54.3 +/- 7.4 years) with suspected coronary artery disease and without a history of myocardial infarction undergoing coronary angiography, the relation between plasma Lp(a) levels and other lipoproteins and the severity and extension of coronary lesions was studied. The coronary angiograms were evaluated in a blinded manner according to three scores: vessel score (0 to 3 points for 0 to 3 vessels with stenoses > or = 70%), stenosis score (0 to 32 points; number and severity of coronary stenoses or lesions), and extent score (0 to 100 points; length-extension of all coronary lesions in relation to the total coronary vessel length). The score values obtained were analyzed for correlations with age and levels of total cholesterol (6.08 +/- 1.26 mmol/L; mean +/- SD), high-density lipoprotein cholesterol (1.04 +/- 0.33 mmol/L), low-density lipoprotein cholesterol (4.18 +/- 1.15 mmol/L), triglycerides (1.88 +/- 1.37 mmol/L), and Lp(a) in plasma (19.5 +/- 22.6 mg/dL). Bivariate correlation analysis resulted in positive correlations between Lp(a) and vessel score (P < .01), stenosis score (P < .01), and extent score (P < .05). With multivariate analyses, besides Lp(a) plasma level (nl), only patient age showed a significant correlation to all three scores used, whereas none of the lipid parameters correlated significantly with all three scores.
Adult↗
Regional myocardial sympathetic dysinnervation in arrhythmogenic right ventricular cardiomyopathy. An analysis using 123I-meta-iodobenzylguanidine scintigraphy.
BACKGROUND: In patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), the frequent provocation of ventricular tachycardia during exercise, the sensitivity toward catecholamines, and the response toward antiarrhythmic drug regimen with antiadrenergic properties suggest an involvement of the sympathetic nervous system in arrhythmogenesis. METHODS AND RESULTS: To analyze the presence, extent, and location of impaired myocardial sympathetic innervation in ARVC, 123I-meta-iodobenzylguanidine (123I-MIBG) scintigraphy was performed in 48 patients with ARVC. For comparison, 9 patients with idiopathic ventricular tachycardia and a control group of 7 patients without heart disease were investigated. In patients with ARVC, the clinical sustained (n = 25; 52%) or nonsustained (n = 23; 48%) ventricular tachycardia originated in the right ventricular outflow tract in 38 patients (79%), whereas in the remaining 10 patients (21%), the site of origin was the apical (n = 5) or inferior (n = 5) right ventricle. In 33 patients (69%), nonsustained or sustained ventricular tachycardia was provocable by exercise (n = 28 of 48; 58%) and/or by isoproterenol infusion (n = 16 of 37; 43%), whereas programmed ventricular stimulation induced sustained or nonsustained ventricular tachycardia in 16 patients each (33% each). With 123I-MIBG scintigraphy, the right ventricle was not visible in any patient. No areas of intense 123I-MIBG uptake ("hot spots") were observed. All patients of the control group and 7 of 9 patients (78%) with idiopathic ventricular tachycardia showed a uniform tracer uptake in the left ventricle. In contrast, only 8 of 48 ARVC patients (17%) showed a homogeneous distribution of 123I-MIBG uptake, whereas 40 patients (83%) demonstrated regional reductions or defects of tracer uptake. In 3 of 48 patients (6%), the defect area was < 15%; in 21 patients (44%), it was 15% to 30%; and in 16 patients (33%), it was > 30% of the polar map area of the left ventricle (mean, 23 +/- 15%; range, 0% to 57%). In 38 of 40 patients (95%) with an abnormal 123I-MIBG scan, reduced tracer uptake was located in the basal posteroseptal left ventricle, involving the adjacent lateral wall in 10, the anterior wall in 2, and the apex in 12 patients. Only 2 patients demonstrated isolated defects of the anterior or lateral wall; one involved the apex. Perfusion abnormalities in the areas of 123I-MIBG defects were excluded by stress/redistribution 201T1 single-photon emission computed tomography scintigraphy and by normal coronary angiograms in all patients. Abnormalities in 123I-MIBG scintigraphy in patients with ARVC correlated with the site of origin of ventricular tachycardia, demonstrating a regionally reduced tracer uptake in 36 of 38 patients (95%) with right ventricular outflow tract tachycardia compared with only 4 of 10 patients (40%) with other right ventricular origins of tachycardia. There was no correlation between the results of 123I-MIBG scintigraphy and the extent of right ventricular contraction abnormalities, right ventricular ejection fraction, biopsy results, coronary anatomy, or left ventricular involvement in ARVC. CONCLUSIONS: In patients with ARVC, regional abnormalities of sympathetic innervation are frequent and can be demonstrated by 123I-MIBG scintigraphy. Sympathetic denervation appears to be the underlying mechanism of reduced 123I-MIBG uptake and may be related to frequent provocation of ventricular arrhythmias by exercise or catecholamine exposure in ARVC. Therefore, in patients with ARVC, the noninvasive detection of localized sympathetic denervation by 123I-MIBG imaging may have implications for the early diagnosis and for the choice of antiarrhythmic drugs in the treatment of arrhythmias.
