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While the advancement of perioperative management has expanded Fontan candidacy, not all patients have a successful postoperative course. Our case was a right isomerism patient who could not leave the ICU due to high central venous pressure and low output syndrome. Initial observation of the monitor ECG showed his rhythm to be supraventricular, however, an echocardiogram indicated simultaneous contraction of the atrium and ventricle, implying a junctional rhythm. While neither central venous pressure nor blood pressure improved with temporary pacing, better central venous and pulmonary venous blood flow patterns during pacing unraveled its positive impact. The patient successfully left the ICU after permanent pacing implantation. Hemodynamic study revealed a beneficial impact of atrial pacing in securing cardiac output and ventricular preload, lowering central venous pressure, and shortening blood transit time, which is partly attributed to the optimization of the fenestration function in reservation of the preload. Our case emphasizes the significant advantage of atrial pacing in a failing Fontan patient with junctional rhythm by reducing venous congestion and maximizing the benefit of fenestration.

The effects of intravenous lidocaine on the refractory periods of the atrium, AV node and right ventricular myocardium were studied using His bundle recordings and the extrastimulus technique with and without atrial and ventricular pacing The drug was administered in an intravenous bolus dose of 1 mg/Kg followed by an infusion of 100 micrograms/Kg/min The AH, HV intervals and resting sinus cycle length as well as functional and effective refractory periods of atrium, AV node and right ventricle were measured before and 5 min afrer bolus injection of lidocaine Neither of the refractory periods nor AH and HV intervals changed significantly following administration of lidocaine The result of this first study in children is in agreement with previous reports of the effects of lidocaine on the cardiac conduction system in adults

Here we report two young patients with atrial fibrillation/atrial flutter complicated with cardiogenic cerebral embolism. Electrophysiological study revealed a large area of low-voltage zone or area of electric silence in both sides of the atrium during restoration of sinus rhythm, and the echocardiogram showed loss of mechanical function of the atrium. The electrical-mechanical dysfunction of the atrium was considered to be the cause of embolic event in this type of patient who was "very low" stroke risk atrial fibrillation or atrial flutter. The idiopathic, fibrotic atrial cardiomyopathy may be underlying in these patients.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with increased risks of stroke and heart failure. However, the exact mechanisms of left atrium remodeling and AF-related biological behaviors are not completely understood.The transcripts of left atrium in permanent atrium fibrillation patients (n = 7) were compared with those of healthy heart donors (n = 4) in sinus rhythm using Agilent 4x44K microarrays. Differently expressed genes were analyzed based on Gene Ontology and KEGG and Biocarta pathway analysis databases.We identified 567 down- and 420 up-regulated genes in atrial fibrillation. The majority of the down-regulated genes participated in metabolic processes, particularly that for fatty acids. The most remarkable up-regulating effects were immune and platelet activation. In addition, atrial remodeling including structural, contractile, electrophysiological, neurohormone, and oxidant stress was also observed, suggesting various pathophysiology changes in fibrillating atrium. Nine AF closely related genes were validated by real-time RT-PCR.Some AF specific genes were determined which may be a complement to the mechanism of left atrium remodeling. Metabolic changes and inflammation could promote or aggravate atrial fibrillation.

Sustained atrial fibrillation (AF) was induced by atrial burst pacing, and monophasic action potentials (MAPs) were recorded. MAP alternans was observed at a cycle length (CL) of 167.5 ± 28.2 msec before burst pacing and 201.3 ± 40.2 msec after burst pacing. AF > 5 minutes duration was induced in 1 dog in the control condition but in all 8 dogs after burst pacing. The difference in RA MAPD80 of the first spontaneous beat and steady-state sinus rhythm was significantly larger after atrial burst pacing than before atrial burst pacing (31.5 ± 15.9 msec versus 8.2 ± 9.0 msec) In 4 dogs, late phase 3 early afterdepolarization was observed after rapid atrial pacing. Rapid atrial pacing-induced electrical remodeling includes APD alternans during rapid atrial pacing and also causes an increase in the MAPD of the initial several beats and the development of late phase 3 early afterdepolarizations after a sudden increase in CL.

Thyroid hormone has been shown to modulate the gene expression of cardiac potassium channels, however, it is not known if gene expression is different between the atrium and the ventricle. The long-term effects of thyroid hormone on nuclear thyroid hormone receptors are also not known. Triiodothyronine (T3) at 25 μg/100 g of body weight or propylthiouracil (PTU) at 4 mg/100 g of body weight was given to adult rats via a gastric tube for 14 days. The levels of mRNA of Kv1.2, Kv1.4, Kv1.5, Kv2.1, Kv4.2, erg, LQT1, and minK were assayed by RNase protection assay. The mRNA of nuclear T3-receptor-α1 and T3-receptor-β1 were also assayed for 15 days. After T3 (or PTU), plasma free T3 and free T4 increased (or decreased) significantly. The mRNA levels of Kv1.2 and Kv1.4 were reduced after T3 in the atrium and the ventricle, while PTU increased the levels in both chambers. Kv1.5 was significantly up-regulated by T3 in the atrium and the ventricle (P

