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Biomedical subjects

M Gottwik

Publications and source records attributed to M Gottwik.

At least 55 records · Page 3Linked to original sources

[Measurement and analysis of monophasic action potentials using fractally coated electrodes--II].

The monophasic action potential (MAP) represents a summed signal formed by overlapping action potentials of myocardial cells close to the tip of the lead. Analysis of the MAP therefore provides detailed information about the electrophysiological effects of autonomous nervous and pharmacological influences on the myocardium, for example adrenergic or cholinergic stimulation of the heart. All known MAP recordings were obtained with Ag/AgCl electrodes, which, thanks to their low polarization properties, ensure reliable MAP measurement. Owing to their toxicity and inadequate long-term stability, however, Ag/AgCl electrodes cannot be implanted. With the aim of making MAP measurement available for implantable devices, fractally coated leads were therefore developed. The aim of the present study was to evaluate the in vivo measurement of fractally coated leads which are characterized by negligible polarization, low impedance over a wide frequency range, high biocompatibility and good long-term stability. In addition, as a result of their extremely high Helmholtz capacities (up to 50 mF/cm2), fractally coated leads permit stimulation and virtually undisturbed recording of MAP with the same pair of electrodes. For the evaluation of MAP measurements with fractally coated leads, a quadrupolar catheter enabling simultaneous MAP recordings with 2 Ag/AgCl electrodes and 2 fractally coated leads was devised. The stimulation pulses were always applied via the fractally coated leads. With both types of electrode, with spontaneous excitation and stimulation, the well-known MAP morphology, with amplitudes of between 10 and 25 mV in the ventricle, and between 5 and 10 mV in the atrium, was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Atropine↗

Intravenous recombinant tissue plasminogen activator (rt-PA) and urokinase in acute myocardial infarction: results of the German Activator Urokinase Study (GAUS).

The effects of recombinant tissue plasminogen activator (rt-PA) and urokinase on patency and early reocclusion of infarct-related coronary arteries were investigated in a single blind, randomized multicenter trial in 246 patients with acute myocardial infarction of less than 6 h duration. Both 70 mg of single chain rt-PA with an initial bolus of 10 mg and 3 million units of urokinase with an initial bolus of 1.5 million units were given intravenously over 90 min. The first angiographic study at the end of the infusion revealed a patent infarct-related artery (Thrombolysis in Myocardial Infarction trial [TIMI] grade 2 or 3) in 69.4% of 121 patients given rt-PA versus 65.8% of 117 patients given urokinase (p = NS). Among patients treated within 3 h from symptom onset a patent infarct-related artery was found in 63.9% of 72 patients given rt-PA versus 70% of 70 patients given urokinase (p = NS). There were five cardiac deaths in each group and one fatal intracranial hemorrhage in the rt-PA group. The in-hospital reinfarction rate was 8.9% versus 13.2% for patients treated with rt-PA and urokinase, respectively. There was no difference in left ventricular function at baseline and follow-up catheterization studies. Both drugs were well tolerated and there was no significant difference in cardiovascular or bleeding complications between the two groups. It is concluded that rt-PA and urokinase in the dosages used provide similar efficacy and safety in the treatment of acute myocardial infarction. Reocclusion during the first 24 h may be less frequent after urokinase treatment.

Adult↗

[Intravenous infusion of recombinant tissue-type plasminogen activator (rt-PA) and urokinase in acute myocardial infarct: intermediate results of the G.A.U.S. study (German Activator Urokinase Study)].

