The electrical impulses of atrium arise from the sinus node, subsequently pass through the right and left atrium, and finally arrive at the atrioventricular node. The P wave is the summation of the electrical current generated by depolarization due to its passage through the atrial conduction pathway. It provides many clinical clues that may be useful for diagnosis of atrial, ventricular, or valvular heart diseases. This review article briefly describes the clinical implications, mechanism of genesis, and normal and pathologic features of the P wave.
Atrioventricular Node ; Diagnosis ; Heart Atria ; Heart Valve Diseases ; Sinoatrial Node

The aim of present study is to investigate the effects of cGMP on hyperpolarization activated inward current (If), pacemaker current of the heart, in rabbit sino-atrial node cells using the whole-cell patch clamp technique. When sodium nitroprusside (SNP, 80 muM), which is known to activate guanylyl cyclase, was added, If amplitude was increased and its activation was accelerated. However, when If was prestimulated by isopreterenol (ISO, 1 muM), SNP reversed the effect of ISO. In the absence of ISO, SNP shifted activation curve rightward. On the contrary in the presence of ISO, SNP shifted activation curve in opposite direction. 8Br-cGMP (100 muM), more potent PKG activator and worse PDE activator than cGMP, also increased basal If but did not reverse stimulatory effect of ISO. It was probable that PKG activation seemed to be involved in SNP-induced basal If increase. The fact that SNP inhibited ISO-stimulated If suggested cGMP antagonize cAMP action via the activation of PDE. This possibility was supported by experiment using 3-isobutyl-1-methylxanthine (IBMX), non-specific PDE inhibitor. SNP did not affect If when If was stimulated by 20 muM IBMX. Therefore, cGMP reversed the stimulatory effect of cAMP via cAMP breakdown by activating cGMP-stimulated PDE. These results suggest that PKG and PDE are involved in the modulation of If by cGMP: PKG may facilitate If and cGMP-stimulated PDE can counteract the stimulatory action of cAMP.
1-Methyl-3-isobutylxanthine ; Guanylate Cyclase ; Heart ; Nitroprusside ; Sinoatrial Node*

Human heart rhythm is mainly regulated and controlled by the sinoatrial node. Fibrosis plays an important regulating role in adjusting the structural and functional integrity of the sinoatrial node pacemaker complex. In physiological state, the fibrosis degree of sinoatrial node is negatively correlated with heart rate, positively correlated with age and heart size, and can maintain a relatively stable heart rate. Pathological fibrosis of sinoatrial node can induce various types of arrhythmias which can result in sudden death. Determination of the mechanisms related to sinoatrial node pathological fibrosis could provide a target for clinical treatment of sinoatrial node fibrosis and diagnosis basis for forensic pathologists. This paper reviews the main mechanism of sinoatrial node pathological fibrosis, including abnormal activation of cardiac fibroblast cells in sinoatrial node, hyperplasia of epicardial adipose tissue, calcium clock disorder, artery stenosis, etc., introduces the test methods, diagnostic criteria as well as its role in sudden cardiac death and discusses the potential application, to provide reference for relevant research and application.
Arrhythmias, Cardiac ; Fibrosis ; Heart Rate ; Humans ; Sinoatrial Node

A simplified method of the cardiac conduction system (CCS) is evaluated by the study of 73 forensic cases. The sinoatrial node were observed in all cases (100.0%), atrioventricular node in 70 cases (95.9%) and penetrating bundle (His bundle) in 70 cases (95.9%). We divided the cases into three groups as the group of cardiac death (25 cases), non-cardiac death (24cases) and sudden unexpected death but undeterminable cause of death (24 cases) diagnosed after routine autopsy including routine cardiac examination and toxicological analysis and compared the type and incidence of CCS lesions in each groups. Narrowing of the sinoatrial (SA) or atrioventricular (AV) artery by fibromuscular hyperplasia (FMH) and fatty infiltration in SA or AV node were identified in all groups, lymphocytic infiltration in SA or AN node in cardiac and non-cardiac death group, hemorrhage and fibrosis of SA or AV node were identified in cardiac death group. FMH of the artery of SA or AN node occured more commonly in undeterminable cause of death group (45.1%) than in cardiac (16.0%) and non-cardiac group (20.8%) and severe narrowing (> or =75%) of the artery of SA or AV node was only present in undeterminable cause of death group (29.2%). The results led to the conclusion that this simple technique is very useful in detection of major abnor-malities of CCS with minimal effort and examination of the CCS in death which the routine autopsy and drug screen fail to provide a cause of death can yield a cause of death in a significant percentage of cases.
Arteries ; Atrioventricular Node ; Autopsy ; Cause of Death ; Death ; Death, Sudden* ; Fibrosis ; Hemorrhage ; Hyperplasia ; Incidence ; Sinoatrial Node