3-Iodobenzylguanidine↗
Dynamics of mitral regurgitant flow and orifice area. Physiologic application of the proximal flow convergence method: clinical data and experimental testing.
BACKGROUND: The proximal flow convergence method, a quantitative color Doppler flow technique, has been validated recently for calculating regurgitant flow and orifice area. We investigated the potential of the method as a tool to study different pathophysiological mechanisms of mitral valve incompetence by assessing the time course of regurgitant flow and orifice area and analyzed the implications for quantification of mitral regurgitation. METHODS AND RESULTS: Fifty-six consecutive patients with mitral regurgitation of different etiologies were studied. The instantaneous regurgitant flow rate Q(t) was computed from color M-mode recordings of the proximal flow convergence region and divided by the corresponding orifice velocity V(t) to obtain the instantaneous orifice area A(t). Regurgitant stroke volume (RSV) was obtained by integrating Q(t). Mean regurgitant flow rate Qm was calculated by RSV divided by regurgitation time. Peak-to-mean regurgitant flow rates Qp/Qm and orifice areas Ap/Am were calculated to assess the phasic character of Q(t) and A(t). In the first 24 patients (group 1), computation of Qm and RSV from the color Doppler recordings was compared with the conventional pulsed Doppler method (r = .94, SEE = 29.4 mL/s and r = .95, SEE = 9.7 mL) as well as with angiography (rs = .93 and rs = .94, P < .001). The temporal variation of Q(t) and A(t) was studied in the next 32 patients (group 2): In functional regurgitation in dilated cardiomyopathy (n = 12), there was a constant decrease in A(t) throughout systole with an increase during left ventricular relaxation; Ap/Am was 5.49 +/- 3.17. In mitral valve prolapse (n = 6), A(t) was small in early systole, increasing substantially in midsystole, and decreasing mildly during left ventricular relaxation; Ap/Am was 2.48 +/- 0.26. In rheumatic mitral regurgitation (n = 14), a roughly constant regurgitant orifice area during most of systole was found in 4 patients. In the other patients there was significant variation of A (t) and the time of its maximum; Ap/Am was 1.81 +/- 0.56. ANOVA demonstrated that the differences in Ap/Am were related to the etiology of mitral regurgitation (P < .0001). To verify that the calculated variation in regurgitant orifice area during the cardiac cycle reflects an actual variation, the ability of the method to predict a constant orifice area throughout systole was tested experimentally in a canine model of mitral regurgitation. Five flow stages were produced by implanting fixed grommet orifices of different sizes into the anterior mitral leaflet. A constant regurgitant orifice area was correctly predicted throughout systole with a mean percent error of -1.8 +/- 4% (from -6.9% to +5.8%); the standard deviation of the individual curves calculated at 10% intervals during systole averaged 13.3% (from 3.6% to 19.6%). In addition, functional mitral regurgitation caused by ventricular dysfunction was produced pharmacologically in five dogs, and the color M-mode recordings of the proximal flow convergence region were obtained with the transducer placed directly on the heart instead of the chest, thus ruling out a significant effect of translational motion on the observed flow pattern. The pattern of regurgitant flow variation was identical to that observed in patients. CONCLUSIONS: The proximal flow convergence method demonstrates that regurgitant flow and orifice area vary throughout systole in distinct patterns characteristic of the underlying mechanism of mitral incompetence. Therefore, in addition to the potential of the method as a tool to quantify mitral regurgitation, it allows analysis of the pathophysiology of regurgitation in the individual patient, which may be helpful in clinical decision making. Calculating mitral regurgitant flow rate and volume from the time-varying proximal flow field (ie, without assuming a constant orifice area that would produce overestimation in individual patients) provides excellent agreement with independent te
Adult↗
[Pectoral cardioverter-defibrillator implantation combined with transvenous bipolar defibrillation electrodes].
