Changes in left ventricular inflow and pulmonary venous flow velocities during preload alteration in hypertrophic cardiomyopathy

6. Pandian N, Kreis A, Hrockway B. Isner J. Sachamff A, Boleza E, Cam R, Muller D. Ulba.sound angioscopy: real-time, two-dimensional, intraluminal ul!xasound imaging of blood vessels. Am J Cardiol lY88;62:493494. 7. Hodgson JM, Graham SP, Sarakus AD, Dame SO, Stephens DN. Dhilon PS, Brands D. Sheehan H, Eberle MJ. Clinical percutaneous imaging of coronary anatomy using an over-the-wire ultrasound catheter system. Int J Card ImqLtg lY89;4:18&193. 8. Gussenhoven EJ, Essed CE, Lancce CT, Mastik F, Friccman P, van Egmond FC, Reibex J. Bosch H. van Urk H. Roelandt J, Born N. Arterial wall characteristics determined by intravascular ultrasound imaging: an in vitro study. JAm Coil Cordial 1989:14:947-952. 9. Nishimura RA, Edwards WD, Wames CA, Kc&r GS, Holmes DRJ, Tajik AJ, Yock PG. Intravascular ultrasound imaging: in vitro validation and pathologic correlation. JAm Co// Curdin/ 1990;16:145-154. 10. Potkin BN, Bxtorelli AL, Gessert JM, Nevil e RF, Almagor Y. Roberts WC. Leon MB. Coronary artery imaging with intravawlar high-frequency ultrasound. Ciradofion 19YO$l: 1575-1585. 11. Nissen SE. Grines CL, Gurley JC, Suhlett K, Haynie D, Diaz C. Booth DC. DeMatia AN. Application of n new phased-any ultraound imaging catheter in the assessment of vascular dimensions. In viva comparison to cineangiogmphy. Circularion IYYQ81:66(&65. 12. Tohis JM. Mallcry J, Mahon D, Lehmann K, Zalesky P, Griffith J. Gessert J, Moriuchi M, McRae M, Dwyer ML, Greep N, Henry W. Intravascular ultm

sound imaging of human coronary arteries in viva Analysis of tissue characterizations with comparison to in vitro histological specimens. Circularion 1991;83:913-926. 13. Mallety JA, Tobis JM. Griffith J. Gcssert J, McRae M, Moussabeck 0, Bessen M, Moriuchi M, Henry WL. Assessment of normal and atberosclcmtic arterial wall tbickne?* with an intravascular ultraound imaging catheter. Am Hean J lYYO;llY:l3Y2-1400. 14. Minw GS, Douek P. Pichard AD, Kent KM, Satler LF. Popma JJ. Leon MB. Target lesion calcification in coronary artery disease: an intravascular ultrasound study. J Am Coil Cardiol 19Y2:20:1149-1155. 15. Matar FA, Mint7 GS. Farb A, Douek P, Pichard AD, Kent KM. SatJer LF. Pop ma JJ, Keller MB, Pinnow E. Merritt AJ, Lindsay J Jr, Leon MB. The contribution of tissue removal to lumen improvement after directional coronary atberectomy. Am J Cardiol 1994;74:647650. 16. Honye J, Mahon DJ, Jain A, White CJ. Ramee SR, Wallis JB, Al-Z.&a A, Tobis JM. Morphological effects of coronary balloon angioplasty in viva assessed hy intravascular ultrasound imaging. Circularion 1992;85:1012-1025. 17. Tenaglia AN, Duller CE, Kisslo KB, Stack RS, Davidson CJ. Mechanisms of balloon angioplasty and directional coronary atberectomy as assessed hy intmcoronary ultrasound. J Am Co// Crrrdiol lYY2;20:685-69 I 18. Fitzgerald P, Potts T. Yock P. Contribution of localized calcium deposits to dissection after angioplasty. An observational study using in@avasadar ultrawxnd. Circulation 1992;86?%70.

