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Intravenous (i.v.) injection of 0.1 mg/kg of ADP within one second in 13 rats caused a prompt drop in platelet count to 55.1 plus or minus 3.2% of the preinjection value with a statistical significance (p less than 0.01) at 30 seconds after the injection. At that time, mean arterial pressure and arterial PO2 decreased, while central venous pressure increased. Heart rate decreased with an appearance of sinus bradycardia and variable A-V block. Various respiratory effects such as shallow or slow respiration or apnea appeared. Such changes showed a tendency to recovery within 3 minutes. Splenectomy did not prevent these changes in 6 rats. In 6 thrombocytopenic and leukopenic rats treated with busulfan, these changes did not appear. Intra-arterial injection of the same amount of ADP induced almost no response. When ADP was injected twice 20 seconds apart in 10 rats, the second injection resulted in no effects or slight responses. In contrast, when 10 rats were injected twice 180 seconds apart, both the first and second injections showed the same effects on platelets and cardiopulmonary functions. The results suggests that the effects observed following I.V. ADP are probably due to transient obstruction of coronary and pulmonary microvessels by platelet aggregates. Reduced response following two successive injections may be due either to the reduced platelet count or to a refractory state induced by the first injection. ADP is probably rapidly metabolized in systemic microvascular beds.

Atrial stimulation were performed in 5 normal patients (group A) and 4 patients with electrocardiographic evidence of sinoatrial disease (group B). The technique of premature atrial stimulation was used to calculate sinoatrial conduction time. Rapid atrial pacing was applied to measure maximum sinus node recovery time. In 4 cases both stimulation methods were repeated after intravenous administration of atropine Group A had a sinoatrial conduction time of 56 ms +/- 11 (SD) and a maximum sinus node recovery time of 1122 ms +/- 158. In 3 out of 4 patients with sinus node dysfunction a prolongation of sinoatrial conduction time could be demonstrated (145, 105, and 150 ms). In addition, one showed probable sinus node exit block after premature atrial stimulation. Sinus node recovery time was excessively prolonged in 2 (3880 and 3215 ms) and normal in the other 2 patients with sinoatrial disease (1330 and 1275 ms). Atropine leads to a decrease of sinoatrial conduction time. Results indicate that sinus node recovery time may not be a reliable indicator of sinus node automaticity if sinoatrial conduction is disturbed. The premature atrial stimulation technique makes it possible to study the pattern of sinoatrial conduction and to evaluate its reaction to therapeutic drugs.

Summary Coexistent sino-atrial and atrioventricular block with Wenckebach phenomenon is an extremely unusual cardiac arrhythmia. Observations on the natural history of sinus node dysfunction are rare. For over six years our elderly patient has been followed without symptoms but with increasing severity of atrio-ventricular block.

Twenty-one patients with long-term right bundle branch block and left posterior himiblock were studied electrophysiologically and then followed up prospectively. The group consisted of 19 men and 2 woman aged 61 +/- 2.7 years (mean +/- standard error of the mean). The majority of patients had either hypertensive cardiovascular disease (48 percent) or primary conduction disease (33 percent). Initial electrophysiologic studies revealed A-H intervals of 58 to 152 msec (mean 98 +/- 7.7) and H-V intervals of 40 to 80 msec (mean 52 +/- 2.1). Six patients (29 percent) had prolonged H-V intervals. The follow-up period ranged from 91 to 1,231 days (mean 671 +/-68). Three of 21 patients (14 percent) needed a permanent pacemaker after development of the following symptomatic conduction disease: sinoatrial block on day 3 of follow-up; second degree atrioventricular (A-V) block, site undetermined, on day 118; and second degree A-V block proximal to the His bundle on day 398. One patient died suddenly (on day 571), and two others died of noncardiac causes. In conclusion, combined right bundle branch block and left posterior hemiblock was associated with less trifascicular disease than reported previously. The clinical course of most of the patients was benign and the incidence of sudden death was relatively small. Symptomatic conduction disease occurred but could be definitely related to trifascicular disease in only one patient. These short-term data suggest that prophylactic pacemaker insertion is not routinely indicated in patients with chronic right bundle branch block and left posterior hemiblock.

