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Biomedical subjects

G Breithardt

Publications and source records attributed to G Breithardt.

At least 55 records · Page 3Linked to original sources
PubMed2001

[Acute anterior wall infarct in a 31-year-old patient after administration of methylergometrin for peripartal vaginal hemorrhage].

CASE REPORT: After administration methylergometrine 30 minutes after delivery for peripartal vaginal bleeding a 31-year-old female patient developed an acute anterior wall myocardial infarction. Coronary angiography 7 hours after beginning of the chest pain demonstrated a dissection with a large thrombus in the proximal left anterior descending artery, followed by a complete occlusion in the periphery of the vessel (Figure 1). After applying rtPA intravenously, coronary angiography showed 24 hours later an open vessel without thrombotic material (Figure 2). CONCLUSION: Coronary artery spasm induced by methylergometrine must be regarded as the main reason for the dissection and thrombus formation followed by a myocardial infarction.

Adult↗
PubMed2001

A novel long-QT 5 gene mutation in the C-terminus (V109I) is associated with a mild phenotype.

Mutations in the human minK gene KCNE1 have been linked to autosomal dominant and autosomal recessive long-QT (LQT) syndrome, a cardiac condition predisposing to ventricular arrhythmias. minK and KvLQT1, the LQT1 gene product, form a native cardiac K+ channel that regulates the slowly delayed rectifier potassium current I(Ks). We used single-strand conformation polymorphism and sequencing techniques to identify novel KCNE1 mutations in patients with a congenital LQT syndrome of unknown genetic origin. In 150 unrelated index patients a missense mutation (V109I) was identified that significantly reduced the wild-type I(Ks) current amplitude (by 36%) when coexpressed with KvLQT1 in Xenopus oocytes. Other biophysical properties of the I(Ks) channel were not altered. Since we observed incomplete penetrance (only one of two mutation carriers could be diagnosed by clinical criteria), and the family's history was unremarkable for sudden cardiac death, the 109I allele most likely causes a mild phenotype. This finding may have implications for the occurrence of "acquired" conditions for ventricular arrhythmias and thereby the potential cardiac risk for asymptomatic mutation carriers still remains to be determined.

Alleles↗
PubMed2001

Blocking effects of the antiarrhythmic drug propafenone on the HERG potassium channel.

Propafenone has been shown to affect the delayed-rectifier potassium currents in cardiomyocytes of different animal models. In this study we investigated effects and mechanisms of action of propafenone on HERG potassium channels in oocytes of Xenopus laevis with the two-electrode voltage-clamp technique. Propafenone decreased the currents during voltage steps and the tail currents. The block was voltage-dependent and increased with positive going potentials (from 18% block of tail current amplitude at -40 mV to 69% at +40 mV with 100 micromol/l propafenone). The voltage dependence of block could be fitted with the sum of a monoexponential and a linear function. The fractional electrical distance was estimated to be delta=0.20. The block of current during the voltage step increased with time starting from a level of 83% of the control current. Propafenone accelerated the increase of current during the voltage step as well as the decay of tail currents (time constants of monoexponential fits decreased by 65% for the currents during the voltage step and by 37% for the tail currents with 100 micromol/l propafenone). The threshold concentration of propafenone effect was around 1 micromol/l and the concentration of half-maximal block (IC50) ranged between 13 micromol/l and 15 micromol/l for both current components. With high extracellular potassium concentrations, the IC50 value rose to 80 degrees mol/l. Acidification of the extracellular solution to pH 6.0 increased the IC50 value to 123 micromol/l, alkalization to pH 8.0 reduced it to 10 micromol/l and coexpression of the beta-subunit minK had no statistically significant effect on the concentration dependence. In conclusion, propafenone has been found to block HERG potassium channels. The data suggest that propafenone affects the channels in the open state and give some hints for an intracellular site of action.

Animals↗
PubMed2001

Outcome of women is impaired in patients undergoing emergency coronary artery bypass grafting for failed PTCA.

