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Arterial and venous compliance in obese and nonobese subjects
ing combined Doppler peak and mean gradients (r = 0.89). In the presence of AR, Doppler mean and peak gradients correlated poorly with catheter gradients, but improved from r = 0.56 to 0.74 when electrocardiographic data were incorporated with Doppler peak gradients. Bengur et al ’ reported that Doppler mean gradients of 227 mm Hg consistently predicted catheter peak-to-peak gradients of >75 mm Hg. In contrast, among the 23 examinations in this study, 22 had Doppler mean gradients z-27 mm Hg, but only 6 had catheter peak-to-peak gradients >75 mm Hg. The interval between evaluations, cardiac index, and age did not account for the discrepancy between these 2 studies. Only 2 of the 6 examinations in our study with Doppler mean gradients 227 and catheter peakto-peak gradients >75 mm Hg showed AR. Among 16 evaluations with catheter peak-to-peak gradients
Arterial Shmuel
Doppler peak and mean gradients are useful predictors of catheter peak-to-peak gradients, hut the predictive value diminishes with AR. We present potentially useful equations to predict catheter gradients and guide the timing of intervention.
1. Bengur AR, Snider AR, Sewer GA, Peters J. Rosenthal A. Usefulness of the Doppler mean gradient in evaluation of children with aortic valve stenosis and comparison to gradient at catheterization. Am J Cm-did 1989;64:756-761.
2. Perry GJ, Helmcke F, Nanda NC, Byard C, Soto B. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Cdl Cm-did 1987;9:952-959. 3. Park MK. Electrocardiography 1. In: Park MK, ed. Pediatric Cardiology for Practitioners. 2nd ed. Chicago, IL: Year Book Medical, 1988:34-52.
and Venous Compliance Nonobese Subjects Oren,
MD, Ehud Grossman,
besity and systemic hypertension frequently coexist in the same patient and are considered in0dependent risk factors of cardiovascular disease. Hemodynamic studies have shown that obesity and hypertension exert disparate cardiovascular effects.‘3 Compared with nonobese patients with the same arterial blood pressure, obese patients have lower peripheral resistance. This study assesses arterial compliance and central blood volume as an indirect index of peripheral venoconstriction in obese and nonobese normotensive and hypertensive patients. . . . Thirty-six hypertensive subjects (19 obese and 17 nonobese) and 24 normotensive subjects ( 11 obese and 13 nonobese) were included in the study. Patients were classified as obese when their body mass index was >30 kg/m2, and as nonobese when body mass index was <26 kg/m2. Obese and nonobese subjects were matched as closely as possible for mean blood pressure and age. However, hypertensive patients were older than normotensive subjects (Table I). All hypertensive patients had diastolic pressure values that were consistently >90 mm Hg when measured in the outpatient clinic, and they were either never treated for high blood pressure or were withdrawn from antihypertensive therapy 24 weeks before the study. The protocol of the study was approved by the institution’s clinical investigaFrom the Department
<75 mm Hg and Doppler mean gradients z-27 mm Hg, 12 showed AR and 4 did not.
of Internal Medicine, Section of Hypertensive Diseases, Ochsner Clinic, and Division of Research, Alton Ochsner Medical Foundation, New Orleans, Louisiana. Dr. Oren’s address is: Department of Internal Medicine, Barzilai Medical Center, Ashkelon, Israel. Manuscript receivedjuly 10, 1995; revised manuscript received and accepted November 2, 1995.
in Obese
MD, and Edward
and
D. Frohlich, MD
tion committee, and informed written consent was obtained. Hemodynamic evaluation was performed in the supine position by previously reported methods.4 Briefly, catheters were inserted in an anticubital vein and a brachial artery and were advanced to the level of the superior vena cava and ascending aorta, respectively. Cardiac output was obtained by the indocyanine green dye dilution technique; intraarterial pressure was continuously determined by direct arterial measurement, and the usual hemodynamic indexes were calculated by standard formulas. Central blood volume was assessed from the dye dilution curve by calculating the product of mean transit time and blood flow per second.5 Plasma volume was measured with iodine-125-labeled plasma serum albumin,4 and total blood volume was estimated from the plasma volume and hematocrit. The distribution of blood between peripheral and cardiopulmonary segments of the circulation, as estimated by the ratio of central blood volume to total blood volume, was chosen as an indirect index of the peripheral venoconstriction.5-9 Arterial compliance was estimated by 2 methods: ( 1) pulse pressure divided by stroke volume, as used previously by different investigators ‘OS”; and (2) diastolic blood pressure decay, an exponential analysis of the blood pressure-time curve during diastole, as calculated from the intraarterial pulse tracings. Arterial compliance was estimated using a simple firstorder model of circulation, as previously described and validated.” Three aortic pulse tracings were measured and arterial compliance was the mean of the 3 values. BRIEF
REPORTS
665
significantly higher arterial compliance than their nonobese counterNarmatensive Hypertensive parts (Table II). Arterial compliance estimated from the diastolic Lean Obese Lean Obese blood pressure decay was nega(n = 13) (n= 11) (n = 17) (n = 19) tively correlated with systolic arteAge (vl 392 10 37% 11 47 + 14* 49 -c 10* rial pressure (r = -0.64; p Women/men 6/7 6/S 6/11 5/14
I Characteristics
of the Study
Group
l
l
666
THE
AMERICAN
JOURNAL
OF
CARDIOLOGY”
VOL.
