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136 patients were followed after implantation a DDD pacemaker (PM) for a total of 1,919 patient-months (m = 14.1 months/patient). 22/136 patients had one or more episodes of atrial flutter or fibrillation (AF) postoperatively. In 121/136 patients (group A) AF had not been documented before, in 4 it was unknown at the time of implantation, but was verified retrospectively (group B). 11 patients (group C) had a positive history of previous AF. Post implantation 7.4% in group A and 81.8% in group C developed AF. In patients with sick sinus syndrome (SSS) the incidence was 10/37 (27%), in those with AV block (AV) 6/77 (7.8%) and in cases with both SSS and AV 6/22 (27.3%). The first AF episode occurred during the implantation itself (n = 2) or during the hospital course in 9/22 patients (A: 11%, B/C: 64% early attacks), and later on in 13 with a time delay of 1-24 months (m = 8.5, 8 patients) in group A and 2-15 months (m = 6.6, 4 patients) in groups B/C. 2 patients of group C had no AF episodes post implantation. In the individual patient the number of attacks ranged from 1 to 3 (10.4/100 patient-months) in group A and from 1 to 6 (20.1/100 patient-months) in groups B/C. During AF 16/22 patients had a ventricular rate of 110-185, m = 132 bpm. In 6 patients the tachycardia was mediated by the PM and in 10 by fast intrinsic AV conduction. 1 patient with SSS, 2 with SSS + AV (spontaneous ventricular rate less than 45 bpm) and 3 with AV needed ventricular backup-pacing during AF. In 7 patients a total of 15 attacks of atrial flutter could be terminated by atrial overdrive pacing, in 5 of these episodes by temporary high rate A00 stimulation via the implanted pacemaker lead system. Otherwise AF was converted to sinus rhythm by antiarrhythmic drugs. After termination AF often recurred, but only 3 patients developed chronic atrial fibrillation. In 2 patients a ventricular rate greater than 180 bpm during AF reverted the PM to asynchronous mode, a possible cause of ventricular fibrillation in one. No other complications due to the PM itself have been encountered. AF, therefore, common during DDD pacing, even in patients without any AF history before implant. Both the incidence and the recurrence of AF depend on the presence or absence of previous atrial arrhythmias.(ABSTRACT TRUNCATED AT 400 WORDS)

To investigate a possible dual action of oxyfedrine on beta-adrenergic receptors, hemodynamics and systolic time intervals were studied in 12 healthy volunteers during intravenous infusion of isoprenaline. The dose was titrated to a mean target heart rate of 113 bpm corresponding to an average dose of 6.16 micrograms/min. After return to baseline hemodynamics, oxyfedrine was administered as an intravenous bolus of 8 mg and the protocol was repeated. Compared to baseline, the percentage changes induced by isoprenaline at doses of 2.73 and 6.16 micrograms/min before and after (in parentheses) oxyfedrine were: heart rate: +33/+83% (+19/+62%); cardiac output: +90/153% (+30/+71%); systolic blood pressure: +16/+20% (+6/+7%); stroke volume: +42/+38% (+10/+6%); peripheral vascular resistance: -50/-63% (-31/-50%); cardiac work: +86/+148% (+19/+54%); pre-ejection period: -40/-56% (-27/-45%); isovolumic contraction time: -56/-79% (-29/-63%); systolic ejection rate: +67/+103% (+27/+52%); tension time index: +32/+50% (+7/+20%). Thus, the dose-dependent hemodynamic effects of isoprenaline were significantly attenuated by oxyfedrine pre-treatment with a shift of the dose-response curve to the right; this was attributed to a beta-antagonistic property of oxyfedrine. The results indicate that, in view of its well-known beta-stimulating effects, oxyfedrine exerts a dual action on adrenergic beta-receptors consistent with partial agonistic activity. Thereby, the different profiles of hemodynamic and metabolic actions of oxyfedrine compared to those of pure beta-agonistic agents can be explained as well as its beneficial therapeutic effects in patients with coronary heart disease.