It has been demonstrated that successful cavotricuspid isthmus ablation of typical atrial flutter combined with atrial fibrillation (AF) sometimes influences the preablation history of paroxysmal AF. However, the effectiveness of only isthmus ablation on AF itself is unclear. Endocardial catheter mapping during induced AF was performed around the tricuspid annulus using duodecapolar clectrode catheters in 39 patients with drug-refractory paroxysmal AF. Isthmus ablation was performed in 16 patients (41%) in whom catheter mapping during AF showed an organized activation pattern around the tricuspid annulus. During a mean follow-up of 12.3 months, isthmus ablation was successful in preventing AF in 12 (75%) patients, 8 without medication and 4 with a previously ineffective drug. This success group had a significantly higher F wave amplitude in lead V1 (0.29+/-0.10 vs 0. 15+/-0.04 mV, p < 0.01), a higher left ventricular ejection fraction (74+/-9 vs 58+/-2%, p < 0.05), and a smaller left atrial dimension (35+/-6 vs 43+/-4 mm, p < 0.05) than the failure group. Isthmus ablation may be effective in preventing paroxysmal AF with an organized activation pattern around the tricuspid annulus. F wave amplitude, left ventricular ejection fraction, and left atrial dimension were significant predictors of success.

The effects of intravenous MS-551, a new class III antiarrhythmic drug, on atrium and ventricle were evaluated in 6 patients with ventricular tachyarrhythmias (4 males and 2 females; mean age 45 +/- 21 years) in an electrophysiologic study. Two patients had sustained ventricular tachycardia (VT) and 4 patients had ventricular fibrillation (VF). Electrophysiologic study was performed before and after the administration of MS-551 (loading infusion 0.3 mg/kg for 5 min + 0.01 mg/kg/min). The QT and QTc intervals were significantly prolonged by MS-551 from 359 +/- 52 to 411 +/- 63 msec (p = 0.01) and from 410 +/- 36 to 452 +/- 47 (p = 0.0172), respectively. No effect was observed on the sinus cycle length, QRS duration, or AH and HV intervals in sinus rhythm. The effective refractory periods of the right atrium (AERP) were significantly prolonged at paced cycle lengths of 600 (from 222 +/- 19 to 250 +/- 23 msec, p = 0.0009), 400 (from 207 +/- 15 to 228 +/- 15, p0.0001) and 300 (from 193 +/- 10 to 205 +/- 8 msec, p = 0.0127) msec. Similarly, the right ventricular ERP (VERP) were significantly prolonged at paced cycle lengths of 600 (from 240 +/- 23 to 268 +/- 23 msec, p0.0001), 400 (from 225 +/- 22 to 250 +/- 24 msec, p = 0.0007), and 300 msec (from 213 +/- 14 to 228 +/- 18 msec, p = 0.0071). MS-551 prolonged AERP and VERP in a "reverse" use-dependent manner without changing the conduction time in patients with ventricular tachyarrhythmias. MS-551 prevented the induction of VT in 1 patient and VF in only 1 patient in this electrophysiologic study. Further evaluation of the therapeutic potential of MS-551 using higher dosages is necessary.

We performed a total repair for a 1-year-old boy with left isomerism, a common atrium, incomplete atrioventricular septal defect and hemiazygos continuation. The operation performed was intraatrial rerouting with a baffle and mitral repair. The postoperative course was uneventful. However, two and a half years after the total repair, the patient revealed obstruction of the systemic atrium constructed by the baffle and the left ventricular outflow tract. Reoperation to relieve these obstructions was successful.

We evaluated the relationship between changes in the atrioventricular (AV) intervals and right atrial monophasic action potential duration at 90% repolarization (RA-MAPD 90 ) in humans. In 4 patients, RA-MAPD 90 was measured during AV reciprocating tachycardia (AVRT, n = 2) or AV node reentrant tachycardia (AVNRT, n = 2) and atrial or ventricular pacing at similar cycle lengths. In 10 patients, RA-MAPD 90 was measured during continuous atrioventricular sequential pacing at AV intervals of 0, 50, 100, 150, 200, 250, 300, 350 msec for 90 sec at a cycle length of 333-400 msec. In patients with AVRT, the RA-MAPD 90 during tachycardia was shorter than RA-MAPD 90 during RA or RV pacing. In patients with AVNRT, RA-MAPD 90 during tachycardia was similar or longer than RA-MAPD 90 during RA or RV pacing. As the AV interval was increased from 0 msec to 150 msec, the peak right atrial pressure decreased from 8-12 mmHg to 2-3 mmHg. RA-MAPD 90 decreased to its minimal value at an AV interval of 150 msec. The maximal difference in the RA-MAPD 90 obtained by changing the AV interval was 22.5 ± 3.0 msec. We conclude that 1) a very short AV or VA interval causes an increase in RA-MAPD 90 which correlates with an increase in RA pressure, and 2) RA-MAPD 90 during supraventricular tachycardia is different from RA-MAPD 90 during atrial or ventricular pacing. Thus, a contraction-excitation feedback mechanism may exist in the human atrium. (Jpn Heart J 36 : 439-450, 1995)

