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

Atrial myxoma is the most common primary cardiac tumor, and surgical removal is the treatment of choice. Atrial flutter-fibrillation is common after the surgical excision of such tumors, whereas sinus node dysfunction is a rare complication. We detected postoperative sinus node dysfunction and atrial tachycardia after the excision of a left atrial myxoma in a 63-year-old woman. The patient underwent the implantation of a permanent pacemaker two weeks after the operation. The patient underwent successful catheter ablation of macroreentrant right atrial tachycardia 16 months after the operation with no recurrence of atrial tachycardia over the next four months.
Catheter Ablation ; Female ; Heart Neoplasms ; Humans ; Middle Aged ; Myxoma ; Recurrence ; Sick Sinus Syndrome ; Sinoatrial Node ; Tachycardia

Recent evidence indicates that the voltage (cyclic activation and deactivation of membrane ion channels) and Ca2+ clocks (rhythmic spontaneous sarcoplasmic reticulum Ca2+ release) jointly regulate sinoatrial node (SAN) automaticity. Since the intact SAN is a heterogeneous structure that includes multiple different cell types interacting with each other, the relative importance of the voltage and Ca2+ clocks for pacemaking may be variable in different regions of the SAN. Recently, we performed optical mapping in isolated and Langendorff-perfused canine right atria. We mapped the intracellular calcium (Cai) and membrane potentials of the intact SAN simultaneously. Using previously described criteria of the timing of the late diastolic Cai elevation (LDCAE) relative to the action potential upstroke to detect Ca2+ clock activity, we demonstrated that the sinus rate increased and the leading pacemaker shifted to the superior SAN with the robust LDCAE during beta-adrenergic stimulation. We also showed that the LDCAE was caused by spontaneous diastolic SR Ca2+ release and was closely related with heart rate changes. We conclude that the Ca2+ and voltage clocks work synergistically to generate SAN automaticity.
Action Potentials ; Calcium ; Heart Rate ; Membrane Potentials ; Membranes ; Sarcoplasmic Reticulum ; Sinoatrial Node ; Sympathetic Nervous System

BACKGROUND: Extended transseptal approach can provide an excellent view of the mitral valve but the safety of this approach is controversial because this incision requires transection of the sinus node artery, which in most cases and can result postoperative arrhythmia. The purpose of this study was to evaluate perioperative and longterm conduction disturbances and the cardiac rhythms of patients who underwent an extended transseptal approach for mitral valve surgery. MATERIAL AND METHOD: Postoperative cardiac rhythms were analyzed in the 164 consecutive patients who received mitral valve replacements with a extended transseptal approach between March 1992 and July 2003. RESULT: Of the 84 patients in normal sinus rhythm, 34 (39%) had developed transient junctional rhythm and atrial fibrillation after operation, lasting less than 72 hours in most of cases. No intractable arrhythmias occurred. Most of these arrhythmia were not detected at the time of discharge and only 8 patients (9%) had atrial fibrillation at discharge. Postoperative PR intervals increased for 1 week, then decreased within 2 weeks postoperatively, and returned to normal range by 6 months postoperatively. During the postoperative period, 4 of the 78 patients with preoperative atrial fibrillation developed normal sinus thythm. CONCLUSION: The postoperative arrhythmias were temporary and showed no significant complications after extended transseptal approach for the mitral valve surgery.
Arrhythmias, Cardiac ; Atrial Fibrillation ; Coronary Vessels ; Humans ; Mitral Valve* ; Postoperative Period ; Reference Values ; Sinoatrial Node*

BACKGROUND: The arterial baroreflex is a key mechanism for maintaining blood pressure homeostasis. Low-dose atropine (LDA) causes bradycardia, either by acting on the sinoatrial node or due to its effect on central muscarinic receptors, which increases vagal activity. We evaluated the effect of LDA on baroreflex sensitivity (BRS) in healthy awake subjects. METHODS: We assessed changes in RR interval (RRI) and systolic blood pressure (SBP), power spectral densities of heart rate variability (HRV) and systolic blood pressure variability (SBPV), and spontaneous BRS by using transfer function analysis before and after LDA (2microgram/kg) in 17 healthy volunteers. RESULTS: LDA induced not only bradycardia but also increased of the high-frequency (HF) component of HRV, RMSSD (root mean squared successive difference interval), and pNN50 (percentage of sinus cycles differing from the preceding cycle by > 50 ms). The HF and LF components of SBPV remained unchanged. Spontaneous BRS determined by transfer function analysis increased significantly (P < 0.05), and changes in BRS were significantly associated with changes in the HF component of HRV (P < 0.05). CONCLUSIONS: LDA increased vagal cardiac function and arterial baroreflex in awake subjects. This result suggests that increased vagal cardiac function by LDA application is related to baroreflex increase.
Atropine* ; Baroreflex* ; Blood Pressure ; Bradycardia ; Healthy Volunteers ; Heart Rate ; Homeostasis ; Receptors, Muscarinic ; 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*