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Biomedical subjects

W Bleifeld

Publications and source records attributed to W Bleifeld.

At least 73 records · Page 4Linked to original sources
PubMed1988

[Thrombocyte function in unstable angina pectoris].

In a prospective study, platelet aggregation in platelet-rich plasma after ADP stimulation (0.5, 1.0 and 10 mumol/l) and collagen (1 and 5 micrograms/ml) was measured in 36 patients with coronary heart disease, 18 with angina at rest during the eight hours preceding the time of blood sampling, and 18 patients with stable, exercise-dependent angina, matched for age and sex. In addition, c-AMP was determined, before and (as a measure of platelet adenylate cyclase activity) after stimulation of this enzyme by prostaglandin E1 (10 mumol/l for 30 sec). There were no differences between all the tested ADP and collagen concentrations with regard to platelet aggregation. c-AMP levels were also similar. Thus, in patients with unstable angina there was no evidence for generalized hyperaggregation of platelets in comparison with control subjects who had stable exercise-dependent angina.

Adenosine Diphosphate↗
PubMed1988

Recombinant single-chain urokinase-type plasminogen activator during acute myocardial infarction.

Recombinant single-chain urokinase-type plasminogen activator was intravenously administered in 2 different doses in 24 patients with acute myocardial infarction and angiographically proved occlusion of the infarct-related artery. Patients with first infarction without contraindications of thrombolysis were treated within the first 4 hours after the onset of symptoms. Group A (12 patients) received 20 mg of rscu-PA as a bolus followed by 60 mg infused over 1 hour and group B received 10 mg as a bolus and 30 mg as infusion. The 2 groups showed no significant difference in age, sex, height, weight, time between onset of symptoms and start of therapy, peak values and course of infarct-related enzymes. Time to reperfusion was 43 minutes in group A versus 67 minutes in group B (p less than 0.005). The rate of reperfusion 90 minutes after start of treatment was 91% in group A and 50% in group B (p less than 0.001). Plasma levels of fibrinogen, plasminogen and alpha-2-antiplasmin did not differ significantly in both groups. Systemic lytic state (fibrinogen less than 100 mg/dl) occurred in 33% of group A and in 9% of group B. Intravenous infusion of 80 mg (but not 40 mg) of rscu-PA led to reperfusion of the occluded coronary artery in nearly all patients. Approximately one-third of the patients treated with this dose demonstrated systemic lysis.

Adult↗
PubMed1988

Improved survival up to four years after early coronary thrombolysis.

The long-term prognosis after thrombolytic therapy in patients with acute myocardial infarction (AMI) is unknown. This question was investigated in a 4-year follow-up study of 227 patients. According to the status of reperfusion at the end of the acute catheterization, the patients were divided into a patent (n = 171) and an occluded (n = 56) group. Both hospital and 4-year mortality rates were significantly reduced in the patent group by 13 and 14%, respectively (p less than or equal to 0.005 for both). Baseline variables known to be important for prognosis did not differ between the 2 groups. Patients with a patent infarct artery who underwent early acute coronary artery bypass grafting (CABG) had a greater survival (p less than 0.10) and better left ventricular function (p less than 0.01) than did patients with a patent infarct artery who did not undergo CABG. This difference was associated with a lower frequency of fatal reinfarction and cardiogenic shock in the CABG group. Thus, survival is improved up to 4 years after successful thrombolysis and appears to be further enhanced by early CABG.

Cardiac Catheterization↗
PubMed1988

Unstable angina: current concepts of medical management.

Unstable angina describes a clinical syndrome bridging the gap between stable angina and acute myocardial infarction. By definition, patients with angina of new onset, of a crescendo pattern, and with angina at rest are included in this high-risk group. The underlying pathogenetic mechanisms are complex and include initial atherosclerotic plaque rupture, release of vasoactive substances, and intracoronary thrombus formation. The currently established medical approach of the acute phase consists of heparin for anticoagulation and nitrates combined with beta-blockers for the relief of pain. Calcium antagonists are indicated, if anginal symptoms persist. The effect of thrombolytic therapy is still under investigation. Angina refractory to medical treatment and angina at rest are associated with a particularly unfavorable prognosis and prompt early catheterization. The long-term prognosis of the patient is markedly improved by chronic platelet inhibitory treatment with aspirin.