To give some explanation for atrial malsensing in dual chamber pacing that occurs only during exercise, atrial electrograms from 33 patients were telemetrically recorded and analyzed in both the time and frequency domains. During exercise, an overall decrease from 6.4 +/- 1.9 to 5.6 +/- 1.9 mV (-11%) in the atrial signal amplitude was noted. Despite considerable variability among patients, marked changes occurred in 15 patients whose signals diminished by 11 to 49%. Slew rates showed a similar decrease from 1.35 +/- 0.45 to 1.18 +/- 0.45 V/s (-10.8%), with individual changes of as much as -51%. Signal attenuation in the time domain correlated well with frequency data, exhibiting a highly significant reduction of signal energy between 25 and 105 Hz. However, spectral distribution changed from rest to exercise, with a relative increase of signal energy in the range between 5 and 25 Hz and a decrease at higher frequencies. Individual changes differed widely when low (15 to 65 Hz) and high (65 to 115 Hz) frequencies were compared, but in a group of 11 patients signal attenuation in the high frequency band was more pronounced (-45%) than in the low frequency band (-23%). The clinical impact of the change in frequency distribution during ergometry was visualized by computer simulation of two different (low and high bandpass) filters. Although in individual patients, both characteristics may be favorable with respect to atrial sensing, it was observed in 11 patients that high pass filtering attenuates signal amplitudes by 10 to 24% in excess of the variation without filtering.(ABSTRACT TRUNCATED AT 250 WORDS)

The electrophysiological effects of nicainoprol, a new antiarrhythmic drug, were evaluated in a heterogeneous group of 23 patients aged 59 +/- 15 (mean +/- standard deviation) years. Nicainoprol was administered intravenously as a bolus of 1-2 mg/kg followed by continuous infusion at two dose levels. Electrophysiologic study was performed before and during the infusion at a steady-state drug level on each dose. The sinus node recovery time was unaltered in patients with normal sinus node function and was markedly prolonged in three of six patients with sinus node dysfunction. The intranodal conduction time (p less than 0.01) and the infranodal conduction time (p less than 0.001) increased, and the QRS duration (p less than 0.05) lengthened significantly even during 1 mg/kg/h. During 2 mg/kg/h, these times were further prolonged and, in addition, the intra-atrial conduction time (p less than 0.05), atrioventricular nodal effective and functional refractory periods (p less than 0.01), as well as the Wenckebach cycle length (p less than 0.001) also increased significantly. Similar depressant effects on the retrograde ventriculoatrial conduction system were also produced by nicainoprol. Retrograde His-atrioventricular nodal conduction was blocked in six of eight patients with this condition and was prolonged in the remaining two. Sustained supraventricular tachycardia was induced in seven patients, five of whom received nicainoprol during the tachycardia. The termination of supraventricular tachycardia was exclusively due to ventriculoatrial block in all five subjects, three with orthodromic circus movement tachycardia and two with atrioventricular nodal reentrant tachycardia of the slow-fast type. The reinducibility of supraventricular tachycardia could be prevented in five of seven patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The treatment of multi-morbid patients suffering from peripheral arterial occlusive disease (PAOD) is rendered difficult due to concomitant diseases such as coronary heart disease, chronic obstructive pulmonary affection, arterial hypertension or diabetes mellitus. Haemodilution can be a clinically efficient therapy for some of the concomitant diseases as well. It is, however, necessary to use a weak colloidal solution which has no additional volume effect as an iso-oncotic substance. Hydroxyethyl starch 200/0.5 6% meets all these demands. In a double-blind, placebo-controlled study over a period of 6 weeks a marked and significant increase of almost 40% in painfree walking distance was achieved for 19 of 37 multi-morbid patients with PAOD II by moderate hypervolaemic haemodilution with venesections. Besides the clinical improvement, blood fluidity also increased through a reduction in haematocrit, plasma viscosity, and erythrocyte aggregation.

