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Biomedical subjects

M Leschke

Publications and source records attributed to M Leschke.

At least 91 records · Page 5Linked to original sources
PubMed1994

[Percutaneous transluminal therapy of local arterial vascular occlusion after heart catheterization studies].

We analyzed the incidence and management of a vascular occlusion at the arterial puncture site following diagnostic or interventional cardiac catheterization. During the study period 26,245 cardiac catheterization procedures were performed for diagnostic (n = 18,895) or interventional (n = 7350) purposes at our institution. A total number of 35 arterial occlusions (0.13%) was identified. In the early phase of our analysis 14 patients (40%) with peripheral vascular obstruction after cardiac catheterization underwent surgical repair. Three patients (9%) could be treated conservatively. In 18 patients (51%) acute vascular occlusion could be managed by additional intravascular manipulations: 18 patients underwent successful percutaneous transluminal balloon dilatation, in nine patients in combination with intravascular thrombolysis. In three patients additional stent-implantation was necessary in the presence of a large occlusive dissection. The procedure was primarily successful in 16/18 patients. No significant complication occurred. In two patients reocclusion led to operative thrombectomy and patch reconstruction in one and to a second catheter-based approach in the other patient. Both reinterventions were successful. Thus, in experienced hands catheter-based therapy of acute arterial obstruction following diagnostic or interventional cardiac catheterization is very effective and should be considered as therapy of first choice in these patients.

Aged↗
PubMed1994

Possible transmission of sarcoidosis via allogeneic bone marrow transplantation.

Allogeneic bone marrow transplantation (BMT) was performed in a 34-year-old man for non-Hodgkin's lymphoma. Two years before bone marrow harvest, pulmonary sarcoidosis was diagnosed in the donor. After steroid therapy, disease of the donor was in clinical remission with only minor radiological signs at the time of BMT. On day 90 after BMT, active sarcoidosis was diagnosed in the recipient. Besides radiologic signs and increased angiotensin converting enzyme levels, diagnosis was proved by characteristic histologic changes in lung and liver biopsies. Immunosuppressive therapy was changed from high dose cyclosporine to high dose methylprednisolone and symptoms promptly resolved within 10 weeks. This case indicates the possibility of transmission of sarcoidosis by marrow transplantation.

Adult↗
PubMed1994

[PTCA in the acute state of myocardial infarct: hospital course of 785 consecutive patients].

Rapid reperfusion of the occluded coronary artery is essential for the reduction of mortality and complications of acute myocardial infarctions. Intravenous thrombolytic therapy using various thrombolytic substances has proven to be effective and easy to perform and has gained widespread acceptance for treatment of acute myocardial infarction. Because of several contraindications, as well as failure to achieve patency of the infarcted vessel in 25-30% of patients, severe bleeding complications, a time interval of 6 or more hours after suspected onset of myocardial infarction, and a high rate of recurrent ischemia, this treatment is currently limited to a small percentage of patients with acute myocardial infarction. Immediate percutaneous transluminal coronary angioplasty (PTCA) can be applied to nearly every patient presenting with acute myocardial infarction. Therefore, we offer immediate PTCA as the primary treatment to all of our patients presenting with acute myocardial infarction. Between January 1987 and December 1991, immediate PTCA was performed in 785 of 903 (87%) consecutive patients (aged 23-86 years, mean 61 +/- 10). 82% (640/785) of the patients were men. Anterior myocardial infarction was present in 372 patients (47%), inferior infarction in 413 patients (53%). 245 patients (31%) had 1-vessel disease, 221 patients (28%) two-vessel disease and 319 patients (41%) had three-vessel disease. 97 patients (12%) were in cardiogenic shock. In 675/785 patients (86%) the infarct related vessel was occluded (TIMI < or = 1). 86% of patients had a patent infarct related vessel (TIMI > or = 2) leaving the catheterization laboratory. The overall in-hospital mortality was 6.9% (54/785 patients), after exclusion of high-risk patients (age > 75 years, cardiogenic shock, PTCA under cardiopulmonary resuscitation) mortality decreased to 2.5%. Recurrent ischemia necessitated immediate repeat PTCA in 4.4% of the patients, in 8.1% of patients another elective PTCA was performed during hospitalization and 9.7% of patients were sent to surgery (4.0% on an emergency basis). 87% of all patients presenting with acute myocardial infarction could be treated successfully with immediate PTCA. With respect to the severely ill group of patients the primary success rate is high, the rate of reocclusion is low, and the overall mortality is extremely low. From our data, it is obvious that immediate PTCA compared to thrombolytic therapy is the superior treatment of myocardial infarction.