There is an ongoing debate whether female gender is associated with increased cardiovascular morbidity and mortality, especially after coronary interventions. The impact of gender on the outcome of patients undergoing emergency coronary artery bypass grafting (CABG) for failed PTCA was analyzed. Clinical and procedural data of all patients who underwent PTCA and subsequent emergency CABG at our institution from 1989 to 1998 were assessed. During these 10 years, 6681 PTCA procedures were performed, 1312 in women (19.6%). Subsequently, 110 patients underwent emergency CABG of whom 32 were females (29.1%). Postoperatively, 9 women and 5 men died (mortality 12.7%). Women presented with higher age (61.2 +/- 2.1 vs. 58.3 +/- 1.0 years, n.s.), smaller height (1.61 +/- 0.01 vs. 1.76 +/- 0.01 m, p < 0.0001), lower weight (67.7 +/- 2.4 vs. 82.1 +/- 1.2 kg, p < 0.0001), smaller body surface area (1.70 +/- 0.04 vs. 1.98 +/- 0.02 m2, p < 0.0001), and higher comorbidity as expressed by their Cleveland score (7.9 +/- 0.3 vs. 7.1 +/- 0.2, p = 0.013). The risk for failure of PTCA with subsequent emergency CABG was higher in women than in men (2.4% vs. 1.5%, p = 0.012, odds ratio 1.66) as well as for postoperative death (28.1% vs. 6.4%, p = 0.004, odds ratio 4.39). Women had longer in-hospital stays (19.7 +/- 4.2 vs. 12.9 +/- 1.3 days, p = 0.044). Logistic regression analyses found lower weight (p = 0.003), higher number of diseased coronary vessels (p = 0.024) and higher Cleveland score (p = 0.023) to be independent predictors of operative mortality. A Kaplan-Meier model (follow-up 5.3 +/- 2.5 years) showed an increased in-hospital mortality in women (p = 0.0034, log rang test), but a comparable long-term survival. Women had an increased risk for failure of PTCA and a markedly higher operative mortality after emergency CABG. In multivariate analyses, however, gender was not an independent predictor of postoperative death.

Angioplasty, Balloon, Coronary↗
PubMed2001

Torsade de pointes induced by ajmaline.

Ajmaline, a reserpine derivative, is an effective class I antiarrhythmic agent. Herein we report two cases of ajmaline-induced abnormal QT prolongation accompanied by polymorphic ventricular tachycardia of the torsade de pointes type. Since ajmaline is increasingly used for the acute termination of wide complex tachycardia and as a diagnostic tool after syncope and in patients with idiopathic ventricular tachyarrhythmias, our observations suggest that caution should be exercised with regard to the effects of the drug on the QT interval and its potency to induce proarrhythmia of the torsade de pointes type.

Ajmaline↗
PubMed2001

[Detection of circulating cerebral microemboli by transcranial Doppler ultrasonography].

Thromboembolic events represent a major complication of cardiovascular diseases and interventions. Although general risk factors and predictors for thromboembolic events are well known from population-based studies, hardly any therapeutic consequences for the individual patient can be drawn, e.g. for a well-balanced therapy with anticoagulants. A new approach towards an optimised therapy adapted to the individual risk of each patient may be based on the detection of circulating microemboli by transcranial Doppler sonography. With this technique, gaseous or solid microparticles circulating in the blood can noninvasively be detected. Due to their small size, they do not induce thromboembolic events themselves. However, several studies demonstrate that they indicate an increased thromboembolic activity and correlate directly with manifest stroke or emboli. From a transcranial Doppler probe positioned on the temporal plane at the patient's skull, the middle cerebral artery's blood flow is recorded and is analysed acoustically and optically for circulating microemboli. This technique has already been used for risk stratification of high-risk patients and therapeutic decision-making in neurologic routine, e.g. for the indication to anticoagulate the patient or for carotis surgery. Data to evaluate its value in cardiology are limited and based on few clinical studies. In this review, the basic principles and the methodological and technical background for the detection of microemboli, as well as current limitations, are discussed. Furthermore, clinical studies and their results evaluating this technique in patients with cardiological diseases and during cardiovascular interventions are reviewed.

