Biomedical subjects
Publications and source records attributed to W Kupper.
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Coronary sinus blood flow, great cardiac vein flow, myocardial oxygen consumption and myocardial lactate extraction were measured in 38 patients (12 female, 26 male) at rest and during supraventricular pacing until angina or av block occurred. 17 patients without significant coronary artery stenosis in the angiogram built the control group (group I). 15 patients had 2- or 3-vessel disease (group II), 6 exhibited an isolated LAD-stenosis of 80 to 95% cross section area (group III). There were no significant differences at rest between the 3 groups. Whereas pressure-heart rate product, coronary sinus blood flow and great cardiac vein flow, increased significantly during pacing in group I and II, there was only a slight increase in great cardiac vein flow from 77 +/- 22 to 83 +/- 19 ml/min in group III. Flow/beat only in this group declined significantly from 1.07 +/- 0.2 at rest to 0.68 +/- 0.1 ml during pacing (p less than 0.001). Coronary reserve capacity of these patients is probably reduced at rest, and flow during pacing can increase only insufficiently. Because rate-pressure product during pacing rose significantly, myocardial oxygen demand rose as well. The fact of a significant myocardial lactate production during pacing in group III indicates that increased myocardial oxygen demand in this group could not be adequately supplied. Also patients in group II produced lactate during pacing in contrast to patients of group I. So, if blood flow in the individual may be similar in patients with and without coronary artery disease, simultaneous measurements of myocardial lactate extraction can discriminate between both groups.
Coronary venous blood flow measured by continuous thermodilution, myocardial oxygen consumption and lactate extraction rate were estimated at rest and during graded heart rate exercise in 21 patients with compensated aortic valve stenosis and in 10 patients without heart disease. Significant differences between the groups were found only in coronary sinus flow, however not in coronary perfusion related to 100 g of left ventricular muscle mass. As regards indication for operation patients with aortic valve stenosis were differentiated according to transvalvular pressure differences. Pressure gradients of more than 90 mm Hg (n = 5) were associated with significant lowering of weight-related myocardial perfusion and oxygen consumption and high lactate production during stimulation. This evidence of myocardial ischaemia was also seen in 3 out of 11 patients with a pressure gradient between 51 and 90 mm Hg. The rest of the patients showed no significantly different measurements in comparison with the control group. Thus insufficient myocardial perfusion during exercise is likely in patients with transvalvular pressure differences of more than 90 mm/Hg and possible when the difference is more than 50 mm Hg.
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In 20 patients with idiopathic hypertrophic obstructive and nonobstructive cardiomyopathy (IHSS), biphasic Thallium-201 myocardial scintigraphy was performed. Regional myocardial Thallium-201 kinetics of these patients were analysed by a semiquantitative computerized method and compared with those of 6 normal subjects. In 12 of 18 with IHSS and no coronary artery disease 26 regions of interest with irreversible and 6 regions of interest with reversible Thallium-201 defects could be detected. Most of the Thallium-201 defects were localized in the interventricular septum. The defects were not related to the age of the patients and there was no relationship between the occurrence of reversible Thallium-201 defects and pathological myocardial lactate extraction rate during maximal atrial pacing measured in 14 patients. The percentage (6.8%) of irreversible defect regions in patients with LV outflow obstruction at rest (n = 13) was more than twice higher compared to those (n = 5, 3.2%) without LV outflow obstruction or no provocative pressure gradient, resp. These data suggest that IHSS is often associated with regional ischemic myocardial fibrosis despite normal coronary arteries. Therefore in these patients Thallium scintigraphy cannot be used as a noninvasive screening method to exclude or prove coronary artery disease.
In 848 coronary arteriograms performed in a two-years period 21 patients (2.5%) showed a myocardial bridging of the left anterior descending artery. Resting- and/or stress-ECG were abnormal in half of the patients. Regional lactate-metabolism measured in the great cardiac vein at rest and during maximal atrial pacing was normal (29 +/- 12 resp. 24 +/- 9%). Thermodilution of great cardiac vein bloodflow at rest and during atrial pacing also demonstrated normal values (94 +/- 33 resp. 138 +/- 30 ml/min). Biphasic 201-Thallium myocardial imaging revealed no case of reversible perfusion defect, but surprisingly frequent (5 of 16 patients) clearly irreversible defects limited to the interventricular septum. We conclude that muscle bridges do not cause myocardial ischemia at rest or during exercise.
Experiences from 233 coronary sinus blood flow measurements with the Ganz continuous thermodilution technique are reported. Experimental studies revealed: 1. Because of incomplete isolation of the external thermistor against injectate one has to take into account a systematic error in the range of 3--4%. 2. If flow exceeds 200 ml/min, injection rate must be increased from 30--40 ml/min to 60--70 ml/min for complete mixing of blood and injectate. Then flow rates up to 450 ml/min may be measured precisely. 3. Using the double thermistor catheter experimental studies indicated complete mixing of blood and injectate between injection orifice and first external thermistor. 4. To avoid right atrial admixture the external thermistor should be positioned 3 cm deep into the coronary sinus. 5. It is easier to obtain an identical catheter position within the great cardiac vein, when repeated measurements at different days are necessary. Compared with other measuring methods of myocardial blood flow this technique is inexpensive and simple. It permits rapid changes in coronary sinus blood flow to be studied. The possibility to determine simultaneously myocardial substrate utilisation is of great advantage.
