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Biomedical subjects

G Breithardt

Publications and source records attributed to G Breithardt.

At least 379 records · Page 21Linked to original sources

Effects of beta-blockade on the incidence of ventricular tachyarrhythmias during acute myocardial ischemia: experimental findings and clinical implications.

Myocardial ischemia and infarction are the most common substrates for life-threatening ventricular tachyarrhythmias. Experimental and clinical evidence suggests that enhanced activity of the sympathetic nervous system plays an important role in the genesis of ischemia-related arrhythmias. In animal experiments, beta-blockers display significant antifibrillatory effects during the acute phase of myocardial ischemia. Preconditions for their antifibrillatory effects are high serum- and tissue-concentrations, and absence of a significant partial agonist activity. During the delayed phase of ischemic arrhythmias which starts 6-8 h after coronary occlusion, beta-blockers gain significance as antiarrhythmic and potentially antifibrillatory drugs, if sympathetic activity is enhanced. The presently available evidence suggests that the potentially antifibrillatory effects of beta-blockers are at least one of the major mechanisms by which these drugs may decrease mortality when given prophylactically in patients after myocardial infarction. However, it remains to be explained why beta-blockers, in a great number of prospective randomized trials, have reduced the incidence of sudden death only by an average of about 30%. This may be the result of their "specific" mechanisms acting in the setting of acute myocardial ischemia with enhanced adrenergic tone, whereas in the remaining patients other mechanisms such as a chronic arrhythmogenic substrate may be operative. A clearer separation of these various mechanisms seems mandatory in order to allow a more specific "targeted" administration of beta-blockers. This is the more important since none of the available prospective studies that used antiarrhythmic agents has shown an improvement of prognosis, but, instead showed a worsening of the mortality rate.

Adrenergic beta-Antagonists↗

Holter monitoring versus programmed ventricular stimulation.

Both Holter monitoring and programmed ventricular stimulation are useful techniques for guiding antiarrhythmic therapy. However, they are not both appropriate for all patients. Holter monitoring is only useful in patients who have consistent and frequent ventricular ectopic beats, and programmed ventricular stimulation requires that the patients have an arrhythmia that is reproducible and inducible. Patients for whom these techniques are used to identify agents that are effective for control of their arrhythmias generally have a better prognosis than those patients for whom an effective agent is not found. Programmed ventricular stimulation may have a better predictive value than Holter monitoring, but the comparison may not be valid, because the procedures are used in different types of patients.

Arrhythmias, Cardiac↗

Diagnostic value of electrocardiographic variables to predict the presence of ventricular late potentials.

To test the hypothesis that the presence of ventricular late potentials in the highly amplified, averaged and filtered surface electrocardiogram (ECG) can be predicted from the conventional surface ECG, 211 patients with and without previously documented sustained ventricular tachycardia outside the acute phase of myocardial infarction were studied. The presence of left ventricular akinesia or aneurysm was significantly correlated with the ECG score (based on Q wave duration, R wave duration and amplitude ratio). The mean ECG score in patients without ventricular tachycardia was 3.4 +/- 3.5 points compared with 5.5 +/- 3.9 points (p less than 0.001) in patients with ventricular tachycardia. The presence of late potentials was positively correlated with the ECG score in the whole cohort of patients. This was also the case in the subgroup of patients without a history of sustained ventricular tachycardia. In contrast, in patients with ventricular tachycardia, the presence of late potentials was independent of their ECG score. Using linear discriminant function analyses to predict the presence of late potentials, a history of ventricular tachycardia alone and the ECG score alone had a high predictive power (high standardized coefficients). If combinations of variables were analyzed including estimates of left ventricular function (presence of aneurysm or akinesia; ejection fraction), the ECG score and a history of ventricular tachycardia still ranked highest. The influence of ejection fraction if used in combination with other variables for the prediction of late potentials was relatively small (standardized coefficient of 0.4). In conclusion, the surface ECG can be used in patients previously free of sustained ventricular tachycardia to predict the presence of ventricular late potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗

Signal averaging.

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Death, Sudden↗

[Anti-tachycardia surgery in ventricular arrhythmia].

