Echocardiographic Changes After Successful Renal Transplantation in Young Nondiabetic Patients

Echocardiographic Changes After Successful Renal Transplantation in Young Nondiabetic Patients

Echocardiographic Changes After Successful Renal Transplantation in Young Nondiabetic Patients· Luis Cueto-Garcia, M.D., F.C.C.P.;]aime Herrera, M.D.;...

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Echocardiographic Changes After Successful Renal Transplantation in Young Nondiabetic Patients· Luis Cueto-Garcia, M.D., F.C.C.P.;]aime Herrera, M.D.; Jaime Arriaga, M.D.; Carolina Laredo, M.D.; and Eduardo Meaney, M.D. Eighteen young nondiabetic patients with chronic renal failure were studied by M-mode echocardiography before and three to 67 weeks after a successful renal transplant. Left ventricular mass (LVM~ cardiac output (CO), and stroke work, which were increased before the operation, decreased afterward, in some cases to normal values. Both regression of the LVM and normalization of CO were detected as early as three weeks postoperatively and probably

resulted from changes in the end-diastolic volume, mean systemic blood pressure, and hematocrit as a consequence of normal renal function. Because all the patients had normal left ventricular function and only moderate dilatation of the left ventricle, it is not known whether these striking beneficial changes after SRT also will occur in patients with significant dilatation or dysfunction of the left ventricle.

pericardial, myocardial, and valvular abnorV arious malities have been documented in patients with

chronic renal failure (CRF);1-7 and the effects ofchronic hemodialysis on the uremic patient's heart also have been studied extensively.v" However, little is known of the effects of successful renal transplantation (SRT) on the hearts of these patients. Because M-mode echocardiography (MME) allows sequential noninvasive cardiac evaluation,'?" it was used to study 18 young, stable, nondiabetic patients before and after SlIT

100

leo

r ......

110

Patients

*From the Departments of Cardiology, Nephrology and Surgery, Instituto Nacional de Nutrici6n, Mexico, D. F. Presented at the 1\velfth National Meeting on Cardiology, Nov 13-16, 1981, Morelia, Mexico. Manuscript received April 22; revision accepted July 30 Reprint requests: Dr. Cueto-Garcia, Llama 124, Jardinesdel Pedregal, Mexico D. F., Mexico 01900

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170

I

MATERIALS AND METHODS

The ten male and eight female patients, who had SRTs from related living donors, were studied by MME one week before and three to 67 weeks after the operation. Their average age was 28.8 years, and the duration of CRF ranged from three to 120 (mean 34) months. All patients were receiving chronic hemodialysis before the SRT and had Cimino-Brescia arteriovenous shunts that were still open when the postoperative echocardiographic study was performed. Seventeen patients had systemic hypertension (systolic pressure>150 mm Hg or diastolic pressure >95 mm Hg), and eight of these had hypertensive retinopathy. All 17 were receiving at least one antihypertensive drug before the SKI: Three patients were taking digitalis preoperatively but were free ofcongestive signs at the time of the preoperative MME. Postoperatively, only one patient was taking antihypertensive medication and none was receiving inotropic drugs; all patients were receiving immunosuppressive treatment. The body surface area. heart rate, and hematocrit value were determined at the time of each echocardiogram. Also, the mean blood pressure (MBP) was calculated from standard cuff measure-

180

140

110

Q

§ ID

110

110 100

10 10

eo PlEOP

POSTOP

FIGURE 1. A significant fall in mean systemic blood pressure was observed after the SKI: EchocardIographIc Changes after Renallt'anspIantation (Cueto-Gatcla et 8/)

-Left ventricular mass (LVM) (in grams) = (LVID(d) + 2 LVWI1- LVID(dytx 1.05;14 -Percent shortening fraction of the left ventricle (SF) = LVID(d)- (LVID(s)/LVID(d»x 100; -LAD/ARD ratio; -The relative size of the right ventricle, expressed as a percentage of the size of the left ventricle; -The end-diastolic volume (EDV), end-systolic volume (ESV), and the stroke volume," -The cardiac output (CO) = SV x heart rate; -The stroke work (SW), in 'ilm per beat =(MBP x 1.36 x SW)/ 100; and -The relative left ventricular wall thickness (R/Th ratio) = LVID(d)/2 LVWI:18 The preoperative and postoperative tracings were obtained following the recommendations for optimal reproducibility, 11-18and paired t-test analyses were used for the evaluation of the preoperative and postoperative values. The Student's t-test was used to evaluate the differences between the CRF patients and 30 normal volunteers.

