Biomedical subjects

F Solti

Publications and source records attributed to F Solti.

At least 19 recordsLinked to original sources

PubMed2000

Investigating the dual nature of endothelin-1: ischemia or direct arrhythmogenic effect?

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide, which may also elicit severe ventricular arrhythmias. The aims of our study were to compare the effects of total left anterior descending coronary artery (LAD) occlusion to intracoronary (ic.) ET-1 administration and to investigate the pathomechanism of ET-1 induced arrhythmias in 3 groups of anesthetized, open-chest mongrel dogs. In group A (n=10) a total LAD occlusion was carried out for 30 min, followed by a 60 min reperfusion period. In groups B and C ET-1 was administered into LAD for 30 min at a rate of 30 pmol/min (n=6) and 60 pmol/min (n=8). Epi- and endocardial monophasic action potential (MAP) recordings were performed to detect electrophysiologic changes and ischemia Blood samples for lactate measurements were collected from the coronary sinus (CS) and from the femoral artery. Infrared imaging was applied to follow epimyocardial heat emission changes. At the end of the ET-1 infusion period coronary blood flow (CBF) was reduced significantly in groups B and C (deltaCBF30MIN B: 21+/-2%, p<0.05; C: 35+/-2%, p<0.05), paralleled by a significant epimyocardial temperature decrease in group C (deltaT30MIN: -0.65+/-0.29 degrees C, p<0.05). Two dogs died of ventricular fibrillation (VF) in the reperfusion period in group A. Ventricular premature contractions and non-sustained ventricular tachycardic episodes appeared in group B, whereas six dogs died of VF in group C. Significant CS lactate level elevation indicating ischemia was observed only in group A from the 30th min occlusion throughout the reperfusion period (control vs. 30 min: 1.3+/-0.29 vs. 2.2+/-0.37 mmol/l, p<0.05). Epi- and endocardial MAP durations (MAPD90) and left ventricular epicardial (LV(EPI)) upstroke velocity decreased significantly in group A in the occlusion period. ET-1 infusion significantly increased LV(EPI) MAPD90 in group B and both MAPD90-s in group C. In conclusion, ischemic MAP and CS lactate changes were observed only in group A. Although ET-1 reduced CBF significantly in groups B and C, neither MAP nor lactate indicated ischemic alterations. ET-1 induced major ventricular arrhythmias appeared before signs of myocardial ischemia developed, though reduced CBF presumably contributed to sustaining the arrhythmias.

Animals↗

PubMed2000

Fundamental electrophysiological differences between low-dose intracoronary endothelin-1 infusion and myocardial ischemia revealed by multiple monophasic action potential recording.

The supposed direct arrhythmogenic property of endothelin-1 (ET-1) has not yet been clearly proven. Our study aimed to characterize the electrophysiological changes during left anterior descending artery (LAD) occlusion and intracoronary (i.c.) ET-1 infusion, and to differentiate between the supposed direct and ischemic arrhythmogenic actions of ET-1 in a canine model. Changes of monophasic action potential duration (MAPD90) and upstroke velocity (UV) are capable of detecting local ischemic changes. Left and right ventricular endo- (LVEND, RVEND) and epicardial (LVEP, RVEP) monophasic action potentials were recorded. MAPD90, monophasic action potential dispersion (MAPDISP) and UV were determined. In group A (n = 8) 30 min LAD occlusion was followed by a 60 min reperfusion period. In groups B and C ET-1 was administered into the LAD at rates of 30 (n = 8) and 60 pmol/min (n = 10), respectively. In group A after the LAD occlusion both MAPD90 and UV decreased significantly in the LAD region (LVEP and LVEND 18 +/- 3% and 10 +/- 1%, p < 0.05, and 65 +/- 4% and 52 +/- 8%, respectively, p < 0.05; control and 30 min values in all groups), whereas the increase in MAPDISP remained unchanged. No severe arrhythmias were noticed in this group. In group B, both MAPD90 and MAPDISP increased significantly (LVEP and LVEND 11 +/- 4% and 18 +/- 3%, p < 0.05; MAPDISP 200 +/- 40%, p < 0.05), whereas UV remained unchanged at the end of the infusion. Early afterdepolarizations (EADs) were present in three instances. In group C both MAPD90 and MAPDISP increased significantly (LVEP and LVEND 12 +/- 5% and 26 +/- 8%, respectively, p < 0.05; MAPDISP 215 +/- 30%, p < 0.05) and UV decreased slightly in the LAD region. EADs were observed in five instances. Severe arrhythmias were observed in both groups B and C. We concluded that MAP prolongation, increased MAP dispersion and development of EADs all contribute to the arrhythmogenic action of ET-1. The lack of the almost prompt decrease of UV and MAPD90 which was observed in group A in groups B and C strongly supports the probability of a direct arrhythmogenic effect of ET-1.