UNLABELLED: Recurrent sustained ventricular tachycardia (VT) is associated predominantly with ischemic heart disease, mostly in the chronic phase after myocardial infarction. Potentially life-threatening and drug-refractory ventricular tachycardias are called malignant VT. In the Federal Republic of Germany, VT develops in about 3,000 to 5,000 patients per year from the 100,000 who survive a myocardial infarction. About 10% of these patients prove to be medically-refractory or additionally are considered candidates for aneurysmectomy or coronary revascularization. Overall, for the Federal Republic of Germany, there is a need for approximately 500 to 1000 antitachycardia operations each year. The morphologic substrate for malignant VT are ischemically-damaged inhomogeneously-structured arrhythmogenic areas. The morphology results in electrical inhomogeneity which predisposes to electrophysiologic reentry phenomena. NATURAL HISTORY: The survival rate of patients with malignant VT who are not surgically treated is 70% at one year and 20 to 40% at four years (Figure 1). In those in whom the tachycardia can be medically controlled, the prognosis is 10.5 times more favorable than in those with medically-refractory arrhythmias. In one study of 45 patients with recurrent, sustained VT, only 20% of those with medical refractoriness were free of renewed arrhythmic events after 30 weeks as compared to 90% whose treatment had been designated effective (p less than 0.0004) (Figure 2). According to a further study, for patients with drug-refractory VT, the probability for sudden death within four years was 55% as compared with 5% for those with medically-controlled VT (p less than 0.0002). SURGICAL TREATMENT: The concept of surgical treatment of malignant VT encompasses delineation of the arrhythmogenic area by means of endocardial mapping and surgical ablation. Arrhythmogenic areas are located mostly in the transition zone between the viable muscle and an aneurysm at the left ventricular endomyocardial septum. With mapping, by means of local measurements of activity times, impulse spread throughout the heart can be recorded in a cartographic system. The left ventricular endocardial activation should be determined during sinus rhythm and tachycardia and, with normothermic extracorporeal circulation the left ventricle is incised, mostly in the aneurysmatic antero-apical area, prior to sequential interrogation of the endocardial surface (Figure 3). As an alternative to point-for-point mapping, by means of multi-terminal electrodes, electrocardiograms can be obtained simultaneously from multiple positions. During tachycardia, the earliest activation can be found in the arrhythmogenic area (Figure 4); during sinus rhythm, in these areas, delayed, low-amplitude and fragmented signals are present (Figure 5). Macroscopically, endomyocardial fibrosis is a common finding. The arrhythmogenic morphologic substrate is either reduced or rendered a homogeneous scar without electrical activity. In this regard, techniques for endomyocardial resection have been described by Harken and Josephson. As an alternative procedure. Guiraudon introduced the encircling endomyocardial resection with which the pathologic reentry circuit can be blocked and the microvascular blood flow to arrhythmogenic areas eliminated. One modification, the partial encircling resection, appears to yield comparable effectiveness with less damage to left ventricular function (Figure 6).(ABSTRACT TRUNCATED AT 400 WORDS)

Electrocardiography↗

[Catheter ablation in ventricular tachycardia].

The basis for management of ventricular tachycardia (VT) is pharmacologic treatment which is effective, however, in only about 20 to 30% of the patients. With respect to this problem, alternative therapeutic modes have been developed which include, in addition to antitachycardia stimulation, electrical, palliative therapy such as the implantable automatic defibrillator, definitive measures such as map-guided antitachycardia surgery and catheter ablation. The goal of catheter ablation is the selective destruction of heart structures which are the morphologic correlate for initiation of propagation of VT. Catheter ablation was discovered by chance by Fontaine after a defibrillation during an electrophysiologic study in which a defibrillating electrode in the proximity of a catheter at the His bundle induced complete AV-block. This effect of destruction in the AV-conduction system by direct current as a therapeutic measure was further developed by Gallagher and Scheinman. The mechanism held responsible is coagulation by the electrode of neighboring tissue and barotrauma. The technique, which was initially used for ablation of the His bundle in supraventricular tachycardia, can also be used for ablation of accessory pathways or the site of origin of VT which generally lies endocardially in marginal regions of myocardial infarctions. CATHETER MAPPING: In sinus rhythm and induced VT, endocavity catheter mapping is carried out after heparinization with electrocardiograms recorded from at least six to ten sites in the right and left ventricles. At the site of early activation, detailed mapping is used for identification of the site of earliest activation, then pace-mapping is performed during sinus rhythm and VT. The morphology of the stimulated QRS complexes is compared with that of the spontaneous VT. In patients in whom VT cannot be induced, localization is carried out by pace-mapping alone. CATHETER ABLATION: After localization, in intubation narcosis and with continuously monitored arterial blood pressure, the suspected site of origin of the VT is subjected to an initial shock during sinus rhythm by means of a distal electrode of a catheter in stable contact with the endocardium. For mapping and ablation, the same catheter is used. After each subsequent shock, assessment is performed to determine if the distal electrode pair still conducts local ventricular signals and if ventricular stimulation is possible. The shock energy delivered is 100, 200 or 400 Joules. At the time of shock discharge, the remaining electrodes or catheters are disconnected. In the case of bradycardia or tachycardia after the shock, immediate connection to an external stimulation generator is established. At the time of the shocks, relaxation is provided by succinylcholine. All shocks are delivered from the anode. The integrity of the catheter is tested after each shock, no catheter is used more than three or four times. At the earliest, ten minutes after shock delivery, induction of clinical VT is attempted with programmed stimulation and if induction is possible, at the same site a maximum of two more shocks are delivered or, after renewed mapping, another shock is delivered to a different site. Induced non-clinical VT is not subjected to ablation.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrioventricular Node↗

Ten years electrophysiologically guided direct operations for malignant ischemic ventricular tachycardia--results.

