Biomedical subjects
Publications and source records attributed to M Tauchert.
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The possibility of maintaining preload reduction and enhancement of exercise tolerance during an interval treatment with 100 mg/day of slow-release isosorbide-5-mononitrate (IS-5-MN) was investigated in 12 patients (aged 57 +/- 5.0 years) with angiographically confirmed coronary artery disease and chronic stable angina pectoris. The effects of a single dose (acute test) were compared with those following an 8-day (chronic) regimen of mononitrate administration. Two hours after administration of 100 mg sustained-release IS-5-MN, mean resting pulmonary artery pressure (PAP), measured with a Swan-Ganz catheter, was reduced by 32% (p less than 0.001) and at submaximal exercise level (50 W, 3 min) by 37% (p less than 0.001). At individually highest comparable work loads mean PAP was reduced by 37% (p less than 0.001), and at maximal work load the PAP reduction was 14% (p less than 0.05). At the end of 1 week of therapy with sustained-release IS-5-MN a slight, clinically irrelevant reduction of hemodynamic effect was recorded. Work capacity increased after 1 h by 79% (264 +/- 154 vs. 472 +/- 180 W x min, p less than 0.01), still significantly above base-line 10 h after nitrate administration. No difference from baseline was demonstrable 24 h after medication. During interval therapy the improved work capacity was fully maintained (chronic, 1 h: 280 +/- 119 vs. 532 +/- 160 W x min, p less than 0.001). There was no significant difference between the plasma IS-5-MN levels at acute and chronic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary embolectomy as an emergent surgical treatment after massive pulmonary embolism often is necessary in cardiogenic shock (CS) and even without previous diagnostic. If complete dissolution of the thromboembolus is possible or spreading of microemboli may occur is unknown. Therefore we studied 21 patients surgically treated by embolectomy, ten of these with consecutive cardiogenic shock (CS) and twelve patients after repetitive microembolism and cava-blocking. Besides lung-functional parameters for special CO-diffusion capacity (DLCO), differentiated in membrane (DM) and vascular (VC) component (Roughton and Forster), we measured mean pulmonary artery pressure (PAP) at rest and at exercise. Patients after repetitive embolism showed considerably more diminution of DLCO (-31%) than those after single massive embolic event (-15%) even concomitant by CS (-10%). Repetitive microembolism lowered VC by 21%. Slight decrease of DM was found after CS. Mean pulmonary artery pressure was elevated at rest (26 mm Hg) and exercise (33 mm Hg) after repetitive microembolism and normal after massive embolism or CS. Pulmonary embolectomy may prevent disturbances of DLCO or PAP even after CS. Damage of vascular integrity (VC) was found after microembolism. Pulmonary embolectomy seems to remove total embolic material and therefore seems to be optimal.
The possibility of maintaining preload reduction and enhancement of exercise tolerance during an interval treatment with 50 mg/day of sustained-release isosorbide-5-nitrate (IS-5-N) was investigated in 13 patients (aged 54.4 +/- 7.9 years [mean +/- standard deviation]) with angiographically confirmed coronary artery disease and chronic stable angina pectoris. The effects of a single dose (acute test) were compared with those following an 8-day (chronic) regimen of mononitrate administration. Two hours after administration of 50-mg sustained-release IS-5-N, mean resting pulmonary arterial pressure (PAP), measured with a Swan-Ganz catheter, was reduced by 27% (p less than 0.01), and at submaximal exercise level (50 W, 3 minutes) by 34% (p less than 0.001). At individually highest comparable work loads mean PAP was reduced by 28% (p less than 0.01), and at maximal work load the PAP reduction was 21% (p less than 0.05). At the end of 1 week of therapy with sustained-release IS-5-N a slight, clinically irrelevant reduction of hemodynamic effects was recorded. Work capacity increased after 1 hour by 60% (408 +/- 104 vs 653 +/- 147 W x min, p less than 0.001)--still significantly above baseline 10 hours after nitrate administration. No difference from baseline was demonstrable 24 hours after medication. During interval therapy the improved work capacity was fully maintained (chronic, 1 hour: 417 +/- 93 vs 679 +/- 160 W x min, p less than 0.001). During interval therapy with sustained-release IS-5-N, hemodynamics and exercise tolerance were durably improved.(ABSTRACT TRUNCATED AT 250 WORDS)
Testing of the chronic therapeutic effects of antianginal drugs is commonly performed by stress electrocardiography. It is well known that this type of testing is easy to be disturbed by the influence of circadian rhythmus and placebo. However, by hemodynamic measurements such as the determination of pulmonary arterial pressure each patient can serve as his own control in therapeutic studies if the reproducibility of these parameters is acceptable. In 29 patients with coronary heart disease the reproducibility of the following parameters was tested at rest and during exercise and found to be acceptable: heart rate, mean arterial pressure, mean pulmonary arterial pressure, and working capacity. In additional studies the application of these parameters on the control of chronic therapy with antianginal drugs was performed. The results were: 1. A 1-week placebo treatment does not influence the parameters. 2. Long-term therapy with 3 x 20 mg of ISDN or IS-5-N daily over 4 weeks does not induce tolerance, whereas the dosage of 3 x 60 mg ISDN resp. 3 x 50 mg IS-5-N induces a remarkable degree of tolerance. 3. A 4-week therapy with 3 x 4 mg or 3 x 8 mg molsidomine daily resp. 4 mg or 8 mg molsidomine retard does not induce significant attenuation of the hemodynamic effects. 4. On a single-dose therapy with 50 mg IS-5-N retard ("interval-therapy") the therapeutic effects are maintained over at least 1 week.