Angina, Unstable↗
PubMed1988

Quantitation of coronary venous adenosine in patients: limitations evaluated by radioimmunoassay.

Experimental studies have shown that adenosine is rapidly released in response to myocardial ischaemia. To evaluate whether coronary venous adenosine release is a metabolic characteristic of myocardial ischaemia in patients, adenosine concentrations were measured by a highly sensitive and specific radioimmunoassay. In three patients with normal coronary arteries and in seven with obstructive coronary artery disease coronary venous adenosine content was measured at rest and during atrial pacing. When whole blood or plasma were extracted immediately with perchloric acid the adenosine content was found to be lower than that previously reported. Recovery studies showed that the importance of time and temperature at low adenosine concentrations had been underestimated in preceding studies. In patients with coronary artery disease coronary venous adenosine concentration increased from 106.3(48.8) nmol.litre-1 to 114.9(57.0) nmol.litre-1 (NS) during pacing and was 130.4(63.3) nmol.litre-1 (NS) 2 min after pacing. Even in the presence of lactate production enhanced adenosine release was not consistently evidenced. Furthermore, venous adenosine content did not increase in five patients undergoing coronary artery occlusion during angioplasty of the left anterior descending coronary artery. The extremely short half life of coronary venous adenosine appears to preclude its use as an index of myocardial ischaemia in patients.

Adenosine↗
PubMed1988

Anti-ischemic effects of slow-release formulations of nifedipine, isosorbide-5-mononitrate and their combination in patients with coronary heart disease.

Eighteen patients (2 females, 16 males) with coronary artery disease and a positive bicycle exercise test were treated with 50 mg slow-release isosorbide-5-mononitrate (ISMN SR) once daily, 20 mg nifedipine SR twice daily and a combination of both drugs during 2 weeks in a randomized double-blind sequence. Fifteen patients completed the study. The efficacy of each therapy was assessed by ECG stress testing after each treatment period. Both substances were equally effective in the reduction of ischemic ST depression: 0.40 +/- 0.22 mV with placebo, 0.31 +/- 0.16 mV during nifedipine SR and 0.31 +/- 0.29 mV during ISMN SR, 0.28 +/- 0.21 mV during the combination. However, during monotherapy with either nifedipine SR or ISMN SR 6 patients did not improve. The alternative monotherapy was effective in 3 out of 6 patients. Combination treatment gave further advantage only to one third of the patients. We conclude that both nifedipine and ISMN in slow-release formulations are equally effective in the treatment of myocardial ischemia. In the individual patient, however, therapy failure may occur. These patients should be switched to another monotherapy. If both monotherapies are ineffective, combination treatment should be considered.

Coronary Disease↗
PubMed1988

[Randomized double-blind study comparing tissue-type plasminogen activator with placebo in acute myocardial infarct].

In a double-blind randomised trial 129 patients with first myocardial infarction of less than 6 h duration were allocated to treatment with human recombinant tissue-type plasminogen activator (rt-PA) given intravenously over 90 min, or to placebo infusion. Coronary angiography at the end of this infusion showed that the infarct-related vessel was patent in 61% of 62 assessable coronary angiograms in the rt-PA-treated group compared with 21% in the control group. Treatment with rt-PA was not accompanied by any major complications. In the rt-PA group the circulating fibrinogen level at the end of the catheterisation was 52 +/- 29% (mean +/- SD) of the starting value.

Adult↗
PubMed1988

[Electrophysiologic properties of accessory atrioventricular pathways. Comparison with myocardial tissue and relation to site].