Angioplasty, Balloon, Coronary↗
PubMed2001

Load-induced changes in repolarization: evidence from experimental and clinical data.

The high incidence of arrhythmias in patients with heart failure, hypertension, valvular heart disease, or mitral walve prolapse suggests a strong link between wall motion abnormalities and arrhythmias. A potential common mechanism underlying these observations may be that overload leads to electrophysiologic changes and facilitates arrhythmias. This article summarizes the interaction between changes in atrial and ventricular loading conditions and repolarization. Most experimental and clinical studies demonstrated 1) a reduction of action potential duration and refractoriness, 2) development of early afterdepolarizations, and 3) ectopic beats originating from these afterdepolarizations. Discrepancies between studies are related to different study designs, i.e., varying magnitude, velocity, and timing of increased load, the level of repolarization at which action potential duration is measured as well as different animal species. Direct effects of increased load on repolarization are most likely caused by activation of stretch-activated nonselective cation ion channels and changes in calcium handling. Current antiarrhythmic drug therapy is aimed at electrical disorders as the primary cause of arrhythmias. If mechanical disorders play a central role in the genesis of cardiac arrhythmias, future treatment should be directed at restoring a more normal mechanical function of the heart. Additional studies will further clarify the nature and clinical significance of load-related changes in repolarization and arrhythmogenesis.

Animals↗
PubMed2001

In vivo recording of monophasic action potentials in awake dogs--new applications for experimental electrophysiology.

INTRODUCTION: Despite enormous developments in the field of clinical and experimental electrophysiology there is still a gap in evaluating repolarization in the awake animal. Numerous previous studies have used monophasic action potentials (MAP) to assess repolarization in vitro and in vivo in anesthetized animal models. However, an approach for recording MAP in awake dogs without interference of anesthesia has not yet been developed. METHODS AND RESULTS: We developed an experimental technique to record MAP in conscious dogs by means of conventional rubber introducers which were implanted into the internal jugular vein. In seven awake dogs, atrial as well as ventricular MAP were simultaneously measured without complications. Pacing thresholds were low and stable over time ranging from 0.2 to 4.0 mA. The MAP amplitudes ranged from 10 to 30 mV for ventricular and from 5 to 15 mV for atrial MAP. Continuous MAP recordings of stable amplitude could be made from the same endocardial site for periods of up to one hour. Antegrade and retrograde AV-nodal conduction properties could be assessed. Programmed stimulation was performed to simultaneously determine local refractory periods and MAP duration at cycle lengths from 500 to 200 ms. CONCLUSION: In awake, unsedated dogs the measurement of MAP via rubber introducers permits safe, long-term recording of MAP. Such recordings may be useful for safety pharmacological studies in evaluating cardiovascular and non-cardiovascular drugs with regard to their effects on repolarization. In various canine in vivo models including in vivo models of long QT syndrome, heart failure or sudden cardiac death, the present technique permits electrophysiological measurements without interference of anesthesia.

Action Potentials↗
PubMed2001

Pulmonary beta adrenoceptor density in arrhythmogenic right ventricular cardiomyopathy and idiopathic tachycardia.

