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Biomedical subjects

H Gülker

Publications and source records attributed to H Gülker.

At least 19 recordsLinked to original sources
PubMed1992

Nd:YAG laser-photocoagulation: acute electrophysiological, hemodynamic, and morphological effects in large irradiated areas.

Laser-photocoagulation (LPC) of arrhythmogenic myocardium has been reported to successfully ablate ventricular tachycardia. The purpose of this study was to investigate the acute hemodynamic and electrophysiological effect of continuous laser energy (Nd:YAG, 1060 nm) applied via a 0.4-mm quartz fiberoptic on the epicardial surface of the heart in nine dogs. A total of 51 +/- 2.3 pulses was delivered in each animal to induce homogeneous tissue necrosis. Applied energy was 12.3 +/- 2.7 J/mm2, irradiated surface measured 12.6 +/- 3.0 cm2, lesion depth was 6.3 +/- 1.2 mm (range: 5.0-8.1 mm), lesion volume was 8.1 +/- 2.8 cm3 (6.8% of left ventricular [LV] mass). After LPC, epicardial stimulation threshold significantly rose from 1.0 +/- 0.3 to 10.2 +/- 4.9 mA in the border zone to nontreated tissue and from 0.9 +/- 0.4 to 32 +/- 15.7 mA in the center of the lesions. Loss of epicardial activation in the irradiated areas could be demonstrated by epicardial mapping. Ventricular extrasystoles during LPC were seen in all dogs, ventricular tachycardia in seven, and ventricular fibrillation in two dogs. After LPC, cardiac output and LV dP/dtmax significantly decreased by 14.2% and 11.2%. LPC induced predictable homogeneous tissue edema, eosinophilic staining, contraction band necrosis, and sharp demarcated hemorrhagic border zones with a sharp electrical border zone to nontreated tissue and loss of epicardial activation. During LPC, various arrhythmogenic effects could be observed. However, no persistent arrhythmic activity developed after LPC. The results confirm the feasibility of epicardial LPC of the myocardium. Although not rested in this study, LPC of arrhythmogenic tissue may also be feasible as a treatment modality of ventricular tachycardia.

Animals↗
PubMed1992

Efficacy and tolerability of slow-release gallopamil in patients with stable exercise-inducible angina pectoris.

The anti-ischemic properties and tolerability of a slow-release formulation (SR) of gallopamil were investigated in 118 patients with exercise-inducible ST-segment depression and stable angina pectoris in this double-blind, randomized, placebo-controlled, multicenter study. After a placebo run-in period (A) of 2-7 days and a 7-day open therapy period (B) with gallopamil SR, the patients were randomized to a double-blind 7-day period (C) to receive placebo or gallopamil SR 100 mg twice a day. Each patient was submitted to gradual upright bicycle ergometry and electrocardiography (ECG) at rest on the last 2 days of each period at 6 and 12 h postadministration (p.a.) In period C, exercise time and exercise tolerance remained significantly prolonged at 6 and 12 h after gallopamil SR administration in comparison with the placebo values. Additionally the sum of ST-segment depression and maximal ST-segment depression were significantly reduced by gallopamil SR at 6 h p.a. as were the frequency of angina attacks and nitroglycerin consumption. Four patients were withdrawn from the study because of gallopamil-related adverse events, which, however, were not serious. Constipation was noted in 2.5% of the patients. These data suggest that gallopamil SR is effective in reducing exercise-inducible ST-segment depression and increasing exercise tolerance with no serious adverse effects in patients with stable angina pectoris.

Adult↗
PubMed1992

[Left atrial myxoma].

Left-atrial myxomas produce a broad array of clinical symptoms depending on their location, size, and morphology. The clinical presentation is characterized by obstruction of blood flow, systemic embolism, and unspecific systemic effects. Within 6 weeks, three patients presented in our clinic with left-atrial myxomas. Primary differential diagnoses were infective endocarditis, circulatory collapse, and transient ischemic attack of unknown origin. In all cases diagnosis was made with echocardiography (m-mode, 2D, TEE). In this review the etiology, epidemiology, and pathology are reported briefly. The variety of clinical symptoms with the corresponding differential diagnosis is presented systematically and discussed with our patients. Diagnostic, therapeutic, and prognostic aspects are summarized.

Adult↗
PubMed1992

[Biophysical aspects of high frequency catheter ablation. Studies of the significance of sudden changes in impedance].

