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Rheological therapy aims at an improvement of organ perfusion however, it has to be stressed that the tonus of the blood vessels also plays an important role for both the blood distribution and the rheology in the micro- and the macrocirculation. Conventional rheotherapy consists of attempts to influence nutrition and life style, to apply drugs such as purin derivatives, vasodilatating or defibrinising substances and hypervolaemic (using infusion therapy), hypovolaemic, e.g., blood letting, erythrocytapheresis and--the most widely distributed- -isovolaemic haemodilution. With the introduction of centrifugal devices, and approximately 10 years later with the introduction of hollow fibre and flat sheet membrane techniques, a considerable increase of therapeutical efficacy was achieved. These technologies were successfully applied for the treatment of cellular and plasmatic hyperviscosity syndromes. The treatment of less severe diseases of the micro- and macrocirculation, vessel stenosis, vessel wall sclerosis, malformation of the blood vessel architecture, pathological clinical-chemical blood parameters and maldistribution have hardly been taken into consideration. Our group at Köln investigated different plasma differential separation techniques and demonstrated, that adsorption as well as filtration could be applied. These different techniques being 6-10 times more effective as conventional haemodilution techniques have in common high molecular weight proteins determining the viscosity of plasma and thus whole blood viscosity is removed, however differences among the different elimination techniques do exist. The rheological and clinical importance of such differences has to be determined. Applying filtration techniques for both primary and secondary separations, the concept of Rheohaemapheresis was developed. A corresponding quality program was also introduced into our clinical routine. Rheohaemapheresis is supported from the currently introduced concept of the synergetic consideration of the microcirculation. Age related macular degeneration, so far without generally accepted therapy, is a most advanced indication based on several pilot studies and a prospective, randomised controlled trial. Other diseases of the microcirculation have also successfully been treated.

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Rheological therapy attempts to favorably influence the blood flow mechanics for the treatment of diseases, mainly of the microcirculation but also of the macrocirculation. Hemapheresis, originally used only for the elimination of an excess of cellular or plasmatic components, was shown to also influence the hemorheology favorably. As extracorporeal therapy affects the rheology much more than conventional hemorheotherapy, not only cellular or plasmatic hyperviscosity syndromes but also many more diseases associated with organ perfusion problems due to diseases of the micro- and macrocirculation, especially in the elderly, were and are increasingly considered to be indicated. Technical progress led away from plasma exchange as an unspecific and unselective procedure to plasma differential separation using precipitation. adsorption, and filtration. With our recent development, we demonstrated that rheohemapheresis is the most advanced technical procedure. The mechanism of action can well be related to a synergetic consideration of rheology. However. one has to keep in mind that the elimination of blood components such as lipids, immunoglobulins, and endothelial factors may well contribute to the explanation and understanding of the positive clinical effects observed. These speculative aspects need further investigation.

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The efficacy and tolerance of the standardized hawthorn (crataegus) extract WS 1442 were tested in a multicenter utilization observational study. We monitored 1,011 patients with cardiac insufficiency stage NYHA II, treated with this extract (Crataegutt novo 450, 1 tablet b.i.d.) over a period of 24 weeks. During and at the end of the observation period a significant improvement in clinical symptoms (reduced performance in the exercise tolerance test, fatigue, palpitation and exercise dyspnea) was observed. Ankle edema and nocturia disappeared by 83%, and by half of the patients respectively manifesting these symptoms before treatment. The improvement and economization of cardiac performance were additionally shown by a reduction in blood pressure, an increased maximal exercise tolerance and a reduction in the difference in the pressure/heart rate product (PHRP). The positive effects of WS 1442 were further demonstrated by an improved ejection fraction and an increased percentile shortening fraction measured using M-mode echocardiography. The stabilizing effect of the hawthorn extract on the heart rate was shown by a slower rest pulse, as well as by an increase in the number of day and night normorhythmic patients, as documented by long-term ECG. The reduction in the number of patients showing ST depressions, arrhythmias and ventricular extrasystoles at the maximum exercise level is regarded as an indication for an improved myocardial perfusion. Fourteen side effects were noted. In two cases (abdominal discomfort and facial pains accompanied by tachycardia) a possible relationship with the hawthorn therapy, was postulated which however was considered unlikely by the treating physicians. Almost 2/3 of the patients felt better or much better following the 24 weeks of treatment. More than 3/4 of the participating physicians noted a good or a very good efficacy, and 98.7% noted a good or a very good tolerance. High-dose hawthorn therapy is an efficient, well-tolerated and easily regulated therapeutic alternative for patients suffering from cardiac insufficiency stage NYHA II.