The density of cardiac beta-adrenoceptors (Bmax) was measured in eighteen patients [2 with atrial septal defect (ostium secundum), 4 with aortic valve disease, 3 with mitral valve disease, 1 with aortic and mitral valve disease, 5 with a history of myocardial infarction, and 3 with angina pectoris] following mild to moderate cardiac failure. Measures were obtained by cardiac catheterization prior to cardiac surgery and also during the surgical procedures. On the basis of symptoms immediately preceding surgery, the severity of the condition in each patient was categorized as either Class I (n = 5) or Class II (n = 13) following the New York Heart Association (NYHA) functional classification system. The Bmax was measured using right atrial appendage tissue obtained during cardiac surgery. [125I]-iodocyanopindolol was used for the assay. The Bmax of atrial cell membranes in patients with NYHA class II was significantly lower than that of class I (34.1 +/- 2.5 vs 55.4 +/- 9.3 fmol/mg protein, M +/- SE, p0.05). Correlation coefficients between the Bmax and hemodynamic parameters measured just prior to cardiac surgery were examined, but only that between Bmax and the minimum value of the time derivative of left ventricular pressure (max negative dp/dt) was significant (r = -0.552, p0.05). Further study is needed to understand and clarify the relationship between Bmax and dp/dt min.

Percutaneous transluminal coronary angioplasty of coronary artery occlusions forms a routine part of cardiological practice. However, only a few angiographic variables which might predict success have been investigated and identified. Video densitometry was used to assess structural features of the occlusion that have not been investigated previously. The sharpness and eccentricity of the tapering, the presence of any distal vessel and the presence of a reservoir or atrium in which the end of the wire could become trapped were measured. Other measurements taken from the cineangiogram included the minimum radius of curvature of the artery immediately before the occlusion, the number of bends and the distance traversed before the occlusion. The number, size, location and angle of branching of side branches from the artery in question were noted. The number of bridging collaterals and presence of distal opacification were noted. There was a significantly higher success rate in patients with less than 3 bends before the occlusion (p = 0.01) and a distance down the artery to the occlusion of less than 27 mm (p < 0.05). An atrium was present in 36% and was associated with an unsuccessful outcome (p = 0.02). Distal opacification, despite occlusion of the artery, was found to be associated with failure to cross the lesion (p < 0.05). The angle of branches of the artery was only found to be important near (within 7.5 mm) the occlusion (p < 0.05). None of the video densitometric measurements of the fine structure of the stump of the coronary artery were found to be helpful.

The cardiovascular effects of 2-amino-N-(2,6-dimethylphenyl)-N-[3- (3-pyridyl)propyl]propionamide dihydrochloride (Ro 22-9194) were investigated in the canine isolated atrial preparation perfused with arterial blood from another donor dog. Intravenous administration of Ro 22-9194 (0.3-3 mg/kg) reduced heart rate and systemic arterial blood pressure of the donor dog. Simultaneously, in the isolated atrium perfused with donor's blood, negative chronotropic and inotropic responses were induced in a dose-dependent manner. Direct administration of Ro 22-9194 (1-300 micrograms) into the sinus node artery of the isolated atrium induced negative chrono- and inotropic responses and a transient increase in coronary blood flow in a dose-related manner. Mexiletine (1-300 micrograms) also induced negative chrono- and inotropic responses. The potency of Ro 22-9194 for negative cardiac effects was similar to that of mexiletine. The negative cardiac effects of Ro 22-9194 were not modified by atropine in doses which significantly inhibited the cardiac effects of acetylcholine. Ro 22-9194 did not affect the cardiac responses to norepinephrine and to acetylcholine significantly. These results suggest that Ro 22-9194 has non-cholinergic cardiac depressant properties with its vasodilating action, and it has neither anti-adrenergic nor anti-cholinergic actions on the dog heart.

Although arrhythmogenic right ventricular dysplasia (ARVD) is believed to involve primarily the right ventricle, left ventricular abnormalities have also been described. We report a case of ARVD with abnormalities of the sinus node, right atrium and atrioventricular node. The biopsies taken from the right atrium and the right ventricle showed replacement of myocardium by fibrous tissue. The pathologic changes of this disease process may extend into the atrium and atrioventricular node.

