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Of 68 patients successfully resuscitated within a period of 18 months 52 (38 men and 14 women; mean age 63 [32-90] years) were interviewed about their experience shortly after discharge. 37 reported to have been aware of the life-threatening nature of the acute episode; recurrent depressions were noted by 20; a positive change in attitude towards their life had resulted in 24 patients; 49 praised their doctors and nurses; 40 were appreciative of the medical technology used. All but one of the 52 patients would again choose to be resuscitated. After 12 months 38 patients were again interviewed (31 men and 7 women); 16 had died in the meantime. 21 of the 38 felt physically stronger than before, 25 were more cheerful and 34 were living more intensely. 36 of the 38 patients thought the interviews had been helpful and they would have liked more intensive psychiatric care even during their hospital stay.

The haemodynamic effects of nifedipine, verapamil and diltiazem were measured and compared in an open randomized parallel investigation on 44 patients with coronary heart disease and compensated myocardial function. Each set of parameters was measured during a control phase and serially after a single dose (nifedipine in retard form, 20 mg; verapamil, 160 mg; diltiazem, 120 mg) over a period of 180 minutes at rest and after a standardized exercise. All three drugs produced a significant fall in systemic arterial pressure of 10-14% and of left-ventricular stroke work of 10-20% from the initial level. The main differences between the three drugs concerned heart rate and stroke volume. Nifedipine produced a significant rise in heart rate, while it fell by 8-10% below the control value after verapamil and diltiazem. On the other hand, verapamil caused a significant fall in stroke-volume index, while after nifedipine and diltiazem it remained unchanged. These results suggest differential therapeutic use of the various calcium antagonists.

Investigations concerning changes of dipeptidyl-peptidase IV-positive (DP IV+) lymphocytes in the peripheral blood (PBL) were undertaken in 22 patients with primary biliary cirrhosis (PBC) under therapy with ursodeoxycholic acid (750 mg/day). We found that 4-8 weeks after therapy beginning the number of DP IV+ PBL was raised from a low initial suppressed level of 5-12% into a range of 18-33% corresponding to that of a healthy. Concurrently liver function parameters of the patients were improved significantly. The identity of DP IV+ and CDw26+ of peripheral T-cells could be shown by combination of the cytochemical DP IV-staining with the indirect immunofluorescence of the lymphocyte marker CDw26. These results show that the UDCA-therapy in patients with PBC has a direct effect on the immune system and a positive influence on the immuno-regulative capacity.

Investigations concerning changes of dipeptidyl-peptidase IV-positive (DP IV+) lymphocytes in the peripheral blood (PBL) were undertaken in 22 patients with primary biliary cirrhosis (PBC) under therapy with ursodeoxycholic acid (750 mg/day). We found that after 4-8 weeks of therapy the number of DP IV+ PBL was raised from an initially low, suppressed level of 5-12% to 18-33% corresponding to the range observed in healthy subjects. Concurrently liver function parameters of the patients were significantly improved. The identity of DP IV+ CD 26+ peripheral T-cells could be shown by the combination of cytochemical DP IV-staining with the indirect immuno-fluorescence of the lymphocyte marker CD 26. These results show that the UDCA-therapy in patients with PBC has a direct effect on the immune system and a positive influence on the immuno-regulative capacity.

Of 68 patients successfully resuscitated within a period of 18 months 52 (38 men and 14 women; mean age 63 [32-90] years) were interviewed about their experience shortly after discharge. 37 reported to have been aware of the life-threatening nature of the acute episode; recurrent depressions were noted by 20; a positive change in attitude towards their life had resulted in 24 patients; 49 praised their doctors and nurses; 40 were appreciative of the medical technology used. All but one of the 52 patients would again choose to be resuscitated. After 12 months 38 patients were again interviewed (31 men and 7 women); 16 had died in the meantime. 21 of the 38 felt physically stronger than before, 25 were more cheerful and 34 were living more intensely. 36 of the 38 patients thought the interviews had been helpful and they would have liked more intensive psychiatric care even during their hospital stay.

