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Biomedical subjects

W Bleifeld

Publications and source records attributed to W Bleifeld.

At least 55 records · Page 3Linked to original sources

[Dipyridamole-thallium 201 tomography following acute myocardial infarct: significance for stratifying cardiac risk factors].

For the purpose of risk stratification 80 consecutive patients (mean age 58 +/- 7) with a chest pain syndrome after documented myocardial infarction underwent tomographic vasodilation-redistribution thallium-201 perfusion imaging, using 0.56 mg/kg intravenous dipyridamole. Tomograms were analyzed for size and location of reversible and fixed perfusion defects and correlated to angiographic characteristics, left ventricular ejection fraction and wall motion, collateral status, and 1-year prognosis as measured by cardiac events within 14 +/- 3 months. No serious side effects were noted with the diagnostic use of intravenous dipyridamole. According to the perfusion pattern three subgroups of post-infarction patients were identified: 1) by ischemia at a distance with redistribution in non-infarct related territories (n = 48), 2) by peri-infarctional ischemia with redistribution in the territory of the "infarct artery" (n = 9), and 3) by exclusively fixed defects without redistribution (n = 23). Ischemia at a distance was associated with a larger reversible defect than peri-infarctional ischemia (p less than 0.05) and the pattern without redistribution (p less than 0.005); the fixed defect size, however, was similar in all three subgroups. In addition, the severity of coronary artery disease (Gensini score and number of diseased vessels) and the degree of collateralization was higher in presence of a redistribution pattern (p less than 0.05), although no significant differences in global and regional function were noted as a function of thallium-201 redistribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Decreasing length of stay in the hospital by coronary angiography with 5-French catheters].

The use of 5-French (F) coronary angiography catheters as opposed to 7-F may reduce arterial injury at the puncture site. Therefore, a decrease in time to recuperation after coronary angiography with the Judkins technique seems possible. In 199 patients undergoing coronary angiography with 5-F catheters, management, imaging, and complications were investigated. In 18 patients the diagnosis of a valvular defect was confirmed; in 128 patients coronary artery disease (lesions greater than 70%) was found. Three patients had idiopathic dilative cardiomyopathy. Coronary lesions of less than 70% with normal left ventricular function were found in 50 patients ("normals"). After coronary angiography with 5-F catheters bedrest was recommended for 4 h, as compared to 24 h after a 7-F catheter procedure. Successful coronary artery imaging with 5-F catheters was achieved in 168 patients (84%). In 31 patients (27 coronary artery disease, 1 aortic stenosis, 3 normals) selective imaging was not achieved, and the 5-F catheter had to be replaced by a 7-F catheter. Aortic (systolic 147 +/- 24 vs 132 +/- 20 mm Hg, p = 0.002; diastolic 74 +/- 13 vs 70 +/- 11, p = 0.05) and left ventricular pressures (systolic 149 +/- 26 vs 131 +/- 20 mm Hg, p = 0.001; enddiastolic 18 +/- 8 vs 14 +/- 8 mm Hg, p = 0.035) were higher in this group, whereas no relations to age, sex, and diagnosis emerged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Non-Q wave and Q wave myocardial infarct: correlation with regional myocardial perfusion, wall function and prognosis within 1 year].

The pathophysiologic substrate and the prognostic value of pathologic Q-waves after an acute myocardial infarction are still unclear. To elucidate this problem we stratified 52 postinfarction patients into those with Q-infarctions (n = 23) and those with non-Q-infarctions (n = 29). The localization and the extent of reversible and irreversible perfusion defects were assessed using dipyridamole-thallium-201 tomography (SPECT); in addition, coronary morphology, left ventricular wall motion, and prognosis were followed for 1 year. The Q-wave group showed a total defect size of 44.0 +/- 15.3% and a reversible defect size of 13.9 +/- 10% of the left ventricular myocardium. This was not significantly different from the non-Q-wave group, with a mean total defect of 35.2 +/- 20.7% and a mean reversible defect of 16.6 +/- 12.9%. However, the size of the irreversible defects in Q-wave infarctions was larger than in non-Q-wave infarctions (30.6 +/- 18.2% vs 18.6 +/- 17.5%; p less than 0.02). In addition, the relative portion of the reversible defect was larger in non-Q-infarctions than in Q-infarctions (55.9 +/- 25.7% vs 35.7 +/- 21.3%; p less than 0.01). Q-wave infarctions had a significantly lower LVEF of 55.7 +/- 15.4%, as compared to non-Q-infarctions (66.2 +/- 11.9%) (p less than 0.02). The extent of disease, as measured by coronary score and regional wall motion, was similar, but non-Q-wave infarctions were associated with a higher reinfarction rate (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Prerequisites for pacemaker electrodes for individual programming of a low stimulation impulse (comparison of an Elgiloy and a steroid-dependent pacemaker electrode)].

