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Effects of cardiac contraction and cavity pressure on myocardial blood flow
J W Doucette1, M Goto, A E Flynn
1Department of Pediatrics, University of California, San Francisco 94143.
Insights
Cardiac contraction significantly impacts coronary blood flow dynamics. When regional contraction is abolished, left ventricular pressure (LVP) becomes a key factor in regulating myocardial inflow and flow distribution.
Area of Science:
- Cardiovascular Physiology
- Myocardial Blood Flow Dynamics
Background:
- Regional impairment of cardiac contraction can disrupt the relationship between force generation and left ventricular pressure (LVP).
- This disruption may influence the phasic pattern and transmural distribution of coronary blood flow.
Purpose of the Study:
- To investigate the effects of abolishing local cardiac contraction and altering cavity pressure on myocardial inflow and transmural flow.
- To determine the roles of contraction and LVP in regulating coronary flow patterns.
Main Methods:
- Utilized anesthetized, open-chest dogs with maximal coronary vasodilation.
- Studied a region of the left ventricular free wall, manipulating local contraction and LVP.
- Measured phasic myocardial inflow and net transmural flow, including normalized amplitude (NAmp) and inner-to-outer flow ratio.
Main Results:
- With contraction present, NAmp was similar at normal and low LVP, but varied significantly when contraction was absent.
- The inner-to-outer flow ratio was not consistently different between normal and low LVP with contraction present.
- However, the inner-to-outer flow ratio was significantly higher at low LVP compared to normal LVP when contraction was absent.
Conclusions:
- Cardiac contraction is the primary determinant of phasic amplitude and transmural distribution of myocardial flow under global function.
- Abolishing regional contraction allows LVP to play a significant role in modulating coronary flow patterns, particularly under low-pressure conditions.
Abstract:
Regional impairment of cardiac contraction uncouples force generation from left ventricular pressure (LVP) and may alter the determinants of the phasic pattern and transmural distribution of coronary flow. In anesthetized, open-chest dogs with maximal coronary vasodilation, we studied the effects of abolishing local contraction and changing cavity pressure on phasic myocardial inflow and net transmural flow in a region of left ventricular free wall. With contraction present, the normalized amplitude of distal phasic coronary velocity (NAmp) was not significantly different at normal vs. low LVP (1.00 vs. 0.92 +/- 0.09, respectively, intracoronary lidocaine, however, NAmp varied with LVP (1.62 +/- 0.25 at normal LVP, 0.85 +/- 0.22 at low LVP, P < 0.0001). With contraction present, inner-to-outer flow ratio was not consistently different at normal vs. low LVP (0.47 +/- 0.15 vs. 0.64 +/- 0.28, respectively, P = NS) but was consistently higher at low than at normal LVP with contraction absent (1.01 +/- 0.30 vs. 1.84 +/- 0.38, respectively, P < 0.0001). During uniform global function, contraction is the main determinant of phasic amplitude and transmural distribution of myocardial flow. When regional contraction is abolished, allowing passive deformation of the wall during systole, LVP assumes a powerful role.