Ultimately, implantable cardioverter-defibrillators (ICD) will one day be implantable like present pacemakers. However, due to the size of the pulse generator and the low defibrillation efficacy of monophasic shocks, only a few selected patients have been implanted transvenously-pectorally. Therefore, we have prospectively investigated whether a transvenous-pectoral approach is in general feasible with a new downsized ICD capable of delivering biphasic shocks. Out of 33 patients, 76% received a bipolar transvenous defibrillation lead system. In the first 13 consecutive patients, a randomized crossover study showed that this high efficacy was above all achieved by a superior defibrillation efficacy of the biphasic waveform in comparison to the monophasic waveform (69% vs. 23%; p = 0.03). Not a single patient could be defibrillated exclusively with the monophasic waveform. In a further 15 consecutive patients, a crossover study showed that a position of the transvenous anode within the Vena anonyma instead of the Vena cava superior is, in general, not superior (87% vs. 80%; p = 0.67). Only one patient could be exclusively defibrillated with the V. anonyma position. Intraoperatively, no complications occurred and all but one patient received a pectoral implantation of the pulse generator. Postoperatively, in five patients local complications related to the ICD system were seen; two needed a surgical revision. In two patients movements of the left shoulder joint were temporarily restricted. Thus, in the majority of patients a new downsized ICD capable of biphasic shocks can be implanted transvenously-pectorally like a pacemaker.
Adult↗
[High frequency catheter ablation of left-sided manifest accessory conduction pathways during sinus rhythm and in continuous atrial fibrillation].
Atrial fibrillation is frequently initiated during radiofrequency catheter ablation of accessory pathways. It has been generally believed that initiation of atrial fibrillation may complicate the localization of accessory pathway. Therefore, most centers currently perform cardioversion in order to continue the ablation session. The purpose of the present study was to assess the feasibility and the electrophysiologic criteria for successful radiofrequency catheter ablation of left sided accessory pathways during atrial fibrillation in patients with WPW-syndrome. Radiofrequency ablation was performed in 87 patients with left-sided manifest accessory pathways during atrial fibrillation (n = 16) or during sinus rhythm (n = 71). The criteria for localization of accessory pathways were recording of stable accessory pathway potentials, local ventricular activation preceding the onset of the intrinsic flection of the unipolar electrogram and a QS pattern of the unipolar electrogram. Overall, the accessory pathways were successfully interrupted in 85/87 patients (98%). During the first ablation procedure, abolishing of accessory pathways was achieved in 15 of 16 patients (94%) during atrial fibrillation compared to 64 of 71 patients (90%) during sinus rhythm (n.s.). The total procedure time and fluoro time was significantly shorter during atrial fibrillation than during sinus rhythm (161 +/- 91 min vs. 216 +/- 128 min, p < 0.05, and 31 +/- 24 vs. 41 +/- 26 min. p < 0.05, respectively). Thus, it is feasible and very effective to perform radiofrequency ablation of left-sided manifest accessory pathways during atrial fibrillation. Precise localization of accessory pathway during atrial fibrillation seems even easier than during sinus rhythm as indicated by shorter procedure and fluoro times in the atrial fibrillation group.
Adolescent↗
[Problems with anti-arrhythmia therapy in atrial fibrillation].