UNLABELLED: To determine the effects and the underlying mechanisms of sudden rise of impedance during radiofrequency (RF) catheter ablation, 60 RF applications were delivered to isolated preparations of ventricular myocardium at three different power levels (mean: 3.7, 11.3, 19.3 watts). Pulse duration was 30 s, current voltage and catheter tip temperature were continuously monitored. Impedance rise occurred during 34 of 60 applications; the incidence of impedance rise increased at higher power levels. Impedance rise was significantly more often observed when the preparations were superfused with heparinized blood compared to saline solution (p less than 0.05). Catheter-tip temperature during radiofrequency application without impedance rise was significantly lower compared to applications with impedance rise (mean = 108 degrees C vs. 121 degrees C, p less than 0.01). The increase of catheter-tip temperature and maximal-tip temperature following impedance rise was significantly higher in blood when compared to saline solution (mean = +48 degrees C vs. +13 degrees C (p less than 0.001), Tmax: 121 degrees C vs. 245 degrees C). Following impedance rise, insulation defects of the electrode catheter and vaporized crater formation of the myocardium was often observed. CONCLUSIONS: During radiofrequency catheter ablation impedance rise occurs following overheating of the catheter electrode (greater than 110 degrees C). After impedance rise, catheter-tip temperature markedly increases. Insulation defects of the catheter and vaporized craters in the myocardium frequently occur after impedance rise. The results have important implications for the clinical use of RF-currents for catheter ablation; energy application should be immediately stopped after the occurrence of impedance rise.

Animals↗
PubMed1991

[Percutaneous endocardial Nd-YAG laser energy: experimental studies of ablation of the ventricular myocardium].

The in vitro and in vivo effects of endocardial laser ablation were assessed. Energy was supplied by a Nd-YAG laser (wavelength approximately 1064 nm) and transmitted via a quartz core fiber (phi: 0.4 mm) housed within a specially designed 7 F catheter. In vitro, the effects of increasing output power (5, 10, 20, 40 watt) and impulse duration (1, 2, 4, 8 s) on lesion size were assessed in myocardial preparations of canine hearts. Preparations were superfused with saline or blood, respectively; the distance of the optical fiber to the endocardium was 5 mm. Lesion size increased in diameter (range: 0-4.0 mm) and depth (range: 0-5.2 mm) in a power- and time-dependent manner. Superfusion with blood significantly enhanced the diameter of the lesions, whereas depth of the lesions significantly decreased. In 16 anesthetized mongrel dogs, a total of 52 laser impulses (output power: 10, 20, 40 w; impulse duration: 1, 2, 4 s; energy: 10-160 J) were delivered to apical and apico-inferior sites of the left ventricle. Postmortem, 40 lesions with a diameter of 2.6-19.4 mm and a depth of 3.7-16.2 mm were found. 19 lesions revealed central vaporized craters with a depth up to 11.2 mm. Perforation of the left ventricle occurred in two cases following 80 and 160 J, respectively. In vitro and in the intact animal (in apical and apico-inferior sites of the left ventricle) endocardial laser ablation is feasible to induce distinct myocardial lesions in a power- and time-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

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↗
PubMed1990

Constant-flow ventilation during experimental left ventricular failure.

The efficacy of constant-flow ventilation (CFV) was investigated in dogs with normal heart function (control phase, n = 8) and after development of left ventricular failure (LVF phase, n = 8). Heated, humidified and oxygen-enriched air (inspired oxygen fraction (Fio2) = 0.4) was continuously delivered via two catheters positioned within each mainstem bronchus at two flow rates (1.2 and 1.6 l/kg/min). Conventional mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP) of 0.5 kPa was used as reference ventilation. During control, neither CMV with PEEP nor CFV revealed severe impairment of cardiopulmonary performance. Alveolo-arterial PO2 difference (P(A-a)O2) increased significantly during CFV1.2 and CFV1.6, indicating a higher degree of ventilation-perfusion (VA/Q) inhomogeneity. Acute left ventricular failure (LVF) was induced by proximal occlusion of the left anterior descending (LAD) coronary artery. Cardiac output (CO), maximum velocity of pressure development (dP/dtmax) and mixed venous PO2 decreased (P less than or equal to 0.05), whereas left ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) increased (P less than or equal to 0.05). Extravascular lung water (EVLW), as determined by thermal-dye technique, increased from 10.1 ml/kg to 20.9 ml/kg (P less than or equal to 0.01). Oxygenation, but not CO2 elimination, deteriorated in the LVF phase. There were no haemodynamic differences between CMV with PEEP and CFV1.2, but cardiopulmonary performance deteriorated with CFV1.6. Gas exchange was significantly more impaired during CFV1.2 and CFV1.6 due to increased VA/Q mismatching. However, there were no significant differences for P(A-a)O2 values between CFVControl and CFVLVF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Radiofrequency coagulation of ventricular myocardium: improved prediction of lesion size by monitoring catheter tip temperature.

