Sinus node dysfunction and impairment of global atrial conduction time after high rate atrial and ventricular pacing in dogs.

It has been shown in animals and humans that AF shortens the atrial refractory period and impairs its rate adaptation. The aim of the study was to evaluate the effects of high rate pacing on sinus node function and intraatrial conduction. Eight dogs were subjected to rapid atrial pacing (AP) at a rate of 400 beats/min for 16 days. After a complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Sinus node recovery time (SNRT) was measured after pacing at 150, 160, and 170 beats/min. P wave duration was measured on a surface ECG recorded at a paper speed of 200 mm/s. Measurements were performed at baseline, immediately after AP or VP, and four weeks after termination of AP or VP. SNRT immediately after AP and VP was significantly prolonged at all three pacing rates (P < 0.03). P wave duration increased significantly after either type of pacing (AP: 74.3 +/- 6.4 ms, VP: 70.0 +/- 3.8 ms) compared with baseline values (60.6 +/- 6.2 ms, P < 0.05). Rapid AP and VP induces sinus node dysfunction and prolongs intraatrial conduction time. The effects of sustained AP and VP on sinus node function and atrial myocardium returned toward control values 4 weeks after cessation of pacing. The authors hypothesize that reversible electrical remodeling occurs both in the sinus node and in the atrial myocardium.

Role of endogenous adenosine in vasovagal syncope.

Adenosine may be a potential mediator in the pathogenesis of vasovagal syncope. Intravenous adenosine increases sympathetic discharge and provokes vasovagal syncope in sensitive subjects. No data are available for endogenous adenosine. The authors compared the results of head-up tilt-table testing (HUT) (45 minutes at 60 degrees) of three arbitrary groups of subjects: sensitive (n = 25, age 34 y, vasovagal syncope, positive HUT), moderately sensitive (n = 28, age 34 y, vasovagal syncope, negative HUT), and nonsensitive (n = 19, age 30 y). A positive test result produced syncopal symptoms with hypotension and/or bradycardia. Single-lead electrocardiogram (ECG) was recorded, and arterial pressure was measured noninvasively. Fourier transform was used for power-spectral heart rate variability (HRV) analysis of 5-minute ECG data. In the nonsensitive and moderately sensitive groups, HUT was repeated with intravenous dipyridamole, an adenosine transport blocker. In the sensitive group, HUT was repeated with oral theophylline, an adenosine receptor blocker, or placebo. In the moderately sensitive group, a third HUT was performed with dipyridamole and oral theophylline. If adenosine plays a role in vasovagal syncope, then dipyridamole would induce more positive HUT responses, a positive HUT response would be prevented by theophylline, and hemodynamic and HRV data in positive HUT responses induced by dipyridamole should reproduce those observed during spontaneous positive HUT responses. Dipyridamole induced positive HUT responses in 57% of the moderately sensitive group and 21% of the nonsensitive group (p < 0.05). Theophylline treatment was not efficient in preventing HUT-induced syncope in sensitive subjects; however, it prevented dipyridamole-induced syncope in 75% of the moderately sensitive group. Dipyridamole immediately increased arterial pressure, heart rate, and total HRV in all (p <0.05). In sensitive subjects, these responses were different: small for arterial pressure and for total and low-frequency HRV, and large for heart rate. It is concluded that endogenous adenosine, like exogenous adenosine, may induce vasovagal syncope. However, the mechanism of adenosine-induced syncope is probably different from that of HUT-induced vasovagal syncope.

Left atrial systolic function in relation to electrical and mechanical remodeling in a canine model.

Rapid atrial activation causes electrical remodeling that promotes the occurrence and maintenance of atrial fibrillation. The aim of this research was to compare the relationship between mechanical remodeling and atrial electrophysiology. Eight dogs (beagles) were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After a complete recovery of electrical variables and left ventricular function evaluated by echocardiography, they underwent high-rate ventricular pacing (VP) at 240 beats/min of equal duration. In half of them, the study was started by VP and in the other half by AP. Left atrial systolic function was assessed by transesophageal echocardiography. Atrial effective refractory period (AERP) at a basic cycle length of 400 ms decreased significantly after either type of pacing (AP: 115 +/- 17 ms, VP: 136 +/- 22 ms) compared with baseline values (153 +/- 23 ms); the difference between tachycardias was significant too (p < 0.02). Significant increases (p < 0.05) in left atrial dimensions (LA-A) (AP: 2.41 +/- 0.23 cm ,VP: 2. 43 +/- 0. 34 cm vs. basal: 2. 16 +/- 0. 21 cm) indicated atrial dilatation after either type of pacing, the differences between two groups being insignificant. Atrial reversal pulmonary venous flow (AR velocity) decreased in AP (-0.13 +/- 0. 02 m/s) and VP (-0. 17 +/- 0. 04 m/s). The difference was highly significant as compared to basal values (-0.25 +/- 0.05 m/s) and also with respect to both tachycardias (p < 0.01). In both groups, atrial remodeling occurred in a relatively short period of time. The echocardiographic findings suggested that left atrial systolic function was significantly more disturbed in the AP group than in the VP group. Mechanical changes are an important substrate of electrical remodeling, yet the deterioration of electrical variables was more pronounced in AP than in VP.