The effects of recombinant tissue plasminogen activator (rt-PA) and urokinase on patency and early reocclusion of infarct-related coronary arteries were investigated in a single blind, randomised multicenter trial in up to now 125 patients with acute myocardial infarction of less than six hours duration. Both, 70 mg of single-chain rt-PA with an initial bolus of 10 mg, and 3 million U of urokinase with an initial bolus of 1,5 million U were given intravenously over 90 minutes. The first angiogram at the end of the infusion revealed a patent infarct-related artery (TIMI grade 2 or 3) in 68% of 62 patients with rt-PA vs. 63% of 63 patients with urokinase (n.s.). Twenty-four hours later patent infarct-related arteries occurred in the same frequency in the rt-PA group and in the urokinase group (71.5% vs. 74.6%, n.s.), although additional recanalisation procedures in sequence with the first angiography were performed more frequent in the rt-PA group. There were two cardiac deaths in either group. In-hospital reinfarction rate was 9.7% vs. 17.5% for patients treated with rt-PA and urokinase, respectively. Both drugs were well tolerated, no significant difference of cardiovascular or bleeding complications could be observed between the two groups. It is concluded that rt-PA and urokinase in the dosages used provide similar efficiency and safety in the treatment of acute myocardial infarction.

Adult↗

Delay of development of transmural irreversible ischaemic injury in canine myocardium.

During the course of experimentally induced myocardial ischaemia affected tissue initially suffers reversible ischaemic injury or, if ischaemia persists, injury of increasing severity before becoming irreversibly damaged. This state is characterized by tissue necrosis and referred to as myocardial infarction. The purpose of this study was to investigate whether it is possible to delay or perhaps even prevent the development of irreversible ischaemic injury. Ischaemia was induced by coronary artery occlusion (CAO) in canine hearts for 90 min or 24 h. The drug used for intervention was hyaluronidase. Ischaemic damage was assessed by p-NBT staining and ultrastructural evaluation of tissue biopsies. Development of irreversible ischaemic damage was prevented during 90 min of CAO. However, progression of reversible to irreversible ischaemic injury could not be prevented during 24 h of CAO. In conclusion, it is possible to prevent the development of irreversible ischaemic injury by a suitable intervention during the early stages of ischaemia in the canine heart and thus to gain time for additional intervention in the early treatment of myocardial infarction.

Animals↗

[Mechanically-induced intraventricular block caused by a right-heart floating catheter--frequency and electrophysiologic findings].

During the course of 2,434 right heart catheterizations with 2,019 floating 3F Grandjean catheters and 415 5F Swan-Ganz catheters we observed 7 patients (0.3%) with catheter-induced infranodal conduction impairment: right bundle branch block (RBBB) in 3 patients, left anterior fascicular block (LAFB) and subsequent RBBB in 1 patient, and complete heart block in 3 patients with pre-existing left bundle branch block (LBBB). There was no apparent difference regarding the incidence of blocks between the two types of catheters. Three patients (one with LAFB + RBBB and two with LBBB) underwent electrophysiologic studies. All three patients exhibited a prolongation of the HV-interval due to coexisting pathologic changes of the right bundle. LBBB patterns disappeared during distal His bundle pacing in two patients, indicating a proximal site of block and suggesting incomplete involvement of the right bundle. Additional mechanical trauma, probably in this region, produced the blocks. Thus, use of balloon tipped or flexible catheters does not provide complete protection against transient lesions of the conduction system.

Adult↗

[Complete revascularization surgery in patients with coronary disease with severely reduced left ventricular function. Discrepancies in the evaluation of results].

Clinical data, function and compliance of left ventricle as well as regional wall motion were analysed in 17 patients with preoperatively limited left-ventricular function and signs of myocardial ischaemia after complete revascularisation surgery. Recatheterisation after 5.2 months on average after surgery showed improvement by one NYHA class, an increase of mean left-ventricular enddiastolic pressure, which was interpreted as "improved status of ischaemia", a decrease of left-ventricular compliance by 30%, of enddiastolic volume by 14% and of endsystolic volume by 20% (P less than 0.05). Loss of function occurred in 3 out of 92 bypasses. Up to the time of reporting, 22.4 months postoperatively, all patients have survived in a relatively satisfactory clinical state. All parameters of left-ventricular function as well as regional wall motion showed a tendency for improvement after surgery in the majority of patients. However, pre- and postoperative mean values were not significantly different (P greater than 0.05). Thus, despite clearcut improvement of clinical state and "ischaemia index", improvement of left-ventricular function and regional wall motion are not consistently demonstrable. The reasons of this discrepancy cannot be ascertained by this investigation. The quality of the surgical intervention and the sensitivity of parameter assessment cannot be held responsible.