The prevalence of atrial fibrillation increases with age, with rates of 2-5% among people over the age of 60 years. Patients may be highly symptomatic or may suffer from hemodynamic compromise or thromboembolic complications. However, antiarrhythmic drug treatment implies problems like the choice of the suitable drug, the individual benefit/risk profile, and alternative treatment strategies. Experimental and clinical data support the concept that atrial fibrillation in the clinical setting in most cases is due to multiple reentrant wavelets. A critical number of three to six simultaneously circulating reentrant wavelets seems to be necessary for the maintenance of atrial fibrillation. Consequently, antiarrhythmic drugs may terminate or prevent atrial fibrillation by prolonging the refractory period or slowing conduction velocity, thereby leading to conduction block. In clinical practice, antiarrhythmic therapy may act by slowing of the ventricular rate due to depression of atrioventricular nodal conduction or by termination and/or prevention of atrial fibrillation. Digitalis is commonly used for the control of the ventricular rate. Betablocking drugs and verapamil are effective in this respect during exercise performance. For antiarrhythmic conversion and prophylaxis of recurrences of atrial fibrillation, class Ia (e.g., quinidine), Ic (e.g., flecainide and propafenone), and class III (e.g., amiodarone and sotalol) drugs of the Vaughan Williams classification are useful. Presently, no general concept exists whether medical or electrical cardioversion should be used as a first line approach for termination of atrial fibrillation. In the individual patient with atrial fibrillation, the potential benefit of restoring sinus rhythm must be weighed against the morbidity and mortality of the arrhythmia and the morbidity and mortality of the antiarrhythmic agents used.(ABSTRACT TRUNCATED AT 250 WORDS)
Anti-Arrhythmia Agents↗
[The pro-arrhythmic effects of anti-arrhythmia agents].
Proarrhythmia is defined as the provocation of new cardiac arrhythmias or the aggravation of preexisting arrhythmias by antiarrhythmic drugs. The possible types of manifestation of proarrhythmia are manifold. With respect to prognosis, drug-induced ventricular tachyarrhythmias seem to be of particular importance. Monomorphic ventricular tachycardia and ventricular tachycardias of the torsade de pointes type have to be distinguished. The former seem to be mainly based on reentrant mechanisms, while the later is supposed to result from triggered activity. Drug-induced monomorphic tachycardia is most often observed during therapy with drugs which slow conduction (class I agents, proarrhythmic potency: IC > IA > IB). Patients with depressed left ventricular function and previously documented life-threatening tachyarrhythmias are the most susceptible candidates. Torsade de pointes can be preferentially observed during therapy with antiarrhythmic drugs which prolong myocardial repolarization (i.e. class IA and class III agents). Electrolyte abnormalities and/or bradycardia are factors which often predispose to the development of this particular type of proarrhythmia. The physician who prescribes antiarrhythmic drugs must be aware of the different types and clinical manifestations of proarrhythmia. This is necessary to assess the degree of proarrhythmic risk and to determine the benefit/risk ratio before the start of drug therapy.
Anti-Arrhythmia Agents↗
[Drug prevention of recurrence in paroxysmal and chronic atrial fibrillation].
In many patients with paroxysmal or chronic atrial fibrillation, long-term antiarrhythmic drug therapy is performed to prevent recurrences of atrial fibrillation or to reduce the incidence of paroxysmal attacks of atrial fibrillation. The results of several studies on the efficacy of antiarrhythmic drugs in patients with paroxysmal atrial fibrillation have revealed that the incidence of recurrent attacks of atrial fibrillation can be reduced and the duration of arrhythmia free intervals can be prolonged by antiarrhythmic drug therapy. However, complete prevention of atrial fibrillation can be achieved only in a minority of patients. At present, there is no evidence that antiarrhythmic drug treatment of patients with paroxysmal atrial fibrillation might worsen the prognosis by an increase in cardiac mortality induced by antiarrhythmic drugs. In patients with chronic atrial fibrillation, the recurrence rate of the arrhythmia can be significantly reduced by antiarrhythmic drug therapy within the first year of treatment. However, there is evidence that antiarrhythmic drugs might worsen the prognosis when compared to patients with atrial fibrillation not treated with antiarrhythmic drugs. Accordingly, the indication for antiarrhythmic drug therapy to prevent recurrences in patients with chronic atrial fibrillation has to be made restrictively and should be largely based on the symptomatic status of the patients. Antiarrhythmic drug therapy seems to be indicated only in patients who are significantly symptomatic or compromised by the arrhythmia. In patients without or with only mild symptoms, medical therapy with the aim to slow the ventricular response with digitalis, calcium antagonists or betablocking agents seems to be more adequate. Currently, with respect to efficacy and safety, there is no antiarrhythmic drug that has been proved to be superior to others and that can thus be recommended as the drug of first choice for patients with paroxysmal or chronic atrial fibrillation to prevent recurrences. The choice of the optimal antiarrhythmic drug should be made by taking individual factors (e.g., etiology of the arrhythmia, patient compliance, liver and renal function of the patient, additional medical therapy) into account. Major problems during long-term antiarrhythmic drug therapy may arise in patients with pre-existing sinus node dysfunction or conduction disturbances of the atrioventricular node. In addition, the conversion of atrial fibrillation with relatively slow ventricular rates to the atrial flutter with fast ventricular rates that is occasionally observed during treatment with class I-antiarrhythmic drugs may complicate long-term therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
Anti-Arrhythmia Agents↗
[Quality assurance in interventional electrophysiology (ablation, automatic defibrillators)].