Changes in Left Ventricular Inflow and Pulmonary Venous Flow Velocities Durin Preload Alteration in Hypertrophic Ca cp lomyopathy Takashi

Oki, Koichi

MD, Nobuo Fukuda, MD, Arata Iuchi, MD, Tomotsugu Tabata, Kiyoshige, MD, Takashi Fujimoto, MD, Kazuyo Manabe, MD, Hirotsugu Yamada, MD, and Susumu Ito, MD

ypertrophic cardiomyopathy (HC) is known to cause congestive heart failure due to left ventricuH lar (LV) diastolic dysfunction despite a normal systolic

MD,

and HC groups in age (mean age 46 + 18 and 48 ? 14 years, respectively) or percent fractional shortening of the left ventricle obtained from a transthoracic M-mode function.1-3 It is clinically important to determine the echogram (42.0 + 5.5% and 43.9 + 4.9%, respectively). severity of pulmonary congestion in this disease, and to Patients with HC were divided into 2 groups according evaluate the influence of preload aIteration.“-g Recently, to LV inflow velocity and LV end-diastolic pressure. In transesophageal pulsed Doppler echocardiography has the 30 patients in group A, LV inflow velocity showed enabled accurate recording of pulmonary venous tlow a decrease in peak early diastolic velocity and a comvelocity. This flow velocity and LV inflow velocity have pensatory increase in peak atria1 systolic velocity, and been used to evaluate hemodynamic events in the left LV end-diastolic pressure was normal or slightly eleatrium and left ventricle in various heart diseases.1c’-16 vated (14 + 4 mm Hg). In the 12 patients in group B, This study investigates the hemodynamic changes dur- LV inflow velocity showed pseudonormalization, and LV end-diastolic pressure was markedly elevated (21 + 8 ing preload alteration in HC using the 2 flow velocities, mm Hg). Three of the 12 patients in group B had LV and clarifies the mechanism of congestive heart failure outflow obstruction. due to LV diastolic dysfunction. . . . A system to apply negative and positive pressure to We evaluated 42 untreated Japanese patients with HC the lower half of the body (Toshiba Corp., Tokyo, Japan) was used. In this system, the air intake and exhaust of of the asymmetric septal hypertrophy type. The thicknesses of the ventricular septal and LV posterior walls the motor fan providing 2 m3/min of air-blasting volume at end-diastole were 215 mm and ~11 mm, respectively, are connected to a stainless steel container via an elecand their ratio was >1.3. The diagnosis of HC was con- tromagnetic valve. The lower half of the subject’s body firmed in each patient by echocardiographic demonstra- (beneath the iliac crest) was placed in the tightly sealed tion of a hypertrophied nondilated left ventricle in the stainless steel container, and lower body negative presabsence of any other cardiac or systemic disease capa- sure (LBNP) of -40 mm Hg and positive pressure ble of producing this finding. The control group con- (LBPP) of +40 mm Hg were applied. Loading condisisted of 25 subjects who had no significant organic heart tions at atmospheric pressure (0 mm Hg) defined the condisease after echocardiography and/or cardiac catheter- trol state. All subjects underwent transesophageal pulsed Doppler echocardiography to record LV inflow and pulization for chest pain, dyspnea, or precordial murmurs. There was no significant difference between the control monary venous flow velocities before and during preload alteration. We initially increased lower body pressure to +40 mm Hg, and then decreased it to 0 and -40 From The Second Deportment of Internal Medicine, Tokushimo Unimm Hg stepwise, every 3 minutes. During each stage, versity School of Medicine, 2-50 Kuromotcxho, Tokushima 770, blood pressure and heart rate were measured, and echoJapan. Manuscripr received August 2 1, 1995; revised manuscript Doppler recordings were obtained. Inter- and intraobreceived October 16, 1995, and accepted October 17. 430