In 16 patients with acute transmural myocardial infarction the effect of 8 mg of intravenous oxyfedrine followed by an infusion of 0.3 mg/kg body weight per hour on haemodynamics of the pulmonary and systemic circulation and dynamic cardiac indices was investigated. Cardiac rate, systemic arterial blood pressure, minute volume, cardiac output, and tension-time index remained unchanged on the whole. On the other hand oxyfedrine produced a persistant significant decrease of the mean and diastolic pulmonary artery pressure, pulmonary capillary pressure, and of the contraction and pressure-increase time. These effects were also demonstrable in patients previously treated with digitalis. No cardiac arrhythmias were observed. The positive inotropic effect of oxyfedrine is suggested as reason for these changes.

Milrinone exerts positive inotropic and dose-dependent vasodilatory effects that promote haemodynamic improvement after intravenous administration to patients with heart failure. Bolus doses of 12.5-75 micrograms kg-1 markedly increase cardiac output and cause a substantial reduction in cardiac filling pressure and in systemic vascular and pulmonary vascular resistance. There is no evidence of tolerance to these effects which are maintained during continuous infusion for up to 48 h. In contrast, there are minimal effects on heart rate or systemic blood pressure, except at very high doses. At lower filling pressures, milrinone increases cardiac output more markedly than equally hypotensive doses of pure vasodilators. This response is accompanied by an increased left ventricular dP/dtmax and a shift in the left ventricular performance is associated with a lower myocardial energy requirement. Despite a fall in mean arterial pressure and transcoronary driving pressure, coronary venous flow is increased and there is a reduction in the arterio-coronary venous oxygen difference. This reflects a global improvement in left ventricular diastolic function, characterized by accelerated early relaxation and greater chamber distensibility. Improved performance of the right ventricle is due primarily to reduced right ventricular afterload as milrinone produces minimal inotropic effects on the right ventricle.

The effects of the calcium-channel-blocking agent Gallopamil (D 600) were assessed in 20 patients with stable exertional angina pectoris in a randomized placebo-controlled double-blind protocol using serial exercise tests. Both after a single oral dose and during long-term treatment over 3 weeks, Gallopamil caused a dose-dependent increase in exercise duration and a reduction in ischemic ST segment depression that became clinically relevant using single doses of 50 mg. Since the rate-pressure product was not significantly affected by Gallopamil, its anti-anginal action cannot adequately be explained by a reduction in myocardial oxygen consumption as a result of this mechanism. The only side effects observed were asymptomatic second-degree sinoatrial block in one and first-degree atrioventricular block in another patient, each on 150 mg gallopamil daily. It thus seems justifiable to study the effectiveness of higher doses.

The serum activities of LDH, alpha-HBDH, CK, GOT and GPT wer investigated in 124 patients who had undergone cardiac catheterization with angiocardiography or coronary angiography. The determinations were made before and 2, 16 and 40 hours after the investigation. There was no significant influence on the enzyme activities. Lengthy intracardial catheter manipulation, trans-septal puncture and ventriculography may cause transient clinically unimportant increases in activity, especially of CK within normal limits. Distinctly pathological enzyme values were only measured in individual cases of intramyocardial contrast media depots after ventriculogram.

In a randomized double-blind crossover trial 30 patients with chronic stable angina were studied to compare the antianginal actions of gallopamil (150 mg/day) and nifedipine. With the initial nifedipine dose of 60 mg/day, the trial had to be stopped because of severe exacerbation of angina in 3 patients of the nifedipine group. Twenty-one patients were entered into a second protocol with the nifedipine dose reduced to 30 mg/day. Compared to the preceding placebo period, the exercise time to onset of angina (+ 30%, P less than 0.01) and the total exercise time (+ 18%, P less than 0.01) were prolonged by gallopamil but not by nifedipine (+ 20 and 13%, respectively, not significant) with no significant difference between the test drugs. Four patients became free of angina during exercise testing with gallopamil therapy and one patient with nifedipine. Both agents significantly reduced ST depression at maximal comparable workload by 77% (gallopamil) and 52% (nifedipine) compared with placebo; the difference between the drugs reached borderline significance (P = 0.055). The increase in heart rate and the rate-pressure product at maximal comparable workload was less with gallopamil than with nifedipine (P less than 0.01). In contrast to nifedipine, very few side effects were reported with gallopamil. Thus, gallopamil is an effective antianginal agent whose therapeutic to toxic ratio appears to be superior to that of nifedipine.

