Related Experiment Videos
Coronary vasodilatory capacity is impaired in patients with dilated cardiomyopathy
S Weismüller1, J Czernin, K T Sun
1Department of Molecular and Medical Pharmacology, UCLA School of Medicine 90095-1735, USA.
Insights
Patients with dilated cardiomyopathy have reduced coronary vasodilatory capacity. This may be due to increased extravascular forces or elevated catecholamines causing coronary vasoconstriction, impacting myocardial blood flow.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Nuclear Cardiology
Background:
- Left ventricular enlargement and altered coronary vasomotor tone can increase wall stress.
- This may impact myocardial blood flow and vasodilatory capacity in dilated cardiomyopathy.
Purpose of the Study:
- To investigate myocardial blood flow and coronary vasodilatory capacity in patients with dilated cardiomyopathy.
- To test the hypothesis that increased wall stress affects myocardial blood flow.
Main Methods:
- Dynamic nitrogen 13-ammonia positron emission tomography (PET) was used to measure myocardial blood flow at rest and during dipyridamole stress.
- A two-compartment model was employed in 10 patients with dilated cardiomyopathy and 10 healthy controls.
- Coronary artery disease and left ventricular hypertrophy were excluded.
Main Results:
- Resting myocardial blood flow was similar between groups.
- Hyperemic myocardial blood flow was significantly lower in dilated cardiomyopathy patients compared to controls (1.57 vs. 1.92 mL/g/min, p < .05).
- Myocardial flow reserve did not differ significantly between the groups.
Conclusions:
- Coronary vasodilatory capacity is reduced in patients with severe nonischemic dilated cardiomyopathy.
- Potential mechanisms include increased extravascular compressive forces or elevated serum catecholamines leading to coronary vasoconstriction.
- These factors may contribute to impaired myocardial blood flow regulation in this patient population.
Abstract:
Increases in wall stress because of left ventricular enlargement and/or alterations in coronary vasomotor tone might affect myocardial blood flow and vasodilatory capacity in patients with dilated cardiomyopathy. To test this hypothesis myocardial blood flow was measured at rest and during intravenous administration of dipyridamole (0.56 mg/kg) using dynamic nitrogen 13-ammonia positron emission tomography (two-compartment model) in 10 patients with dilated cardiomyopathy (mean left ventricular ejection fraction 28 +/- 8% 1 woman, 9 men; 47 +/- 13 years of age). Ten age and gender matched healthy volunteers served as controls. Coronary artery disease was ruled out by coronary angiography and left ventricular hypertrophy by two dimensional-echocardiography. Baseline heart rate (70 +/- 13 v 64 +/- 12 bpm), systolic blood pressure (111 +/- 20 v 114 +/- 12 mm Hg) and rate pressure product (7,686 +/- 1264 v 7,306 +/- 1,645) were similar in patients and controls. During dipyridamole administration, the rate pressure product increased similarly in both groups. Myocardial blood flow at rest did not differ between groups of patients and volunteers (0.69 +/ -0.27 v 0.67 +/- 0.17 mL/g/min) but correlated with the rate pressure product only in controls (myocardial blood flow, 0.18 + 0.000068214; rate pressure product, .67; P < .05). Hyperemic myocardial blood flow was lower in patients (1.57 +/- 0.39 v 1.92 +/- 0.31 mL/g/min, p < .05, whereas myocardial flow reserve did not differ between groups of patients and controls (2.57 +/- 1.15 v 3.02 +/- 0.94). Coronary vasodilatory capacity is reduced in patients with severe nonischemic cardiomyopathy. Increases in extravascular compressive forces or increased serum catecholamine levels, which in turn induce coronary vasoconstriction, might account for this finding.