Sinoatrial Block
Adams-Stokes Syndrome
Sinoatrial Node
Heart Block
Tachycardia, Sinoatrial Nodal Reentry
Conduction disturbances and increased atrial vulnerability in Connexin40-deficient mice analyzed by transesophageal stimulation. (1/24)
BACKGROUND: Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. METHODS AND RESULTS: Fifty-two mice (18 Cx40(+/+), 15 Cx40(+/-), and 19 Cx40(-/-) mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40(-/-) mice compared with Cx40(+/-) and Cx40(+/+) mice (287.8+/-109.0 vs 211.1+/-61.8 vs 204.4+/-60.9 ms; P<0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40(-/-) mice than in Cx40(+/-) or Cx40(+/+) mice (93. 3+/-11.8 vs 83.9+/-9.7 vs 82.8+/-8.0 ms, P<0.05). Analysis of 27 Cx40(-/-) mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40(+/-) and 31 wild-type (Cx40(+/+)) mice. Furthermore, in Cx40(-/-) mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. CONCLUSIONS: This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis. (+info)Development of sinus node disease in patients with AV block: implications for single lead VDD pacing. (2/24)
OBJECTIVE: To investigate the incidence of sinus node disease after pacemaker implantation for exclusive atrioventricular (AV) block. DESIGN: 441 patients were followed after VDD (n = 219) or DDD pacemaker (n = 222) implantation for AV block over a mean period of 37 months. Sinus node disease and atrial arrhythmias had been excluded by Holter monitoring and treadmill exercise preoperatively in 286 patients (group A). In 155 patients with complete AV block, a sinus rate above 70 beats/min was required for inclusion in the study (group B). Holter monitoring and treadmill exercise were performed two weeks, three months, and every six months after implantation. Sinus bradycardia below 40 beats/min, sinoatrial block, sinus arrest, or subnormal increase of heart rate during treadmill exercise were defined as sinus node dysfunction. RESULTS: Cumulative incidence of sinus node disease was 0.65% per year without differences between groups. Clinical indicators of sinus node dysfunction were sinus bradycardia below 40 beats/min in six patients (1.4%), intermittent sinoatrial block in two (0.5%), and chronotropic incompetence in five patients (1.1%). Only one of these patients (0.2%) was symptomatic. Cumulative incidence of atrial fibrillation was 2.0% per year, independent of the method used for the assessment of sinus node function and of the implanted device. CONCLUSIONS: In patients undergoing pacemaker implantation for isolated AV block, sinus node syndrome rarely occurs during follow up. Thus single lead VDD pacing can safely be performed in these patients. (+info)Atrio-sinus interaction demonstrated by blockade of the rapid delayed rectifier current. (3/24)
BACKGROUND: Proper pacemaking of the heart requires a specific organization of the sinoatrial (SA) node. The SA node drives the surrounding atrium but needs to be protected from its hyperpolarizing influence, which tends to suppress pacemaker activity. It has been suggested that the hyperpolarizing atrial influence is minimal at the site of the central nodal area. METHODS AND RESULTS: Atrio-sinus interaction was assessed by specific depolarization of the SA node by blocking the HERG-encoded rapid delayed rectifier current (I(K,r)) with the drug E-4031. In the SA node, E-4031 (1 micromol/L) changed action potential configuration drastically but never resulted in pacemaker arrest. In the atrium, E-4031 did not affect the membrane resting potential, thereby leaving the normal hyperpolarizing load on the SA node intact. When the SA node was sectioned into strips and subsequently separated from the atrium, spontaneous electrical activity of the strip containing the primary pacemaker ceased on I(K,r) blockade. When not separated from the atrium, I(K,r) blockade never resulted in pacemaker arrest. A similar effective atrio-sinus interaction was demonstrated in computer simulations. CONCLUSIONS: Our results demonstrate that the atrium provides an effective hyperpolarizing load on the central SA nodal area and is at least one of the controlling mechanisms for normal pacemaking function. The present study can be of help in understanding why patients with long-QT2 syndrome secondary to a mutation in HERG do not show sinus arrest. (+info)Comparative study of sinoatrial conduction time and sinus node recovery time. (4/24)
Atrial stimulation were performed in 5 normal patients (group A) and 4 patients with electrocardiographic evidence of sinoatrial disease (group B). The technique of premature atrial stimulation was used to calculate sinoatrial conduction time. Rapid atrial pacing was applied to measure maximum sinus node recovery time. In 4 cases both stimulation methods were repeated after intravenous administration of atropine Group A had a sinoatrial conduction time of 56 ms +/- 11 (SD) and a maximum sinus node recovery time of 1122 ms +/- 158. In 3 out of 4 patients with sinus node dysfunction a prolongation of sinoatrial conduction time could be demonstrated (145, 105, and 150 ms). In addition, one showed probable sinus node exit block after premature atrial stimulation. Sinus node recovery time was excessively prolonged in 2 (3880 and 3215 ms) and normal in the other 2 patients with sinoatrial disease (1330 and 1275 ms). Atropine leads to a decrease of sinoatrial conduction time. Results indicate that sinus node recovery time may not be a reliable indicator of sinus node automaticity if sinoatrial conduction is disturbed. The premature atrial stimulation technique makes it possible to study the pattern of sinoatrial conduction and to evaluate its reaction to therapeutic drugs. (+info)Sinus node dysfunction in acute myocardial infarction. (5/24)
