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Biomedical subjects

H Blanke

Publications and source records attributed to H Blanke.

At least 19 recordsLinked to original sources
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↗
PubMed1991

[Chronic thromboembolic cor pulmonale in pacemaker-associated right atrial thrombi. Pulmonary thromboendarterectomy with removal of the electrodes as a life-saving measure].

Life-threatening chronic cor pulmonale occurred in a 22-year-old woman with congenital 3 degrees atrioventricular block, 6 years after implantation of a pacemaker and 3 1/2 years after removal of the pacemaker (the electrodes were too firmly attached to be removed). The emboli originated from the right-atrial thrombi which had formed around the electrodes left in situ. The embolic source shrank during systemic administration of urokinase, initially 600,000 IU in 60 min, then 100,000 IU per hour, and pulmonary perfusion improved transiently. Nonetheless the patient became breathless on the slightest physical exertion. Recurrent syncopal attacks with marked increase of pulmonary artery pressure necessitated pulmonary thrombendarterectomy and removal of the electrode and wires. Thereupon the patient's condition clearly improved so that 6 months postoperatively her exercise tolerance was again unimpaired.

Adult↗
PubMed1990

[The coincidence of acute intermittent porphyria and Crohn's disease].

In the course of four weeks, tetraparesis developed in a 28-year-old man with Crohn's disease for the last six years, treated with glucocorticoids and sulphasalazine. The cause was acute intermittent porphyria which had been previously overlooked because of the similar abdominal symptoms of Crohn's disease. Treatment with glucose, propranolol and haemarginate failed to bring about any improvement, but there was a remission of the porphyria. This case demonstrates that diagnosis of acute intermittent porphyria in the presence of Crohn's disease is difficult, and if delayed therapeutic measures in the face of persisting neurological complications are of little benefit.

Acute Disease↗
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↗
PubMed1989

[Results of left heart catheterization study in 64 patients with nocturnal disorders of respiratory control (sleep apnea)].

Sleep apnea (SA) is associated with increased morbidity of the cardiovascular system, the interaction between the disordering of respiratory coordination and cardiovascular regulation being largely unknown. In 64 patients (age: mean = 54.1; range: 35-67 years) with an increased apnea index (AI greater than 10), a cardiac catheterisation investigation was performed to exclude coronary heart disease (CHD) or cardiomyopathy. CHD was excluded in 39 patients, 6 patients had coronary single-vessel disease, 9 patients coronary two-vessel, and 10 three vessel disease. In 10 patients, cardiomyopathy was detected, while high-grade impairment of the left ventricular ejection fraction (greater than 30%) was observed in five patients. With the exception of a single patient, CHD was observed only in patients in the over-fifty age group. Arterial hypertension was seen in 84% of the patients with, and in 69% of the patients without, CHD. The patient groups with and without coronary heart disease did not differ with respect to apnea index, ten minute index, or the average duration of the 30 longest apneic episodes. Anginal complaints, observed in a total of 72% of the patients, were one of the major indications for coronary angiography. These results do not support the assumption that SA is primarily a consequence of underlying cardiac disease, but do indicate that SA must be considered a cardiac risk factor, especially in view of the fact that pronounced nocturnal changes in blood gases and haemodynamics, together with malignant arrhythmias, are found in conjunction with this disturbance of breathing.

Adult↗
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↗
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↗
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

Influence of pressure on permeability of normal and diseased muscular arteries to horseradish peroxidase. A new catheter approach.

The effects of different distending pressures on permeability of dog and human arteries to horseradish peroxidase (HRP) were studied. A new catheter was employed to achieve the distention of defined vessel segments to the desired pressure. Normal dog brachial arteries were studied both post mortem and in vivo. Mildly to moderately diseased human coronary arteries were studied post mortem. A predictable linear relationship between pressure and penetration of HRP into the dog arterial media was found, using pressures of 0, 150, 300 and 500 mm Hg. Postmortem vessels were consistently less permeable than those studied in vivo. Full penetration of the media by HRP was achieved by application of 300 mm Hg pressure for 45 sec with the new catheter. When human coronary lesions were examined under these same conditions, plaques were readily demonstrated to be permeable to HRP, even to a depth of many hundreds of micrometer. Thus, penetration of arterial wall thickness by HRP (Mr 40,000 dalton) is related to the distending pressure applied. Human coronary plaques also show ready penetrance by HRP. The new catheter described allows the application of these pressures to defined segments of the arterial tree.

