Hemodynamic changes in pulmonary circulation induced by effort in the elderly

phy that risk factors for ECAD were age, systemic hypertension, smoking, serum HDL cholesterol (inverse association) and uric acid (inverse association), and Framingham type A score (inverse association).7 Risk factorsnot significantlv assnciat~rlwith EC&V?::‘crc sex, diabetesmelhtus, family history of CAD, percent ideal body weight, history of myocardial infarction and angina pectoris, hemoglobin, serum total and low-density lipoprotein cholesterol, and serum triglycerides. These investigatorsalso reported that the B-mode score (extent of carotid atherosclerosis) was strongly and independently associatedwith CAD in patients aged >50 years8 The relation between ECAD, diagnosed by carotid duplex ultrasonography,and serum total and HDL cholesterol, measured8 years before the carotid studies and concurrently, was investigated in 1,189 elderly persons in the Framingham Study.gThere was a strong association between the degree of ECAD and serum total cholesterol measured 8 years before the carotid studies in both men and women. There was a strong association between the degree of ECAD and serum HDL cholesterol, measured8 years before the carotid studies and concurrently, for women but not for men. The present study performed in 1,063 elderly patients showed that significant prognostic variables for ECAD in the multivariate logistic regression model were: (1) cigarettesmoking, (2) serum total cholesterol, (3) serum HDL cholesterol, (4) diabetes mellitus, and (5) prior CAD. There was a tendency for age to be associated with ECAD (p = 0.06). Systemic hypertension (p =

0.001) and serum triglycerides (p = 0.021) were significant risk factors for ECAD by univariate analysis, but not after multivariate analysis. The variable systemic hypertension became nonsignificant when the variable of pior CAD was entered in me togtstic regression model. Other risk factors not associated with ECAD were sex and obesity.

1. Amnow WS, Schoenfcld MR, Paul P. Risk factors fur extracranial internal or cmnmon carotid arterial disease in persons aged 60 years and older. Am J Car-di01 1989:63:881-8X2. 2. Aronow WS, Schoenfeld MR. Forty-five-month follow-up of extracmnial carotid ,atet-ial disease for new coronary events in elderly patients. Coi-onary Artmy Dis 1992;3:249-251. 3. Aronow WS, Herzig AH, Etienne F, D’Alba P, Ronquillo J. 41-month followup OF risk factors correlated with new coronary events in 708 elderly patients. J Am Geriatr Sot 1989;37:501-506. 4. Master AM, Laser RP, Beckman G. Tables of average weight and height of Americans aged 65 to 94 years. Relationship of weight and height to suwival. JAMA 1960;172:658&662. 5. Candclisc L, Bianchi F, Galligoni F, Albanese V, Bonelli G, Bona L, Inz~lari D, Mwiani F, Rasura M, Rognoii F, Sangiovanni G, Fiescbi C. It&a multicenter smdy on reversible cerebral ischemic attacks: ITI--influe~~~ of age ‘and risk factors on cerebrovascula atherosclerosis. Stroke 1984;15:379-382. 6. Ford CS, Grouse JR III, Howard G, To& JF, Ball MR, Frye J. The role of plasma lipids in carotid bifurcation atherosclerosis. Ann NeLlrol 1985;17:301-303. 7. Grouse JR, Took JF, McKinney WM, Dignan MB, Howard 6, Kahl FR, McMahan MR, Harpold GH. Risk factors for extracranial carotid artcry atherosclerosis. Smke 1987;18:99&996. 8. Craven ‘IE, Ryu .IE, Espeland MA, Kahl FR, McKinncy WM, To& JF, McMam hau MR, Thompson Cl, H&s G, Crows JR m. Evaluation of the associations between carotid artery atherosclerosis and coronary xtety stenosis: a case-control study. Circulation 1990;82:123&-1242. 9. O’Leary DH, Anderson KM, Wolf PA, Evans JC, Poehlman NW. Cholesterol and carotid atherosclerosis in older pewxs: the Framingham Study. Ann Eph~iol 1992;2:147-153.

