Author + information
- Alexander C. Egbe, MD, MPH∗ (, )
- Sushil A. Luis, MBBS,
- Ratnasari Padang, MBBS, PhD and
- Carole A. Warnes, MD
- ↵∗Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street Southwest, Rochester, Minnesota 55905
We thank Dr. Cremer and colleagues for their letter regarding our recent paper about the outcomes in patients with moderate mixed aortic valve disease (MAVD) (1). We agree with Cremer and colleagues that we cannot make strong recommendations based on a single-center retrospective study, and we clearly highlighted this limitation in the paper. Let us address the concerns raised in their letter.
The reason for the small sample size of 251 patients was because of the strict entry criteria for the study. All 251 patients met both velocity and valve area criteria for moderate aortic stenosis plus at least 2 criteria for moderate aortic regurgitation. There were 856 patients with moderate-to-severe MAVD followed at our institution within the study period. However we studied only a “pure” cohort of patients with moderate MAVD while excluding those with more than moderate stenosis or regurgitation because arguably those patients already had an indication for aortic valve replacement (AVR) if they were symptomatic.
Similarly, the primary message of the study was that asymptomatic patients with moderate MAVD behaved similarly to asymptomatic patients with severe aortic stenosis with regard to the development of symptoms and need for AVR, hence the need for vigilance in follow-up. Almost 40% of them will become symptomatic and require AVR within 3 years from the time of diagnosis, similar to patients with severe aortic stenosis. This is in sharp contrast to the observed event rates in isolated moderate aortic stenosis or regurgitation. Additionally, about 11% of patients with moderate MAVD (mostly those with severe left ventricular hypertrophy) will become symptomatic (subjective report by the patient, and objective documentation of symptoms and decline in exercise capacity on stress test) even in the absence of progression of lesion severity. Of necessity, AVR must be a hard endpoint, particularly when predicated by the development of symptoms. Although we cannot yet prove that early AVR improves prognosis, the rapidity of symptom development underscores the need for careful follow-up before the development of class III symptoms, which poses a higher risk for operation, with additional concerns about the long-term prognosis for patients with both hypertrophied and dilated left ventricles, often with concomitant diastolic dysfunction. We agree that consideration of early AVR was only speculative, and prospective studies are needed; our major clinical message was the need for meticulous surveillance.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation