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Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 325 records · Page 18Linked to original sources
PubMed1990

[Acute myocardial uptake of lidocaine, mexiletine and amiodarone].

To assess acute myocardial uptake of antiarrhythmic drugs, we measured drug concentrations simultaneously in the aorta and in the coronary sinus during diagnostic cardiac catheterization. Measurements were taken 1, 2, 3, 4, 5, 7, and 10 minutes after intravenous bolus application of lidocaine (n = 10, 25 mg), mexiletine (n = 5, 25 mg and n = 10, 100 mg), or amiodarone (n = 10, 25 mg). Drug levels were measured by high-pressure liquid chromatography. Maximal concentrations were observed after 2-5 min. After 3-5 min coronary sinus levels exceeded aorta levels, indicating the end of net myocardial drug uptake. In contrast to lidocaine and amiodarone, no mexiletine was found in the coronary sinus 15 s after the end of drug application, obviously indicating a high myocardial drug content. Furthermore, the data provide an explanation for the acute efficacy of amiodarone. The myocardial uptake may result in various pharmacodynamic effects of antiarrhythmic drugs.

Amiodarone↗
PubMed1990

Silent myocardial ischemia: a special aspect of coronary artery disease.

Silent myocardial ischemia is a serious progressive disease which deserves continuous surveillance. It is characterized by painless ST-segment depression based on coronary artery disease. The mechanisms responsible for producing this condition do not differ from stable angina pectoris. The prognostic implications of silent ischemia are not yet completely clarified. However it could be argued that patients die--whether or not angina pectoris is present--because they develop myocardial infarction or ischemic ventricular arrhythmias. Complex ventricular arrhythmias seem to occur not at a higher rate than in patients with angina pectoris. On the other hand there is no doubt about a present arrhythmogenic potential of a silent myocardial ischemia, but there is so far no clinical evidence that the prognostic significance is different to symptomatic myocardial ischemia. In order to reduce or eliminate ischemic episodes intensive combination medical therapy should be used. If symptoms recur or ischemic changes are persistent, consideration should be given to revascularisation. Nevertheless, the optimal way of treating silent ischemia is still to be defined.

Angina Pectoris↗
PubMed1990

[Long-term follow-up of pacemaker therapy].

The use of pacemakers has been a major advance in the treatment of different forms of bradycardias and tachyarrhythmias. The main objectives for cardiac pacing in heart block are to improve the chances of survival and to prevent disabling symptoms, especially Stokes-Adams attacks. The long-term follow-up results of cardiac pacing are affected by different factors, in particular age and underlying heart disease; major technical aspects include pulse generator, lead and electrode longevity, and the pacing mode (VVI, atrioventricular sequential pacing, rate response stimulation, etc.). - Sinoatrial dysfunction is a relatively benign condition. Hence, pacing should probably not be adopted as a routine measure but should be reserved for patients with clinical (troublesome) symptoms. Based on earlier studies it can be concluded that patients with complete heart block and second degree atrioventricular block (Mobitz Type II) should be treated with pacemakers from the prognostic point of view. During chronic rate-responsive pacing improvement of exercise capacity can be expected in patients with sinus node disease and after His-bundle ablation. In patients with complete AV-block or bradycardia rate-responsive pacing can increase exercise tolerance and improve clinical symptoms as well. The automatic implantable cardioverter/defibrillator prevents sudden death over a long-term follow-up period in a high risk group of patients suffering from life-threatening ventricular tachyarrhythmias.

Arrhythmias, Cardiac↗
PubMed1990

New aspects of the clinical use of anti-arrhythmia agents with special reference to acute therapy of ventricular tachycardia (lidocaine vs. ajmaline).