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BACKGROUND: The most important complications of deep vein thrombosis are pulmonary embolism and postthrombotic syndrome. While the medicine of lethal pulmonary embolism is reduced to less than 2% by conventional anticoagulation, fibrinolytic therapy aims at a reduction of the greater than 50% incidence of postthrombotic syndrome. The optimal therapeutic regimen concerning risks and effect has not been established yet. RESULTS: A review of 26 studies involving ultrahigh-dose streptokinase (UHSK), urokinase (UK), and tissue-type plasminogen activator (rt-PA) shows the highest success rate for UHSK (45% complete and 40% parital patency), whereas there are lower rates for UK (25% and 40%) and low-dose locoregionally applied rt-PA (22% and 44%). The studies were not directly comparative, however. Published data concerning complications range from 1.7% mortality for UHSK to 0.9% for UK and 0.0% for rt-PA. Success criteria, however, are varying and not well defined. The influence of fibrinolytic therapy on the incidence of postthrombotic syndrome has not been established prospectively, but a reduction by 40 to 50% can be assumed. Calf vein thromboses are not indication for lytic therapy. In patients with iliacal vein thromboses there is an increased risk of pulmonary embolism using UHSK. CONCLUSIONS: UHSK can be regarded the standard concerning success rate in deep vein thromboses. DATA involving locoregional therapy with rt-PA are inconsistent and worse, but bleeding complications might be less frequent. Large prospective studies evaluating the impact on incidence and severity of the postthrombotic syndromes, which involve a controlled application of compression therapy are needed.

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Only few cases of myocardial infarction complicating dobutamine stress echocardiography have been reported. We observed a 42-year-old woman in whom acute inferior wall infarction developed 10 minutes after discontinuation of dobutamine stress echocardiography with up to 20 micrograms/kg/min dobutamine. The right coronary artery, which had had a 50% stenosis in the prior angiography, showed proximal complete occlusion on the immediately performed recatheterization. Thrombolysis in myocardial infarction study flow grade 3 was rapidly accomplished by intracoronary thrombolysis with recombinant tissue type plasminogen activator. For recurrent unstable angina, the patient received coronary bypass grafting on the same day. The case shows that myocardial infarction not preceded by regional wall motion abnormalities is a possible complication of dobutamine stress echocardiography. Post-test monitoring even after negative tests is recommended.

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Ninety-five patients with syndrome X were studied by brain single-photon emission computed tomographic examination; 72 (76%) had pathologic findings suggestive of cerebral perfusion abnormalities. These findings support the hypothesis of a vascular disorder not confined to cardiac vessels.