The rapid development of interventional electrophysiology during the recent years has lead to an increasing number of procedures and a wide-spread use of these techniques. Interventional electrophysiology includes catheter ablation of supraventricular and ventricular tachycardias and implantation of cardioverter-defibrillators. Measures for quality assurance aim at improving the quality of training in clinical electrophysiology as well as at giving recommendations for the personnel needed. The specific recommendations for implantation of defibrillators include the qualification of the personnel and technical prerequisites as well as recommendations for accepted indications, probable indications as well as for no indications. For catheter ablation, specific recommendations have been given as well which include the technical and personnel requirements. The presently available recommendations and guidelines help that the various elements of quality assurance obtain increasing attention and are going to affect the quality of results.
Catheter Ablation↗
[Significance of temperature-controlled energy generation in high-frequency catheter ablation of accessory conduction pathways].
Radiofrequency catheter ablation has become an established treatment modality for definite cure of patients with WPW-syndrome or concealed accessory pathways. On-line monitoring of the induced tissue effects plays an important role concerning the efficacy and safety of this procedure. In a 50 year-old man with recurrent atrioventricular tachycardia, endocardial catheter mapping revealed a left anterolateral concealed accessory pathway. A temperature-guided radiofrequency pulse with a preselected temperature of 70 degrees C was applied during tachycardia when stability of the local electrogram, continuous ventriculoatrial activity during orthodromic tachycardia, and registration of a Kent-potential indicated electrogram criteria for a successful ablation. However, orthodromic tachycardia did not terminate, and catheter tip temperature only reached a plateau of 45 degrees C with maximal power output of 50 watts indicating an insufficient catheter tip-tissue-contact. Therefore, the bending of the catheter curve was slightly straightened during energy application without pushing the catheter forward in order to achieve a better tip electrode contact with the tissue. Simultaneously, a sudden increase in catheter tip temperature was observed accompanied by termination of the tachycardia indicative of the successful ablation of the accessory pathway. At present, a control of radiofrequency catheter induced tissue effects can be best achieved by temperature-guided energy application whereas monitoring of current, voltage, and impedance are insufficient in this respect. In the present case, correction of the catheter placement during energy application could be achieved because of the on-line monitoring of the catheter tip temperature thereby allowing successful ablation of the accessory pathway with a single radiofrequency pulse.
Bundle of His↗
[Transvenous subcutaneous implantation technique of the cardioverter/defibrillator].
For years the high efficacy of implantable cardioverter-defibrillators (ICD) to prevent sudden cardiac death was impaired by the substantial perioperative mortality of the therapy. With the introduction of transvenous-subcutaneous defibrillation leads, thoracotomy could be abandoned and perioperative mortality was reduced to less than 1%. Despite frequent lead complications as dislocations, conductor fractures and isolation failures, long-term efficacy in termination of ventricular tachyarrhythmias remained approximately 98% and prevention of sudden cardiac death was not impaired. All nonthoracotomy defibrillation lead systems involve an endocardial right ventricular lead usually introduced from the left cephalic vein or directly via the subclavian vein. This lead has a pace/sense tip and at least one defibrillation electrode located in the right ventricle. Additionally, a second transvenous electrode and/or a subcutaneous patch or array electrode or the pulse generator shell has to be used for defibrillation. In combination with the biphasic defibrillation waveform, virtually all patients can be defibrillated using a combination of these electrodes. In most patients defibrillation is possible with transvenous electrodes alone and there is no need for an additional subcutaneous electrode. Smaller pulse generators have already been implanted in a subpectoral position--in many patients allowing a single incision approach as used for pacemaker implantation. Ultimately, with even smaller pulse generators ICDs should be implantable like present pacemakers in local anesthesia. This overview covers the history, models, practical aspects of implantation and testing, efficacy and complications of transvenous/subcutaneous defibrillation leads. Figures show the impact of the surgical approach on the frequency of de novo ICD implantations, X-rays of nearly all current bipolar and tripolar transvenous subcutaneous ICD lead systems, transvenous-epicardial hybrid systems and various complications. Additional figures cover lead complications not visible on X-rays. Defibrillation thresholds are compared for various lead configurations. Sensing amplitudes and pacing thresholds are compared for bipolar and pseudobipolar sense/pace leads as well as for different cardiac diseases. Tables summarize the main characteristics of current transvenous and subcutaneous ICD leads and external devices for intraoperative testing of ICD leads as well as the complications of transvenous/subcutaneous leads in three multicenter studies.
