Urinary cGMP concentrations in severe primary pulmonary hypertension

BACKGROUND Prognostic evaluation of patients with primary pulmonary hypertension (PPH) requires right heart catheterisation. The development of accurate non-invasive methods for monitoring these patients remains an important task. Cyclic guanosine monophosphate (cGMP) is an indicator of the action of natriuretic peptides and nitric oxide on target cells. Plasma and urinary cGMP concentrations are raised in patients with congestive heart failure in whom they correlate closely with haemodynamic parameters and disease severity. The aim of the present study was to determine whether the urinary concentration of cGMP could be used as a non-invasive marker of haemodynamic impairment in patients with severe PPH. METHODS Urinary cGMP concentrations were measured in 19 consecutive patients with PPH, seven with acute asthma, and 30 normal healthy controls. RESULTS Patients with PPH had higher urinary cGMP concentrations than asthmatic patients or normal healthy controls (p = 0.001). Urinary cGMP concentrations were higher in patients with severe haemodynamic impairment—that is, those with a cardiac index (CI) of ⩽2 l/min/m2 (p = 0.002)—and urinary cGMP concentrations were inversely correlated with CI (r = –0.69, p = 0.002) and venous oxygen saturation (r = –0.65, p = 0.003). CONCLUSION Urinary cGMP concentrations may represent a non-invasive indicator of the haemodynamic status of patients with severe PPH.

[1]  B. Puschendorf,et al.  Is measurement of cyclic guanosine monophosphate in plasma or urine suitable for assessing in vivo nitric oxide production? , 1998, Circulation.

[2]  P. Poole‐Wilson,et al.  Value of natriuretic peptides in assessment of patients with possible new heart failure in primary care , 1997, The Lancet.

[3]  B. Groves,et al.  A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. , 1996, The New England journal of medicine.

[4]  F. Murad,et al.  Nitric Oxide and Cyclic GMP Signaling , 1996, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[5]  S. Rich,et al.  Neurohormonal activation in patients with right ventricular failure from pulmonary hypertension: relation to hemodynamic variables and endothelin levels. , 1995, Journal of the American College of Cardiology.

[6]  R. Frydman,et al.  Urinary cGMP levels during pregnancy with and without uterine contractions. , 1995, European journal of obstetrics, gynecology, and reproductive biology.

[7]  K. Kugiyama,et al.  Localization and Mechanism of Secretion of B‐Type Natriuretic Peptide in Comparison With Those of A‐Type Natriuretic Peptide in Normal Subjects and Patients With Heart Failure , 1994, Circulation.

[8]  F. Brénot Primary pulmonary hypertension. Case series from France. , 1994, Chest.

[9]  J. Mair,et al.  Clinical significance of urinary cyclic guanosine monophosphate in diagnosis of heart failure. , 1994, Clinical chemistry.

[10]  W. MacNee,et al.  Atrial natriuretic peptide in stable and decompensated chronic obstructive pulmonary disease. , 1993, Thorax.

[11]  S. Rich,et al.  The effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. , 1992, The New England journal of medicine.

[12]  B. Groves,et al.  Atrial natriuretic peptide and urinary cyclic guanosine monophosphate in patients with chronic heart failure. , 1992, Journal of the American Society of Nephrology : JASN.

[13]  E H Bergofsky,et al.  Survival in Patients with Primary Pulmonary Hypertension: Results from a National Prospective Registry , 1991 .

[14]  J. Mair,et al.  Release of cyclic guanosine monophosphate evaluated as a diagnostic tool in cardiac diseases. , 1991, Clinical chemistry.

[15]  A. Morice,et al.  Atrial natriuretic peptide in primary pulmonary hypertension. , 1990, The European respiratory journal.

[16]  F. Roudot-thoraval,et al.  Atrial natriuretic factor in chronic obstructive lung disease with pulmonary hypertension. Physiological correlates and response to peptide infusion. , 1989, The Journal of clinical investigation.

[17]  R. Schrier,et al.  Enzymatic and binding effects of atrial natriuretic factor in glomeruli and nephrons. , 1989, Kidney international.

[18]  R. Zimmerman,et al.  Atrial stretch, not pressure, is the principal determinant controlling the acute release of atrial natriuretic factor. , 1988, Circulation research.

[19]  O. Burghuber,et al.  Human atrial natriuretic peptide secretion in precapillary pulmonary hypertension. Clinical study in patients with COPD and interstitial fibrosis. , 1988, Chest.

[20]  D. Buff Primary pulmonary hypertension. , 1987, Annals of internal medicine.

[21]  C. Brun-Buisson,et al.  Atrial natriuretic peptide concentrations and pulmonary hemodynamics in patients with pulmonary artery hypertension. , 1987, The American review of respiratory disease.

[22]  E H Bergofsky,et al.  Primary pulmonary hypertension. A national prospective study. , 1987, Annals of internal medicine.

[23]  T. Carr,et al.  Proton magnetic resonance imaging to stage activity of interstitial lung disease. , 1987, Chest.

[24]  H. Imura,et al.  Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function. , 1987, Circulation.

[25]  O. Kohmoto,et al.  Plasma concentrations of α-human atrial natriuretic polypeptide and cyclic GMP in patients with heart disease , 1987 .

[26]  O. Kohmoto,et al.  Plasma concentrations of alpha-human atrial natriuretic polypeptide and cyclic GMP in patients with heart disease. , 1987, American heart journal.

[27]  S. Hunt,et al.  Heart-lung transplantation: successful therapy for patients with pulmonary vascular disease. , 1982, The New England journal of medicine.

[28]  A. Broadus,et al.  Kinetic parameters and renal clearances of plasma adenosine 3',5'-monophosphate and guanosine 3',5'-monophosphate in man. , 1970, The Journal of clinical investigation.