In 45 patients (15 female, 30 male; age 34 +/- 12 years) with Wolff-Parkinson-White syndrome: 1) the relation between electrophysiologic properties and location of accessory pathways and 2) the relationship between electrophysiologic properties of accessory pathways and adjacent atrial and ventricular myocardium was studied. Location of the accessory pathways was determined by catheter mapping of the coronary sinus and the tricuspid valve ring. There was no linear correlation between antegrade and retrograde effective refractory periods of accessory pathways and adjacent myocardial tissue. According to their location, accessory pathways were divided into right lateral (n = 4), anteroseptal (n = 6), posteroseptal (n = 10), left posterolateral (n = 8), and left lateral (n = 17). While analysis of variance revealed no differences between subgroups concerning retrograde effective refractory periods, antegrade effective refractory periods were significantly different (p less than .01). Moving in a clockwise direction around the mitral valve ring, antegrade effective refractory periods of the accessory pathways decrease from anteroseptal (321 +/- 30 ms) to posteroseptal (290 +/- 38 ms), left posterolateral (258 +/- 21 ms) and left lateral (246 +/- 27 ms), (Spearman R = 0.70m, p less than .01). Antegrade effective refractory periods of septally located accessory pathways (301 +/- 38) were significantly longer than of pathways located in the free wall of the ventricles (251 +/- 24, p less than .01).

Adult↗
PubMed1988

[Avulsion of a calcified leaflet as a complication of aortic valvuloplasty].

Valvuloplasty was recently introduced as a palliative treatment of calcific aortic stenosis in elderly patients. Embolisation of valvular material has not been described as complication yet. We describe the detachment of a large calcific fragment resulting in acute, severe aortic incompetence in a 76-year-old patient. During immediate operative valve replacement the calcific embolus was recovered from the abdominal aorta.

Aged↗
PubMed1988

[Myocardial perfusion with 201-thallium tomography in the post-infarct phase: prognostic significance and 1-year follow-up].

An individualized post-infarction risk stratification has impact on therapeutic decision making and prognosis after acute myocardial infarction. For evaluation of the cardiac risk profile 80 consecutive post-infarction patients were subjected to biphasic thallium-201 tomography after dipyridamole infusion for maximal coronary vasodilation. By correlating the extent and localization of reversible and irreversible perfusion defects with coronary angiography and one-year follow-up data of 94% of the patients, several univariate parameters with prognostic implications for a risk profile were identified. A stepwise logistic regression model selected the combination of 1) an irreversible defect of greater than 30% of left ventricular myocardium with less than 25% redistribution in the total defect, and 2) a reversible defect of greater than 6% of myocardium with 25% redistribution in the total defect to give optimal sensitivity of 100% and a specificity of 97% for cardiac events such as recurrence of angina, reinfarction, interventional coronary revascularization, and death within one year post infarction. Thus, the semiquantitative tomographic analysis of post-infarction myocardial perfusion allows an efficient individual risk stratification with a non-invasive technique.

Adult↗
PubMed1988

[Comparison of the acute hemodynamic effect of nisoldipine (Bay k 5552) and nifedipine in patients with ischemia-induced left ventricular impaired function].

Calcium channel blockers of the dihydropyridine type have different sites of action that may cause negative inotropic effects in some patients; therefore, their use as systemic vasodilators in left heart failure may be limited. In 10 patients with coronary heart disease we compared the acute peripheral and central hemodynamic effects of i.v. nisoldipine vs. i.v. nifedipine intraindividually, using a sequential crossover protocol. All patients were subjected to right heart catheterization, arterial pressure monitoring, and simultaneous radionuclide angiography. The infusion of either calcium channel blocker was titrated to a similar steady-state reduction of mean arterial pressure by 15 +/- 3% and 15 +/- 2%, respectively, which reduced systemic vascular resistance by 25 +/- 5% and 17 +/- 2%, respectively. The required equally effective dosage was 0.17 +/- 0.06 micrograms/min/kg for nisoldipine and 0.58 +/- 0.1 micrograms/min/kg for nifedipine. In contrast to nifedipine, the administration of nisoldipine was associated with an increase in cardiac index by 0.45 +/- 0.33 l/min/m2 (p less than 0.05), stroke volume index by 3.91 +/- 3.0 ml/m2 (p less than 0.05), and left ventricular ejection fraction by 4.6 +/- 2.8% (p less than 0.05). Mean pulmonary capillary wedge pressure decreased with nisoldipine from 11.8 +/- 3.4 to 8.0 +/- 3.4 mm Hg (p less than 0.005) and mean pulmonary artery pressure decreased from 20.4 +/- 4.06 to 16.1 +/- 3.2 mm Hg (p less than 0.005), but was unaffected by nifedipine. Left and right ventricular endsystolic and enddiastolic volumes were not significantly altered by either drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Intracoronary thrombus in patients with unstable angina pectoris].

