Relation of arterial pressure waveform to left ventricular and carotid anatomy in normotensive subjects

travels toward the heart (l,2). la the functional ~at~~i~~ between the left v

reflected waves fall in the diastolic portion of the central arterial waveform

crease that enhances coronary

nerate a pressure in- on CM).

From the Department of Medicine, The New ?ork Hospital-Cornell Medical Center. New York, New York and *Institute of Clinical Medicine, University of Sassari, Sassari, Italy. This study was suppofled in part by Grant PIL 18323 from the National Heart, Ltmg, and Blood Institute, National Institutes of Health, Bethesda, Maryland; the Michael Walk Heart Founda- tion, New York and the Helen W. Buckner Cardiac Research Fund, New York. Dr. Saba is the recipient of a research grant from the Regione Autonoma della Sardegna, Italy.

Manlnscript received December 18. 1992; revised miaurssripl received May 7. 1993, accepted July 15, 1993.

me: Dr. M.q 9. &man, Division of Cad&q, Box 222, The New York Hospital-Cornell Medical Center, 525 East 68 Street. New York, New York 10021.

return of ~~~~ct~d

the central systole rather

further a~6~~~ti~~ systolic pressure (2 this phenomenon to left ve~tr~~~~a~

ith higher vascubr ~~~ed~c~~ index sf cardiac ~yd~~~~~~ Is

crease in systolic wall stres

small aumbers of

1874 SA&A ET AL.

PRESSURE WAVEFORMS AND CARBIOVASCULAR ADAPTATION

noninvaSive, high fidelity recording of central pressure wavefms and ultrasound evaluation of carotid and kft vent&& structure to examine these relations in normo-

tensive, apparently normal,

subjects.

The

pressure 440190 mm Hg on repeated measure-

ments), with a mean age of 47 f: 15 yews (tange 26 to 8%

formulas. Endaystolic

sis i1 system (OTE. Bio-

prd~. With the subject rextension, the common

Two-dimensionally guided -mode trxiogs of the common carotid artery (app imately 1 cm pmimal carotid bulb) with a simu~taueoMs e~e~tro~ar~iog~m a

pressure waveform from the ~o~t~~~t~~~~ carotid artery

Suitable frames

BS been validated in

The transducer is internally calibrat

10 mm Hg) and ‘stem absolute changes in

over a range olF mm Hg. To obtain actu

pressure values, the waveform tracings were also externally calibrated. On the basis of the observation that mean arterial pressure does not significantly vary within the capacitance

ells (X,33), b~~bi~~ artery pressure was measured and menus s~~ygmoma~ometer with the patient

v and

meam

ssigned to the planimetricalIy corn es-derived mean blood pressure of the carotid waveforms. after calibration, carotid peak systolic and end-diastolic pressures were cal- culated by computer.

m

d

1876 SABA ET AL. JACC Vol. 22, NC. 7

F’RESSURE \VAVEFORMS AND CARDIOVASCULAR ADAPTATION Decamher 1993:1873-80

tid

ventricular mass index was positively nl

0.02) to the augmentation index (Fig. 31, whereas relations of VecntricMlar mss to measures of arterial st

attain statisticat significance. Because left v

diastolic chamber sizes were similar, relative wall thickness 2, Total periphml resistance was bjects owiaag to the ~~~~e~ man blood ~~SsM~e ~~~~s~ stroke volun1e alrd cardiac Output did mt differ

Au carotid artery St~~tM~e ard su MSS. Carotid artery ahsolute and relative wall thicknesses were larger in group 2 than in group 1 (Table 4, Fig. 2). All measures of regional arterial stiffness (except Young’s mod- ulus, which did not attain statistical significance) were in-

0.01 vs. wbjecki with type c bear. Vdecs ~~~~~~4~~~ 111% menn wutuss ” or numbr of subjeck Al * ~14~~~i~~~~4~jl~414 index: BBP v ditrstolic bk?od ssurc; F - hirle; M j*, mdc; MAP = mm ertcd pnwsubx W = pulse pmss'3m; SW = systolic blood pWMre.