77
MARCH
15,
1996
The present study agrees with the recent study of Raison et al,17 in which they compared obese with nonobese hypertensive patients, and found that obese patients were characterized by higher values of blood flow velocity and by lower values of vascular resistance. In conclusion, the present study shows that, compared with their’nonobese counterparts, obese patients have higher stroke volume, cardiac output, central blood volume, and total blood volume, and lower peripheral resistance. The ratio of central blood volume to total blood volume, as an index of peripheral venous distensibility, did not differ between the 2 groups, whereas arterial compliance was better in obese patients and correlated with body mass index only in the hypertensive population.
1. Messerli FH, Sundgaard-Riise K, Resisin E, Dreslinski F, Dunn FG, Frohlich ED. Disparate cardiovascular effects of obesity and arterial hypertension. Am J Med 1983;74:808-812. 2. Messerli FH. Cardiovascular effects of obesity and hypertension. Lancer 1982;1:1165-1168. 3. Messerli FH. Cardiopathy of obesity-a not-so-Victorian disease. N Engl J Med 1986;314:378-380. 4. Messerli FH, De Carvalho JGR, Christie B, Frohlich ED. Systemic and regional hemodynamics in low, normal and high cardiac output borderline hypertension. Circulation 1978;58:44-448.
5. Uhych M, Frohlich ED, Tarazi RC, Duston HP, Page IH. Cardiac output and distribution of blood volume in central and peripheral circulations in hypertensive and normotensive man. Br Heart J 1969;31:570-574. 6. Safar ME, London GM. Venous system is essential hypertension. Clin Sci 1985;69:497-504. 7. London GM, Safer ME, Simon AC, Alexander JM, Levenson JA, Weiss YA. Total effective compliance, cardiac output and fluid volume in essential hypertension. Circulation 1978;51:995-1000. 8. Simon AC, Safar ME, Weiss YA, London GM, Millie2 PL. Baroreflex sensitivity and cardiopulmonary blood volume in normotensive and hypertensive patients. Br Heart J 1977;39:799-805. 9. Schmieder RE, Messerli FH, de Carvalho JGR, Husserl FE. Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis. Am J Kidney Dis 1987;9:55-59. 10. Simon AC, Safar MA, Levenson JA, Kheder AM, Levy BI. Systolic hypertension: hemodynamic mechanism and choice of antihypertensive treatment. Am J Cardiol 1979;44:505-511. 11. Tarazi RC, Margii F, Dustan HP. The role of aortic distensibility in hypertension. In: Miller P, Safar MD, eds. International Symposium on Hypertension. Monaco, 1975, Boehringer Ingelheim:l33-135. 12. Fitzpatrick MA, Hinderliter AL, Egan BM, Julius S. Decreased venous distensibility and reduced renin responsiveness in hypertension. Hypertension 1986;8(suppl II)%36-11-43. 13. Reisin E, Frohlich ED, Messerli FH, Dreslinski GR, Dunn FG, Jones MM, Batson HM Jr. Cardiovascular changes after weight reduction in obesity hypertension. Ann Intern Med 1983;98:315-319, 14. Ventura H, Messerli FH, Oigman W, Suarez DH, Dreslinski GR, Dunn FG, Reisin E. Impaired systemic arterial compliance in borderline hypertension. Am Heart J 1984;109:132-136. 15. Simon AC, Levenson J, Maarek B, Bouthier J, Safar ME. Evidence of early changes of the brachial artery circulation in borderline hypertension. J Cardiovasc Phannacol 1986;8(suppl5):536-538. 16. Simon AC, Safar ME, Levenson JA, London GM, Levy BI, Chau NP. An evaluation of large arteries compliance in man. Am J Physiol 1979;237:H550H554. 17. Raison JM, Safar ME, Cambien FA, London GM. Forearm hemodynamics in obese, normotensive and hypertensive subjects. J Hypertens 1988;6:299303.
