Adatia, Ian

Atz, Andrew M.

Wessel, David L.

Elsevier - Publisher Connector 

Pulmonary vascular response to oxygen and inhaled nitric oxide 

JACC February 1996 ABSTRACTS- Oral 325A 
hess (WT; external diameter - -  Internal diameter,'extemal diameter), number 
of layers, and measurements of the !ntima, media, and adventitia~ All PH pa- 
t/onto had > 2 visible layers, whereas no control patient had a visible intima 
Patients with PH had a thicker media (0.32 ~ 0.17 vs 0.15 ± 0.01 mm, p < 
0.05) and %WT (29 ± 3 vs 16 4- 2%, p < 0.05) than contnois, We conclude 
that IVUS allows for direct visualization of structural changes in small pul- 
monary arteries in patients with PH and may complement hemodynarni¢ and 
pulmonary wedge angiogmphy evaluation in these patients. 
4:15 
r~8--2-~ Pulmonary Response to Oxygen and Vascular 
Inhaled Nitric Oxide 
Andrew M. Nz, lan Adatie, David L. Wessel. Children's Hospital, Harvard 
Medical School, Boston, MA 
We compared the effects of known inhaled pulmonary vasodilate~s, oxygen 
(02) and tnhabd nitric oxide (INO) in 58 pulmonary hypertensive patients at 
cardiac catheterization. In 42, measurements were made at room air (RA), 
100% 02, return to RA, and with INO (80 ppm at RA). Results (mean :l: 
SEM): 
n = 42 PAp PVR BP SVR 
*p < 0.05 ..m. mHg U.m 2 mmH 0 U.rr~ 
RA 64.1±3.5' 17.8±2.3 78±2.3 23.6-4-1.7 
02 55.7 ~: 3.4 11.44.1.6" 80 ± 2.4 24.8:1:1.6 
RA 61.9±3.6 18.3±2.4 78~2.6 23.6 :E 1.8 
NO+RA ~'~.0 + 3.2" 12.0±1.8" 78±2.7 24.7:t:1.8 
A reduction in PVR of _> 20=/o was considered responsive. A response Was 
seen in 35/42 with 02 alone. Of the 7 nonresDondars, 3 showed a response 
to NO + RA, In the NO + RA group, response was seen in 29142 with 9 of the 
13 nonrespondere respondl~ to 02. An additional 16 patiente were studied 
while olt supplemental 02 (FiO2 0.4-0.95). The addition of INO at 80 ppm 
caused.additional pulmonary vasodilation i  14/16 (12 with • 20% reduction 
in PVR). Results (mean • SEM): 
n = 16 PAp (mmHg) PVR (U:m 2) 
02 6,?..2 ± 4.9 ~1.1 ± 3.8 
NO + 02 S3.6 :t: 4.9 15.34- 3.4 
Conclusion. INO and 02 ere both effective pulmonary vesedllalors, Com- 
bination therapy can produce additional vasodilation, This suggests that the 
most comprehensive and specific t~ting of pulmonary vasoreactivity should 
include combination treatment with INO and supplemental 02. 
4:30 
~-~ Aerolized Prostscyclin (aePGl=) for Preoperative 
Evaluation and Postoperative Treatment of 
Pulmonary Hypertension (PHT) 
Ingrem Schulze-Nelck, Frank Uhlemann, Jan NOmbefg, Felix Berger, 
Christian Opilz 1, Franz X, Kleber ~, Peter E. Lange. German Heart Institute, 
Bert/n, Germany; t Cardiovascular Catheterization Laboratory, Humboldt 
Un'~emity, Berlin, Germany 
We examined the effects of aePGl~ in patients with PHT as an alternative 
to inhaled nitric oxide (/NO), Dudng routine catheterization for evalu~.~, n of 
pulmonary vesoreactivity, aePGI2 versus/NO was compalred In 9 cyanct~ 
patients with congenital intmcardiae shunting lesions and 3 patiante w'dh 
primary PIN', who inhaled aePQI2 during spontaneous breathing (patient 
group A). AePGI~ was used postopsretively in 3 patien~3~, In whom ongoing 
iNO-Therepy for PHT or right vantricalar ¢,'ysrunction had to be in tem~ for 
technical reasons (patient group B), These ventilated patients had pamisting 
PHT after termination of INO therapy. No acute side effects escun'ed in either 
group. Group A: 5/12 patients howed no vasorea¢tivity. In2/3 patients with 
primary PHT, ~ ~ignifk:~nt drop in pulmonary arte~ resistance occured (-33 
:E 12%) with crmcommitant increase in cardiac output. In 5/9 patients with 
shunt lesions, tho relative puknor,ay vascular esistance (Rp:Rs) d~¢masnd 
with INO from 96:1= 32% to 62 =1= 33% systenlin resistonce, and to ER :E 
41% systemic resistance with aePGl,~ (p < 0.02). Thus, aePGl= showed a 
ma~ked effect in 7/12 patients and in all pa~ente whom/NO w~s elfective. 
Group B: Cardiac index (+21 + 17%), systemic oxy~#,-~lon and left a~l  
pressure Impreved; se~tml vanous i~ssum and pulmonary artmy p , -~ 
(-45:1: 19%) dacroesed 2 rain aftor applloat~n of aePGl~ and remalnod 
tow 20-30 rain a~er appr~ w~ stopped. AePG~ ~ pulmon~ 
vascular e~mnse ancl impmvad caro~ac funcUon. Thla etast,~esmed to be 
