Is overactivity of the sympathetic system demonstrable in Syndrome X?

Is overactivity of the sympathetic system demonstrable in Syndrome X?

S122 Abstracts W e d n e s d a y a f t e r n o o n , A p r i l 26, 1995 P22-485 P22-487 DIAGNOSIS OF CARDIAC SARCOIDOS1S BY I-123 MIBG AND TL-201 ...

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S122

Abstracts W e d n e s d a y a f t e r n o o n , A p r i l 26, 1995

P22-485

P22-487

DIAGNOSIS OF CARDIAC SARCOIDOS1S BY I-123 MIBG AND TL-201 SPECT IMAGING. Haruto Fujioka, Satoshi O h a s h i , Keiko Kobayashi, Chic Hatsumi, Naoaki T a m u r a , Hiroyuki Sato, Hiroshi Yzmlaguclti. Cardiology, Internal Medicine, J u n t e n d o University School of Medicine, Tokyo, JAPAN. Tile major(77%) c a u s e of d e a t h in s a r c o i d o s i s pattents(pts) is c a r d i a c event in J a p m l . On the o l h e r h a n d , primaaN c a r d i a c involvement is not oRen recognized clinically, a l t h o u g h it may b e d e m o n s t r a t e d a t a u t o p s y in 2 0 - 3 0 % of c a s e s of s a r c o i d o s i s , m a s t of w h t e h d e m o n s t r a t e generalized s a r c o i d o s i s . It is useful to k n o w the p r e s e n c e of c a r d i a c s a r c o i d o s i s ( C S ) in the em'ly p h a s e , b e c a u s e t h i s d i s e a s e is c a p a b l e of In'eating. In fltis s t u d y , we investigate file u s e f u l n e s s of I-123 MIBG(MIBG) mid TI-201{TI) SPECT in d e t e c t i n g CS. All pts(n=30, male; 11 } were d i a g n o s e d .as s a r c o i d o s i s by hilar l y m p h o a d e n o p a t h y or b y uveitis. 111MBq of MIBG a n d TI were injected at r e s t a n d d u a l SPECT i m a g i n g w a s done. Exteni score(ES) a n d severity score(SS) were c a l c u l a t e d u s i n g norn~l bull's eye lnap, all(:[ c o m p a r e d to r e s u l t s of echocardiogrtui~ (UCG) electrocardtogram(ECG) a n d Holter ECG (Holter). 3 0 pts were divided into 2 g r o u p s . Pts in g r o u p A (n=l l) h a d abnornhalittes in E C G o r Holter, pts in g r o u p B /n=19) did not h a v e either. All pts in g r o u p A revealed a h n o r m a l a c c u m u l a t i o n of both MIBG a n d TI, a n d only 3 of t h e m h a d UCG abnornh31ities. In g r o u p B, 2 pts h a d a b n o r m a l a c c u m u l a t i o n ol TI, 10 pLs h a d that of MIBG. The former 2 pts were i n c l u d e d m the latter 10 pts. N o b o d y in this grotq~ h a d rely UCG a b n o r m a l i t y . "From c a l c u l a t e d ES a n d SS (both MIBG a n d TI), nificanfly high s c o r e s were recognized in g r o u p A, in both a n d SS, w h e r e a s r e m a i n e d low in g r o u p B on lhe average. T h o u g h , i n g r o u p B, a few pts h a d significa3~tly high s c o r e s , almost e q u a l to those in g r o u p A. In g r o u p A, ES a n d SS of MIBG t e n d e d to h e high, c o m p a r e d to those of Ti. We recognized s c i n t i g r a p h i c a b n o r m a l i t i e s in all pts who h a d ECG a b n o r m a l i t i e s , a n d also recognized h i g h ES a n d SS in a few pts who did not d e m o n s t r a t e a b n o r m a l ECG. S c i n t i g r a p h i c a b n o r m a l i t i e s , TI is of c o u r s e b u t e s p e c i a l l y M[BG, have possibilities to indicate m y o c a r d i a l i n v o l v m e n t b y s a r c o i d o s i s w h i c h is not able to b e d e t e c t e d b y UCG, ECG or Holter.

Assessment of Diastolic Filling Reveals Early Cardiotoxicity Following Bone Marrow Transplantation. SS. Lele, I'lL Thomson, J$. Atherton, FA. Khafagi, ST Durrant, MP. Frenneaux. Royal Brisbane Hospital, Brisbane, Australia

P22 -486

P22-488

Venoennstriction during Lower Body Negative Pressure in Patients with Neurocardiogenic Syncope H L Thomson, S S Lele, J Atherton, K N Wright, G W Muehle, W J McKenna, M P Frenneaux, Departments of Cardiology Royal Brisbane Hospital Brisbane Australia, and St George's Hospital London U.K.