Adult↗
PubMed1992

[Chronic intermittent urokinase therapy in therapy-refractory angina pectoris].

To assess the effect of urokinase-induced reduction of fibrinogen concentration on myocardial perfusion, urokinase infusions were administered for 3 months to 24 men (mean age 59 +/- 10 years) in the inoperable end-stage of coronary heart disease with treatment-resistant angina pectoris. Initially 500,000 IU urokinase were infused i.v. daily until a fibrinogen concentration of 150-200 mg/dl was reached. Treatment was then continued as out-patients at a dosage of 500,000 IU two to four times per week. After 12 weeks the fibrinogen concentration had fallen from 348 +/- 88 to 211 +/- 52 mg/dl and plasma viscosity from 1.44 +/- 0.08 to 1.33 +/- 0.09 mPa.s (P for each less than 0.01). Up to the end of 12 weeks after the end of treatment the frequency of anginal attacks fell significantly from 3.2 +/- 1.6 to 0.7 +/- 0.4 daily (P less than 0.01), while ergometric exercise capacity increased by 76%. Thallium myocardial scintigraphy demonstrated an increased perfusion in all but three of 19 patients, global in 10, regional in 6. These results indicate that in patients with treatment-resistant angina due to coronary heart disease chronic intermittent urokinase infusion provides a promising treatment alternative.

Aged↗
PubMed1992

Reduced peripheral and coronary vasomotion in systemic hypertension.

In 53 patients with a history of arterial hypertension and 16 normotensive control subjects, coronary blood flow reserve by means of the argon method, and peripheral vascular flow reserve by means of venous occlusion plethysmography, were studied. The coronary flow reserve, expressed as the ratio of coronary vascular resistance under resting conditions to the minimal coronary vascular resistance after the administration of dipyridamole, was 4.34 +/- 0.89 in the normotensive group and 2.18 +/- 0.60 in the hypertensive group. There was no significant difference in forearm peak flow after 3 min of arterial occlusion between normotensive and hypertensive patients, while the peripheral minimal vascular resistance was significantly higher in hypertensive patients (8.8 +/- 3.8 mmHg x ml.min-1 x 100 ml-1 tissue) as compared to normotensive subjects (6.37 +/- 2.37 mmHg x ml.min-1 x 100 ml-1 tissue). Parallel to the reduction in coronary reserve, the peripheral flow reserve, expressed as the ratio of peripheral resting vascular resistance to peripheral minimal vascular resistance after 3 min of arterial occlusion, was significantly lower (P less than 0.01) in hypertensive subjects (3.85 +/- 2.28) as compared to normotensive subjects (5.31 +/- 1.72). These data suggest that in hypertensives an impaired vasodilator reserve of both coronary and peripheral microcirculation exists.

Angina Pectoris↗
PubMed1990

Blood rheology as a contributing factor in reduced coronary reserve in systemic hypertension.

The influence of blood fluidity on coronary reserve in patients with essential hypertension and normal coronary arteries was examined. The coronary reserve, expressed as the ratio of coronary vascular resistance under resting conditions to the coronary vascular resistance after administration of dipyridamole, was 4.1 +/- 1.5 in 10 normotensive patients with normal coronary arteries, whereas the mean value was only 2.4 +/- 0.8 in 35 hypertensive patients. When compared with the normotensive control group the 35 hypertensive patients had significantly higher levels of hematocrit (45.9 +/- 3.7 vs 42.3 +/- 3.6; p less than or equal to 0.01) and plasma viscosity (1.39 +/- 0.07 vs 1.32 +/- 0.06 mPas; p less than 0.01). Plasma fibrinogen (291 +/- 67 vs 251 +/- 25 mg/dl) and whole blood viscosity at a shear rate of 2 s-1 (7.77 +/- 1.1 vs 7.21 +/- 1.28 mPas) and at a high shear rate of 100 s-1 (4.23 +/- 0.57 vs 3.91 +/- 0.64 mPas) demonstrated a trend without statistical significance toward higher values in hypertensive patients. When the hypertensive group was further divided according to the coronary reserve (less than 2.5, severely impaired coronary reserve; greater than 2.5 less than 3.8, moderately impaired coronary reserve), the parameters of blood fluidity clearly correlated inversely with coronary reserve. This suggests a major importance of rheologic abnormalities on impaired coronary reserve in hypertensive patients.