To assess the importance of voltage, current, impedance and catheter tip temperature for the prediction of the size of tissue injury induced by transcatheter radiofrequency application, radiofrequency pulses (500 kHz) were delivered both in vitro and in vivo to isolated ventricular preparations and the intact canine heart, respectively. Radiofrequency coagulations were performed using unipolar electrode configuration. Besides measurements of current and voltage which were used to calculate the delivered power and tissue impedance, the catheter tip temperature was monitored during each application using specially designed 6F USCI catheters with a built-in nickel/chromium-nickel thermoelement. Lesion dimensions were measured and the correlation between lesion volume and delivered radiofrequency energy, maximum changes in catheter tip temperature and the integral of the temperature curve were calculated. First, in a pilot in vitro investigation, 50 radiofrequency coagulations (3.2 W-22.4 W, pulse duration 10 s) were performed in ventricular preparations from freshly excised dog hearts. The correlation between applied radiofrequency energy and lesion volume was 0.87; the correlation between maximal catheter tip temperature and lesion volume was 0.82; the correlation between temperature integral and lesion volume was 0.9. In the intact dog heart, 44 radiofrequency pulses were delivered to the left and right ventricular endocardium in 12 anaesthetized dogs (exposure time: 10 s). Delivered power ranged between 5.6 W and 24.6 W; tissue impedance varied between 92 omega and 364 omega; lesion volume measured 0-273 mm3; developed peak temperatures ranged from 16.25 degrees C to 196 degrees C. The calculated integral beneath temperature curves measured 126-1971 degrees C.s. The correlation between applied radiofrequency energy and lesion volume was 0.32; the correlation between maximal catheter tip temperature and lesion volume was 0.61. Temperature integral correlated best with the assessed volume of myocardial necrosis (r = 0.7). No significant arrhythmogenic or haemodynamic side-effects were observed. Macroscopic examination showed a central depression surrounded by a zone of homogeneous coagulation. Vaporization and crater formation up to a depth of 4 mm were observed following three radiofrequency discharges. In two of these cases, rapid changes and oscillation of catheter tip temperature were observed. Thus, monitoring of catheter tip temperature during radiofrequency energy application improves the prediction of lesion size. In addition, temperature monitoring might improve the safety of the procedure with respect to the risk of perforation.

Animals↗
PubMed1989

[Ion regulation disorders and cardiac arrhythmia. The relevance of sodium, potassium, calcium, and magnesium].

1. Among the dysionemias hyper- and hypokalemia are particularly important for clinical arrhythmogenesis. Disorders in sodium- and calcium concentrations, however, are relevant only in single cases. The impact of magnesium concentration disorders on cardiac rhythm is not yet totally elucidated. 2. In hypokalemia tachycardic arrhythmias are most important, while bradycardic and tachycardic arrhythmia can be caused by hyperkalemia. An important factor in arrhythmogenesis is the rate of development of hypo- or hyperkalemia. Hypokalemically-induced arrhythmia can be suppressed by potassium substitution. 3. Although the importance of a magnesium dysionemia for arrhythmogenesis has not been confirmed, magnesium can be used for the treatment of arrhythmias with good results. Besides an antiarrhythmic efficacy, an antifibrillatory activity is suggested in acute myocardial ischemia.

Animals↗
PubMed1989

Electrophysiologic, haemodynamic and antiarrhythmic effects of the new class Ic agent 1-(2'-biphenyloxy)-2-tert.-butylamino-propanol-2-hydrochloride.

The electrophysiological, antiarrhythmic and haemodynamic profile of the new compound GK 23-G (1-(2'-biphenyloxy)-2-tert.-butylamino-propanol-2-hydrochloride, proposed INN: bipranol) was examined using dogs models relevant to conditions in humans. In the first part of the study, dose-related effects of cumulatively increasing doses of GK 23-G (0.2-12.8 mg/kg) on intracardiac conduction, ventricular refractoriness and on haemodynamic parameters of the non-ischemic heart were determined in six anesthetized mongrel dogs. In the second part of the study, antiarrhythmic actions of bipranol on "delayed reperfusion ventricular arrhythmias" following release of coronary artery occlusion after 2 h of obstruction were investigated in another six dogs. The results show: GK 23-G causes a significant prolongation of HV-time, QRS-duration and ventricular refractory period at mid-range and high doses (greater than or equal to 3.2 mg/kg). QT-time does not change. Atrial refractory period is significantly lengthened at the maximum dose of 12.8 mg/kg. There are no significant changes in heart rate, systolic and diastolic aortic pressure and cardiac output. Up to 12.8 mg/kg, GK 23-G does not influence left ventricular contractility (dp/dtmax). In acute myocardial necrosis "delayed reperfusion arrhythmias" are almost completely abolished at a dose of 1.6 mg/kg + 50 micrograms/kg x min. Thus, because of its antiarrhythmic potency, further experimental and clinical testing of the new compound seems promising.

Animals↗
PubMed1989

[Anti-arrhythmia effects of calcium antagonists].

Calcium antagonists such as verapamil/diltiazem predominantly delay av-nodal conduction. Thus, the most important clinical indications for their application are the av-nodal-reentrant-tachycardia as well as the slowing of rapid ventricular response in intraatrial tachyarrhythmias. To reestablish sinus rhythm in atrial fibrillation, verapamil should be combined with chinidin. Usually, ventricular arrhythmias cannot be suppressed by calcium antagonists, but they may be indicated in exercise-induced ventricular arrhythmias and tachycardias arising from the right ventricular outflow tract. Verapamil/diltiazem are effective in ischemia-induced tachyarrhythmias, especially ventricular fibrillation, because of the reduction of ischemia-related conduction delay in the ischemic zone. The effectiveness of calcium antagonists in the secondary prevention of myocardial infarction can not yet be definitively defined.

Arrhythmias, Cardiac↗
PubMed1988

Termination of malignant ventricular tachycardias by use of an automatical defibrillator (AICD) in combination with an antitachycardial pacemaker.

We implanted an "Automatic Implantable Converter-Defibrillator" (AICD) and as far as useful an antitachycardial pacemaker (Intertach) in addition in 11 patients suffering from malignant ventricular tachycardias via a median sternotomy. In eight cases a coronary artery disease and in three cases a dilatative myopathy was the intrinsic disease. During surgery in all patients we attempted to trigger ventricular tachycardias and their termination by programmed stimulation. This procedure was successful in nine patients who received an antitachycardial pacemaker system. After the wounds healing, repeated induced ventricular tachycardias in all patients, who received a combination of the systems, could be terminated by the antitachycardial pacemaker prior to an intervention of the implanted defibrillator.

Cardiac Pacing, Artificial↗
PubMed1988

[Experimental and initial clinical experiences with the new class Ib anti-arrhythmia agent barucainide].

Barucainide is a new class Ib-antiarrhythmic compound which causes a reduction of the upstroke velocity and shortens the duration of the action potential in a dose-dependent fashion. The electrophysiological, hemodynamic and antiarrhythmic effects of the new drug were analyzed in experimental and clinical investigations. The results show that barucainide, in a dose range varying between 0.125-4.0 mg/kg i.v. fails to exert any significant effect on cardiac conduction and refractory times, heart rate, arterial blood pressure, cardiac output and left ventricular contractility. In a standardized animal model of ventricular arrhythmia, barucainide proved to be superior to lidocaine with respect to its antiarrhythmic potency. In a group of patients displaying chronic, otherwise therapy-resistant ventricular arrhythmias, the drug was effective in the majority of cases. Tolerance was excellent over a maximum observation period of 18 months. According to our first experimental and clinical observations, further testing of barucainide appears promising. The drug may be of particular value for treatment of ventricular arrhythmias in cases with left ventricular dysfunction, heart failure and severe conduction disturbances.

Adult↗
PubMed1988

[Results of thrombolytic therapy in acute myocardial infarct].

Acute thrombosis of highly stenosed coronary arteries often results in acute myocardial infarction. The rationale for thrombolytic therapy is to restore blood flow before irreversible myocardial cell damage develops. In this review the results of more than 60 interventional studies in which reperfusion or "patency" rates, left ventricular function, infarct size, as well as intrahospital and long-term mortality following thrombolytic therapy were assessed, are reported and analyzed with respect to the patterns of applying thrombolytic therapy (different thrombotic agents and percutaneous transluminal coronary angioplasty). The results show that a significant reduction in infarct size, improvement in left ventricular function, and decrease in early- as well as late-mortality can be achieved when successful recanalization is established within four hours after onset of symptoms. Thrombolytic efficacy with respect to patency rates is highest after intravenous application of so-called fibrin-selective thrombolytic agents (rt-PA) and APSAC (71% and 73%), intracoronary application of streptokinase (69%), and primary percutaneous transluminal coronary angioplasty (88%). By contrast, intravenous infusion of streptokinase results in recanalization of only 56% of occluded vessels. However, the improved reperfusion rates after treatment with rt-PA or intracoronary application of streptokinase are associated with a relatively high incidence of reocclusion (up to 20%). Patients' prognosis after successful initial thrombolysis is essentially influenced by additional interventions, e.g., percutaneous transluminal coronary angioplasty and surgical revascularisation. At present, several questions about the ideal thrombolytic agents or the optimal timing of additional interventions need to be clarified. Further studies are necessary to answer these questions.