ments as follows: MBP = diastolic pressure + ([systolic pressure - diastolic pressure]/3) Echocardiographic Technique and Data Collection M-mode echocardiograms were obtained with a 2.25 MHz transducer with an Echo IV (Electronics for Medicine) or Ekoline 20A (Smith Kline & French) machine attached to a Honeywell strip-chart recorder. The tracings were made with the patient in the left lateral decubitus position, with care taken to position the patient and transducer during the postoperative MME as they had been positioned for the preoperative examination. The left ventricular internal diastolic dimension (LVID(d», left ventricular internal systolic dimension (LVIS(d», left ventricular wall thickness (LVWIj, interventricular septal thickness (IVST), aortic root dimension (ARD), left atrial dimension (LAD), EF slope, and right ventricular internal diastolic dimension (RVID(d» were calculated according to the recommendations of the American Society of Echocardiography," From these values, the following derived echocardiographic data were calculated:

Table I-Left Ventricular Echocardiographic MetJIUrementa Before (B) and After (A) Succeuful Renal Tranaplant Case

TIme Postop (weeks)

1

57

2

52

3

64

4

62

5

57

6

66

7

6

8

25

9

33

10

44

11

8

12

6

13

8

14

28

15

26

16

3

17

8

18

8

Means

31.16± 23.59*

LVID(d) LVID(d) (cm) B 5.1 A 4.1 B 4.4 A4.4 B 5.8 A5.5 B 4.6 A 4.9 B 6.4 A 5.6 B 5.3 A 4.3 B 4.7 A4.9 8 4.2 A3.8 85.3 A4.2 8 4.7 A4.7 85.2 A3.9 8 4.9 A4.3 86.1 A5.0 B 5.1 A 4.1 84.2 A 4.1 B 4.3 A2.8 B 5.0 A4.6 B 5.5 A4.5 B 5.04±0.62 A 4.48±0.7 p <0.0025

LVID(s) (em)

LVWf(cm)

SF (%)

2LVWf

3.5 3.6 3.4 3.4 4.4 3.8 3.4 2.7 5.9 5.1 3.9 2.8 3.4 4.0 3.1 2.5 3.7 2.2 3.5 3.5 3.1 2.9 3.5 3.3 4.3 3.4 2.6 3.3 2.7 3.2 3.5 2.2 3.0 3.9 3.6 3.5

0.9 1.0 1.3 0.9 1.0 1.0 1.4 1.0 1.1 0.8 1.1 1.1 1.3 0.9 1.5 0.8 1.0 1.0 1.0 0.9 1.1 0.8 1.2 1.1 1.3 1.3 1.0 0.9 1.1 0.8 1.3 1.2 1.1 0.8 1.2 0.9

31 12 23 23

22 19 21 40 30 35 22

2.83 2.05 1.69 2.44 2.90 2.75 1.64 2.45 2.90 3.50 2.40 1.95 1.80 2.70 1.40 2.37 2.65 2.10 2.35 2.60 2.36 2.43 2.04 1.95 2.35 1.92 2.55 2.28 1.90 2.56 1.65 1.16 2.57 3.50 2.29 2.50

3.58±0.7 3.29±0.7 NS

1.16±0.16 0.95±0.14 p <0.0005

29.1±9.12 26.5± 10.0 NS

2.22±O.46 2.41±O.54 NS

24

31 26 45 7 9 26 35 28

18 26 34 30 48 26 26 40 26 29

23 30 32 49 20 36

*SD. CHEST I 83 I 1 I JANUARY, 1983

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Table !--AtItJIomic .ntl Hemotlr/ntJmic DtJItJ Derived From Table1 Cue

1 2 3 4 :5 6

7 8 9 10 11 12 13 14 15 16 17 18 Means

EF (IfJ)

868 A32 854 AM 856 A67 B60 A83 B22 A24 B60 A 73 863 A46 B59 A 71 866 A85 859 A59 B 79 A59 864 ASS B65 A69 887 A48 873 A52 846 A50 B78 A66 B 72 A53 B 62.8% 14.1· A 58.1% 15.7 NS

LVM (g) 206

166 271 161 293 268 323

221

393 208

287 205

292

192 314 108 252

172

9IY1

179 278 112

285 205

453

329 237 143 197 l.22

261

123

261

207 343

167 286.6± 64.4 182.7± 55.7

p
EDV (ml)

