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A case of QT interval prolongation with ventricular tachycardia and torsade de pointes is reported. Arrhythmias occurred in a baby with persistent 2:1 atrioventricular block and long QT interval 2 days after birth and were self-limiting. No structural cardiac defect was present. Serum levels of sodium, potassium, magnesium and calcium were in the normal range. Finally, the pathogenetic mechanism of cardiac block is discussed.

In 1980 Sedaghatian described an Iranian infant who died shortly after birth. At autopsy, he was found to have subacute myocarditis, cortical necrosis of kidneys, and adrenal and pulmonary hemorrhage. His skeletal abnormalities included mild rhizomelic shortness of his limbs and platyspondylyl and "laciness" of the iliac wings. In 1987 Optiz et al. described another Iranian infant with a similar perinatal course and roentgenograms. This infant was born to first cousins, suggesting an autosomal recessive single gene defect. We report our findings of another infant with a lethal course.

Antiarrhythmic agents alter cardiac conduction, refractoriness, and action potential duration in a rate dependent fashion. A simple in vivo model was developed to measure these variables over a wide range of cycle lengths. Complete heart block was produced in dogs using an 8 French hexapolar ablation catheter, anterior skin electrode, and radiofrequency current (30 W, 13.6 +/- 2.6 seconds). Ventricular pacing and monophasic action potential recordings were performed using a single combination catheter. QRS and action potential durations were measured at multiple cycle lengths and after an abrupt change in paced cycle length. Ventricular effective refractory periods were also measured at multiple cycle lengths. Data obtained during flecainide and d-Sotalol infusions are presented. This simple model allows detailed in vivo evaluation of the electrophysiological effects of antiarrhythmic agents and combinations.

A patient is reported in whom exercise induced reversible ischemic left anterior fascicular block and far advanced right bundle branch block. Master's two step exercise test for pre-operative check-up revealed significant ST elevation in leads V1-5, negative U waves in leads V3-5 and fascicular blocks with retrosternal anginal chest pain. Long acting nitrate and nicorandil relieved the fascicular blocks.

Balloon pulmonary valvuloplasty is a safe and effective treatment for congenital pulmonic valve stenosis. This report describes a child who developed complete atrioventricular (AV) block following balloon pulmonary valvuloplasty. The child was treated with a 10-day course of systemic corticosteroids. The heart block gradually resolved during the first week following the procedure and has not recurred. Heart block is a known complication of right heart catheterization and has been described following balloon pulmonary valvuloplasty. Systemic corticosteroids have been used to treat AV block of various etiologies and may have contributed to the child's recovery in this case.

The underlying mechanism of atrioventricular block (AVB) in acute inferior myocardial infarction (AIMI) is not clearly understood. In 33 (27 males and 6 females) of 123 patients with AIMI, second and/or high degree AVB was observed. In 14 of the 33 patients (42%), AVB transiently appeared within 24 hours after the onset of AIMI. In 13 patients (39%) AVB appeared after 24 hours. In the remaining 6 patients (18%), AVB appeared within 24 hours and disappeared thereafter. Among these 3 groups, there were no significant differences in age, sex, serum enzymes, the appearance of high degree AVB, pump failure or Forrester's classification II, III and IV and the necessity of temporary pacing. One mg of atropine sulfate was administrated intravenously 35 times in 19 patients. When AVB improved or the ventricular rate increased more than 30%, the drug was regarded as effective. Atropine was more effective when administrated after 24 hours (11%, less than or equal to 24 hours vs 60%, greater than 24 hours, p less than 0.05), and in patients with a slight degree of AVB (28% in high degree vs 80% in second degree, p less than 0.05) and rapid ventricular rate during high degree AVB (0%, less than 40/min vs 45%, greater than or equal to 40/min, p less than 0.05). In the 6 patients not responding to atropine, 250 mg of aminophylline was given intravenously for 15 min. The effect was not seen in 4 patients, including 3 patients to whom it was administrated within 3 days after the onset of AIMI, and one patient to whom it was given on the 5th day. Aminophylline improved atrioventricular conduction on the 5th to 10th day after the onset of AIMI in 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

