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Acute pulmonary vasoreactivity test with sildenafil or nitric monoxide before left ventricular assist device implantation

Imamura, Teruhiko (författare)
University of Tokyo, Japan
Kinugawa, Koichiro (författare)
University of Tokyo, Japan
Hatano, Masaru (författare)
University of Tokyo, Japan
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Kato, Naoko (författare)
University of Tokyo, Japan
Minatsuki, Shun (författare)
University of Tokyo, Japan
Muraoka, Hironori (författare)
University of Tokyo, Japan
Inaba, Toshiro (författare)
University of Tokyo, Japan
Maki, Hisataka (författare)
University of Tokyo, Japan
Kimura, Mitsutoshi (författare)
University of Tokyo, Japan
Kinoshita, Osamu (författare)
University of Tokyo, Japan
Shiga, Taro (författare)
University of Tokyo, Japan
Yao, Atsushi (författare)
University of Tokyo, Japan
Kyo, Shunei (författare)
University of Tokyo, Japan
Ono, Minoru (författare)
University of Tokyo, Japan
Komuro, Issei (författare)
University of Tokyo, Japan
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 (creator_code:org_t)
2013-04-05
2013
Engelska.
Ingår i: Journal of Artificial Organs. - : Springer Verlag (Germany). - 1434-7229 .- 1619-0904. ; 16:3, s. 389-392
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • There has been no established medical therapy to ameliorate pulmonary hypertension (PH) owing to left heart disease (LHD-PH). It has recently been shown that the left ventricular assist device (LVAD) can improve LHD-PH and therefore has the potential to become a major bridge tool for heart transplantation (HTx). However, some patients still have persistent PH even after LVAD treatment. It is essential to demonstrate the reversibility of end-organ dysfunction, including PH, prior to implantable LVAD treatment, especially in Japan, because implantable LVAD treatment is indicated only as bridge to transplantation. Here we report a patient with LHD-PH whose PH was demonstrated to be reversible by the acute pulmonary vasoreactivity test (APVT) with nitrogen monoxide (NO) and the phosphodiesterase-5 inhibitor sildenafil. Both inhaled NO and sildenafil reduced pulmonary vascular resistance, but pulmonary capillary wedge pressure was increased by NO, which was conversely decreased under increased cardiac output by sildenafil. After the patient was listed as an HTx recipient, pulmonary vascular resistance recovered down to an acceptable range with LVAD treatment. Based on these findings, we suggest that the APVT with sildenafil may be a useful and safe tool to predict improvement of PH after LVAD treatment.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Hälsovetenskap (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Health Sciences (hsv//eng)

Nyckelord

Heart failure; Transplantation; Pulmonary hypertension; Out of proportion

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