Therapeutically effective doses of beta-acetyldigoxin in healthy subjects produced no or only minor S-T depression both at rest and under maximal cycle-ergometry, in individual instances the S-T segment never being depressed by more than 0.1 mV. On the other hand, similar exercise in patients with latent coronary insufficiency produced marked, significantly and dose-dependent S-T segment depressions under increasing digitalisation within the therapeutic range, and in some of the patients there was also decreased exercise tolerance before anginal symptoms. It is concluded that the so-called digitalis effect is definitely of diagnostic significance in the recognition of latent coronary insufficiency, contrary to previously held belief.

Right atrial pacing at different rates was performed on 15 women and 11 men with persistent angina with normal resting and exercise ECG. In 21 subjects there developed during bicycle exercise unequivocal S-T depression of myocardial ischaemia at maximal frequency. In 16 of them the diagnosis was confirmed by rate-dependent attacks of angina. These results demonstrate that, especially in the elderly, the maximal rate (+/-15%) thought to give a full load to cardiovascular functions is not suitable for diagnosing with certainty coronary insufficiency on exercise. In such patients rate-stimulation test may help in recognising the basic disease. On the other hand, in younger patients, capable of marked increase in heart rate on maximal exercise, rapid atrial stimulation has no diagnostic advantage. This test is indicated in those subjects who during ergometric exercise have an insufficient increase in heart rate because of a general reduction in exercise tolerance.

Right atrial pacing at different rates was performed on 15 women and 11 men with persistent angina with normal resting and exercise ECG. In 21 subjects there developed during bicycle exercise unequivocal S-T depression of myocardial ischaemia at maximal frequency. In 16 of them the diagnosis was confirmed by rate-dependent attacks of angina. These results demonstrate that, especially in the elderly, the maximal rate (+/-15%) thought to give a full load to cardiovascular functions is not suitable for diagnosing with certainty coronary insufficiency on exercise. In such patients rate-stimulation test may help in recognising the basic disease. On the other hand, in younger patients, capable of marked increase in heart rate on maximal exercise, rapid atrial stimulation has no diagnostic advantage. This test is indicated in those subjects who during ergometric exercise have an insufficient increase in heart rate because of a general reduction in exercise tolerance.

The influence of the calciumantagonistic agent Gallopamile (D 600) on cardiac conduction and sinus node function was studied by using His bundle recordings and atrial stimulation in 13 patients with normal sinus rhythm. Intravenous administration of a single dose of 4 mg produced a significant increase in the atrioventricular conduction time by 30 %. On atrial stimulation second degree a-v block occurred at lower stimulation rates in all patients after Gallopamile. The impulse propagation in atrial tissue and within the His-Purkinje system was not affected, even in patients with diseased conduction system. There was an impairment in sinus node automaticity, the sinus node recovery time was increased by 58 % of the control value.

Therapeutically effective doses of beta-acetyldigoxin in healthy subjects produced no or only minor S-T depression both at rest and under maximal cycle-ergometry, in individual instances the S-T segment never being depressed by more than 0.1 mV. On the other hand, similar exercise in patients with latent coronary insufficiency produced marked, significantly and dose-dependent S-T segment depressions under increasing digitalisation within the therapeutic range, and in some of the patients there was also decreased exercise tolerance before anginal symptoms. It is concluded that the so-called digitalis effect is definitely of diagnostic significance in the recognition of latent coronary insufficiency, contrary to previously held belief.

ST-segmental depression below the isoelectric line in the ECG occurring under a therapy of sub-therapeutical and therapeutical digitalising doses, very often involves an increase of pre-existent stress stenocardia with cardiovascularily compensated patients having a coronary heart disease. For this purpose, 13 patients of both sexes with latent coronary insufficiency were examined. The patients were treated with beta-Acetyldigoxin i.v. and were controlled under bicycle ergometric test-conditions before as well as during the different saturation phases with digitalis (0.66 +/- 0.03 mg, 1.20 +/- 0.07 mg and 1.54 +/- 0.10 mg beta-Acetyldigoxin) in a miximum of 4 functional tests alltogether. Dose-depent depression of the ST-segment accurred regularly accompanied by a reduction of the T-wave amplitude. A comparative valuation of myocardischemic and glycoside conditioned repolarisation disorders in the ECG demonstrated formalanalytically no differences concerning differential diagnosis. With the appearance of digitalis conditioned ST-T-changes an increase of angina pectoris could be proved. There were hints that the so-called adhesive signs of digitalis are an expression of myocardial ischemia and therefore principally of diagnostic value.