This experiment was carried out to evaluate the effect of ginsenosides from stems and leaves (GSL) on the sinus node dysfunction (SND) by observing the changes of the electrophysiological parameters of sinus node in limited period. Anesthetized rabbits were randomly divided into 3 groups. In the acute experiment, GSL, 50 mg/kg, iv, was given to the GSL group (G), n = 12. Normal saline (NS), the same volume, to the control group (C), n = 12. After GSL was administered 30-50 mg/kg.d for 14 days, iv, another data were obtained from chronic experimental group (CE), n = 15. The results show that the parameters, spontaneous cycle length (SCL), maximal sinus node recovery time (SNRTmax), corrected sinus node recovery time (CSNRT) were shorter in G group and CE group than C group respectively (P less than 0.05, P less than 0.01). It was suggested that GSL exerted protective effects on the experimental sinus node dysfunction.

Despite the high incidence of leukaemic infiltration of the heart, only 8 cases of atrioventricular block due to leukaemia have been reported in the literature. Improvement in the heart block associated with disappearance of the leukaemic infiltrate has not been reported. A rest thallium-201 study was used in a 65-year-old man to demonstrate leukaemic infiltration of the heart which was associated with complete heart block. After chemotherapy, when the tumour burden was reduced and the leukaemia in remission, his heart block resolved, and a follow-up thallium scan was normal.

A 32-year-old woman with systemic lupus erythematosus was found to have a fetus with heart block and fetal ascites at 23 weeks gestation. Treatment with high-dose corticosteroids ameliorated the early signs of heart failure, although the fetal heart rate gradually fell from 48 beats/min to 42 beats/min by 34 weeks. Sudden deterioration of the fetal state occurred at 35 weeks, and this only partially responded to digitalisation. Neonatal death occurred on Day 18 from the consequences of severe birth asphyxia. The relationship and pathogenesis of anti-Ro antibodies, congenital heart block and hydrops fetals are discussed, together with the in utero management of this condition.

In order to create and evaluate a model sensitive to QT-dependent proarrhythmic effects of drugs, a long QT syndrome was produced in chronically instrumented dogs with bradycardia and hypokalemia. Bradycardia (mean cycle length: 1495 +/- 78 msec) was provided by permanent atrioventricular block and hypokalemia (K+ = 2.6 +/- 0.05 mmol/l) by high doses of diuretics. To evaluate that model, six of these conscious dogs were subjected to quinidine, flecainide, lidocaine, propranolol and sotalol infusions. In crossover design, drugs were infused i.v. at rates allowing stable and nontoxic drug plasma levels during the experiment. Four-lead ECGs were recorded for arrhythmias for 30 min before (base line) and 75 min after onset of infusion. Ventricular cycle length was increased dramatically by sotalol, lidocaine and propranolol (+618 +/- 192, +388 +/- 125 and +329 +/- 114 msec, respectively) and QT interval was increased by sotalol, quinidine and flecainide (+56 +/- 8, +31 +/- 7.9 and +20 +/- 5.7 msec, respectively). Quinidine and sotalol, but not flecainide, propranolol or lidocaine, exhibited significant arrhythmogenic activities. During quinidine infusion, most dogs exhibited some ventricular arrhythmias whose most severe forms were runs of ventricular tachycardia. These arrhythmias were suppressed by pacing at high rates. During sotalol infusion, five out of six dogs exhibited typical "torsades de pointes." This incidence was not related to the slowing effects of sotalol on idioventricular pacemakers, because a similar incidence was obtained in five complementary dogs paced at 40 bpm. It could be related to dose, because torsades de pointes occurred only once in another group of five dogs receiving half the dose used in the controlled study. Only quinidine and sotalol, but not propranolol, flecainide or lidocaine, are clinically associated to torsades de pointes. They were also the only drugs associated with proarrhythmic events in the present study, a fact suggesting that QT-dependent arrhythmogenic effects of drugs can be reliably evaluated in conscious hypokalemic dogs with complete atrioventricular block.