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server variabilities of measurements of TAME I Heart Rote and Mean Blood Pressure During Preload Alteration pulsed Doppler indexes were calculatLBNP (-40 mm Hg) Control State LBPP (+40 mm Hg) ed as the differences in 2 measurements of the same subjects by ‘2 different Normal controls (n = 25) observers and by 1 observer divided by Heart rate (beats/min) 69i 18 68* 12 70 f 20 Mean BP (mm Hg) 92i 13 90 * 5 93* IO the mean value, respectively. They Hypertrophic cardiomyopathy were 0.5% to 1.5% for all the values. Group A (n = 30) The equipment used for transesoHeart rote (beats/min) 71 * 11 70* 14 70* 17 phageal echocardiography was a comMeon BP [mm Hg) B6* IO 86 zt 8 88 +z 7 mercially available Toshiba SSH-16OA Group B (n - 12) 67* 12 Heart rate (beots/min) 78 zt 9* 66* 10 (Toshiba Corp., Tokyo, Japan; 5 MHz 8B* 13 9oi 15 Mean BP [mm Hg) 87* 14 probe) and an Aloka SSD 870 (Aloka *p co.05 versus control state. Co., Ltd., Tokyo, Japan; 5 MHz probe). Values ore expressed os mean * SD. Peak early diastolic velocity, peak atriBP = blood pressure; LBNP = lower body negative pressure; LBPP = lower body positive pressure. al systolic velocity, and their ratio were determined from LV inflow velocity. Values are expressed as mean f SD. Mean values The time-velocity integral between the start of the LV inflow and the peak of the early diastolic wave of LV were compared between groups by analysis of variance inflow velocity, and that between the peak and the end (ANOVA) and Scheffe’s test. A 2-tailed paired Stuof the early diastolic wave were obtained (Figure 1). The dent’s t test was used to compare the measurements takpeak first and second systolic velocities, peak early dias- en in the control state and during preload alteration. A tolic velocity, and peakatrial systolic velocity were mea- linear regression coefficient was obtained to show the sured from pulmonary. venous flow velocity. The time- degree of correlation among variables. ‘Differences at p velocity integral for the second systolic wave, and that for co.05 were considered statistically significant. the early diastolic wave of pulmonary venous flow velocThe control group and group A had no significant ity were obtained (Figure 1). Both waveforms were re- changes in heart ,rate or mean blood’ pressure during corded while the patients lay in the left lateral decubitus LBNP and LBPP (Table I). In group B, however, heart position. The mean values for 5 consecutive heart beats rate increased significantly during LBNP were used. All patients with HC underwent left-sided carIn the control group and group A, peak early diasdiac catheterization to determine LV end-diastolic pres- tolic velocity decreased significantly during LBNP and sure within 6 hours after transesophageal echocardiogincreased significantly during LBPP (Table II and Figures 2 and 3, top). No significant changes in peak atriraphy. There was no ditference between the 2 examinations with regard to heart rate and blood pressure. None al systolic velocity during preload alteration were seen of the 42 patients had mitral regurgitation of grade 23+ in these groups. Therefore, the A/E ratio in both of by Sellers’ classification” on left ventriculography. Before these groups was significantly higher during LBNP and beginning the studies, the examinations were explained was significantly lower during LBPP than during the to all subjects, and their consent was obtained. control state. Although LV inflow velocity in group B

FIGURE 1. Pammeters from pulmanary venaus fkxv (PVFj and left ventricular inflow (LVIF) vehiies. A = Peak atrial systolic vebci af LVIF; E = Peak eady diast& vekxii af LVIF; ECG = ebctracardiimm; ID = timevekxii integral af earty diastolic r of PVF; IEa = time-velocity ral between shrt af left ventricu ?a r inflow and Peak aI early diastdic wave of LVIF; IEd = time-vekxii integml between Peak and end af early diastolic WOW of LVIF; IS2 = time-vekxity

LVIF

-A A-b

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431

,

LBNP and increased during LBPP, but it did not change in group B during IBNP (-40 mm Hg) Control State LBPP (+40 mm Hg) LBPP. Peak early diastolic velocity decreased significantly during LBNP Normal controls [n = 25) and increased significantly during 51 * 10* 68 f 7 77 f 1s E Id4 46 * 5 47 * 5 47 f 5 A km/s1 LBPP in group A, whereas it decreased 0.9 * 0.1 0.7 f 0.1 0.6 + 0.1’ WE significantly during both LBNP and Hypertrophic cardiomyopathy LBPP in group B. Peak atria1 systolic Group A (n = 30) velocity decreased significantly during 29 * 17* 561t 19 69 it 15* E (cm/4 55i 16 57zt 18 58* 15 LBNP and increased significantly durA km/s) 2.1 * 0.2t 1.1 f 0.1 1 .o * 0.3 A/E ing LBPP in both groups with HC, but Group B (n = 12) was unchanged in the control group. In 42 zt ll* 63 i 9 64 zt 8 E icdsl summary, parameters of pulmonary 41 i6 38 * 8 25 i 8’ A IdsI venous flow velocity in group B were 1.0 * 0.1* 0.6 zt 0.1 0.4 f 0.1* A/E similar to those in group A during l p
II

Parameters

of Left Ventricular

Inflow

Velocity

During

Preload

Alteration

l

Control

state

LBPP

(+40

mm Hg)

velocities during lowar body left ventricular inflow change in peak atrial syspulmonary venous flow systolic vekxii (PVSt).