Action Potentials↗

PubMed1998

Intrapericardial infusion of endothelin-1 induces ventricular arrhythmias in dogs.

OBJECTIVES: Recently, extremely high levels of endothelin-1 (ET-1) were detected in the pericardial fluid of patients with heart disease; however, the pathophysiological importance of this finding is not known. The present study was designed to characterize ET-1 levels in canine pericardial fluid and to investigate the effects of local high concentrations of exogenous ET-1 in vivo. METHODS: In anesthetized, open-chest dogs ET-1 (Groups 1 and 2: 11 and 33 pmol.kg-1.min-1; n = 6 and 6, respectively) or physiological saline (Group 3, n = 5) were infused into the closed pericardial sac for 40 min. In serial pericardial fluid and aortic blood plasma samples, ET-1 levels were measured by radioimmunoassay, and analysed by high-performance liquid chromatography (HPLC). Systemic arterial blood pressure, heart rate, cardiac output (CO), standard ECG and right ventricular endocardial monophasic action potentials (MAPs) were recorded. RESULTS: Basal pericardial fluid ET-1 levels were significantly higher than respective plasma levels (342 +/- 210 vs. 8.0 +/- 5.2 pmol.l-1, n = 14, P < 0.001. In HPLC analysis pericardial fluid ET-1 was indistinguishable from ET-1(1-21). Infusion of exogenous ET-1 into the pericardial space induced ventricular arrhythmias in all instances, which were associated with 9.7-fold increase in pericardial fluid ET-1 levels. Ventricular tachycardias developed in 9 of 12 animals. The arrhythmogenic effect of ET-1 was more apparent in dogs with the larger dose. Before the onset of arrhythmias, intrapericardial infusion of ET-1 increased QT time (Group 1: 207 +/- 18 to 230 +/- 23 ms, P < 0.01; Group 2: 220 +/- 12 to 277 +/- 17 ms, P < 0.01) and MAP duration at 90% repolarization (at 300 ms cycle length) (Group 1: 192 +/- 9 to 216 +/- 9 ms, P < 0.01; Group 2: 205 +/- 9 to 255 +/- 9 ms, P < 0.001). Hemodynamic variables did not change significantly prior to the onset of ventricular tachyarrhythmias. In Group 3, arrhythmias were not observed and all electrophysiological and hemodynamic parameters remained unchanged. CONCLUSIONS: Administration of exogenous ET-1 into the pericardial space induces ventricular arrhythmias associated with prolongation of QT time and MAP duration. Whether pericardial fluid ET-1 under pathophysiological conditions can ever reach sufficiently high levels to induce ventricular arrhythmias remains to be elucidated.

Action Potentials↗

PubMed1998

Verapamil reduces the arrhythmogenic effect of endothelin.

In a previous study we established that endothelin-1 (ET-1) can induce characteristic ventricular tachycardias (VT) with significant prolongation of QT and QTc time. In this investigation we studied the role of CA2+ channels in the pro-arrhythmic effects of ET-1. In 24 anesthetized, open-chest mongrel dogs, ET-1 was administered into the left anterior descending coronary artery at a comparatively low dose (60 pmol/min) for 30 min. Twelve dogs received the Ca(2+)-channel blocker verapamil (0.4 mg/kg) before ET-1 application. The following parameters were recorded continuously over the infusion period: systemic arterial blood pressure, coronary blood flow, surface ECG leads, epicardial atrial and ventricular electrograms, and right and left ventricular endocardial monophasic action potentials (MAP). Electrophysiologic studies were performed by programmed electrical stimulation of the heart. Blockade of myocardial Ca2+ channels attenuated the arrhythmogenic action of ET-1. After verapamil administration to ET-1-treated dogs, sustained VT did not appear and ventricular fibrillation (VF) developed only in two dogs. In the control group serious and sustained VT and VF developed in nine animals. It is noteworthy that verapamil did not prevent ET-1-induced prolongation of QT time. The results appear to prove that myocardial Ca2+ channels are involved in the proarrhythmic effect of ET-1.

