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Biomedical subjects

W Kasper

Publications and source records attributed to W Kasper.

At least 91 records · Page 5Linked to original sources
PubMed1988

[X-ray changes in the thoracic organs in acute heart infarct].

Chest X-rays were used to evaluate the hemodynamic status of 86 patients with acute myocardial infarction. The chest films, divided into three groups depending on the degree of pulmonary venous hypertension revealed: grade 1, pulmonary-venous congestion; grade 2, interstitial pulmonary edema; grade 3, diffuse alveolar edema. On clinical examination, four grades of congestive heart failure were distinguished in acute myocardial infarction. In 69% of our patients radiological and clinical grading of left ventricular failure led to precisely the same conclusions. Pulmonary capillary wedge pressure was measured in 31 patients with acute infarction. Radiological criteria of the degree of pulmonary vascular congestion, when related to pulmonary capillary wedge measurements, provide a basis for consistent therapy of left ventricular failure secondary to acute myocardial infarction.

Adult↗
PubMed1987

Evaluation of long-term oral levodopa therapy in chronic congestive heart failure.

To evaluate the long-term effects of orally administered levodopa, 11 patients with chronic congestive heart failure (NYHA III-IV) were studied during maintenance therapy (30 +/- 1 days) and after withdrawal from levodopa. The daily levodopa dose was 4 g in six patients; because of side effects the levodopa dose was reduced to 2-3 g in the remaining patients. After withdrawal of levodopa, mean pulmonary capillary wedge pressure and mean right atrial pressure increased significantly (from 19 +/- 2 to 24 +/- 3 and from 7 +/- 2 to 9 +/- 2 mmHg, respectively). Effective renal plasma flow was 329 +/- 57 during levodopa therapy and decreased significantly to 252 +/- 27 ml/min after withdrawal of levodopa. The number of ventricular premature contractions and couplets increased during levodopa therapy and decreased again significantly after withdrawal of levodopa. No significant differences between on and off levodopa were observed in resting heart rate, arterial blood pressure, cardiac index, stroke work index, systemic vascular resistance, sodium and water excretion, or creatinine clearance. Seven patients improved on levodopa therapy by one NYHA class; four of these seven patients deteriorated again by one NYHA class after withdrawal of levodopa. Regarding both clinical and hemodynamic changes after withdrawal of levodopa, three patients were classified as responders to long-term levodopa therapy. All three responders received 4 g levodopa per day. Average dopamine plasma level was 5.3 +/- 0.8 ng/ml in the responder group and 2.0 +/- 0.5 ng/ml in the nonresponder group. Long-term administration of oral levodopa is associated with beneficial clinical and hemodynamic response in only a minority of patients with chronic congestive heart failure.

Administration, Oral↗
PubMed1987

[Hemodynamic effect of intravenous diltiazem and nifedipine in acute myocardial infarct. A randomized study].

In a prospective, randomized trial of 28 patients with acute myocardial infarction nifedipine or diltiazem were administered intravenously and hemodynamic parameters and drug plasma levels measured for 24 hours. Both drugs lowered arterial blood pressure and peripheral resistance. Only diltiazem reduced heart rate and the heart rate x arterial pressure product, as pointer to a reduction in myocardial oxygen consumption. On the other hand, nifedipine is more likely to cause a (reflex) increase in heart rate. In no patient was there evidence of drug-induced hemodynamic impairment. Left ventricular filling pressure was reduced in those patients in whom it had been elevated. While a steady-state plasma concentration was quickly reached with nifedipine, in some patients diltiazem infusion produced a continuous rise in plasma concentration and, in two patients with posterior-wall infarction, high-grade a-v block (reversible after discontinuation of the drug). The results indicate that under ECG control both drugs can be used intravenously without much risk. The hemodynamic profile of diltiazem (reduction in peripheral resistance and heart rate) would seem to be particularly favorable in acute infarction, while nifedipine is preferred in acute infarction plus hypertension. The possible effect on a-v conduction is to be watched on intravenous administration of diltiazem, while in normotensive patients nifedipine may cause an undesirable (reflex-mediated) sympathetic activation.

Adult↗
PubMed1987

Determination of aortic valve orifice area in aortic valve stenosis by two-dimensional transesophageal echocardiography.