Antiarrhythmic treatment is based on the hypothesis that ventricular premature beats (VPBs), in the presence of underlying cardiac disease and impaired ventricular function, may predispose to sudden cardiac death. The effectiveness of treatment, however, has not been proven. For acute treatment of paroxysmal ventricular tachycardia, on comparison of the effectiveness of lidocaine and ajmaline, some new aspects have been rendered. VENTRICULAR PREMATURE BEATS (VPB): Isolated VPBs can be found in 40 to 75% of healthy subjects; if their number is substantial, investigation is warranted. For VPBs with subjective symptoms, beta-receptor blockers or specific antiarrhythmic agents, if necessary in combination, may be given. In several studies it has been shown that the prognosis of patients with frequent and complex VPBs, that is couplets and salvos, without heart disease is not compromised. In one long-term study over an average of 6.5 years, sudden death was observed in only one of 70 subjects who had 566 VPBs/24 hours, 60% additionally couplets and 26% salvos in the Holter ECG. Accordingly, treatment for the sake of prognosis is not warranted. For patients with mitral valve prolapse or only mildly impaired ventricular function and asymptomatic arrhythmias, treatment is not necessary since it has not been shown to be beneficial. Coronary artery disease is the most frequent cause of ventricular arrhythmias and sudden death. In numerous studies in patients after myocardial infarction, a relationship has been recognized between frequent and complex VPBs and overall mortality as well as sudden death. Particularly at risk are patients with very frequent and complex VPBs with additional impairment of ejection fraction to less than 30 to 40% but this group only accounts for 10% of patients after infarction. Only in one interventional study, carried out with aprindine, there was a significant reduction in overall mortality from 12.5 to 7.8% with an adverse reaction rate, however, of 21%. In high-risk patients with a low ejection fraction and numerous, complex VPBs as well, in a further study with aprindine, after one year, there was no decrease in overall mortality as compared with the placebo group. The cause for the insufficient effectiveness of the antiarrhythmic agents in various interventional studies has been attributed to a limited number of patients, rigid dosing regimens, inadequate suppression of VPBs and a high incidence of adverse reactions. In the multicenter, randomized, placebo-controlled CAST study with newer substances, a total of 2309 patients with essentially asymptomatic VPBs at a rate of more than 6/hour and an ejection fraction less than 55% or 40% admitted more than 90 days after infarction, respectively, were followed from six days to two years after myocardial infarction to determine if the significant suppression of VPBs in patients with coronary artery disease with antiarrhythmic agents leads to a reduction in arrhythmia-associated deaths. Flecainide, encainide and moricizine led to a significant suppression of VPBs in 75% of the patients. After an average of ten months, the rate of arrhythmia-induced deaths of 4.5% in those treated with encainide or flecainide was significantly higher than the 1.2% observed in the placebo group. These results appear attributable to a proarrhythmic effect of the class IC drugs during long-term treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Ajmaline↗
PubMed1990

[Indications for pacemaker therapy in ophthalmoplegia plus and Kearns-Sayre syndrome].

Mitochondrial myopathies can affect the skeletal muscle, the central or peripheral nervous system, and they may be associated with chronic progressive external ophthalmoplegia (CPEO). In 7/29 patients with mitochondrial myopathies and CPEO a cardiac involvement (Kearns-Sayre syndrome) was found: incomplete right bundle branch block (n = 1), right bundle branch block (n = 1), left anterior fascicular block and right bundle branch block (n = 2), complete atrioventricular block (n = 3); congestive cardiac failure (ejection fraction 40%) (n = 2); 3/10 patients had prolonged infranodal conduction on His-bundle electrography (HV-interval 60 ms). The cardiac involvement in ophthalmoplegia plus is characterized by progressive impairment of fascicular conduction. The need for prophylactic pacemaker implantation appears to exist in patients with bifascicular block and prolonged His-ventricle conduction.

Adolescent↗
PubMed1990

[Computer-assisted contour detection in a complete heart cycle by levocardiography with adaptive raster tracking--validation of the method].