Angina Pectoris↗
PubMed1990

[Acute effects of extracorporeal LDL cholesterol and fibrinogen elimination on blood rheology and microcirculation].

Long-term intermittent heparin-induced extracorporeal low-density lipoprotein (LDL)-cholesterol precipitation was performed in three men - aged 32, 52 and 56 years - with severe familial hypercholesterolaemia and angiographically demonstrated coronary heart disease. This significantly lowered by 65-70% their LDL-cholesterol concentration and by 48-54% their fibrinogen concentration. Fibrinogen elimination reduced plasma viscosity by 13-14% and clearly raised the transcutaneously measured partial pressure of oxygen by 33-50%. Clinically the improved microcirculation achieved a decrease in angina symptoms: the walking distance of the 52-year-old man increased from about 100 m to 4000 m, the daily need of glyceryl trinitrate falling from an average of 12 to 4 aerosol doses.

Adult↗
PubMed1990

[Rheologic changes in the postprandial phase].

In this study, the postprandial changes of blood rheology and lipid parameters after a lipid-enriched test meal (75% lipids) versus a normal lipid composition control meal (30% lipids) were monitored. Six healthy volunteers were given a high lipid test meal (85 g lipids, 3800 kJ) as well as a control test meal (30% lipids, 3730 kJ) after 7 days. 3-6 hours after ingestion of the test meal, triglyceride levels peaked with an increase of about 120% after the lipid-enriched test meal and of about 55% after the control meal. The mean levels of plasma viscosity increased from 1.25 mPas to 1.29 mPas 3 hours after ingestion of the lipid-enriched test meal, whereas the blood rheology parameters, such as plasma viscosity and red blood cell aggregation, were nearly unchanged after the control meal with normal lipid composition. The changes of plasma viscosity after the lipid-enriched test meal were caused by an increase of triglyceride levels and an increase of fibrinogen levels in the postprandial phase by nearly 60% (mean value). Two different rheological reaction patterns have been demonstrated. Whereas 5 individuals showed the increase of blood rheology parameters mentioned above, one person had a very pronounced increase of plasma viscosity from 1.34 to 1.42 mPas and fibrinogen levels from 155 mg/dl to 280 mg/dl after the lipid-enriched test meal. This marked postprandial increase of blood viscosity may contribute to a flow limitation of myocardial microcirculation in patients with coronary artery disease.

Adult↗
PubMed1990

[The significance of rheologic mechanisms in atherogenesis].

Beside the well-known risk factors for atherogenesis fibrinogen is an independent risk factor. High plasma fibrinogen levels predispose to hypercoagulability and thrombotic processes. Furthermore, rheological mechanisms, interfering with cell-to-cell contacts, and fluid-dynamic factors, facilitate local endothelial lesions resulting in atherosclerosis. Plasma fibrinogen, as the major contributing factor to plasma viscosity and red-blood-cell aggregation can limit oxygen supply and blood flow in microcirculation even in the absence of apparent coronary artery disease. Pharmacological interventions, in order to decrease elevated fibrinogen levels, do improve myocardial ischemia in patients with severe coronary artery disease.

Arteriosclerosis↗
PubMed1989

[Effect of fenofibrate on fibrinogen concentration and blood viscosity. Consequences for myocardial microcirculation in coronary heart disease?].

The effect of fenofibrate (a clofibrate derivative) on fibrinogen concentration, blood viscosity and myocardial microcirculation was examined in 35 patients with coronary heart disease (n = 27) or hypertension (n = 8). After eight weeks' administration of 250 mg fenofibrate daily cholesterol and triglycerides levels decreased significantly, as did the fibrinogen concentration, from a mean of 300.7 +/- 75.1 mg/dl to 252.3 +/- 61.2 mg/dl (P less than 0.01). Plasma viscosity and erythrocyte aggregation were also significantly lowered (from 1.43 +/- 0.09 to 1.37 +/- 0.07 mPas and 15.0 +/- 3.1 to 13.5 +/- 2.2, respectively; P less than 0.01). In eight of twelve subjects selected from the whole group thallium myocardial scintigraphy demonstrated, after eight weeks of treatment with fenofibrate, a global (in two) or regional (in six) increase in blood flow. Reduction of fibrinogen concentration may in coronary heart disease achieve an improvement in myocardial microcirculation with decreased myocardial ischaemia.