Two-dimensional transesophageal echocardiography was used to measure aortic valve orifice area in 24 patients with aortic valve stenosis (AS) and 15 patients without aortic valve disease. Using transesophageal echocardiography, orifice area could be measured in 20 of 24 patients with AS. With transthoracic echocardiography, orifice area could be determined in only 2 of 24 patients. In patients with AS, orifice area determined by transesophageal echocardiography was 0.75 +/- 0.34 cm2 and that calculated with Gorlin's formula was 0.75 +/- 0.32 cm2. In normal aortic valves, orifice area was 3.9 +/- 1.2 cm2 by transesophageal echocardiography. A good correlation was demonstrated between aortic valve orifice area determined using transesophageal echocardiography and calculated orifice area using Gorlin's formula in patients with AS: r = 0.92, standard error of estimate = 0.14 cm2. The absolute difference between orifice area measured with both methods ranged from 0.0 to 0.4 cm2 (mean 0.09 +/- 0.1). In 4 patients orifice area could not be determined with transesophageal echocardiography. The orifice could not be identified in 2 patients because an appropriate cross-sectional view of the aortic valve could not be achieved and in 2 patients with pinhole stenosis (aortic valve orifice area 0.3 cm2). These data show that aortic valve orifice area can be measured reliably using 2-dimensional transesophageal echocardiography.

Aged↗
PubMed1987

Alinidine in heart patients: electrophysiologic and antianginal actions.

The electrophysiological properties of alinidine were studied in 18 patients. Four of these patients were pretreated with intravenous propranolol, 0.2 mg kg-1, and atropine, 0.04 mg kg-1, to induce autonomic blockade. Alinidine produces a sustained bradycardiac effect at a dose of 40 mg intravenously. The sinus node recovery time increased in patients with and without autonomic blockade, while the corrected sinus node recovery time was unaffected by alinidine in patients without autonomic blockade and increased in patients with autonomic blockade. The effective refractory period of the right atrium, the atrioventricular node and the right ventricle, as well as the functional refractory period of the atrioventricular node, were unaffected by alinidine in both groups of patients. Intraatrial, atrioventricular and intraventricular conduction was also not altered by this drug. Thus the electrophysiological profile of alinidine differs from other bradycardia-inducing agents such as beta-blockers or calcium antagonists. Furthermore we evaluated alinidine efficacy in 14 patients with angiographically proven coronary artery disease and stable angina during a 10-week placebo-controlled randomized double-blind trial. Alinidine (40 mg three times a day) reduced the number of anginal attacks and the average number of nitroglycerine capsules consumed. The double product was slightly lowered during rest but more pronounced during exercise. This effect was mainly due to decreased heart rate. The ischaemic ST-segment depression was diminished. Exercise tolerance was clearly improved in 6, slightly improved in 2, and unchanged in 4 patients.

Adult↗
PubMed1987

Hierarchy of levels of ischemia-induced impairment in regional left ventricular systolic function in man.

We tested the hypothesis that different subsets of ischemia-induced wall motion disorders are characterized by specific patterns of abnormal regional left ventricular systolic function. Regional contraction was quantitatively assessed from two-dimensional echocardiograms by an automated integrative analysis considering the time course of wall motion during the entire contraction sequence in 20 patients with chronic myocardial infarction, in 13 patients with impending myocardial infarction (less than 2 hr after the onset of symptoms), and in nine patients during transient myocardial ischemia. Wall motion abnormalities were detected in all patients by the integrative analysis. In contrast, the sensitivity for detecting wall motion abnormalities was 80% during chronic infarction, 77% during impending infarction, and 56% during transient ischemia if only end-diastolic and end-systolic frames were compared for assessment of overall regional systolic function. There were distinct differences in the time course of abnormal wall excursion between the three groups. Chronic infarction was characterized by a monophasic contraction pattern, with abnormal synergy in regional contractile events occurring predominantly during early systole. In contrast, transient ischemia caused predominantly mid-to-late systolic abnormal synergy followed by late systolic shortening corresponding to a polyphasic contraction pattern. During impending infarction, an intermediate temporal contraction pattern was present with both early and mesosystolic abnormal synergy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Early clinical evaluation of the intravenous treatment of acute myocardial infarction with anisoylated plasminogen streptokinase activator complex.

