Biomedical subjects
Publications and source records attributed to H Bahawar.
In implantable cardioverter-defibrillator therapy with endocardial lead systems, certain clinical variables are associated with defibrillation energy requirements. Because of the weak correlation coefficients, these variables cannot predict defibrillation thresholds in individual patients.
Antiarrhythmic drug effects may include cardiodepression. This risk is theoretically well recognized but clinically rather poorly defined. To evaluate the risks of ajmaline treatment, we monitored hemodynamic parameters and end-systolic pressure-volume relations (ES-PVR) to evaluate potential negative inotropic effects. Twelve patients (nonischemic CAD) underwent hemodynamic analysis with and without the influence of ajmaline, 1 mg/kg i.v., both (a) at rest (paced constant heart rate of 90 beats/min) and (b) during tachycardia of 160 beats/min. With ajmaline, LV pump function was found to have diminished moderately; ejection fraction by 23 and 10%, stroke volume by 10 and 0%, cardiac work by 5 and 16%, and dP/dtmax by 14 and 19%, respectively. While preload increased under the influence of ajmaline (LVEDP by 17 and 30%, respectively), the LV volumes increased (EDV by 18 and 12%, and ESV by 58 and 21%, respectively), and afterload remained unchanged. Ajmaline caused the loops of the ESPVR to move rightward and the slope k to decrease, thus indicating loss of inotropy under the influence of the antiarrhythmic agent. In essence, ajmaline's negative inotropic components were defined by the conductance technique, but they failed to induce clinically relevant cardiodepression in the above NYHA class II patients. This technique proved to be sensitive, useful, and safe in the assessment of inotropic effects by analyzing the ESPVR within the routine of the catheterization laboratory.
To evaluate cardiodepressive risks of antiarrhythmic treatment with ajmaline, we monitored, in addition to conventional hemodynamic parameters, end systolic pressure-volume relations (ESPVR) to assess potential negative inotropic effects. Twelve patients (CAD without ischemia; EF = 60 +/- 3%) underwent hemodynamic analysis with and without the influence of ajmaline (1 mg/kg, i.v.) both 1) at rest (paced heart rate of 90 bpm) and 2) during tachycardia of 160 bpm. As a result, LV-pump function was found to have diminished moderately: EF by 23% vs 10%, respectively; stroke volume by 10% vs 0%; cardiac work by 5% vs 16%, and dP/dtmax by 14% vs 19%. While preload increased under the influence of ajmaline (LVEDP by 17% vs 30%), the LV-volumes increased (EDV by 18% vs 12%; ESV by 58% vs 21%), afterload remained unchanged. Ajmaline caused the loops of the ESPVR to move rightward and the slope k of the ESPVR to decrease, thus indicating loss of inotropy during the influence of the antiarrhythmic agent. Thus, ajmaline showed a tendency to generate cardiodepressive effects in patients with normal LV-function, and to depress contractility in single cases that clinically had no consequences. The conductance technique proved useful and safe in the assessment of inotropic drug effects by analyzing the ESPVR within the catheterization laboratory routine.
To evaluate the risk of ischemia in 17 patients with significant coronary artery disease, the influence of enoximone was analyzed under the following conditions: (1) at rest (RC) and during exercise (ExC) under control conditions and (2) at rest (RE) and during exercise (ExE) after administration of enoximone (0.75 mg/kg, intravenously). During ExC all patients had ischemia (angina, and ST segment alterations); metabolic markers of ischemia (MMI) increased, as did the mean pulmonary artery pressure, from 19 to 41 mm Hg. However, during ExE ischemia was abolished (no angina, decrease in mean pulmonary artery pressure to 24 mm Hg, and improvement in MMI) and there was some improvement in left ventricular pump function, whereas pre- and afterload decreased (pulmonary artery pressure by 40%, systemic vascular resistance by 10%), and heart rate, arterial pressure, and myocardial oxygen consumption (MVO2) were all unchanged (p greater than 0.05). Comparative hemodynamics at RE vs RC showed a decrease in pulmonary artery pressure (by 25%) and pulmonary vascular resistance (by 19%) and an increase in heart rate (by 11%), whereas arterial pressure and MVO2 were unchanged (p greater than 0.05). Enoximone did not induce changes in plasma catecholamine, prostaglandin, or thromboxane levels (p greater than 0.05), whereas the atrial natriuretic factor decreased (by 15%), probably because of unloading of the atria during exercise. We concluded that enoximone induces beneficial hemodynamic effects in coronary artery disease without causing ischemia, probably by enhancing myocardial contractility, vasodilation, and improved diastolic properties.