Blood Viscosity↗
PubMed1988

[Hyperfibrinogenemia and pathological plasma viscosity. Pathogenetic factors in unstable angina pectoris?].

Plasma viscosity and erythrocyte aggregation, as the most important rheological factors in the microcirculation, and fibrinogen were measured in the blood of groups of patients in various stages of coronary-heart disease. Patients with unstable angina had viscosity and fibrinogen levels, even before any manifest infarction, that were higher than those of patients with stable angina. Plasma viscosity and hyperfibrinogenaemia (1.39 +/- 0.08 mPa.s in 48 patients and 394.4 +/- 82.7 mg/dl, respectively, in 33) were comparable to the values in patients with acute myocardial infarction (1.37 +/- 0.09 mPa.s [n = 45] and 390.2 +/- 126.9 mg/dl [n = 27], but significantly higher (P less than 0.02) than in those with stable angina (1.33 +/- 0.08 mPa.s [n = 78] and 295.3 +/- 68.6 mg/dl [n = 44], respectively). This abnormal viscosity in unstable angina plays a part in increasing myocardial ischaemia because oxygen delivery is already diminished and capillary flow slowed down. It thus contributes to progression of the angina and must be taken into account as an additional pathogenetic factor in the clinical instability.

Angina Pectoris↗
PubMed1988

Blood rheology and hypertension in hemodialysis patients treated with erythropoietin.

Fifteen hemodialysis patients suffering from stable anemia were treated with recombinant human erythropoietin (r-HuEPO). Within 16 weeks, hematocrit values increased from 23.7 +/- 1.2 to 35.7 +/- 0.2%. Simultaneously, mean predialytic blood pressure rose significantly from 131/79 to 139/85 mm Hg. Three out of 15 patients developed frank hypertension and had to be put on antihypertensive therapy. When the hematocrit was lowered again from 36.3 +/- 1.8 to 30.5 +/- 1.2% in these 3 patients, blood pressure was attenuated and the antihypertensive medication could be reduced or abolished. With rising hematocrit values, whole blood viscosity increased at both low (+42%) and high shear rates (+33%) without reaching the values seen in healthy subjects. By contrast, plasma viscosity was already elevated in hemodialysis patients prior to r-HuEPO treatment and showed only a slight, but insignificant increase during r-HuEPO treatment. Since whole blood viscosity is one factor that determines vascular resistance, it is conceivable that the development of hypertension during correction of the renal anemia is, at least partly, due to an increment of blood viscosity.

Adult↗
PubMed1987

[Significance of the thrombin-antithrombin III complex in the diagnosis of pulmonary embolism and deep venous thrombosis--comparison with fibrinopeptide A, platelet factor 4 and beta-thromboglobulin].

In 22 patients with suspected pulmonary embolism and 19 patients with suspected deep vein thrombosis, thrombin-antithrombin III complex (TAT) as an indicator of thrombin activation was measured using a newly developed ELISA. For comparison fibrinopeptide A (FPA), as a marker of an activated coagulation, as well as platelet factor 4 (PF4), and beta-thromboglobulin (beta-TG), as markers of platelet activation, were determined. In all patients in whom pulmonary embolism was confirmed by perfusion lung scan and in 15 of 16 patients in whom deep vein thrombosis was confirmed by phlebography, TAT exceeded the upper limit of normal (3.0 ng/ml). FPA was increased in 71% of the pulmonary embolism patients, PF4 in 53%, and beta-TG in 59%. The data for the patients with deep vein thrombosis were comparable. PF4 and beta-TG were increased in more than 25% of the normal controls, FPA in 17%, and TAT in 9%. TAT is very sensitive in detecting an activation of the coagulation system in patients with suspected thromboembolic events. The test, however, is not specific for thromboembolism; it only indicates an activation of the coagulation system. Acute pulmonary embolism or deep vein thrombosis would appear to be unlikely if TAT is normal. The measurement of TAT is easier and less susceptible to disturbances than that of FPA, PF4, and beta-TG.

Antithrombin III↗