One of the rare causes of syncope is "swallowing syncope," or "deglutition syncope." We have reported a case of atrioventricular block induced by swallowing.

Theophylline increases sinus rate, but as yet its use has not been investigated in patients with chronic atrioventricular conduction disturbances. Resting electrocardiogram, 24-h Holter recording and treadmill test were performed in 17 patients with chronic atrial fibrillation and a slow ventricular response not related to drugs (age: 75 +/- 8 years). Then slow-release theophylline was administered (700 mg daily) and after 5 days these investigations were repeated with the same methods. Theophylline increased mean resting heart rate (51 +/- 6 versus 67 +/- 13 beats.min-1, P less than 0.01), mean 24-h heart rate (51 +/- 6 versus 68 +/- 14 beats.min-1, P less than 0.01) and minimal 24-h heart rate (32 +/- 6 versus 42 +/- 11 beats.min-1, P less than 0.01). Cardiac pauses greater than 2.5 s were present in 13 patients during control recording; after theophylline they disappeared in 11 and markedly decreased in the remaining two. The longest R-R interval decreased in all patients (3218 +/- 943 versus 2121 +/- 518 ms, P less than 0.01). The daily number of wide QRS complexes increased in 16 out of 17 patients (428 +/- 752 versus 1146 +/- 1464 ms, P less than 0.01). Exercise heart rate, evaluated at the end of first and second stage, was higher after theophylline than during control test (P less than 0.01). These data suggest that oral theophylline can represent a valid therapy in most patients with atrial fibrillation and a slow ventricular response.

Experimental data have suggested a relation between Torsades de Pointes and early post-depolarization (EPD). We have studied the effect of intravenous verapamil in three patients with atrioventricular block (AVB) and Torsades de Pointes (TP), to obtain indirect evidence of slow membrane channel involvement in the TP mechanism. In two cases TP were completely suppressed and in one there was marked, albeit partial, suppression. In two cases verapamil did not shorten QT, while in the third suppression verapamil was related to junctional escape acceleration and QT shortening. In one of the cases where QT was not changed, the abolition of long pauses may have played a role in TP suppression. The affect of verapamil on TP in our patients is consistent with a combination of mechanisms, including direct membrane effects (EPD inhibition) and junctional pacemaker acceleration. Verapamil might be of therapeutic value in this clinical setting.

The clinical course and outcome of 55 fetuses with complete atrioventricular (AV) block detected prenatally were studied to identify factors that affect the natural history of this lesion. In 29 fetuses (53%) complete AV block was associated with complex structural heart defects, usually left atrial isomerism (n = 17) or discordant AV connection (n = 7). The other 26 fetuses had normal cardiac anatomy; in 19 cases the mother had connective tissue disease or tested positive for antinuclear antibodies. Six fetuses showed progression from sinus rhythm or second degree block to complete AV block. Of the 55 pregnancies, 5 were terminated and 24 fetuses or neonates died; at the end of the neonatal period 26 fetuses were still alive. Fetal or neonatal death correlated significantly with the presence of structural heart defects (4 of 29 surviving, p less than 0.001), hydrops (0 of 22 surviving, p less than 0.001), an atrial rate less than or equal to 120 beats/min (1 of 12 surviving, p less than 0.005) or a ventricular rate less than or equal to 55 beats/min (3 of 21 surviving, p less than 0.001). Mean atrial and ventricular rates were higher in surviving than in nonsurviving fetuses (142 +/- 8 vs. 127 +/- 21 beats/min, p less than 0.002; 64 +/- 8 vs. 52 +/- 8 beats/min, p less than 0.001, respectively). A slow atrial rate, however, was frequently associated with left atrial isomerism.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular (AV) block may be induced by ischaemia as a result of production of adenosine, a metabolite that accumulates during hypoxia and ischaemia. Adenosine antagonism has been shown to reverse experimental AV node block in dogs. Recently, theophylline has been shown to be highly effective in diminishing the frequency and severity of bradycardia in newborn infants with apnoea-bradycardia spells. We report here a case of acute inferior wall myocardial infarction who developed atropine resistant AV block which was reversed by aminophylline, a competitive, antagonist of adenosine.