OBJECTIVE: In recent in vivo studies using positron emission tomography (PET) our group demonstrated that the myocardial beta adrenoceptor (betaAR) density is reduced in arrhythmogenic right ventricular cardiomyopathy (ARVC) and idiopathic right ventricular outflow tract tachycardia (RVO-VT) associated with an increased presynaptic catecholamine washout. It was hypothesised that the reduction of myocardial betaAR density is secondary to an increase of local catecholamines in the myocardium resulting from the presynaptic dysfunction since circulating plasma catecholamines were demonstrated to be unchanged in these conditions. To further prove this hypothesis of an organ-limited adrenergic nervous dysfunction of the heart, this study aimed to investigate betaAR density in another thoracic organ, the lung. METHODS: Pulmonary and myocardial betaAR density was measured in 7 ARVC patients, 8 RVO-VT patients and in a group of healthy controls (n = 13) using the non-selective beta-blocker [11C]-CGP 12177 and PET. RESULTS: Pulmonary betaAR density was similar in controls (12.4 +/- 1.7 pmol/g tissue), ARVC (11.6 +/- 1.7 pmol/g tissue, p = ns) and RVO-VT (12.8 +/- 2.0 pmol/g tissue, p = ns), whereas myocardial betaAR density was significantly reduced in ARVC (6.3 +/- 1.1 pmol/g tissue, p = 0.006) and RVO-VT (6.8 +/- 1.2 pmol/g tissue, p=0.02) as compared to controls (8.8+/-1.5 pmol/g tissue). CONCLUSION: The unchanged pulmonary betaAR density in the presence of a previously described significant reduction in myocardial betaAR density in the same patient principally supports our pathophysiological hypothesis that the myocardial betaAR density may be reduced in ARVC and RVO-VT because of an increase in local synaptic catecholamine levels due to an organ-limited presynaptic adrenergic dysfunction of the heart. Since in the present study only pulmonary betaAR density was measured, future functional studies excluding pulmonary betaAR desensitisation are required to finally prove the unchanged pulmonary sympathetic innervation in ARVC and RVO-VT.

Adult↗
PubMed2001

Signal characteristics of multichannel epicardial electrograms in chronic ischaemic and scarred myocardium: electromechanical mismatch indicates viability in regions of myocardial dysfunction.

BACKGROUND: To predict the outcome after myocardial revascularisation, a clear separation between hibernation and/or repetitive stunning on the one hand and myocardial scarring on the other hand is of importance. METHODS AND RESULTS: A total of 44 patients was included in this study. In 35 patients with chronic myocardial ischaemia and an indication for coronary bypass-surgery, epicardial mapping of local activation was performed. Nine patients with LV aneurysm and an indication for antitachycardia surgery were also included. For simultaneous recording of the local electrograms during sinus rhythm, a sock electrode with 102 bipolar leads was used. The regional myocardial contraction pattern was assessed from preoperative angiograms and regional myocardial metabolism (viability) from 18F-FDG PET, respectively. The results were projected on the grid of the intraoperative position of the sock electrode. This enabled regional comparison of electrogram characteristics to local contraction patterns and viability. For the characterisation of local electrograms, peak-to-peak amplitude and duration of activation were calculated using custom-made automated computer-algorithms. Dysfunctional but viable areas showed normal or almost normal electrographic signal characteristics. In contrast, dysfunctional and non-viable myocardium showed a distinct reduction of local amplitudes and prolongation of signal duration. These changes were even more intense in areas of LV aneurysms. CONCLUSIONS: In patients with chronic ischaemic myocardium, a mismatch between mechanical function and local electrogram characteristics was observed in areas with preserved metabolism. Thus, normal epicardial electrograms in regions of myocardial dysfunction may be an indicator for myocardial viability.

Adult↗
PubMed2001

Antitachycardia pacing for rapid VT during ICD charging: a method to prevent ICD shocks.