The frequency, clinical course, and prognosis of sinus node dysfunction in 431 patients with acute myocardial infarction admitted to the coronary care unit were studied. Sinus node dysfunction occurred in 20 patients. In 13, the principal manifestation consisted of severe sinus bradycardia. In the remaining 7, periods of bradycardia alternating with episodes of supraventricular tachycardia were noted. Though several of the patients with sinus bradycardia required intravenous atropine or temporary pacing, normal sinus rhythm returned in virtually all during follow-up. The clinical course of patients with both bradycardia and tachycardia was less benign, during the acute phase and during follow-up; 5 of the 6 survivors required continued antiarrhythmic therapy or permanent pacing. The differences in the clinical course between these two groups of patients may reflect distinct underlying pathological changes. The findings in this study suggest that in contrast to sinus bradycardia, the occurrence of bradycardia-tachycardia syndrome during the acute phase of myocardial infarction may have important prognostic implications. (+info)Sinoatrial block complicating legionnaire's disease. (6/24)
A 59 year old woman presented with acute onset of fever, chills, diaphoresis, vague chest discomfort, and was found to be hypotensive and tachypnoeic. An electrocardiogram demonstrated sinoatrial block with a junctional rhythm between 50 and 80 beats/min. All cultures were negative and imaging studies unrevealing. Her urine tested positive for Legionella pneumophila antigen serotype 1 and she improved with antibiotic therapy. (+info)Sinoatrial node dysfunction and early unexpected death of mice with a defect of klotho gene expression. (7/24)
BACKGROUND: Homozygous mutant mice with a defect of klotho gene expression (kl/kl) show multiple age-related disorders and premature death from unknown causes. METHODS AND RESULTS: The kl/kl mice subjected to 20-hour restraint stress showed a high rate (20/30) of sudden death, which was associated with sinoatrial node dysfunction (conduction block or arrest). Heart rate and plasma norepinephrine of kl/kl mice, unlike those of wild-type (WT) mice, failed to increase during the stress. Intrinsic heart rate after pharmacological blockade of autonomic nerves in kl/kl mice was significantly lower than that in WT mice (380+/-33 versus 470+/-44 bpm; n=7). The sinus node recovery time after an overdrive pacing (600 bpm, 30 seconds) in kl/kl mice was significantly longer than in WT mice (392+/-37 versus 233+/-24 ms; n=6). In isolated sinoatrial node preparations, the positive chronotropic effect of isoproterenol was significantly less, whereas the negative chronotropic effect of acetylcholine was significantly greater in kl/kl than in WT mice. There was no degenerative structural change in the sinoatrial node of kl/kl mice. The precise localization of klotho was analyzed in newly prepared klotho-null mice with a reporter gene system (kl(-geo)). Homozygous kl(-geo) mice showed characteristic age-associated phenotypes that were almost identical to those of kl/kl mice. In the kl(-geo) mice, klotho expression was recognized exclusively in the sinoatrial node region in the heart in addition to parathyroid, kidney, and choroid plexus. CONCLUSIONS: In the heart, klotho is expressed solely at the sinoatrial node. klotho gene expression is essential for the sinoatrial node to function as a dependable pacemaker under conditions of stress. (+info)Quinine-induced arrhythmia in a patient with severe malaria. (8/24)
It was reported that there was a case of severe malaria patient with jaundice who presented with arrhythmia (premature ventricular contraction) while getting quinine infusion was reported. A man, 25 years old, was admitted to hospital with high fever, chill, vomiting, jaundice. The patient was fully conscious, blood pressure 120/80 mmHg, pulse rate 100 x/minute, regular. On admission, laboratory examination showed Plasmodium falciparum (++++), total bilirubin 8.25 mg/dL, conjugated bilirubin 4.36 mg/dL, unconjugated bilirubin 3.89 mg/dL, potassium 3.52 meq/L Patient was diagnosed as severe malaria with jaundice and got quinine infusion in dextrose 5% 500 mg/8 hour. On the second day the patient had vomitus, diarrhea, tinnitus, loss of hearing. After 30 hours of quinine infusion the patient felt palpitation and electrocardiography (ECG) recording showed premature ventricular contraction (PVC) > 5 x/minute, trigemini, constant type--sinoatrial block, positive U wave. He was treated with lidocaine 50 mg intravenously followed by infusion 1500 mg in dextrose 5%/24 hour and potassium aspartate tablet. Quinine infusion was discontinued and changed with sulfate quinine tablets. Three hours later the patient felt better, the frequency of PVC reduced to 4 - 5 x/minute and on the third day ECG was normal, potassium level was 3.34 meq/L. He was discharged on 7th day in good condition. Quinine, like quinidine, is a chincona alkaloid that has anti-arrhythmic property, although it also pro-arrhythmic that can cause various arrhythmias, including severe arrhythmia such as multiple PVC. Administration of parenteral quinine must be done carefully and with good observation because of its pro-arrhythmic effect, especially in older patients who have heart diseases or patients with electrolyte disorder (hypokalemia) which frequently occurs due to vomiting and or diarrhea in malaria cases. (+info)Sinoatrial block is a type of heart conduction disorder that affects the sinoatrial node, which is the natural pacemaker of the heart. In a sinoatrial block, the electrical impulses that originate in the sinoatrial node are delayed or blocked, resulting in a slower than normal heart rate or pauses between heartbeats.