The results of biphasic 201thallium (201Tl) scanning were compared with those of coronary arteriography, left ventricular angiogarphy and stress ECG in 56 patients with coronary artery disease and six with no evidence of heart disease. There were 104 201Tl defects, 50 of them reversible. The defects were always located in the area supplied by a critically stenotic coronary artery. Correlation of regional wall motion with 201Tl activity demonstrated that in all forms of abnormal wall motion there was either ischaemia or fibrosis. The resting LV angiogram thus does not make it possible to distinguish between myocardial ischaemia and fibrosis. Taking the LV angiogram as a standard, the rate of false-positive 201Tl scintigrams was 5%, that of false-negative ones 23%. The biphasic 201Tl scintigram was more sensitive than the stress ECG in detecting myocardial ischaemia. It furthermore made it possible to localize the ischaemic (or fibrotic) region within the LV and to estimate its size.
In a 45-year-old female patient with Prinzmetal angina pectoris coronary angiograms and a 201thallium scintigram were performed during an ergotamine-induced episode of angina. The spontaneous and the ergotamine-induced attacks were characterized by transient ST elevation in the posterior wall ECG leads. The coronary angiogram during the attack showed spasm of the circumflex branch of the left coronary artery. In the 201thallium scintigram a large defect in myocardial thallium uptake was noticed in the posterior wall of the left ventricle. Angina and ECG abnormalities disappeared within 4 minutes. However, the scintigraphic defect disappeared only after 6 hours. The slow recovery of myocardial thallium uptake is thought to represent an alteration of the myocardium after a brief 4 minute interruption of regional coronary arterial blood flow. The diagnostic approach in patients with Prinzmetal angina is discussed.
The size of infarction was determined in 21 patients with acute myocardial infarction aged 42 to 76 years using serial analyses of the serum concentrations of the total creatine kinase (CK) and of the CK-MB isoenzyme. CK-MB isoenzyme concentrations reached their maximum in serum three hours earlier on average and returned to the initial value 10 to 12 hours before the total CK. CK-MB isoenzyme concentrations reached a maximum of 12.4% of maximum total CK activity. In 17 uncomplicated cases the infarct weight determined from total CK (40 +/- 23 g) and from CK-MB isoenzyme (35 +/- 23 g) was only different by 5 g (r = 0.92). In 4 patients with infarction and defibrillation or reanimation use of total CK led to an overestimation of the infarct size by more than double. The determination of the infarct size from CK-MB isoenzyme values proves that without extracardial CK release, estimation of the infarct size can also be done sufficiently exactly from the total CK concentrations. In complicated cases, however, the specific myocardial CK isoenzyme makes determination of the infarct size possible
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27 patients (8 women, 19 men) aged 39-79 (mean 61) years with acute transmural mycoardial infarction and limitation of left ventricular function were treated in the acute stage for 24-72 (mean 55) hours with intravenous infusions of sodium nitroprusside in concentrations of 10-200 microng/min. Haemodynamic measurements before and 12 hours after onset of treatment showed a significant reduction in mean arterial pressure by 19%, in end-diastolic pressure in the pulmonary artery by 33% and in the total peripheral resistance by 32%, whereas stroke volume and cardiac index rose by 12% and 17%, respectively. The percentage improvement was most marked in those patients most severely affected. The mortality rate of cardiogenic shock was reduced to 25%. In a control group with haemodynamically similar left ventricular failure the mortality rate was 55%. However, the total mortality was nearly unchanged as the number of sudden unexpected deaths after the fourth day rose from 23 to 50%. Further investigations will show how these sudden deaths, mainly due to arrhythmias, can be prevented.
The left ventricular hemodynamics of 70 patients with acute myocardial infarction were determined from measurements of pulmonary arterial end-diastolic pressure, cardiac index, mean arterial pressure and heart rate during the acute phase(first study, 5 hours after admission), 4 to 6 weeks later (second study, during convalescence) and in 35 percent of all subjects 6 to 12 months after the acute infarction (third study). Serial analysis of serum creatine kinase was carried out during the acute phase. The peak CK value normalized for body surface area was used as a rough index of the extent of the acute myocardial necrosis. The condition of all survivors of the acute stage improved. Patients with only slightly reduced left ventricular performance during the acute stage recovered to nearly normal during convalescence. The condition of patients with greatly reduced left ventricular function also improved but remained impaired during convalescence. In all patients the main changes in left ventricular hemodynamics occurred within the first 4 to 6 weeks; there was almost no further alteration during the following 9 months.
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