50 consecutive patients with acute myocardial infarction and symptoms of less than 4 hours duration were treated with anisoylated plasminogen streptokinase activator complex (APSAC) 30U intravenously as a bolus injection over 5 minutes. An open infarct-related artery was found in 32 patients (64%) when the first coronary angiography was taken 66 +/- 21 minutes after APSAC. Complete reperfusion was subsequently seen in 10 of 18 patients with an occluded infarct-related artery 74 +/- 16 minutes after injection of APSAC. Thus, a patient infarct-related artery was seen in 42 patients (84%) within 68 +/- 20 minutes. A control coronary angiography was performed in 37 patients (74%) after 25 +/- 19 days. Reocclusion was found in 5 patients. The minimal cross-sectional area of the residual coronary stenosis increased from 1.3 +/- 0.9 mm2 to 1.8 +/- 1.9 mm2. Patients with residual thrombi after coronary thrombolysis (n = 13) demonstrated an increase of the minimal cross-sectional area of the residual stenosis from 1.2 +/- 0.8 to 2.6 +/- 2.3 mm2, whereas those without residual thrombi showed only minor changes of the minimal cross-sectional area (1.3 +/- 0.9 to 1.2 +/- 1.2 mm2). Thus, APSAC demonstrated a high patency rate and a low reocclusion rate after intravenous administration. The prolonged fibrinolytic activity of APSAC leads to a further regression of the residual coronary stenosis among patients with coronary thrombi after reperfusion.

Adult↗
PubMed1987

[Relation between spontaneous and electrically inducible ventricular arrhythmias in patients with coronary heart disease].

In a prospective study, 267 patients with invasively diagnosed coronary artery disease were studied by programmed electrical stimulation (PES) and induced ventricular arrhythmias were compared to spontaneous arrhythmias occurring during 24 h Holter registration. In 89 patients (33%) no evidence of myocardial infarction was present, 61 patients (23%) were studied for 6 weeks to 3 months, 36 patients (13%) for 3-6 months and 81 patients (31%) for more than 6 months after myocardial infarction. PES was performed in the right ventricular apex with 1 and 2 extrastimuli during pacing with 100, 120 and 140 beats/min. Endpoint of the study was defined by the induction of 4 repetitive ventricular responses (RVR). Within 72 hours after PES a 24 h Holter registration was performed in all patients. During PES, 15 patients (6%) were not inducible for any RVR. Single RVR (1-2) were induced in 146 patients (55%) and 3-5 RVR in 68 patients (25%). Ventricular tachycardia and ventricular fibrillation were induced in 38 patients (14%); 6 patients showed a sustained, monomorphic tachycardia. Altogether, the incidence of RVR was higher when a history of myocardial infarction was present. With increasing time after infarction the incidence of inducible 3-5 RVR remained stable; however, the number of greater than 6 RVR decreased. During Holter registration, 54/255 patients (21%) showed no spontaneous ventricular arrhythmias, 70 patients (28%) had arrhythmias of Lown-class I/II, 84 patients (33%) of Lown-class III. Complex arrhythmias were observed in 47 patients (18%) (Lown-class IVA: 33 patients, IVB: 14 patients).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

The sliding rail system (monorail): description of a new technique for intravascular instrumentation and its application to coronary angioplasty.

The sliding rail technique is a new technique for intravascular instrumentation, especially coronary stenosis dilatation. The so-called monorail balloon catheter is the first device which can be used according to this technique. The monorail catheter has a single lumen shaft and only a short central tube within the distal balloon part. With the guidewire inserted into the tube, the balloon can be advanced or retracted on the guidewire as on a sliding rail. The most relevant improvements for coronary dilatation are steerability, contrast flow and rapid and easy exchangeability of balloon catheters and other intracoronary devices. These characteristics are felt to result in a more simple and time- and fluoroscopy-saving dilatation procedure. A special transfusion catheter may also improve procedural safety. The first clinical results in 69 patients with a success rate of 96%, an emergency bypass rate of two patients (one infarction) and a stenosis improvement of 58% confirm the theoretically conceived advantages.

Adult↗
PubMed1987

[Relation between hemodynamics and ventricular arrhythmia in patients with heart valve diseases].