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A 57-year-old man with a cough and increasing exertional dyspnoea for the past 6 weeks was found on examination to have a loud systolic murmur and cardiomegaly with pulmonary congestion. Echocardiography revealed congenitally corrected transposition of the great arteries (cTGA: atrioventricular and ventriculoarterial discordance): a morphologically right ventricle with a tricuspid valve on the left, a morphologically left ventricle with bicuspid a-v valve on the right, the aorta arising ventrally from the left-sided (morphologically right) ventricle. The tricuspid valve showed an Ebstein-like anomaly with obvious regurgitation. Transoesophageal and contrast echocardiography defined valvar anatomy, attachment of the great arteries and cardiac chambers to the venous and arterial circulations, as well as absence of a left to right shunt. Angiography revealed a coronary anatomy typical for cTGA. The exertional dyspnoea responded to diuretics and low doses of ACE inhibitor. Follow-up monitoring of the valvar regurgitation and appropriate endocarditis prophylaxis were recommended. As the haemodynamics in cTGA is normal, in the absence of additional anomalies, it is a congenital cardiac defect which can, though rarely, present first in adulthood. Life expectancy depends on the nature of any additional defects and the degree of commonly associated tricuspid valve regurgitation. As this case demonstrates, echocardiography can largely define the anomalies.

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The possibility of maintaining preload reduction and enhancement of exercise tolerance during an interval treatment with 100 mg/day of slow-release isosorbide-5-mononitrate (IS-5-MN) was investigated in 12 patients (aged 57 +/- 5.0 years) with angiographically confirmed coronary artery disease and chronic stable angina pectoris. The effects of a single dose (acute test) were compared with those following an 8-day (chronic) regimen of mononitrate administration. Two hours after administration of 100 mg sustained-release IS-5-MN, mean resting pulmonary artery pressure (PAP), measured with a Swan-Ganz catheter, was reduced by 32% (p less than 0.001) and at submaximal exercise level (50 W, 3 min) by 37% (p less than 0.001). At individually highest comparable work loads mean PAP was reduced by 37% (p less than 0.001), and at maximal work load the PAP reduction was 14% (p less than 0.05). At the end of 1 week of therapy with sustained-release IS-5-MN a slight, clinically irrelevant reduction of hemodynamic effect was recorded. Work capacity increased after 1 h by 79% (264 +/- 154 vs. 472 +/- 180 W x min, p less than 0.01), still significantly above base-line 10 h after nitrate administration. No difference from baseline was demonstrable 24 h after medication. During interval therapy the improved work capacity was fully maintained (chronic, 1 h: 280 +/- 119 vs. 532 +/- 160 W x min, p less than 0.001). There was no significant difference between the plasma IS-5-MN levels at acute and chronic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

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Pulmonary embolectomy as an emergent surgical treatment after massive pulmonary embolism often is necessary in cardiogenic shock (CS) and even without previous diagnostic. If complete dissolution of the thromboembolus is possible or spreading of microemboli may occur is unknown. Therefore we studied 21 patients surgically treated by embolectomy, ten of these with consecutive cardiogenic shock (CS) and twelve patients after repetitive microembolism and cava-blocking. Besides lung-functional parameters for special CO-diffusion capacity (DLCO), differentiated in membrane (DM) and vascular (VC) component (Roughton and Forster), we measured mean pulmonary artery pressure (PAP) at rest and at exercise. Patients after repetitive embolism showed considerably more diminution of DLCO (-31%) than those after single massive embolic event (-15%) even concomitant by CS (-10%). Repetitive microembolism lowered VC by 21%. Slight decrease of DM was found after CS. Mean pulmonary artery pressure was elevated at rest (26 mm Hg) and exercise (33 mm Hg) after repetitive microembolism and normal after massive embolism or CS. Pulmonary embolectomy may prevent disturbances of DLCO or PAP even after CS. Damage of vascular integrity (VC) was found after microembolism. Pulmonary embolectomy seems to remove total embolic material and therefore seems to be optimal.