The effects of potassium canrenoate on arrhythmias induced by long-term progressive digoxin toxicity were studied in eight conscious beagle dogs. Sinus bradycardia and sinoatrial block, as well as atrioventricular (A-V) conduction disturbances, were consistently alleviated by administration of potassium canrenoate. Premature supraventricular (including junctional) and ventricular depolarizations as well as ventricular tachycardias were also suppressed. Although potassium canrenoate always terminated the digitalis-induced arrhythmias, it usually converted the rhythm to sinus arrhythmia rather than to normal sinus rhythm. Equimolar sodium canrenoate, but not potassium chloride, had similar reversal effects on arrhythmias induced by long-term digoxin intoxication. These data indicate that canrenoate, a diuretic agent with reported positive inotropic effects, may be useful in the treatment of digitalis-induced arrhythmias in man.

Sino-atrial conduction was investigated using premature atrial depolarization in 25 patients seven of whom had sino-atrial block. The results obtained in this investigation were evaluated plotting the test cycle (expressed as difference between the basic sinus cycle and the test cycle as a percentage of the basic sinus cycle) as a function of the return cycle (expressed as difference between the return cycle and the basic cycle as a percentage of the basic sinus cycle). In normal subjects, premature atrial depolarizations elicited in the last 10–20% of the spontaneous sinus cycle, produced a progressive prolongation of the return cycle and the points correlating the return cycle index to the test cycle index fell above the diagonal of the plotting system. After earlier premature atrial depolarizations, the return cycle remained of the same length, and the points correlating the return cycle index to the test cycle index fell along a line parallel to the y-axis ('plateau'). The mean value of the returning cycles (as expressed above) corresponding to the test cycles (as evaluated above) included in the first 5% of the 'plateau' can be defined as 'the sino-atrial conduction index'. This index, the sum of conduction into and out of the sinus node, was found to range from 79 to 185 ms. By assuming similar anterograde and retrograde conduction, the sino-atrial conduction time ranged from 39.5 to 97.5 ms (mean value = 70 ms). In the patients with sino-atrial block, fully compensatory pauses were observed for atrial premature depolarizations elicited up to the last 25–35% of the atrial cycle, and a slow and progressive divergence from the diagonal of the plotting system was seen instead of the 'plateau'. In these patients the sino-atrial conduction index ranged from 151 to 297 ms (mean 253 ms). By assuming similar antegrade and retrograde conduction, the sino-atrial conduction time ranged from 75.5 to 148.5 ms (mean value = 126.5 ms) with a statistically significant difference with respect to normal subjects (P = 0.001).

The relationship of depressed sinus node function to coronary artery disease (CAD) was evaluated. The sinus node artery (SNA) was easily identified in all of 80 unselected normal coronary arteriograms. Angiographic disease of, or significant obstruction proximal to, the SNA was seen in 21% of 80 unselected CAD patients. Heart rate and sinoatrial recovery times (SART) were obtained in 50 consecutive unmedicated patients prior to arteriography. There was no difference between the SART of 23 CAD patients free of SNA involvement (1092 msec +/- 55 sem) and 18 normals (1070 +/- 40 msec). Nine patients with SNA involvement had shorter SART (941 +/- 52 MSEC) than normals (P less than 0.05) or other CAD patients (NS). Similar results were obtained for heart rate. No patient with SNA involvement had a prolonged SART or sick sinus syndrom (SSS). six of the 50 patients studied were symptomatic with SSS. Five of these SSS patients had CAD but none had angiographic evidence of SNA involvement. Obstructions involving the SNA were common in CAD but were not associated with altered heart rate or SART. Patients with SSS exhibited no angiographic evidence of SNA involvement. Therefore, it is unlikely that SSS is related to CAD of the SNA.

The present study was carried out to see if lignocaine in therapeutic anti-arrhythmic dosages given to pacemaker-treated patients involved any risks of exit block. We conclude that such risk does not exist. However, we consider that lignocaine is contraindicated in patients with AV block II and III not treated with a pacemaker.