Electrocardiographic alterations and onset of angina pectoris during an acute treatment period with lidoflazine -3 to 4 mg/kg b.w. by oral application- was investigated in 20 patients with latent coronary insufficiency under increasing heart rate condition by atrial pacing. Significant changes in the repolarisation phase mainly due to prolongation of the QTc-interval already appeared 90 to 120 min after oral administration. The onset of test-induced agina pectoris and ischaemic ST-segmental depression in the ECG were not influenced by lidoflazine. Exceeding a rate of 140 min-1 produced a delay of atrioventricular conduction time under drug influence whereas significant changes of intraventricular conduction did not appear. Under frequent heart rates bundle branch block developed in a few individuals that might be drug-induced. In addition, there were some signs of digitalis-potentiation by lidoflazine.

Compound BQ 22-708 is a pyridopyridazine with marked antihypertensive effects on experimentally induced hypertension. At this study hemodynamic reactions were controlled in 5 patients with resistent hypertension, two of them with the complication of hypertensive, two of them with the complication of hypertensive crisis, after oral administration of a mean dose of 11 mg BQ 22-708 (range 5 to 15 mg). Mean arterial pressure was reduced by 40 mm Hg. The onset of drug activity occurred 10 to 20 minutes after application. Maximum was reached after 90 to 180 minutes, whereas the antihypertensive effect lasted for about 5 to 6 hours. Peripheral resistance was reduced by about 50%. Heart rate and cardiac output increased. In patients with normal cardiac function stroke volume remained constant, whereas in patients with heart insufficiency an increase occurred. BQ 22-708 led to a slight reduction in pulmonary artery pressure and pulmonary capillary wedge pressure. Right atrial mean pressure remained unchanged. Additional treatment with a beta-adrenergic-blocking-agent or a drug with Ca-antagonistic-activities is indicated for inhibition of BQ-related increase of heart-rate.

Haemodynamic investigations were performed in 40 patients with acute myocardial infarction before and after intravenous application of 6 mg propranolol. Cardiac index was significantly decreased caused by reduction of cardiac frequency and stroke volume. Pulmonary capillary pressure increased significantly. As a consequence pulmonary and peripheral vascular resistance increased. Arterial blood pressure remained largely unaffected. Propranolol showed a haemodynamically beneficial decrease of left ventricular stroke work without signs of negative cardiodepression at a cardiac index of more than 3.0 l/min . m2. At a cardiac index of less than 3.0 l/min . m2 a haemodynamically detrimental lowering of cardiac index to ranges of insufficiency of 2.0 l/min . m2 on average occurred. Thus cardiac index is an important factor for the decision of use of beta-blocking agents in acute myocardial infarction. Indiscriminate use of beta-blocking substances should not be accepted.

Hypertension presents many unsolved therapeutical problems. On this reason further examinations on new antihypertensive agents are needed. BQ 22-708 is a pyridopyridazine with peripheral vasodilating activities, which has been shown in animal experiments marked antihypertensive properties of dihydralazine-type. A hemodynamic study revealed now similar effects in man, as could be demonstrated in 5 patients with resistent hypertension and additional hypertensive crisis in two cases. At these patients BQ 22-708 in doses between 5 and 15 mg reduced the mean arterial pressure by 48 mm Hg, but at the same time increased heart rate. Peripheral resistance was significantly reduced by 30-60%. Cardiac output increased. Stroke volume remained unchanged in patients without heart failure, but in those with cardiac insufficiency increased. There was a slight but non-significant reduction in pulmonary artery pressure and capillary wedge pressure, wheras right atrial pressure remained unchanged. The onset of drug activity was noticed 10-20 minutes after application of a single dose BQ 22-708 and lasted for about 5-6 hours. Therefore BQ 22-708 may prove to be useful in the therapy of resistent hypertension.