In patients with ICDs, rapid VTs are usually treated with shocks. It is unknown, if antitachycardia pacing (ATP) delivered once for rapid VT during capacitor charging can avoid painful shocks without increasing the risk of syncope. In patients in whom rapid monomorphic VT (cycle length 300-220 ms) could be reproducibly induced during predischarge ICD testing, the success of cardioversion (defibrillation threshold plus 10 J) and a single ATP attempt (burst with 8 or 16 stimuli) was compared using a randomized crossover study design. Consciousness of the patients was checked by the signal from a button constantly pushed by the patient. In 20 patients (ejection fraction 0.50 +/- 0.19) rapid VTs (253 +/- 26 ms) were reproducibly induced. A single burst successfully terminated 11 (55%) of 20 rapid VTs, 6 episodes could not be terminated with a single burst pacing and 3 VTs accelerated. Rapid VTs not terminated by ATP were significantly faster than those that could be terminated (246 vs 258 ms, P = 0.026). Cardioversion (19 +/- 3 J) terminated the VTs in all cases. No patient suffered syncope during rapid VTs. A single ATP may terminate rapid VT with cycle lengths < 300 ms in 55% of patients without increasing the risk of syncope. Therefore, in rapid VTs one attempt of ATP may be suitable as an additional therapy option during ICD capacitor charging to avoid painful shocks without compromise of safety. Thus, future ICDs should implement the option of ATP during charging of capacitors.

Adult↗
PubMed2001

Clinical value of electrocardiographic parameters in genotyped individuals with familial long QT syndrome.

Rate corrected QT interval (QTc) and QT dispersion (QTd) have been suggested as markers of an increased propensity to arrhythmic events and efficacy of therapy in patients with long QT syndrome (LQTS). To evaluate whether QTc and QTd correlate to genetic status and clinical symptoms in LQTS patients and their relatives, ECGs of 116 genotyped individuals were analyzed. JTc and QTc were longest in symptomatic patients (n = 28). Both QTd and JTd were significantly higher in symptomatic patients than in asymptomatic (n = 29) or unaffected family members (n = 59). The product of QTd/JTd and QTc/JTc was significantly different among all three groups. Both dispersion and product put additional and independent power on identification of mutation carriers when adjusted for sex and age in a logistic regression analysis. Thus, symptomatic patients with LQTS show marked inhomogenity of repolarization in the surface ECG. QT dispersion and QT product might be helpful in finding LQTS mutation carriers and might serve as additional ECG tools to identify asymptomatic LQTS patients.

Adult↗
PubMed2001

Implantation of a dual chamber pacing and sensing single pass defibrillation lead.

Dual-chamber ICDs are increasingly used to avoid inappropriate shocks due to supraventricular tachycardias. Additionally, many ICD patients will probably benefit from dual chamber pacing. The purpose of this pilot study was to evaluate the intraoperative performance and short-term follow-up of an innovative single pass right ventricular defibrillation lead capable of bipolar sensing and pacing in the right atrium and ventricle. Implantation of this single pass right ventricular defibrillation lead was successful in all 13 patients (age 63 +/- 8 years; LVEF 0.44 +/- 0.16; New York Heart Association [NYHA] 2.4 +/- 0.4, previous open heart surgery in all patients). The operation time was 79 +/- 29 minutes, the fluoroscopy time 4.7 +/- 3.1 minutes. No perioperative complications occurred. The intraoperative atrial sensing was 1.7 +/- 0.5 mV, the atrial pacing threshold product was 0.20 +/- 0.14 V/ms (range 0.03-0.50 V/ms). The defibrillation threshold was 8.8 +/- 2.7 J. At prehospital discharge and at 1-month and 3-month follow-up, atrial sensing was 1.9 +/- 0.9, 2.1 +/- 0.5, and 2.7 +/- 0.6 mV, respectively, (P = NS, P < 0.05, P < 0.05 to implant, respectively), the mean atrial threshold product 0.79, 1.65, and 1.29 V/ms, respectively. In two patients, an intermittent exit block occurred in different body postures. All spontaneous and induced ventricular arrhythmias were detected and terminated appropriately. Thus, in a highly selected patient group, atrial and ventricular sensing and pacing with a single lead is possible under consideration of an atrial pacing dysfunction in 17% of patients.

Aged↗
PubMed2001

Prolonged QRS duration increases QT dispersion but does not relate to arrhythmias in survivors of acute myocardial infarction.

QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2-3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%-15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 +/- 7 vs 78 +/- 1 ms, JT disp 80 +/- 6 vs 79 +/- 2 ms, mean +/- SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction.

Aged↗