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The possibility of maintaining preload reduction and enhancement of exercise tolerance during an interval treatment with 50 mg/day of sustained-release isosorbide-5-nitrate (IS-5-N) was investigated in 13 patients (aged 54.4 +/- 7.9 years [mean +/- standard deviation]) with angiographically confirmed coronary artery disease and chronic stable angina pectoris. The effects of a single dose (acute test) were compared with those following an 8-day (chronic) regimen of mononitrate administration. Two hours after administration of 50-mg sustained-release IS-5-N, mean resting pulmonary arterial pressure (PAP), measured with a Swan-Ganz catheter, was reduced by 27% (p less than 0.01), and at submaximal exercise level (50 W, 3 minutes) by 34% (p less than 0.001). At individually highest comparable work loads mean PAP was reduced by 28% (p less than 0.01), and at maximal work load the PAP reduction was 21% (p less than 0.05). At the end of 1 week of therapy with sustained-release IS-5-N a slight, clinically irrelevant reduction of hemodynamic effects was recorded. Work capacity increased after 1 hour by 60% (408 +/- 104 vs 653 +/- 147 W x min, p less than 0.001)--still significantly above baseline 10 hours after nitrate administration. No difference from baseline was demonstrable 24 hours after medication. During interval therapy the improved work capacity was fully maintained (chronic, 1 hour: 417 +/- 93 vs 679 +/- 160 W x min, p less than 0.001). During interval therapy with sustained-release IS-5-N, hemodynamics and exercise tolerance were durably improved.(ABSTRACT TRUNCATED AT 250 WORDS)

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Testing of the chronic therapeutic effects of antianginal drugs is commonly performed by stress electrocardiography. It is well known that this type of testing is easy to be disturbed by the influence of circadian rhythmus and placebo. However, by hemodynamic measurements such as the determination of pulmonary arterial pressure each patient can serve as his own control in therapeutic studies if the reproducibility of these parameters is acceptable. In 29 patients with coronary heart disease the reproducibility of the following parameters was tested at rest and during exercise and found to be acceptable: heart rate, mean arterial pressure, mean pulmonary arterial pressure, and working capacity. In additional studies the application of these parameters on the control of chronic therapy with antianginal drugs was performed. The results were: 1. A 1-week placebo treatment does not influence the parameters. 2. Long-term therapy with 3 x 20 mg of ISDN or IS-5-N daily over 4 weeks does not induce tolerance, whereas the dosage of 3 x 60 mg ISDN resp. 3 x 50 mg IS-5-N induces a remarkable degree of tolerance. 3. A 4-week therapy with 3 x 4 mg or 3 x 8 mg molsidomine daily resp. 4 mg or 8 mg molsidomine retard does not induce significant attenuation of the hemodynamic effects. 4. On a single-dose therapy with 50 mg IS-5-N retard ("interval-therapy") the therapeutic effects are maintained over at least 1 week.

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Fluctuating mononitrate plasma levels in the course of 24 h are a prerequisite for prevention of nitrate tolerance in patients with angina pectoris undergoing longterm treatment. In 12 patients with angiographically proven coronary artery disease (54 +/- 7 years) effects of 50 mg Isosorbide-5-mononitrate (IS-5-MN) in a slow-release (SR) formulation on hemodynamics and exercise tolerance were evaluated after a first dose and at the end of a 1-week treatment period with 50 mg given once-daily. 1 and 2 h after medication mean pulmonary artery pressure (PAP) at rest was reduced by 30% (p less than 0.001) and 25% (p less than 0.01 respectively. During submaximal bicycle exercise (50 W, 3 min) PAP was significantly reduced by IS-5-MN by 35% (1 and 2 h after medication). At the end of exercise (discontinuation), drug-induced reductions of PAP were 19% (1 h) and 21% (2 h) (p less than 0.05), respectively. IS-5-MN led to a marked increase of exercise capacity (base-line: 396 +/- 119 W x min); 1 h: 646 +/- 153 W x min (p less than 0.01). At stress testing 2, 4 and 10 h post medication improvements were 67% (p less than 0.01), 49% (p less than 0.01) and 28% (p less than 0.01), respectively. 24 h after medication baseline values were reached again. After a 1-week treatment with 50 mg IS-5-MN SR daily, beneficial effects of the drug on hemodynamics and working capacity could be demonstrated. Again, significant effects could be shown up to 10 h after drug administration. Thus, IS-5-MN SR administered once daily proved effective in intermediate-term treatment of patients with coronary artery disease with regard to hemodynamics and exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