Blood Pressure↗

Effects of AR-L 115 BS (Sulmazol), a new cardiotonic agent, in coronary artery disease: improved ventricular wall motion, increased pump function and abolition of pacing-induced ischemia.

AR-L 115 BS (Sulmazol) is a new noncatechol, nonglycosidic cardiotonic agent. In 17 patients with significant coronary artery disease, the influence of AR-L 115 BS on hemodynamics and regional wall motion was investigated under the following conditions: 1) control, 2) the immediate postpacing period without medication, and 3) the postpacing period under the peak influence of AR-L 115 BS, 2 mg/kg intravenously. During the postpacing phase without medication, all patients developed ischemia (angina, ST segment alterations, increase of mean left ventricular end-diastolic pressure from 13 to 30 mm Hg), left ventricular pump function diminished and overall regional wall motion showed a tendency to decrease (p greater than 0.05). However, during the postpacing period with AR-L 115 BS medication, ischemia was abolished (no angina; mean left ventricular end-diastolic pressure decreased to 13 mm Hg; hemodynamic variables returned to control levels and left ventricular pump function showed some improvement while overall regional wall motion showed tendencies to improve. A comparison of alterations of hemodynamics and regional wall motion during the postpacing phase without medication with those under the influence of AR-L 115 BS shows that overall left ventricular pump function and regional wall motion improved while angina and an increase in left ventricular end-diastolic pressure were prevented. It is concluded that AR-L 115 BS improves left ventricular pump function and regional wall motion in coronary artery disease without inducing ischemia, probably by means of a reduction in extravascular resistance.

Angina Pectoris↗

[Efficacy of nicorandil (SG-75), a substance with nitro-properties and long-term effects in coronary patients: improvement of LV-function and wall motility without pacing-induced myocardial ischemia].

Following trials in Japan, Nicorandil (SG-75) has been introduced as a new antianginal drug with coronary dilatory properties. The effects of 20 mg SG-75 administered sublingually were studied in 9 patients with coronary artery disease and reproducible pacing-induced myocardial ischemia (MIS) (rise in left ventricular enddiastolic pressure, changes in ST-segment, and angina). Changes in heart rate, arterial pressure and angiographic left ventricular ejection parameters, contractility, parameters derived from left ventricular function (ejection fraction, cardiac index, stroke work index) and cardiac work (left ventricular stroke work index, left ventricular work), myocardial oxygen consumption, cardiac efficiency (LVeff), and regional wall motion (RWM) were investigated for the following hemodynamic phases: 7th and 14th minute after SG-75, the immediate postpacing phase without medication (PPP), and the postpacing phase under the influence of SG-75 (PPP + SG). In the 7th and 14th minute after SG-75 and in the absence of stress, there was no variation from control values (p less than 0.05). In the 15th and 16th minute after SG-75 (serum-level control), under pacing stress equivalent to that measured in the PPP, the MIS observed in the absence of medication did not now occur. Moreover, in the PPP + SG-75 phase the following mean parameter changes were noted: ejection fraction +21%, cardiac index +37%, left ventricular stroke work index +48%, left ventricular work +52%, and LVeff +60%; RWM also improved. Prophylaxis of ischemia and improved hemodynamics under the influence of SG-75 were probably due to a decrease in preload (left ventricular enddiastolic pressure -41%) and afterload (stroke volume ratio -29%). Similar changes might have been expected after nitroglycerin, if given under equivalent conditions. Since no harmful effects, either subjective or objective, were apparent during or after application of SG-75, this seems to be a promising drug for the antianginal therapy of the future.

Aged↗

[Mechanism and effects of the cardiotonic AR-L 115 BS in coronary heart disease: improved ventricular function and regional wall motility without angina pectoris].

