Reduction in membrane component of diffusing capacity is associated with the extent of acute pulmonary embolism

Acute pulmonary embolism (PE) often decreases pulmonary diffusing capacity for carbon monoxide (DL,CO), but data on the mechanisms involved are inconsistent. We wanted to investigate whether reduction in diffusing capacity of alveolo-capillary membrane (DM) and pulmonary capillary blood volume (Vc) is associated with the extent of PE or the presence and severity of right ventricular dysfunction (RVD) induced by PE and how the possible changes are corrected after 7-month follow-up. Forty-seven patients with acute non-massive PE in spiral computed tomography (CT) were included. The extent of PE was assessed by scoring mass of embolism. DL,CO, Vc, DM and alveolar volume (VA) were measured by using a single breath method with carbon monoxide and oxygen both at the acute phase and 7 months later. RVD was evaluated with transthoracic echocardiography and electrocardiogram. Fifteen healthy subjects were included as controls. DL,CO, DL, CO/VA, DM, vital capacity (VC) and VA were significantly lower in the patients with acute PE than in healthy controls (P<0·001). DM/Vc relation was significantly lower in patients with RVD than in healthy controls (P = 0·004). DM correlated inversely with central mass of embolism (r = −0·312; P = 0·047) whereas Vc did not. DM, DL,CO, VC and VA improved significantly within 7 months. In all patients (P = 0·001, P = 0·001) and persistent RVD (P = 0·020, P = 0·012), DM and DL,CO remained significantly lower than in healthy controls in the follow-up. DM was inversely related to central mass of embolism. Reduction in DM mainly explains the sustained decrease in DL,CO in PE after 7 months despite modern treatment of PE

Chronic thromboembolic pulmonary hypertension: epidemiology, pathogenesis and natural history

Nadciśnienie płucne zakrzepowo-zatorowe (CTEPH) to postać nadciśnienia płucnego spowodowana częściowym zamknięciem tętnic płucnych przez zorganizowane skrzepliny z często towarzyszącą przebudową drożnych oporowych tętniczek płucnych. Stanowi ono tak zwaną grupę 4 w aktualnie obowiązującej klasyfikacji nadciśnienia płucnego. Z wielu względów jest to szczególne schorzenie. Wyjątkowość CTEPH wynika z wciąż istniejących, istotnych wątpliwości dotyczących przyczyn i mechanizmu jego rozwoju, a jednocześnie - z możliwości skutecznego leczenia znacznego odsetka pacjentów metodą chirurgiczną za pomocą endarterektomii tętnic płucnych. Ten złożony zabieg może przywrócić choremu wydolność wysiłkową, jakość życia i przewidywany okres przeżycia, bardzo ograniczone w przypadku braku możliwości zastosowania swoistej terapii CTEPH.Chronic thromboembolic pulmonary hypertension (CTEPH) is a type of pulmonary hypertension induced by the partial obliteration of pulmonary arteries by organized thromboemboli, usually with coexisting remodeling of still patent pulmonary arterioles. It is compatible with group 4, according to the current classification of pulmonary hypertension. CTEPH has several peculiarities. They include persistent incertainties regarding its causes and pathogenesis, but also the possibility of highly effective surgical treatment in a significant proportion of patients by means of pulmonary endarterectomy. This complex intervention may restore exercise capacity, quality of life and life expectancy, otherwise all significantly limited by CTEPH

Centrilobular nodules in high resolution computed tomography of the lung in IPAH patients — preliminary data concerning clinico-radiological correlates