When the dislen

ass index or !xxIy s

es and Arterial Pressttr te %yst0lic Peak of the Ciroup 2 Group 1 (1 A and (type C beats, a&,

AI % O.0) 0.0)

(n = 25) (n = 4:) p Valtsc s____l___

Al -0.11 c 0.M 0.14 z-o.s!I

Atie (yrl 362 10 542 14 c O.Qoo1

Gender (ME) 2213 26116 < 0.03

Smoking history (% smokers) 16 26 HS

Height (m) 1.76 + 0.0s 1.69 f 0.10 < 0.002 Body mass index (kglm*) 24.6 2 4.5 25.6 + 3.7 NS Body surfacle area (mZ) 1.92 f 0.22 I.83 + 0.21 NS Brachial SW (mm Hg) 116 2 9 123 t 10 $8 ?z 9 74 ?: 110 c 0.03 Brachial PP (mm Wg) 48 1- g MAP (mm Ng) 8428 Carotid SBP (mm Mg) 107 z!z 10 Carotid BBP (mm Hg) 672 10 71 f. 12 NS Carotid PP (mm Hg) 40 + 12 47 + 16 NS

Unless otherwise identified, values presented are mean value I- SQ or number of subjects. Abbreviations as in Table 1.

1878 SABA ET AL.

W%JRE WAVeFORMS AND CARDIOVASCULAR ADAWATION

4, R&&on of Augmentation Index to Carotid Artery

GKNJp 1 Group 2 (AI s O.@ (AI B 0,O)

(i-l = 25) (n = 42) p value wall tikness (mln~ 0.62 9 0.17 0.73 ” 0,15 < 0.01 DiaWJic dirnc~sion (mm) 5.77 f 0.71 5.50 c a60 NS IWive wali tikness 0.22 t 0.05 0.27 k 0,06 C 0*0006 Ep (dyn&cm*~10-6, 0.37 * OS18 0.53 t OS31 < OS01 E (dyne&mz per mm~lO? 0.63 u 0.19 0.75 r O-37 NS

l&t

ventricular wall thicknesses

index between

two groups (Table 5).

V+zatriculw Anatomy in R&ion to Augmenttltion Index After Comction for UldM Arterial Pressure by Analysis of Covtianca

A~usted Mean vahles+ Adjusted Mean WINS* for Group 1 (n = 25) for Gpaup 2 (n = 42)

(AK s 0.0) (AI > O.(1)

1.71 1.72 1.71 I .70

poskrior wall thickriess (cm) 0.7% 0.76 0.w 0.83$

stulie thickness (cml 0.78 0.80 0.880 0.8%

65 6% 8311 831

0.3 1 0,32 0.33 0.33

Ttiti @@heal titiarlce (dyRewl& ‘3) I,434 I.454 l.561 1,551 and for gender. age and mean arterial pressun of subjects. rsus group 1 after adjus t for gender and age. #p < 0.05 versus group 1 after adjustment aerial pressure. §p < 0.85 versus group I after adjustment for gender and age. IIp < 0.001 versus @WP 1 PAer @iustment fw gender and age. ?Jp < 0.001 versus group 1 after adjustment for gender, age and mean arterial paessun. Abbreviations as in Tables 1 and 3.

ventricuhx mass because the tension imposed portant stimusus to iation between late systolic pressure peaks and left v~~~~r~~u~ar relative wa1 thickness did not remain statistically significant after adjust- ment for gender and age.

Prospective evaluation will be required to determine whether subjects with a dominant late systolic arterial

eak are more likely ta develop fran systolic ~y~er~e~sio~, or t early systolic peak. The observation that the pulsa#e ~omp~~e~t

of

carotid artery, was also found in the

late19 to the pressure waveform. Similar to left ventricular findings, both the absolute and relative wall thicknesses of the common carotid artery were in- creased in subjects with a dominant late systolic pressure peak, whereas the internal diameters were similar in the two groups. All measures of regional arterial stiffness were increased in group 2 subjects, ~~~~~d~rn~ measures that take into account the curvilinear press -vohune relation (p’ and /31W), the influences of distend pressure (ploo) or t

effect of compensatory increases in wall thickness (Young’s modulus).

The observed differences in carotid artery structure and stiffness between the two groups appear to be primarily

We thank Virginia Burns for assistance in preparation of the nmuscript.

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