Animals↗

PubMed1998

Potential pathophysiologic role of endothelin-1 in canine pericardial fluid.

Recently, extremely high levels of endothelin-1 (ET-1) were detected in the pericardial fluid of patients undergoing cardiac surgery. This study was designed to assess the pathophysiologic importance of this finding by infusing ET-1 into the closed pericardial sac of anesthetized dogs. Systemic arterial blood pressure, heart rate, and standard ECG were recorded. Intrapericardial infusion of ET-1 (11 and 33 pmol/kg/min; n = 4/4) for 40 min induced ventricular arrhythmias in all instances. The lower dose of ET-1 induced a substantial number of ventricular extrasystoles, couplets, and triplets. In one instance, ventricular extrasystoles accelerated into nonsustained ventricular tachycardia (VT). In animals receiving the higher dose, nonsustained VTs occurred regularly, whereas sustained VTs were detected in two of four animals. Before the onset of arrhythmias, QT time was significantly prolonged [ET-1 (11 pmol/kg/min) 180 +/- 12 to 198 +/- 10 ms, p < 0.05; ET-1 (33 pmol/kg/min) 192 +/- 15 to 233 +/- 13 ms, p < 0.01]. Hemodynamic variables did not change significantly before the onset of ventricular arrhythmias. Our results show that administration of exogenous ET-1 into the pericardial space induces ventricular arrhythmias associated with prolongation of QT time.

Anesthesia↗

PubMed1998

Bradycardia increases the arrhythmogenic effect of endothelin.

The effect of permanent bradycardia on the proarrhythmic action of endothelin-1 (ET) was investigated in 24 open-chest anesthetized mongrel dogs. In 12 dogs, permanent bradycardia was induced by radiofrequency ablation of the AV node and the hearts were paced at 70 beats/min. ET (60 pmol/min) was infused into the left anterior descending coronary artery. Blood pressure, coronary blood flow (CBF), and atrial and ventricular epicardial surface ECG were recorded continuously. Polymorphous ventricular tachycardia developed in every dog with permanent bradycardia, and ventricular fibrillation terminated the experiments in 11 cases. Bradycardia prolonged the basal QT but there was no difference in the frequency corrected QTc time between the two groups. ET prolonged the QT time in a similar fashion in both groups. In the control group, six dogs developed sustained ventricular tachycardias and ventricular fibrillation occurred in nine cases. EADP was found in six cases of eight registered. Signs of myocardial ischemia did not accompany the development of arrhythmias. We conclude that permanent bradycardia augments the direct proarrhythmic effect of ET in dogs.

Animals↗

PubMed1998

Mechanism of endothelin-induced malignant ventricular arrhythmias in dogs.

The development of ventricular tachyarrhythmias caused by low-dose intracoronary infusion of endothelin-1 (ET-1) has recently been observed in dogs. The aim of the present study was to investigate the pathomechanism of ET-1-induced ventricular arrhythmias in 32 anesthetized, open-chest mongrel dogs in group A (n = 14) without, in group B (n = 14), and in group C (n = 4 control) with atrioventricular node ablation. The coronary blood flow (CBF) was measured in the left anterior descending (LAD) coronary artery by an electromagnetic flowmeter. Standard ECG, atrial and ventricular electrograms, and in groups B and C endocardial and epicardial monophasic action potentials (MAPs) were recorded. ET-1 was administered into the LAD at a low dose (30-60 pmol/min). At the time of the appearance of premature beats, CBF was only slightly decreased. The effective ventricular refractory period did not change significantly. Onset of spontaneous polymorphic and monomorphic sustained ventricular tachycardia (sVT) was observed in five dogs without bradycardia and in nine dogs with bradycardia. VTs in dogs with complete AV block were longer and slower. In most of the cases, ventricular fibrillation occurred. ET-1 treatment resulted in a significant increase in MAP 90% duration (255 +/- 9 vs. 290 +/- 8 ms endocardial, 244 +/- 10 vs. 292 +/- 12 epicardial; p < 0.05) at 70 beats/min ventricular pacing. In eight cases (group B), third-phase early afterdepolarization could be recorded. According to our results, the mechanism of ET-1-induced arrhythmias appears to be based on prolongation of MAP duration and development of afterdepolarizations.

Action Potentials↗

PubMed1996

[Intermittent Romano-Ward syndrome].