Guinea pig right atria were perfused in vitro at 30°C. When the temperature was lowered to about 20°C, atrial activity ceased and the resting potential of atrial fibers decreased significantly. When activity was restored during hypothermia by electrical stimulation, both the resting and the action potentials were similar to those recorded at 30°C. Blockade of receptors by atropine or propranolol reduced the effects of electrical stimulation on the membrane potentials, and the reduction was greatest when both drugs were present. In particular, propranolol reduced the amplitude of the action potential. Strophanthidin also reduced the increment in resting potential induced by electrical stimulation at low temperature. Norepinephrine restored atrial activity, but the action potential and its rate of rise were small and the resting potential remained low. We concluded that (1) electrical stimulation restored atrial activity by simultaneously depolarizing the membrane to threshold, liberating autonomic mediators, and stimulating the sodium-potassium pump and (2) norepinephrine removed the sinoatrial block induced by low temperature by increasing the slow calcium and sodium currents.

The effect of ventricular premature contractions on atrioventricular (A–V) conduction of the following sinus beat was studied in 25 patients with use of His bundle electrography. Facilitation of A–V conduction (shortening of the A–H interval) in the postextrasystolic beat was observed in 17 patients. This facilitation was believed to be due to a longer recovery period of the A–V node after its premature retrograde (and frequently concealed) depolarization by the ventricular premature contraction. Slowing of A–V conduction (prolongation of the A–H interval) after interpolated or repetitive ventricular premature contractions occurred in five patients. In these instances, after retrograde depolarization by the ventricular premature contraction, the A–V node was still partially refractory and conduction of the postextrasystolic beat was delayed. Retrograde P waves without resetting of the A–V node were documented; in these cases, the interval after the retrograde P wave was fully compensatory, suggesting retrograde and antegrade sinoatrial block.

The tachycardia-bradycardia syndrome consists of paroxysmal atrial fibrillation, flutter or tachycardia followed by sinoatrial block or sinus arrest resulting in Stokes-Adams attacks. Detailed histologie findings of the conduction system of 2 patients with this entity correlated well with the clinical observation of cardiac rhythm disturbances in the sinus node, atria and atrioventricular (A-V) junction. Eight other patients with the syndrome were studied clinically. The mechanisms (as revealed by the electrocardiogram) producing the bradycardia phase include depression of pacemaker function (arrest) or of conduction (exit block) of the sinus impulse, or both, plus depression of A-V junctional impulse formation. Proper therapy usually requires electrical pacing in conjunction with administration of digitalis or propranolol, or both. Our findings suggest that the term “sick sinus syndrome” is an inaccurate and inappropriate synonym for the tachycardia-bradycardia syndrome.

The clinical spectrum of the sick sinus syndrome (SSS) is described in a series of 56 patients who demonstrated either persistent unexplained sinus bradycardia (group I: eight patients); sinus arrest (group II: 15 patients); or bradycardia with episodic supraventricular tachyarrhythmias (group III: 33 patients). Coronary disease was the most common form of heart disease where etiology could be determined, but in 25 patients no clear etiologic diagnoses could be established. Thirty-three patients showed associated electrocardiographic conduction disturbances. Symptoms were common and were produced by both bradycardia and tachycardia. Eight patients in the bradycardia-tachycardia group experienced cerebral embolization. Despite bother-some symptoms, only six of the 56 patients died over an average follow-up of 7 years, and only one of these deaths appeared related to an arrhythmia. Drug therapy of bradycardia was generally ineffective, but digitalis was frequently helpful in patients with tachycardia. Electrical pacing was uniformly successful in treating symptoms of bradycardia but was disappointing in preventing tachyarrhythmias.

Permanent pervenous atrial pacing from the coronary vein has been attempted in 14 patients. Several types of arrhythmias including symptomatic bradycardia, "bradytachy" syndrome, and refractory ventricular tachyarrhythmia-fibrillation have been successfully treated with pervenous atrial pacing in 10 patients for 1 to 30 mo. Longterm atrial pacing was unsuccessful in four patients; in two of these four this was due to high atrial pacing thresholds. To date there has been no evidence of pacemaker perforation or pacemaker-induced coronary vein thrombosis. It is concluded that permanent pervenous atrial pacing from the coronary vein is a reliable method of atrial pacing without resorting to thoracotomy.

