78 results match your criteria: "Pulmonary Hypertension Clinic[Affiliation]"

The assessment of pulmonary hypertension.

Clin Chest Med

September 2001

Department of Cardiovascular Diseases, Pulmonary Hypertension Clinic, Mayo Clinic, Rochester, Minnesota, USA.

The goals of evaluating pulmonary hypertension are detection, definition of severity and the nature of the hemodynamic lesion and its consequences, diagnosis of causal or associated conditions, and determination of optimal therapy. These objectives are reliably achieved by a disciplined approach employing multiple diagnostic tools. This chapter outlines the fundamental background and guidelines for assessing pulmonary hypertension, including consideration of several new and less frequently used methods to elucidate the physiologic mechanism.

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Medical management of primary pulmonary hypertension.

Eur Respir J

November 1996

Dept of Internal Medicine IV (Pulmonary Medicine), Pulmonary Hypertension Clinic of the Vienna General Hospital, University of Vienna, Austria.

Primary pulmonary hypertension (PPH) is a poorly understood, progressive disease that is characterized by elevation of pulmonary artery pressure and vascular resistance, leading to right ventricular failure and death within 2-3 yrs after diagnosis. Based upon the concept that vasoconstriction and thrombotic occlusion of resistance vessels precipitate this process, vasodilator therapy and anticoagulation have become the main strategies for improving survival in these patients. Whereas, a few years ago, medical therapy of primary pulmonary hypertension was perceived as a bridging therapy to lung or heart lung transplantation, modes of therapy are being clinically tested at this time to offer an alternative to the surgical treatment of this disease.

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Two patients had potentially serious drug interactions (phenytoin, digoxin) that were probably attributable to changes in pharmacokinetics and pharmacodynamics caused by high-dose calcium channel blocker therapy (diltiazem) in the treatment of pulmonary hypertension. Even in the approved normal dosages for the treatment of angina and hypertension, calcium channel blockers are known to cause significant changes in the metabolism of other drugs. Currently, no data exist on the effects of the very high dosages of these drugs, administered to patients with pulmonary hypertension, on the metabolism and clearance of other agents, although, based on our experience and literature reports, recommendations for monitoring therapy can be made.

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