Fluctuating mononitrate plasma levels in the course of 24 h are a prerequisite for prevention of nitrate tolerance in patients with angina pectoris undergoing longterm treatment. In 12 patients with angiographically proven coronary artery disease (54 +/- 7 years) effects of 50 mg Isosorbide-5-mononitrate (IS-5-MN) in a slow-release (SR) formulation on hemodynamics and exercise tolerance were evaluated after a first dose and at the end of a 1-week treatment period with 50 mg given once-daily. 1 and 2 h after medication mean pulmonary artery pressure (PAP) at rest was reduced by 30% (p less than 0.001) and 25% (p less than 0.01 respectively. During submaximal bicycle exercise (50 W, 3 min) PAP was significantly reduced by IS-5-MN by 35% (1 and 2 h after medication). At the end of exercise (discontinuation), drug-induced reductions of PAP were 19% (1 h) and 21% (2 h) (p less than 0.05), respectively. IS-5-MN led to a marked increase of exercise capacity (base-line: 396 +/- 119 W x min); 1 h: 646 +/- 153 W x min (p less than 0.01). At stress testing 2, 4 and 10 h post medication improvements were 67% (p less than 0.01), 49% (p less than 0.01) and 28% (p less than 0.01), respectively. 24 h after medication baseline values were reached again. After a 1-week treatment with 50 mg IS-5-MN SR daily, beneficial effects of the drug on hemodynamics and working capacity could be demonstrated. Again, significant effects could be shown up to 10 h after drug administration. Thus, IS-5-MN SR administered once daily proved effective in intermediate-term treatment of patients with coronary artery disease with regard to hemodynamics and exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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The optimal dose of nitrates is still controversial, as chronic usage of too high a dose may result in a decrease in vascular response. The dose should be determined to reduce preload acutely, and not to decrease the activity during chronic therapy. To determine this dose, 50 patients with angiographically confirmed coronary artery disease were studied. The effects on heart rate and mean systemic and pulmonary arterial pressures at rest and during exercise, and work capacity and duration were measured. The patients were classified into 5 groups, receiving placebo or isosorbide-5-mononitrate, 5, 10, 20 and 50 mg, respectively, as a single oral dose. Placebo had no effect on the measured parameters. All doses of isosorbide-5-mononitrate reduced mean pulmonary arterial pressure: 10 mg--by 16% at rest and 24% during exercise; 20 mg--24% and 34%, respectively (a near maximal effect); and 50 mg--27% and 38%. Similar results were found also for work capacity: 10 mg increased work capacity by 33%; 20 mg--79%; and 50 mg--56%. Thus, the therapeutically optimal single dose is about 20 mg. Higher doses produce no additional benefit and increase the risk for tolerance development.
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To test the clinically supposed development of tolerance during chronic molsidomine therapy we studied a total of 11 patients with angiographically-proven coronary heart disease at rest and during ergometric exercise (supine position; submaximal, i.e. 50 W for 3 min, and maximal exercise). Pulmonary arterial pressure (PAPmean, floating catheter), arterial blood pressure (RR, cuff method), work capacity (W x min) and duration of exercise loading (sec) were measured at rest and on exercise before and during chronic (4 weeks) oral therapy with 3 x 4 mg day-1 of molsidomine. Acute administration of 4 mg molsidomine reduced the mean arterial resting pressure by 12% and under submaximal exercise loading by 8%. After molsidomine, the PAPmean was reduced by 35% at rest; following a period of treatment of 4 weeks no significant decrease in efficacy could be discerned (PAPmean reduction by 31%). Under submaximal and maximal exercise the PAPmean dropped by 44% and 37%, respectively (35.5 +/- 6.7 cf. 19.9 +/- 4.5 mmHg; 39.2 +/- 6.5 cf. 24.8 +/- 7.0 mmHg), whilst simultaneously the work capacity increased by 93% (281 +/- 108 cf. 545 +/- 254 W x min). After 4 weeks treatment with 12 mg day-1 of molsidomine, the PAPmean of 22.4 +/- 6.6 mmHg and 30.1 +/- 9.9 mmHg under identical exercise loading conditions, remained significantly below the exercise load value prior to the onset of medication. The molsidomine-induced increase in the exercise tolerance was maintained throughout the long-term medication (537 +/- 268 W x min). With a four-week treatment with daily doses of molsidomine there was a persistent effect on the pulmonary arterial pressure and the work capacity. Thus development of tolerance during high dose, long-term molsidomine therapy is not to be expected.