A case of a 29 year old female patient with sinoatrial block, first degree A-V heart block and Adams-Stokes seizures since the age of 11 is reported. The mechanism of the syncopal attacks was established by continuous radioelectrocardiographic monitoring as episodes of sinoatrial heart block or arrest, or both. There was no evidence of inflammatory, degenerative or congenital heart disease, and the patient had never received drugs assocated with the production of Adams-Stokes seizures. From the etiologic standpoint exaggerated vagal effects undoubtedly played a role; the existence of a congenital abnormality of the conduction system must, however, be taken into consideration. Treatment with artificial pacemaker stimulation proved effective and prevented further Adams-Stokes attacks.

Fatty infiltration has only rarely been reported as a cause of a cardiac conduction defect. A case of chronic sinoatrial block and atrial fibrillation with severe fatty infiltration of the myocardium and the conduction system is reported. The literature on conduction defects due to fatty infiltration is reviewed.

Six patients with symptoms due to sinoatrial block are described in whom no relief or improvement in block occurred when they were treated with isoprenaline or ephedrine. All six patients were treated by ventricular cardiac pacing with complete relief of symptoms. Despite the theoretical disadvantages of parasystole and loss of accrochage in treating these patients by ventricular pacing they have survived for periods of 18 months to over five years.

A new technique for the transvenous implantation of a specially designed atrial sensing electrode is described. In combination with a ventricular stimulating electrode and an atrial-controlled pacemaker, the method enables synchronization of atrial with ventricular activity. The atrial sensing electrode is put into the right atrial appendage through a preshaped radiopaque Teflon applicator catheter. Two hooks on the electrode tip provide for safe and secure anchoring of the electrode tip to trabeculae of the atrial appendage. The technique has been used for synchronous P wave pacing in 12 patients with complete atrioventricular block, most of them suffering from AdamStokes attacks. Three additional patients with sinoatrial block were treated by means of anchored atrial electrodes. Observation periods of up to 39 months showed no dislocation of any of the anchored atrial electrodes, and performance in all patients was faultless.

In the conventional postmortem coronary angiogram and vessels are illustrated by a "compact" filling with contrast medium. In the case of the double contrast technique, a thin film of contrast medium is brought about the inner surface of the arteries. Gas injected under controlled pressures into the vessels acts as a further control against the surrounding media. The method is suitable for a more precise illustration of the subepicardial and large intramural coronary arteries. Of particular advantage is the high transparency of the x-ray pictures and the possibility to make the coronary ostia visible. The evaluation of x-ray pictures produced at different controlled pressures permits conclusions about pressure-volume relations of defined vessel sections, which then can be analysed histologically.

Lithium is known to produce T wave changes in the ECG, whereas effect upon the conducting system of the heart has not been described. In our patient lithium produced sinoauricular block and possibly tachycardia. The correlation between lithium treatment and tachyarrhythmias is discussed. When during lithium treatment block is found, the treatment should preferably be stopped, but if this is not possible it is important to realize that digitalis should not be used as a prophylactic drug against tachycardia, as it worsens the block and therefore increases the frequency of arrhythmia, even leading to Adams-Stokes attacks.

Twenty-one patients with long-term right bundle branch block and left posterior himiblock were studied electrophysiologically and then followed up prospectively. The group consisted of 19 men and 2 woman aged 61 +/- 2.7 years (mean +/- standard error of the mean). The majority of patients had either hypertensive cardiovascular disease (48 percent) or primary conduction disease (33 percent). Initial electrophysiologic studies revealed A-H intervals of 58 to 152 msec (mean 98 +/- 7.7) and H-V intervals of 40 to 80 msec (mean 52 +/- 2.1). Six patients (29 percent) had prolonged H-V intervals. The follow-up period ranged from 91 to 1,231 days (mean 671 +/-68). Three of 21 patients (14 percent) needed a permanent pacemaker after development of the following symptomatic conduction disease: sinoatrial block on day 3 of follow-up; second degree atrioventricular (A-V) block, site undetermined, on day 118; and second degree A-V block proximal to the His bundle on day 398. One patient died suddenly (on day 571), and two others died of noncardiac causes. In conclusion, combined right bundle branch block and left posterior hemiblock was associated with less trifascicular disease than reported previously. The clinical course of most of the patients was benign and the incidence of sudden death was relatively small. Symptomatic conduction disease occurred but could be definitely related to trifascicular disease in only one patient. These short-term data suggest that prophylactic pacemaker insertion is not routinely indicated in patients with chronic right bundle branch block and left posterior hemiblock.