A sinoatrial block can be classified as first-, second-, or third-degree, depending on the severity of the block. In a first-degree sinoatrial block, the electrical impulses are slowed but still conducted through to the atria. In a second-degree sinoatrial block, some of the electrical impulses are blocked, resulting in dropped beats or an irregular heart rhythm. In a third-degree sinoatrial block, also known as sinus node arrest, there is a complete failure of the sinoatrial node to generate impulses, resulting in a prolonged pause followed by a ventricular escape rhythm.
Sinoatrial blocks can be caused by various factors, including aging, heart disease, medication side effects, and electrolyte imbalances. In some cases, a sinoatrial block may not cause any symptoms and may only be detected during a routine electrocardiogram (ECG). However, in more severe cases, a sinoatrial block can lead to symptoms such as palpitations, dizziness, syncope (fainting), or shortness of breath. Treatment for a sinoatrial block depends on the underlying cause and may include medication adjustments, pacemaker implantation, or other interventions.
Adams-Stokes syndrome is a medical condition characterized by a series of episodes of sudden loss of consciousness (syncope) due to a significant decrease or temporary cessation of heart function (cardiac standstill or severe bradycardia). These episodes are often associated with convulsive movements and may be triggered by certain positions or activities that increase the obstruction to blood flow from the heart.
The syndrome is named after English physicians Robert Adams and William Stokes, who independently described the condition in the 19th century. It is most commonly caused by heart block or sick sinus syndrome, which are electrical conduction disorders of the heart. Other causes may include structural heart diseases, such as hypertrophic cardiomyopathy or coronary artery disease.
Treatment for Adams-Stokes syndrome typically involves addressing the underlying cause. In some cases, a pacemaker may be required to regulate the heart's electrical activity and prevent further episodes of syncope.
The sinoatrial (SA) node, also known as the sinus node, is the primary pacemaker of the heart. It is a small bundle of specialized cardiac conduction tissue located in the upper part of the right atrium, near the entrance of the superior vena cava. The SA node generates electrical impulses that initiate each heartbeat, causing the atria to contract and pump blood into the ventricles. This process is called sinus rhythm.
The SA node's electrical activity is regulated by the autonomic nervous system, which can adjust the heart rate in response to changes in the body's needs, such as during exercise or rest. The SA node's rate of firing determines the heart rate, with a normal resting heart rate ranging from 60 to 100 beats per minute.
If the SA node fails to function properly or its electrical impulses are blocked, other secondary pacemakers in the heart may take over, resulting in abnormal heart rhythms called arrhythmias.
Heart block is a cardiac condition characterized by the interruption of electrical impulse transmission from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This disruption can lead to abnormal heart rhythms, including bradycardia (a slower-than-normal heart rate), and in severe cases, can cause the heart to stop beating altogether. Heart block is typically caused by damage to the heart's electrical conduction system due to various factors such as aging, heart disease, or certain medications.
There are three types of heart block: first-degree, second-degree, and third-degree (also known as complete heart block). Each type has distinct electrocardiogram (ECG) findings and symptoms. Treatment for heart block depends on the severity of the condition and may include monitoring, medication, or implantation of a pacemaker to regulate the heart's electrical activity.
Tachycardia is a heart rate that is faster than normal. In sinoatrial nodal reentry tachycardia (SANRT), the abnormally fast heart rhythm originates in the sinoatrial node, which is the natural pacemaker of the heart. This type of tachycardia occurs due to a reentry circuit within the sinoatrial node, where an electrical impulse travels in a circular pattern and repeatedly stimulates the node to fire off abnormal rapid heartbeats. SANRT is typically characterized by a heart rate of over 100 beats per minute, palpitations, lightheadedness, or occasionally chest discomfort. It is usually a benign condition but can cause symptoms that affect quality of life. In some cases, treatment may be required to prevent recurrences and manage symptoms.