Relapsing polychondritis is a rare systemic disease, characterized by recurrent inflammation of articular cartilaginous tissues, with frequent involvement of other organs and systems. While the cause remains unknown, an autoimmune pathogenesis appears likely; the natural history is not completely defined. The authors describe an interesting case with cardiovascular involvement and a good response to cyclosporin A.

The effects of dibutyryl cyclic AMP (DBcAMP) on ventricular vulnerability during complete atrioventricular block (CAVB) were studied one week after transarterial electrical ablation of the AV junction in 18 closed-chest dogs. All dogs exhibited CAVB and a stable ventricular escape rhythm with a mean cycle length of 1812 +/- 638 ms. After the administration of DBcAMP at a rate of 0.1 mg/kg/min for 30 min, the ventricular cycle length was significantly shortened, and the QTc interval was slightly prolonged, although the QT interval did not change. The ventricular fibrillation threshold after the administration of DBcAMP was significantly increased (from 12.2 +/- 3 84 to 18.4 +/- 5.08 mA, p less than 0.01). Thus, it was demonstrated that DBcAMP exhibited suppressive effects on the ventricular vulnerability in the experimentally induced CAVB.

The clinical aspects of the influence of cardiac glycosides on the sinus node and atrioventricular junction in health and dysfunction are reviewed. It has been shown that digitalis drugs do not produce any effect on sinus node automatism including that in dysfunction. Cardiac glycosides suppress enhanced atrioventricular conduction and do not affect it provided it remains within normal. The mechanisms by which cardiac glycosides may act are discussed: extracardiac, cholinomimetic (in the acute test and direct one) and influencing heart conduction components (when used continuously).

Drugs influencing hepatic microsomal enzyme systems, such as mexiletine, may affect the elimination pattern of theophylline. The three patients reported here had a history of asthma and premature ventricular contractions, and were receiving theophylline therapy. A few days after starting the coadministration of mexiletine and theophylline, theophylline serum concentrations increased about twofold over concentrations during theophylline therapy. In one case, theophylline serum concentrations increased by 2.6 fold, and the patient developed nausea and anorexia. Mexiletine serum concentrations did not change. It seems that with mexiletine therapy, lower doses of theophylline may be required and careful monitoring of serum concentrations is necessary.

Cardiac manifestations are reported in 0.3%-4.0% of European patients with Borrelia burgdorferi (B.b.) infection. Usually symptoms disappear within 6 weeks. We report a case with persistent impairment of atrioventricular (AV) conduction. Diagnosis was confirmed by demonstration of IgM antibodies and increase of IgG antibody titers against B.b. in serum, by isolation of the spirochete from skin biopsy material and by the typical clinical combination of erythema migrans, Bannwarth syndrome (meningoradiculitis), and complete heart block. Despite immediate antibiotic therapy with ceftriaxone, first degree AV block and second degree block Wenckebach with atrial pacing at 100 beats/minute persisted for 2 years. We conclude, that Lyme carditis can cause long-standing or irreversible AV conduction defects despite adequate and early antimicrobial therapy.