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The optimal dose of nitrates is still controversial, as chronic usage of too high a dose may result in a decrease in vascular response. The dose should be determined to reduce preload acutely, and not to decrease the activity during chronic therapy. To determine this dose, 50 patients with angiographically confirmed coronary artery disease were studied. The effects on heart rate and mean systemic and pulmonary arterial pressures at rest and during exercise, and work capacity and duration were measured. The patients were classified into 5 groups, receiving placebo or isosorbide-5-mononitrate, 5, 10, 20 and 50 mg, respectively, as a single oral dose. Placebo had no effect on the measured parameters. All doses of isosorbide-5-mononitrate reduced mean pulmonary arterial pressure: 10 mg--by 16% at rest and 24% during exercise; 20 mg--24% and 34%, respectively (a near maximal effect); and 50 mg--27% and 38%. Similar results were found also for work capacity: 10 mg increased work capacity by 33%; 20 mg--79%; and 50 mg--56%. Thus, the therapeutically optimal single dose is about 20 mg. Higher doses produce no additional benefit and increase the risk for tolerance development.

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To test the clinically supposed development of tolerance during chronic molsidomine therapy we studied a total of 11 patients with angiographically-proven coronary heart disease at rest and during ergometric exercise (supine position; submaximal, i.e. 50 W for 3 min, and maximal exercise). Pulmonary arterial pressure (PAPmean, floating catheter), arterial blood pressure (RR, cuff method), work capacity (W x min) and duration of exercise loading (sec) were measured at rest and on exercise before and during chronic (4 weeks) oral therapy with 3 x 4 mg day-1 of molsidomine. Acute administration of 4 mg molsidomine reduced the mean arterial resting pressure by 12% and under submaximal exercise loading by 8%. After molsidomine, the PAPmean was reduced by 35% at rest; following a period of treatment of 4 weeks no significant decrease in efficacy could be discerned (PAPmean reduction by 31%). Under submaximal and maximal exercise the PAPmean dropped by 44% and 37%, respectively (35.5 +/- 6.7 cf. 19.9 +/- 4.5 mmHg; 39.2 +/- 6.5 cf. 24.8 +/- 7.0 mmHg), whilst simultaneously the work capacity increased by 93% (281 +/- 108 cf. 545 +/- 254 W x min). After 4 weeks treatment with 12 mg day-1 of molsidomine, the PAPmean of 22.4 +/- 6.6 mmHg and 30.1 +/- 9.9 mmHg under identical exercise loading conditions, remained significantly below the exercise load value prior to the onset of medication. The molsidomine-induced increase in the exercise tolerance was maintained throughout the long-term medication (537 +/- 268 W x min). With a four-week treatment with daily doses of molsidomine there was a persistent effect on the pulmonary arterial pressure and the work capacity. Thus development of tolerance during high dose, long-term molsidomine therapy is not to be expected.

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In twelve patients with coronary heart disease and hemodynamically significant coronary artery stenoses (LAD: 11, LAD plus RCA: 1) the effect of intracoronary nifedipine, 0.2 mg, on PTCA-related myocardial ischemia was evaluated. The severity of angina pectoris during balloon inflation was not significantly reduced by nifedipine, whereas the sum of ST segment alterations in Einthoven and Goldberger leads on inflation was significantly decreased by the drug. Before inflation intracoronary nifedipine lowered the systolic arterial blood pressure significantly, whereas diastolic and mean aortic pressure and heart rate remained unchanged. At the end of the inflation period heart rates were significantly faster after nifedipine, and the heart rate-blood pressure product higher with nifedipine. No significant correlations could be calculated between the extent of ST segment alterations and any of the hemodynamic parameters. From our results we conclude that, besides the possibility of ventricular afterload reduction, the beneficial cardioprotective effect of intracoronary nifedipine may mainly be attained by the local "cardioplegic" action of this substance.

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