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Biomedical subjects

M Gottwik

Publications and source records attributed to M Gottwik.

69 records · Page 4Linked to original sources
PubMed1982

[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↗
PubMed1981

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↗
PubMed1981

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↗
PubMed1981

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↗
PubMed1980

[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↗
PubMed1979

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↗
PubMedDate not supplied

Development of collaterals. Application of external subcritical fixed constrictors in a canine model.

A canine model for a standardized induction of collaterals is presented with a fixed external constrictor that is not designed to induce an occlusion of the coronary artery and at least over the timespan of 6 weeks does not impair perfusion under resting conditions in the myocardium-at-risk. The coronary constriction was standardized by a reduction of the postocclusive reactive hyperemia of 50%. Flow measurements were performed by flowmeter and by radioactive microspheres acutely and after an interval of 6 weeks of constriction. The results showed an increase of the collateral flow from 21.2 +/- 11.8 ml/100 g/min-1 to 42.8 +/- 16.2 ml/100 g/min-1 (p less than 0.05). The regional perfusion exhibited a transmyocardial gradient in favour of the subepicardial layers with 49.3 +/- 25 ml/100 g/min-1 as compared to 33.1 +/- 17.3 ml/100 g/min-1 (p less than 0.05) of the endocardial layers. Reactive hyperemia, as determined by flowmeter, was decreased by 21% after 6 weeks on account of slow progression of the coronary constriction due to intimal reactions, whereas reactive hyperemia, as determined by the microsphere method, increased by 9% due to additional collateral channels.

Animals↗
PubMedDate not supplied

The relationship between the perfusion deficit, infarct size and time after experimental coronary artery occlusion.

It is well known that coronary occlusions of short duration do not produce infarcts in the dog heart, but permanent occlusions always do. The aim of this paper was to investigate with quantitative direct measurements the determinants of infarct size within these two extremes. We measured left ventricular MV2, coronary and collateral blood flow and infarct size after occlusion times varying between 45 minutes and 24 hours. MVO2 was kept low in one group by establishing low heart rates with a synthetic opiate. In another group, MV2 was kept elevated by giving synthetic catecholamines (dobutamine) that stimulated contractility and heart rate. Under the described experimental conditions LV-coronary blood flow reflected the true demand for blood and oxygen. The ratio of collateral blood flow over coronary blood flow (both measured with tracer microspheres) was therefore a good approximation of the supply-demand ratio (SD). Since collateral flow was inhomogeneously distributed across the left ventricular wall, the SD-ratio showed similar variations. As the collateral blood flow increased with elapsed time after coronary occlusion, the SD-ratio improved. Since high LV-O2-demand increased coronary flow but exerted practically no influence on collateral flow, this situation influenced the SD-ratio in a negative way. Decreased O2-demand had the opposite effect. The SD-ratio is thus a valid expression of the relative and absolute blood flow deficit as influenced by the local and general O2-demand. We found significant and characteristic correlations between the SD-ratio and infarct which was only influenced by time. A blood flow deficit of 90% (i.e., collateral flow = 10% of required flow) produced a 50%-infarct (relative to the risk-region) with a 45-min occlusion but a 90%-infarct with occlusion times of 3 hrs and longer. If the perfusion deficit is only 0.5 (collateral flow = 50% of required flow), no infarct is detectable at occlusion times shorter than 3 hrs. Small perfusion deficits of only 20% below required flow caused infarctions at 24 hrs and longer. In the group where the SD-ratio was closer to unity because of a low overall LV-O2-consumption (bradycardia), infarcts at t = 24 hrs were significantly smaller than in the group with a high LV-MVO2.

Animals↗
PubMedDate not supplied

Experimental myocardial infarction in a closed-chest canine model. Observations of temporal and spatial evolution over 24 hours.

Myocardial infarction was induced in 7 mongrel dogs by transfemoral intraluminal occlusion of the left anterior descending coronary artery. Perfusion area at risk was determined by post-mortem coronarography and infarct size by macrohistological staining with para-nitrophenoltetrazolium. Regional flow was determined by injection of radioactive microspheres 0.2 hours, 12 hours, and 24 hours post occlusion. Infarct size as determined by planimetry of post-mortem angiograms and macrohistological stains at identical magnification revealed 74.5 +/- 12.1% infarcted tissue of the perfusion area at risk. The flow of the necrotic tissue was below 13 Ml/100 g min without exception, indicating a threshold perfusion for maintenance of myocardial viability. Accordingly, a flow of less than or equal to 10 ml/100 g min identified 93% of the entire infarcted myocardium, resulting in 71 +/0 20% as compared to the perfusion area at risk. Based on the good agreement of macrohistological and flow data, the evolution of myocardial injury was determined by flow measurements. The results indicated a different progression of the borders of critical flow in the subendocardial and subepicardial layers, whereas in the subendocardium 85% of the tissue at risk was identified by the critical flow at 0.2 hours and 97% at 12 hours, the subepicardial flow changed at a different pace: only 53% showed subcritical perfusion at 0.2 hours, 61% at 12 hours with a final increase of 39% from 12 to 24 hours.

Animals↗
PubMedDate not supplied

Heart valve replacement with the new all-pyrolytic bi-leaflet St. Jude medical prosthesis.

Since February 1978, seventy-nine St. Jude medical prostheses have been implanted in seventy-two patients with an overall mortality of 8.5%. Clinical, hemodynamic and hematological findings are presented. Twenty-two patients have been catheterized postoperatively, and findings are presented. In vitro comparisons have made between the St. Jude and other prostheses.

Adolescent↗