Cardiac arrhythmias in the conscious dog after excision of the sinoatrial node and crista terminalis.

Euler, David E.; Jones, Stephen B.; Gunnar, William; Loeb, Jerod M.; Murdock, David K.; Randall, Walter C.

doi:10.1161/01.cir.59.3.468

Cited by 30 publications

(10 citation statements)

References 31 publications

(15 reference statements)

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“…8C). The dog SAN is considered to be similar to the human SAN and, in the dog, total ablation of SAN pacemaker function requires the destruction of a block of tissue ∼ 4 cm long and 1.5 cm wide extending from the lateral junction of the superior vena cava with the right atrial appendage, along the crista terminalis to the inferior vena cava [26,43]. Once again, this corresponds to the distribution of SAN tissue as described in the present study (Fig.…”

Section: San and Superior Vena Cavasupporting

confidence: 57%

Extended atrial conduction system characterised by the expression of the HCN4 channel and connexin45

Yamamoto

Dobrzynski

Tellez

et al. 2006

Cardiovascular Research

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Section: San and Superior Vena Cavasupporting

confidence: 57%

Extended atrial conduction system characterised by the expression of the HCN4 channel and connexin45

Yamamoto

Dobrzynski

Tellez

et al. 2006

Cardiovascular Research

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“…This observation underscores the notion that an extensive region of tissue has to be ablated to stop sinus rhythm, ie, that only a small number of cells within the SAN region is sufficient for SAN function, and that the location of this activity within the SAN is flexible. 5,7,27,28 …”

Section: Molecular and Functional Regionalization Of The San Into An mentioning

confidence: 99%

Formation of the Sinus Node Head and Differentiation of Sinus Node Myocardium Are Independently Regulated by Tbx18 and Tbx3

Wiese

Grieskamp

Airik

et al. 2009

Circulation Research

275

321

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Abstract-The sinus node (or sinoatrial node [SAN]), the pacemaker of the heart, is a functionally and structurally heterogeneous tissue, which consists of a large "head" within the right caval vein myocardium and a "tail" along the terminal crest. Here, we investigated its cellular origin and mechanism of formation. Using genetic lineage analysis and explant assays, we identified T-box transcription factor Tbx18-expressing mesenchymal progenitors in the inflow tract region that differentiate into pacemaker myocardium to form the SAN. We found that the head and tail represent separate regulatory domains expressing distinctive gene programs. Tbx18 is required to establish the large head structure, as seen by the existence of a very small but still functional tail piece in Tbx18-deficient fetuses. In contrast, Tbx3-deficient embryos formed a morphologically normal SAN, which, however, aberrantly expressed Cx40 and other atrial genes, demonstrating that Tbx3 controls differentiation of SAN head and tail cardiomyocytes but also demonstrating that Tbx3 is not required for the formation of the SAN structure. Our data establish a functional order for Tbx18 and Tbx3 in SAN formation, in which Tbx18 controls the formation of the SAN head from mesenchymal precursors, on which Tbx3 subsequently imposes the pacemaker gene program. Key Words: heart development Ⅲ progenitors Ⅲ Hcn4 Ⅲ Cx43 Ⅲ transgenic mice T he sinoatrial node (SAN) or sinus node is the most upstream component of the cardiac conduction system. As the primary pacemaker, it serves to initiate and control the rate of electric impulses for the ordered stimulation and contraction of the cardiac chambers. The critical importance of the SAN is reflected in dysfunctions that arise on aging and disease, including sick sinus syndrome, leading to implantation in about one-half of all pacemaker recipients in the United States. 1 The SAN consists of a small group of primitive variably sized myocytes with little contractile filaments and intermingled fibroblasts at the junction of the right venous entrance and the atrium. 2 They form an elongated "comma-shaped" structure that is subdivided into a large "head" in the right superior caval vein bordering the atrium, and a "tail" along the terminal crest. 3,4 The leading pacemaker usually originates from a small number of cells within the SAN, but its location shifts under altered physiological conditions, a phenomenon that likely contributes to both controllability and stability of pacemaker activity. 2,5,6 For example, ␤-adrenergic stimulation in rat causes dominant pacemaker activity to shift cranially into the SAN head region, 7 supporting the notion that functional specialization correlates with structural regionalization in the SAN.The mechanisms underlying the functional regionalization, as well as the pathological mechanisms underlying SAN dysfunction, are only insufficiently understood. Histological studies initially indicated that the mouse SAN forms at approximately embryonic day (E)10 to E11 from myocardium of t...