Concealed AV junctional extrasystoles are described which, conducted in a restrograde manner to the sinoatrial junction, interfere with sinus impulses, thus simulating a second-degree, 2:1, sinoatrial block.

Analysis of the long-term survival of pacemaker carriers showed a parallelism between two curves: that of the survival in patients treated with a pacemaker as from the second month, and that of a control group with the same age and physical structure. Treatment in the first few years was made problematical by defects in surgical technique: while in 17% of reoperations, the reason was straightforward substitution of the pacemaker owing to wear on the battery, 83% were the consequences of complications. Of these, 23% consisted of shifts in the intracavitary probe, electrode failures, or increase in the threshold. The frequency of infections due to implantation or reoperation was 7,4%, in certain cases with fatal outcome. Bearing in mind that mortality from Adam-Stokes disease was 50% prior to the introduction of pacemakers, it can be maintained that this therapy represents a considerable step forward in cardiology. Mortality was 27% in all patients submitted to implantation.

Twenty-three children underwent electrophysiological studies during routine postoperative catheterization two months to five years after complete correction of tetralogy of Fallot. The aim of the study was to investigate the whole conduction system, including sinus node function, suing His bundle recordings and atrial pacing. H-V intervals were normal at rest and with pacing in twenty-two patients, including four patients with evidence of bifascicular block on the surface ECG. One patient with cardiomegaly and evidence of diffuse myocardial damage had a prolonged H-V interval but did not develop a block at this level during pacing A-H interval was slightly prolonged in four patients and normal in all others. The threshold of pacing-induced atrioventricular block ranged from 75 to 240/min and was somewhat age dependent (r = -0.55). Two patients fell below the 95% confidence limit of this regression and are considered abnormal. One returned to normal after intravenous injectionof atropine. Corrected sinus node recovery time ranged from 60 to 2000 msec. Three patients had values above 500 msec which are considered abnormal. These patients had other minor signs of sinus node dysfunction, i.e., episodes of sino-atrial block at rest or intermittent sinus bradycardia. Thus, while the His Purkinje system performed satisfactorily in all patients, sinus node dysfunctional and A-V node dysfunction were demonstrated in a few patients after correction of tetralogy of Fallot.

Out of a pacemaker population of 392 patients, 90 (23%) have been found to have sinoatrial syndrome. Their ages ranged from 22 to 86 years, and averaged 66 for men and 70 for women. The male-to-female ratio was 1: 1.6. Before pacemaker implantation, syncopal attacks had occurred in 54%, dizziness without syncope in 31% and tachyarrhythmias in 57%. Atrial or paroxysmal supraventricular tachycardia had been recorded in 33%, atrial fibrillation or flutter in 28%, and ventricular tachycardia in 11%. First and/or second degree AV block was found in 36%. Coronary heart disease was present in 61% and 20% had had myocardial infarction. Cardiomyopathy and previous carditis were other associated heart diseases. Sinoatrial syndrome was the only manifestation of heart disease in 20%. Follow-up time after pacemaker implantation ranged from 3 months to 7 years, mean 23 months. Syncopal attacks were stopped in 48 of 49 patients, dizziness was relieved in all 28 patients and tachyarrhythmias were controlled by combined drug treatment in 43 of 51 patients. Nineteen patients died during the follow-up, most of them of cerebrovascular events or myocardial infarction. Associated coronary heart disease was especially frequent in this group. The death of one patient was caused by a run-away pacemaker. Other pacing failures were due to electrode movement or premature battery exhaustion. There was no mortality associated with pacemaker implantations or replacements. These results strongly support the view that pacemaker treatment most effectively controls symptoms of sinoatrial syndrome when drug treatment fails.