The total mortality for 1977 of 706 prospectively examined patients with an average age of 68 in an intensive care ward was 15%. 42% of the patients were 70 years old with a lethality of 19%, which was not essentially higher than the 51 to 70 year-old patients with 16%. In 139 patients with a recent myocardial infarction the lethality was 20%. Infarct patients over 70 years old died in 27%, between 51 and 70 years old in 17% and under 51 years of age in 7% of cases. Resuscitation measures were essential in 93 cases and led to a lasting success in 25%.

Nitroglycerin bound to cellulose (Nitroglin) was investigated in patients with coronary heart disease as to the oral long-term effects in a dosage of 10 mg (n = 10) and 20 mg (n = 10) in comparison with 40 mg sustained release isosorbide dinitrate (n = 10) and placebo (n = 10). Haemodynamics were evaluated in a randomised double blind protocol. All true medications showed comparable maximal effects on right heart atrial pressure, pulmonary artery and pulmonary capillary pressure taking place with certainty between the first and fourth hour. Differences were seen for the duration of action: 10 mg cellulose bound nitroglycerin showed a sustained action until the end of the sixth hour, 20 mg until the eighth hour. The 20 mg dosage was aequipotent to the action of 40 mg of sustained action isosorbide dinitrate. However, the high dosage of 20 mg cellulose bound nitroglycerin cannot be recommended universally as diminutions of cardiac output by 30-40% may occur. Cellulose bound nitroglycerin is an oral long-term nitrate with therapeutic relevance besides the sustained action isosorbide dinitrate.

It can be noted, a consequently discovered and treated hypertension is one of the most important achievements of modern medicine within the last 20 years. The earlier treatment begins, the better it success of treatment in avoiding complications on the basis of arterio sclerosis and expectation of life. For elderly hypertensives it is particularly important, what is good in younger decades too - but in higher age the acute threat of life by hypertension is much more pronounced.

60 patients with chronic atrial fibrillation and flutter were randomly allotted to two groups and treated alternately with two different therapy regimes. 30 patients (group I) received lidoflazine in increasing dosage up to 480 mg/24 h and in cases where there was no conversion to sinus rhythm propafenon in a maximal daily dosage of 1800 mg orally. The duration of treatment was limited to 4 days for each substance. 30 patients (group II) were treated in the reverse order, i.e. propafenon and in cases of ineffectiveness with lidoflazine. Atrial fibrillation could be overcome in 21 patients in group I and in 23 patients in group II. The combined success rate in both groups was 73%. The conversion rates for the individual substances were 41% for propafenon (17 out of 41 patients) and 59% for lidoflazine (27 out of 46 patients). The difference was not statistically significant. Successive use of both substances leads to an increased conversion rate. Dangers arising from therapy are a conduction inhibitory action and depression of sinus node function as far as propafenol is concerned and the risk of ventricular ectopy and tachyarrhythmia in lidoflazine.

The haemodynamic effects of nifedipine, verapamil and diltiazem were measured and compared in an open randomized parallel investigation on 44 patients with coronary heart disease and compensated myocardial function. Each set of parameters was measured during a control phase and serially after a single dose (nifedipine in retard form, 20 mg; verapamil, 160 mg; diltiazem, 120 mg) over a period of 180 minutes at rest and after a standardized exercise. All three drugs produced a significant fall in systemic arterial pressure of 10-14% and of left-ventricular stroke work of 10-20% from the initial level. The main differences between the three drugs concerned heart rate and stroke volume. Nifedipine produced a significant rise in heart rate, while it fell by 8-10% below the control value after verapamil and diltiazem. On the other hand, verapamil caused a significant fall in stroke-volume index, while after nifedipine and diltiazem it remained unchanged. These results suggest differential therapeutic use of the various calcium antagonists.