A method for computer-assisted edge detection in a full heart cycle of the left ventricular cineangiogram is presented. Left ventricular cineangiograms were acquired in the 30 degrees RAO position on cinefilms with 50 frames/s. A selected heart cycle was digitized with a spatial resolution of 512 x 512 pixels and a grey-value range from 0 to 255. In the first frame of the heart cycle a raster was calculated from contour points marked by an operator. The raster was automatically adapted to the left ventricular contour in the following frames. The contour points were determined on the adaptive raster by a gradient method. The automatic calculation of all contours of the systolic contraction was possible in 28 of 30 cineangiograms, operator interaction was necessary in two cineangiograms. The calculation of the diastolic contours requested operator interaction in 4 of 30 cineangiograms. The mean deviation of the calculated from the true contours ranged from -1.2 +/- 1.9 mm to 0.9 +/- 2.9 mm. The correlation coefficients between volumes calculated from the computer-determined and manually drawn contours ranged from r = 0.98 to r = 1.0 at beginning of systole, midsystole, endsystole, middiastole, and enddiastole with a standard error of the estimate between 2.8 ml and 5.2 ml. A repeated automatic determination of the contours after an independent remarking of the starting points resulted in a linear correlation of the calculated volumes with a correlation coefficient of r = 1.0 and a standard error of the estimate between 1.3 ml and 4.7 ml. The correlation coefficient for the ejection fraction was r = 0.99 with a standard error of the estimate of 1.9%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Role of antitachycardia devices in the treatment of ventricular tachyarrhythmias.

Chronic recurrent ventricular tachycardia (VT) can be terminated reproducibly by programmed endocardial right ventricular stimulation. However, antitachycardia pacing is associated with possible acceleration of VT, while frequent occurrence of VT and discomfort of the patient can limit treatment with an automatic implantable cardioverter/defibrillator (AICD; Cardiac Pacemakers Inc.). The combined use of antitachycardia pacing (Tachylog pacemaker; Siemens-Elema) and AICD was therefore evaluated in 6 of 35 patients (aged 50 to 70 years, mean 60.1 +/- 7.7) in whom AICD had been implanted because of VT, which could be terminated by temporary overdrive pacing. With the interactive mode of the Tachylog, termination of VT by the pacemaker as well as by the AICD was assessed after implantation. In the automatic mode, the Tachylog functioned as a bipolar ventricular inhibited (VVI) device with antitachycardia burst stimulation: 2 to 5 stimuli, interval 260 to 300 ms, 1 to 2 interventions. During follow-up of 32 +/- 17 months, the Tachylog terminated VT reliably 50 to 505 times per patient. When burst stimulation accelerated VT, termination was achieved by AICD discharge. Thus, drug-resistant VT can be terminated by antitachycardia pacing avoiding patient discomfort. In case of acceleration, VT can be controlled by the AICD. A universal pacemaker should combine antibradycardia and antitachycardia pacing with backup cardioversion/defibrillation mode.

Electric Countershock↗
PubMed1989

[Increased atrial natriuretic peptide in essential hypertension--relation to right atrial pressure behavior].

The role of atrial natriuretic peptide (ANP) in the pathogenesis of essential hypertension has not yet entirely been clarified. We investigated whether the increase of ANP in essential hypertension may be explained by elevated right atrial pressures and/or a different relationship between right atrial pressures and ANP secretion. Patients with stable essential hypertension undergoing right and left heart catheterization because of suspected coronary heart disease had significantly higher ANP levels than normotensives: 58.7 +/- 6.7 pg/ml in hypertensives versus 42.0 +/- 4.1 pg/ml in normotensives (p less than 0.01). Matching hypertensives with normotensives at identical levels of left ventricular enddiastolic pressure revealed significantly higher mean pulmonary artery pressures in hypertensives. Right atrial diastolic pressure (v-wave) after matching for LVEDP was 4.8 +/- 0.5 mm Hg in hypertensives and 3.1 +/- 0.2 mm Hg in normotensives (p less than 0.05). In addition, at any given mean right atrial pressure hypertensives showed higher ANP levels than normotensives. These results demonstrate that hypertensives exhibit raised pressures in the pulmonary artery independent of left ventricular pressure load. The elevation in right atrial pressures and the steeper relationship between these pressures and ANP are a suitable explanation for raised ANP levels in hypertension. ANP in essential hypertension may represent a counterregulation against elevated pulmonary resistance.