BRIEF REPORTS
667
Arterial Shmuel
Doppler peak and mean gradients are useful predictors of catheter peak-to-peak gradients, hut the predictive value diminishes with AR. We present potentially useful equations to predict catheter gradients and guide the timing of intervention.
1. Bengur AR, Snider AR, Sewer GA, Peters J. Rosenthal A. Usefulness of the Doppler mean gradient in evaluation of children with aortic valve stenosis and comparison to gradient at catheterization. Am J Cm-did 1989;64:756-761.
2. Perry GJ, Helmcke F, Nanda NC, Byard C, Soto B. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Cdl Cm-did 1987;9:952-959. 3. Park MK. Electrocardiography 1. In: Park MK, ed. Pediatric Cardiology for Practitioners. 2nd ed. Chicago, IL: Year Book Medical, 1988:34-52.
and Venous Compliance Nonobese Subjects Oren,
MD, Ehud Grossman,
besity and systemic hypertension frequently coexist in the same patient and are considered in0dependent risk factors of cardiovascular disease. Hemodynamic studies have shown that obesity and hypertension exert disparate cardiovascular effects.‘3 Compared with nonobese patients with the same arterial blood pressure, obese patients have lower peripheral resistance. This study assesses arterial compliance and central blood volume as an indirect index of peripheral venoconstriction in obese and nonobese normotensive and hypertensive patients. . . . Thirty-six hypertensive subjects (19 obese and 17 nonobese) and 24 normotensive subjects ( 11 obese and 13 nonobese) were included in the study. Patients were classified as obese when their body mass index was >30 kg/m2, and as nonobese when body mass index was <26 kg/m2. Obese and nonobese subjects were matched as closely as possible for mean blood pressure and age. However, hypertensive patients were older than normotensive subjects (Table I). All hypertensive patients had diastolic pressure values that were consistently >90 mm Hg when measured in the outpatient clinic, and they were either never treated for high blood pressure or were withdrawn from antihypertensive therapy 24 weeks before the study. The protocol of the study was approved by the institution’s clinical investigaFrom the Department
<75 mm Hg and Doppler mean gradients z-27 mm Hg, 12 showed AR and 4 did not.
of Internal Medicine, Section of Hypertensive Diseases, Ochsner Clinic, and Division of Research, Alton Ochsner Medical Foundation, New Orleans, Louisiana. Dr. Oren’s address is: Department of Internal Medicine, Barzilai Medical Center, Ashkelon, Israel. Manuscript receivedjuly 10, 1995; revised manuscript received and accepted November 2, 1995.
in Obese
MD, and Edward
and
D. Frohlich, MD
tion committee, and informed written consent was obtained. Hemodynamic evaluation was performed in the supine position by previously reported methods.4 Briefly, catheters were inserted in an anticubital vein and a brachial artery and were advanced to the level of the superior vena cava and ascending aorta, respectively. Cardiac output was obtained by the indocyanine green dye dilution technique; intraarterial pressure was continuously determined by direct arterial measurement, and the usual hemodynamic indexes were calculated by standard formulas. Central blood volume was assessed from the dye dilution curve by calculating the product of mean transit time and blood flow per second.5 Plasma volume was measured with iodine-125-labeled plasma serum albumin,4 and total blood volume was estimated from the plasma volume and hematocrit. The distribution of blood between peripheral and cardiopulmonary segments of the circulation, as estimated by the ratio of central blood volume to total blood volume, was chosen as an indirect index of the peripheral venoconstriction.5-9 Arterial compliance was estimated by 2 methods: ( 1) pulse pressure divided by stroke volume, as used previously by different investigators ‘OS”; and (2) diastolic blood pressure decay, an exponential analysis of the blood pressure-time curve during diastole, as calculated from the intraarterial pulse tracings. Arterial compliance was estimated using a simple firstorder model of circulation, as previously described and validated.” Three aortic pulse tracings were measured and arterial compliance was the mean of the 3 values. BRIEF
REPORTS
665
significantly higher arterial compliance than their nonobese counterNarmatensive Hypertensive parts (Table II). Arterial compliance estimated from the diastolic Lean Obese Lean Obese blood pressure decay was nega(n = 13) (n= 11) (n = 17) (n = 19) tively correlated with systolic arteAge (vl 392 10 37% 11 47 + 14* 49 -c 10* rial pressure (r = -0.64; p Women/men 6/7 6/S 6/11 5/14
I Characteristics
of the Study
Group
l
l
666
THE
AMERICAN
JOURNAL
OF
CARDIOLOGY”
VOL.
