LAUSR

It is abundantly clear that clinical outcomes after interventions for left-sided heart valve disease are related to preoperative left ventricular hypertrophy (LVH) and myocardial fibrosis. The timing of treatment is influenced by the detection of changes in left ventricular (LV) geometry and long-axis function and pulmonary vascular resistance, with the goal of avoiding persistent symptoms and irreversible progression to heart failure. It is important to diagnose adverse remodelling preoperatively and to assess its consequences for LV function and reserve, and also important to monitor responses after valve surgery to confirm that hypertrophy is regressing and that function is maintained or improved. Kammerlander et al.1 report that two thirds of their patients attending for follow-up on average 50 months after surgery for aortic or mitral valve disease, fulfilled diagnostic criteria for heart failure with preserved ejection fraction (HFpEF). More than half of the patients were in atrial fibrillation and their natriuretic peptide levels were very high, exceeding levels usually observed in patients with HFpEF alone. More importantly, only 12.5% of them had been diagnosed to have heart failure, so their symptoms and need for increased treatment were unrecognized. And most importantly, patients with this syndrome had an increased mortality that was similar to patients with heart failure with reduced ejection fraction (HFrEF), who had been recognized. Over a follow-up of 7 years their risk of dying was 1.8 times higher than patients who had also had valve interventions but who did not have heart failure. Their study serves as a timely reminder that full recovery after valve