Adult↗
PubMed1989

[Captopril versus digoxin in the treatment of mild to moderately severe heart failure].

In a randomized and double-blind study of 116 patients with chronic heart failure (NYHA classes II or III) the effectiveness of captopril + hydrochlorothiazide (HCT) (group 1) and of digoxin + HCT (group 2) were compared. Treatment was effected for a 12-month period with a combination of 50 mg captopril (twice 25 mg daily, oral) and HCT, or 0.2 mg digoxin (twice 0.1 mg daily, oral) and HCT. In a pretreatment phase over 3-4 weeks the patients of group 1 were given an average HCT dose of 37.7 mg daily, whereas those of group 2 received 34.9 mg per day. At the end of the 12-month treatment period the patients in the captopril/HCT group had improved significantly more--by the criteria of echocardiographic intracardiac diameters, exercise tolerance and NYHA class--than those in the digoxin/HCT group. Change by a mean of one NYHA class had occurred in 61 patients (51.8%) of group 1 and in 47 (40.7%) of group 2 (P les than 0.01). These findings suggest that treatment of patients with mild to moderately severe chronic heart failure in sinus rhythm best be initiated with an angiotensin-converting enzyme inhibitor together with a diuretic rather than a digitalis-diuretic combination.

Blood Pressure↗
PubMed1989

Acute induction of sustained ventricular tachycardia: a new porcine model.

In this study we evaluated the possibility of initiating long-lasting ventricular tachycardias acutely, using isolated porcine hearts and thus avoiding an open-chest operation model. This set-up was designed especially to investigate defibrillating or antitachycardiac pacing devices, which terminate these malignant arrhythmias if medical treatment fails. The experiments were performed on 42 pigs, weighing 20-25 kg. After thoracotomy their hearts were removed and adapted to a Langendorff perfusion system. Supplied with their own blood, beating hearts were manipulated in three different ways: direct current impulses (4.5 V, 750 ms) or programmed ventricular stimulation, creation of a small myocardial infarction, and application of antiarrhythmic drugs (ajmalin, lidocaine, sotalol). Out of all possibilities the combination of ajmalin (mean concentration 0.041 micrograms/ml) and a small anteroapical myocardial infarction (3-6 cm2) along with direct current impulses (4.5 V), led to sustained ventricular tachycardias in the highest proportion (93%) of trials (P less than 0.001). The heart rate was 251 beats per minute on average. Lidocaine trials were less successful (53%), while programmed ventricular stimulation and sotalol failed to induce ventricular tachycardias. This study supports the evidence that the combination of ajmalin and a small myocardial infarction with direct current impulses is a reliable model for sustained ventricular tachycardias in isolated pig hearts. Although it is a rather artificial organ model, tachycardias can be induced acutely without any long-term pretreatment. Animal models based on chronic myocardial infarctions will therefore be unnecessary for the investigation of defibrillating systems and antitachycardiac pacing devices.

Animals↗
PubMed1989

Control of antiarrhythmic drug therapy by electrophysiologic testing.

Pioneering electrophysiological studies in the 1970s by Wellens and Josephson showed that in the majority of patients who have survived an episode of sustained ventricular tachycardia, the arrhythmia can be initiated and terminated by programmed electrical stimulation in the catheterization laboratory. Later work demonstrated that this method can also be applied to patients who have survived an episode of cardiac arrest due to ventricular fibrillation, not associated with acute myocardial infarction. As a consequence, serial electrophysiologic testing can be recommended to assess the efficacy of antiarrhythmic agents for the guidance of long-term treatment of these patients. This report focuses on some aspects of this method such as the recommended indications at present, differences in the electrophysiologic protocols among various authors, the results to be obtained by serial electrophysiologic testing, and finally discusses the question--not yet resolved--whether an improvement of outcome can thereby be achieved.

Anti-Arrhythmia Agents↗