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Published on: February 7, 2015
Determinants of myocardial blood flow response to cold pressor testing and pharmacologic vasodilation in healthy
John O Prior1, Thomas H Schindler, Alvaro D Facta
1Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, B2-085J CHS, 10833 Le Conte Ave, Box 956948, Los Angeles, CA 90095-6948, USA.
Insights
Myocardial blood flow response to cold pressor testing in healthy individuals is independent of baseline factors but linked to HDL cholesterol and vasodilator capacity. This reflects the coronary endothelium
Area of Science:
- Cardiovascular Physiology
- Non-invasive Cardiac Imaging
Background:
- Myocardial blood flow (MBF) response to sympathetic stimulation, like cold pressor testing (CPT), is influenced by endothelial factors and altered by coronary risk factors.
- Determinants of CPT-induced MBF changes in low-risk individuals are not fully understood, particularly concerning baseline hemodynamics, MBF, and vasodilator capacity.
Purpose of the Study:
- To define the determinants of myocardial blood flow (MBF) response to cold pressor testing (CPT) in healthy volunteers.
- To investigate the relationship between CPT-induced MBF changes and baseline hemodynamic, metabolic, and lipid profiles, as well as pharmacologically stimulated vasodilator capacity.
Main Methods:
- Fifty healthy volunteers underwent MBF measurement using (13)N-ammonia and PET at baseline, during CPT, and during pharmacologic hyperemia.
- Evaluated associations between MBF response to CPT and age, gender, heart rate, blood pressure, rate-pressure product (RPP), plasma substrates, lipids, and vasodilator capacity.
Main Results:
- CPT increased heart rate, blood pressure, and MBF (Delta MBF=0.23+/-0.09 ml/min/g).
- MBF response to CPT was independent of baseline hemodynamics and metabolic factors but associated with HDL cholesterol and the change in RPP.
- Changes in coronary vascular resistance during CPT correlated with changes in pharmacologic vasodilation capacity.
Conclusions:
- The myocardial blood flow response to cold, reflecting endothelium-dependent vasomotion, is independent of gender, age, and resting conditions in healthy individuals.
- HDL cholesterol levels modulate MBF response to CPT even in the absence of coronary risk factors.
- Coronary vascular resistance changes during CPT are linked to overall vasodilator capacity.
Purpose:
Response of myocardial blood flow (MBF) to sympathetic stimulation with cold is modulated by endothelium-related factors and is typically altered in the presence of coronary risk factors. Determinants of flow response to cold pressor testing (CPT) in normal volunteers at low risk for CAD remain less well defined, especially relative to baseline conditions such as hemodynamics and MBF, plasma substrate and lipid levels, and total pharmacologically stimulated vasodilator capacity.
Methods:
In 50 normal volunteers (42+/-13 years; 31 women) without coronary risk factors, insulin resistance, or family history of diabetes/premature CAD, MBF was measured with (13)N-ammonia and PET at baseline, during CPT, and during pharmacologic hyperemia.
Results:
Sympathetic stimulation with CPT raised heart rate and blood pressure and thus MBF (Delta MBF=0.23+/-0.09 ml/min/g). MBF response, defined in absolute flow units as the difference between CPT and baseline, was independent of age, gender, heart rate, and blood pressure and rate-pressure product (RPP) at baseline as well as plasma substrate and lipid levels with the exception of an association with HDL cholesterol (rho=0.40, p=0.005) but depended on the change in RPP from rest (rho=0.33, p=0.019). Finally, changes in coronary vascular resistance in response to CPT were associated with changes in pharmacologic vasodilation (rho=0.56, p<0.0001).
Conclusion:
MBF response to sympathetic stimulation with cold (NO-mediated endothelium-dependent vasomotion), reflecting the functional state of the coronary endothelium, was independent of gender, age, and resting heart conditions. It was modulated by HDL cholesterol levels, even in healthy volunteers, and also related to pharmacologically stimulated vasodilator capacity at the coronary vascular resistance level.
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