sek~tve, and vms comparaMa to iNO. Tl'mmfom. aePGle seukhm~,-~;ant • 
crmicaify useful agemalim to iT~O. FB1hm studies wgl have te evaluate the 
benelgs of either ; ~ c  ~',at=gy. 
4:45 
~ - ]  H emodynam|c and Histologic Evaluation of the 
Pulmonary Vascular Bed and Clinical Outcome in 
ChildrenWit. h Congenital Heart Disease (CHD): is 
m nero a uold Stanoard? 
R.M.F. Berger, C.A. Wagenvoort, R.J. van Suylen, J. Hess. Sophia 
Children's Hospital/Universily Hnsp#al Rotterdam, The Nethedands 
Hemudynamic and histologic data of a selected group uf 52 children (2.6 :l: 
4.4 ym) with compax CHD were assessed to determine the relation between 
tung morphology and hemodynamlo data, and outcome. Pulmonary artery 
pressures (PAP) showed significant correlations with medial hypertrophy and 
musculansatlon of artedoles, however, the correisUon coefficients were all 
< 0.5. Pulmonanj bloodflow, shuntsize, the ratio of pulmonary (Rp) to sys- 
temic (Rs) vascular esistance were not correlated with histology. Concentric 
laminar intimal fibrosis (CLIF), dilatation lesions (DL), fibrinoTd necrosis (FN) 
and plexitorm lesions (PL) were not present in cases with diastolic PAP < 
25 mmHg or Rp < 6 WU.m 2. In patients with diast. PAP > 25 mmHg or 
Rp • 6 WU.m ~ vascular changes could not be predicted accurately from 
hemodynemic data, including mspons to vasedilatom. Short-term outcome: 
45 patients were opatated, 16 died pedoperatively, 12 in relation to acute 
pulmonary hypertensive crises (APHC). These children showed increased 
medial hypedrephy and musculadsation i  mlaltrm to the sundvere (p = 
0.003). The occurence of APHC was not correlated with any of the homo- 
dynamic parameters. Mid-term ~me:  17 patiente died unrelated to oper- 
ation, 16 without signs of pulmonary vascular disease (PVD). One patient, 
who showed "utffavoureble" hemodynamlca, but only medial hypertrophy 
of arteMes and veins, died of progressive PVD. 19 patients were still alive 
(fo!l~'~'-t,'p 57• 29 month:). 6 showed s~gns of PVD. OdginN hemodynBmic 
d~ta did not differ signif'mantiy npatients with or without PVD. DL and PL 
were not assoclaled with signs of PVD at foi~w up (p = 0.257). The presence 
of CLIF (p = 0.027) or FN (p = 0,037) was associated with PVD at follow up, 
however the predictive value was low. 
Thus, although diasL PAP < 25 mmHg or Rio < 6 WU.m ~ predict favourabte 
lung histology with respect o long term prognosis, they do not predict risk of 
A.PMP,. In contrr,,% di~, PAP • 25 mmHg or Rp > 6 WU.n-~- do not predict 
lung histology. The value of both hemodynamic and histelogic evaluation of 
pulmena,,y vesculature is limited with respect o mid-term (5 yr) prognosis in 
the individual child. 
Pharmacology of  Clotting and Platelets 
Wednesday, March 27, 1996, 4:00 p.m.--5:00 p.m. 
Orange County Convention Center, Room 208 
4:00 
~69"~ The Extent and Mechanlam of ACT ProlongaUon 
With GPIIb/llla Blockade 
Sandeep Khurene, Darius Aliabadi, Mark Pica, Randall McPherson, Gerald 
C. "nmmi~, Robert D. Sat/an. ~lliam Beaumont Hospital Royal Oak, MI 
To assess the degree of Activated Clotting Time (ACT) prolongation at- 
tdbctable to c7E3 Fab during PTCA, we measured the ACT with and without 
different concentrations (0, 2.5, 5 and 10/~g/mL) of c7E3 added to whole 
blood of lOtS before or after PTGA (25 pts; 100 ACT obsenra~ns). The ACT 
increased by 6% for each 2.5/LghnL c7E3 (!) < 0.001 repeated measures 
ANOVA). A mere detailed analysis (mpeetod measures ANGOVA with log 
ACT as covadale) revealed that the eWect of 07E3 was more pronounced at 
h]qher baseline AGT (p < 0.02) suggesting synargy between hepadn and 
¢?~3. We also pedom~l t h ~  tTEG) on non heparin~ad 
wholo bload (n = 12) to measure the effeot of c7E3 on the dynamic otestic 
modulus ((3, dYnea.cm'a), ~, measure ot dot strength. On TEG, both the 
to davelup a "time" clot and maximal ctot strength (G) were dose dependanW 
Impaired by ¢7E3 es ~'.hown i  the tig (p < 0.001). 
Ehsdc/S:len ~on W BI~d 
. r ,~  ~ p.71~*o 
° %, .= = 
o 10n'cg~L " 
• 
.M 
- -  911 190 290 380 
mSB.INE,CT ~) 


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Pulmonary vascular response to oxygen and inhaled nitric oxide

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