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Both the clinical picture and the prognosis of patients with congestive heart failure (CHF) are characterized by impaired exercise tolerance and dyspnoea, and the impact of respiratory muscle dysfunction on these symptoms has been evaluated since the early 1990s [1, 2, 3, 4]. These studies proved that weakness of respiratory muscles expressed as maximum inspiratory pressure Pimax is not only a predictor of worse outcome in patients with CHF [5] but also an independent risk factor for cardiovascular events in an elderly normal population [6]. Several factors may contribute to this respiratory muscle weakness, among which are at cellular level a metabolic impairment and structural abnormalities of myocytes [7, 8] , and at tissue level an altered blood flow [9] and switch from type I into type II fibers [10]. Recent studies found structural tissue changes in the diaphragm of heart failure rats, with degradation of sarcomer and mitochondria and expansion of intermyofibrillar spaces [11]. At level of the entire organism, these processes result in general loss of skeletal muscle which impairs chemo- and baroreflex control independently from the peripheral chemoreceptors. This dysfunction of feedback may limit exercise and aggravate dyspnoea, as it was outlined in the “muscle hypothesis of CHF” [12]. Recently, a close relation between inspiratory muscle strength and pulmonary hypertension has been described in patients with left [13] and right [14] ventricular dysfunction.
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