Function and Dysfunction of the Sinus Node: Clinical Studies in the Evaluation of Sinus Node Function

Jordan, Jay L.; Yamaguchi, Iwao; Mandel, William J.

doi:10.1007/978-94-009-9715-8_1

Cited by 10 publications

(6 citation statements)

References 93 publications

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“…Moreover, staining with di-4-ANEPPS, as in our previous study of the in the rabbit SAN,13 may cause a transient effect on pacemaking and conduction properties of the canine SAN. However, our observation of pacing-induced SAN dysfunction is in agreement with several clinical observations 30,34,35…”

Section: Discussionsupporting

confidence: 93%

“…Thus, because of exit block, estimation of SAN recovery time using only atrial electrograms is not a reliable estimate of recovery of SAN intrinsic activity. Our data showed that atrial pacing induced SAN dysfunction attributable to exit block (Figures 5 and 6), which is consistent with clinical evidence 31-34. Two general hypotheses of pacing-induced SAN dysfunction have been proposed34: (1) suppression is caused by release of neurotransmitters; and (2) overdrive pacing directly disrupts ionic mechanisms of the pacemaker automaticity.…”

Section: Discussionsupporting

confidence: 88%

“…Our data showed that atrial pacing induced SAN dysfunction attributable to exit block (Figures 5 and 6), which is consistent with clinical evidence 31-34. Two general hypotheses of pacing-induced SAN dysfunction have been proposed34: (1) suppression is caused by release of neurotransmitters; and (2) overdrive pacing directly disrupts ionic mechanisms of the pacemaker automaticity. It is well known that atrial overdrive pacing does result in a release of autonomic neurotransmitters, presumably acetylcholine (ACh) 35,36.…”

Section: Discussionsupporting

confidence: 88%

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Structural and Functional Evidence for Discrete Exit Pathways That Connect the Canine Sinoatrial Node and Atria

Fedorov

Schuessler²,

Hemphill³

et al. 2009

Circulation Research

117

178

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Abstract-Surface electrode recordings cannot delineate the activation within the human or canine sinoatrial node (SAN) because they are intramural structures. Thus, the site of origin of excitation and conduction pathway(s) within the SAN of these mammals remains unknown. Canine right atrial preparations (nϭ7) were optically mapped. The SAN 3D structure and protein expression were mapped using immunohistochemistry. SAN optical action potentials had diastolic depolarization and multiple upstroke components that corresponded to the separate excitations of the node and surface atrial layers. Pacing-induced SAN exit block eliminated atrial optical action potential components but retained SAN optical action potential components. Excitation originated in the SAN (cycle length, 557Ϯ72 ms) and slowly spread (1.2 to 14 cm/sec) within the SAN, failing to directly excite the crista terminalis and intraatrial septum. After a 49Ϯ22 ms conduction delay within the SAN, excitation reached the atrial myocardium via superior and/or inferior sinoatrial exit pathways 8.8Ϯ3.2 mm from the leading pacemaker site. The ellipsoidal 13.7Ϯ2.8/4.9Ϯ0.6 mm SAN structure was functionally insulated from the atrium. This insulation coincided with connexin43-negative regions at the borders of the node, connective tissue, and coronary arteries. During normal sinus rhythm, the canine SAN is functionally insulated from the surrounding atrial myocardium except for 2 (or more) narrow superior and inferior sinoatrial exit pathways separated by 12.8Ϯ4.1 mm. Conduction failure in these sinoatrial exit pathways leads to SAN exit block and is a modulator of heart rate. The clinical signs of SAN dysfunction include bradycardia, sinus pauses, sinus arrest, sinus exit block, and reentrant arrhythmias. 3,4 Although the syndrome may have many causes and commonly affects elderly persons, it usually is idiopathic. 5 Studies of human SAN function are complicated by the inability of epior endocardial mapping to detect the origin and slow propagation of action potentials (APs) within the SAN before it activates adjacent atrial myocardium. 6,7 Sinus rhythm (SR) is physiologically controlled by autonomic modulation of pacemaker ion channels, 8 calcium handling, 9 and shifts of the leading pacemaker site. 10 -12 Anatomic structure and electrophysiological heterogeneity play important roles in SAN excitation under various conditions. 6 Recently, we investigated activation patterns in the rabbit SAN using optical mapping, 13 which is the only available technology that allows the resolution of simultaneous changes in the activation pattern and AP morphology from multiple sites. In that study, we demonstrated that the rabbit SAN is functionally insulated from the atrial septum. 13 However, the rabbit SAN is essentially a 2D structure 14 in contrast to the 3D structure of the canine 7,15,16 and human 17,18 SANs. Bromberg et al 7 suggested that the canine SAN may be functionally insulated from the surrounding atrial myocytes, except for a limited number of exit si...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 88%

