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Biomedical subjects

M Leschke

Publications and source records attributed to M Leschke.

100 records · Page 6Linked to original sources
PubMed1987

[Heparin-induced thrombopenia].

Cutaneous necroses, acute renal failure and an adrenocortical insufficiency appeared during heparin therapy in a 47 year old patient with myocardial infarction. The thrombocytes fell to 73,000/microliter and displayed intensified spontaneous aggregation. In histological investigation of the cutaneous necroses, intensive thromboses of the cutaneous and subcutaneous blood vessels were found. The findings indicate a thromboembolic etiology of the acute renal failure and the adrenocortical insufficiency. This case involves a complex example of a heparin-induced thrombopenia with thromboembolic complications.

Acute Kidney Injury↗
PubMed1987

Blood rheology in hypertension and hypertensive heart disease.

Blood rheology was studied in 50 patients with a long history of essential hypertension, together with severe left heart hypertrophy (mass-volume relationship greater than 1.6) and angina pectoris, as well as in 17 patients with renoparenchymal hypertension. The rheologic findings were compared with those of 34 normotensive patients in whom coronary artery disease (CAD) was excluded by coronary angiography. Based on angiographic findings, the patients with essential hypertension could be differentiated into two groups: 20 hypertensive patients with normal coronary arteries and 30 hypertensive patients with coexistent CAD. In renoparenchymal hypertension, increased plasma viscosity (1.39 +/- 0.08 mPas) secondary to elevated fibrinogen levels (406.8 +/- 84.6 mg/100 ml) was found. Whole blood viscosity at low and high shear rates and the elastic component of blood were significantly more elevated in patients with renal hypertension than in patients with essential hypertension. In 30 patients with essential hypertension and coexistent CAD, higher levels of plasma viscosity (1.37 +/- 0.08 mPas, p less than 0.05) and fibrinogen (294.1 +/- 55.1 mg/100 ml, p less than 0.02) were found than in patients with essential hypertension and normal coronary arteries (1.32 +/- 0.07 mPas and 259.8 +/- 44.9 mg/100 ml, respectively). Hypertensive patients with normal coronary arteries, however, showed significantly higher levels of plasma viscosity, red blood cell aggregation, and whole blood viscosity than did normotensive controls. It is conceivable that increased blood viscosity in hypertensive patients with normal coronary arteries contributes to angina pectoris and to the reduction in coronary reserve that is observed in hypertensive patients (1).

Blood Viscosity↗
PubMed1987

Effect of intravenous nifedipine on hemodynamics and left ventricular function in acute myocardial infarction.

Twenty-one patients with acute myocardial infarction were treated 7.6 +/- 4.9 h after the onset of symptoms with intravenous nifedipine for 48-72 h. No other vasoactive medication was given. Three patients with hypertension did not respond to nifedipine and were excluded from the analysis. In the remaining 18 patients, arterial blood pressure decreased significantly, whereas the heart rate remained unchanged. The mean pulmonary artery and capillary pressure showed a slight but significant decrease. Cardiac index increased significantly. In nine patients, two-dimensional and M-mode echocardiography could be analyzed. The left ventricular ejection fraction increased significantly from 50 +/- 3% to 56 +/- 1%. There was a significant decrease in systemic peripheral resistance index, systolic wall stress, and the calculated myocardial oxygen consumption. These hemodynamic effects persisted throughout the study period. The therapy was well controllable, and there were no significant side effects. Nifedipine improves left ventricular function without an increase in myocardial oxygen demand. This effect is primarily due to afterload reduction.

Acute Disease↗
PubMed1986

[Hemorheologic therapy applications in coronary heart disease].

A significant correlation was found between heightened plasma viscosity and increased red blood cell aggregation and the severity of coronary artery disease. At low shear rates and exhausted vasomotion these rheological factors can cause a reversible loss of fluidity. The reduced fluidity may induce a limitation in microcirculatory flow due to the viscus resistance. Rheological treatments aim at restoration of impaired perfusion by decreasing plasma viscosity and thus diminishing red blood cell aggregation. Further therapeutic measures tend to improve red blood cell deformability. Because of limited coronary reserve in coronary artery disease hemodilution therapy is contraindicated except the cases with polyglobulia. Thrombolytic therapy in acute myocardial infarction causes a significant reduction of plasma viscosity and red cell aggregation for at least 72 hours. This improvement in blood fluidity may beneficially influence the reperfusion of ischemic areas. A therapy with orally active hemorheological drugs (pentoxifylline and buflomedil) can be discussed as an additive treatment in severe angina pectoris refractory to specific medical therapy, since these drugs increase fluidity and inhibit platelet aggregation. The defibrination may cause thrombotic and bleeding complications in the early phase of treatment. Coronary small vessel disease represents a rare type of coronary heart disease. This disease is defined by normal epicardial coronaries and reduced coronary artery reserve. In disorders of coronary microcirculation with abnormal rheology (Waldenstrom's macroglobulinemia) rheological treatment is a rational and causal therapy.

Blood Viscosity↗
PubMed1984

[Serum levels and urine excretion of L-carnitine in patients with normal and impaired kidney function].