Colour-coded M-mode Doppler echocardiography is a simultaneous registration of the conventional M-mode echocardiogram and of the pulsed wave colour-coded Doppler echocardiogram with simultaneous analysis of several sample volumes along the ultrasound cursor with a high timely resolution, guided by the two-dimensional imaging. Within 9 months, 36 foetuses with arrhythmias were prospectively examined (24 foetuses with atrial premature beats, 9 foetuses with supraventricular tachycardia, and 3 foetuses with complete heart block). The classification of arrhythmia by the colour-coded M-mode Doppler echocardiography was always possible at first examination. The most important advantage of this method is the simultaneous registration of the information of conventional M-mode and Doppler echocardiography. Therefore, the intervals between atrial and ventricular contractions can also be analysed even when the angle of insonation to the foetal heart is unfavourable, since contractions cannot only be identified by wall movements but also by the flow velocities. Furthermore, the duration of regurgitation of atrioventricular valves can be exactly measured by colour-coded M-mode Doppler echocardiography. In foetal supraventricular tachycardia, it appears that severity of congestive heart failure is correlated with the duration of atrioventricular valve regurgitation up to a holosystolic insufficiency. Thus, it seems possible, that the duration of insufficiency of atrioventricular valves is a good parameter for evaluation of cardiac function and for modifying antiarrhythmic treatment in cases of supraventricular tachycardia.

In 50 patients with chronic congestive heart failure (CCHF, III or IV class), aged 62.8 +/- 9.1 years, who were treated with digoxin (Dx) and furosemide (F) (investigation A), continuous 24-hour ecg registration was performed according to Holter. Next, this treatment was extended by two-week administration of nifedipine (N) or isosorbide dinitrate (S) (investigation B), followed by one-month addition of captopril (Cp) (investigation C). During the last two weeks Dx, F, N or Dx, F, S were administered with Cp being withdrawn (investigation D). At the end of each stage of the treatment ecg registration was repeated according to Holter. At the same time, during the investigation A there were performed determinations of blood serum sodium, potassium and digoxin concentrations, two-dimensional echocardiography and evaluation of submaximal exercise tolerance. In 96 per cent of patients with CCHF, treated with Dx and F, cardiac rhythm disturbances were found. In 53.3 per cent life-threatening ventricular arrhythmias occurred, including unstable ventricular tachycardia in 11.1 per cent of patients. Addition of N or S to the classical treatment did not decrease either patient number or amounts of cardiac rhythm disturbances in individual classes according to Lown. Also Cp did not affect numbers of patients with cardiac rhythm disturbances, but it decreased numbers of patients with life-threatening ventricular arrhythmias from 53.3 per cent to 28.9 per cent (from 24/45 to 13/45). At the same time, Cp significantly decreased numbers of ventricular arrhythmias in class 3 and 4a (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial arrhythmia is not uncommon in congenital atrial septal defect. Its incidence increases with age and the hemodynamic compromise of right ventricle. In the literature, atrial fibrillation is the most common presentation in middle-aged adults with congenital atrial septal defect, followed by atrial flutter and paroxysmal supraventricular tachycardia. However, atrial tachycardia with block has rarely been reported. We here report a case of 61-year-old male with congenital secundum atrial septal defect who presented atrial tachycardia with block without taking digitalis. Normal sinus rhythm restored after six-day use of Verapamil and Quinidine.

The effect of the 1,4-dihydropyridine calcium antagonist nisoldipine (Bay k 5552) on the atrio-ventricular (AV) conduction was studied in 9 patients with AV blocks. The impuls propagation through the AV node (A-H time) and the bundle of His (H-V time) was determined before, 1-3 min and 10-15 min after the intravenous injection of nisoldipine (1.5 micrograms/kg body weight). Except for one patient, A-H and H-V times almost remained unaffected by the calcium antagonist. In this patient with an AV block II, Mobitz type I, A-H time transiently increased from 290 to 410 ms. Nisoldipine did not aggravate an AV block I or II to an AV block II or III, respectively. Furthermore, ventricular heart rates did not change significantly. It is concluded that, in general, nisoldipine does not impair the impulse propagation of the AV node in patients with AV blocks although a transient increase of the A-H time may occur.

A 56-year-old woman, who had received an aortic valve replacement suffered from complete left bundle branch block and advanced atrioventricular block. On the basis of marked systemic inflammatory findings on admission and histopathological findings on previous cardiac surgery, this patient was considered to have conduction disturbances that were a consequence of myocardial involvement of Takayasu's aortitis. The conduction disturbances improved rapidly after treatment with steroids.