The individual programming of cardiac pacemakers to pulse amplitudes of 2.5 volts and less reduces unnecessary energy consumption by the pacing impulse. In order not to impair the safety margin, electrodes must reveal a low chronic pacing threshold associated with a small standard deviation. For 3 months after implantation we investigated these conditions in 10 patients with a steroid-eluting lead and in 10 patients with a conventional elgiloy lead. During the study period patients with a steroid-eluting lead had a significantly lower pacing threshold. Twelve weeks after implantation all steroid-patients had 0.8 volts pacing threshold at 0.5 ms pulse width. In contrast to the conventional lead the steroid-eluting lead had a significantly lower impedance. Since voltage enters squared into the energy consumption formula, patients with a steroid-eluting lead needed significantly less energy for an effective stimulation of the myocardium 4 and 12 weeks after implantation. R-wave amplitude was not different in both groups. Our investigation demonstrates that immediately after implantation all patients with a steroid-eluting lead can be programmed at 2.5 volts pulse voltage or individually even lower. The saved energy results either in an extended pulse generator longevity or allows the implantation of a smaller pulse generator with a reduced battery capacity.

Aged↗

[Arrhythmia as an indicator for reperfusion following acute myocardial infarct?].

For the purposes of the European double blind and randomized study 27 patients with acute myocardial infarction underwent thrombolysis with rt-PA (60 mg over 90 minutes i.v.) or placebo. To evaluate whether arrhythmias, especially ventricular arrhythmias indicate coronary reperfusion after thrombolysis a 24 hour Holter monitoring was performed from the beginning of the rt-PA or placebo infusion. Typical reperfusion arrhythmias were thought to be idioventricular rhythms (rate less than 110/min), ventricular tachycardia (rate greater than 110/min) or bradycardic rhythm disturbances (rate less than 50/min). The effect of thrombolysis on reperfusion of the infarct related artery was evaluated 90 minutes after the infusion by coronary angiography. After 90 minutes of rt-PA or placebo infusion in 16/16 patients treated with rt-PA and 2/11 patients, who received placebo, was the infarct artery patent. 16/18 patients with a patent artery presented a total of 105 arrhythmic events. 47% of the arrhythmias obviously due to reperfusion were classified as idioventricular rhythms. In contrast only 3/9 patients with an occluded infarct artery presented 25 arrhythmic events. The time of occurrence was not different during the running rt-PA infusion compared to placebo. The following interval up to 24 hours showed no difference in incidence and type of the arrhythmias. No relationship was found between reperfusion arrhythmias and salvage of myocardium during 90 minutes of rt-PA or placebo infusion.

Arrhythmias, Cardiac↗

[Effects of low-dose acetylsalicylic acid on thrombocytes in health subjects and in patients with coronary heart disease].

The effects on platelet function of a four-week administration of aspirin at a low dosage (100 mg daily) were compared in two groups, 14 healthy young volunteers and 14 patients with coronary heart disease. In both groups there occurred a clear inhibition of platelet aggregation with collagen (1 and 5 micrograms/l) and arachidonic acid (1 mmol/l) during the aspirin period. The inhibitory effect reached its maximum after three days, remaining at maximum for the remainder of the four weeks. Platelet functions returned to normal within eight days of discontinuing aspirin. The inhibitory effects went together with a definite in-vitro decrease in thromboxane synthesis. In both groups there was no change in aggregation velocity with adenosine diphosphate (ADP) as aggregation-inducing substance, while the frequency of irreversible aggregation decreased with submaximal concentrations of ADP (0.5 and 1.0 mumol/l). The results indicate that low-dose aspirin causes a definite inhibition of platelet function, in a similar manner, in both healthy subjects and patients with coronary heart disease.

Adenosine Diphosphate↗

Isoelectric focusing of creatine kinase MM isoforms and its application for diagnosis of acute myocardial infarction.

