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Coronary perfusion related changes in myocardial contractile force and systolic ventricular stiffness
T Iwamoto1, X J Bai, H F Downey
1Department of Physiology, University of North Texas Health Science Center at Fort Worth 76107-2699.
Insights
Increased coronary blood flow boosts heart muscle strength, stiffness, and oxygen use. These changes in contractile force and stiffness, not heart chamber size, drive the oxygen consumption increase.
Area of Science:
- Cardiovascular Physiology
- Cardiac Metabolism
Background:
- The relationship between coronary perfusion and myocardial oxygen consumption (MVO2), known as the Gregg phenomenon, remains debated.
- Understanding this mechanism is crucial for managing cardiac health and oxygen supply to the heart muscle.
Purpose of the Study:
- To investigate how coronary perfusion pressure and flow affect myocardial contractile force and systolic ventricular stiffness.
- To elucidate the role of these mechanical properties in mediating changes in myocardial oxygen consumption.
Main Methods:
- Utilized a canine model with selective left anterior descending coronary artery perfusion.
- Measured regional myocardial segment length, developed force, and calculated MVO2.
- Assessed systolic myocardial stiffness using the slope of the force-length curve during ejection (delta F/delta SL).
Main Results:
- Increased coronary perfusion pressure led to higher developed force, systolic stiffness (delta F/delta SL), and MVO2, with no change in end-diastolic length.
- Elevated coronary blood flow (via adenosine infusion) at constant pressure also increased developed force, systolic stiffness, and MVO2, without altering end-diastolic length.
- The relationship between MVO2 and delta F/delta SL was steeper with increasing flow in the perfusion pressure variation protocol.
Conclusions:
- Enhanced coronary blood flow directly increases myocardial contractile force, systolic ventricular stiffness, and MVO2 in the intact, ejecting heart.
- Changes in myocardial contractile force and systolic stiffness, rather than end-diastolic length, are the primary drivers of coronary blood flow-related MVO2 alterations.
Objective:
The mechanism by which changes in coronary perfusion alter myocardial oxygen consumption (MVO2; Gregg phenomenon) is controversial. This study examined the effect of coronary perfusion on myocardial contractile force and systolic ventricular stiffness in the intact, ejecting heart.
Methods:
During selective perfusion of the left anterior descending coronary artery, coronary blood flow was changed with or without concurrent changes in coronary perfusion pressure in 19 alpha chloralose anaesthetised dogs. Regional myocardial segment length (end diastolic length; end systolic length) and developed force were measured with piezoelectric crystals and with a miniature force transducer, respectively. MVO2 was calculated from coronary flow and arteriovenous O2 difference. The slope of the force-length curve during ejection period (delta F/delta SL) was used as an index of systolic myocardial stiffness.
Results:
When coronary perfusion pressure was varied from 60 to 180 mm Hg (protocol 1, n = 11), maximum developed force (Fmax), delta F/delta SL, and MVO2 increased with perfusion pressure while end diastolic length, segmental shortening, and other haemodynamic variables stayed constant. When coronary blood flow was increased at constant perfusion pressure by infusion of either a low dose or a high dose adenosine (protocol 2, n = 8), Fmax, delta F/delta SL, and MVO2 increased while end diastolic length, segmental shortening, and other haemodynamic variables stayed constant. MVO2 and delta F/delta SL increased more steeply with flow in protocol 1.
Conclusions:
(1) Increased coronary blood flow enhances myocardial contractile force, systolic ventricular stiffness, and MVO2 in the intact, ejecting heart. (2) Coronary blood flow induced changes in myocardial contractile force and systolic ventricular stiffness, but not end diastolic length, are probably responsible for coronary blood flow related changes in MVO2.