UNLABELLED: The use of new cardiotonic drugs, such as AR-L 115 BS (ARL), in patients with coronary artery disease (CAD) might be limited by their aggravating myocardial ischemia (MIS). Accordingly, we investigated ARL's (2 mg/kg BW i.v.) hemodynamics, myocardial oxygen consumption (MVO2) and regional wall motion (RWM) in 30 patients with CAD presenting with pacing-induced MIS (angina, rise of LVEDP, lactate production). ARL improved LV-pump function in 13 group-1 patients (average increases: cardiac index by +25%; LV-work by +17%; dp/dtmax by +30%; coronary sinus flow by +39%), while there was a decrease in preload (LVEDP by -44%) and afterload (AOMP by -9%) and cardiac efficiency by -25%. Such ARL-effects required a rise of MVO2 by +41% but did not induce MIS. These beneficial results were corroborated by significant hemodynamic improvements also in 17 group-2 patients when comparing the non-medicated immediate post-pacing period (PPP) with MIS versus the ARL-medicated PPP (= PPP + ARL) without MIS, where RWM improved by an overall average of 26 +/- 11% in the phase PPP + ARL. CONCLUSION: In CAD ARL improves hemodynamics and RWM. The mechanism is pre- and afterload reduction, increase in contractility, MVO2 and CSF without MIS being induced.

Cardiotonic Agents↗

Hemodynamic properties of St. Jude medical and Björk-Shiley valvular prostheses in mitral position in the pulse duplicator.

A general lack of standardization of the pre-clinical testing of artificial valves leads to an actual comparison of different prosthetic models at the time of a first clinical trial, frequently with contradictory results. Therefore, a pulse duplicator was developed in order to compare different valves of comparable size under identical standardized conditions in aortic and mitral positions. Comparison of Björk-Shiley and St. Jude medical prostheses in the duplicator revealed a linear relationship between pump setting and stroke volume delivered (r less than or equal to 0.9) for both valves. Pressure loss across the mitral valves showed a linear relationship to stroke volume (less than or equal to 0.9) and frequency (less than or equal to 0.9). The gradient, expressed per milliliter stroke volume, for identical frequencies appeared as the simplest and most suitable parameter for comparison of the hydraulic function of different valves. Using this parameter, the valves showed individual differences over a wide physiological range of testing. The differences, however, are of a magnitude that can hardly be detected under clinical testing conditions.

Aortic Valve↗

The importance of the collateral circulation for myocardial survival.

In acute coronary occlusion the survival time of ischemic myocardium depends critically upon collateral blood flow and on oxygen uptake at the moment of, and during, occlusion. There are good reasons to believe that ischemic myocardium provides the stimulus for near-maximal vasodilation of collateral blood vessels. Under these conditions the determinants of collateral blood flow are: a) the anatomically fixed hydraulic resistance of the collaterals proper, b) the arterial driving pressure, c) extravascular resistance (radial stress, pressure transmission across the LV wall, tissue pressure) and d) size of the ischemic bed. Under ideal conditions (maximal dilation of collaterals) overall collateral resistance is 3.5 resistance units, i.e. theoretically a perfusion pressure of 350 mmHg is needed to drive 100 ml of blood per minute through 100 g of tissue. Small ischemic beds receive a relatively larger amount of collateral flow and vice versa. This delays necrosis (but does not prevent it) following occlusion of small coronary arteries. The reason for this is the more favorable ratio of epicardial circumference (of the ischemic area) to ischemic volume because canine collaterals are exclusively located on the epicardial surface.-Tissue pressure in acute occlusion is distributed in such a way that subendocardial collateral flow is lower than subepicardial flow. This leads to an earlier onset of irreversible damage in the subendocardium, earlier damage to subendocardial microvessels, i.e. earlier subendocardial no-reflow phenomenon. Flow "offered" to but not "taken" by the subendocardium is at the disposal of the subepicardium which thereby increases its chances of survival. As a rule subendocardial flow decreases as a function of time after occlusion and subepicardial flow increases. In certain cases even subepicardial flow is too low shortly after occlusion. In this case it decreases further with time and a truly transmural infarct develops.