CK MM isoforms (MM 3 having the highest isoelectric point, followed by MM 2, MM 1, and MM X) were measured in 35 patients with acute myocardial infarction (AMI) by isoelectric focusing on agarose gel. Blood samples were analysed every 2 h for the first 12 h, then every 4-8 h until 72 h after AMI. In the first sample, obtained 2.1 h after the onset of chest pain, the ratio of the isoforms MM 3:1 was 0.7 (range 0.2-1.8), equivalent to a normal value. Before the total CK exceeded normal, in 86% of the patients the ratio MM 3:1 rose to 2.2 (range 0.3-3.3). The maximal individual ratio MM 3:1 was 4 (range 0.9-12) after 7 h. It fell below 1 again after 27 h. Thus, the ratio MM 3:1 was useful in the early diagnosis of AMI by enzymatic methods and to estimate the time elapsed since the onset of infarction. Twenty patients with an open infarct vessel (angiographic data after thrombolytic therapy) showed similar peak enzyme activities as ten non-reperfused patients. They differed significantly in the time to the peak activity, mostly for CK MM 3 and CK MB (p less than 0.0005). A higher ratio CK MM 3:1 and a shorter time to the maximum CK MM 3 activity in reperfused patients helps to assess the success of thrombolytic therapy.

Animals↗

Bleeding after thrombolysis in acute myocardial infarction.

232 consecutive patients with acute myocardial infarction were treated either with 2 x 10(6) IU urokinase as an intravenous bolus injection, or 250,000 IU streptokinase intracoronary, or 60 mg recombinant tissue-type plasminogen activator (rt-PA) over 90 min. All patients enrolled had chest pain for more than 30 min and less than 3 h before admission and a typical electrocardiogram. Contra-indications to thrombolytic treatment were absent. All bleeding complications occurring within 24 h after admission were assumed to be due to thrombolytic therapy. Bleeding complications occurred in 14 patients (6.5%). Only seven patients received a blood transfusion (3%). No correlation was evident between previous hypertension, diabetes mellitus, smoking, sex, age, fibrinogen level before and 24 h after thrombolytic therapy and bleeding complications. The risk of bleeding was not significantly different between the different thrombolytic regimens despite marked differences in the fall of the fibrinogen level. The decrease of fibrinogen following thrombolytic therapy did not influence the patency rate of the infarct vessel. Thrombolytic therapy in acute myocardial infarction is a safe treatment even among patients advanced in years and with medically controlled hypertension and diabetes mellitus, irrespective of the kind of thrombolytic treatment.

Female↗

Effects of aspirin and prostaglandin E1 on in vitro thrombolysis with urokinase. Evidence for a possible role of inhibiting platelet activity in thrombolysis.

The formation of thrombi in vivo includes the activation of both platelets and the coagulation cascade. Conventional thrombolytic therapy is primarily directed toward the dissolution of fibrin. To evaluate the possibility that platelet activity impairs the lysis of thrombi, we studied the effects of aspirin and platelet-deaggregating prostaglandin E1 on thrombolysis with urokinase. Combined platelet and fibrin thrombi were produced in vitro by adding CaCl2 and collagen (1 microgram/ml) to citrated platelet-rich plasma (250,000 platelets per microliters). Urokinase (500-10,000 units/ml) caused a dose-dependent weight loss of the thrombi that was maximal at 2,000 units/ml. The addition of aspirin (10-200 micrograms/ml) to platelet-rich plasma before thrombus formation markedly enhanced thrombolysis with urokinase. This effect was most pronounced at 20 micrograms/ml aspirin. However, when aspirin was added after completion of thrombus formation, no significant effect on thrombolysis was noted. Prostaglandin E1 (1-100 mumol/l) improved the lysis with urokinase of the combined platelet and fibrin thrombi. This effect was maximal at 20 mumol/l prostaglandin E1. When pure fibrin thrombi were produced in platelet-free plasma, prostaglandin E1 was without effect on lysis. Thus, in vitro lysis with urokinase of combined platelet and fibrin thrombi was enhanced by the addition of platelet-deaggregating prostaglandin E1 and by pretreatment with aspirin.

Adult↗

Catheter atherectomy: functional results in peripheral arterial disease.

In 10 patients with peripheral arterial disease (PAD) atherectomy was performed with the Simpson atherectomy catheter. PAD was diagnosed by clinical evaluation, oxzillography, Doppler ultrasound examination, treadmill walking, and angiography. Eight patients belonged to stage II and 2 to stage IV. Two stenoses were located in the iliac artery, and the others in the superficial femoral artery or popliteal artery or both. The treadmill walking distance before the intervention ranged from 24 to 67 m before and 105 to 115 m after the procedure (speed 2 mph; gradient 12.5%). After atherectomy, the walking distance improved by 35% to 126%. No patient in stage II perceived pain. In these patients treadmill exercise was terminated because of dyspnea. The ankle/arm ratio (Doppler ultrasound) ranged from 0.4 to 1.0 before atherectomy with a mean improvement of 0.15 afterward (stages II and IV). Control angiography within three to six months in 4 patients did not reveal any significant change at the site of the original stenosis.