Introduction: Inhomogeneity of lung attenuation pattern is observed in high resolution chest computed tomography (HRCT) in some IPAH patients despite lack of interstitial lung disease. Such radiological changes are described either as ill-defined centrilobular nodules (CN) or as focal ground glass opacities (FGGO). There is no consensus in the literature, whether they indicate the distinct type of IPAH, or pulmonary venoocclusive disease (PVOD) with subtle radiological changes. Thus the aim of the present pilot study was to assess the frequency and clinical significance of inhomogenic lung attenuation pattern in IPAH. Material and methods: 52 IPAH patients (38 females, 14 males, mean age 41 years ± 15 years), entered the study. All available chest CT scans were reviewed retrospectively by the experienced radiologist, not aware about the clinical data of the patients. Results: CN were found in 10 patients (19%), FGGO — in 12 patients (23%). No lymphadenopathy or interlobular septal thickening suggestive of PVOD were found. The significant differences between CN and the remaining patients included: lower mean age — 31 and 43.5 years, (p = 0.02), lack of persistent foramen ovale (PFO) — 0% and 43% (p = 0.03), and higher mean right atrial pressure (mRAP) — 12.5 mm Hg and 7.94 mm Hg (p = 0.01). No significant survival differences were observed between the groups of CN, FGGO and the remaining patients. Conclusion: Centrilobular nodules in IPAH were combined with lack of PFO, higher mRAP and younger age of patients.  INTRODUCTION: Inhomogeneity of lung attenuation pattern is observed in high resolution chest computed tomography (HRCT) in some IPAH patients despite lack of interstitial lung disease. Such radiological changes are described either as ill-defined centrilobular nodules (CN) or as focal ground glass opacities (FGGO). There is no consensus in the literature, whether they indicate the distinct type of IPAH, or pulmonary venoocclusive disease (PVOD) with subtle radiological changes. Thus the aim of the present pilot study was to assess the frequency and clinical significance of inhomogenic lung attenuation pattern in IPAH. MATERIAL AND METHODS: 52 IPAH patients (38 females, 14 males, mean age 41 years ± 15 years), entered the study. All available chest CT scans were reviewed retrospectively by the experienced radiologist, not aware about the clinical data of the patients. RESULTS: CN were found in 10 patients (19%), FGGO — in 12 patients (23%). No lymphadenopathy or interlobular septal thickening suggestive of PVOD were found. The significant differences between CN and the remaining patients included: lower mean age — 31 and 43.5 years, (p = 0.02), lack of persistent foramen ovale (PFO) — 0% and 43% (p = 0.03), and higher mean right atrial pressure (mRAP) — 12.5 mm Hg and 7.94 mm Hg (p = 0.01). No significant survival differences were observed between the groups of CN, FGGO and the remaining patients. CONCLUSION: Centrilobular nodules in IPAH were combined with lack of PFO, higher mRAP and younger age of patients.

Low DLCO in idiopathic pulmonary arterial hypertension — clinical correlates and prognostic significance

INTRODUCTION: Decreased diffusing capacity of the lung for carbon monoxide (DLCO) is observed in some idiopathic pulmonary arterial hypertension (IPAH) patients, but its clinical significance is uncertain. We aimed to assess clinical correlates and prognostic significance of low DLCO in IPAH patients. MATERIAL AND METHODS: In the group of 65 IPAH patients the cut off value for low DLCO was set up based on histogram as &lt; 55% of predicted value. Demographic data, exercise capacity, lung function tests, hemodynamic parameters and survival of the patients were compared depending on DLCO value. RESULTS: Low DLCO was found in 18% of the patients, and it was associated with male sex, older age, worse functional status and exercise capacity, and higher prevalence of coronary artery disease. Low DLCO carried a 4-fold increase of death risk in 5-year perspective. CONCLUSIONS: Low DLCO was a marker of worse functional capacity and increased risk of death in studied IPAH patients.INTRODUCTION: Decreased diffusing capacity of the lung for carbon monoxide (DLCO) is observed in some idiopathic pulmonary arterial hypertension (IPAH) patients, but its clinical significance is uncertain. We aimed to assess clinical correlates and prognostic significance of low DLCO in IPAH patients. MATERIAL AND METHODS: In the group of 65 IPAH patients the cut off value for low DLCO was set up based on histogram as &lt; 55% of predicted value. Demographic data, exercise capacity, lung function tests, hemodynamic parameters and survival of the patients were compared depending on DLCO value. RESULTS: Low DLCO was found in 18% of the patients, and it was associated with male sex, older age, worse functional status and exercise capacity, and higher prevalence of coronary artery disease. Low DLCO carried a 4-fold increase of death risk in 5-year perspective. CONCLUSIONS: Low DLCO was a marker of worse functional capacity and increased risk of death in studied IPAH patients