Nine patients of mean age 47.8 years, with suspected sinus node dysfunction, underwent extensive electrophysiological studies. Sinus bradycardia(6the electrophysiological study, AH and HV intervals were prolonged in 2/9 and 1/9 patients, respectively. Maximal sinus node recovery times were prolonged in 7/9 patients, ranging from 1,330 msec to 12,330msec. Sinoatrial conduction times measured by atrial premature stimulation technique were prolonged in 5/7 patients, ranging from 137msec to 310 msec. And sinoatrial conduction time measured by continuous pacing technique also revealed prolonged value in 4/6 patients ranging from 140 msec to 195 msec. The effective refractory periods, of atrium were prolonged in 6/8 patients (320 msec to 470 msec). The effective and functional refractory periods of AV node were prolonged in 3/8 patients (440 csec to 490 msec) and 4/8 patients (530 msec to 560 msec), respectively. Retrograde VA conduction could be observed in 3/7 patients and ventricular effective refractory periods were normal in 7/7 patients. Atrial flutter was induced in 1/9 patients by electric stimulation during electrophysiological study. Above data suggest that the electrophysiological study is very useful in assessing the sinus node function and other electrophysiological properties in sick sinus syndrome patients and also suggest that the data could be utilized in choosing the proper mode of artificial pacemaker for each patient.
Atrial Flutter ; Atrioventricular Node ; Electric Stimulation ; Humans ; Pacemaker, Artificial ; Sick Sinus Syndrome* ; Sinoatrial Node

The incidence of intraoperative arrhythmia is extremely high, and some arrhythmias require clinical attention. Therefore, it is essential for the anesthesiologist to evaluate risk factors for arrhythmia and understand their etiology, electrophysiology, diagnosis, and treatment. Anesthetic agents reportedly affect normal cardiac electrical activity. In the normal cardiac cycle, the sinoatrial node initiates cardiac electrical activity through intrinsic autonomous pacemaker activity. Sequential atrial and ventricular contractions result in an effective cardiac pumping mechanism. Arrhythmia occurs due to various causes, and the cardiac pumping mechanism may be affected. A severe case may result in hemodynamic instability. In this situation, the anesthesiologist should eliminate the possible causes of arrhythmia and manage the condition, creating hemodynamic stability under proper electrocardiographic monitoring.
Anesthesia ; Anesthetics ; Arrhythmias, Cardiac* ; Diagnosis ; Electrocardiography ; Electrophysiology ; Hemodynamics ; Incidence ; Risk Factors ; Sinoatrial Node

BACKGROUND: It is very important to evalute the function of the atrioventricular conduction system in selecting appropriate pacemaker, pacing and sensing mode in sick sinus syndrome. It has been reported that atrioventricular conduction abnormalities were commonly accompanied with sinus node dysfunction (SND). However, there were several long term follow-up studies indicating that incidence of AV conduction abnormalities was as low as below 1% a year in patients with SND implanted pacemaker. This study was performed to evaluate the properties of the AV conduction system in patients with SND. SUBJECT AND METHODS: Patients subjected to this study were fifty-eight who underwent electrophysiologic study on suspicion of SND. Sinus node recovery time (SNRT) was defined as the longest time among the times that sinus rhythm reappeared after rapid atrial pacing for 45 seconds with several cycle lengths, and corrected SNRT (cSNRT) was worked out by subtracting sinus cycle length (SCL) from SNRT. Criteria for sinus node dysfunction were 1550 msec or more on SNRT, 550 msec or more on cSNRT and group A (23 cases, 58+/-13 yrs) was defined as SND not retrieved to normal after intravenous administration of atropine 1-2 mg, group B (21 cases, 52+/-14 yrs) was retrieved to normal and group C (14 cases, 54+/-13 yrs) was normal control group. Abnormalities of the AV conduction system were defined as 150 msec or more on AH interval, 500 msec or more on AVblock cycle length (AV-BCL), 450 msec or more on AV nodeeffective refractory period (AVN-ERP). RESULTS: SCL in group A, B, C was 1197+/-340 msec, 1215+/-273 msec, and 898+/-129 msec, respectively at baseline and 886+/-218 msec, 798+/-106 msec, and 722+/-110 msec respectively after atropine administration, showing a significant prolongation of SCL in group A and B at baseline (p<0.001) and group A after atropine administration (p<0.05). SNRT in group A, B, C was 3520+/-1817 msec, 3180+/-2390 msec, and 1282+/-116, respectively at baseline and 4155+/-4281 msec, 1237+/-210 msec, 1020+/-245 msec, respectively after atropine administration, showing a significant prolongation of SNRT in group A and B at baseline (p<0.001) and group A after atropine administration (p<0.05). AH intervals at baseline and after atropine administration were 107+/-27 msec and 100+/-20 msec in group A, 101+/-21 and 91+/-14 in group B, and 118+/-32 and 83+/-23 in group C, showing no significant difference between 3 groups. AV-BCLs at baseline and after atropine administration were 428+/-151 msec and 453+/-301 msec in group A, 525+/-140 and 370+/-53 in group B, and 461+/-120 361+/-94 in group C, showing no significant difference between 3 groups. AVN-ERP was 315+/-57 msec in group A, 343+/-132 msec in group B, 347+/-132 in group C, showing no significant difference between 3 groups. There was no significant difference in the incidences of cases with abnormal AH interval, AV-BCL, AVN-ERP, HV interval between 3 groups. AV block greater than second degree was observed in one patient of group A but none of group B and C. CONCLUSIONS: Atrioventricular conduction abnormalities in patients with sinus node dysfunction were not more common than control subjects. Therefore, atrial pacing rather than ventricular or dual chamber pacing may be safely selected as a permanent pacing mode for sick sinus syndrome with no combined significant AV block.
Administration, Intravenous ; Atrioventricular Block ; Atropine ; Humans ; Incidence ; Sick Sinus Syndrome* ; Sinoatrial Node*

