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Editorial

Phosphodiesterase Type 5 Inhibition

A Support of the Left Ventricular Assist Device Bridge to Transplant

Marc J. Semigran, MD

From the Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Marc J. Semigran, MD, Heart Failure and Cardiac Transplantation Unit, Massachusetts General Hospital, Bigelow 800, Fruit Street, Boston, MA 02114. E-mail msemigran@partners.org

Key Words: heart-assist device • heart failure • pulmonary heart disease • transplantation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The development of right heart failure has been a clinical concern of physicians caring for patients after cardiac transplantation since the inception of the field.¹ Although the problem of "fixed" pulmonary vasoconstriction that does not respond to the reduction of left ventricular filling pressure seems to have diminished since the early days of transplantation, there are still some patients in whom this remains a problem. Data from the International Society of Heart Transplantation Registry suggests that right ventricular (RV) dysfunction accounted for 50% of all cardiac complications and 19% of all early deaths among heart transplantation patients,² with persistent pulmonary vasoconstriction a major contributing factor to early RV dysfunction. The cause of the increase in vasoconstriction is unknown, although it may be a result of humoral factors, including cytokines, promoting changes in vascular smooth muscle gene expression. The hallmark of this problem is a lack of sensitivity to endogenous and exogenous vasodilators, be they nitric oxide (NO) released from pulmonary vascular endothelium or exogenous agents acting through NO, endothelin, or prostaglandin signaling pathways.³ Heart failure patients with fixed pulmonary hypertension can be disqualified from consideration for transplant surgery, given their worse prognosis for early survival. One alternative for these patients is to attempt to reverse the vasoconstriction with a combination of pharmacological agents and reduction of one of the presumed stimuli to vasoconstriction, an elevated pulmonary venous pressure. Variable success in reducing "fixed" pulmonary vasoconstriction has been reported with the use of inotropes such as milrinone and dobutamine in combination . . . [Full Text of this Article]