22 pateints with a fixed, sometimes therapy-resistant (N = 18) hypertension were treated with a new antihypertensive agent, the pyridopyridazine derivative BQ 22-708 and hemodynamically investigated. 14 hypertensives received single oral doses of between 5 and 15 mg, 8 other patients also received additional treatment with a beta-receptor blocker (0.8 mg pindolol i.v.) or calcium antagonist (10 mg verapamil i.v.). In hypertension which is only poorly controllable or resistant, therapy with BQ 22-708 combined with beta-receptor offers a genuine alternative medication.

A retrospective determination of survival time over a total control phase of eight years was done in 53 patients who had been admitted to an internal intensive care unit in 1970 because of cardial pulmonary edema. The hospital survival rate amounted to 55%. 27% of the patients were still alive six months after discharge; after a year there were only 20%. Three of the 53 patients reached the 8th control year. The most unfavorable short- and long-term prognosis by far was evidenced by pulmonary edema resulting from an acute myocardial infarction with a hospital lethality of 80%; none of these patients survived longer than two years (n = 19). Irrespective of the nature of the basic disease, comparable rates were found for those types of pulmonary edema connected with a higher grade insufficiency of the right heart and corresponding increase of the central venous pressure over 20 cm water column (n = 13). In contrast, the pulmonary edema in consequence of a cor hypertonicum had a fairly good prognosis, because the 50% survival rate amounted to four years in this group (n = 21). All attempts to quantify the life prognosis in cases of pulmonary edema possess only speculative significance for the interests of the individual case. Nevertheless, they are indispensable for the correct choice of therapeutic procedure in medical borderline situations.

In 20 infarct patients, whose age varies from 43 to 78 years (m 59.6), continuous hemodynamic measurements were made to determine the cardiovascular effects of propranolol without and during a simultaneous infusion treatment with nitroglycerin. In cases of compensated ventricular function and pulmonary wedged pressures of 15 mm Hg or less (N = 10), a mean intravenous propranolol dose of 6.1 +/- 1.3 mg led to a significant reduction of the LVSWI and a simultaneous increase of the PCP by 31% of the control value (P less than or equal to 0.005). A simultaneously performed infusion treatment with nitroglycerin at a mean dose of 3.0 +/- 1.6 mg/h resulted in totally cutting off the propranolol-induced PCP increase, whereas a decrease of the heart rate and the LVSWI due to a beta-receptor-blockade remained completely unchanged. In the case of pre-existing congestion insufficiency of the left ventricle (N = 10) and of a pulmonary wedged pressure of above 15 mm Hg, the administration of a mean dose of propranolol of 5.8 +/- 1.1 mg for protection of the myocardium resulted in a partly disquieting decrease of the volume of cardiac output (P less than or equal to 0.005) which was 28% of the control value for the CI an 12% for the SVI. Correspondingly the left ventricular stroke work decreased to 18%. Nitroglycerin has a reducing influence on these changes, but not down to the initial level. In cases of sufficient ventricular function, propranolol has a favorable influence on the myocardial O2-metabolism via its depressor effect on heart rate and contractility. By means of nitroglycerin, an increase of the pulmonary wedged pressure occurring under this condition can be inhibited. However, in the case of a pre-existing congestion insufficiency, propranolol can lead to a partly disquieting depression of the circulation, which, apart from the hemodynamic risks, makes a rather unfavorable influence on the myocardial O2-metabolism seem likely.

In an open clinical trial, 30 compensated cardiac patients with essential hypertension were selected and randomly distributed. Treatment was given by means of two combinations of active agents, one containing 0.15 mg reserpine, 15 mg mefruside and 150 mg inositol nicotinate and the other 0.10 mg reserpine, 10 mg mefruside and 125 mg alpha-methyldopa. A randomized control group of 30 patients with essential hypertension received 0.15 mg reserpine, 15 mg mefruside and 150 mg isositol nicotinate exclusively over the same treatment period. By substituting only 125 mg alpha-methyldopa for 150 mg inositol nicotinate, the reserpine-mefruside portion can be reduced by one third while still obtaining the same antihypertensive effect.