Animals↗

Hemodynamics alterations induced by isoproterenol and pacing after aortic valve replacement with the Björk-Shiley or St. Jude medical prosthesis.

Stress evaluation was carried out in 26 patients approximately 7 months after aortic valve replacement with Björk-Shiley valves (13 patients) and St. Jude medical valves (13 patients). During isoproterenol infusion (0.3 micrograms/kg/min), cardiac output increased by a factor of 1.5 and aortic valve area decreased by 50% for both valve groups, while transvalvular gradients (rest: 7 +/- 2 vs 10 +/- 5 mm Hg, p greater than 0.05) increased by 42 +/- 18 vs 51 +/- 18 mm Hg (p greater than 0.05), i.e., to levels of moderate aortic stenosis. However, during pacing stress these values progressively decreased with rising heart rates. In other postoperative evaluations that included ergometric stress with isoproterenol and pacing, induced hemodynamic changes after aortic valve replacement were predictable and consistent with regard to both direction and magnitude, and they differed characteristically according to the type of stress used. We conclude that no functional differences between Björk-Shiley and St. Jude medical valves can be claimed. Standardized evaluation with isoproterenol is a sensitive stress test of prosthetic valvular hemodynamics. Because of the apparent magnification of residual obstruction after aortic valve replacement, it has advantages over pacing.

Aortic Valve↗

[Echo parameters of chronic aortic regurgitation (author's transl)].

Staging and timing of aortic-valve replacement, with respect to long-term prognosis is crucial in patients with isolated chronic aortic regurgitation (AR). To compare angiographic and M-mode echocardiographic parameters we echoed 39 patients one day before cardiac catheterisation: The angiography was used to divide the collective into four grades (G I-G IV). End-diastolic volume (EDV), stroke volume (SV) and regurgitant volume (RV) were used as echo parameters of the left ventricular volume, ejection fraction (EF) and circumferential fiber shortening (VCF) as parameters of left ventricular function. AR of G II and G III could be differentiated by an increase of EDV from 145 +/- 28.2 to 304 +/- 33.5 ml (p < 0.001), whereas EDV in G I-G II were similar to normal and G IV was similar to G III. EF and VCF were able to differentiate G III and G IV by a decrease from 67 +/- 8% to 54 +/- 7% (p < 0.001) and 1.01 +/- 0.24 to 0.88 +/- 0.31 (p < 0.01) respectively. Thus echo measurements predicted AR greater than G II from an increase of the EDV by more than 110% and a regurgitant volume of more than 3 1/min. G III and G IV could be differentiated by EF und VCF. These quantitative echo parameters were highly sensitive (92%) and specific (96%) whereas all other M-mode echo signs (oscillations of the mitral valve leaflet and interventricular septum, amplitude of oscillations, aortic root diameter, diastolic separation of the cusps) could be used only as qualitative indices, some with high specificity. Echocardiography allows a non-invasive assessment of the severity of AR based on parameters of left ventricular volume and function and thereby assist the accurate timing of aortic valve replacement.

Adult↗

Recovery of the heart after normothermic ischemia. Part II: Myocardial function during postischemic reperfusion.

Contraction and relaxation of the canine myocardium were examined during normothermic ischemia in an isolated heart model. Decrease in the development of tension depends on the duration of ischemia. Deficient functional recovery was observed after ischemic periods extending beyond 30 minutes, in spite of reperfusion periods of over 1 hour. A decrease in compliance was observed during the anoxic period, but a persistent defect of relaxation occurred only after 60 minutes of ischemia. After this period there was also a disturbance in the autoregulative mechanisms of coronary perfusion and an uncoupling of O2-consumption and mechanical efficiency. A prolonged reperfusion period of the heart beating empty allowed ultrastructural recovery of the damaged myocardium. In contrast, functional recovery of the myocardium, as determined by several parameters of contraction and relaxation, did not correlate with ultrastructural recovery and was not improved by prolonged reperfusion.

Animals↗