Angioplasty, Balloon↗
PubMed1988

[Preventive antifibrillatory treatment of sudden cardiac death in acute myocardial infarct].

The pathophysiological basis of sudden cardiac death due to ventricular arrhythmias in acute myocardial infarction has been extensively investigated in experimental as well as in some clinical studies. Numerous clinical studies have been performed with the aim to establish the feasibility of antifibrillatory prophylaxis of sudden cardiac death by pretreatment with antiarrhythmic drugs. Using class I-antiarrhythmic drugs the reported findings were contradictory. While the antiarrhythmic efficacy of Lidocaine and other, newer class I-antiarrhythmic drugs is well established, the antifibrillatory effects of these drugs in the early phase of acute myocardial infarction remain uncertain. In clinical studies with the endpoint of mortality in patients at risk, longterm administration of orally effective class I-antiarrhythmic drugs did not prove to be superior to placebo. However, beta-sympatholytic agents have been shown to reduce mortality in patients at risk in several large clinical studies. The basic mechanism seems to be primarily a reduction in sudden cardiac death which is caused predominantly by ventricular fibrillation. The antifibrillatory properties of beta-blockers was demonstrated as well by a reduction in the number of episodes of ventricular fibrillation. The recognition of patients at risk who profit most from chronic beta-blocker therapy remains the main problem when treatment of numerous low-risk patients is avoided. In the ISIS I-study with Atenolol intravenous administration of a beta-blocker in the early phase of acute myocardial infarction has been shown to be beneficial if hemodynamic monitoring, for example using flow-directed heart catherization is performed. In general this does not apply to the treatment with calciumantagonists, especially with Verapamil and Nifedipine. These drugs do not improve prognosis of acute myocardial ischemia, obviously because of hemodynamic side effects. The antifibrillatory efficacy of Verapamil-type calciumantagonists, shown in the experimental model, could not be demonstrated in the clinical setting. Nevertheless, further clinical studies performing longterm prophylactic treatment of patients at risk before the onset of myocardial ischemia seem to be worthwhile. Concerning class III-antiarrhythmic agents, clinical experience in the setting of acute myocardial infarction is limited; hence a final conclusion about their antifibrillatory efficacy under clinical conditions at present is impossible.

Anti-Arrhythmia Agents↗
PubMed1988

[The incidence of ventricular arrhythmia following direct current ablation, high-frequency current ablation and laser photo-ablation].

Incidence and severity of ventricular arrhythmias (VA) following transvenous catheter ablation have so far not been fully elucidated. In the present study we evaluated the comparative incidence of postablation ventricular arrhythmias following high voltage-direct current electrical ablation (DCA), radiofrequency-ablation (RFA), and laser-photoablation (LPA). Experiments were performed on a total of 26 anesthetized mongrel dogs (BW: 20-30 kg). DCA (n = 14; 150-200 J) and RFA (n = 7; 38.5-72.5 J) were performed unipolarly via a 6F USCI catheter, LPA (n = 5; 40-80 J) was delivered through a quarz core fiber (diameter 0.4 mm) housed within a special designed catheter. Energies were delivered to various sites of free wall and apical endocardium of the left ventricle. Immediately after DCA fast runs of ventricular tachycardia (VT) developed in 13 out of 14 dogs degenerating into ventricular fibrillation in two animals. Mean cycle length of induced VT was 298 +/- 86 ms. Persistent VA, morphologically mainly characterized by an accelerated idioventricular rhythm interrupted by runs of ventricular salvoes, occurred in 12 animals (mean rate: 78 +/- 13 VPB/min 3 h after ablation). During VT early endocardial activations were recorded from the ablation site. No significant correlation between total applied energy (150-550 J) and incidence of arrhythmogenic effects was observed. RFA and LPA induced ventricular salvoes and runs of non-sustained ventricular tachycardia, in one animal ventricular fibrillation occurred during RFA; however, no persistent arrhythmic activity developed after RFA and LPA, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