To study the factors controlling the release of atrial natriuretic factor (ANF), we analyzed the peripheral plasma ANF concentration in 34 patients with heart disease who underwent cardiac catheterization. A significant positive correlation between plasma ANF concentration and pulmonary arterial pressure (systolic, r = 0.87; diastolic, r = 0.75; mean, r = 0.85; each p less than 0.001) was found in all the patients examined. There were significant positive correlations between plasma ANF concentration and systolic right ventricular pressure (r = 0.86, p less than 0.001), pulmonary capillary wedge pressure (r = 0.50, p less than 0.01) and mean right atrial pressure (r = 0.39, p less than 0.05). A weak but significant negative correlation was found between plasma ANF concentration and stroke volume index (r = -0.43, p less than 0.05). The correlation coefficient between plasma ANF concentration and mean pulmonary arterial pressure was significantly stronger than those between plasma ANF concentration and pulmonary capillary wedge pressure, and between plasma ANF concentration and mean right atrial pressure (p less than 0.05 and p less than 0.01, respectively). In 10 patients with mitral valvular disease, significant correlations with plasma ANF concentration were also found for pulmonary arterial pressure (systolic, r = 0.80; diastolic, r = 0.82; mean, r = 0.82; each p less than 0.01). These findings suggest that pulmonary arterial pressure may play an important role in the mechanism of release of ANF from atrial cardiocytes.

Analysis of beat to beat changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in 30 consecutive patients undergoing diagnostic cardiac catheterization. The group consisted of 9 normal subjects, 18 with coronary artery disease and 3 with congestive cardiomyopathy. The recordings of aortic pressure were made during atrial pacing and ventricular pacing at a rate 5 to 10 beats/min above each individual's sinus rhythm. During ventricular pacing, LV ejection time was the longest when an atrial contraction preceded a ventricularly paced beat by a physiologic interval and was approximately similar to that obtained during atrial pacing (maxET). When the atrial systole occurred with or followed the ventricularly paced contraction, LV ejection time was decreased (minET). Since maxET occurred in the presence of an effective atrial contraction to ventricular filling and minET in the absence of this contraction, the atrial contribution to ventricular filling was calculated as (maxET-minET)/maxET X 100 (%). LV volumes at end-systole (V1), before atrial contraction (V2) and at end-diastole (V3) were obtained according to the area-length method by tracing the silhouette of left ventriculograms using a computer system. The atrial contribution was calculated from LV volumes using the formula (V3-V2)/(V3-V1) X 100 (%). There was a good correlation (r = 0.88) between the atrial contributions calculated from LV ejection times and those calculated from LV volumes. In the patients with coronary artery disease and with congestive cardiomyopathy, the atrial contribution was significantly greater than in the normal subjects. The measurement of LV ejection time during ventricular pacing may be a clinically useful screening procedure to identify patients in whom physiologic pacing may be indicated.

The effects of potassium chloride were studied on pacemaker activity in the sinoatrial (SA) node and on contractility in isolated, blood-perfused atrial and left ventricular preparations of dogs, which were suspended in the bath and perfused with arterial blood from the carotid artery of the heparinized support dog. Potassium chloride given directly into the sinus node artery in a dose range of 100 micrograms--1 mg produced a dose-related positive chronotropic and a negative inotropic effect in isolated atrium preparations. Potassium chloride into the cannulated anterior descending branch of the left coronary artery caused only a negative inotropic effect in isolated ventricular preparations. A larger dose of potassium chloride caused temporary atrial or ventricular arrest. These effects of potassium chloride were not modified by pretreatment with atropine or propranolol.

This study used an isolated right atrial preparation, cross-perfused with arterial blood from a support dog. We investigated the effects of dibutyryl cyclic AMP (DBcAMP) on heart rate and arterial blood pressure of the support dog and on the sinus rate and atrial contractile force of the isolated perfused atrium. DBcAMP was injected into the external jugular vein of the support dog or into the sinus node artery of the isolated atrium. DBcAMP to the support dog induced a small increase and/or decrease in arterial blood pressure at a dose of 3 or 10 mg/Kg i.v. It produced a decrease, with or without an increase in blood pressure, at a dose of 30 mg/Kg i.v., and a dose-dependent increase in heart rate in the support dog. In the isolated atrium, positive chronotropic and inotropic effects were observed. Direct injection of DBcAMP (3-30 mg) into the sinus node artery of the isolated atrium induced positive chronotropic and inotropic effects, after initial brief negative effects, in a dose-dependent manner. DBcAMP did not change norepinephrine-induced positive chronotropic and inotropic effects in the isolated atrium. These results demonstrate that DBcAMP induces a decrease in systemic arterial blood pressure with increases in sinus rate and atrial contractile force, and acts additively with the norepinephrine-induced positive cardiac effects in the dog heart.