UNLABELLED: During the recent 10 years period worldwide more than 1000 patients underwent an electrophysiologically guided direct operation for malignant ventricular tachycardia in the setting of chronic ischemic heart disease. The published results of these operations as regards relief of ventricular tachycardia and survival are highly variable. The data presented here are largely based on a multi-institutional registry series (n = 665) and the combined Düsseldorf-Birmingham/Alabama (DUS-UAB) ventricular tachycardia surgery experience (n = 216). DATA: Survival (hospital deaths included) was 75% one year after operation and 45% at 5 years (DUS-UAB). The respective data of the registry series were 78% and 55%. The most prevalent mode of death in both analyses was acute/subacute/chronic heart failure. More extensive encircling procedures (incisional/cryo) for ventricular tachycardia ablation and the combination of encircling cryoablation and endocardial resection increased the risk of progressive left ventricular dysfunction and death; however, by multivariate analysis the severity of the underlying ischemic heart disease (indicated by NYHA functional class, LVEDP, No. of previous infarcts, and extensiveness of coronary disease) and the absence of a discrete left ventricular aneurysm were more powerful predictors for early and late postoperative mortality than the use of alternative surgical techniques for ventricular tachycardia ablation. Survival was particularly poor after the return of spontaneous sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗

Pathophysiological mechanisms of ventricular tachyarrhythmias.

The pathophysiological background for ventricular tachyarrhythmias based on experimental and clinical evidence is presented. Sudden cardiac death may occur as the first manifestation of coronary artery disease without antecedent complaints or it may occur in patients with a previous myocardial infarction. In the latter situation, a circumscribed area of cardiac tissue may be responsible for the genesis and maintenance of a ventricular tachyarrhythmia which may be called the 'arrhythmogenic substrate'. This zone of electrically abnormal ventricular myocardium is usually located at the border of a previous myocardial infarction, and is characterized by islands of relatively viable muscle alternating with areas of necrosis and, later, fibrosis. The consequent fragmentation of the propagating electromotive forces leads to the development of high-frequency components that can be recorded directly or non-invasively using signal-averaging techniques. These signals have been called ventricular late potentials. The 'arrhythmogenic substrate' may be present permanently or may rise acutely and be present only transiently in the case of extensive ischaemia or acute myocardial infarction. In the setting of a chronic 'arrhythmogenic substrate', this electrically abnormal tissue may be triggered by spontaneously occurring ventricular ectopic beats or salvoes or by programmed ventricular stimulation, as well as by transient episodes of ischaemic causing spontaneous arrhythmias. These trigger factors modify the 'arrhythmogenic substrate' in such a way that ventricular tachyarrhythmias are sustained. It is apparent that sudden cardiac death is due to a wide spectrum of pathophysiological mechanisms which may be interrelated. There is obviously no single parameter that helps the clinician to predict the propensity for sudden cardiac death in the individual patient.

Coronary Disease↗

Efficacy of flecainide in pacing-induced sustained ventricular tachyarrhythmias: correlation to clinical parameters and tachycardia-characteristics.

Seventy-two patients with sustained ventricular tachycardia or syncope of unknown origin underwent electrophysiologic evaluation before and after therapy with flecainide (200-300 mg day-1). In all patients, sustained ventricular tachycardia or ventricular fibrillation was inducible during control electrophysiologic study. During flecainide therapy, sustained ventricular tachycardia (VT) was no longer inducible in 18 patients (25%) whereas in 54 patients, VT was still inducible. In five of the latter patients, VT became more difficult to induce (overall efficacy 32%). The rate of VT decreased from 214 +/- 49 beats min-1 during the control electrophysiologic study to 178 +/- 48 beats min-1 during flecainide (P less than 0.01). The ERP of the right ventricle increased from 251 +/- 27 ms during the control study to 267 +/- 34 ms on flecainide (P less than 0.01). Mean ejection fraction and mean LVEDP did not differ between responders and non-responders, yet the presence of a left ventricular aneurysm correlated with a lack of antiarrhythmic response to flecainide. VT rate as well as VT morphology during the control study discriminated between responders and non-responders; 11% of patients with VT-rate less than or equal to 230 beats min-1 responded to oral flecainide compared with 31% with a VT rate greater than 230 beats min-1 at control. 26% with induced monomorphic VT responded, compared with 100% with induced VF during the control study. 18 of 23 responders were discharged on flecainide. During a mean follow-up of 26 +/- 18 months, two patients experienced a recurrence of VT and in one patient, flecainide had to be discontinued due to side-effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