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Central Pressure More Strongly Relates to Vascular Disease and Outcome Than Does Brachial Pressure

The Strong Heart Study
Originally publishedhttps://doi.org/10.1161/HYPERTENSIONAHA.107.089078Hypertension. 2007;50:197–203

Abstract

Brachial blood pressure is predictive of cardiovascular outcome; however central pressure may better represent the load imposed on the coronary and cerebral arteries and thereby bear a stronger relationship to vascular damage and prognosis. Relations of brachial and central pressures to carotid artery hypertrophy (intimal-medial thickness and vascular mass), extent of atherosclerosis (plaque score), and incident cardiovascular events were examined in the Strong Heart Study. Central pressures were calculated using radial applanation tonometry. Among 3520 participants, central and brachial pulse pressures were more strongly related to vascular hypertrophy and extent of atherosclerosis than were systolic pressures. Central pulse pressure was more strongly related to all 3 arterial measures than was brachial pulse pressure (r=0.364 versus 0.309 for plaque score; P<0.001 for comparison of Spearman correlation coefficient; r=0.293 versus 0.249 for intimal-medial thickness; P<0.002; r=0.320 versus 0.289 for vascular mass; P<0.05). Among the 2403 participants free of clinical cardiovascular disease at baseline, 319 suffered fatal or nonfatal cardiovascular events during mean follow-up of 4.8±1.3 years. After adjustment for age, gender, current smoking, body mass index, cholesterol:HDL ratio, creatinine, fibrinogen, diabetes, and heart rate, central pulse pressure predicted cardiovascular events more strongly than brachial pulse pressure (hazards ratio=1.15 per 10 mm Hg, χ2=13.4, P<0.001 versus hazards ratio=1.10, χ2=6.9, P=0.008). In conclusion, noninvasively-determined central pulse pressure is more strongly related to vascular hypertrophy, extent of atherosclerosis, and cardiovascular events than is brachial blood pressure. These findings support prospective examination of use of central blood pressure as a treatment target in future trials.

Hypertension, defined as sustained elevation of brachial blood pressure, is a major risk factor for cardiovascular disease, and reduction of brachial blood pressure decreases cardiovascular events, particularly stroke.1 Available evidence suggests a greater importance of lowering systolic than diastolic pressure.2,3 In addition, pulse pressure predicts outcome4–10 and may be more strongly related to cardiovascular events than systolic pressure,6–8,11 depending on the age of the population studied.12–14 Although antihypertensive agents differ in their ability to reduce pulse pressure,15,16 the efficacy of targeting pulse pressure as a treatment goal has not been proven. Furthermore, pulse wave velocity, a measure of vascular stiffness, has been related to cardiovascular risk in hypertensive patients,17,18 the elderly,19,20 patients with end-stage renal disease,21,22 and population-based samples.23,24 Central aortic pressure can now be reliably determined by noninvasive techniques,25 and potential evidence of greater prognostic importance of central aortic than brachial pressures has been obtained in treated hypertensive patients.26 However, the applicability of this observation to population-based samples has not been assessed.

Although mean pressure is relatively similar in different large arteries,27,28 central aortic and brachial systolic and pulse pressures may differ considerably based on pulse wave velocity, a direct measure of arterial stiffness that influences timing of reflected waves returning from the periphery to the central aorta.29 The resultant amplification of brachial compared with central pulse pressure is most pronounced in young and nonhypertensive individuals.29 Central aortic pressures should more accurately reflect loading conditions of the left ventricular myocardium, coronary arteries, and cerebral vasculature and thereby, in theory, better relate to cardiovascular target organ damage and to cardiovascular events than brachial pressures. Likewise, vascular stiffness may better summate chronic damage to blood vessels from aging, hypertension, and diabetes than brachial or even central aortic blood pressure. Thus the present study was undertaken to examine the relations of central and brachial blood pressures and conduit arterial stiffness to carotid artery hypertrophy and extent of atherosclerosis, signs of systemic atherosclerosis, and to cardiovascular events in the longitudinal population-based Strong Heart Study.