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“…These procedures often resulted in early appearance of coronary sinus or atrioventricular junctional rhythms that were later replaced by atrial escape rhythms.23 24,26,28,30,31 Jones et a132 performed stepwise excisions of right atrial tissue segments beginning at the sinoatrial node and extending caudally along the sulcus terminalis to the junction of the inferior vena cava and inferior right atrium. In the acute open-chest canine preparation they found atrial, atrioventricular, and ventricular ectopic pacemakers to emerge.…”

Section: Short-term Effects Of Lasingmentioning

confidence: 99%

Modification of sinus node function by epicardial laser irradiation in dogs.

et al. 1990

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This study tested the feasibility of neodymium:YAG laser photocoagulation of selected sinus node areas to depress sinus rate responsiveness. In 14 open-chest dogs, origin of the sinus impulse (0 point) was electrically mapped from the epicardium before and during isoproterenol infusion. Epicardial laser photocoagulation was applied to the 0 point observed during isoproterenol infusion and stepwise to remapped new 0 points until a 30±5% decrease in heart rate occurred. Long-term effects were assessed by Holter monitoring and electropharmacologic testing preoperatively and up to 10 weeks or 6 months. Mean (± SEM) percent decreases were observed at 10 weeks in the following parameters: average 24-hour heart rate, 17.4+±5.0%; maximum heart rate on Holter, 30.5+±3.5%; heart rate during pharmacologic autonomic blockade, 32.7±3.5%; and maximum heart rate on isoproterenol, 23.1±4.6% (all p<0.01). Curves with pacemaker recovery time plotted against control cycle length remained unchanged. Holter monitoring did not show excessive bradycardic episodes even after administration of propranolol. In three control dogs (sham operation), sinus node function remained unchanged. Histologic study of the irradiated area showed replacement by inflammatory cells, fibrosis, and cartilage formation with surrounding normal cells and occasional cells resembling pacemakerlike cells at the caudal end of the sinoatrial node. This study suggests that 1) map-guided graded laser photocoagulation of sinus node regions showing earliest activation during catecholamine stimulation successfully limits maximum heart rates without causing significant bradycardia, 2) the effects are long lasting, and 3) the remaining pacemaker behaves like the sinus node. Laser modification of sinus node function could become a form of nonpharmacologic heart rate control in patients with coronary artery disease undergoing surgery and in the syndrome of inappropriate sinus tachycardia. (Circulation 1990;81:350-359) P harmacologic control of excessive sinus tachycardia in humans is occasionally limited by side effects inherent to the drugs used, patient intolerance, or treatment failure related to the nature of the disease.12 Therapeutic options for severe cases of drugresistant sinus tachycardia today include total surgical exclusion of the sinus node region or cryosurgical ablation.34 Both procedures usually result in atrial or Supported by grants from the Heineman Medical Research Center of Charlotte, NC, Inc, and HL-30558-06 from the National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Maryland.Address for correspondence: Laszlo Littmann, MD, Laser and Applied Technologies Laboratory, Carolinas Heart Institute, PO Box 32861, Charlotte, NC 28232.Received April 11, 1989; revision accepted September 13, 1989. atrioventricular junctional escape rhythms and necessitate implantation of a permanent pacemaker. The functional anatomy of the sinus node region in humans and dogs is unique in that it shows widespread distribution and rate differ...

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Cardiac arrhythmias in the conscious dog after excision of the sinoatrial node and crista terminalis.

Cited by 30 publications

References 31 publications

Extended atrial conduction system characterised by the expression of the HCN4 channel and connexin45

Extended atrial conduction system characterised by the expression of the HCN4 channel and connexin45

Formation of the Sinus Node Head and Differentiation of Sinus Node Myocardium Are Independently Regulated by Tbx18 and Tbx3

Modification of sinus node function by epicardial laser irradiation in dogs.

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