A case report of patient with cardiac sarcoidosis is presented. Advanced atrioventricular (AV) block and abnormalities of radionuclide imaging were improved by steroid therapy. We stress the effectiveness of steroid therapy together with usefulness of radionuclide techniques.

In this study involving 45 patients with the normal function of the sinus node and 10 patients showing signs of its damage (n-10), intravenous administration of ethmozine in a dose of 150 mg (1.5-2 mg/kg) exerted atropine like action. In four cases with dysfunction of the sinus node the drug significantly increased the time of the restoration of sinus node function. Ethmozine induced a Stage II sinoatrial block in 3 out of 10 patients with sinus node dysfunction. The above data suggest that ethmozine produces an atropine-like effect on the sinus node. In some patients with sinus node dysfunction, ethmozine may impair the function of the sinus node which calls for caution while employing the drug in such cases. The inhibitory effect of the agent on the sinoatrial conduction in the patients studied suggests that ethmozine may prove an effective antiarrhythmic drug for treating patients with paroxysmal sinoatrial tachycardia.

The effects of quinidine on sinus nodal and A-V nodal function were assessed in 20 patients (age: 60 +/- 7 years) with sinus bradycardia and a prolonged A-H interval. Electrophysiological studies were performed twice in each patient. In the first study, the measurements of sinus and A-V node function were evaluated both in the basal state and after autonomic blockade (propranolol 0.2 mg kg-1 and atropine 0.04 mg kg-1). Oral quinidine was administered for 3-4 days (1200 mg day-1) and the study was then repeated using the same methods. Comparison of data obtained in the two studies in the basal state allowed us to evaluate the overall effect of quinidine. Comparing the results obtained following autonomic blockade, the direct action of the drug could be assessed. In the basal state quinidine did not significantly change the function of either node. In contrast, after autonomic blockade, significant changes were noted after quinidine. In 3 patients with sinus rate less than 50 beats min-1 and an abnormal intrinsic heart rate, quinidine induced marked depression of sinus automaticity. These data suggest that: (1) in patients with sinus bradycardia and prolongation of the A-H interval, oral quinidine has a direct depressant effect on sinus and A-V nodal function, but this effect is counteracted by autonomically mediated actions; (2) in patients with moderate or severe bradycardia and an abnormal intrinsic heart rate, the drug can induce marked depression of sinus automaticity.

The atrioventricular block was produced in dogs 24 hours after the occlusion of the left descending coronary artery by formalin injection into the atrioventricular node or the bundle of His. The intensity and duration of the ectopic foci inhibition produced by ethmozine and by its diethylamine analogue (ethmozine DAA) were compared. It was shown that intravenous infusion of 3 mg/kg ethmozine reduced the frequency of the ectopic ventricular excitations by 28% (n = 6), 0.5 mg/kg ethmozine DAA - by 46% (n = 7), and 1 mg/kg ethmozine DAA - by 78% (n = 8). In 50% of the animals 1 mg/kg ethmozine DAA completely suppressed the ectopic activity. Duration of the drugs action was determined by the time necessary for the attainment of 50% of the maximal effect in the inhibition of ectopic exitation frequency (for 3 mg/kg ethmozine it was 32.7 +/- 2.5 min, for 0.5 mg/kg ethmozine DAA - 5.1 +/- 7.2 min, and for 1 mg/kg ethomozine DAA - 55.0 +/- 9.8 min). The results obtained suggest that the ethmozine DAA action is more intensive and of longer duration than ethmozine, and effective at the late stage of experimental myocardial infarction.

A 55-year old male patient, with dizzy spells during everyday activity and a complete right bundle branch block as the sole electrocardiographic abnormality, reproducibly demonstrated tachycardia-dependent Mobitz Type II- and 2:1 second degree atrioventricular block. An electrophysiologic study revealed a provocable block within the distal portion of the bundle of His without evidence of a split His potential. Because of the truly tachycardia-dependent AV-block, beta-blocker medication was initiated to prevent high sinus rates during everyday activity. This therapy abolished symptoms totally.