Biomedical subjects
Publications and source records attributed to J Nitsch.
Digital subtraction angiography, using a time interval difference mode in relation to a suitable mask, provides a means of showing the myocardium in every phase of the cardiac cycle. The endo- and peri-cardial contours and the thickness of the myocardium in both ventricles can be demonstrated accurately. Artifacts are usually due to displacements of the heart or to tachycardia.
Regional cardiac free fatty acid metabolism of 41 patients with coronary artery disease (CAD) and of 10 controls with normal coronary arteries was studied by means of I-123 phenylpentadecanoic acid (IPPA), a radioiodinated palmitic acid analog, and sequential single photon emission tomography (SPECT). All patients and controls underwent symptom--limited bicycle exercise, with the tracer being injected at peak stress. More than 99% of left ventricular segment of controls showed homogeneous tracer uptake and release, indicating homogeneous free fatty acid turnover in normal myocardium. Homogeneous postexercise uptake was followed by decreasing segmental activity in 75.1% of normally perfused segments in patients with CAD. Sixty-five percent and 88.6% of segments, assigned to the perfusion bed of 50%-75% and greater than 75% obstructed vessels had decreased IPPA release and/or reduced IPPA uptake. Patients with exercise induced ischemia had focal metabolic abnormalities in jeopardized myocardium for significantly longer time than clinical or electrocardiographic signs of ischemia (p less than 0.01). All patients with CAD and a negative stress test had metabolic abnormalities, but exhibited, compared to ECG--positive patients, less pronounced segmental metabolic aberrations. These findings indicate reduced cardiac utilization and delayed oxidation of IPPA, associated with exercise-induced ischemia in CAD. The metabolic changes suggest a marked sensitivity to ischemia as well as prolonged postischemic abnormalities of cardiac fatty acid metabolism in jeopardized myocardium.
The interaction of intravenous (i.v.) nitroglycerin (glyceryl trinitrate) on the anticoagulant effect of heparin was studied in 27 patients. The heparin dose was adjusted (800-1400 IU/h) to achieve partial thromboplastin time (PTT) of more than 100 s (130 +/- 28 s). While the heparin infusion was continued at the same dosage, the patients received 2-5 mg/h nitroglycerin i.v. (Perlinganit without propylene glycol [15 patients] or Gilustenon with propylene glycol [12 patients]). During combined heparin and nitroglycerin (NG) administration PTT decreased significantly (60 +/- 23 s; P less than 0.01). After withdrawal of NG, PTT increased to the initial levels (126 +/- 30 s). The drug interaction was seen in both groups--with or without propylene glycol. In nine of the 27 patients plasma heparin levels were measured; they remained unchanged during NG administration. The results indicate that i.v. NG induces heparin resistance. After NG is withdrawn, a rebound increase in PTT may occur. Adequate monitoring of PTT and heparin dosage adjustment are thus required during combined heparin and NG administration.
A maculopapular exanthema developed in a 60-year-old man with coronary heart disease while being treated for angina with the calcium antagonist diltiazem. Epicutaneous and scratch tests were positive, both for the immediate type (type I) and the delayed type (type IV), proving that the drug had caused the allergic reaction. The exanthema quickly disappeared once the drug had been discontinued. Anti-anginal treatment was continued without further complications with nifedipine.
Experiences in i.v. digital subtraction angiocardiography (DSAC) including so-called parametric imaging for morphological delineation of the right ventricle are illustrated. 32 patients with different anatomical and haemodynamic disturbances of the right ventricle were subjected to these examinations. Special emphasis is placed on pulmonary stenosis, particularly on its infundibular manifestations. For visualisation of muscular or fibrous bulging or other changes of the outflow tract of the right ventricle, analysis of the amplitudes is very suitable to produce cumulative pictures of ventricular wall motion during a cardiac cycle. Obstructive wall alterations within the infundibular part become visible even if they occur only during certain phases of the myocardial action, usually in late systole than otherwise.
In the present study the prognostic value of ANP measurement was investigated in 52 patients undergoing coronary angiography. 22 normotensive and 30 hypertensive subjects were included. A significant inverse correlation between left ventricular ejection fraction (EF) and plasma ANP was found in normotensives, but not in hypertensives. In patients with chronic myocardial infarction, there was no difference in ANP levels compared to patients without infarction in either group, provided that EF was normal. However, hypertensives showed a 35% increase in ANP compared to normotensives. This was true for subjects with and without myocardial infarction. These results show that in normotensives ANP levels have a prognostic value on a statistical rather than an individual basis. This does not apply to hypertensives, whose ANP level is increased by factors other than impaired ejection fraction.