TA-064 is a new cardiotonic agent which is also effective orally, according to investigations conducted in Japan. We analyzed computer-assisted alterations of pressure-volume relationships serially and of indirect myocardial oxygen consumption (MVO2) estimations on line during TA-064 influence in 16 patients with congestive cardiomyopathy: left ventricular function was moderately decreased in seven patients (group A) and drastically decreased in nine (group B). Results showed that TA-064, 8 micrograms/kg/min intravenously, exerted positive inotropic effects in both groups and induced mean maximal delta percentage changes at about 5 minutes of infusion as follows: left ventricular stroke work index +65% and +47%; dP/dtmax +61% and 59%; left ventricular efficiency +62% and 53%; MVO2 +31% and +11% (p less than 0.05). TA-064, 20 mg by mouth induced serum levels (group A = 23.8 +/- 12ng/ml and group B = 26.4 +/- 20 ng/ml) corresponding to the effects with dosages of 1 to 2 ng/kg/min intravenously (p greater than 0.05), thus implying that significant changes in left ventricular function require higher oral dosages. We conclude that TA-064 improves left ventricular function, primarily via a contractility increase, also in group B patients without toxic side effects. On-line indirect MVO2 assessment and analysis of serial pressure-volume relationships helped to provide a more complex definition of the mechanism and efficiency of the cardiotonic agent under study.
Using a dynamic and symmetrical cardiac phantom different echocardiographic mathematical models (Simpson 7 slices, area-length method, Simpson 2 slices and method according to Teichholz) were compared. 9 different end-diastolic (EDV) and end-systolic (ESV) volumes, 9 different stroke volumes (SV) and ejection fractions (EF) were used. EDV and ESV varied between 39-298 ml; SV between 29-100 ml and EF between 14-46%. In addition 10 fixed volumes of the same shape were evaluated using the same echocardiographic mathematical models. While symmetrical fixed volumes can be assessed correctly (r = 0.97-0.98), apart from the formula according to Teichholz (r = 0.89, significant underestimation of volumes), the correlation coefficients decrease using a dynamic cardiac phantom. In the modification of Simpson with 7 slices the best correlation was found for all parameters (EDV: r = 0.93; ESV: r = 0.94; EF: r = 0.87; SV: r = 0.81). The biplane area-length method has no advantages over Simpson's rule with 2 slices in the short axis; for symmetrical models both methods are comparable, both having high correlation coefficients (for volumes r = 0.85 and r = 0.88; for EF 0.78 and 0.84). Using the method according to Teichholz symmetrical volumes can be well assessed (r = 0.90), for the determination of EF the correlation coefficient decreases to r = 0.65 and for stroke volume to 0.33, reflecting no significant correlation to the actual SV. Possible causes for a poorer correlation are discussed for moving objects as opposed to the fixed volumes.
UNLABELLED: According to investigations conducted in Japan, TA-064 is a new cardiotonic agent, which is also effective orally. We analyzed computer-assisted alterations of pressure-volume relations serially and of MVO2 online (Bretschneider) during TA-064 influence in 16 patients with congestive cardiomyopathy: LV-function of 7 patients was only moderately decreased (group A) and in 9 patients massively (group B). RESULTS: 1) TA-064, 8 micrograms/kg/min, i.v. had positive inotropic effects in both groups and induced mean maximal delta% changes at about the 5th minute of infusion as follows: LVSWI + 65% and 47%; DP/DTmax + 61% and 59%; LV-efficiency + 62% and 53%; MVO2 + 31% and + 11% (p less than 0.05). 2) TA-064, 20 mg p.o. induced serum levels (A: 23.8 +/- 12 and B: 26.4 +/- 20 ng/ml) corresponding to the effects with the dosages 1-2 micrograms/kg/min, i.v. (p greater than 0.05), thus implying that significant changes in LV-function require higher p.o. dosages. 3) TA-064 i.v. on the 6th day of exposure to the medication produced less LV-function improvement than on day 1 (p greater than 0.05). CONCLUSIONS: In both groups A and B TA-064 improves LV-function primarily via increased contractility, without toxic side effects. For a more complex definition of the efficiency and mechanism of cardiotonic agents, the validity and importance of using on-line MVO2 assessment and analysis of serial pressure-volume relations is stressed.
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.
A precondition for quantitative angiography is strict standardization of all geometric parameters, i.e., position of the patient and radiation-source-object-image geometry. Correction for respiratory and cardiac cycles is equally important. When all these variables are controlled, the absolute size of a vessel can be a major source of error, since border recognition becomes progressively difficult with decreasing vascular diameter. Finally, contrast density, independent of vascular geometry, will induce errors by virtual magnification of minimal diameters. The results in this paper show the influences of image intensifier position, angulation of the imaging device, and contrast concentration on the geometry of model coronary stenoses when evaluated with computer-assisted quantitative methods. Increase of object-image intensifier distance led to an underestimation of size which increased with decreasing vascular diameter. Decrease in contrast concentration led to a significant overestimation of actual size, up to 20% (p less than 0.05). This effect could be confirmed in human coronary arteriograms (n = 11, p less than 0.05). In conclusion, realistic contrast-perfused calibration devices will have to be developed to replace wire or plaster models in order to control systemic errors that may impede the measurement of absolute vascular size.