Late cardiac damage of anthracycline therapy for acute lymphoblastic leukemia in childhood.

Long-term leukemia survivors (46) underwent cardiac evaluation, including physical examination, ECG, exercise testing, and echocardiography. They were 2-17 years old at diagnosis and 5-23 years old after treatment. Thirty-four survivors received anthracyclines (AC) (mean 203 mg/m2), 12 of them had also alkylating agents (AA) and 12 had no AC. Exercise tolerance was bellow predicted values in 21 (48%) survivors and 21 survivors had ECG abnormalities, which were more frequent in those treated with AC. Concomitant AC with AA was correlated with prolonged isovolumic relaxation time (IVRT) and influenced significantly the volume of left atrium (p = .02). Sixteen (52%) survivors had IVRT > or = 90 ms. There were no significant differences in other parameters of diastolic or systolic function. Despite the lack of clinical symptoms in the survivors treated with lower doses of AC, subtile abnormalities in myocardial function were found, mainly manifest as abnormal diastolic function. Prolonged IVRT may be a sensitive indicator for early detection of AC cardiotoxicity.

Unusual ECG variations in left-sided pneumothorax.

A patient with spontaneous left-sided pneumothorax and unusual, phasic voltage variations in the electrocardiogram (ECG), which fluctuated depending on respiration, was observed. After intercostal tube drainage, these variations disappeared. The respiratory changes in the thorax seem to be a cause of these ECG findings.

Tachycardia induced cardiomyopathy in dogs; relation between chronic supraventricular and chronic ventricular tachycardia.

Long-standing ventricular tachycardia (VT) and supraventricular tachycardia (SVT) can produce a reversible left ventricular dysfunction. The onset of cardiomyopathy and the severity of posttachycardic changes depend at least on three parameters of tachycardia, including its type (VT or SVT), rate and duration. Ten dogs (beagles) were paced at 180 beats/min for 3 weeks. Two pacing modalities, supraventricular and ventricular, were used in each dog. In half of them, the study was started by ventricular, and in the other half by supraventricular high-rate pacing. The alternate pacing modality was applied after complete recovery of left ventricular function. Ventricular function and morphology were evaluated by radionuclide ventriculography, echocardiography and Swan-Ganz catheterisation. Posttachycardic changes were studied in sinus rhythm after cessation of pacing. Left ventricular ejection fraction (LVEF) fell significantly after either type of tachycardia (SVT: 53 +/- 5%, VT: 48 +/- 7%, P < 0.05) compared with baseline values (69.5 +/- 2.3%). Significant increases (P < 0.05) in end-systolic (SVT: 2.1 +/- 0.3 cm, VT: 2.4 +/- 0.2 cm vs. 1.6 +/- 0.3 cm) and end-diastolic dimensions (SVT: 3.0 +/- 0.3 cm, VT: 3.3 +/- 0.4 cm vs. 2.7 +/- 0.3 cm) indicated ventricular dilation in paced animals. Left ventricular pulmonary capillary wedge pressure increased significantly after either type of tachycardia as compared with baseline values (SVT: 7.5 +/- 1.2 mmHg, VT: 8.4 +/- 1.1 mmHg vs. 1.9 +/- 1.5 mmHg, P < 0.05); the difference between tachycardias was not significant. The present study demonstrates that chronic SVT and VT result in left ventricular dysfunction in a relatively short time, even if the heart rate is not very high. Deterioration of left ventricular ejection fraction and dilation of the left ventricle are more marked in chronic VT than in chronic SVT.

Cardiac involvement in Emery-Dreifuss muscular dystrophy: role of a diagnostic pacemaker.

Emery-Dreifuss muscular dystrophy is an X-linked recessive myopathy. Its progression is slow, and it rarely leads to cessation of walking; therefore, it has often been called "benign." On the other hand, cardiac involvement is often severe and sudden death is not uncommon. We describe a family with four affected males, two of whom died suddenly. The case of an affected man with first-degree AV block, incomplete right bundle branch block, and left anterior fascicular block is described in detail. The prophylactic insertion of a diagnostic pacemaker enabled us to follow the progress of conduction disturbances without leaving the patient unprotected. While AV and intraventricular conduction defects were more prominent before pacemaker implantation, sinus node dysfunction became more important during the follow-up.

Spontaneous shifts in the sinus node pacemaker complex.

Shifts in sinus node pacemaker complex may occur spontaneously, but occurrence of clinically relevant shifts is very rare. In this report, three patients (2 are siblings) with a history of palpitations and nearly permanent shifts in sinus node pacemaker complex are presented. Often, but not always, the pacemaker shifts followed spontaneous sinoatrial exit blocks. The shifts were probably related to varying vagal tone, since they were eliminated by atropine and exercise. The experience with these patients suggests that sinus pacemaker shifts can be a cause of symptomatic nonrespiratory sinus arrhythmia. A 4-year follow-up period showed no changes in symptoms or in heart rhythm; therefore, a benign course of the disease can be expected.