Hemodynamic Changes in Pulmonary Effort in the Elderly

Circulation

Induce

Federico Cacciapuoti, MD, Maria D’Avino, MD, Diana Lama, MD, Ugo Bianchi, MD, Nicob Perrone, MD, and Salvatore Gentile, MD ge-relatedchangesin vascular tissue were previously reported.1,2Moreover, mild dilfuse connective tissue proliferation of the aging lung can contribute to reduced reserve of the pulmonary vascular bed.3 These morphologic changes may induce some hemodynamic impairment of the aging pulmonary circulation. Unlike the systemic circulation, relatively little is known regarding the effects of effort on pulmonary hemodynamits in healthy, elderly subjects. Difficulties in selecting elderly subjectswithout pulmonary vascular, cardiac and lung disease,and the absenceof an effective, noninvasive method for the measurementof pulmonary herno-. dynamics are the causesfor this poor knowledge.4 In the present study, we evaluated the pulmonary hemodynamits in an elderly cohort, free of cardiovascular and lung disease,at rest and during submaximal supine exercise. The study group comprised 47 healthy subjects (31 men and 16 women, age range 32 to 7.5 years). The subjects were selected retrospectively from 3,422 patients who underwent cardiac catheterization for suspected coronary disease. Patients with coronary artery From the Cattedra di Gerontologia e Geriatria, First Facolta di Medicina, Universitk “Federico II,” Piazza L. Miraglia, 2, 80138 Napoli, Italia. Manuscript received December 9, 1992; revised manuscript received January 6, 1993, and accepted January 7.

disease were excluded from the study, as well as those with an ejection fraction <50%. Electrocardiograms and echocardiograms were within the normal range in all 47 subjects. All subjects had systolic blood pressure 1140 mm Hg and diastolic blood pressure 580 mm Hg. On chest x-ray, the cardiothoracic ratio was 10.5, with no signs of pulmonary congestion or hypertension, or both. The forced expiratory volume and vital capacity were normal. In addition, subjects had an arterial oxygen tension 270 mm IIg and an arterial oxygen saturation 290% at catheterization. Nine subjects were smokers (II packlday), 5 were exsmokers,and the remaining 33 were nonsmokers.With referenceto age, the study cohort was divided in 2 groups: Group I comprised 27 subjects (21 men and 6 women) with an age range between 32 and 60 years (mean 50 _+9). Group II comprised the remaining 20 subjects (10 men and 10 women) with an age range between 61 and 15 years (mean 67 + 4). All subjects gave informed consent and underwent new right-sided cardiac catheterization to evaluate the pulmonary hemodynamic responseto effort I week afler baseline hemodynamic measurements.For this procedure, a SFr Swan-Ganz balloon-tipped catheter was inserted in the pulmonary artery and placed in the wedge position. Supine dynamic exercise BRIEFREPORTS

monary artery pressure (mm Hg), wedgepressure (mm Hg), difSerencebetween mean pulmonary artery and wedge pressure (mm Hg), pulmonary vascular resistance (dyneslslcm-5), and pulmonary-to-systemic vascular. resistance ratio X 1,000. Values were expressed as mean f I SD. An unpaired Student’s t test was used to compare mean values obtained in the 2 study groups at rest and during effort. Linear regressionanalysis was pegormed to evaluate the relation betweenage andpulmonary hemodynamic changesat rest. Furthermore, the

was peqormed with a bicycle placed at the foot of the bed, so that the subject could leg pedal in a recumbent position. The stress test was peflormed following the standard protocolsg6and was stopped at 90% of the predicted mean age-spec$c heart rate. Both at rest arid during the last minute of exercise, the following parameters were evaluated: heart rate (beatslmin), systolic, diastolic and mean blood pressure (mm Hg), cardiac index (literslminlm2), cardiac output (literslmin), systemic vascular resistance (dyneslslcm-5), mean pul-

I

r

TABLE I Systemic Hemodynamics

(mean k 1 SD) Rest

Effort

Group I HR (beatsimin) SBP (mm Hg) DBP (mm Hg) mBP (mm Hg) WP (mm Hg) Cl (L/min/m’) CO (L/min) SVR (dynes/s/cm-5)