A new cardiotonic compound, 5-methyl-6-(4-pyridinyl)-2H-1,4-thiazine-3(4H)-one X hydrochloride (ZSY-27), was investigated in cross-circulated dog atrial muscle preparations. When ZSY-27 was intravenously administered to the donor dog, a dose-dependent depressor effect with slight sinus tachycardia was induced in the donor dog. At the same time, a significant dose-dependent increase in developed tension was usually observed in an isolated atrium perfused with donor's arterial blood, but there were no significant changes in sinus cycle length and sinoatrial conduction time. The ZSY-27-induced positive inotropic effect was not significantly influenced by treatment with propranolol in doses which completely inhibited norepinephrine-induced positive chronotropic and inotropic effects. When ZSY-27 was injected into the cannulated sinus node artery of the isolated atrium, dose dependent positive chronotropic and inotropic effects were induced. The dominant increases in developed tension by ZSY-27 were similar to effects of other phosphodiesterase inhibitors, such as papaverine and aminophylline. From these results, it is concluded that ZSY-27 has non-adrenergic, cardiotonic properties with a depressor effect.

The presence or absence of ventriculoatrial (VA) conduction in the human heart is assessed by investigating whether 1:1 retrograde atrial capture is observed during constant cycle length ventricular pacing. In this study, a new pacing protocol for assessing VA conduction was designed in which the ventricular extrastimulus was delivered during basic ventricular and atrial simultaneous pacing (VE-VASP method). The effect of this pacing protocol on VA conduction was investigated in 12 patients who showed no evidence of VA conduction with the constant cycle length ventricular pacing method. In 5 of 12 patients, intact VA conduction was demonstrated with the VE-VASP method, while VA conduction was not observed in the remaining 7 patients. These results suggest that VE-VASP method sometimes demonstrates the presence of intact VA conduction in patients who show no evidence of VA conduction during constant cycle length ventricular pacing.

Left atrial and left ventricular infarction with various atrial arrhythmias, multiple systemic arterial thromboembolism, and a large mural thrombus over the left atrial infarction is reported. In ischemic heart disease, systemic arterial thromboembolism may develop due to atrial infarction which is often overlooked in antemortem as well as in postmortem examinations. When a clinical diagnosis of atrial infarction is made, the possibility of a Stokes-Adams syndrome, thromboembolism, and rupture of the atrium should also be investigated.

The study comprised 67 subjects, mean age 43.7 years, with suspected sick sinus syndrome, in whom rapid atrial pacing before and after combined atropine and propranolol was performed by Narula's method. Three groups were formed: group I--with normal sinus node recovery time (SNRT) and corrected sinus node recovery time (CNRT) before and after the autonomic blockade; group II--with functional disorders of the sinus node and group III--with intrinsic sinus node dysfunction. After autonomic blockade in groups I and II mean SNRT, CNRT, post-stimulation cycle lengths (except No. 2 and Nos. 5, 6, 10, respectively) shortened, whereas HR rose. In contrast, in group III mean SNRT, CNRT, post-stimulation cycle lengths (Nos. 1, 2, 6, 10) and HR increased. Significant differences in post-stimulation cycle lengths were observed between groups I and III as well as groups II and III. In conclusion, rapid atrial pacing after combined atropine and propranolol helps us to diagnose latent sick sinus syndrome and extrinsic sinus node dysfunction more precisely, and significant differences in post-stimulation cycle lengths between the groups confirm diagnostic value.

The electrophysiological effects of intravenous administration of diphenylhydantoin (DPH) (5 mg/Kg, maximum 250 mg) were studied in 20 patients with sinus node dysfunction (SND). DPH shortened spontaneous cycle length (SCL) in 3 patients and lengthened it in 3. Maximum corrected sinus node recovery time (max CSRT) was prolonged in 7 patients and shortened in 3. Estimated sinoatrial conduction time was prolonged in 3 patients and shortened in 2 of 10 patients in whom this measurement was possible. However, these changes were not statistically significant. Neither were there any significant changes in PA, AH and HV intervals nor refractory periods of the atrium, the AV node and the ventricle. DPH prolonged SCL and/or max CSRT in 9 of 20 patients with SND, and it was suggested that DPH has depressant effects on the sinus node in some patients with SND. Thus, this drug should be used with caution in the treatment of ventricular arrhythmias accompanied by sinus node dysfunction.

The distribution of norepinephrine (NE), cyclic AMP (cAMP) and cyclic GMP (cGMP) and the activities of related enzymes in the atrioventricular (A-V) conducting tissue of the bovine heart were examined. The concentration of NE in the atrium was about twice that in the ventricle. In the A-V conducting tissue, the concentration of NE was highest in the atrioventricular node (AVN) and lowest in the false tendon (FT), with intermediate levels in the bundle of His (HIS) and the right and left bundle branches (RLBB). The activity of monoamine oxidase (MAO) in the atrium was about 2.2 times that in the ventricle. In the A-V conducting tissue, the activity of MAO was highest in the HIS and lowest in the FT. The activity of catechol-o-methyltransferase (COMT) in the atrium and ventricle was similar, and that in the HIS was slightly, but not significantly, higher than that in other regions of the A-V conducting tissue. The concentration of cAMP in the ventricle was about twice that in the atrium. In the A-V conducting tissue, the concentration of cAMP was higher in the AVN and FT than in the HIS and RLBB. The distribution of adenylate cyclase (AC) was similar to that of NE. The phosphodiesterase (PDE) activity in the atrium and ventricle was similar. No significant difference was found in the level of PDE activity in different regions of the A-V conducting tissue. The concentration of cGMP was slightly, but not significantly, higher in the A-V conducting tissue than in the atrium or ventricle. In the A-V conducting tissue, the concentration of cGMP was highest in the FT and the concentrations in the HIS, RLBB and AVN were similar. These findings suggest that in the A-V conduction tissue, the regions that have the higher spontaneous pacemaker rates have higher NE content and AC activity, that is sensitivity to NE. Furthermore, the sensitivity for muscarinic cholinergic stimulation is higher in the conducting tissue (especially in the FT) than in the atrium and ventricle.

