Respiratory muscle dysfunction in congestive heart failure—The role of pulmonary hypertension
Introduction
In patients with congestive heart failure (CHF), exercise intolerance and dyspnoea have been attributed partially to the dysfunction of the skeletal and possibly of the respiratory musculature [1], [2], [3], [4]. Moreover, the inspiratory muscle strength was assessed by static maximal inspiratory mouth occlusion pressure (Pimax) or using tests more independent from patients aptitude; and Pimax serving as a significant and independent prognostic marker [5], [6]. Several pathomechanisms have been suggested to contribute to respiratory muscle dysfunction in CHF. In severe CHF, a general atrophic loss of skeletal muscle mass in patients has been reported [3], [7]. Moreover, even in early stages of CHF, peripheral muscle function is impaired due to structural and metabolic abnormalities of skeletal myocytes [7]. Hammond et al. [8] reported on respiratory muscle weakness in patients with congestive heart failure and proposed blood flow reduction to be responsible for the inspiratory muscle weakness. Moreover, in CHF the increase in ventilatory drive has been an inconsistent finding. Its potential contribution to respiratory muscle dysfunction remains a matter of debate [4], [11], [12]. However, no data were provided as for the relationship between respiratory muscle strength and pulmonary hemodynamics. The relation between hemodynamics and respiratory muscle strength was first studied by Nishimura et al. [9] who showed an inverse relationship between cardiac index and maximal inspiratory mouth occlusion pressure (Pimax). Recently, additional data were reported on the association of respiratory muscle dysfunction with the severity of idiopathic pulmonary arterial hypertension [10]. However, comprehensive data on respiratory muscle strength in relation to pulmonary hemodynamics in a large CHF population is lacking.
Therefore, the present study was designed to investigate the relationship between pulmonary hypertension, respiratory muscle dysfunction, and ventilatory drive in CHF patients with a wide range in disease severity.
Section snippets
Study population
This study enrolled 532 consecutive CHF patients (159 female, age 59 ± 12 years, NYHA functional classes I–IV) from two tertial referral centers in Germany (German Heart Institute, Berlin, and University Hospital, Heidelberg). All patients were electively short-term hospitalized for comprehensive invasive and non-invasive evaluation.
The diagnostic classification of underlying cardiac disorder was based on left heart catheterization and coronary angiography. As inclusion criteria, left ventricular
Results
Invasive hemodynamic assessment was compatible with CHF (Table 1). In 65% of the 532 CHF patients, PAPm was > 25 mm Hg at rest (Table 1). The close correlation between PAPm and PCWPm (r = 0.61; p = 0.0015), together with the PVR (6.2 ± 4.5 WU) and the TPG (9 ± 6 mm Hg) indicates a postcapillary component of PH.
Discussion
The present study provides first evidence of a close relation between respiratory muscle dysfunction, increased ventilatory drive and pulmonary hypertension in 532 patients with various degrees of chronic left ventricular failure.
The major findings are:
- 1.
Inspiratory muscle dysfunction (reduction in Pimax) is more pronounced in patients with severe CHF.
- 2.
There is a close inverse correlation between inspiratory muscle strength and PAPm as well as PCWP. This occurs in parallel with a reduction in VC.
- 3.
Acknowledgement
The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [29].
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