Intracoronary thrombi were found in 20 of 52 patients (38%) who had coronary angiography because of treatment-resistant unstable angina. Unrelated to the angiographic finding, eight patients (15%) sustained a myocardial infarction, and two died during their hospital stay. Only one patient (5%) with and six patients (19%) without intracoronary thrombi were stabilized and discharged from hospital. The remaining patients either had an aortocoronary bypass (n = 31) or transluminal balloon angioplasty (n = 13). These findings underline the importance of intracoronary thrombus formation in the pathogenesis of treatment-resistant unstable angina.

Adrenergic beta-Antagonists↗
PubMed1987

[Fibrinolysis in acute myocardial infarct].

Fibrinolysis has opened up a new avenue in the treatment of acute myocardial infarction (AMI). In principle, the rate of reperfusion depends on the type of compound used, the mode of administration and the time between onset of symptoms and the beginning of treatment. With intracoronary streptokinase the reperfusion rate is of the order of 85%. Intravenous urokinase administered as a bolus results in a reopening rate of 50-60%; a similar rate of reperfusion is achieved with rt-PA as infusion, while i.v. streptokinase produces about 50% reopened coronary vessels. The final infarct size is decreased in 70% of patients if fibrinolysis is initiated within 2.5 hours after the onset of symptoms and followed by reopening of the occluded vessel. This results in a lowering of in-hospital mortality, which in various studies is of the order of 45-60%.- Bearing in mind the contraindications, fibrinolysis should be initiated within 3 hours. Hemodynamic improvement by a decrease of infarct size may also be achieved beyond 3 hours in large anterior myocardial infarctions and in posterior infarctions with cardiogenic shock. Early initiation of thrombolysis is of major importance in improving left ventricular function and lowering mortality following acute myocardial infarction. Therefore, prehospital thrombolytic therapy should be considered. - In the postinfarction phase coronary angiography is indicated in patients with angina at rest, stable angina of ECG signs of ischemia. In this situation transfer to a specialized cardiology division for possible percutaneous transluminal angioplasty is indicated. - Reocclusion after successful thrombolysis occurs in 20-30%, and it is therefore important to avoid reinfarction to improve the long term prognosis after AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticoagulants↗
PubMed1987

Comparison of the acute hemodynamic response to intravenous nisoldipine (Bay k 5552) and intravenous nifedipine for left ventricular dysfunction secondary to myocardial infarction.

Dihydropyridine calcium blocking drugs exert potentially dangerous negative inotropic action in selected patients with severe left ventricular dysfunction. In 10 patients peripheral and central hemodynamic effects of nisoldipine were intraindividually compared with nifedipine using a sequential crossover protocol. The drugs were titrated to a similar steady-state reduction of mean arterial pressure by 15 +/- 3% and 15 +/- 2% and systemic vascular resistance by 25 +/- 5% and 17 +/- 2%, respectively. The equi-effective dosage was 0.17 +/- 0.06 microgram/min/kg for nisoldipine and 0.58 +/- 0.1 microgram/min/kg for nifedipine. In contrast to nifedipine, administration of nisoldipine was associated with increases in cardiac index of 0.45 +/- 0.33 liters/min/m2 (p less than 0.05), stroke volume index of 3.91 +/- 3.0 ml/m2 (p less than 0.05) and left ventricular ejection fraction of 4.6 +/- 2.8% (p less than 0.05). Mean pulmonary capillary wedge pressure decreased with nisoldipine from 11.8 +/- 3.4 to 8.0 +/- 3.4 mm Hg (p less than 0.005) and mean pulmonary arterial pressure from 20.4 +/- 4.06 to 16.1 +/- 3.2 mm Hg (p less than 0.005); these variables were unaffected by nifedipine. Thus, intraindividual comparison revealed no cardiodepressive action of nisoldipine, whereas with nifedipine the conceptually beneficial effect of afterload reduction appears to be offset by intrinsic negative inotropic action. Due to higher vasospecificity and more effective unloading, nisoldipine appears to be superior to nifedipine in patients with left ventricular dysfunction secondary to ischemic heart disease.

Aged↗