In this study plasma levels of atrial natriuretic peptide and of the catecholamines epinephrine and norepinephrine were investigated in hypertensive patients (HT) (n = 30). 22 normotensive patients (NT) served as controls. Hypertensives showed an elevated ANP-level in comparison with controls (46.8 +/- 3.3 vs. 36.8 +/- 3.3 pg/ml, M +/- SEM, p less than 0.01). When patients with myocardial infarction or with reduced ejection fraction were excluded, the same relation was demonstrated (49.3 +/- 3.2 vs. 33.6 +/- 2.0 pg/ml, p less than 0.01). Plasma norepinephrine was 230.8 +/- 52.3 pg/ml in HT compared with 138.0 +/- 19.6 pg/ml in NT (p less than 0.05). Epinephrine was 70.8 +/- 10.5 vs. 54.8 +/- 9.7 pg/ml in HT and NT. To exclude an increased left ventricular enddiastolic - and hence left atrial - pressure as the cause for the elevation of ANP and norepinephrine, HT and NT were matched for the same levels of enddiastolic pressure (LVEDP) (n = 18). For each level of LVEDP ANP was higher in HT than in NT (p less than 0.01). The same held true for norepinephrine (p less than 0.05) and to a lesser extent for epinephrine (p = 0.09). Our results demonstrate that patients with essential hypertension exhibit markedly elevated levels for ANP and catecholamines which is not due to myocardial failure. We propose that the increased secretion of the vasodilatory hormone ANP serves as counterregulation against the vasoconstrictor norepinephrine. The endocrine function of the heart may play a pivotal role in the modulation of sympathetic activity.
UNLABELLED: Only the free protein-unbound drug concentration in plasma is pharmacologically active. The concentration of some drugs in saliva is equal to the free drug level. We compared concentrations (in plasma before, 30 and 60 min after the morning dose, in saliva before, 30, 60, 90 and 120 min after the morning dose) of amiodarone (n = 8, 2 x 200 mg orally per day) and flecainide (n = 16, 2 x 100 mg) administered as chronic antiarrhythmic treatment. Drug levels were measured by "high performance liquid chromatography". RESULTS: Just prior to the first morning dose, amiodarone concentrations in plasma were 1.0-2.9 (2.0 +/- 0.6) micrograms/ml, in saliva 0.02-0.25 micrograms/ml; flecainide in plasma 80-560 (316 +/- 163) ng/ml, in saliva 630-3700 (1749 +/- 963) ng/ml. After the morning dose we found maximal flecainide plasma levels of 462 +/- 203 and saliva levels of 3218 +/- 2857 ng/ml. The highest flecainide concentrations in the saliva (13,400 and 11,300 ng/ml) were found in two patients 30 and 60 min after the morning dose. Flecainide, but not amiodarone, is excreted actively in the saliva, probably indicating an enteroenteric circulation. This should be considered to reduce life-threatening flecainide intoxications by gastric and intestinal lavage and suction. The concentration of flecainide in the saliva does not represent the non-protein-bound free drug level in the plasma.
A high frequency ultrasound system processor was used for an intraoperative evaluation of coronary blood flow velocity and volume. In 12 patients with symptomatic coronary heart disease, morphology and hemodynamic parameters of the coronary artery system were examined intraoperatively. Optimal imaging was possible by keeping the ultrasound transducer at a constant distance of a few millimeters from the surface of the heart and the pericardial space between them filled with saline solution. Using this technique, large areas of the cardiovascular system were reproducible up to a peripheral vascular diameter of 2-3 mm. Blood flow velocity (20 to 33 cm/s) and blood volumes (33 to 94 ml/min) provide quantitative information on the degree of stenosis intraoperatively after coronary anastomosis during bypass surgery. All images were of outstanding quality and precision. This method is highly valuable for the intraoperative determination of blood flow parameters.
In 42 patients with heart failure who were on long-term treatment with flecainide (2 X 100 mg daily by mouth) plasma concentration of flecainide was measured before the morning dose and compared with the clinical grade of heart failure or left ventricular ejection fraction (in the levo-angiogram). Mean plasma flecainide concentration was 415 +/- 244 ng/ml (110-1035 ng/ml), mean ejection fraction 55 +/- 17.7% (24-84%) (r = -0.60). In seven patients with plasma concentrations over 700 ng/ml (870 +/- 150 ng/ml) in clinical grade III or IV, ejection fractions were 24, 25, 25, 30, 33, 37 and 44%, respectively. In two patients (ejection fraction of 24 and 25%, respectively) the morning plasma concentration was around 1000 ng/ml. The results point to possible high plasma flecainide concentrations--at times in the toxic range--in patients who are in heart failure. In patients with marked reduction in left ventricular pumping function who are on long-term flecainide treatment, a reduction in dosage or monitoring of plasma flecainide concentration is indicated.