Effects of salmon calcitonin on SA node pacemaker activity and contractility were investigated in isolated atrium and papillary muscle preparations which were perfused with arterial blood led from a carotid artery of the support dog. Calcitonin at a dose range from 0.005 to 0.16 units was injected into the cannulated sinus node artery, which dose-relatedly caused a negative chronotropic and inotropic effect in atrium preparations. This negative effect was not modified by treatment with atropine. On the other hand, in the isolated paillary muscle preparations, an intraarterial calcitonin caused little negative inotropic effect even at higher dose level of 0.16 units. From these results, it is concluded that 1) in chronotropy, calcitonin causes a negative chronotropic effect, and 2) in inotropy calcitonin causes a negative inotropic effect on the atrium but not on the ventricle.

Electrophysiologic and histopathologic studies were performed on an 83-year-old man with partial atrial standstill. In the electrophysiologic study, no atrial electrical activity was recorded in the right atrium, but f waves were seen in the coronary sinus electrogram. Although the high right atrium and the atrial septum could not be activated by electrical stimuli of up to 10 V, the low atrium could be stimulated. The pathologic examination showed that there was extensive fatty infiltration into the sinus node and fibrosis in the atrial muscle. In the low right atrium, the musculature was partially preserved.

To clarify the mechanism of stress-induced ST segment elevation in patients with previous anterior myocardial infarction, we examined myocardial lactate metabolism during atrial pacing in 32 patients with previous anterior myocardial infarction (MI group) and 11 control subjects (control group). In the MI group, atrial pacing resulted in new or additional ST segment elevation in leads with Q waves in 15 patients (ST elevation group), ST segment depression in 7 (ST depression group), but induced no appreciable ST segment changes in the remaining 10 patients (ST unchanged group). In all patients, the ST segment changes were identical to the results of exercise stress testing which was carried out prior to the atrial pacing. Lactate extraction ratio increased moderately during the atrial pacing in the control group (p

Electrophysiological studies were performed to see the effects of lidocaine on the conduction system, particularly sinus node and atrium in 40 patients of SSS, using HBE recordings, rapid atrial pacing and atrial extrastimulus technique. Sinus cycle length, PA (P'A), AH, HV intervals, calculated SACT, and refractory periods of atrium, AV node and His-Purkinje system did not change after lidocaine. Only maximum CSRT was significantly increased with lidocaine. These results were not affected by pretreatment of atropine. In conclusion, the combining rapid atrial pacing with lidocaine may be useful to manifest the masked sinus node abnormalities. It was suggested that lidocaine directly depressed sinus node automaticity in SSS patients, without affecting perinodal tissue. Therefore, lidocaine should be used with caution in patients with known or suspected SSS.

The electrophysiological effects of intravenous propranolol (0.15 mg/kg) were studied in 26 patients with sinus node dysfunction (SND group) and 9 patients with normal sinus node function (control group). Spontaneous cycle length and AH interval were significantly increased in the control and SND groups after propranolol. PA and HV intervals, calculated sinoatrial conduction time and refractory periods of the atrium, AV node and ventricle were not significantly changed in either group. Maximum corrected sinus node recovery time (max CSRT) was not changed in the control group, but it was significantly prolonged in the SND group. These results of the overdrive suppression test were in disagreement with those of previous studies. Propranolol lengthened spontaneous cycle length (by more than 200 msec) and/or max CSRT (by more than 1000 msec) in 8 of 26 patients with SND. Thus, it is suggested that propranolol should be used with caution in patients with SND.

Ventriculo-atrial (VA) conduction was studied in 133 patients with various kinds of arrhythmias using intracardiac electrograms and programmed stimulation. One-to-one VA conduction was observed during RV pacing at the rate just above the sinus rate in 6 of 31 patients (19.4%) with advanced AV block, in 7 of 26 patients (26.9%) with impaired AV nodal conduction, in 25 of 71 patients (35.2%) with normal AV nodal conduction and 3 of 5 patients (60%) with enhanced AV nodal conduction. However, the differences between these groups were not significant. There was no significant difference in either the AH block rate during RA pacing or the antegrade functional refractory period (FRP) of the AV node in patients with or without VA conduction, and the VA block rate during RV pacing was not significantly correlated with the AH block rate or the FRP of the AV node. VA conduction time (S-HRA) also showed no significant differences between these groups. The mean VA conduction time during RV pacing at rates of 60 to 80 bpm was 208 +/- 87 msec, ranging from 100 to 395 msec. In conclusion, AV conduction disturbances may influence VA conduction, but VA conduction cannot be predicted from antegrade conductivity.