Exertional syncope in a patient with aortic stenosis and right coronary artery disease.

A female with advanced aortic valvular stenosis and moderate right coronary artery disease experienced an exertional syncope during 24-h ambulatory electrocardiographic monitoring. A progressive bradycardia with 90-s sinus node arrest (cardio-inhibitory response) and premonitory angina pectoris with significant ST segment changes were demonstrated. Our report supports the concept of a neurocardiogenic (vasovagal) mechanism of exertional syncope in patients with aortic stenosis. The predominant left ventricular inferior-wall myocardial ischaemia in our patient might be an additional stimulus to left ventricular mechanoreceptors, resulting in a profound cardio-inhibitory response.

Unusual subclavian steal phenomenon.

A patient who had undergone myocardial revascularization with a saphenous vein graft to the left anterior descending artery and a left internal thoracic (mammary) artery graft to the 1st diagonal branch presented with an unusual form of subclavian steal syndrome. Occlusion of both the left subclavian and the left anterior descending arteries caused retrograde flow through the internal thoracic artery to the distal subclavian artery; the blood flow was supplied by the vein graft via the distal left anterior descending artery and diagonal branch.

Complete cure after a seemingly unsuccessful operation for Wolff-Parkinson-White syndrome.

A 48-year-old man with Wolff-Parkinson-White syndrome and poorly tolerated atrial fibrillation underwent surgical dissection of an accessory pathway. After operation electrocardiogram revealed a very unfavorable outcome: sinus rhythm with persistence of delta waves alternated with sequences of complete atrioventricular block. Therefore, an early reoperation was planned. Fortunately, in the next days conduction through the accessory pathway and signs of atrioventricular block disappeared. Complete cure was observed during long-term follow-up.

Romano-Ward syndrome: case report, family study and signal averaged electrocardiogram.

A family with the Romano-Ward syndrome is described. A 28-year-old woman had episodes of syncope due to self-terminating ventricular tachycardia torsades de pointes. During lidocaine treatment she developed a sustained ventricular tachycardia and cardiopulmonary resuscitation was necessary. Propranolol reduced ventricular ectopic activity, but the QTc interval remained prolonged. A "threshold" in QT duration for the generation of complex ventricular arrhythmias was observed in the patient. There were no late ventricular potentials noted in the signal averaged ECG in the patient and in members of her family.

Reversible congestive cardiomyopathy due to chronic ventricular tachycardia.

A patient with congestive cardiomyopathy, induced by ventricular tachycardia, is presented. The patient had chronic ventricular tachycardia, which persisted 4 months and was eventually successfully treated by an antitachycardia pacemaker. A severe left ventricular dysfunction persisted after treatment for some days and then gradually resolved. After 3 months the indices of left ventricular function returned to normal values. The tachycardia-induced ventricular dysfunction seems to be a reversible disorder.

Longitudinal dissociation in the His bundle.

A patient with hypertensive heart disease, in whom atrial premature beats with a decrease in the amplitude and widening of his bundle potential, prolongation of the H-V interval, and right bundle branch block pattern suggested intrahisian longitudinal dissociation, is described.

Paradoxical elevation of pulmonary vascular resistance after nifedipine in primary pulmonary hypertension. A case study.

The case of a 55-year-old woman with primary pulmonary hypertension is described who developed 2 hours after sublingual administration of a 10 mg capsule of nifedipine a severe rise in pulmonary arterial and right atrial pressures accompanied with dyspnoea and cyanosis. The event lasted for two hours and subsided without intervention. With repeated nifedipine intake in the form of orally administered slow-release tablets no complications occurred. The authors ascribe the marked rise in pulmonary vascular resistance to rapid reduction of plasma nifedipine concentration after sublingual administration, due to a faster drug resorption compared to oral intake. The necessity of cautious introduction of vasodilating drugs in pulmonary hypertension and of gradual dosage increase is stressed.

Pericardial mesothelioma.

The case of a 44-year old man, never exposed to asbestos, who died from a pericardial mesothelioma is described. The diagnosis was made by surgical examination. Two weak transient episodes of amelioration, the first accomplished with pronison administration and the other one by radiotherapy, were registered.

Detection of electrocardiographically imperceptible ventricular pre-excitation by phase imaging.

The sequence of ventricular contraction was studied by radionuclide phase imaging in 25 patients with Wolff-Parkinson-White syndrome. The studies were performed when no signs of precontraction were present in the electrocardiogram; in these cases pre-excitation was either intermittent or suppressable by injection of ajmaline. In 11 of the 16 patients with free wall accessory pathways, precontraction could be detected in spite of electrocardiographically absent pre-excitation. Discrete precontraction was seen also in 2 of the 9 patients with paraseptal accessory pathways. We conclude that antegrade conduction through the accessory pathway does not need to be completely blocked if signs of pre-excitation are absent on the electrocardiogram, and that phase imaging is, at least in some patients (especially those with free wall accessory pathways), a more sensitive technique for detection of pre-excitation (precontraction) than the electrocardiogram.