See 1 more Smart Citation

Structural and Functional Evidence for Discrete Exit Pathways That Connect the Canine Sinoatrial Node and Atria

Fedorov

Schuessler²,

Hemphill³

et al. 2009

Circulation Research

117

178

View full text Add to dashboard Cite

show abstract

“…The syndrome was present in approximately 1 in 600 patients older than 50 years attending a Belgian provincial cardiovascular disease detection center; 23 however, this may be underestimated because the prevalence in asymptomatic individuals is not known. In addition, up to 40% of new pacemaker implants are related to this disorder 24,25 . Sick sinus syndrome is associated with adverse long‐term outcomes, including high rates of syncope, heart failure, and stroke 26,27 .…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Vein Isolation for Atrial Fibrillation in Patients with Symptomatic Sinus Bradycardia or Pauses

Khaykin

Marrouche

Martin

et al. 2004

Cardiovasc electrophysiol

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“…It is largely a disease of the elderly and its incidence increases in an exponential manner with age (Mandel et al, 1999 ; Adan and Crown, 2003 ; Dobrzynski et al, 2007 ). Although human SND can be induced by a number of different pathophysiological mechanisms such as drug effects, autonomic imbalances, cardiomyopathy and electrophysiological alterations, SAN structural abnormalities have been commonly observed in these dysfunctions and are significantly associated with HF, SAN ischemia, and inflammatory conditions (Jordan et al, 1978 ; Adan and Crown, 2003 ; Sanders et al, 2004 ; Kottkamp, 2012 ). In 1907, Keith and Flack saw a “definite increase in the amount of fibrous tissue” present in the SAN from pathological hearts (Keith and Flack, 1907 ).…”

Section: Fibrosis In San Dysfunctionmentioning

confidence: 99%

Fibrosis: a structural modulator of sinoatrial node physiology and dysfunction

et al. 2015

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Heart rhythm is initialized and controlled by the Sinoatrial Node (SAN), the primary pacemaker of the heart. The SAN is a heterogeneous multi-compartment structure characterized by clusters of specialized cardiomyocytes enmeshed within strands of connective tissue or fibrosis. Intranodal fibrosis is emerging as an important modulator of structural and functional integrity of the SAN pacemaker complex. In adult human hearts, fatty tissue and fibrosis insulate the SAN from the hyperpolarizing effect of the surrounding atria while electrical communication between the SAN and right atrium is restricted to discrete SAN conduction pathways. The amount of fibrosis within the SAN is inversely correlated with heart rate, while age and heart size are positively correlated with fibrosis. Pathological upregulation of fibrosis within the SAN may lead to tachycardia-bradycardia arrhythmias and cardiac arrest, possibly due to SAN reentry and exit block, and is associated with atrial fibrillation, ventricular arrhythmias, heart failure and myocardial infarction. In this review, we will discuss current literature on the role of fibrosis in normal SAN structure and function, as well as the causes and consequences of SAN fibrosis upregulation in disease conditions.

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Function and Dysfunction of the Sinus Node: Clinical Studies in the Evaluation of Sinus Node Function

Cited by 10 publications

References 93 publications

Structural and Functional Evidence for Discrete Exit Pathways That Connect the Canine Sinoatrial Node and Atria

Structural and Functional Evidence for Discrete Exit Pathways That Connect the Canine Sinoatrial Node and Atria

Pulmonary Vein Isolation for Atrial Fibrillation in Patients with Symptomatic Sinus Bradycardia or Pauses

Fibrosis: a structural modulator of sinoatrial node physiology and dysfunction

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