cardiomyopathy was relatively good. However, cautious 1. Report of the WHO/ISFC task force on the definition and classification of Br HeartJ 1980;44:672-673. observationof nondilated cardiomyopathy is needed,be- 2.cardiomyopathy. Keren A, Billingham ME, Weintrub D, St&on EB, Popp RL. Mildly dilated cause 2 casesdeteriorated to dilated cardiomyopathy. congestive cardiomyopathy. Circulation 1985;72:302-309. Although the reason for this deterioration is uncertain, 3. Kurozumi H, Toyama S, Yokota Y, Fukuzaki H. Clinical study of patients mildly dilated left ventricle: early dilated cardiomyopathy? JpnJ Med somecaseswith “latent” dilated cardiomyopathy“J2may with Ultrawnics1989;16:433-437. be included in nondilated cardiomyopathy. 4. Curtius JM, Stechern V, Kuhn H, Loogen F. Echokardiographische VerlaufsKeren et al2describedcaseswith “mildly dilated con- beobachtung bei Latenter Kardiomyopathie. Z Kardiol1984;73:695-700. Kurozumi H, Matsuoka N, Hayakawa M, Inoh T. Significance of blood gestivecardiomyopathy.” However, their caseswere very 5.pressure on echocardiographic examination: evaluation in normal persons. JpnJ different from ours in many aspects.First, the prognosis MedUharonics1990,17(suppl):153-154. 6. Colan SD, Borow KM, Neumann A. Left ventricular endsystolic wall stressof their caseswas very poor, and, second,their caseshad velocity of fiber shortening relation: a load independent index of myocardial severecongestiveheart failure with a low ejection fraction contractility. J AmCONCardiol1984;4:715-724. equal to that of dilated cardiomyopathy. Therefore, it is 7. Borow KM, Neumann A, Arensman FW, Yacoub MH. Left ventricular and contractile reserve after cardiac transplantation. Circuhtion possiblethat mildly dilated congestivecardiomyopathy is contractility 1985;71:866-873. another disease.Although cardiac transplantation should 6. Moore GW, Hutchins GM, Bulkley BH, Tseng JS, Ki PF. Constituents of be considered for their cases,it is unnecessaryfor ours human ventricular myocardium: connective tissue hyperplasia accompanying hypertrophy. AmHeartJ 198O;lOOz610-616. becauseof their relatively goodprognosis.Further studies 9.musclar Kurozumi H, Yokota Y, Fukuzaki H. Role of afterload in progression of are warranted in regard to the precise hemodynamic dilated cardiomyopathy: evaluation with force-velocity relation. Jpn Circ J 1989;53:20-26. mechanism and long-term prognosis of nondilated car- 10. Ross J Jr. Afterload mismatch and preload reserve: A conceptual frame work diomyopathy. for analysis of ventricular function. frog Cardiwosc Dis 1976;18:255-264. 11. Hirota Y, Shim&u G, Kaku K, Saito T, Kino M, Kawamura K. Mechanism For the calculation of end-systolicwall stress,we used of compensation and dccompensation in dilated cardiomyopathy. AmJ Cordial a peak systolic cuff pressure, becauseReicheck et all3 1984;54:1033-1038. demonstratedan excellent correlation betweenpeak sys- 12. Kurozumi H, Yokota Y, Miki T, Emoto R, Nakanishi 0, Fukuzaki H. A trial tolic cuff pressure and invasive endsystolic pressure. diagnosis of latent dilated cardiomyopathy. J Cardiol1987;17:779-784. 13. Reichek N, Wilson J, Sutton MS, Plappert TA, Goldberg S, Hirshtield JW. However, the difference between the 2 pressuresmay Noninvasive determination of left ventricular end-systolic stress: validation of the affect the selection of patients. 1982;65:99-106. method and initial application. Circulation
Increased Atrial Natriuretic Coarctation Repair
Factor Response to Exercise After
Robert D. Ross, MD, Sandra K. Clapp, MD, Stephen Gunther, MD, Stephen M. Paridon, MD, Richard A. Humes, MD, Zia Q. Farooki, MD, and William W. Pinsky, MD trial natriuretic factor (ANF) is primarily secreted A in responseto stretching of the atria1 tissue.’ Recent evidencesuggeststhat owing to its natriuretic and vasore-
From the Division of Pediatric Cardiology, Department of Pediatrics, Children’s Hospital of Michigan, Wayne State University School of Medicine, 3901 Ekaubien Boulevard, Detroit, Michigan 48201. This study was supported in part by the American Heart Association of Michigan, Lathrup Village, Michigan. Manuscript receivedDecember 6,199 1; revisedmanuscript receivedand acceptedJanuary 13,1992.