133 69

85 85

39 39

85

55

118

20

97

262

176 149 80

104 118 74 55

149 74 104 104 141 59

118

80 227

125 133

69

74

69 80 22 125

176 166 91 134± 52 96.4

±43

p
If a posterior pericardial effusion was present, the distance between the epicardium and pericardium was meas~ at the end eXdiastoleand the amountf1fluidcalculated using the semiquantitative technique.-

REsuU'S The calculated body surface areas and heart rates of the patients changed little between tracings; the former averaged 1.58±0.18 (SD) ml preoperatively and 1.59±0.16 rnl postoperatively, and the latter averaged 79 ± 12 (SD) beats per minute preoperatively, and 72.6± 16 beats per minute postoperatively. Because there were no significant changes in the heart rate, the absolute values fOr chamber size and cardiac performance could be compared. II The MBP declined from 133.8± 19.0 (SD) mm Hg preoperatively to 102.2 ± 12.5 mm Hg postoperatively (Fig 1), and the

SV (ml)

43 47

195 166

·SD.

58

ESV (ml)

39

90 22 46

46 110 III

58 98

57

205

133

43 90 58 65 54

59 22 39 64 30

44

39

16 51 11 43 43 30

24

43 36 80 39

18

36 20

98 63

61 61 III 35

75

44

147 86

115 33 54 36

33

37 11

43

11

27 59 42 43

52.2± 41.9 40.6± 27.8

p
98

117 119 48 81.9± 31.1 55.8± 29.5

p
sw

CO (Umin)

(g/mIbeat)

9.3 1.9 3.3 2.5 7.5 6.2 3.9 5.1 4.5 3.4 7.4 5.1 5.7 5.4 3.3 2.1 7.4 4.2 5.4 3.9 7.5 2.1 6.6 4.4 14.7 7.6 7.1 2.3 4.3 2.3 2.8 0.8 8.8 7.3 7.1 4.2 6.47± 2.83 3.93± 1.93

135

p
22

79 73 169 161 110 138 90

64

179 76 115 69 86

52

204 94 124 80

181 44 153 17

346

133

208 42 69

46 70 20

151 148

243 65

150.6 ±70.6 74.6 ±44.2

p
hematocrit value increased from 24.8± 11.6 (SO) percent to 38.7 ± 7.6 percent.

Anatomic Data Normal values in this laboratory for the LVIO(d) are 4.3 ± 0.6 (SD) em, with 5.5 cm being the upper limit of normal. Preoperatively, three patients had an LVID(d) >5.5 em. After the Sm: the LVIO(d) either did not change or decreased less than 3 mm in three patients. In seven patients, the ~VID(d) decreased 3 mm to 1 em, and seven patients had a decrease of at least 1 em, ID one patient, the LVID(d) increased slightly «3 mm), These and the other MME data on the patients are shown in 'Iables 1 and 2. The mean preoperative LVWT in our patients was greater than that found in our control group (1.16±0.16 [SD] em vsO.77 ±O.11 em), In 17 patients, Echoc8nIographI Ch8ngeI8fter AenIJ1tanIpIantatIon (~.

et III)

Table 3-CarditJc MeaaunmaentB Before and After SBT

LAD (em) ABD (em) LAD/ARD (em) RVID(d) (em) IVST (em) RVID(d)/ LVID(d) (%) EF slope (mm/sec)

