BACKGROUND: Non-cirrhotic portal fibrosis (NCPF) is an important cause of portal hypertension (PHT) and variceal bleeding, especially in the developing countries. While the hepatic parenchyma and liver functions are normal, the patho-anatomic defect in these patients is pre- and peri-sinusoidal in nature. AIM: To study the systemic and pulmonary hemodynamic alterations in patients with NCPF and compare them with compensated cirrhotic patients. PATIENTS AND METHODS: Patients with NCPF (n = 20, mean age 29.3 +/- 9.8 year) and matched Child's A cirrhotic patients (n = 17, age 34.1 +/- 9.8 year) who had bled in the past, underwent hemodynamic measurements using a balloon tipped catheter. RESULTS: In NCPF patients, the hepatic venous pressure gradient (HVPG) was significantly lower than in the cirrhotic patients (4.9 +/- 1.5 mmHg vs. 15.7 +/- 4.5 mmHg; P < 0.01). NCPF patients had hyperdynamic circulation and peripheral vasodilatation comparable to cirrhotic patients; cardiac output (8.0 +/- 1.2 l/min vs. 8.4 +/- 1.9 l/min; P = 0.4), cardiac index (5.4 +/- 0.8 l/min/m(2) vs. 5.5 +/- 1.9 l/min/m(2); P = 0.86), mean arterial pressure (88.2 +/- 14.1 mmHg vs. 89.9 +/- 17.3 mmHg; P = 0.73), systemic vascular resistance (852.8 +/- 204.3 dynes . s/cm(5) vs. 854.1 +/- 189.9 dynes . s/cm(5); P = 0.98) and pulmonary vascular resistance (41.6 +/- 18.1 dynes . s/cm(5) vs. 41.3 +/- 17.9 dynes . s/cm(5); P = 0.95) were comparable in the two groups. CONCLUSIONS: NCPF associated portal hypertension leads to a hyperdynamic state with high cardiac index and low systemic and pulmonary vascular resistance comparable to compensated cirrhosis. These novel observations suggest a primary role of portal hypertension in the development of hyperdynamic state.
BACKGROUND: Non-cirrhotic portal fibrosis (NCPF) is an important cause of portal hypertension (PHT) and variceal bleeding, especially in the developing countries. While the hepatic parenchyma and liver functions are normal, the patho-anatomic defect in these patients is pre- and peri-sinusoidal in nature. AIM: To study the systemic and pulmonary hemodynamic alterations in patients with NCPF and compare them with compensated cirrhotic patients. PATIENTS AND METHODS: Patients with NCPF (n = 20, mean age 29.3 +/- 9.8 year) and matched Child's A cirrhoticpatients (n = 17, age 34.1 +/- 9.8 year) who had bled in the past, underwent hemodynamic measurements using a balloon tipped catheter. RESULTS: In NCPF patients, the hepatic venous pressure gradient (HVPG) was significantly lower than in the cirrhotic patients (4.9 +/- 1.5 mmHg vs. 15.7 +/- 4.5 mmHg; P < 0.01). NCPF patients had hyperdynamic circulation and peripheral vasodilatation comparable to cirrhotic patients; cardiac output (8.0 +/- 1.2 l/min vs. 8.4 +/- 1.9 l/min; P = 0.4), cardiac index (5.4 +/- 0.8 l/min/m(2) vs. 5.5 +/- 1.9 l/min/m(2); P = 0.86), mean arterial pressure (88.2 +/- 14.1 mmHg vs. 89.9 +/- 17.3 mmHg; P = 0.73), systemic vascular resistance (852.8 +/- 204.3 dynes . s/cm(5) vs. 854.1 +/- 189.9 dynes . s/cm(5); P = 0.98) and pulmonary vascular resistance (41.6 +/- 18.1 dynes . s/cm(5) vs. 41.3 +/- 17.9 dynes . s/cm(5); P = 0.95) were comparable in the two groups. CONCLUSIONS: NCPF associated portal hypertension leads to a hyperdynamic state with high cardiac index and low systemic and pulmonary vascular resistance comparable to compensated cirrhosis. These novel observations suggest a primary role of portal hypertension in the development of hyperdynamic state.