All subjectswere instructed to have a light breakfast and arrive at 7:30 A.M. for the study. After obtaining informed consent,an intravenous heparin lock was inserted in the left arm, and patients were allowed to rest for 20 minutes. They were seated on an electronically braked bicycle (BOSCH No. ERGSSl), where baseline heart rate and blood pressure were recorded. The exercise protocol began with 3 minutes of peddling in an unloaded state. The work rate was then increasedeach minute by a consistentincrement to achievethat subject’s predicted maximal work rate in 10 to I2 minutes. Right arm blood pressure was obtained every 3 minutes during exercise,at maximum exerciseand during recovery, using an automated sphygmomanometer (Colin STBP680) with simultaneous auscultatory confirmation. Blood samples for ANF were obtained at rest, peak exercise and after 1.5minutes of recovery. Each 5 ml blood specimen was collected in a prechilled glass tube containing I mglml of bisodium ethylenediamine tetraacetate.Plasma was separatedby centrijiigation at 2,500 X gfor 10 minutes at 4” C and stored at -70°C until assay. The radioimmunoassayfor ANF was adaptedfrom the method of Tan et al4 as described previously.5 Student’s t test was used to compare variables between the groups where the variances were equal. The Wilcoxan rank sum test wasperformedfor comparisons where the variances were unequal. Stepwise multiple
1370
MAY 15. 1992
laxant properties,ANF may be involved in the regulation of blood prcssure.2Becausechildren who haveundergone repair of coarctation of the aorta have a propensity for either resting or exercise-related hypertension later in life, this study was designedto evaluate the responseof ANF to dynamic exercisemany years after coarctation repair and compare the results with those of an agematched control group. This study included 31 patients who had undergone repair of coarctation of the aorta, and 16 control subjects who were healthy volunteers or clinic referrals with normal cardiovascular examinations. All patients had been operatedon at Children’s Hospital of Michigan and were asymptomatic without medications. Most of thesepatients (27) underwent an end-to-end anastomosis, whereasthe remainder had subclavianjlap (2) or patch (2) angioplasty. The responsesof plasma norepinephrine and renin activity in most patients appear elsewhere.’
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 69
regression analysis was usedfor each group to evaluate which variables predicted ANF at maximal exercise. ANF data are presented as mean f SD, and a p value 2 SD from predicted means based on age and sex). No control subject was hypertensive. The blood pressure responseto exerciseis shown in Figure 1. The only difference betweengroups was at 5 minutes of recovery when mean diastolic blood pressure of patients was significantly greater than that of control subjects. The responseof ANF to exerciseis shownin Figure 2. There was no difference betweenbaselineconcentrations of ANF for patients and control subjects. The ANF of patients increased significantly from baseline to peak exercise, and this difference was maintained at IS minutes of recovery. In contrast, the concentrationsof ANF
200
in the control group were unchangedfrom baseline to peak exerciseand recovery. The difference betweenthe 2 groups becamesignificant at 15 minutes of recovery. Stepwise multiple regression analysis for predictors of peak exerciseANF wasperformed using thefollowing independentvariables: age,yearsfrom repair (inpatients only), baselinesystolic and diastolic pressures,peak systolic and diastolic pressures, baseline and peak heart rates, and percentageof maximally predicted work rate. For patients, the multiple regression model that best explained the variancefor peak ANF concentration was: ANF= -193.9 + 2.4 (restingsystolic bloodpressure) + 1.2 (peak diastolic blood pressure) - 0.8 (peak heart rate) (multiple r = 0.85, ti = 0.72;~
Increased Atrial Natriuretic Coarctation Repair
Factor Response to Exercise After
Robert D. Ross, MD, Sandra K. Clapp, MD, Stephen Gunther, MD, Stephen M. Paridon, MD, Richard A. Humes, MD, Zia Q. Farooki, MD, and William W. Pinsky, MD trial natriuretic factor (ANF) is primarily secreted A in responseto stretching of the atria1 tissue.’ Recent evidencesuggeststhat owing to its natriuretic and vasore-
From the Division of Pediatric Cardiology, Department of Pediatrics, Children’s Hospital of Michigan, Wayne State University School of Medicine, 3901 Ekaubien Boulevard, Detroit, Michigan 48201. This study was supported in part by the American Heart Association of Michigan, Lathrup Village, Michigan. Manuscript receivedDecember 6,199 1; revisedmanuscript receivedand acceptedJanuary 13,1992.
