Current therapy of pulmonary hypertension.
Pulmonary arterial hypertension (PAH) affects vascular proliferation and remodeling in small pulmonary arteries and results in right ventricular failure and death due to a progressive increase in pulmonary vascular resistance. Recent advances in understanding of the molecular mechanisms involved in PAH suggest that endothelial dysfunction plays a major role. Impaired production of vasoactive mediators, such as prostacyclin and nitric oxide, accompanied with prolonged overexpression of vasoconstrictors such as endothelin-1, affects vascular tone and reinforces vascular remodeling. As the latter substances represent logical pharmacological targets, new drugs affecting these mechanisms have evolved during the past 2 decades and led to umpteen placebo-controlled trials in bygone years. Prognosis and quality of life of patients suffering from PAH seem to improve due to these new treatment strategies resulting in a reduction of mortality and morbidity, but there is still a substantial need for further long-term and head-to-head trials.
Baumhäkel
Magnus
M
Cremers
Bodo
B
Böhm
Michael
M
D000959:Antihypertensive Agents / Q000008:administration & dosage*; D002986:Clinical Trials as Topic / Q000639:trends*; D065128:Endothelin Receptor Antagonists; D006801:Humans; D006976:Hypertension, Pulmonary / Q000175:diagnosis / Q000628:therapy*; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage*; D010879:Piperazines; D010818:Practice Patterns, Physicians' / Q000639:trends*; D011687:Purines; D000068677:Sildenafil Citrate; D013450:Sulfones; D014665:Vasodilator Agents / Q000008:administration & dosage*
D000959:Antihypertensive Agents; D065128:Endothelin Receptor Antagonists; D010726:Phosphodiesterase Inhibitors; D010879:Piperazines; D011687:Purines; D013450:Sulfones; D014665:Vasodilator Agents; D000068677:Sildenafil Citrate