Related Experiment Videos
Coronary vascular reserve in left ventricular hypertrophy secondary to chronic aortic regurgitation
Insights
Severe chronic aortic regurgitation (AR) significantly reduces coronary vascular reserve, particularly in patients with left ventricular hypertrophy. This reduced reserve correlates with increased left ventricular mass and wall thickness.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Severe chronic aortic regurgitation (AR) can lead to significant cardiac remodeling.
- The impact of AR on coronary vascular reserve (CVR) is not fully understood.
Purpose of the Study:
- To investigate coronary vascular reserve in patients with severe chronic aortic regurgitation.
- To determine the relationship between CVR and left ventricular (LV) remodeling in AR.
Main Methods:
- Coronary sinus flow and contrast-agent-induced hyperemia measured by continuous thermodilution in 11 AR patients and 19 controls.
- Left ventricular dimensions and mass assessed echocardiographically.
- Coronary arteries evaluated for abnormalities.
Main Results:
- Patients with AR exhibited increased resting coronary flow and decreased CVR compared to controls.
- Decreased CVR correlated with increased LV mass (r=-0.86) and LV wall thickness (r=-0.83).
- LV wall thickness, not LV volume, was the critical factor related to CVR.
Conclusions:
- Coronary vascular reserve is diminished in proportion to left ventricular hypertrophy in chronic AR.
- LV wall thickness is the primary determinant of reduced CVR in AR.
- No significant correlation found between CVR and angina pectoris in this cohort.
Abstract:
Coronary vascular reserve was studied in 11 patients with severe chronic aortic regurgitation (AR). Nineteen patients with the chest pain syndrome and normal findings on cardiac catheterization served as control subjects. Resting coronary sinus flow and contrast-agent-induced hyperemia were measured by continuous thermodilution. Left ventricular (LV) dimensions and mass were obtained echocardiographically. All patients had normal coronary arteries. Resting coronary flow was increased and coronary reserve was decreased in patients with AR compared with the control subjects: 310 +/- 38 versus 121 +/- 13 ml/min and 56 +/- 9 versus 86 +/- 7.5%, respectively. The decrease in coronary vascular reserve correlated with the increase in LV mass (r = -0.86, p = 0.001) and LV wall thickness (r = -0.83, p = 0.002) and with the decrease in LV volume/mass ratio (r = 0.761, p = 0.007). There was no significant correlation between the decrease in coronary vascular reserve and LV volume (r = 0.255), LV peak wall stress (r = 0.292), LV systolic pressure (r = -0.495), aortic or LV diastolic pressure (r = 0.322 and -0.318, respectively), or aortic-LV diastolic gradient, nor with the voltage on the electrocardiogram (limb leads r = -0.60, precordial leads r = -0.118). Thus, coronary vascular reserve is decreased in proportion to the degree of left ventricular hypertrophy in patients with chronic AR. Patients with angina pectoris tended to have a lower coronary vascular reserve than those without angina (median 26 versus 76%, difference not significant). LV wall thickness and not LV volume is the critical component of left ventricular mass related to coronary reserve. No significant correlation between the decrease in coronary vascular reserve and the presence of angina pectoris was demonstrated.