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Full-root Aortic Valve Replacement by Stentless Aortic Xenografts in Patients with Small Aortic Roots
Published on: May 21, 2017
Coronary reserve in patients with aortic valve disease before and after successful aortic valve replacement
F R Eberli1, M Ritter, J Schwitter
1Division of Cardiology, University Hospital, Zurich, Switzerland.
Insights
Patients with aortic valve disease have reduced coronary flow reserve due to elevated resting coronary blood flow. Aortic valve replacement improves coronary flow reserve by decreasing resting flow and reducing left ventricular hypertrophy.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Aortic valve disease can impair coronary circulation.
- Coronary vasodilator capacity is crucial for myocardial oxygen supply.
Purpose of the Study:
- To investigate coronary reserve in patients with aortic valve disease before and after aortic valve replacement.
- To compare coronary hemodynamics between preoperative patients, postoperative patients, and healthy controls.
Main Methods:
- Coronary sinus thermodilution technique used to determine coronary reserve.
- Study included 37 preoperative patients, 18 postoperative patients, and 7 controls.
- Coronary flow and resistance ratios (dipyridamole/rest) were calculated.
Main Results:
- Preoperative patients had diminished coronary flow reserve compared to postoperative patients and controls.
- Elevated resting coronary sinus blood flow was observed in preoperative patients.
- Maximal coronary blood flow did not differ significantly among the groups.
Conclusions:
- Reduced coronary vasodilator capacity in aortic valve disease is primarily due to elevated resting coronary blood flow.
- Aortic valve replacement leads to regression of left ventricular hypertrophy and improves coronary flow reserve.
- Decreased resting flow post-surgery is key to improved coronary flow reserve.
Abstract:
In patients with aortic valve disease and normal coronary angiograms coronary reserve was determined by the coronary sinus thermodilution technique. Three groups of patients were studied: 37 preoperative patients; 18 different patients 12-52 months after aortic valve replacement and seven control subjects with no cardiac disease. Coronary flow ratio (dipyridamole/rest) was diminished in preoperative compared with postoperative patients (1.66 +/- 0.44 vs 2.22 +/- 0.85; P less than 0.05) as well as with controls (2.80 +/- 0.84; P less than 0.01), and corresponding coronary resistance ratio (dipyridamole/rest) was higher in preoperative patients than in both other groups (0.61 +/- 0.17 vs 0.48 +/- 0.14; P less than 0.05 vs 0.37 +/- 0.10; P less than 0.01). Differences in the flow ratio, but not in the resistance ratio, were significant (P less than 0.05) in patients after aortic valve replacement compared with controls. Total coronary sinus blood flow at rest was elevated in preoperative compared with both postoperative patients and controls (252 +/- 99 vs 169 +/- 63; P less than 0.01; vs 170 +/- 35 ml.min-1, P less than 0.05), whereas flows after maximal vasodilation did not differ among the three groups (416 +/- 184 vs 361 +/- 150 vs 488 +/- 235 ml.min-1). Postoperative patients showed a distinct, though not total regression of left ventricular angiographic muscle mass index and wall thickness. Nine of the 18 postoperative patients showed a normal coronary flow reserve and nine showed subnormal response. These two subgroups did not differ with respect to preoperative macroscopic and microscopic measures of hypertrophy. Thus in aortic valve disease, the reduced coronary vasodilator capacity is mainly due to an elevated coronary flow at rest, while the maximal coronary blood flow achieved is identical to that of postoperative patients and controls. With regression of left ventricular hypertrophy, flow at rest decreases and this leads to a distinct improvement of coronary flow reserve.
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