Control Group

Preoperative

Postoperative

2.83 ± 0.48· 2.67 ± 0.48* 1.05 ± 0.09* 1.06±O.45* 0.81±0.16*

3.58±O.72t 2.68 ± 0.63* 1.38±O.241 1.68± O.SO* 1.12±0.29*

3.15±0.66 2.77±0.53 1.18±0.26 1.90±0.50 1.15±0.32

42.8 ±9.10§

34.16± 13.161

45.70±15.50

98.5

75.60±25.00*

81.50±26.70

±30.~

*p
the LVW'T did not change or decrease after SRT; in nine, the decrease was 3 mm or more. In the remaining patient, the LVW'T increased 1 mm. The normal R/Th ratio in our laboratory is 2.86±0.65 (SD). Before the SRl: the ratio in the CRF patients was 2.22 ± 0.46, which is significantly below normal. Postoperatively, the R!Ib ratio increased to 2.41±O.54. The normal values for LAD, ARD, and the LAD/ ARD ratio are shown in Table 3. In ten patients, the ARD was normal preoperatively and did not change significantly after the SRl: whereas the LAD, and thus, the LAD/ARD ratio, were often above normal both before and after the operation. Before the operation, the LVM was above normal, with a mean value of 286.6±64.4 (SD) g (normal = 127 ± 30 g). In all patients, the LVM decreased between 25 and 206 g postoperatively (Fig 2 and 3). The decrease was significant, even in patients studied soon after the operation; all seven patients three to eight weeks after the SRT had a decrease of >50 g (Table 2). Both the preoperative and the postoperative values for RVID(d) were higher than those in the normal control population. Before the SKI: the relation between the sizes of the right and left ventricles (RVID(d)/LVID(d)) was below normal; afterward, it increased to normal (Table 3). Function Data The EF slope increased from 75.6±25.0 mmlsec preoperatively to 81.5 ± 26.7 mm/sec after the SRl: Thus, whereas the preoperative value was significantly below normal, the mean postoperative value was similar to that found in the control group. Before the SRl: the stroke volume and cardiac output were above normal as a consequence of an increased end-diastolic volume and normal shortening fraction. Also, because 17 of the patients were hypertensive and most had an increase in stroke volume, the calculated stroke work was abnormally high. After the SKI: the end-diastolic volume decreased significantly

100

471 410

4.

---

at

~

I 2

400 575

180

118 !GO

111

Z

~

I-

I&.

~

250

2_

200 175

110 125 100

PRIOP

POI'OP

2. The LVM was above normal limits (brolcen line) in all patients before SRT and decreased afteJ'W8J"tL with ten patients having normal values at the postoperative MME. FIGURE

CHEST I 83 I 1 I JANUARY, 1883

II

110 140

134

110

......

120

~

110

E ...., 11.I

~

100

.0

~

80

W

10

I !

81

Pericardial Effusions Five patients had pericardial effusions, the largest of which was calculated to be 830 ml, before the 8m: Postoperatively, only two patients had evidence of effusions. In one, the anterior clear space persisted, but the posterior effusion disappeared (Fig 3). DISCUSSION

a-.

The principal cause of death in patients with CRF is cardiovascular disease, and therefore, the cardiac anatomy and function of these patients must be characterized. Despite the fact that MME provides information on myocardial, pericardial, and valvular anatomy and function, this technique has not been used hereto80

IV

50

40

FIGURE

without a Significant change in the end-systolic volume. These changes decreased the stroke volume, and because the heart rate did not change, the cardiac output fell to within the normal range. The stroke work also decreased signi6cantly (Table 2 and Fig 4). Valuesfor the shortening and ejection fractions were normal before and after the 8m:

95

BV

10

50 3A (upper~ Echocardiographic tracing of a patient before Sm: showing increased LVID(d) and Lvwr with normal shortening fraction; there is a significant pericardia1 effusion. B (lower). Postoperatively, LVM has decreased, and the posterior pericardia1 effusion has disappeared. There is a residual anterior clear space.

82

20

sa

ElY

40

ElY

10

o

PREOP P08TOP 4. Changes in end-diastolic (upper value), SV (middle value), and end-systolic values (lower value); significant decrease in SV after SKI' is the consequence of changes in end-diastolic volume. FIGURE

fore in the evaluation of the cardiac changes produced bySm: The changes observed in the LVID(d), and consequently, in the end-diastolic volume, are significant in comparison with the modest changes observed during hemodialysis. For example, Vaziri and Prakash" found a mean predialysis value of 5.0±0.64 cm and a postdialysis value of 4.7 ± 0.5 cm. However, signi6cant _changes, such as those observed in this study, have been documented in patients after correction of LV volume overload. Thus, Schuler et alJ7 reported a decrease in LVID(d) from 6.49±0.84 cm to 5.1 ±0.76 cm after aortic valve replacement, and Gaasch et alf.8 had similar results. Changes in LV mass also have been shown experimentally after removal of LV volume EchocardIograph Changes after Renal 1l'anIpIantaIIo (Cueto-GarcIa et tJI)