72.3 122.5 69.10 90.3 6.80 3.30 5.90 1,174

Group I

Group II

f 3.2 f 4.5 2 2.07 f 2.6 z!z1.32 k 0.17 f 0.63 2 117

75.4 127.5 72.4 95.6 7.00 3.20 5.6Q 1,465.5

-+ 3.6 k 5.0 t- 4.4 -+ 3.6 2 0.66 r 0.17 ir 0.17 + 73.0

167.9 172.5 84.2 109.5 7.80 8.30 15.2 616.9

+- 8.6 +- 7.1 t 2.5 2 7.2 F 1.21 2 1.13 YL1.8 zk 53.2

Group II 138.1 188.0 90.2 122.5 8.70 8.00 14.90 789

2 * 2 2 2 f f 5

5.2 5.0 5.4 6.8 0.81 0.39 1.29 61

Groups I and II are younger and older subjects, respectively. Differences between groups not significant. Cl = cardiac index; CO = cardiac output; DBP = diastolic blood pressure; HR = heart rate; mBP = mean blood pressure; SBP = systemic blood pressure; SVR = systemic vascular resistance: WP = wedge pressure. I

I

TABLE II Pulmonary Hemodynamics

(mean + 1 SD) Effort

Rest Group I mPAP (mm Hg) mPAP - WP (mm Hg) PVR (dynes/s/cm-5) PVR/SVR x 1,000

11.7 4.90 66.3 56.1

Group I

Group II

k 1.3 -+ 0.46 2 7.0 k 5.5

15.9 8.80 131.0 89.4

f 1.0* 2 0.58* f 8.27 +- 4.8t

13.2 5.3 32.1 50.8

2 1.3 F 0.6 z. 4.4 + 6.5

Group II 18.12 9.40 87.8 80.6

-c l.lO* f 0.55 2 4.5t f 4.3t

*p <0.05; tp
I

mPA P 20-t n-47 rz 0.94 18-

.

Y=-2,22+.,9x

.

P
FIGURE 1. Correlation between age and value of mean pulmonary artery preb sure (mPAP).

8-

6-

4

‘ 30

I 40

I

I 50

,

I 60

I

1 70

YEARS

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THE AMERICANJOURNALOF CARDIOLOGY VOLUME71

JUNE 15,199X

I

percent changes in theseparameters induced by efort sure across the pulmonary vascular bed was related to in each group were calculated and compared by un- age (r = 0.75; p ~0.001) (Figure 2). Pulmonary vascupaired Student’s t test. All subjects were found to have lar resistance was also closely related to age (r = 0.77; normal coronary flow, and right and left ventricular p ~0.001) (Figure 3). Finally, the pulmonary-to-systnem.‘r..Pm,--.l--i:;i;&fiLc: ,&& x <,Q$(jLyignificantly in“CIOLCbIUI hemodynamics.Differences in body +&e area in the LlllllL 2 groups were notsigni$cant (I.77 f 0.15 n$ in group creased with age (r = 0.71; p
8

FIGURE 2. Correlation between age and difference in pressure vascular bed (mPAP - W.P,).

I”

*

E

7

E 8

3 80

40

30

60

70

YEARS

VZ-35.20

FlGURE 3. Correlation between pulmonary vascular resistance

+ 2.25

X

age and (P.V.R.).

BRIEFREPORTS

PVR/SVR

FIGURE 4. Correlation between age and pulmonary-to-systemic vascular reektame ratio (PVR/SVR) x 1,000.