The incidence and severity of ventricular arrhythmias were compared with hemodynamic findings of cardiac catheterization, in 160 patients with mitral and aortic valve disease. All patients underwent right and left heart catheterization, as well as M-mode and 2D-echocardiography, and 24-hour ambulatory electrocardiographic monitoring. Out of 160 patients, 68 had mitral valve disease and 92 had aortic valve disease. In mitral regurgitation the degree and frequency of ventricular arrhythmias showed a positive correlation to the degree of regurgitation (rs = 0.44, rs = 0.56, respectively) and a negative correlation to left ventricular ejection fraction (rs = -0.49, rs = -0.57) and to cardiac index (rs = 0.48, rs = 0.53). In aortic valve disease the incidence and severity of ventricular arrhythmias were not related to the type of valve lesion, to the transvalvular pressure gradient nor to the degree of regurgitation. In aortic stenosis, the degree of arrhythmia showed a negative correlation to left ventricular ejection fraction (rs = 0.55) and a positive correlation to left ventricular endsystolic volume index (rs = 0.40) and to peak systolic left ventricular wall stress (rs = 0.59). In aortic regurgitation the number of ventricular arrhythmias showed a negative correlation to left ventricular ejection fraction (rs = -0.43) and a positive correlation to left ventricular endsystolic volume index (rs = 0.43) and to peak systolic left ventricular wall stress (rs = 0.37). These data demonstrate that the incidence and severity of ventricular arrhythmias, in patients with aortic valve disease and mitral regurgitation, are strongly associated with the impairment of left ventricular function.

Adult↗
PubMed1986

Automated monoclonal radioimmunoassays for pirenzepine, a selective muscarinic receptor antagonist, in plasma and urine.

Sensitive and specific monoclonal radioimmunoassays (RIA) for pirenzepine, a muscarinic receptor (M1) antagonist, were developed and validated for rapid automated routine analysis of plasma and urine samples from clinical studies. Three discrete stable hybridoma clones secreting monoclonal antibodies (MAb) to pirenzepine were produced by fusing the myeloma line X63-Ag8.653 to spleen cells of BALB/c mice immunized with pirenzepine-5-N-propionate-protein conjugates. Of three carrier proteins investigated (HSA, BSA and edestin), optimal humoral immune responses and affinity of hybridoma antibody were attained using HSA. All three MAb displayed high affinity to pirenzepine (Ka = 0.6-1.2 X 10(9) l/mol) but showed differing cross-reactivities with its 4'-N-desmethyl metabolite (less than 1%, 6% and 40% respectively). The MAb with essentially zero metabolite cross-reactivity, 58-7/7, was selected for RIA development. In comparison, eight rabbit polyclonal antisera raised against pirenzepine-5-N-propionate-HSA or pirenzepine-5-N-butyrate-HSA possessed a similar range of affinities to the MAbs, but none approached MAb 58-7/7 in specificity. The bridge length had no significant effect on antisera characteristics. Competitive solid-phase RIAs for pirenzepine in human plasma and urine were established using MAb 58-7/7 and [3H]pirenzepine as tracer. All fluid transfers were automated using a programmable sample processing system (Microlab 2,000). Detection limits were 0.25 ng/ml (plasma) and 4 ng/ml (urine) in 0.1 ml sample. The coefficient of within-assay variation was 4% or better in the range 2-100 ng/ml (plasma) or 30-1,000 ng/ml (urine), the between-assay CV was 5.3% or better in the range 5-90 ng/ml (plasma) or 40-660 ng/ml (urine). Excellent correlation was observed between the plasma monoclonal RIA and the hitherto used polyclonal RIA (n = 106, r = 0.994), and between the urine monoclonal RIA and HPLC (n = 82, r = 0.998). We expect that these assays will prove valuable in pharmacokinetic and pharmacological investigations of pirenzepine.

Animals↗
PubMed1986

Coronary thrombolysis during acute myocardial infarction by intravenous BRL 26921, a new anisoylated plasminogen-streptokinase activator complex.

The safety and fibrinolytic efficacy of a new anisoylated plasminogen-streptokinase activator complex (APSAC) was tested in 50 patients with acute myocardial infarction (AMI) less than 4 hours in duration. APSAC (30 mg) was given intravenously as a bolus injection 151 +/- 47 minutes after clinical symptoms. Coronary angiography was then performed to assess coronary artery patency: 28 patients had an inferior AMI and 22 an anterior AMI. A patent infarct-related artery was found in 32 patients (64%) on first coronary angiography 66 +/- 21 minutes after administration of APSAC. Subsequent reperfusion was observed in 10 patients after 74 +/- 16 minutes (84%). Bleeding complications or hematomas were observed in 18 patients, of whom 3 required blood transfusions. Marked hypofibrinogenemia was observed within 24 hours in most patients. A control coronary angiogram was recorded in 37 patients (74%) after 25 +/- 19 days and showed reocclusion in 5 patients.

Adult↗