The effects of DJ-7141, a new alpha-2 agonist, on an isolated atrial preparation cross-perfused with arterial blood from a support dog were investigated. In the isolated atrium, a selective injection of DJ-7141 (1-100 micrograms) into the sinus node artery induced dose-dependent positive chronotropic and inotropic effects. The positive cardiac effects of DJ-7141 were not only inhibited by propranolol and by imipramine, but reversed to negative effects, whereas the positive cardiac effects of norepinephrine were blocked by propranolol and potentiated by imipramine. Tetrodotoxin (TTX) did not modify the cardiac responses to DJ-7141. After propranolol treatment, the negative chronotropic and inotropic responses to DJ-7141 were not influenced by atropine, which completely blocked acetylcholine-induced cardiac responses. When DJ-7141 was injected into the support dog at a dose of 10-300 micrograms/Kg i.v., it induced a brief increase in femoral arterial blood pressure and a long-lasting decrease in heart rate in the support dog and increases in atrial rate and contractile force in the isolated atrium. These results suggest that the new alpha-2 agonist, DJ-7141, induces indirect positive chronotropic and inotropic effects due to a tyramine-like action and direct negative cardiac effects in the isolated dog heart, and that the tyramine-like effect may be partially responsible for the increase in blood pressure seen with DJ-7141 in in situ dogs.

Disopyramide has been successfully used to treat a variety of supraventricular and ventricular arrhythmias. The electrophysiologic effects of this drug were studied following diagnostic cardiac catheterization in 14 children aged 7 months to 14 years, suffering from congential heart disease. Surface EKG, intra-atrial, and His bundle electrogram as well as right atrial pacing with the use of extrastimulus technique were obtained before and after a single intravenous dose of disopyramide (2 mg/Kg, max 50 mg). The drug significantly prolonged the HV interval, effective and functional refractory periods of the atrium and the AV node. The most consistent change was the prolongation of the atrial refractory periods. The electrophysiologic effects of this drug on the conduction system have been variable and this variability has been attributed to the degree of vagal tone. The findings in this age group are similar to adults with simultaneous cholinergic blockade. This might be due to the direct depressant effects of disopyramide on the atrial and AV nodal tissue, and point to the potential usefulness of this drug in the pediatric age group.

Eight patients with atrial flutter (AF) and rapid atrial tachycardia (AT) (5 common AF, 1 uncommon AF and 2 AT) were treated with transesophageal atrial pacing (TEAP). In 5 patients no antiarrhythmic agent was used during this study, and in 3 patients procainamide was administrated intravenously. Conversion to sinus rhythm was successfully achieved in 7 patients (5 common AF and 2 AT). Two patients were converted to sinus rhythm immediately after pacing, and transient atrial fibrillation was induced before conversion to sinus rhythm in 5 patients. TEAP failed to terminate the arrhythmia in 1 patient with uncommon AF. Administration of procainamide reduced the atrial rate in 2 common AF and 1 AT, which were successfully converted to sinus rhythm by TEAP, but induced a rapid ventricular response in 2 patients, one of whom also developed hypotension before conversion. No significant complication due to TEAP was observed in this study. In conclusion, TEAP is a noninvasive method with fewer complications and has nearly the same high efficacy for converting AF and rapid AT to sinus rhythm as DC cardioversion or transvenous atrial pacing.

The effects of intravenous administration of mexiletine on the refractory periods of the atrium and atrioventricular (AV) node were studied using His bundle recordings and the extrastimulus technique with atrial pacing. The drug was administered to 10 children with heart disease in an intravenous bolus dose of 3 mg/Kg, injected over a 5-min period, followed by an infusion of 1 mg/Kg/hr of mexiletine, achieving a mean therapeutic plasma concentration of 0.762 +/- 0.270 microgram/ml. The AH and HV intervals, the resting sinus cycle length, and the functional and effective refractory periods of the atrium and AV node were measured before and 5 min after initiation of the mexiletine infusion. The sinus cycle length was reduced significantly. However, neither the refractory periods nor the AH and HV intervals changed in a significant manner. Except for the heart rate, these results are similar to those reported in adults without conduction disturbances. In adults, mexiletine did not affect the sinus cycle length. However, in children, it consistently increased the heart rate. The lack of side effects in children is in contrast to adults, who usually suffer from gastrointestinal and neurologic symptoms upon receiving comparable doses parenterally.