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were significant positive correlations TAME III Parameters of Pulmonary Venous Flow Velocity During Preload Alteration between the changing time-velocity LBNP (-40 mm Hg) Control State LBPP (+40 mm Hg) integral in the first half of the early diastolic wave of LV inflow velocity Normal controls (n = 25) and that in the second systolic wave of 39 f a 38 f a 37 f 7 PVSi [cm/s] 40 f 9* 56 i 9 62 zt 10t PVSz [cm/s] pulmonary venous flow velocity (FigPVD (cm/s) 52 f 7 50 f 7 50 f 5 ure 4), and between the changing time10 f 2 11 i3 12*3 PVA (cm/s) velocity integral in the second half of Hypertrophic cardiomyopathy the early diastolic wave of LV inflow Group A (n = 30) velocity and that in the early diastolic 29 f 8 30 f 7 28 f a PVSI (cm/s) 47 * 22* 62 zt 21 68 f 14t PVS2 (cm/s) wave of pulmonary venous flow veloc40 f a 46 zt 10’ PVD [cm/s) 30 f 9’ ity (Figure 5) during preload alteration. PVA (cm/s) 19 * 77 27 zt 8 32 zt 51 There were no significant correlations Group B (n = 12) between any parameters in group B PVSI (cm/s) 46 * 9 50 f 9 40 zt Bt 43 * 137 54* 10 53 *6 PVSz (cm/s) (Figures 4 and 5). PVD (cm/s) 42 i 10t 53 f 7 44 f at . . . 11 * 10’ 50 * 7 56i 117 PVA [cm/s) In general, LBNP and LBPP are l p
LBNP

(-40

nun

Hg)

Control

state

LIBPP

(+40

nml Hg)

FIGURE 3. Recordin s of changes in left ventricular 4 in w (bp] and puhnonary venous Row &Warn] velocities during lower body negolive (IBNP) and positive (IBPP) pressure in a patient in grou 6. Peak atria1 systolic vekxity I& of left ventricukr inflow decreases durin IBPP, although peak early diisdic vebcii (E) decreases during IBNP and is unchanged during IBPP. Peak second systolic velocity ~SZ) of pulmonary venous flow does not thongs during IBPP, although it decreases markedly during IBNP. Peak early diastolic v$oc’ (PvD) decreases significan $ * bob IBNP and IBPP. Ptr%ial s stdic velocity (WA) decreases J*unng LBNP and increases durin&B;PVS; ;rk first sys-

BRIEF REPORTS

433

Changes in LV inflow velocity during preload alteration in group A were similar to responses in the control group. In pulmonary venous flow velocity, however, peak early diastolic and atria1 systolic velocities changed in addition to the peak second systolic velocity. Furthermore, there were positive correlations between the changing time-velocity integral in the early diastolic wave of pulmonary venous flow velocity and that in the second half of the early diastolic wave of LV inflow velocity, as well as between the changing time-velocity integral in the second systolic wave of pulmonary venous flow velocity and that in the first half of the early diastolic wave of LV inflow velocity. Therefore, LV inflow during early to mid-diastole involves not only reserved blood in the left atrium, but also a conduit from the pulmonary vein to the left ventricle. Compliance of the pulmonary venous system is 2 to 3 times greater than that of the left ventricle dur-

s

AIEa

I

(cm)

n = 60 :group

y = 0.35x-o r - 0.82

E 3 s

ing ventricular diastole. t* In group A, end-diastolic compliance of the left ventricle was low due to LV hypertrophy, and an “atrial kick” was augmented in compensation. With more preload, therefore, left atrial contraction tends to increase regurgitant blood flow into the pulmonary vein rather than blood inflow into the left ventricie.t0,16 In conclusion, the aforementioned results suggest that LV inilow and pulmonary venous llow velocities during preload alteration in HC provide important information on the mechanism of congestive heart failure due to LV diastolic dysfunction and on the evaluation of the efficacy of preload reduction therapy for this disease; however, acute changes in pressure lead to immediate catecholamine changes and reflexes that are unrelated to responses to chronic therapy.

A or.lv) 01

p< 0.001

FtGURE

4. Correiation

between

infkw (AlEa) and thot in the second systol~ wave of pulmonary venous fkw (Ah) during lower body negative (LBNP) and positive (IBPP) pressure in the 2 groups of po(;ents with hypertrophic cardiiyapathy.

