Diastolic dysfunction is a diabolically dysfunctional subject: scarcely any two accounts agree, and the very mention of it can cause British cardiologists to foam at the mouth. I spent ages about ten years ago trying to devise a study of the natural history of hypertension in relation to left ventricular hypertrophy, diastolic filling, aortic pressure wave velocity and B-type natriuretic peptide release, oddly enough with the aim of using valsartan as the intervention. As a result I became a better and wiser person, but these investigators actually did the trial (VALIDD). All they have discovered so far is that any blood pressure lowering agent improves diastolic filling velocity.

Neurodegeneration will get us all in the end. Actually, I’ve probably got the tense wrong in that sentence. Wouldn’t it be marvellous if you could introduce the right genes to the cells concerned and reverse the process? This paper describes initial success in 12 patients with advanced Parkinson’s disease, using a glutamic acid decarboxylase (GAD) gene carried by an adenovirus vector. Lots of bigger trials must surely follow.