Two cases are described to have intermittent long QT syndrome. This type of long QT syndrome is not easy to recognize and the result could be fatal in case taking I/A type antiarrhythmic drugs. The first patient who was investigated had got "chinidin syncope" two years earlier, the second one had symptoms of syncope and dizziness for 3 months. The long QT syndrome was diagnosed in both cases by Holter monitoring. For these reason this paper underline the value of Holter monitoring as a diagnostic tool to establish the diagnosis of long QT syndrome. The monophasic action potential showed early after depolarisations in both cases.

Action Potentials↗

PubMed1996

[Clinical importance of monophasic action potential registration in long QT syndrome].

For more than 30 years, the monophasic action potential has been used as an experimental tool for the study of myocardial repolarisation. With recent improvements in catheter design, the utility of the tool as a means to identify the bases for ventricular arrhythmias in humans has been greatly improved. Abnormalities of repolarisation leading to ventricular arrhythmia formation can be identified and specific pharmacological therapies may be evaluated. The pathomechanism of major arrhythmias (ventricular tachycardia, ventricular fibrillation) occurring in long QT syndrome (LQTS) is not yet fully elucidated. The authors have recorded the monophasic action potentials (MAP) of the right ventricle in three patients with LQTS and with previous episodes of major ventricular arrhythmias. The changes in MAP duration and after depolarisation in response to spontaneous arrhythmias, programmed electrostimulation, atrial pacing and isoproterenol treatment were studied. In all of the three patients the early afterdepolarisation was present, which in two cases exhibited pause-dependent features. Thus in these patients dual chamber pacemaker implantatious were performed. These were the first permanent recordings of MAP during electrophysiological examination in Hungary and also the first evidences that the early afterdepolarisation does play a pathogenic role in the development of idiopathic LQTS. Further evaluation of the technique by cardiac electro-physiologists may improve both the diagnosis and the treatment of ventricular arrhythmias dependent upon afterdepolarisation formation.

Action Potentials↗

PubMed1995

[Experience with a transvenous pacemaker-cardioconverter-defibrillator without subcutaneous patch].

Sudden cardiac death caused by malignant ventricular arrhythmias is one of the main causes of cardiovascular mortality. Implantation of cardioverter-defibrillators has resulted in the reduction of the incidence of sudden cardiac death caused by malignant ventricular arrhythmias from the yearly 10-30% to 1%. For the very first time in Hungary, the authors applied only transvenous lead configuration for automatic cardioverter defibrillators in three patients. The indications of the implantation were ventricular fibrillation in one case, ventricular tachycardias refractory to drug treatment in two cases. Ventricular arrhythmias were secondary to coronary heart disease in two patients, dilatative cardiomyopathy in one patient. Preoperative, intraoperative and postoperative electrophysiological studies were regularly taken. Using Biotronik Phylax 03 device with a right ventricular electrode and a superior vena cava electrode and without subcutaneous patch the intraoperative defibrillation thresholds were 6, 11 and 12 J respectively. The fractally iridium coating increases the surface of the electrodes that has a very good effect on defibrillation threshold. During a mean follow-up of six months the occurring spontaneous ventricular arrhythmias (1 ventricular fibrillation and 5 ventricular tachycardias) were terminated by Phylax 03 with cardioversion-defibrillation or overdrive stimulation. The authors' results of intraoperative testing and clinical experiences show that the Phylax 03 biphasic system due to low defibrillation thresholds without subcutaneous patch can safely be applied with only transvenous implant technique in patients with major ventricular arrhythmias to prevent sudden cardiac death and to terminate ventricular tachycardia.

Arrhythmias, Cardiac↗

PubMed1995

Ventricular tachycardias induced by intracoronary administration of endothelin-1 in dogs.

In 12 anesthetized, open-chest mongrel dogs, endothelin-1 (ET-1) was infused into the left anterior descending coronary artery through an indwelling catheter at a dose of 30 pmol.min-1 for 30 min (n = 8). In four dogs the ET-1 dose was increased to 60 pmol/min for 10 min. Programmed electrical stimulation was used for electrophysiologic studies. Coronary blood flow was reduced by 32% on average without any ischemic ECG signs. QT time (186 +/- 3 ms vs. 218 +/- 6, p < 0.05, and 225 +/- 9, p < 0.05, p < 0.05). Ventricular irritability increased in all cases; ventricular extrasystoles, and nonsustained and sustained tachycardias occurred and, in 11 cases, ventricular fibrillation terminated the experiments. In two dogs, early afterdepolarization was recorded. Therefore, ET-1 is capable of inducing fatal ventricular arrythmias at least partly independent of its vasoconstrictor effect. QT prolongation appears to have a pathophysiologic role in this arrythmogenic effect.

