Severe symptomatic aortic stenosis is commonly encountered in clinical practice, affecting close to 5% of individuals older than 65 years of age, and carries a dismal prognosis if left untreated.(1,2) Chronically increased left ventricular afterload triggers a compensatory myocardial response, ultimately leading to ventricular hypertrophy, aimed at reducing chronically increased wall tension an restore cardiac performance.(3) Hypertrophy ultimately results in maladaptive changes and ultimately leads to heart failure and eventually increased risk of cardiac mortality. Myocardial fibrosis and altered myocardial perfusion appear to play a role in progressive cardiac decompensation.
Microvascular function in patients undergoing Transcatheter Aortic Valve Implant (TAVI) for severe symptomatic aortic stenosis: association with myocardial fibrosis