[Cooled tip ablation of left ventricular outflow tract tachycardia through the aortic sinus of valsalva]. / Gekühlte HF-Stromkatheterablation epikardialer Ausflusstrakttachykardien über die Sinus valsalvae der Aorta.

BACKGROUND: Monomorphic tachycardia with an epicardial site of the arrhythmic focus in the left ventricular outflow tract (LVOT) usually cannot be ablated by an endocardial approach. We describe the use of cooled tip catheter ablation through the aortic sinus of valsalva to treat LVOT tachycardia. METHODS: In seven patients (four males, one with valvular cardiomyopathy, six patients without heart disease) with sustained and non-sustained ventricular tachycardia (VT) an epicardial focus of LVOT tachycardia could be identified by pace-mapping and earliest local activation within the aortic sinus of valsalva. Coronary angiography served to define the position of the coronary arteries with respect to the ablation catheter. High frequency current was delivered using a closed-loop cooled tip catheter system (Chilli Cool(R), Boston Scientific). ECG, Holter-ECG, echocardiography and transesophageal echocardiography were performed after the procedure and 3 months later. RESULTS: Foci were located in the left (two patients), in the right (three) and in the a coronary aortic sinus (two). Successful ablation could be achieved in six patients. No procedure-related complications could be observed during a mean follow-up of 4.2 months. CONCLUSION: Monomorphic VT with epicardial origin in the LVOT can be successfully treated by cooled tip ablation through the aortic sinus of valsalva. The use of a cooled tip ablation system may be favourable in several ways: 1) it allows the creation of deep lesions necessary to reach remote foci; 2) due to lower temperatures at the catheter/tissue interface surface tissue damage may be reduced; 3) lower catheter temperature may additionally reduce the risk of local clot formation which is crucial for all left-sided procedures and especially for ablation in the sinus of valsalva.

[Therapy with implanted cardioverter-defibrillator: Is a replacement of the impulse generator due to battery depletion also necessary without the occurrence of a tachyarrhythmia episode?]. / Therapie mit implantierbaren Kardioverter/Defibrillatoren: Ist ein Austausch des Impulsgenerators bei Batterieerschöpfung auch ohne stattgehabte Tachyarrhythmie-Episode notwendig?

The aim of this retrospective study was to evaluate the necessity of the replacement of an implantable cardioverter/defibrillator (ICD) in patients with pulse generator battery depletion without an adequate, spontaneous arrhythmia episode during the life-time of the first implanted device. In this study 213 patients with implanted ICDs were enrolled. In 62 patients an elective generator replacement due to battery depletion was performed. Both patient groups (Group A: patients with generator replacement n = 62 and Group B: patients without replacement n = 151) were not different with regard to main clinical characteristics, such as underlying heart disease and left ventricular function. In both groups there was a predominance of male patients (Group A: 89%; Group B: 83%). The mean age was 58 +/- 11 years and 59 +/- 11 years in Group A and Group B, respectively. Coronary artery disease was present in 66% and 68% of the patients. There was a comparable left ventricular ejection fraction: Group A: 30.5 +/- 9% vs Group B: 31.9 +/- 9%. The follow-up time was much longer in Group A patients compared to Group B patients (50.5 +/- 14 vs. 16.5 +/- 11 months). For the total patient group there was a 5 year event-free probability of 23%, no differences were found between both groups. The subanalysis in Group A patients revealed no difference in the probability of ICD-shock occurrence prior to or after the replacement of the pulse generator. In 48/62 (77%) of Group A patients adequate ICD discharges were documented. In 15/62 (24%) patients shock occurred before and after generator replacement. In 6/62 (10%) of Group A patients, the first adequate ICD-therapy was documented after generator replacement. The results of this study indicate the necessity of an ICD-pulse generator replacement even in patients without an adequate device discharge during the life-time of the first implanted device.

Tedisamil (KC 8857) is a new specific bradycardic drug: does it also influence myocardial contractility? Analysis by the conductance (volume) technique in coronary artery disease.

To determine whether inotropism influences the bradycardic action of tedisamil, hemodynamic assessment was performed in 13 patients with ischemic coronary artery disease including analysis of end-systolic pressure-volume relationships after an infusion of tedisamil, 0.3 mg/kg, at rest, and during paced tachycardia stress. Slope Emax fell by 14% at rest (13 patients) and by 10% during tachycardia (6/13 patients), whereas loops of end-systolic pressure-volume relationships moved rightward; all parameter changes indicated a lack of significant inotropism loss with tedisamil (p > 0.05). Although the mean heart rate decreased from 77.5 to 64.7 beats/min and QTc duration increased by 14% (p < 0.05), filling pressure and dp/dtmin remained unchanged and vascular resistance increased by 30%. Parameters of left ventricular pump function (ejection fraction, stroke volume, left ventricular efficiency) decreased slightly (between 3% and 13%), whereas left ventricular volumes increased (end-diastolic volume by 6%, end-systolic volume by 23%). The respective parameter changes during tachycardia were comparable in tendency, and angina could no longer be induced during postdrug pacing stress. We concluded that the bradycardic effects of tedisamil are selectively generated without impairing either ventricular pump function or contractility in a clinically relevant fashion, whereas the postdrug anginal threshold appears elevated. Thus tedisamil can be used safely in ischemic coronary artery disease.

[Is the bradycardic effect of tedisamil at the expense of the loss of the inotropic effect? A pressure-volume analysis with the conductance (volume) catheter technique in patients with coronary artery disease]. / Wird die bradykardisierende Wirkung von Tedisamil mit Inotropie-Einbusse erkauft? Eine Druck-Volumen-Analyse mit der Conductane-(Volumen-)Kathetertechnik bei Patienten mit koronarer Gefässkrankheit.

UNLABELLED: To exclude or prove potential inotropic influences from tedisamil's bradycardiac effects, our hemodynamic evaluation in 13 patients (pat.) with coronary artery disease (CAD) included analyses of end-systolic pressure-volume relationships (ESPVR) after tedisamil, 0.3 mg/kg infusion at rest and during tachycardia induced by atrial pacing. Slope Emax [mm HG/ml] fell by 14% at rest (13 pat.) and by 10% during paced tachycardia (6/13 pat.) while loops of ESPVR tended to move rightward towards larger volumes (p > 0.05): all parameter changes indicated lack of significant inotropy loss with tedisamil. While mean heart rate decreased from 77.5 to 64.7 b/min and QTc duration increased by 14% (p < 0.05), filling pressure as well as dP/dtmin remained unchanged and vascular resistance rose by 30%. Parameters of LV-pump function (ejection fraction, stroke volume) decreased slightly (between 3 and 13%), while LV-volumes increased (end-diastolic by 6%, end-systolic by 23%). The respective parameter changes during paced tachycardia were comparable in tendency. CONCLUSION: Tedisamil's bradycardic effects are selectively generated without impairing either ventricular pump function or contractility in a clinically relevant fashion. Thus, tedisamil can be used safely in CAD.

Antiischemic and hemodynamic effects of an oral single dose of 150 mg of the phosphodiesterase inhibitor enoximone in patients with coronary artery disease--relation to plasma concentration.

The hemodynamic and antiischemic effects of a 150-mg single oral dose of the PDE inhibitor enoximone were correlated with the plasma levels of enoximone and its sulfoxide metabolite. Twenty-one patients with angiographically documented coronary artery disease were investigated by exercise testing 1 and 2 hours after drug administration. The control group consisted of 15 patients with proven coronary artery disease and stable reproducible angina pectoris on exercise. The enoximone group included 14 responders with therapeutic plasma concentrations 2 hours after drug intake and significantly reduced mean pulmonary artery pressures on exercise (from 42.4 +/- 8.6 to 30.9 +/- 11.2 mmHg, p less than 0.05). Compared to basal exercise values, responders showed a reduced ST-segment depression by 1 hour after drug intake (2.1 +/- 1.2 vs. 1.3 +/- 3 mm, p less than 0.05) and minimal values after 2 hours (0.9 +/- 1.0 mm, p less than 0.01) at comparable workloads. There were no significant changes in heart rate, blood pressure, cardiac output, and systemic vascular resistance. No significant improvement in the hemodynamic parameters and ST-segment depression was found in nonresponders with plasma concentrations below 100 ng/ml and 500 mg/ml for enoximone and its metabolite, respectively. In summary, oral administration of enoximone in patients with coronary artery disease led to favorable acute hemodynamic and antiischemic effects at sufficiently high plasma levels of enoximone and its sulfoxide metabolite.

[Alinidine in multi-vessel coronary disease: reduction of stress-induced ischemic reaction]. / Alinidine bei koronarer Mehrgefässerkrankung: Reduktion der belastungsinduzierten Ischämiereaktion.

