Modulation of the arterial coronary blood flow by asynchronous activation with ventricular pacing

G. Amitzur, D. Manor, A. Pressman, D. Adam, H. Hammerman, R. Shofti, R. Beyar, S. Sideman

Research output: Contribution to journalArticle

Abstract

This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfusion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfusion pressure. Four pacing sites were used: right atrium (RA(p)), mid-right ventricle (RV(p)), mid-left ventricle (LV(p)), and left ventricular apex (Apex(p)). Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricular (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Results: BFV was decreased in the LAD during RV(p) and Apex(p) pacing by 9.7%-12.9% versus RA(p) and by 11.6%-14.6% versus LV(p) (P <0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the atrial pacing, and higher by 14.1% ± 6.1% only in LV(p) versus RA(p) pacing in the LAD (P <0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P <0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%-45.5%, P <0.02). Normalized oscillatory flow amplitude (OFA(n)) was reduced in RV(p) pacing compared to RA(p) and LV(p) pacing (16.2 ± 3.5 and 21.7% ± 4.1%, respectively, P <0.03). The variations in blood flow and OFA(n) disappeared with adenosine-mediated maximum vasodilatation. Summary: (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV(p), Apex(p)). (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.

Original languageEnglish (US)
Pages (from-to)697-710
Number of pages14
JournalPACE - Pacing and Clinical Electrophysiology
Volume18
Issue number4 I
DOIs
StatePublished - 1995
Externally publishedYes

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Blood Flow Velocity
Perfusion
Pressure
Blood Vessels
Arteries
Adenosine
Heart Ventricles
Heart Atria
Vasodilation
Arterial Pressure
Homeostasis
Thorax
Dogs
Injections

Keywords

  • asynchronous activation
  • coronary flow
  • ventricular pacing

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Modulation of the arterial coronary blood flow by asynchronous activation with ventricular pacing. / Amitzur, G.; Manor, D.; Pressman, A.; Adam, D.; Hammerman, H.; Shofti, R.; Beyar, R.; Sideman, S.

In: PACE - Pacing and Clinical Electrophysiology, Vol. 18, No. 4 I, 1995, p. 697-710.

Research output: Contribution to journalArticle

Amitzur, G, Manor, D, Pressman, A, Adam, D, Hammerman, H, Shofti, R, Beyar, R & Sideman, S 1995, 'Modulation of the arterial coronary blood flow by asynchronous activation with ventricular pacing', PACE - Pacing and Clinical Electrophysiology, vol. 18, no. 4 I, pp. 697-710. https://doi.org/10.1111/j.1540-8159.1995.tb04664.x
Amitzur, G. ; Manor, D. ; Pressman, A. ; Adam, D. ; Hammerman, H. ; Shofti, R. ; Beyar, R. ; Sideman, S. / Modulation of the arterial coronary blood flow by asynchronous activation with ventricular pacing. In: PACE - Pacing and Clinical Electrophysiology. 1995 ; Vol. 18, No. 4 I. pp. 697-710.
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abstract = "This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfusion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfusion pressure. Four pacing sites were used: right atrium (RA(p)), mid-right ventricle (RV(p)), mid-left ventricle (LV(p)), and left ventricular apex (Apex(p)). Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricular (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Results: BFV was decreased in the LAD during RV(p) and Apex(p) pacing by 9.7{\%}-12.9{\%} versus RA(p) and by 11.6{\%}-14.6{\%} versus LV(p) (P <0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16{\%}-28{\%} in the CFX for the three ventricular pacing sites versus the atrial pacing, and higher by 14.1{\%} ± 6.1{\%} only in LV(p) versus RA(p) pacing in the LAD (P <0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50{\%}-64{\%} (P <0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6{\%}-45.5{\%}, P <0.02). Normalized oscillatory flow amplitude (OFA(n)) was reduced in RV(p) pacing compared to RA(p) and LV(p) pacing (16.2 ± 3.5 and 21.7{\%} ± 4.1{\%}, respectively, P <0.03). The variations in blood flow and OFA(n) disappeared with adenosine-mediated maximum vasodilatation. Summary: (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV(p), Apex(p)). (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.",
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T1 - Modulation of the arterial coronary blood flow by asynchronous activation with ventricular pacing

AU - Amitzur, G.

AU - Manor, D.

AU - Pressman, A.

AU - Adam, D.

AU - Hammerman, H.

AU - Shofti, R.

AU - Beyar, R.

AU - Sideman, S.

PY - 1995

Y1 - 1995

N2 - This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfusion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfusion pressure. Four pacing sites were used: right atrium (RA(p)), mid-right ventricle (RV(p)), mid-left ventricle (LV(p)), and left ventricular apex (Apex(p)). Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricular (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Results: BFV was decreased in the LAD during RV(p) and Apex(p) pacing by 9.7%-12.9% versus RA(p) and by 11.6%-14.6% versus LV(p) (P <0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the atrial pacing, and higher by 14.1% ± 6.1% only in LV(p) versus RA(p) pacing in the LAD (P <0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P <0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%-45.5%, P <0.02). Normalized oscillatory flow amplitude (OFA(n)) was reduced in RV(p) pacing compared to RA(p) and LV(p) pacing (16.2 ± 3.5 and 21.7% ± 4.1%, respectively, P <0.03). The variations in blood flow and OFA(n) disappeared with adenosine-mediated maximum vasodilatation. Summary: (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV(p), Apex(p)). (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.

AB - This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfusion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfusion pressure. Four pacing sites were used: right atrium (RA(p)), mid-right ventricle (RV(p)), mid-left ventricle (LV(p)), and left ventricular apex (Apex(p)). Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricular (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Results: BFV was decreased in the LAD during RV(p) and Apex(p) pacing by 9.7%-12.9% versus RA(p) and by 11.6%-14.6% versus LV(p) (P <0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the atrial pacing, and higher by 14.1% ± 6.1% only in LV(p) versus RA(p) pacing in the LAD (P <0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P <0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%-45.5%, P <0.02). Normalized oscillatory flow amplitude (OFA(n)) was reduced in RV(p) pacing compared to RA(p) and LV(p) pacing (16.2 ± 3.5 and 21.7% ± 4.1%, respectively, P <0.03). The variations in blood flow and OFA(n) disappeared with adenosine-mediated maximum vasodilatation. Summary: (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV(p), Apex(p)). (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.

KW - asynchronous activation

KW - coronary flow

KW - ventricular pacing

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