overload." The changes in the end-diastolic volume

observed in the present cases also resemble those found by Schuler et al27 and because the ejection fraction did not change, the cardiac output fell to normal levels. The findings before SRT indicate that the principal determinant of the abnormally high cardiac output in uremic patients is an increased stroke volume. Other authors state that an increased heart rate is the chief cause of high cardiac output in CRF. 30,31 Also, according to the present results, and in disagreement with the reports of others.I-" the arteriovenous shunt is not a significant factor in the hemodynamic changes observed in the uremic patient, as the end-diastolic volume and the cardiac output decreased after the SRT while the shunt was still open. Whereas the changes in LVID(d) in our patients resemble those observed after correction of severe aortic regurgitation, the changes in LVWf and LVM are quite different. Thus, the correction of left ventricular overload without associated lesions does not produce an early decrease in LVM27 and because of this, the LVWf tends to increase after surgery in those cases. For example, Schuler et al" found an LVWf of 1.49±0.18 em in the early postoperative period, which is significantly higher than the preoperative value of 1.26 ± 0.13 em. By contrast, in this series, the LVWf decreased in one half of the patients after SRT and did not change in the others. It is believed that the measured LVWf did not increase after SRl; despite a significant decrease in LV volume, because of an early decrease in LVM. Because in all of our patients the SRT brought a significant fall in the systemic blood pressure and the ED~ and because both factors are known to influence the LVM,7,12.27-31,33-37 it is impossible to determine the contribution of each factor to the LVM regression. Decreases in the LVM after the relief of pressure overload have been reported occasionally in both clinical and experimental settings. 33-37 Changes in LVM after medical treatment of essential hypertension have been attributed to changes in the LVWl: From all these considerations, it appears that the pattern of LVM regression observed in our patients, ie, a significant regression in LVWf and ED~ is unique. Because the number of cases in this series is small, and the intervals for the postoperative study were not assigned systematically, the rate at which these significant changes take place is unknown. However; from the few patients studied within eight weeks of the Sm: it appears that the changes begin soon after the operation. Because all of the present patients had normal left ventricular function and only moderate left ventricular dilatation with an appropriate degree of hypertrophy, the results may not be applicable to uremic patients with poor left ventricular function or inappropriate

hypertrophy. 3 The changes observed in EF slope are difficult to interpret without left ventricular pressure measurements but may reflect changes in left ventricular compliance; Kleiger et al3 have suggested that a decreased EF slope in patients with kidney disease probably results from decreased compliance. The lack of significant decrease in the LAD/ARD ratio in our patients is similar to findings in other types of left ventricular disease in which, despite normalization of left ventricular hemodynamics, left atrial enlargement persists. In this institution, renal transplantation is reserved for young, nondiabetic patients. Therefore, caution is given that these findings on MME before and after SRT may not be applicable when the operation is performed on older patients with Significant vascular disease. REFERENCES 1 Langendorf R, Pirani CL. The heart in uremia: an electroeardiographic and pathologic study. Am Heart J 1974; 37:282-307 2 Cruz lA, Bhatt GR, Cohen HC, Glick G. Echocardiographic detection eX cardiac involvement in patients with chronic renal failure. Arch Intern Med 1978; 138:720-24 3 Kleiger R, de Mello VR, Malone D, Fernandes J, Thanavaros, Conners J~ Left ventricular function in end-stage renal disease. South Med J 1981; 74:819-25 4 Yoshida K, Shina A, Asano ~ Hosoda S. Uremic pericardial effusion: detection and evaluation ~ uremic pericardial effusion by echocardiography. Clin Nephroll980; 13:260-68 5 Luft FC, Gilman JK, Weyman AE. Pericarditis in the patient with uremia: clinical and echocardiographic evaluation. Nephron 1975; 15:17-28 6 Kersting It: Brass H, Heints R. Uremic cardiomyopathy: studies on cardiac function in the guinea pig. Clin Nephrol 1978; 10:109-13 7 Capelli J~ Kasparian H. Cardiac work demands and left ventricular function in end-stage renal disease. Ann Intern Med

1977; 86:261-67

8 Cohen MV, Dfaz ~ Scheurer J. Echocardiographic assessment of left ventricular function in patients with chronic uremia. Clin Nephrol 1979; 12:156-62 9 Vaziri ND, Prakash R. Echocardiographic evaluation of the effect ofhemodialysis on cardiacsize and function in patients with endstage renal disease. Am J Med Sci 1979;278:201-06 10 Cueto L, Aniaga J. Ecocardiografia en medicina interna modo M: el estado del miocardio (la de 3 partes). Rev Inv Clin (Mex) 1979; 31:169-76 11 Ehsani AA, Hagberg JM, Hudson RC. Rapid changes in left ventricular dimension and mass in response to physical conditioning and disconditioning. Am J Cardioll978;42:52-56 12 Cueto L, Aragon M, 1ioyo R La secuencia cUnica eeocardi0gni6ca y hemodin4mica en la Bsula arteriovenosa cerebral. Arch Inst Cardiol Mex 1979; 49:634-47 13 Sahn DS, de Marla A, Kisslo J, Weyman A. The Committee on M-Mode Standardization eX the American Society of Ech~ diography: recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978; 58:1072-83 14 Bennett DH, Evans DW. Correlations of the left ventricular mass determined by echocardiographic measurements. Br Heart J 1974; 36:981-84 15 Feigenbaum DH, Popp LR, Wolfe SB, et all Ultrasonic measureCHEST I 83 I 1 I JANUARY, 1983