Defibrillators, Implantable↗
[Coronary angiography and intravascular ultrasound examination of a 60-year-old patient with familial HDL deficiency (Tangier disease)].
A 60-year-old homozygous patient with familial high density lipoprotein deficiency (Tangier disease) was examined by coronary angiography and intravascular ultrasound because of typical angina pectoris. We found a normal left ventricular function, moderately diffuse coronary sclerosis without stenosis, and no critical stenosis of peripheral arteries. Intravascular ultrasound revealed normal thickness and the three-layer appearance of the arterial intima, media, and adventitia within the peripheral arteries, and showed a single, discrete arteriosclerotic lesion in one iliac artery segment. The lack of severe atherosclerosis was remarkable insofar as massive foam cell formation in reticuloendothelial tissues and the virtually complete absence of circulating HDL is characteristic of Tangier disease and had been previously demonstrated in this patient.
Arteriosclerosis↗
[Therapy of AV nodal reentry tachycardia with catheter ablation of the fast retrograde pathway].
AV-nodal reentrant tachycardia (AVNRT) is a common cause of recurrent supraventricular tachycardia. Currently, catheter ablation of either slow or fast pathway are nonpharmacologic options for the treatment of patients with AVNRT. Radiofrequency (RF) catheter ablation of the fast pathway was attempted in 35 patients (aged 46.7 +/- 15 years; 12 m, 23 f) with recurrent AVNRT. RF energy (25-50 watt, 30-90 s) was delivered to the anterior right atrial septum. The catheter was placed posterior to the largest His bundle deflection. AV conduction was monitored during continuous pacing of the high right atrium while the RF current was applied. RF-ablation was acutely successful using a mean of 6.5 +/- 6.2 impulses in 31 patients. Late spontaneous block of the slow pathway occurred in one patient (pat. 17) with an unsuccessful initial attempt of fast pathway ablation. PQ and AH interval increased significantly after the ablation procedure (PQ: from 149 +/- 27 to 208 +/- 34 ms, AH: from 76 +/- 22 to 131 +/- 38 ms; p value: < 0.0001). Acute interruption of retrograde VA conduction was the result in 23 patients. Six patients (17%) had a recurrence of AVNRT during a follow-up period of 11.9 +/- 7.5 months. Five of 6 patients underwent a second successful procedure. Complete AV block occurred in 3 of the first 10 consecutive patients and in none of the subsequent 25 patients (overall incidence: 8.6%). Thus, RF ablation of the fast retrograde pathway is an effective method for the curative treatment of AVNRT.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Ventricular tachycardia.
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Anti-Arrhythmia Agents↗
Comparison of frequency of aggravation of ventricular tachyarrhythmias after implantation of automatic defibrillators using epicardial versus nonthoracotomy lead systems.
