Pharmacologic testing of the reversibility of an increased pulmonary vascular resistance before heart transplantation with prostaglandin I-2 (prostacyclin)

Citation
M. Trautnitz et al., Pharmacologic testing of the reversibility of an increased pulmonary vascular resistance before heart transplantation with prostaglandin I-2 (prostacyclin), Z KARDIOL, 88(2), 1999, pp. 133-140
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
ZEITSCHRIFT FUR KARDIOLOGIE
ISSN journal
03005860 → ACNP
Volume
88
Issue
2
Year of publication
1999
Pages
133 - 140
Database
ISI
SICI code
0300-5860(199902)88:2<133:PTOTRO>2.0.ZU;2-K
Abstract
An increased pulmonary vascular resistance (PVR) or an increased transpulmo nary gradient (TPG) is a risk factor for increased 3-day and 3-month mortal ity after heart transplantation (HTx). The reversibility of increased PVR o r TPG under pharmacologic testing is supposed to indicate a decreased proba bility of right ventricular failure/death after transplantation. We tested the response of an increased PVR (> 2.5 Wood units, WU) and/or of an increa sed TPG (> 15 mm Hg) in 29 right heart catheterizations (thermodilution cat heter) of 23 patients (51 +/- 8 years, mean NYHA-class 3.1 +/- 0.6, ischemi c n = 8, dilated cardiomyopathy n = 15). Increasing doses of prostaglandin I-2 (PGI(2), mean maximum dose 13.5 +/- 6.4 ng/kg/min) were applied stepwis e over at least 10 min at the maximum dose level. We analyzed any dependenc e of the reversibility of PVR and TPG under prostaglandin I-2 on hemodynami c values, echocardiographic parameters, demographic data, and laboratory fi ndings. A decrease of PVR to a range usually accepted as no contraindicatio n for HTx (less than or equal to 4 WU) was found in each patient without sy mptomatic systemic hypotension during application of PGI(2) (baseline value : 4.7 +/- 1.3 WU, during PGI,: 2.3 +/- 0.6 WU). An unresponsive, fixed incr eased PVR or TPG was not observed using PGI(2). In 62% of investigations, b oth PVR and TPG decreased below 2.5 WU and 15 mm Hg, respectively. The exte nt of reversibility of PVR and TPG was individually different and did not d epend on the mean pulmonary artery pressure, mean capillary wedge pressure, cardiac output, mean systemic artery pressure or echocardiographic paramet ers (EDD, FS, ES-distance), sodium, urea or bilirubin levels, medication, a ge of the patients or the duration of the disease. The baseline PVR correla ted inversely with its percentile value during PGI(2) (r = -0.76, p < 0.05) . Tn advanced heart failure, PGI(2) decreases PVR in ranges of lower risk c oncerning orthotopic HTx, without causing an intolerable systemic hypotensi on. The individual extent of reversibility of PVR and TPG under PGI, is not influenced by basic hemodynamic parameters or the patient's demographic pr ofile.