Study of atrio-ventricular conduction across the atrio-ventricular node using rapid atrial stimulation revealed a particular kind of block in 10 patients; the characteristics of the Wenckebach phenomenon were associated with a 2/1 block. One P wave was blocked, and the PR interval of the conducting sequence became progressively longer until the cycle was broken by two consecutive blocked P waves. By recording the potentials in the bundle of His, it proved possible to localise the conduction defect to the A/V node in 9 cases. The defect appeared in various clinical forms: atrial tachysystole, incomplete atrio-ventricular block, both chronic and acute, and atrio-ventricular conduction that was apparently normal. Study of the transmission through the node of progressively increasing atrial stimuli showed that there was a strong tendency towards diminishing conductivity which appeared to favour dispersion of the incoming impulses centrally within the node.

Thirty-four patients (mean age 64 years) with this syndrome are reviewed. Common symptoms relate to transient cerebral ischemia with syncope, episodes of rapid palpitations, or both. Usually no definite etiology was found but ischemic heart disease was present in 12 of the 34. Thirty patients had objective evidence of other cardiac disease besides, the sinoatrial block. Additional conduction disturbances were present in 14 subjects. Calcification was found in the mitral or aortic annulus in nine cases. It is likely that sinoatrial block is only symptomatic and important if other processes are present which may decrease the automaticity of lower pacemaker areas. This may take the form of associated cardiac disease or excessive vagal tone as in three cases of reversible chronic sinoatrial block with peptic ulcer. Treatment with drugs alone is almost always unsuccessful. Long-term cardiac pacing either alone or in combination with drugs usually alleviates the major symptoms.

An arrhythmia displaying the phenomenon of exit block around a junctional pacemaker in a patient with atrial tachycardia and complete A-V block at the junctional level is described. The importance of the exit block concept for a rational interpretation of cardiac arrhythmias is discussed.

Seventeen patient with sinoatrial block and 16 healthy volunteers were investigated with recently developed autonomic tests of atrial pacemaker function. Only one patients was found to be entirely normal in comparison with normal subjects, while another patients had supernormal responses. Fifteen patients had reduced responses relative to the controls implying impaired atrial pacemaker function or sinoatrial disease. It is suggested that while in some cases sinoatrial block may be of physiological origin, it is more often due to sinoatrial disease. The latter group are liable to Adams-Stokes syncope and may have additional atricventricular conduction abnormalities. The possible mechanisms and treatment of sinoatrial block are discussed relative to the autonomic and pacemaker function abnormalities described.

Sinoatrial (SA) conduction can be tested in man by premature atrial stimuli. The difference between the post-extrasystolic pause and the spontaneous sinus cycle is a sign of the sinoatrial delay. Extern atrial stimuli provoked over the esophagus showed analogous results to intracardiac tests. The sinoatrial conduction time estimated by the esophagus method is about 20 ms higher. In 30 normal persons it was 95 +/- 36 ms (x +/- 2 SX). 7 patients with sick sinus syndrome showed aberrations as in the intracardiac test. Different types of sinoatrial block should be distinguished. Type I measured by the esophagus method had a "SAE time" over 130 ms. Type II always had compensating postextrasystolic pauses due to higher SA delay. Type III of other authors could not be observed; there are doubts about the rightness of this type. In 2 patients SA blocks over several sinus cysles could be induced by premature stimuli. This feature osberved for the first time has been declared as type IV. In 28 patients with different diseases of the heart type I could be found 12 times and type II 6 times; SA block was not known previously. The calculation of the SA time by atrial stimuli via the esophagus offers a riskless and simple method for the further differential diagnosis of disturbances of the cardiac rhythm.

Summary Two patients in whom profound sinus bradycardia resulted from the use of lidocaine are described. In one patient, complete AV block also occurred in association with sinus bradycardia. While congestive failure and the associated hepatic insufficiency may have contributed to excessive blood levels of lidocaine in one patient, these factors were not evident in the other. The occurrence of sinoatrial block in isolated rabbit heart preparations during exposure to lidocaine suggests that a similar mechanism may be responsible for instances of “sinus bradycardia” and “sinus arrest” in patients with heart disease. The development of sinoatrial block in conjunction with suppression of latent pacemakers in the AV junction and the ventricles may result in particularly dangerous arrhythmias and should be borne in mind when using lidocaine in patients with heart disease.