The time of onset of 4,471 episodes of ventricular tachycardia (VT) or fibrillation (VF) in 40 of 65 patients with an implantable cardioverter-defibrillator (ICD) with endocardial defibrillation electrodes (group 1) and in 53 of 123 with epicardial defibrillation electrodes (group 2) was analyzed to examine whether the incidence of VT/VF immediately after surgery is greater than during further follow up and whether the site of lead placement exerts an influence on the occurrence of these arrhythmias. Actuarial survival rates free of VT/VF were 77, 65, and 54% at 1, 3 and 6 months, respectively, for group 1, and 84, 66 and 52%, respectively, for group 2. The probability of VT/VF was increased only during the first week after surgery; in that week, 12.8% of all patients had VT/VF, without significant differences between groups 1 and 2. Until the end of the first month, this percentage increased to 23%, whereas only 12 to 15% of patients had VT/VF during subsequent months. In 19 patients with third-generation devices capable of terminating tachycardias by overdrive pacing, 326 of 412 VT/VF episodes occurring in the first week after surgery were terminated by antitachycardia pacing, and only 86 had to be terminated by cardioversion or defibrillation. No postoperative exacerbation of inappropriate ICD therapies was observed in any group; 2 to 5% of patients per month received ICD therapies for atrial fibrillation or sinus tachycardia. Patients who received appropriate ICD therapies in the first week after surgery were at high risk of recurrence of VT/VF.(ABSTRACT TRUNCATED AT 250 WORDS)
Defibrillators, Implantable↗
Clinical experience with antitachycardia pacing and improved detection algorithms in a new implantable cardioverter-defibrillator.
OBJECTIVES: This study was conducted to assess the effectiveness of antitachycardia pacing modes and detection algorithms in patients with a new third-generation implantable cardioverter-defibrillator. METHODS: Twenty-three of 42 consecutive patients had coronary artery disease, 14 had dilated cardiomyopathy, 2 had prior valve replacement and 3 had arrhythmogenic right ventricular dysplasia. The mean ejection fraction was 41 +/- 14%; there were 31 men (74%) and 11 women, with a mean age of 53 years. On the basis of preoperative and postoperative electrophysiologic studies, in 28 patients antitachycardia pacing was postoperatively programmed randomly as "burst" (66%) or autodecremental "ramp" (34%) stimulation with a first coupling interval of 81% of tachycardia cycle length and up to 8 sequences with 3 to 10 stimuli. RESULTS: During a follow-up interval of 6.3 +/- 2.2 months, 15 patients were treated by antitachycardia pacing for a median of 6 (range 1 to 59) hemodynamically stable ventricular tachycardias (175 +/- 12 beats/min). In 5 patients, 22 ventricular tachycardias (9%) were not terminated by antitachycardia pacing but by cardioversion. Seven (3%) of these episodes accelerated (> 50 ms) during antitachycardia pacing. Syncope did not occur during these episodes. In seven patients initial antitachycardia pacing in cases of supraventricular tachycardias delayed charging and redetection prevented inappropriate discharges. Additional detection algorithms were programmed only after inappropriate therapy. The sudden "onset" and "sustained rate duration" criteria were programmed in three patients and the cycle length "stability" criteria in six patients, respectively. After activation of these detection algorithms only two of the seven patients had further inappropriate device discharges. CONCLUSIONS: Thus, antitachycardia pacing by this implantable cardioverter-defibrillator effectively and appropriately terminated 91% of hemodynamically stable ventricular tachycardias. Inappropriate device discharges were prevented in some patients by antitachycardia pacing and additional detection algorithms.
Adult↗
Atrioventricular nodal reentry tachycardia: electrophysiologic comparisons in patients with and without 2:1 infra-His block.
Patients with atrioventricular nodal reentry tachycardia (AVNRT) occasionally may demonstrate a 2:1 infra-His block during tachycardia. However, the electrophysiologic background of this phenomenon has not been established so far. In the present study we compared the electrophysiologic parameters of 10 consecutive patients with a transient 2:1 infra-His block during AVNRT of the common type (Group A) with those of 17 consecutive patients without this phenomenon during tachycardia (Group B). Transient 2:1 infra-His block occurred without termination of the tachycardia in all 10 patients of Group A. The tachycardia sustained despite intermittent or permanent conduction disturbance of the infrahisian tissue in 8 of these 10 patients. In comparison, the electrophysiologic parameters of 17 patients without 2:1 block during AVNRT of the common type (Group B) were analyzed. A significantly longer antegrade (318 +/- 58 ms vs. 259 +/- 50 ms) and retrograde (308 +/- 59 ms vs. 239 +/- 20 ms) AV conduction capacity could be demonstrated in these patients. The tachycardia cycle length did not differ significantly between the two groups, although the mean tachycardia cycle length was 48 ms longer in patients of Group B. These observations demonstrate an advanced conduction capacity in patients with a transient infra-His block during AVRNT of the common type. This study underlines that the reentry circuit in AVNRT is not necessarily dependent on infrahisian tissue.
Adult↗