Methods

Study Population

The study population was drawn from the Strong Heart Study (SHS), a population-based longitudinal study of prevalent and incident cardiovascular disease in American Indians. Details of the study design have been previously published.30 In brief, members of 13 American Indians tribes in Arizona, North and South Dakota, and Oklahoma were invited to participate in serial evaluations, including personal interview, physical examination, and ascertainment of cardiovascular risk factors and prevalent disease. The baseline examination of the SHS cohort was conducted from 1989 to 1991. The 3rd examination in 1996 to 1999, attended by 88% of surviving cohort members, added carotid ultrasonography and radial artery applanation tonometry to the study protocol. The 3943 participants in the 3rd SHS examination included 3197 members of the SHS cohort and 750 additional family members participating in the SHS pilot family study31; 3520 had complete information available regarding brachial and central blood pressures and carotid ultrasonography. Missing data were largely attributable to sonographer unavailability, machine malfunction, or inadequate quality (>5% variability) of radial waveforms. All 3520 participants who underwent carotid ultrasonography and radial applanation tonometry were included in cross-sectional analyses regarding the relations of central and brachial blood pressures to vascular hypertrophy and atherosclerosis. The 2403 of 3197 SHS cohort members who were free of clinically overt cardiovascular disease, including atrial fibrillation, at the 3rd SHS examination were considered in longitudinal analyses.

Blood was drawn at each examination after a 12-hour fast to determine total, low-density and high-density lipoprotein cholesterol, fasting plasma glucose, creatinine, and fibrinogen. Diabetes was defined by the American Diabetes Association criteria32 as fasting plasma glucose ≥7.0 mmol/L (126 mg/dL) or treatment with insulin or oral hypoglycemic agents. Brachial blood pressure was measured in triplicate in the right arm by cuff and mercury sphygmomanometer after the participant had been resting in a seated position for 5 minutes; diastolic pressure was defined as the disappearance of Korotkoff sounds. The average of the last 2 measurements was used as brachial blood pressure. Pulse pressure was calculated as the difference between systolic and diastolic pressures. Hypertension was defined by Joint National Committee 7 criteria33 as systolic pressure ≥140 mm Hg, diastolic pressure ≥90 mm Hg or current use of antihypertensive medication.

The occurrence of fatal and nonfatal cardiovascular events was ascertained during follow-up, as previously described.34,35 Cardiovascular events were determined from medical records, autopsy reports, and informant interviews; all materials were independently reviewed by physician members of the SHS morbidity and mortality committees. Cardiovascular events and causes of death included myocardial infarction, coronary heart disease, sudden death, congestive heart failure, and stroke. Follow-up through December 2003 was 99.8% complete for mortality and 99.2% complete for morbid events. The Indian Health Service Institutional Review Board, Institutional Review Board of the participating institutions, and the participating tribes approved the study. Informed consent was obtained from all of the participants.

Carotid Ultrasonography

All participants underwent carotid ultrasonography using Acuson Sequoia machines equipped with 7 MHz vascular probes on the day of the study visit using a standardized protocol. In brief, the extracranial segments of the left and right carotid arteries were extensively scanned for the presence of discrete atherosclerotic plaque, defined as focal protrusion (intimal-medial thickening) with a thickness exceeding that of the surrounding wall by ≥50%. A plaque score was calculated by the number of left and right segments (common carotid, bulb, internal carotid, external carotid) containing plaque; thus plaque score ranged from 0 to 8. Intimal-medial thickness of the far wall of the distal common carotid artery was measured at end diastole on multiple cycles of M-mode images.36 Intimal-medial thickness was never measured at the level of a plaque; intimal-medial thicknesses are presented as the average of the left and right values. Carotid cross-sectional area, a measure of vascular volume or mass, was calculated as previously described.37 All ultrasound studies were performed by research sonographers and interpreted by a single highly experienced cardiologist who was blinded to the clinical characteristics of the participants.