20

I 30

40

I 50

1

I 60

I

1 70

YEARS

ry diseases.Thus, results were not comparable, and were dependent on different ages and cardiorespiratory protiles, However, Davidson and Feel0 studied pulmonary hemodynamics in elderly subjects without coronary disease, but the observations were obtained only at rest. The increase in pulmonary vascular resistance and pressure recorded at rest in the elderly subjects was dependent on several mechanisms.A prevalent abnormality of the pulmonary vascular bed is likely to occur with age, together with changes in the systemic circu1ation.l’ However, the increasedpulmonary-to-systemic vascular resistanceratio found in older subjects suggeststhat the effects of aging were greater in the pulmonary than in the systemic vascular bed. Furthermore, the small increasein wedge pressurecould be explained by the agedependenttendency toward left ventricular diastolic dysfunction.r2 However, the major decrease in pressure acrossthe pulmonary vascular bed suggeststhat the increasedmean pulmonary artery pressure was prevalent with changes in capillary wedge pressure. During exercise, the efficacy of the p-adrenergic stimulation progressively decreaseswith age,13and this has been hypothesized to be deleterious to cardiovascular performancewith increasingage.Therefore,it hasbeen accepted that a decreasein cardiac output at exercise is a manifestation of the aging process.r4On the contrary,the present results showed that aging per se did not limit the increase in cardiac output during exercise. However, aging probably did alter the mechanisms by which cardiac output is augmented during effort. In younger subjects during a dynamic stress test, the increased cardiac output was due to an increase in heart rate and to a reduction in end-systolic volume, whereas in older subjects ‘this result appearedto be due to intervention of the

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Frank-Starling mechanism, which induces a greater increase in end-diastolic and stroke volumes to compensatefor the age-dependentminor increasein heart rate.r5 This increase in cardiac output was also responsiblefor the decreasein pulmonary vascular resistanceduring exercise in our older subjects.

1. O’Rcwke MF. Aging and Arterial Function. New York: Churchill Livingstone, 1982~185-195. 2. Lakatta EG. Alterations in the cardiovascular system that occur in advanced age. Fed Proc 1979;38:163-167. 3. Frank N, Head I, Ferris B Jr. The mechanical behavior of the lungs in the healthy elderly persons. J Am Znvesr 1957;56:168@1687. 4. Burrows B, Alpert JS, Ross JL. Pulmonary heart disease. J Am Coil Car&l 1987;10:63A-65A. 5. Lowe DK, Rothbaum DA, MC Henry PL, Co~ya BC, Knoebel SB. Myoca~dial blood flow response to isometric (handgrip) and treadmill exercise in coronary artery disease. Circulation 1975;51: 126-131. 6. Bruce RA, Blakmon JR, Jones JW, Strait G. Exercising testing in adult normal subjects and cardiac patients. Pediatrics 1963;32:742-748. 7. Elkins RC, Milnor WR. Puhnonq vascular response to exercise in the dog. Circ Res 1971;29:591-599. 8. Thadani U, Parker JO. Hemodynamic at rest and during and sitting bicycle exercise in normal subjects. Am .I Cardiol 1978;41:52-59. 9. Holmgren AJ, Jonsson B, Sjostrand T. Circulatory data in normal subjects at rest and during exercise in the recumbwt position, with special reference to the stroke volume at different work intesities. Acra Physiol Scand 1960;49:343-363. 10. Davidson WR Jr, Fee EC. Influence of aging on pulmonaq emcdynamics in a population free of coronary a&ry disease. Am J Cardiol 1990;65:1454-1458. 11. Abboud FM, Huston JH. The effects of aging and degenerative vascular disease on the measurement of arterial rigidity in man. J Clin Invest 1961;40:933-938. 12. Yin FCP, Spurgeon HA, Weisfeldt ML, Lakatta EG. Mechanical properties of myocardium from hypertrophical rat hearts. A comparison between hypertrophy induced by senescence and by aortic banding. Circ Res 1980;46:292-298. 13. Lakatta EG. Age-related alterations in the cardiovascular response to adrenergic mediated stress. Fed Proc 1980;39:3173-3179, 14. Brandfonbrener M, Landowne M, Shock NW. Changes in cardiac output with age. Circulation 1955:12:557-566. 15. Rodeheffer RJ, Gerstenblith G, Becker LC, Fleg JL, Weisfeldt ML, Lakatta EG. Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilatation and increased stroke volume compensate for a diminished heart rate. Circulation 1984,69:203-213.

JUNE 15,1993