-10

-8

4

6 LBNP

2

AIEd ‘cm’ )

(-

n = 60
only:

-2

40 mm

0

2

Hg)tl+

LBPP

4

,.,,,.

6

C+ 40 mm

Hg>

i

:

p
FIGURE 5. Correblion between the changing time-vebc’ integml in the second half 3 the diastdic wave of bft venr inflow (AlEd) and hot in

0 group o group

+/

,

6

LBNP

434

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40

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Hg)t[-w

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A

I

2 LBPP

4 (I

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A B

6

40

mm

//

ID

(cm)

8

Hg)

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1. Dodek A, Kawbaum DG, Bristow JD. Pulmonary edema in coronary artery disease without cardiomegaly. Paradox of the stiff heart N EngI J Med 1972;286: 1347- 13.50. 2 Dougherty AH, Naccarelli GV, C&y EL, Hicks CH, Goldstein RA. Congestive hearI failure with normal systolic function. Am J Cardiol 1984$4:77X-782. 3. Bmtsaert DL, Sys SU, Gill&en TC. Diastolic failure: pathophysiology and therapeutic implications. J Am Co/l Cardiol 1993;22:318-325 4. Zoller RI’, Mark AK, Abboud FM, Schmid PG. H&ad DD. The role of lower pressure baroreceptors in reflex va.wconsUicIor responses in man. J C/in Inwsr 1972; 1~2967-2972. 5. Ahmad M. Blomquis( G. Mullins CB, Willerwn JT. L&I venuicular function during lower body negative pressure. Avior Space Environ Med 1977;48:512-515. 6. Stoddard MF. Pearson AC, Kern MJ, Ratcliff J, Mrosek DG, Labovitz AJ. Influence of alteration in preload on the pattern of left ventricular diastolic filling as assessed hy Doppler cchocardiography in humans. Circularion 19X9:79: I226 1236. 7. Thomas JD. Choong CYP. Flachskampf FA, Weyman AE. Analysis of Ihe early ~ransmitral Doppler velocity curve: effect of primary physiologic changes and compensatory preload adjushnent. /Am Co/l Curdiol 1990,16:644-655. 8. Berk MR, Xie G, Kwan OL, Knapp C, Evans I, Kotchen T , Kotchen JM, DeMaria AN. Reduction of left ventricular preload by lower body negative prcswn: ahcs Doppler Iransmival filling patterns. J Am Co/l Cordial 1990.16: 1387-1392. 9. Triulzi MO. Castini D, Ornaghi M, Vitolo E. Effects of preload reduction on mitral flow velocity pattern in normal subjects. Am J Curdiol 1990;66: 99.5-1001. 10. Naito M. Dreifus LS. David D. Michelwn EL, Mardclli J, Kmewo JJ. Reewuation of the role of atrial systole to cardiac hemodynamics: evidence for pulmonary venous regurgitation during abnormal auioventricular sequencing. Am Hearr J 1983:105:295-302.

11. Nishimura RA. Abel MD. Ha& LK, Tajik AJ. Relruion of pulmonary vein to mitral flow velocities by transcsophageal Doppler echocardiography. Effect of different loading conditions. Circulation ly90,8 I: 14X8-1497. 12 Kuecherer HF, Muhiudeen IA. Kusumoto FM, Lee E, Moulinier LE. Cahalan MK, Schiller NB. Estimation of mean left atria1 pressure from hansesophageal pulsed Doppler echocardiography of pulmonary venous flow. Circularion 1990:82: 1127-l 139. 13. Fujimoto T , Oki T , luchi A, Ogawa S, Kageji Y, Hayashi M. Shinohara H. Hosoi K, Kiyoshige K, Fukuda N, Ito S. Changes in blood flow velociry pattem of the superior vena cava and pulmonary vein during lower body negative pressure. in normal subjects. Jprr J Med Ulwuson 1991;18:668-677. 14. Hoffmann R. Iambertz H, JuIIen H, Flachskampf FA, Hamath P. Mitral and pulmonary venous flow under influence of positive end-expiratory pressure ventilation analyzed by tramesophageal pulsed Doppler echocardiography. Am J Cardial 1991;68:697-701. 15. Hoit BD, Shao Y, Gabel M, Walsh RA. Influence of loading conditions and contractile spate on pulmonary venous flow. Validation of Doppler vekximeby. Circularion 1992;86:6.5 1659. 16. Oki T . Fukuda N, Ara N, Iuchi A, Tabata T , Tanimoto M, Manalx K, Kageji Y. Sasaki M. Ito S. Evaluation of left atrial active contraction and relaxation in various myocardial d&aces by tramesophageal pulsed Doppler echocardiography of leh ventricular inflow and pulmonary venous flow. Am J Noninvasive Cardioll994; 8:140-145. 17. Sellers RD, Levy MJ, Amplatz K. Lillehei CW. Left retrograde cardioangiography in acquired cardiac disease. Am J Cordial 1964:14:437~7. 18. Go10 M, Arakawa M, Suzuki T . Tanaka T . Miyamoto H, Yamaguchi M, Takaya T , 110 H, Hirakawa S. A quantitative analysis of reservoir function of the human pulmonary ‘Lvcnous” system for the IeA ventricle. Jpn Circ J 1986;50:222-231.

