Atrial septostomy (AS) is a palliative treatment for right ventricular failure from severe pulmonary arterial hypertension (PAH). We sought to investigate the effect of AS, alone or combined with PAH-specific pharmacotherapy, on the survival of patients with PAH.We performed a retrospective analysis of the functional and haemodynamic changes in patients with PAH following AS, and long-term survival characteristics for the whole group and separately for the subgroup who received post-procedural pharmacotherapy. 50 procedures performed in 34 patients (mean¡SD age 35¡10 yrs) resulted in haemodynamic and symptomatic improvement in most of the patients. Only one (2%) procedure-related death occurred. Due to spontaneous closure of the defect, AS was repeated in 10 patients. In 21 patients, AS was the only form of treatment, while 11 received additional pharmacotherapy after AS. During follow-up (58.5¡38 months), 21 patients died; median survival of the group was 60 months (95% CI 43-77 months). Median survival for patients on pharmacotherapy additional to AS was 83 months (95% CI 57-109 months), which was better than that for patients with AS alone (53 months, 95% CI 39-67 months) (log-rank 6.52; p50.010).In selected patients with PAH, AS is a safe and effective intervention that exerts a beneficial impact on long-term survival. Survival appears to be improved when AS is combined with PAHspecific pharmacotherapy.

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SUMMARY Although ,t-adrenergic blocking agents reduce myocardial oxygen consumption and symptoms of myocardial ischemia in patients with coronary artery disease (CAD), propranolol has been reported to exacerbate coronary artery spasm in some patients with variant angina. To determine whether increased coronary vasomotor tone can be induced by 3-adrenergic blockade, we measured the changes in coronary vascular resistance (CVR) during cold pressor testing (CPT) in 15 patients, nine with severe CAD and six with normal left coronary anatomy, before and after i.v. propranolol (0.1 mg/kg). Coronary blood flow was measured by coronary sinus thermodilution. CVR was calculated as mean arterial pressure divided by coronary sinus blood flow. Heart rate was maintained constant at a paced subanginal rate of 95 + 5 beats/min.Before propranolol, CPT induced significant increases in coronary vascular resistance in patients with CAD (15.0 ± 2.2%, p < 0.02), but no increase in CVR in the normal patients. After propranolol, the CVR change during CPT was augmented for patients with CAD (29 ± 6%, p < 0.01) and for the normal population (9 ± 5%, NS). The potentiated increase in CVR occurred without significant changes in resting CVR or in the magnitude of the hypertensive response to CPT.We conclude that ,B-adrenergic blockade with propranolol can potentiate coronary artery vasoconstriction in some patients with CAD, possibly mediated by unopposed ct-adrenergic vasomotor tone. These changes may be important in patients in whom intense adrenergic stimulation may increase coronary artery tone and adversely influence the balance between myocardial oxygen supply and demand.COMPELLING EVIDENCE suggests that myocardial ischemia may be induced by a reduction in myocardial oxygen supply due to coronary artery spasm. Primary decreases in coronary blood flow associated with abnormal coronary vasomotor reactivity have been found to occur not only in variant angina, I but also in classic and unstable angina,2 3 cold-induced angina,4 exercise-induced angina5 6 and myocardial infarction.7 8 The mechanism of such variation in coronary artery vasomotion is unknown, but several studies have implicated a central role for the adrenergic nervous system. ProtocolThe investigational protocol and consent form were approved by the Human Subjects Committee of the Brigham and Women's Hospital. After the patients gave informed consent, treatment with 3-adrenergic blocking agents was withheld for at least 12-24 hours before cardiac catheterization, and long-acting nitrate preparations were withheld for at least 6 hours before catheterization. Before coronary arteriography, all patients received 0.4 mg of sublingual nitroglycerin and six also received 0.5 mg of i.v. atropine.Fifteen minutes after completion of the diagnostic cardiac catheterization and coronary angiography, a #8F coronary sinus thermodilution pacing catheter (Wilton Webster Laboratories) was inserted into an antecubital vein and advanced under fluoroscopic guidance to the coronary sinus. The lo...

With careful monitoring, BDAS is a safe and useful palliative treatment for selected patients with severe PPH.