The influence of age, sex, and renal function on serum levels and urinary excretion of free carnitine was studied in 187 subjects. Sixty-one subjects with normal renal function (creatinine clearance greater than 100 ml/min) showed a serum carnitine level of 72.2 +/- 23.2 mumol/l. The carnitine values of males (76.8 +/- 23.3 mumol/l, n = 39) were higher (p less than 0.05) than those of females (64.0 +/- 21.0 mumol/l, n = 22). Carnitine levels did not correlate with age. Values in patients with normal renal function did not differ from serum carnitine levels in healthy controls (74.7 +/- 17.5 mumol/l, n = 49). The mean urinary carnitine excretion per day was 163.5 mumol (range 63.7-419.6 mumol) in patients with intact renal function. Extreme impairment of glomerular filtration rate (creatinine clearance less than 20 ml/min) resulted in higher carnitine concentrations in serum (108.9 +/- 39.4 mumol/l, n = 18, p less than 0.05), lower carnitine elimination per day (78.5 mumol, range 14.5 - 424.3 mumol, n = 18, p less than 0.05) and a decreased carnitine clearance (0.8 ml/min, range 0.2 - 3.8 ml/min). These data together with earlier results obtained in dialysis patients suggest that carnitine metabolism in renal failure is altered by reduction of both endogenous carnitine biosynthesis and renal carnitine clearance.

Adolescent↗
PubMed1984

Recent progress in improving data processing in filtration measurements.

Nucleopore filter membranes currently utilized to assess RBC "deformability" do not meet the strict metrological requirements of a measuring gauge. They present different kinds of inhomogeneities introducing an useless information (a background noise) into measurement results and expressed as poor reproducibility. Variance reduction can only be achieved by eliminating aberrant results from a series of parallel measurements made with different membranes. To this end a procedure is proposed to identify aberrant values by an iterative statistical regression analysis of data from filter calibration and measurements on RBC suspensions and to express results as "reduced" initial flow rates for a standard filter resistance.

Erythrocytes↗
PubMed1983

Quantitative assessment of carnitine loss during hemodialysis and hemofiltration.

Carnitine deficiency has been claimed to be responsible for the myo- and cardio-myopathy observed in dialysis patients and has been attributed to the loss of carnitine during dialysis. To quantitate carnitine loss, we determined the carnitine concentrations in 29 patients on chronic hemodialysis, 10 patients on chronic hemofiltration, and 8 patients on CAPD. Mean plasma carnitine levels in hemodialysis and hemofiltration patients (39.8 +/- 2.7 mumoles/liter; N = 39) were significantly lower (P less than 0.01) than in controls (49.8 +/- 2.0 mumoles/liter; N = 43). Hemodialysis or hemofiltration led to a further reduction (33.2 +/- 3.5 mumoles/liter; P less than 0.001). There was no significant difference in the mean plasma carnitine level between CAPD patients (40.0 +/- 5.7 mumoles/liter) and controls. Hemofiltration treatment resulted in a weekly loss of 795 +/- 84 mumoles of carnitine. This was significantly lower (P less than 0.0001) than the urinary carnitine excretion in healthy controls (1534 +/- 134 mumoles per week; N = 27) and the carnitine elimination in the dialysate of CAPD patients (1905 +/- 236.6 mumoles per week; N = 8). It is concluded that carnitine deficiency in dialysis patients cannot be explained by loss into dialysate or filtrate. Because intestinal reabsorption of carnitine does not seem to be impaired, decreased endogenous carnitine synthesis is considered as the most plausible explanation for the moderate degree of carnitine deficiency observed in dialysis patients.

Adult↗
PubMed1983

Quantitative assessment of carnitine loss during haemodialysis and haemofiltration.

Carnitine concentrations were measured in plasma, haemofiltrate, dialysate and urine of patients on regular dialysis treatment and in normal controls. Patients on haemofiltration and on haemodialysis exhibited moderately decreased plasma values, whereas in eight patients on CAPD mean values did not differ from controls. Carnitine loss into the haemofiltrate was significantly lower than urinary carnitine excretion in normal subjects. Major disturbances of intestinal carnitine absorption in patients on regular dialysis treatment were not observed. It is concluded that patients on regular dialysis are in a state of moderate carnitine deficiency and that therapeutically induced carnitine losses or grossly impaired intestinal absorption are not major factors in the development of carnitine deficiency in these patients.

Blood↗
PubMedDate not supplied

Low-dose intermittent urokinase therapy in chronic symptomatic end-stage arterial disease--clinical relevance for patients with coronary artery disease or peripheral arterial occlusive disease.

Symptomatic end-stage arterial disease in coronary artery or peripheral arterial occlusive disease represents an increasing clinical problem as cardiovascular mortality in these patient groups has declined due to improved secondary prevention. While in peripheral arterial occlusive disease amputation with subsequent life-long physical disability is the major problem, patients with end-stage coronary artery disease and refractory angina pectoris repeatedly report to the emergency ward with the clinical symptoms of unstable coronary syndromes, but myocardial infarction is generally ruled out. For these patients long-term intermittent urokinase therapy has been developed as an alternative treatment modality. Potential mechanisms for clinical effectiveness include improvement of rheological blood properties, thrombolysis of non-occluding arterial thrombi and possibly plaque regression. In coronary artery disease urokinase is applied as an intravenous bolus injection of 500,000 IU urokinase three times a week over a period of 12 weeks. This leads to a marked reduction of fibrinogen by about 35% and of clinical symptoms by around 70% accompanied by a reduction of exercise-induced myocardial ischemia. In observational studies in patients with peripheral arterial occlusive disease injections of 500,000 IU of urokinase were usually given daily for a shorter time period of three to four weeks with a clinical success rate, defined as a cessation or marked reduction of rest pain and/or salvage of a limb, of around 50%. Given the state of critical ischemia in both entities of atherosclerotic disease, long-term intermittent urokinase therapy represents a promising antiischemic approach. In particular in patients with peripheral arterial occlusive disease randomized controlled trials with prolonged treatment periods, which are likely to improve clinical results, are warranted.

Arterial Occlusive Diseases↗