Adult↗
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

The proteinase inhibitor complexes (antithrombin III-thrombin, alpha 2antiplasmin-plasmin and alpha 1antitrypsin-elastase) in septicemia, fulminant hepatic failure and cardiac shock: value for diagnosis and therapy control in DIC/F syndrome.

Thrombin (Thr), plasmin (Pl) and elastase (ELP) are serine proteinases which are quickly inactivated by their specific inhibitors (AT III, alpha 2AP, alpha 1AT), if intravascular activation of coagulation and fibrinolytic system or if release from PMN granulocytes by different stimuli (F.I., endotoxin, activated factor XII, a.o.) occurs. The immunological determination of the developing proteinase inhibitor complexes (PIC) AT III-Thr, alpha 2AP-Pl and alpha 1AT-ELP gives information as to whether intravascular coagulation, hyperfibrinolysis or unspecific proteolysis induced by elastase have taken place. Despite the high antiprotease activity in the plasma the a.m. serine proteinases may exert their proteolytic activity towards their specific substrates in vivo. In infectious diseases, fulminant hepatic failure and cardiac shock a complex consumption of coagulation factors and inhibitors may cause severe coagulation defects, microcirculatory disturbances and bleeding tendency. The PICs behaviour was determined in more than 80 patients with infectious diseases, in 5 patients with fulminant hepatic failure (FHF) and 7 patients with cardiac shock. Only in infectious diseases, mainly in septic complications, and septic complications during FHF and cardiac shock, are alpha 1AT-ELP levels found to be highly elevated. After cardiac shock, in FHF and in infectious diseases coagulation and fibrinolysis may additionally be activated. In this case AT III-Thr and alpha 2AP-Pl complexes could be detected in the patients plasma. This indicates that intravascular coagulation and hyperfibrinolysis has additionally taken place. To prevent bleeding complications a replacement therapy with plasma derivatives (AT III, plasminogen concentrate, PPSB and FFP) has been successfully performed in several patients with septic complications and in the 5 patients with FHF and the 7 patients with cardiac shock. No bleeding complication occurred, and the haemostatic balance could be maintained in the treated patients. AT III replacement therapy is necessary to stop DIC, PPSB improves severe coagulation defects, only FFP may additionally provide alpha 1AT, alpha 2AP and factor V. In acute renal failure sometimes plasminogen replacement is necessary to maintain a normal activity of the fibrinolytic system. The complex consumption of coagulation proteins in infectious diseases, FHF and cardiac shock cannot successfully be treated with an anticoagulant such as heparin alone.

Aged↗
PubMed1985

Long-term follow-up after intracoronary streptokinase therapy for acute myocardial infarction.

This article describes the effects on patients treated with intracoronary streptokinase during acute myocardial infarction and long-term follow-up. The mortality and the incidence of cardiac events were assessed during a follow-up period of 35 +/- 5 months. Coronary artery bypass grafting was undertaken in 37% of the patients. Hospital mortality was 11%, (n = 8); none of these deaths was due to myocardial rupture. The postdischarge mortality was 10%; three of these patients experienced sudden death. Serial assessment of left ventricular function in 35 patients showed an increase of angiographic ejection fraction prior to intervention from 50 +/- 4% to 58 +/- 12% (p = 0.005) 36 +/- 53 days later. Gated-blood pool imaging after 16 +/- 7 months (n = 35) and 32 +/- 9 months (n = 31) revealed no change in ejection fraction. Angina pectoris recurred in four of the 35 patients. We studied a historical comparison group, that consisted of 66 patients, who were treated at the same institution prior to the advent of intracoronary intervention techniques; this group was followed for 48 +/- 9 months. Baseline clinical and angiographic parameters were comparable in the two groups. Coronary artery bypass grafting was performed in only 18 of these patients. Mortality during hospitalization and postdischarge was not significantly different in the two groups. Ejection fraction decreased significantly in the comparison group from the first to the second evaluation and remained unchanged during the follow-up period. We conclude that no major adverse effects were associated with intracoronary streptokinase infusion over a long follow-up period. This may be related to the high frequency of coronary artery bypass surgery following reperfusion.

Aged↗