Negative contrast echocardiograms of two-dimensional long axis view of the right ventricle and the atrium were compared with the results of cardiac catheterization and surgical findings in 33 adults with atrial septal defects. Contrast echocardiographic evidence of atrial communication was noted in 30 cases (91%), and, in 28 cases, the negative contrast during one cardiac cycle could be measured. This could be applied even in cases with a small left-to-right shunt or with Eisenmenger's syndrome. No obvious difference in the behavior of negative contrast was documented among the cases with distinct types of septal defects.The maximum negative contrast area and the duration of appearance in one cardiac cycle were related to the pulmonary-to-systemic flow ratio. However, a significant overlap and considerable effects of transducer angulation on measurements were documented. Thus, negative contrast echocardiography may be widely used for the noninvasive identification of a left-to-right shunt in atrial septal defects. However, the method is not appropriate for a precise quantification of three-dimensional shunt flow.

Although many of its effects have not been clarified, it is well known that the carotid sinus reflex has a profound influence on the cardiovascular system. The purpose of this paper is to investigate the effect of the carotid sinus reflex on the canine heart.The present experiments were performed on the in situ canine heart: 1) during sinus rhythm, 2) during electrically driven rhythm, and 3) during electrically driven rhythm after the administration of atropine. Before and during carotid sinus stimulation, the intracellular and surface electrograms, standard lead II electrocardiograms and aortic blood pressure were simultaneously recorded. The intracellular and surface electrograms were obtained from the epicardial surfaces of the right atrium and the left ventricle.Atrium. The duration of the membrane action potential (MAP) shortened during sinus rhythm and electrically driven rhythm. There were no significant changes in the amplitude of the MAP and the membrane resting potential (MRP). The PQ interval in the standard lead II electrocardiogram became significantly prolonged during both types of rhythm. The P amplitudes decreased during sinus rhythm. The shortening of the duration of the MAP was almost entirely inhibited by atropine.Ventricle. The duration of the MAP during sinus rhythm showedsignificant widening. The ST segment in the surface electrogram became significantly elevated during sinus rhythm and during electrically driven rhythm. The QT interval in the standard lead II electrocardiogram prolonged significantly during sinus rhythm, but less so during electrically driven rhythm. The RR interval became significantly prolonged during sinus rhythm. After atropine, the duration of the MAP widened very slightly during electrically driven rhythm.The following possibilities are discussed: Electrical behavior in atrial muscle is mainly mediated by the cholinergic nervous system. The response of the sinoatrial node is caused by cholinergic activity as well as by the decrease in adrenergic activity.The effect of carotid sinus stimulation on intracellular electrograms is more apparent in atrial muscle and in the sinoatrial node than in ventricular muscle.

Complete A-V block was observed in 18.4 per cent of 38 dogs with the anterior septal artery ligation and in 56.5 per cent of 23 dogs in which both anterior and posterior septal arteries were ligated. No complete A-V block appeared when only the posterior septal artery was ligated.In dogs which survived one day or more, A-V conduction disturbances were mostly transient even when both anterior and posterior septal arteries were ligated.Marked histological changes of the A-V conduction tissue were observed in dogs which had suffered from complete A-V block even after normal sinus rhythm was restored.The results of this study indicate that a rather small part of the crosssectional area of the A-V conduction tissue can carry impulses from the atrium to the ventricle in normal way.

(1) The effects of chlorpromazine (CP) on the action potentials (AP's) and contractions of the isolated guinea pig heart were investigated by means of a microelectrode and a strain gauge transducer.(2) CP at concentrations of 2×10-6 to 5×10-1Gm./ml. decreased markedly the pacemaker activity of the sino-atrial node. By the repeated application of the drug to the tissue, however, a considerable tolerance to the drug was developed, and in some preparations the acceleration of the beat rate occurred rather than the deceleration.(3) CP shortened AP-duration of the left atrial muscle and the left ventricular papillary muscle by 10 to 20%, but slight prolongation occurred for a longer treatment with the drug in some preparations.(4) CP definitely decreased the maximum rate of rise of AP's of both atrial and ventricular muscles without significant change in the resting potential.(5) The excitability assumed by the strength-duration curve of the atrium was decreased by the application of CP, and the full-recovery time of the atrium was delayed.(6) Contractile tension of both the atrium and the ventricle was strikingly reduced by the application of CP, but recovery was almost complete.(7) Clinical electrocardiographic abnormalities induced by fairly high dosage of the phenothiazine drugs and antiarrhythmic actions of these drugs were discussed in relation to the results obtained.

The ectopic pacemaker formation by aconitine in the left superior vena cava proximal to the heart was studied in rabbit.(1) Aconitine produced the automatic activities in the isolated strip of vena caval muscle.(2) During the recovery from aconitine poisoning the action potentials with diastolic slow depolarization were recorded from the region of the left superior vena cava near the coronary sinus.(3) In the in situ experiment, tachycardia was produced by the local application to the left superior vena cava near the coronary sinus.(4) From the above-mentioned facts, it was suggested that aconitine induced the ectopic pacemaker in the left superior vena cava proximal to the heart and that the impulse from the ectopic focus spread not only to the periphery but also to the atrium.