All subjectswere instructed to have a light breakfast and arrive at 7:30 A.M. for the study. After obtaining informed consent,an intravenous heparin lock was inserted in the left arm, and patients were allowed to rest for 20 minutes. They were seated on an electronically braked bicycle (BOSCH No. ERGSSl), where baseline heart rate and blood pressure were recorded. The exercise protocol began with 3 minutes of peddling in an unloaded state. The work rate was then increasedeach minute by a consistentincrement to achievethat subject’s predicted maximal work rate in 10 to I2 minutes. Right arm blood pressure was obtained every 3 minutes during exercise,at maximum exerciseand during recovery, using an automated sphygmomanometer (Colin STBP680) with simultaneous auscultatory confirmation. Blood samples for ANF were obtained at rest, peak exercise and after 1.5minutes of recovery. Each 5 ml blood specimen was collected in a prechilled glass tube containing I mglml of bisodium ethylenediamine tetraacetate.Plasma was separatedby centrijiigation at 2,500 X gfor 10 minutes at 4” C and stored at -70°C until assay. The radioimmunoassayfor ANF was adaptedfrom the method of Tan et al4 as described previously.5 Student’s t test was used to compare variables between the groups where the variances were equal. The Wilcoxan rank sum test wasperformedfor comparisons where the variances were unequal. Stepwise multiple
1370
MAY 15. 1992
laxant properties,ANF may be involved in the regulation of blood prcssure.2Becausechildren who haveundergone repair of coarctation of the aorta have a propensity for either resting or exercise-related hypertension later in life, this study was designedto evaluate the responseof ANF to dynamic exercisemany years after coarctation repair and compare the results with those of an agematched control group. This study included 31 patients who had undergone repair of coarctation of the aorta, and 16 control subjects who were healthy volunteers or clinic referrals with normal cardiovascular examinations. All patients had been operatedon at Children’s Hospital of Michigan and were asymptomatic without medications. Most of thesepatients (27) underwent an end-to-end anastomosis, whereasthe remainder had subclavianjlap (2) or patch (2) angioplasty. The responsesof plasma norepinephrine and renin activity in most patients appear elsewhere.’
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 69
regression analysis was usedfor each group to evaluate which variables predicted ANF at maximal exercise. ANF data are presented as mean f SD, and a p value 2 SD from predicted means based on age and sex). No control subject was hypertensive. The blood pressure responseto exerciseis shown in Figure 1. The only difference betweengroups was at 5 minutes of recovery when mean diastolic blood pressure of patients was significantly greater than that of control subjects. The responseof ANF to exerciseis shownin Figure 2. There was no difference betweenbaselineconcentrations of ANF for patients and control subjects. The ANF of patients increased significantly from baseline to peak exercise, and this difference was maintained at IS minutes of recovery. In contrast, the concentrationsof ANF
200
in the control group were unchangedfrom baseline to peak exerciseand recovery. The difference betweenthe 2 groups becamesignificant at 15 minutes of recovery. Stepwise multiple regression analysis for predictors of peak exerciseANF wasperformed using thefollowing independentvariables: age,yearsfrom repair (inpatients only), baselinesystolic and diastolic pressures,peak systolic and diastolic pressures, baseline and peak heart rates, and percentageof maximally predicted work rate. For patients, the multiple regression model that best explained the variancefor peak ANF concentration was: ANF= -193.9 + 2.4 (restingsystolic bloodpressure) + 1.2 (peak diastolic blood pressure) - 0.8 (peak heart rate) (multiple r = 0.85, ti = 0.72;~