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ments of the left ventricle. Arch Intern Med 1972; 129:461-66 16 Gaasch WHo Left venbicuJar thickness to wall thickness ratio. Am J Cardioll979; 43:1189-94 17 Clark RD, ICorcuska K, Cohen K. Serial echocardiographic evaluation of left ventricular function in valvular disease including reproducibility guidelines for serial studies. Circulation 1980; 62:564-65 18 Wong A, Shah PM, 1llylor RD. Reproducibility ofleft ventricular internal dimensions with M-mode echocardiography: effects of heart size, body position and transducer angulation. Am J Cardioll981; 47:1068-74 19 Ditchey ~ Schuler G, Peterson K. Reliability of echocardiographic and electrocardiographic parameten in assessing serial changes in left ventricular mass. Am J Med 1981; 70:104.2-49 20 Horowitz MS, Schultz CS, Stinson ES, Hanison DC, Popp RL. Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 1974; 50: 239-47 21 de Maria AN, Newman A, Schubart PS, Lee G, Mason Dl: Systematic correlation of cardiac size and chamber performance determined with echocardiography and alterations of the heart rate in normal persons. Am J Cardioll979; 43:1-9 22 Parsons FM, Brunner F~ Gurland HS. Combined report on regular dialysis and transplantation in Europe. Proc Eur Dial Thmsplant Assoc 1971; 8:3 23 Gurland HJ. Combined report on regular dialysis and transplantation in Europe. Proc Eur Dial 1hmsplantAssoc 1973; 10:17-21 24 Casaretto AA, Marchiaro TL, Bagdada JD, Hyperlipidemia fOllowingrenal transplant. 'U Amer SocArtifIntern Organs 1973; 19:154-57 25 MeniU JR Cardiovascular problems in patients on long-term hemodialysis. JAMA 1974; 228:1149-53 26 Nichols A), Catto GRD, Edward N, Engeset ), McLeod M. Accelerated atherosclerosis in long-term dialysis and renal transplant patients: fact or fiction? Lancet 1980; 1:276-78

27 Schuler G, Peterson KL, Johnson A, Francis G, Ashburn ~ Dennison G. Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of aortic regurgitation. Am J Cardioll979; 44:585-94 28 Gaasch WH, Andrias ~ Levine HS. Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular mass and function. Circulation 1978; 58:825-36 29 Papadimibiou JM, Hopkins BE, 'Dlylor RD. Regression of left ventricular dilatation and hypertrophy after removal of volume overload. Circ Res 1974; 35:127-35 30 Neff MS, Kim KE, Persoff M, Oneseti G, Swartz C. Hemodynamics of uremic anemia. Circulation 1971; 43:876-83 31 Del Greco It: Simon NM, Roguska J, Walker C. Hemodynamic studies in chronic uremia. Circulation 1969; 40:87-95 32 Bibra H, Castro L, Autenrieth G, McLeod A, Gurland HJ. The effects of arteriovenous shunts on cardiac function in renal dialysis patients: an echocardiographic study. Clio Nephroll978; 5:205-09 33 Sasayama S, Ross J Jr, Franklin 0, Bloor CH, Bishop S, Dilley RB. Adaptations ofthe left ventricle to chronic pressure overload. Cire Res 1976; 35:172-78 34 Henry WL, Bonow RO, Borer JS, Kent KM, Ware JH, Redwood DR. Evaluation of aortic valve replacement in patients with valvular aortic stenosis. Circulation 1980; 61:814-25 35 Hall 0, Hall E, Ogden E. Cardiac hypertrophy in experimental hypertension and its regression following reestablishment of normal blood pressure. Am J Physioll953; 174:175-78 36 Froslich ED, 18razi RC. Is arterial pressure the sole factor responsible for hypertensive cardiac hypertrophy? Am J Cardiol 1979; 44:959-63 37 Schlant RC, Felver JE, Heymesfield SS, Gilbert CA, Shulman NE, Thttle ER Echocardiographic studies of left ventricular anatomy and function in essential hypertension. Cardiovasc Med 1977; 2:477-91

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