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The implantable defibrillator is a device to treat refractory ventricular tachyarrhythmias. This study was done to evaluate the determinants of defibrillator performance which are not known completely. Different defibrillation electrodes were attached to beating and non-beating isolated pig-hearts (n = 15) and the electric field resulting from defibrillation measured over a distance of 3 mm. From 5 to 20 J a non-linear relation was found between delivered shock energies and the amplitudes of the recorded voltage waveforms. Using two patch electrodes maximal amplitudes were monitored apical in the right (4.6 +/- 0.5 V) and left ventricle (2.1 +/- 0.3 V). The atria only showed 10-25% of the maximal amplitudes. The combination of a patch and a catheter electrode showed similar efficiency. Two catheter electrodes reduced the apical (1.2 +/- 0.1 V) and increased the atrial amplitude (0.75 +/- 0.06 V). The recorded amplitudes in myocardium were half as much compared with blood-/sodium chloride indicating the twofold higher resistance of myocardial tissue. These experiments quantify the dependence of the efficiency of automatic implantable defibrillator systems on the sort and localization of the defibrillation electrodes.
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The effect of orally administered activated charcoal on plasma concentrations of flecainide were studied in eight volunteers (24-38 years of age). A single dose of 200 mg flecainide were given at 3 days: control (day 1); simultaneous application of flecainide and 30 g charcoal (day 2); application of 30 g charcoal 90 min after flecainide (day 3). Plasma concentrations were determined by HPLC after 2, 4 and 6 h. Absorption of flecainide was almost completely prevented, when flecainide and charcoal was ingested immediately. When charcoal was taken 90 min after flecainide, the following flecainide plasma levels were found: after 2 h 231 +/- 62 ng/ml (266 +/- 30 ng/ml control; n.s.), after 4 h 199 +/- 49 ng/ml (232 +/- 27 ng/ml control; P less than 0.05) and after 6 h 155 +/- 42 ng/ml (231 +/- 51 ng/ml control; P less than 0.01). Charcoal seems to be effective in prevention of the absorption of flecainide. A drug interaction may occur if charcoal is given therapeutically, for example in hypercholesterolaemia. Charcoal may be indicated as an additional treatment of flecainide intoxication.
The purpose of this study was to assess the contribution of digital subtraction angiography (DSA) to the quantification of aortic valve regurgitation in 21 patients undergoing heart catheterization. The digital image subtraction was used for densitometric evaluation. The regurgitation was derived from the distribution of contrast volumes during diastole in aortic and left ventricular "regions of interest". DSA-measurements were compared with results of conventional cineangiography. Results showed the following correlation between DSA measurements and cineangiographic estimates (grades I-III): regurgitation 1.7-9.8% in grade I (n = 11), 8.9-22.3% in grade II (n = 5), 31.7 and 32.5% in grade II-III (n = 2), 37-42.4% in grade III (n = 3). DSA and digital densitometry seem to be valuable methods for the quantification of regurgitation. Concerning quantitative measurements in left heart catheterization the digital subtraction aortography is superior to conventional cineangiography and will be helpful to characterize patients with aortic regurgitation more completely.
The course of a 20-year-old patient with head injury and fractures of the ribs is reported, in whom sinus tachycardia has now persisted for three years. Antiarrhythmic treatment with calcium antagonists, beta-blocking agents and digitalis did not reduce the rate of the tachycardia. Contusio cordis, as well as different mechanisms of arrhythmias after cerebral trauma are discussed.
The hepatic hemodynamic effect of 20 mg sublingual nifedipine was evaluated in 15 patients (13 men, 2 women) during heart catheterization. The liver blood flow was measured 10 min after administration of nifedipine by continuous thermodilution (Baim coronary sinus flow analyzer). Nifedipine was associated with a decrease in systolic blood pressure (from 156 +/- 14 to 138 +/-13 mmHg), an increase in heart rate (from 73 +/- 13 to 81 +/- 8.6 beats/min), and increase in cardiac output (from 6.0 +/- 1.6 to 6.5 +/- 1.3 l/min). In 2/15 patients no significant change was derived. The liver blood flow increased in 13/15 patients from 218 +/- 171.7 to 336.7 +/- 247.7 ml/min (22%-194%, P less than 0.01). The study demonstrates that the vasodilation of nifedipine involves the hepatic circulation. If the hepatic clearance of drugs is high and flow dependent, nifedipine-induced increase of hepatic blood flow may impair drug clearance.
In eleven patients serum levels of amiodarone and its desethyl metabolite were determined after a single dose of 400 mg amiodarone given with and without subsequent administration of colestyramine. In addition, the elimination half-life was measured in three patients after discontinuation of long-term amiodarone therapy. Mean serum levels of amiodarone at 7 1/2 hours after dosing (n = 11) were 0.42 +/- 0.11 micrograms/ml without colestyramine and 0.21 +/- 0.14 micrograms/ml with colestyramine (P less than 0.01). Elimination half-life after discontinuing long-term amiodarone therapy (n = 3) was 23 1/2, 29 and 32 days, respectively (half-life in eight controls: 35-58 days). The results indicate that colestyramine significantly reduces the enterohepatic circulation of amiodarone. Therefore, colestyramine should be capable of accelerating the regression of dose-dependent side-effects of amiodarone by enhancing its elimination.