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Hemodynamic mechanisms responsible for reduced subendocardial coronary reserve in dogs with severe left ventricular
L Hittinger1, I Mirsky, Y T Shen
1Department of Medicine, Harvard Medical School, Brigham & Women's Hospital, Boston, Mass, USA.
Insights
Reduced subendocardial coronary reserve in left ventricular hypertrophy (LVH) is primarily due to hemodynamic factors like compressive forces, not just structural changes. Lowering these forces in LVH dogs restored coronary flow, supporting this conclusion.
Area of Science:
- Cardiovascular Physiology
- Cardiac Hypertrophy Research
- Coronary Blood Flow Dynamics
Background:
- Left ventricular hypertrophy (LVH) is characterized by reduced subendocardial coronary reserve.
- The underlying mechanisms, whether hemodynamic or structural, remain debated.
Purpose of the Study:
- To investigate whether hemodynamic or structural factors are primarily responsible for reduced subendocardial coronary reserve in LVH.
- To differentiate the roles of altered wall stress versus intrinsic structural changes.
Main Methods:
- Studied 10 conscious dogs with induced LVH via aortic banding.
- Assessed coronary blood flow and myocardial wall stress during near-maximal vasodilation with adenosine.
- Manipulated preload to alter LV wall stress in a subgroup of LVH dogs.
Main Results:
- In LVH dogs, adenosine infusion led to smaller increases in subendocardial blood flow and a greater fall in the subendocardial/epicardial ratio compared to controls.
- LV wall stresses remained elevated during vasodilation in LVH dogs.
- Reducing LV wall stress in LVH dogs normalized the subendocardial/epicardial ratio and subendocardial blood flow.
Conclusions:
- Hemodynamic factors, specifically compressive forces, significantly contribute to reduced subendocardial coronary reserve in LVH.
- Structural alterations alone do not fully explain the diminished coronary reserve in severe LVH.
- Modulating hemodynamic forces can restore coronary flow reserve in LVH.
Background:
Reduced subendocardial coronary reserve is a hallmark of left ventricular hypertrophy (LVH). The goal of this study was to determine whether hemodynamic, as opposed to structural, mechanisms were responsible for the reduced subendocardial coronary reserve.
Methods And Results:
The effects of near-maximal vasodilation with adenosine were examined in 10 conscious dogs with LVH (79% increase in ratio of LV weight to body weight) induced by aortic banding in puppies with and without preload reduction. At baseline, LV end-diastolic pressure, LV end-diastolic circumferential and compressive radial wall stresses, and LV myocardial blood flow were similar in dogs with LVH and sham-operated controls, while LV end-systolic circumferential wall stress tended to be greater in the LVH group compared with the control group. In control dogs, adenosine reduced LV circumferential end-systolic and end-diastolic wall stresses and compressive radial subendocardial wall stress; LV subendocardial blood flow increased (from 1.41 +/- 0.16 to 3.58 +/- 0.27 mL.min-1.g-1) and the ratio of subendocardial to subepicardial blood flow decrease from 1.30 +/- 0.07 to 0.69 +/- 0.05. In dogs with LVH, during adenosine infusion, LV circumferential end-systolic and end-diastolic wall stresses and LV radial subendocardial wall stresses remained elevated, the increase in LV subendocardial blood flow was significantly smaller (from 1.11 +/- 0.11 to 2.27 +/- 0.24 mL.min-1.g-1, P < .05), and the subendocardial/epicardial ratio fell to a lower level (from 1.22 +/- 0.17 to 0.35 +/- 0.03, P < .05). When LV wall stresses during adenosine were reduced in a subgroup of 5 dogs with LVH, the endocardium/epicardium ratio during adenosine infusion was no longer different from that in control dogs (0.63 +/- 0.11), nor was the level of subendocardial blood flow different (3.42 +/- 0.60 mL.min-1.g-1).
Conclusions:
These data suggest that hemodynamic factors, eg, compressive forces, are an important component of the reduced subendocardial coronary reserve as opposed to structural alterations, even in the presence of severe LVH.