Ten patients suffering from an angiographically documented coronary two- or three-vessel disease were examined to evaluate the effects of the specific bradycardiac agent alinidine during a bicycle stress test. Hemodynamic and electrocardiographic parameters were compared before and after an intravenous application of 30 mg of the substance. The alinidine plasma levels 30 min after the injection were 160.6 +/- 22.5 ng/ml) (mean +/- SEM). Alinidine significantly (p less than 0.05) reduced the resting levels of heart rate (8.5%), double product (10.3%), myocardial oxygen consumption (9.1%), and cardiac output (9.0%). During exercise, significantly less ST-segment depression (p less than 0.001) in the EKG was observed after alinidine application in nine out of 10 patients, and the rise of pulmonary artery pressure was significantly reduced (34.7 vs 38.1 mm Hg, mean p less than 0.05). However, alinidine had no effect on the maximum heart rate at the end of exercise. We, therefore, assume that the substance has additional anti-ischemic properties.

Left ventricular muscle mass and diastolic function in patients with essential hypertension under long-term clonidine monotherapy.

To determine whether alterations of left ventricular (LV) structure are associated with improved LV function under chronic clonidine monotherapy (300-450 g/day) of essential hypertension, 11 male patients (age range 47-61 years) were followed for 5.4 +/- 0.9 months using echocardiography and Doppler echocardiography. Blood pressure decreased from a mean of 168/105 to 150/96 mmHg (p less than 0.01), heart rate remained unchanged (73 +/- 10 vs. 71 +/- 10 beats/min). LV muscle mass decreased from 350 +/- 73 to 297 +/- 56 g (p less than 0.02), LV volume/muscle mass ratio increased from 0.58 +/- 0.13 to 0.69 +/- 0.12 ml/g (p less than 0.005). Ejection time increased from 276 +/- 17 to 296 +/- 17 ms (p less than 0.01), whereas no significant change was found for pre-ejection period, ejection fraction, cardiac index and LV dimensions. Doppler analysis revealed improved isovolumic relaxation time (116 +/- 17 vs. 84 +/- 28 ms; p less than 0.05), but no change in isovolumic contraction duration, maximal inflow velocities, time-velocity integrals and their duration, rate of acceleration and deceleration of early and atrial filling, and of their ratios. It is concluded that no reliable improvement in diastolic or systolic LV function is observed in chronic clonidine monotherapy of essential hypertension despite a normalization of blood pressure and a regression of LV hypertrophy.

[Hemodynamic, anti-ischemic, metabolic and neurohumoral effects of enoximone (MDL 17,043) in patients with coronary disease]. / Hämodynamische, antiischämische, metabolische und neurohumorale Effekte von Enoximon (MDL 17,043) bei Patienten mit koronarer Herzkrankheit.

The hemodynamic, anti-ischemic, metabolic, and neurohumoral effects of the phosphodiesterase inhibitor enoximone were investigated in 17 patients (mean age 58 +/- 2 years) with coronary heart disease as established by coronary angiography and positive exercise tests after i.v. application of 0.75 mg/kg body weight. Whereas administration of enoximone resulted in a significant increase in heart rate from 75 +/- 17 to 83 +/- 14 per minute (p less than 0.01), exercise heart rate, blood pressure and myocardial oxygen consumption did not change significantly (p greater than 0.05). At rest, enoximone led to a significant decrease of mean right atrial pressure from 5.7 +/- 2.3 to 3.8 +/- 1.2 mm Hg (p less than 0.01). During exercise there was a significant fall in pulmonary pressure (PAm from 40 +/- 7 to 24 +/- 7 mm Hg, p less than 0.001; PCm from 24 +/- 7 to 14 +/- 6 mm Hg, p less than 0.001) caused by preload reduction and concomitant inotropic increase; there was also a significant rise in cardiac output from 12.7 +/- 5 to 13.8 +/- 5 mm Hg (p less than 0.01) and a decrease of ST-segment depression from 1.97 +/- 0.76 to 0.53 +/- 0.51 mm (p less than 0.001). With improved peripheral and probably coronary blood flow, a concomitant decrease of the metabolic ischemic markers was detected during exercise (potassium 4.44 +/- 0.29 vs. 4.31 +/- 0.30 mval, p less than 0.05; lactate 19 +/- 9 vs. 18 +/- 7 mg/dl; pH 7.28 +/- 0.27 vs. 7.36 +/- 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)