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The action of nifedipine given first intravenously and then orally was studied in nine patients undergoing investigation for angina pectoris who were already receiving atenolol (100-200 mg/daily) and who had been shown to be fully beta blocked (reduction in maximal heart rate by greater than 25%). Intravenous nifedipine 7.5 micrograms/kg reduced both systolic blood pressure and left ventricular pressure (dP/dt) transiently; both values were significantly lower five and 10 minutes after the infusion of nifedipine but were not significantly different from control values at 20 minutes. There was minimal but pronounced depression of atrioventricular nodal function after giving intravenous nifedipine, though this was detected only when sensitive tests of atrioventricular nodal function were used. These effects were also transient, showing no significant change from control values at 20 minutes. Atrioventricular nodal conduction time and sinus rate were unchanged. Radionuclide angiography of patients taking the oral combination of atenolol and nifedipine for chronic angina showed no change in ejection fraction compared with those taking atenolol alone, but there was a small increase in peak ejection rate. Resting blood pressure and heart rate were unchanged and the PR interval did not lengthen. Peak heart rate and systolic blood pressure showed no alteration on exercise testing when the drugs were combined compared with the response with atenolol alone. Despite the negative inotropic influence when nifedipine was given intravenously, the absence of haemodynamic deterioration when oral nifedipine is combined with atenolol has confirmed that this combination can be used safely in patients with normal left ventricular function. The minimal changes in atrioventricular nodal function cannot be detected on the surface electrocardiogram and are not of clinical importance in patients with normal conduction.

The names of Russian physicians do not often spring to mind when recalling the advances of the past century, though a quick glance discloses many contributions, including those of Anitschkow in the pathogenesis of arteriosclerosis, Korotkoff in the measurement of blood pressure, and Elie Metchnikoff, the bacteriologist. Few, however, realise that James Herrick's diagnosis of coronary occlusion in the living patient1 had been anticipated by two years by two physicians from Kiev, Obrastzow and Straschesko. Their original description in Russki Vrach was republished almost simultaneously in German and was cited by Herrick.2 Even before this, however, a Russian physiologist, Alexander Filipovich Samojloff, had written the first book on electro cardiography, which should have been easily accessible to Western physicians because it was written in German and had been issued by a leading German publisher.3 The book is not, however, listed in two important EngUsh bibliographies,45 though it and several other publications by Samojloff were cited by Western contemporaries, and his contributions are proudly acknowledged in the Soviet Union. Who was Samojloff and what was his role in Russian and indeed international physiology?

One hundred years ago, Augustus Desiré Waller recorded the human electrocardiogram for the first time, using a capillary electrometer. Electrocardiography only became clinically relevant in 1901 when Willem Einthoven devised his string galvanometer for this purpose. Sir Thomas Lewis was the key figure in showing the value of the electrocardiography for the diagnosis of disorders of cardiac rhythm and conduction, but many others amplified the technique to encompass the assessment of structural heart disease, especially when due to ischemia. Knowledge of their role and work gives us a better perspective when considering the development of surface electrocardiography.

We present clinical and electrophysiological data on 9 patients with paroxysmal reciprocating sinus tachycardia (PRST) of whom only 6 described palpitations. Sinus node disease was present in 5 and cardiac ischemia and/or hypertension in another 3; the remaining case had apparently coincidental Wolff-Parkinson-White (WPW) syndrome. PRST could be initiated in all cases, and terminated in the 4 in whom it was sustained, by suitably timed atrial premature beats over a zone that was dependent on the effective atrial extrastimulus coupling interval (A1-A2) in the high right atrium (HRA). The sequence of atrial depolarization during PRST was similar to that of sinus beats although minor changes in both the P wave and the configuration of the HRA electrogram were observed in half the cases. During paroxysms, cycle length variation and sensitivity to alterations in vagal tone were common. In 6, paroxysms could be initiated by moderately rapid atrial pacing. Repetitive attacks were usually initiated by increases in the sinus rate and not be an antecedent premature atrial extrasystole. Verapamil suppressed sinus node reentry in 5 patients while small doses of atropine favored initiation in 3. PRST was seen in association with AV reentry tachycardias in the patient who had the WPW syndrome.

Oral amiodarone has been used to treat 21 patients with various supraventricular arrhythmias; 13 had Wolff-Parkinson-White syndrome, which was complicated by atrial fibrillation and re-entry atrioventricular tachycardia in four, and re-entry tachycardia alone in the other nine. The remaining eight patients had paroxysmal atrial fibrillation or flutter without pre-excitation. All were refractory to conventional treatment and had undergone intracardiac electrophysiological study. Fifteen have been controlled with amiodarone, this treatment proving most effective in atrial fibrillation or flutter with or without pre-excitation. Amiodarone was successful in only four of the nine patients with re-entry atrioventricular tachycardia. In two patients who responded well the drug had to be discontinued because of side effects.

Bepridil is an anti-anginal agent with a novel chemical structure. Its main pharmacological effects are an increase in coronary blood flow, a reduction in myocardial oxygen demand, reduction in cardiac work, primarily by a decrease in after-load and a dose-dependent negative chronotropic effect, and anti-arrhythmic properties. These are mainly due to a calcium-antagonistic action. There is evidence that fast sodium channels in heart muscle are also inhibited. Trials have shown that bepridil is effective in the prophylactic treatment of various forms of angina pectoris and accompanying arrhythmias. Pharmacokinetic data justify once-daily administration. The evidence suggests that bepridil is generally well tolerated. This paper reviews already published studies and the results of recent investigations on the pharmacological and clinical efficacy of bepridil.

An atrial aneurysm gave rise to incessant atrial tachycardia in a 21 year old Seychellian soldier. This arrhythmia was suppressed by intravenous adenosine triphosphate and ajmaline. Resection of the aneurysm abolished the arrhythmia and re-established sinus rhythm.

In 9 patients with paroxysmal supraventricular tachycardia the effects of tilting the body on the blood pressure and on responses during tachycardia or pacing revealed important effects that could influence the clinical presentation and the treatment required. Assessment of these reflex responses adds a major dimension to the understanding of the patient with supraventricular tachycardia.

Verapamil was administered by intravenous injection to 181 patients with various cardiac arrhythmias. The automaticity of the cardiac pacemaker was slowed in sinus, idionodal, and idioventricular tachycardia. In atrial fibrillation the drug usually slowed the ventricular response and often made it regular. In some cases atrial flutter was converted to sinus rhythm, the ventricular response being reduced in the remainder. Conversion of paroxysmal supraventricular tachycardia to sinus rhythm was consistently achieved. A favourable response occurred in four patients in whom arrhythmias were associated with pre-excitation syndromes. There were no adverse clinical side effects.