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

BACKGROUND: The most widely utilized indexes of sinus node dysfunction are the sinus node recovery time (SNRT) and the corrected sinus node recovery time (CSNRT), which generally require catheterization. Adenosine has negative chronotropic effect on the sinoatrial node. Non-invasive and reliable sinus node function test with intravenous adenosine was investigated. METHODS AND RESULT: The clinical value of rapid intravenous injection of adenosine for assessing sinus node dysfunction was examined in 14 patients with sick sinus syndrome (SSS) and 31 controls. After prophylactic insertion of a temporary pacemaker in the right ventricle, overdrive suppression test was conducted using the standard technique and CSNRT was measured to evaluate the sinus node function. Then, the CSNRT after administration of an intravenous bolus of adenosine (6 mg and 12 mg) was measured. Post-adenosine corrected sinus node recovery time (ADO: SNRT) was calculated by subtracting the basal sinus cycle length from the longest sinus cycle length. When ADO: SNRT over 550 msec was assumed as an indicator of sinus node dysfunction, intravenous injection of 6 mg of adenosine had a sensitivity of 85% and specificity of 100%, and 12 mg of adenosine had a sensitivity of 100% and specificity of 90% for detection of sick sinus syndrome. There were significant differences in ADO: SNRT between patient and control group (6 mg 1501+/-1081 msec vs 64+/-109 msec; 12 mg 4005+/-2055 msec vs 216+/-315 msec, respectively). CONCLUSION: he ADO: SNRT was a highly sensitive and specific index for diagnosing sick sinus syndrome, and should be considered as an alternative to invasive testing in patients with suspected sick sinus syndrome.
Adenosine* ; Catheterization ; Catheters ; Diagnosis* ; Heart Ventricles ; Humans ; Injections, Intravenous ; Sensitivity and Specificity ; Sick Sinus Syndrome* ; Sinoatrial Node

Surface ECG findings in 29 patients with left isomerism were reviewed. Among the total 46 wave axis distributions, 25(54%) were abnormal axis, not originated from sinus node. Congenital atrioventricular block was found in 2 children. 6 patients showed the bradycardia and junctional escape rhythm intermittently or persistently. 4 of them, not related with heart surgery, were much older than 2 patients who showed these ECG findings after heart surgery. These ECG findings suggested the possibility of occurrence of sinus node or subsidiary pacemaker dysfunction in the patients with left isomerism, especially in the older patients. So we thought that electrophysiologic evaluation is necessary in some patients with left isomerism.
Atrioventricular Block ; Axis, Cervical Vertebra ; Bradycardia ; Child ; Electrocardiography* ; Humans ; Isomerism* ; Sinoatrial Node ; Thoracic Surgery ; United Nations

Hyponatremia is the most common electrolyte abnormality in hospitalized patients and often presents no symptoms. The association between sinus node dysfunction and hyponatremia has rarely been reported. We describe a 77-year-old woman who developed reversible sinus node dysfunction accompanied by pulmonary edema that was associated with hyponatremia.
Aged ; Female ; Humans ; Hyponatremia* ; Pulmonary Edema* ; Sick Sinus Syndrome* ; 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

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*