Successful conversion to sinus rhythm was achieved in 20 out of 26 patients (77%) with chronic atrial fibrillation or flutter of various origin, that had existed for about 40 +/- 13 months. There was a significant relation between the converting dose of Lidoflazine and the duration of atrial fibrillation. In those patients with atrial fibrillation, that preexisted no longer than two years, restoration of sinus rhythm was achieved in 12 of 14 cases (86%) with an average dose of 109 +/- 67 mg Lidoflazine a day, whereas in the group with atrial fibrillation known for more than two years therapeutical success was obtained only in 8 of 12 cases (67%). The dose of conversion was 382 +/- 150 mg/day in this group and produced in a few patients toxic side effects. Two patients relapsed to atrial fibrillation. On this reasons conversion with Lidoflazine should only be done in patients with atrial fibrillation within two years. There were no significant changes related to: heart rate, myocardial function and intraventricular conduction process. In the presence of underlying hypokalaemic disturbances and/or additional therapy with digitalis preparations Lidoflazine may be the cause of developing premature beats. Lidoflazine may be regarded as a relatively safe drug even in large doses, if monitoring of heart rhythm and QTc-interval is available.

More than 400 patients with acute and chronic liver diseases as well as non-hepatic diseases (control group) were examined for the existence of antibodies against mitochondria, smooth musculature and cytoblasts with the help of the immunofluorescence-serological method. The proof of the hepatitis-B antigen was carried out by means of the transmigration-electrophoresis. Auto-antibodytitres larger than 1 : 160 (limiting titres) could be established only in the chronically aggressive hepatitides and the chronically destructing non-purulent cholangitides. Whilst in the chronically destructing non-purulent cholangitides dominate high mitochondrial antibody-titres, in the chronically aggressive hepatitides the antibodies against smooth musculature and/or cytoblasts are dominating. When the hepatitis-B-antigen was present in all groups of diagnosis auto-antibody titres of 1 : 160 were not transgressed. The kind of the antibody-spectrum and the size of the antibody-titres seem to be suitable for the differential diagnosis. High mitochondrial antibody-titres in women are suspicious of a chronically destructing non-purulent cholangitis. High titres of antinuclear antibodies or such ones against smooth musculature might be a reference to the so-called auto-immune form of the chronically aggressive hepatitis. For a still better differentiation of the chronic liver diseases the determination of these antibodies seems to be valuable.

Therapeutic doses of digitalis may give rise to depressions and abnormities of the ST segment. In coronary patients this is occasionally also associated with anginal complaints. In 7 patients the ST segment was investigated at rest and under increasing stress by atrial frequency without and with digitalis at increasing therapeutic dosage. In all patients a glycoside-induced, linearly intensifying depression of the ST segment was demonstrated as a regular and dose-dependent pattern the onset of which was already recognizable at an average effective level of 0,59 mg digoxin. The opinion is held that glycoside-induced ST depressions in the ECG are not in general of insignificant nature but may be the reflection of myocardial ischemia.

Arrhythmias are the expression of disordered stimulus formation or conduction. Focal genesis is due to an abnormal automatism in primary, secondary and tertiary impulse centers. Conduction blockade leads to bradycardial substitute rhythms which are determined by the site of the lesion. Bradycardial arrhythmias with a high degree of risk, with disturbed impulse automatism or with impaired hemodynamics require treatment with a pacemaker. Tachycardial and extrasystolic arrhythmias are treated today according to the differential therapeutic aspects. Treatment is also obligatory for premonitory arrhythmias and an identified Stokes-Adams disease. Ventricular fibrillations, high-grade ventricular bradycardia and asystole are cardiological emergencies.

Herzrhythmusstorungen konnen nicht nur durch primare Herzerkrankungen, sondern auch durch unterschiedliche Einflusse aus dem extrakardialen Bereich hervorgerufen werden. Kardiale und extrakardiale Grunde konnen einzeln oder in Kombination fur das Auftreten von Rhythmuskomplikationen verantwortlich sein.