A prospective study was done in 54 patients with acute spontaneous intracranial haemorrhage, 27 of them with subarachnoid bleeding and 27 with primary intracerebral haemorrhage. The frequency of ventricular arrhythmias was registered by continuous long-term ECG and the incidence of QT prolongation by daily standard ECG registration. Prolongation of frequency-corrected QT-interval (QTc) developed in 9 patients with subarachnoid haemorrhage and in 10 with intracerebral haemorrhage. For assessment of time-relation between QT-interval and ventricular arrhythmias the results of corresponding long-term ECG and standard ECG were used and two groups were defined: group A (149 tapes) = QTc less than or equal to 450 ms, group B (43 tapes) = QTc greater than 450 ms. In group B singular frequent ventricular extrasystoles, couplets and non-persistent ventricular tachycardias occurred more frequently though not significantly so. Persistent ventricular tachycardias occurred significantly more frequently in group B (14% vs. 1%, P less than 0.01). In three tapes of group B, all of them with QTc prolongation of more than 550 ms persistent ventricular tachycardias with typical "torsade de pointes " morphology were seen. The results show that QTc prolongation of more than 450 ms occurs in a third and significant ventricular arrhythmia in nearly half of patients with spontaneous intracranial haemorrhage. Persistent ventricular tachycardias occur almost only in cases of QTc-prolongation. Pronounced QTc prolongation of more than 550 ms is rare. However, it can give rise to torsade de pointes and ventricular fibrillation.

In 34 unselected patients blood concentrations of glucose, lactate, pyruvate and free fatty acids (FFA) were determined after i.v. injection of a pressure agent containing theophylline esterified with norephedrine and theophylline esterified with norepinephrine (Akrinor) with and without beta-adrenergic blockade. After Akrinor a significant increase of FFA concentration of 32% is observed, which can be abolished by beta-receptor blocking agents. Our findings indicate that the Akrinor-induced lipolysis is mainly due to a direct sympathomimetic effect on the beta-receptors of adipose tissue. there are only slight effects on carbohydrate metabolism (decrease of pyruvate concentration, increase of lactate/pyruvate ratio) which are not influenced by beta-receptor blockade. According to our results there are important metabolic differences between Akrinor and the classical catecholamines.

In 12 patients with acute myocardial infarction the hemodynamic effects of a single intravenous injection of 30 mg of pentazocine were investigated. The administration of pentazocine resulted in no significant hemodynamic changes. In particular, there was no increase in peripheral vascular resistance and no evidence of decreased left ventricular function or respiratory depression. In the occasional patients who demonstrated an elevation of pulmonary arterial pressure, it was probably due to a direct effect of the drug on the pulmonary vasculature.

To determine the incidence and significance of angina pectoris in aortic valve disease, clinical, haemodynamic, and angiographic data concerning 111 consecutive patients aged 27-68 years (mean 52) were retrospectively analysed. 14.4% (group A) had significant, 85.6% (group B) had no coronary heart disease. There was a significant difference between the groups regarding the incidence of typical angina pectoris (62.5% vs 31.6%, p less than 0.01) and freedom from chest pain (12.5% vs 32.6%, p less than 0.05). No difference, however, could be found concerning the incidence of atypical chest pain (25% vs 35.8%). Of 12 patients aged over 50 years with coronary artery disease, no patient was free of angina pectoris. 83% had typical, 17% had atypical angina pectoris. Of 4 patients below 45 years with coronary artery disease, however, none had typical angina pectoris, 2 patients had atypical angina, and 2 patients had none. These results demonstrate that typical angina pectoris in patients with aortic valve disease is not a specific indicator of concomitant significant coronary artery disease. On the other hand, absence of chest pain does not predict absence of coronary artery disease, especially in younger patients. We therefore suggest that coronary angiography be carried out in all adult patients in whom aortic valve surgery is being considered.