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In a prospective study of 23 patients the clinical effects of rate-adapted activity-sensed (by mechanical resonance oscillations) pacing (Activitrax system) were tested over a mean period of 8.1 +/- 3.8 months. This form of pacemaker treatment was used when, after exercise and on long-term ECG monitoring, the spontaneous heart rate had not exceeded 85 beats per min and there had been symptoms of decreased exercise tolerance. Lasting improvement in physical exercise tolerance was achieved in 11 of 17 patients after changing from fixed-rate to rate-adapted pacing. Treadmill ergometry, randomised in the fixed-rate or rate-adapted mode, brought about a significant rise in exercise tolerance (P greater than 0.01). Contrary to results after external influences, insufficient rate increases in five patients in the course of static stress was of clinical significance and thus narrow the indications for this type of pacing.

Haemodynamic effects of 5-isosorbide mononitrate (5-ISMN) were studied at rest and on exercise in 31 patients with angiographically confirmed coronary heart disease. A decrease in arterial blood pressure and mean pulmonary artery pressure without significant change in heart rate, cardiac output and stroke volume occurred both at rest and on exercise after 20 mg of 5-ISMN to 12 patients. Administration of 50 mg 5-ISMN to 19 patients achieved greater decrease in mean pulmonary artery pressure; cardiac output and stroke volume were highly significantly reduced at rest, while on exercise both cardiac output and stroke volume remained unchanged. Ten patients, in whom after a single dose of 50 mg 5-ISMN the mean pulmonary artery pressure at rest and on exercise had decreased 28% and 45%, respectively, with a definite rise in exercise tolerance, repeat acute administration of a single dose of 50 kmg 5-ISMN produced a fall in mean pulmonary artery pressure at rest by 20% after 50 mg three times daily for four weeks. On exercise the fall was only 14% below the control levels before treatment. In addition, exercise tolerance was reduced. These results indicate that acute administration of 5-ISMN at rest and on exercise decreases cardiac work load. But on chronic administration of high doses, tolerance to the drug may develop.

The effect of endocardial cardioversion was investigated in 17 patients (aged 26-76 years), ten of them with ventricular tachycardia, either spontaneous or initiated by programmable stimulation. During a total of 14 days of observation there were 33 episodes of spontaneous or induced ventricular tachycardia. A special cardioverter catheter had been placed into the right ventricle and endocardial microshocks were given ranging from 0.05-2.0 J. All patients could feel the shock, but in most instances it was mild to moderate, in only one painful. The tachycardia was slowed in 20% of all microshocks, moderate acceleration occurred in 6%, while in 71% the tachycardia rate remained unchanged. In 7 out of 65 microshocks sinus rhythm occurred spontaneously, after an interval in which the tachycardia slowed. Atrial fibrillation was induced in 6% of cases, but there was no instance of ventricular fibrillation. Reversion directly to sinus rhythm after endocardial cardioversion occurred in 26 of 33 episodes of ventricular tachycardia, while in 7 episodes the tachycardia rate slowed. In no case was it necessary to use external DC cardioversion to terminate a ventricular tachycardia. Threshold values for successful cardioversion of ventricular tachycardia averaged 0.77 (+/- 0.63) J. In one patient, atrial flutter with a relatively high A-V conduction rate was converted into atrial fibrillation by an intra-atrial microshock of 5.0 J. Thus endocardial cardioversion proved effective and safe in terminating ventricular tachycardia, even in patients in whom anti-tachycardic ventricular pacemaker stimulation had failed. The method is apparently not suitable for the conversion of supraventricular tachy-arrhythmias to sinus rhythm.

The haemodynamic and antianginous efficacy of percutaneous nitroglycerin was evaluated in 24 patients with coronary heart disease. Groups of 8 patients each received one, two or four patches (nitroglycerin liberation 5 mg per patch within 24 hours). Prior to application and after 1 and 2 hours cardiac frequency, arterial and pulmonary arterial pressures and exercise tolerance were assessed. Cardiac frequency and arterial pressure showed no relevant changes after application of patches. The mean pulmonary arterial pressure decreased after application of one or two plasters by 18.5 and 22.2% at rest and by 12.7 and 21.1%, respectively, during exercise. The working capacity showed a trend towards improvement only. With four nitroglycerin patches the mean pulmonary arterial pressure at rest was lower by 26.2% and during exercise by 39.1%. The working capacity rose significantly by 48.7%. Comparison of these effects with oral single dosage of 20 mg 5-isosorbide mononitrate (ISMN) showed that two simultaneously administered plasters did not achieve efficacy of 20 mg 5-ISMN, four plasters, however, were more effective.

An automatic, implantable cardioverter-defibrillator (AICD) which generates a high-energy current impulse is now available for the management of treatment-resistant malignant ventricular arrhythmias. Such a device (manufactured by Intec/CPI) was implanted into eight patients with coronary heart disease or dilated cardiomyopathy, and in four after surgery for postinfarction ventricular arrhythmias. All patients had had life-threatening episodes of ventricular fibrillation or tachycardia: the arrhythmias were refractory to multiple drug therapy (mean of 6.8 antiarrhythmia drugs per patient). The threshold energy for converting ventricular fibrillation was 9.6 Joules +/- 5.7. Except for one bacterial infection of the electrodes, there were no serious complications. During a mean observation period of 13.6 months 21 electrophysiologically induced and 105 spontaneous tachyarrhythmias were successfully terminated by the AICD. No malfunctions occurred and there was no death due to an arrhythmia.

The accuracy of ST-segment analysis by means of the Marquette-Laser-Holter system was compared with conventional ECG registration during ergometry. In 26 patients with angiographically confirmed coronary heart disease conventional chest leads and long-term ECGs were recorded simultaneously during standardized exercise. Simultaneously registered ST-segments in V5 and Holter CM5 were compared, with the results correlating well (r = 0.91) for any recorded abnormal repolarizations.

In 500 patients suffering from angina pectoris (454 males, 46 females) in whom coronary angiography had been performed a dipyridamole test was carried out. The test was positive in 319 of 396 patients with stenosing coronary heart disease (sensitivity 80%); ECG changes typical of ischaemia were demonstrated in 51%. The exercise ECG test was positive in only 68% of 229 patients with coronary heart disease. Among 104 patients without stenosing coronary heart disease the dipyridamole test was false-positive in 47, giving a specificity of 55%, while in 17 (16%) there were false-positive ECG-changes. The exercise test was falsely positive in 20 of 38 patients without stenosing coronary heart disease (specificity of 47%). Coronary blood flow was measured with the argon technique in 19 of 47 with a false-positive dipyridamole test and three with a false-positive exercise ECG. Maximal pharmacologically induced coronary blood flow was significantly reduced in all so that the diagnosis of "atypical coronary heart disease" or "small vessel disease" was made. The dipyridamole test or the exercise ECG test were falsely positive in these patients only with regard to the coronary arteriogram, correctly positive, however, in relation to angiographically non-demonstrable coronary blood flow abnormalities. The dipyridamole test is complementary to the exercise ECG test and has comparable accuracy. The same precautions must be observed for both tests.