77
MARCH
15,
1996
The present study agrees with the recent study of Raison et al,17 in which they compared obese with nonobese hypertensive patients, and found that obese patients were characterized by higher values of blood flow velocity and by lower values of vascular resistance. In conclusion, the present study shows that, compared with their’nonobese counterparts, obese patients have higher stroke volume, cardiac output, central blood volume, and total blood volume, and lower peripheral resistance. The ratio of central blood volume to total blood volume, as an index of peripheral venous distensibility, did not differ between the 2 groups, whereas arterial compliance was better in obese patients and correlated with body mass index only in the hypertensive population.
1. Messerli FH, Sundgaard-Riise K, Resisin E, Dreslinski F, Dunn FG, Frohlich ED. Disparate cardiovascular effects of obesity and arterial hypertension. Am J Med 1983;74:808-812. 2. Messerli FH. Cardiovascular effects of obesity and hypertension. Lancer 1982;1:1165-1168. 3. Messerli FH. Cardiopathy of obesity-a not-so-Victorian disease. N Engl J Med 1986;314:378-380. 4. Messerli FH, De Carvalho JGR, Christie B, Frohlich ED. Systemic and regional hemodynamics in low, normal and high cardiac output borderline hypertension. Circulation 1978;58:44-448.
5. Uhych M, Frohlich ED, Tarazi RC, Duston HP, Page IH. Cardiac output and distribution of blood volume in central and peripheral circulations in hypertensive and normotensive man. Br Heart J 1969;31:570-574. 6. Safar ME, London GM. Venous system is essential hypertension. Clin Sci 1985;69:497-504. 7. London GM, Safer ME, Simon AC, Alexander JM, Levenson JA, Weiss YA. Total effective compliance, cardiac output and fluid volume in essential hypertension. Circulation 1978;51:995-1000. 8. Simon AC, Safar ME, Weiss YA, London GM, Millie2 PL. Baroreflex sensitivity and cardiopulmonary blood volume in normotensive and hypertensive patients. Br Heart J 1977;39:799-805. 9. Schmieder RE, Messerli FH, de Carvalho JGR, Husserl FE. Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis. Am J Kidney Dis 1987;9:55-59. 10. Simon AC, Safar MA, Levenson JA, Kheder AM, Levy BI. Systolic hypertension: hemodynamic mechanism and choice of antihypertensive treatment. Am J Cardiol 1979;44:505-511. 11. Tarazi RC, Margii F, Dustan HP. The role of aortic distensibility in hypertension. In: Miller P, Safar MD, eds. International Symposium on Hypertension. Monaco, 1975, Boehringer Ingelheim:l33-135. 12. Fitzpatrick MA, Hinderliter AL, Egan BM, Julius S. Decreased venous distensibility and reduced renin responsiveness in hypertension. Hypertension 1986;8(suppl II)%36-11-43. 13. Reisin E, Frohlich ED, Messerli FH, Dreslinski GR, Dunn FG, Jones MM, Batson HM Jr. Cardiovascular changes after weight reduction in obesity hypertension. Ann Intern Med 1983;98:315-319, 14. Ventura H, Messerli FH, Oigman W, Suarez DH, Dreslinski GR, Dunn FG, Reisin E. Impaired systemic arterial compliance in borderline hypertension. Am Heart J 1984;109:132-136. 15. Simon AC, Levenson J, Maarek B, Bouthier J, Safar ME. Evidence of early changes of the brachial artery circulation in borderline hypertension. J Cardiovasc Phannacol 1986;8(suppl5):536-538. 16. Simon AC, Safar ME, Levenson JA, London GM, Levy BI, Chau NP. An evaluation of large arteries compliance in man. Am J Physiol 1979;237:H550H554. 17. Raison JM, Safar ME, Cambien FA, London GM. Forearm hemodynamics in obese, normotensive and hypertensive subjects. J Hypertens 1988;6:299303.
BRIEF REPORTS
667