Inappropriate sinus bradycardia associated with degenerative changes in the sinoatrial node has been designated as the sick sinus syndrome. Patients can be asymptomatic but often complain of palpitations and syncopal episodes. A 30 year old parturient, whose pulse rate was about 45-55 beats/min, underwent cesarean section under neuroleptanesthesia. Authors report this case with the review of the relevant literatures.
Adult ; Bradycardia ; Cesarean Section ; Female ; Heart Rate ; Humans ; Pregnancy ; Sick Sinus Syndrome* ; Sinoatrial Node ; Syncope

Paroxysmal atrial fibrillation may be induced by coronary spasm presenting with typical angina-like pain and palpitations. It is typically treated using rate or rhythm control strategies, although sustained coronary spasm can induce sinus bradycardia with dizziness and syncope. In the present case, we reached a diagnosis of paroxysmal atrial fibrillation and sinus bradycardia due to coronary artery spasm using the methyl-ergonovine provocation test during angiography. While the treatment of coronary spasm can resolve paroxysmal atrial fibrillation, sinus bradycardia, and variant angina, the mechanism remains unclear, although it may be associated with sinus node ischemia. Similar symptoms, particularly chest discomfort, should be carefully considered in cases of paroxysmal atrial fibrillation.
Angiography ; Atrial Fibrillation* ; Bradycardia* ; Coronary Vasospasm ; Coronary Vessels* ; Diagnosis ; Dizziness ; Ischemia ; Sinoatrial Node ; Spasm* ; Syncope ; Thorax

Clinical EPS was performed in 16 normal adults without evidence of conduction disease on the surface standard 12 lead electrocardiogram in order to provide normal electrophysiological values of the sinus node function and AV conduction. EPS was also performed in 15 patients with sick sinus syndrome and 10 patients with AV conduction disturbance to evaluate the clinical usefulness of EPS in detecting sinus node dysfunction and AV conduction disturbance. The results were as follows. 1) The results of sinus node function test in the normal group were m-SNRT 853+/-198msec(range 800-1,560msec), c-SNRT 230+/-66msec(range 120-370msec), and %m -SNRT/SCL 127+/-11%(range 114-149%). 2) In 15 patients with SSS, the M-SNRT were ranged from 1,270 to 12,330msec and 10 patients(66%) had significantly increased m-SNRT exceeding 1,560msec. The c-SNRT were ranged from 230 to 10,730msec and 13 patients(83%) had significantly increased c-SNRT exceeding 370msec. The % m-SNRT/SCL were ranged from 136 to 770% and 12 patients(80%) had significantly increased % m-SNRT/SCL exceeding 150%. 3) The SACT in normal group were 84+/-14msec(range 70-105msec) measured by continuous atrial pacing method and 80+/-19 msec(range 60-115msec) measured by atrial extrastimulation method. 4) In SSS, the SACT measured by continuous atrial pacing method was ranged from 80 to 1,050msec and 11/12 patients(92%) had significantly increased SACT exceeding 112 msec. The SACT measured by atrial extrastimulation method was ranged from 90 to 310msec and 7/8 patients(88%) had significantly increased SACT exceeding 118 msec. 5) C-SNRT, % m-SNRT/SCL, and SACT were more useful in detecting sinus node dysfunction than m-SNRT. 6) The AV conduction intervals in normal group were PA interval 17+/-6(range 5-25msec), AH interval 96+/-18 msec(range 70-135msec), and HV interval 46+/-7msec(range 35-55msec). 7) Rapid atrial pacing induced Wenckebach type second degree AV block proximal to H at pacing rate of 90 to 190/min in 14/16 normal adults. 2 patients maintained intact AV conduction upto maximum pacing rate of 200/min. 8) His bundle electrogram showed the site of AV block in 9 of 10 patients with AV conduction disturbances. The sites of AV block were AV nodal area 1 case, intraHis bundle 4 cases, and infraHis bundle 4 cases. 9) EPS provided a good supportive information that was useful in selecting pacemaker therapy in a patient with chronic bifascicular block who revealed prolonged HV interval and infraHis bundle block at a pacing rate of 70min. 10) The refractory periods of AV conduction system in normal group were AERP 274+/-54msec (range 170-410msec), AVN-FRp 467+/-74msec(range 285-600msec), AVN-ERP 341+76msec(range 190-460), and V-ERP 280+/-25msec(range 240-320msec).
Adult ; Atrioventricular Block ; Electrocardiography ; Electrophysiologic Techniques, Cardiac ; Humans ; Sick Sinus Syndrome ; Sinoatrial Node*