Left Atrial Pacing Following Mustard's Correction of Transposition of the Great Vessels

The objective of this study was to examine the hypothesis that long-term, rapid atrial pacing produces a model of atrial systolic and diastolic dysfunction but does not alter ventricular function. Eight dogs were atrially paced at 400 beats/min (3:1–5:1 ventricular response) for 6 wk and subsequently instrumented with left atrial (LA) and left ventricular (LV) sonomicrometers and micromanometers. Data were compared with those from six sham-operated controls at matched heart rates and mean LA pressures of 10 mmHg. Dogs with rapid pacing had slightly greater LA volume (10.3 ± 4.0 vs. 7.9 ± 4.4 ml) and reduced ejection fraction (2.2 ± 1.4 vs. 13.0 ± 4.0, P < 0.05), systolic ejection rate (0.3 ± 0.1 vs. 2.8 ± 1.2 vol/s, P < 0.05), and reservoir fraction (0.07 ± 0.04 vs. 0.35 ± 0.06, P < 0.05) compared with controls. LA diastolic chamber stiffness was greater after rapid atrial pacing than before (stiffness constant k c, 5.7 ± 2.3 vs. 3.4 ± 0.6, P < 0.05), and the ratio of transesophageal echo-determined pulmonary venous systolic to diastolic integrated flow (a measure of relative reservoir to conduit function of the LA) was less in rapidly paced dogs compared with control dogs (0.41 ± 0.19 vs. 0.68 ± 0.23, P < 0.05). In contrast, rapid atrial pacing did not influence LV systolic performance or lusitropy, because the LV pressure time derivative and the time constant of LV relaxation were similar in both groups. In this model of isolated atrial myopathy, increased atrial stiffness and enhanced conduit function compensate for impaired atrial booster pump and reservoir functions.

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Left Atrial Pacing

New England Journal of Medicine ◽

10.1056/nejm196806132782418 ◽

1968 ◽

Vol 278 (24) ◽

pp. 1349-1350

Keyword(s):

Left Atrial ◽

Atrial Pacing

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Permanent Left Atrial Pacing:

Pacing and Clinical Electrophysiology ◽

10.1111/j.1540-8159.2004.00434.x ◽

2004 ◽

Vol 27 (3) ◽

pp. 314-317 ◽

Cited By ~ 3

Author(s):

INTISAR MIRZA ◽

SIMON JAMES ◽

PHYLLIS HOLT

Keyword(s):

Left Atrial ◽

Atrial Pacing

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Permanent Left Atrial Pacing with a Specifically Designed Coronary Sinus Lead

Pacing and Clinical Electrophysiology ◽

10.1111/j.1540-8159.1997.tb05433.x ◽

1997 ◽

Vol 20 (11) ◽

pp. 2755-2764 ◽

Cited By ~ 24

Author(s):

CLAUDE DAUBERT ◽

CHRISTOPHE LECLERCQ ◽

HERVE BRETON ◽

DANIEL GRAS ◽

DOMINIQUE PAVIN ◽

...

Keyword(s):

Coronary Sinus ◽

Left Atrial ◽

Atrial Pacing ◽

Coronary Sinus Lead

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Adenosine's role in coronary vasodilation induced by atrial pacing and norepinephrine

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1982.243.4.h536 ◽

1982 ◽

Vol 243 (4) ◽

pp. H536-H545 ◽

Cited By ~ 6

Author(s):

J. P. Manfredi ◽

H. V. Sparks

Keyword(s):

Left Atrial ◽

Myocardial Oxygen Consumption ◽

Atrial Pacing ◽

Coronary Vasodilation ◽

Vascular Conductance ◽

Norepinephrine Infusion ◽

Anesthetized Dogs ◽

The Difference ◽

Arterial Plasma ◽

Metabolic Vasodilation

If adenosine (ADO) mediates metabolic vasodilation in the heart, increases in interstitial ADO (ISF[ADO]) must accompany increases in coronary vascular conductance. We tested this using ADO release, defined as the difference in [ADO] in coronary venous and arterial plasma multiplied by coronary plasma flow, as an index of ISF[ADO]. Pentobarbital-anesthetized dogs received intravenous norepinephrine or left atrial pacing, and the resulting changes in coronary blood flow (delta CBF), conductance (delta C), myocardial oxygen consumption (delta VO2), and ADO release (delta RADO) were measured. If ISF[ADO] and C are coupled, the ratio delta RADO/delta C should be greater than zero. For dogs receiving atrial pacing, the ratios delta RADO/delta C, delta RADO/delta CBF, and delta RADO/delta VO2 equal -2.4 +/- 2.2 nmol . mmHg-1 . ml-1, -0.022 +/- 0.020 nmol/ml, and -0.13 +/- 0.12 nmol/ml, respectively. These values do not differ from zero. For dogs receiving norepinephrine, delta RADO/delta C, delta RADO/delta CBF, and delta RADO/delta VO2 equal 9.7 +/- 1.8, 0.051 +/- 0.017, and 0.44 +/- 0.13, respectively. These values are greater than zero (P less than 0.05). These differences between atrial pacing and norepinephrine infusion rate observed despite similar changes in C, CBF, and VO2. We conclude that ADO may mediate the vasodilation induced by norepinephrine, but not atrial pacing.

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