• Diastolic dysfunction
• echocardiography-exercise

Exertional shortness of breath in the absence of an obvious cardiac abnormality is a perplexing and relatively common clinical scenario especially in older patients. These patients often undergo multiple evaluations by different specialists and end up without a definitive diagnosis and, more importantly, without any specific therapeutic target to improve their symptoms. In some of these patients, exercise intolerance is attributed to respiratory disease, in others to deconditioning or obesity and in many diastolic abnormalities are claimed as the underlying problem without substantiating data. In their article in this edition of Heart, Tan et al describe a study of diastolic function on exercise in a group of patients with treated hypertension without significant diastolic dysfunction at rest whose functional capacity is significantly reduced (see page 948).1 Their findings that these patients exhibit significant abnormalities of diastolic function on limited exercise and that these induced diastolic abnormalities relate to the degree of functional limitation are an important contribution to our understanding of the pathophysiology of functional impairment in older hypertensive patients. This paper also highlights the potential utility of diastolic stress testing as a diagnostic modality in this patient population.

It is not surprising that exercise stress will provoke diastolic abnormalities that are not apparent at rest. Indeed, diastolic abnormalities, as a rule, accompany systolic abnormalities during stress, and demand ischaemia leads first to diastolic, and then to systolic abnormalities. One can roughly divide diastolic function parameters into ‘traditional’ or ‘hard’, and ‘contemporary’ or ‘soft’ indices. Traditional diastolic function indices are usually considered as measures of relaxation, diastolic stiffness and filling pressure (which results from the interaction of relaxation, stiffness and preload). Relaxation occurs first with mitral valve closure, followed by left ventricular (LV) filling along the pressure–volume curve that is defined by LV stiffness, and finally, results …