Action Potentials↗

PubMed1994

Characteristics of long QT with permanent bradycardia.

The study was aimed to investigate the electrophysiological properties of long QT syndrome associated with permanent bradycardia. The investigations were performed in 26 patients suffering from long QT duration (QTC-frequency adapted QT-:484 +/- 34 ms) with permanent, marked bradycardia (heart rate: 42 +/- 7 min-1). Adams Stokes syncopal attack appeared in 12 patients, while in 14 cases ventricular tachycardia attack with syncope could be observed (study group). As control served the data of 30 patients suffering from long lasting marked bradycardia (heart rate: 44 +/- 7 min-1) with normal QT (QTC:420 +/- 28 ms). Each patient was candidate for pacemaker implantation. The following questions were studied: 1. The effect of heart rate on QT duration. The experiments were performed by electrical ventricular stimulation. 2. The effect of sympathetic and parasympathetic-pharmacologic-blockade on QT time. The study was performed under electrical ventricular stimulation by administration of propranolol and atropine. 3. The dispersion of QT time was studied by using electrical heart stimulation and 12 lead ECG recording. Electrophysiological investigations were performed in 14 patients with long QT and permanent bradycardia. On augmentation of the cycle length (bradycardia) the increase in the QT duration was more-out of all proportion-expressed in long QT. On pharmacologic sympathetic blockade in long QT syndrome the QT duration significantly diminished. The QT dispersion was more expressed in patients with prolonged QT interval and on bradycardia the QT dispersion further increased significantly. The irritability of the ventricle was markedly augmented in patients with long QT and bradycardia. Appearance of polymorphous ventricular tachycardia could frequently be observed and could be regularly induced by early ventricular extrastimuli and bradycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Coronary arteriopathy after lymphatic blockade: an experimental study in dogs.

The effects of lymph stasis on the histological and biochemical properties of the coronary arterial wall and on the coronary circulation were studied in 72 dogs. Cardiac lymph stasis was produced in 52 dogs by cardiac lymphatic blockade whereas in 20 dogs only a sham operation was performed. Blockade of cardiac lymph drainage promoted characteristic injury to the coronary arteries including subendothelial edema with plasma inbibition, interstitial and intracellular edema in the tunica media with degeneration in the smooth muscle layer, swelling of the adventitial space with dilated lymph vessels and, later, fibrosis. The biochemical properties of the coronary arterial wall also were adversely affected by cardiac lymph stasis. Thus, the collagen and hexosamine content of the coronary arteries increased and the metabolism of the coronary wall shifted in an anaerobic direction. Whereas coronary blood flow was slightly decreased with lymph blockade, the coronary circulatory reserve capacity and the adaptability of the coronary vascular system was markedly reduced. The histological changes were most apparent in the smaller coronary arteries. The coronary microvasculature was also pathologically altered with the development of numerous coronary arteriovenous microshunts. These findings in conjunction with other experimental and clinical information suggest that impaired cardiac lymph drainage contributes to the pathogenesis and progression of coronary artery disease.

Animals↗

PubMed1993

[Iatrogenic sinus node disease and iatrogenic AV block].

The appearance of long lasting bradycardia due to damage of the sinus node (iatrogen sick sinus syndrome; or the atrioventricular conduction system, iatrogen AV block) is not a rare event after open heart surgery. In the course of 5093 heart operations the development of iatrogen sick sinus syndrome was observed in 234 patients (4.6%) and iatrogen AV block in 91 cases (1.8%). The incidence rate of iatrogen sick sinus syndrome or iatrogen AV block was quite divergent depending mostly on the type of operation. Comparing the data of our earlier (1977-1982) and later (1983-1991) cardiac surgical interventions, the prevalence of iatrogen sinus node disease and iatrogen AV block seems to decrease, mainly due to the progress in techniques of cardiac surgery. With the appearance of iatrogen sick sinus syndrome or AV block, urgent temporary pacing is indicated to prevent the deleterious hemodynamic effect of bradycardia. In the cases of persistent iatrogen sick sinus syndrome and iatrogen AV block, permanent pacemaker implantation is needed. It is remarkable that although the incidence rate of iatrogen sick sinus syndrome is greater than that of iatrogen AV block, in iatrogen sick sinus syndrome the regression is quite frequent, while in iatrogen AV block the 2nd or 3rd degree AV block is usually permanent. We performed pacemaker implantation in 56 cases of iatrogen sick sinus syndrome (24%) and in 57 patients of iatrogen AV block (63%). With pacemaker therapy the outcome of iatrogen sick sinus syndrome and iatrogen AV block is very favourable.

