European journal of internal medicine · 2013
NT-proatrial natriuretic peptide as a possible biomarker of cardiopulmonary involvement in sarcoidosis.
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Magrì Damiano, Agostoni Piergiuseppe, Ricotta Agnese, Pisani Lara, Cauti Filippo Maria, Onofri Alessandro, Bruno Pierdonato, Ricci Alberto, Volpe Massimo, Marchitti Simona, Mariotta Salvatore, Rubattu Speranza
Аннотация
BACKGROUND: Lung diffusion for carbon monoxide (DLCO) has been shown to associate with the risk of pulmonary arterial hypertension development and, most likely, with right ventricular (RV) myocardial dysfunction in sarcoidosis patients. Besides its known role as a marker of left ventricular dysfunction, experimental evidence suggests a role of NT-proAtrial Natriuretic Peptide (NT-proANP) also in modulating pulmonary circulation. We therefore investigated possible relationships between NT-proANP, lung diffusion impairment and RV dysfunction.
METHODS: Thirty-two pulmonary sarcoidosis outpatients and eighteen volunteers underwent full clinical assessment, including full lung function tests and Doppler echocardiography integrated with tissue Doppler imaging (TDI) study. Resting circulating NT-proBNP and NT-proANP plasma levels were also determined.
RESULTS: NT-proANP and RV-myocardial performance index (RV-MPI) were significantly higher in those patients with the greatest DLCO impairment, whereas no differences were found for NT-proBNP values. At multivariable analysis, only DLCO (β: -0.496; standard error: 3.38; p=0.000) and RV-MPI (β: 0.373; standard error: 6.56; p=0.031) remained significantly associated with NT-proANP levels.
CONCLUSIONS: Our finding may support a key role of NT-proANP in the complex mechanisms underlying modulation of lung function. An early increase in pulmonary vascular resistance may stimulate NT-proANP increase, thus explaining its association with signs of early RV myocardial dysfunction. This hypothesis warrants further confirmation.
METHODS: Thirty-two pulmonary sarcoidosis outpatients and eighteen volunteers underwent full clinical assessment, including full lung function tests and Doppler echocardiography integrated with tissue Doppler imaging (TDI) study. Resting circulating NT-proBNP and NT-proANP plasma levels were also determined.
RESULTS: NT-proANP and RV-myocardial performance index (RV-MPI) were significantly higher in those patients with the greatest DLCO impairment, whereas no differences were found for NT-proBNP values. At multivariable analysis, only DLCO (β: -0.496; standard error: 3.38; p=0.000) and RV-MPI (β: 0.373; standard error: 6.56; p=0.031) remained significantly associated with NT-proANP levels.
CONCLUSIONS: Our finding may support a key role of NT-proANP in the complex mechanisms underlying modulation of lung function. An early increase in pulmonary vascular resistance may stimulate NT-proANP increase, thus explaining its association with signs of early RV myocardial dysfunction. This hypothesis warrants further confirmation.