Percutaneous Balloon Aortic Coarctation Joseph

Dilatation in Adults

of

V. de Giovanni, MD, Gregory Y.H. Lip, MD, Khalid Osman, MRCP, Madan Mohan, MRCP, Ismail F. Islim, MRCP, Jayant Gupta, MD, Robert D.S. Watson, MD, and Shyam P. Singh, FRCP

n the past, the traditional treatment for adult patients with coarctation of the aorta had been surgery, with a significant mortality and morbidity.‘T2 Percutaneous balloon angioplasty (PBA), however, is a therapeutic procedure for coarctation of the aorta, which was first described by Singer et aL3 Since then, it has been widely used in children and infants, reducing the requirement for surgery. However, there are few reports of this procedure in adults with coarctation of the aorta. We describe our experience of 27 adult patients who were considered suitable for this procedure. To our knowledge, this represents one of the largest series reported by a European or North American center (Table I). . . . The City Hospital Adult Congenital Cardiology Clinic is a regional referral center that is jointly run by a pediatric and an adult cardiologist. Consecutive patients with coarctation of the aorta who were considered for PBA between 1989 and 1994 were included in this study. All patients were taking antihypertensive therapy. Coarctation gradients before and after dilatation were obtained during the procedure, and follow-up of these patients after the procedure was done in our adult congenital heart disease clinic. Follow-up blood pressure (brachial) and

ankle occlusion pressure were measured using a conventional mercury sphygmomanometer. The peak systolic velocity of the descending aorta was determined, and the peak systolic pressure calculated (using the modified Bernoulli equation [i.e., pressure = 4v2, where v = peak systolic velocity]) as an index of Doppler coarctation gradient using spectral continuous-wave Doppler on a Siemens Sonoline echocardiography machine with a standard 2.5 MHz transducer (Siemens Ultrasound, Inc., Pleasanton, California). Coarctation gradients before and after dilatation and blood pressures are expressed as mean f SD. Paired comparisons were performed using the paired t test, and a p value co.05 was considered statistically significant. Patients were admitted the night before the procedure and informed consent was obtained. We routinely crossmatched 2 units of blood and arranged cardiothoracic surgical cover. On the morning of the procedure, patients were given oral diazepam 10 mg as premeditation. rABlE I Balloon Dilatation of Published Reports

of Coorctation

Total From the Department of Cordiology, City Hospital, Birminghom B 18 7QH, England. Dr. lip is recipient of the Edith Walsh and Ivy Powel! research awards for cardiovascular disease from the British Medical Association. Dr. Gupto is o Rorary International Fellow. Dr. lip’s oddress is: University Depor!ment of Medicine, Ci;v Hospital, Birmingham B 1 8 7QH, Englond. Manuscript received July 3 1, 1995; revised manuscript received October I 1, 1995, and accepted October 17.

Reference

Lababidi Buchler Rico et Kale et Fowzy Phadke

of the Aorta:

Number

Number

of Patients

et al 1984” et al 198720 01 1989’9 al 1 99216 et al 199315 et al 1993’8

1; 2 9; 18; 24; 15;

age mean mean mean mean

27

Aged

yr age age age age

19.0 17.5 25.0 35.5

yr yr yr yr

BRIEF

A Review

of Patients >15

Years

1 2 9 9 24 15

REPORTS

435