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In twelve patients with coronary heart disease and hemodynamically significant coronary artery stenoses (LAD: 11, LAD plus RCA: 1) the effect of intracoronary nifedipine, 0.2 mg, on PTCA-related myocardial ischemia was evaluated. The severity of angina pectoris during balloon inflation was not significantly reduced by nifedipine, whereas the sum of ST segment alterations in Einthoven and Goldberger leads on inflation was significantly decreased by the drug. Before inflation intracoronary nifedipine lowered the systolic arterial blood pressure significantly, whereas diastolic and mean aortic pressure and heart rate remained unchanged. At the end of the inflation period heart rates were significantly faster after nifedipine, and the heart rate-blood pressure product higher with nifedipine. No significant correlations could be calculated between the extent of ST segment alterations and any of the hemodynamic parameters. From our results we conclude that, besides the possibility of ventricular afterload reduction, the beneficial cardioprotective effect of intracoronary nifedipine may mainly be attained by the local "cardioplegic" action of this substance.
Computed axial tomography (CAT) was used in 70 patients with diagnostic problems centering on the heart (47 patients) or the aorta (23). The method proved suitable for the diagnosis, differential diagnosis and serial control of pericardial effusions and also well demonstrated intracardiac tumours. Aortic aneurysms are also easily demonstrated and their extent can be exactly defined. But aortic wall dissection and stenosis of arteries arising from the aorta are not visualized and therefore require angiography.
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We are reporting a series of 13 out of a total of 16 patients in whom sinus nodal activity was recorded with the use of intra-atrial electrodes, during diagnostic His-bundle electrocardiography investigations. The protocol consisted of the simultaneous monitoring of the following intra-atrial points: high right atrium, low lateral right atrium, left atrium and the His-bundle electrogram (HBE), which accompanied the detecting sonde placed as a loop in the superior vena cava, with the electrodes facing the sinus nodal area. This permitted an adequate assessment of the sequence of the depolarizing activity. All patients showed sinus nodal potentials preceding the initiation of the P-wave in the surface-EKG or the atrial potential in the high right atrial lead, respectively, in the range of 60 to 270 msec depending upon the functional status of the sinus node in each patient. Such waves were clearly separated from the initiation of the atrial potential by an isoelectric line and showed functional traits compatible with the S-A nodal functions, as many authors have previously reported in experimental animal models. The text contains a review of the relevant literature and discussion upon the diagnostic significance of this method in the assessment of sinus nodal disease.
In 13 patients in the age range of 34 to 70 years (mean: 53 +/- 10 years), during diagnostic His-bundle investigations, registrations from the sinus nodal area were analyzed with a signal-averaging computer. In 12 patients we were able to get reproducible per-P-potentials with a sino-atrial conduction interval between 56 and 227 ms. The normal sequence of the excitation process from the atrium to the AV node together with the bundle of His and to the ventricles in all patients, and the reproducibility of the signal-averaged pre-P-potentials, which were well outlined from the atrial potential with a reasonable conduction interval, suggest that these signal-averaged pre-P-potentials reflect the sinus nodal activity rather than an ectopic focus. In 5 of 11 comparable cases there was a good correlation between the signal-averaged sino-atrial conduction intervals and those calculated with the extrastimulus technique. In 2 patients this correlation was moderate. The signal-averaging process may be impaired by coarse random noise, frequent atrial or ventricular extrasystoles, and by fluctuations of the baseline of the sinus nodal lead. The fact that the registrations are performed during normal undisturbed sinus rhythm offers a considerable advantage over the extrastimulus technique.
In ten patients with coronary heart disease molsidomine achieved a clear-cut decrease in pre- and after-load of the heart at rest. Due to decreased venous return at rest there was a fall in stroke volume resulting in a fall of systolic and diastolic aortic pressure. But at the same level of standardised exercise, systolic and diastolic arterial pressure and cardiac output were similar with or without molsidomine. Without changing after-load, there was a fall in pulmonary artery mean pressure (P less than 0.005), probably due to an increase in left-ventricular compliance and (or) a fall in pulmonary vascular resistance. A rise in venous capacity or a decrease in venous return during exercise was excluded as a possible mechanism of molsidomine action.