IS OVERACTIVITY OF SYSTEM DEMONSTRABLE

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W E D N E S D A Y P M A P R I L

JOURNAL OF NUCLEAR CARDIOLOGY M a r c h / A p r i l 1995, P a r t 2

Background: We tested the hypothesis that in patients with neurocardiogenic syncope(NCS) there may be a failure of venocoastriction in response to central volume unloading and that this may be a primary abnormality leading to an empty hypercontractile ventricle proposed as the substrate for NCS.. Patients and Method: 16 patients with NCS and abnormal tilt table tests ( 12 male and 13 female age 23-70 mean 45.5 years) and 20 healthy controls with normal tilt table tests (15 male 5 female age 25-70 mean 42.2years ) were studied. We evaluated the forearm venous pressure-volume relationship as a measure of forearm venous tone using a nuclear technique before and during the application of subhypotensive lower body negative pressure(LBNP)(20 mm Hg) Results(expressed as mean + SD): LBNP caused a reduction in venous volume at all venous occluding pressures of 11 +5% compared with baseline in controls vs a mean reduction of 10+7% in patients (p =NS), In one patient LBNP caused an increase in venous volume of 9%. Conclusions: For the group as a whole, forearm venous tone increased normally during subhypotensive LBNP in patients with NCS. The observation of a paradoxical venodilator response in one patient during LBNP(present at 10 and 20 mm Hg LBNP ( sub hypotensive) suggests a primary abnormality of venous control may be present in a subset, deserving study in a larger series.

We hypothesized that abnormalities of diastolic filling during exercise may be an early feature of late anthracycline cardiotoxicity. We assessed 25 consecutive patients surviving one year following bone marrow transplantation (BMT) and 10 age matched controls using radionuclide ventricalography during semi erect cycle exercise. 6 patients had received anthracyclines and melphalan(Group I), 9 cyclophosphamide alone (Group /I) and 11 anthracycline and cyclophosphamide(Group~ prior to BMT. Results Ejection fraction was similar at rest and at peak exercise in the controls and patients (564-5.9 vs 55.54-10.9% p NS at rest and 69.2.-+6.9 vs 62.44-12.3% p NS at peak exercise respectively ). Peak filling rate was similar at rest and at peak exercise in the two groups (3.04.0.7 vs 3.3=1:1.4 EDV/s p NS at rest and 7.8a:1.9 vs 6.34-2.7EDV/s p NS at peak exercise ). TTPF was slightly prolonged at rest in patients compared to controls (133~:28 vs 1844-72 ms p=0.04) and at peak exercise was markedly longer in patients (140.44-39.2 in patients vs 634.38.2 c:ontrols p<0.0001 ). There was a loss of the normal inverse relationship between "[q"PF and HR ( r=0.78 p<0.05 in controls vs r ~ . l l p NS in patients) implying the development of diastolic dysfunction during exercise in some patients. In group I patients TTPF was prolonged at rest and during exercise but fell in all patients during exercise, ha group II patients resting TrPF was normal but increased paradoxically during exercise in one patient and the decrease in TTPF in the remaining patients was markedly attenuated. In group III patients resting TrPF was prolonged and rose on exercise in 3 patients. Conc/us/oNs. The combination of cyclophosphamide and anthracycline produces specific abnormalities of exercise diastolic filling which is known to carry a greater risk for late cardiotoxicity.

THE SYMPATHETIC IN S Y N D R O M E X ?

SD Rosen, S Guzzetti, A Dritsas and PG Camici, M R C Clinical Sciences Centre, RPMS, Hammersmith Hospital, London, UK. Excessive activation of the sympathetic nervous system (SNS) has been suggested as an aetiological factor in syndrome X (SX, anginal pain, ischaemic-like stress ECG and normal coronary arleriogram). To test this hypothesis, we measured and assessed the correlations amongst: plasma catecholamines, corrected maximum resting QT interval (QTc-max), myocardial B-adrenoceptor (gAR) density (using PET with 11C-CGP-12177) and frequency domain parameters of heart rate variability (HRV). Pooled data from 18 SX patients [age, mean (SD), 58 (9) years, range 33-69] was compared to that from 20 controls [(2, age 44 (13) years, range 21-77]. Plasma noradrenaline (NA) was higher in SX than C [2.90 (1.03) vs 1.86 (0.85) riM; p<0.01]. QTc-max was prolonged in SX compared to C [439 (33) ms vs 417 (21) ms, p<0.01]. BAR was non-significantly lower in SX [7.88 (1.92) vs 8.76 (2.06) pmol/g]. Amongst the HRV data, the night-time (midnight to 6 am) decline in the low frequency (LF, ~0.10 Hz) c o m p o n e n t found in C was absent in SX [42(2) normalized units (nu) vs 50(3) nu; p<0.05]. In conclusion: These data confirm that there is altered cardiovascular autonomic regulation in syndrome X, with enhanced sympathetic activation, detectable by the non-invasive methods described.