To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
To determine the possible role of atrial natriuretic factor in right ventricular infarction, serial measurements of this hormone were performed in 21 patients with acute inferior myocardial infarction. All patients underwent enzymatic, electrocardiographic, echocardiographic and coronary arteriographic studies. Ten patients also had right heart hemodynamic measurements. Eight patients had evidence of an associated right ventricular infarction (Group I) and 13 patients did not (Group II). Enzymatically estimated infarct size, presence of left heart failure and arrhythmias were similar in both groups. Mean arterial pressure in Group I (72.1 +/- 4.4 mm Hg) was significantly lower (p = 0.02) than in Group II (89.5 +/- 4.6 mm Hg). Seven (88%) of the eight patients in Group I had elevated right atrial pressures and a higher incidence than Group II of prolonged hypotension (75%) and right ventricular dysfunction (75%) clinically and by echocardiography. Plasma atrial natriuretic factor levels (mean values +/- SEM in pg/ml) for days 1, 2, 3 and 7 after infarction were, respectively: 152 +/- 30, 165 +/- 48, 199 +/- 27 and 189 +/- 31 for Group I versus 55 +/- 9, 55 +/- 11, 61 +/- 13 and 77 +/- 20 for Group II. The difference between groups was significant for days 1 (p less than 0.05), 3 and 7 (p less than 0.01) and not significant for day 2 (p = 0.07). These findings show that atrial natriuretic factor elevation is part of the neurohumoral response to right ventricular infarction and are consistent with the hypothesis that atrial natriuretic factor may play a pathophysiologic role in the right ventricular infarct syndrome.
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