Aged↗

[Lipid-lowering and anti-aggregating effect of low-dose therapy with fish oil].

Fifteen healthy volunteers were treated for 30 days with 5 g daily fish oil in capsule form (MaxEPA). After that time, serum triglycerides had decreased by a mean of 26% (p less than 0.05). This relative decrease in triglycerides was the larger the higher were the baseline levels before the start of therapy (p less than 0.01). Total cholesterol remained unchanged with fish oil. HDL-cholesterol showed a small mean increase by 12% (p less than 0.10). The rate of platelet aggregation after induction with collagen 1 microgram/ml was reduced after 30 days of therapy (p less than 0.05), while no effect on platelets was observed with collagen 5 micrograms/ml or ADP (0.5, 1 and 10 mumol/l) as aggregating agents. In vitro thromboxane synthesis after stimulation with collagen (1 microgram/ml) or arachidonic acid (1 mmol/l) was inhibited cumulatively by fish oil and, after 30 days, reached 56% (p less than 0.02) and 44% (p less than 0.05) of the initial values, respectively. Both the basal and prostaglandin E1 stimulated concentrations of c-AMP in platelet rich plasma remained uninfluenced. Thus, the ingestion of a low dose of fish oil by young and healthy subjects led to significant changes in serum triglycerides and platelet function.

Administration, Oral↗

[Coronary artery spasm as a rare cause of sudden heart arrest].

After successful resuscitation only few patients present without any findings indicative of the causes of their cardiac arrest. We report on a 39-year-old woman who had normal clinical, electrocardiographic, and angiographic findings after she was successfully resuscitated. In contrast to other patients without apparent organic heart disease she had three cardiac arrests within 10 months; each episode was preceded by an ascending epigastric pain. During an attack with epigastric pain a long-term ECG recording documented an increasing ST-segment elevation followed by rapid, non-sustained ventricular tachycardia. Intravenous ergonovine induced a spasm of the right coronary artery with a subtotal vessel occlusion and an ST-elevation in lead III. After medication with a calcium antagonist no coronary vasospasm was demonstrated. For 11 months the patient has been without any complaints.

Coronary Angiography↗

[Sudden heart death in a long distance runner during a marathon].

Sudden cardiac death during running is mainly caused by an acute myocardial infarction and coronary artery disease. Other diseases like myocarditis are rarely documented. Before a marathon a 37-year-old, well-trained long-distance runner had normal findings at a sports medical consultation. During the race he collapsed after 41 km and died despite of immediate resuscitation attempts. At autopsy a 50% stenosis of the descending branch of the left coronary artery, and histologically an active myocarditis were observed (Dallas-classification). The endured extreme stress of the marathon probably resulted in arrhythmias and in sudden cardiac death.

Adult↗

[Requirements in radiologic diagnosis from the internist-cardiology viewpoint].

The article discusses the demands to be made on the various radiological methods in thoracic diagnostics in respect of their informative value for therapeutic consequences, as seen from the viewpoint of internal-cardiological intensive-care medicine. The importance of x-ray thoracic film in one or two planes is emphasised, with special reference to routine imaging. In consideration of the demonstration of essential pathological findings, routine chest x-ray film would be mandatory only the 40th year of age onwards and lateral projection from the 50th year. At any rate, about 50% of routine thorax x-rays in intensive-care wards show changes, the percentage being higher if there is a clinical suspicion of changes. Mention must be made of a so-called time phase lag between the x-ray thoracic findings and changed pulmonary arterial pressure. In diagnosis of pulmonary artery embolism the nuclear medicine methods are compared with pulmonary arterial angiography, taking sensitivity and specificity into account. 90% of pulmonary embolism show only non-specific changes in the chest x-ray. Together with these and perfusion scintigraphy a sensitivity of 98% can be attained, albeit with lower specificity, since perfusion angiography and angiography agree in only about 87% of the cases. The demands to be made on radiological diagnostics must be determined from case to case by the diagnostic effectivity in relation to the technical setup and cost. The cost aspect of the individual methods is of major importance when installing equipment in hospitals.

Cardiology↗