Maximal Inspiratory Pressure and Its Relationship With Clinical Parameters in Pulmonary Hypertension

Abstract Background: Exercise intolerance in patients with PH and salient mechanisms responsible for the reduced exercise capacity in patients with PH, which include cardiopulmonary alterations, but also intrinsic dysfunction of peripheral and respiratory muscle. Maximal inspiratory pressure (MIP) is a simple and readily available parameter reflecting respiratory muscle strength, but its association with clinical characteristics in PH remains unclear. Methods: This study included 64 patients diagnosed with PH via right heart catheterization. Patients were categorized into two groups based on MIP values: ≥70% of predicted (n=26) and <70% of predicted (n=38). Chi-square test was used to evaluate the correlation. Results: Patients with impaired MIP were significantly lower body weight than PH patients with normal MIP(P<0.05). A significant positive correlation was observed between MIP and pulmonary artery oxygen saturation (PaO2) and forced vital capacity (FVC) in PH patients (P<0.05). However, no significant correlations were found between MIP and 6-minute walk distance (6MWD), mean pulmonary artery pressure (mPAP), cardiac index (CI), cardiac output (CO), pulmonary artery wedge pressure (PAWP), pulmonary vascular resistance (PVR), right atrial area, right ventricular basal diameter, RV/LV (basal diameter), main pulmonary artery diameter, right ventricular wall thickness (RVWT), tricuspid annular plane systolic excursion (TAPSE), forced expiratory volume in one second (FEV1), FEV1/FVC ratio, and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels (P>0.05). Conclusion: Our study suggests a positive association between MIP and pulmonary gas exchange parameters (PaO2 and FVC) in PH patients. Interestingly, we found that the difference in 6MWD between the two groups reached the minimal clinically important difference.This finding highlights the importance of respiratory muscle strength in maintaining adequate oxygenation in PH. The underlying mechanisms may involve mitochondrial metabolism, key proteins, skeletal muscle morphology alterations, and skeletal muscle microcirculation. Correcting these functional disturbances will alleviate respiratory muscle endurance and strength deficits, ultimately improving exercise intolerance in patients with PH. Therefore, the patients who have impaired MIP, respiratory muscle training should be considered. This intervention aims to enhance exercise tolerance via increasing the V/Q ratio and respiratory muscle O2 saturation. However, MIP did not correlate with other clinically significant parameters, suggesting its limited value in predicting disease severity or guiding treatment decisions in this population. Further research is necessary to investigate the potential role of MIP as a complementary tool in assessing respiratory function and guiding management strategies in PH. Table 1 Table 2 Correlation anlysis