Bradycardia↗

PubMed1992

[Regulation of blood circulation in the extremities in intermittent claudication].

UNLABELLED: The study was aimed to investigate the characteristics of the limb circulation in patients suffering from intermittent claudication. The study group consisted of 71 patients with intermittent claudication. As control served the data of 60 patients with intact peripheral circulation and 24 patients suffering from rest pain, too. The limb blood flow was measured by the venous isotope dye-dilution method. RESULTS: 1. The limb blood flow will be diminished in intermittent claudication already in resting state. The decrease of the limb blood flow is more expressed in severe claudication (with short claudication distance). 2. The pathological condition of the limb circulation in intermittent claudication can be characterized by the elevation of the limb vascular resistance. 3. The O2 consumption of the limb tissues will decrease in intermittent claudication. The data of the study are indicating that the regulation of the limb circulation will pathologically be changed in claudication. The reserves of the peripheral circulation are diminished and the insufficiency of the limb circulation will be manifested on walking.

Adult↗

PubMed1992

Congenital complete heart block associated with QT prolongation.

The coexistence of congenital complete heart block and QT prolongation represents a special type of arrhythmia. The electrophysiological and clinical characteristics of this syndrome were studied in eight patients suffering from congenital AV block and QT prolongation. Data from 22 patients suffering from congenital complete heart block only, served as a control. In the study group, the appearance of a torsade de pointes type of ventricular tachycardia could regularly be observed and the tachycardial attack could usually be provoked by ventricular extrastimuli. The corrected QT time was markedly prolonged; on ventricular stimulation, at higher pacing rates the QT interval shortened, but remained significantly higher than in the control group. Syncopal attacks--with the character of polymorphic tachycardia--appeared in each patient of the study group while occurring in only three patients from the control group. Patients were given pacemaker implants (using a higher pacing rate) and long-term administration of beta-receptor blockers. The outcome was favourable; no ventricular tachycardia or syncopal attack was observed in the follow-up period.

Adolescent↗

PubMed1991

Lymphatic arteriopathy: damage to the wall of the canine femoral artery after lymphatic blockade.

The effect of lymph stasis on the histological, biochemical, and elastic properties of the femoral artery were studied after regional lymphatic blockade in 36 dogs. Dogs were sacrificed 4-21 days after operation. Histologic changes of the femoral arterial wall (interstitial edema, degeneration in the muscle layer or media, thickened adventitia with dilated lymph vessels, and fibrosis) developed after regional lymphatic blockade. Characteristic metabolic alterations of the arterial wall (anaerobic catabolism of carbohydrate, increased lactate and glycosamine content) accompanied the morphological changes. Distensibility of the femoral artery decreased and greater elastic stiffness developed after regional lymphatic blockade. These results in conjunction with other experimental and clinical data support the concept that insufficient lymphatic transport within the blood vessel wall may contribute to the genesis and progression of arteriopathies.

Animals↗

PubMed1990

Atrial standstill: an indication for rate responsive pacing.

Atrial standstill (atrial paralysis) is a rare reason for permanent bradycardia. A case of atrial standstill is presented. A 35-year-old man had suffered from bradycardia since his childhood. For 2 years he had complaints (diminishment of his working capacity, and dyspnea occurred with effort) as well. On admission, a slow (38/min) junctional escape rhythm could be detected. There were no signs of atrial mechanical activity (atrial contraction) according to chest x ray, echocardiography, and the atrial pressure curve. The electrophysiological study revealed that the atria could not be electrically stimulated, and no P wave (A wave) could be recorded on right atrial electrograms. The patient received a rate responsive pacemaker. After pacemaker implantation, he became symptom-free; his working capacity improved markedly and his heart size decreased. Owing to the permanent bradycardia and the lack of atrial stimulation, the atrial standstill represents an indication for ventricular rate responsive pacing. Atrial standstill, permanent bradycardia, and the inability to stimulate the atrium are indications for ventricular rate responsive pacing.

Adult↗