It was really surprising to see such a large audience, in a large auditorium, attending a non-sponsored, and non-technological symposium, only focusing on a good old traditional clinic. It seems that there are still people interested in understanding the cause of symptoms before trying to cure them.
Everybody is trying to convince us that they have been able to win the battle against the disabling symptoms of heart failure, thanks to the newest pharmacological and non-pharmacological therapy, or thanks to more innovative devices and aggressive approaches. However, there are still many unsolved issues in heart failure, and one of the most intriguing, but still obscure, ones is simply the cause of shortness of breath.
Four experts gave very interesting and stimulating talks, each presenting and proposing alternative explanations for the origin of dyspnoea: lung, heart, peripheral circulation, or skeletal muscle?
Very elegantly, Maria Tokmakova (Plovdiv, Bulgaria) argued in favour of the role of the lung. Indeed, a complex of several abnormalities were described from an anatomical point of view, relating to the composition, functional, regulatory control: increased bronchial hyper-reactivity, reduced diffusion capacity, restrictive pattern, reduced diffusion capacity, V/Q mismatch, abnormal breathing pattern, hyperventilation, reduced respiratory muscle strength: but at least some of these abnormalities may be improved by peripheral intervention such as physical training programmes.
An outstanding lesson was given by Lin-Bun Tan (Leeds UK): starting from the bedside, going to basic science and physiology Dr Tan outlined the central role of the heart in the pathophysiology of heart failure.
Back to the periphery again was the statement of G. Jondeau (France) in his lecture. Based on solid physiological issues, he reanalysed the ventilatory response to exercise and the haemodynamic changes in the skeletal muscle to outline the role of peripheral blood flow.
This message was reinforced in the last talk, given by myself. I went deeply in to the muscle: not only an effect of deconditioning, but also intrinsic abnormalities, are contributing factors. Impaired deossification systems, increased ROS accumulation, cytokine over-expression, apoptotic factors: all lead to increased systemic peripheral resistance, skeletal muscle dysfunction and hypoperfusion, and reflex hyperactivation. Exercise training has an anti-oxidative effect, with increased radical scavenger enzyme activity in skeletal muscle.