Applanation Tonometry

Radial arterial pressure waveforms were obtained by applanation tonometry using a solid state high-fidelity external Millar transducer; central arterial waveforms and pressures were calculated by the use of the SphygmoCor device using a generalized transfer function (AtCor Medical, Sydney, Australia) and calibration using the brachial mean and diastolic pressures obtained immediately before the procedure. Orientation and pressure applied to the transducer were adjusted to optimize applanation of the artery between the transducer and the underlying tissue. Applanation tonometry has been validated to yield accurate estimates of intraarterial pulse pressure by comparison with simultaneous invasive pressure recordings.25,38,39 Arterial stiffness was estimated from pressure-diameter relations of the common carotid artery. Minimum (end-diastolic) and maximum (peak-systolic) diameters were obtained from carotid ultrasonography performed immediately before applanation tonometry with the position of the subject and ambient environment unchanged. The arterial stiffness index (beta)40,41 was calculated according to the formula: ln(Ps/Pd)/([Ds −Dd]/Dd), where Ps and Pd are aortic systolic and diastolic pressures, respectively, and Ds and Dd are carotid systolic and diastolic diameters, respectively.

Statistical Analyses

Data are presented as percents or mean±standard deviation. Means of continuous variables were compared using Student’s t test for independent samples or Mann-Whitney U test in the setting of skewed distribution. Brachial and central pressures were compared by paired sample t test. Categorical variables were compared by χ2 analysis. Bivariate relations were analyzed using Spearman correlation coefficient. Differences in the strengths of association between central and brachial blood pressures and measures of carotid hypertrophy and atherosclerosis were compared by calculation of z statistics for comparison of correlations within a single sample. Relations of central and brachial blood pressures and arterial stiffness to cardiovascular events were determined in Cox regression analyses with adjustment for age, gender, current smoking, body mass index, total:HDL cholesterol ratio, serum creatinine, fibrinogen, diabetes, and heart rate in all models. Two-tailed P<0.05 was considered significant. Statistical analyses were performed with SPSS, version 11.0 (SPSS Inc).

Results

Study Population

Participants (n=3520) who underwent both radial artery applanation tonometry and carotid ultrasonography during the third SHS examination were used in cross-sectional analyses. The average age at the time of examination was 58±14 years (range from 18 to 88 years); 61% were women; body mass index was 31.5±6.8 kg/m2. Hypertension was present in 48.3% of the population, 49.0% of women and 47.2% of men (P=0.29); 70% of hypertensive participants took antihypertensive medications at the time of study. Diabetes mellitus was present in 46.5% of women and 38.1% of men (P<0.001); 35.3% of men and 25.2% of women were active smokers (P<0.001). Carotid ultrasound findings and brachial and central blood pressures are presented in Table 1. Carotid atherosclerosis was present in 53% of women and 60% of men (P<0.001). As expected, brachial systolic and pulse pressures were higher than their central aortic counterparts (P<0.001 for both comparisons). The ratio of central aortic to brachial pulse pressure increased with age (r=0.156, P<0.001), consistent with the known diminution of pulse pressure amplification with aging.

TABLE 1. Carotid Ultrasound and Blood Pressure Findings in the Entire Population

VariableMean±SD
Intimal-medial thickness, mm0.72±0.19
Mass, mm215.35±4.56
Plaque, %56.2
Plaque score, n1.33±1.61
Brachial systolic pressure, mm Hg130±19
Brachial pulse pressure, mm Hg55±17
Central systolic pressure, mm Hg120±19
Central pulse pressure, mm Hg41±16
Arterial stiffness index4.58±2.45

Relations of Central Aortic and Brachial Blood Pressures to Carotid Hypertrophy and Atherosclerosis

The relations of central aortic and brachial blood pressures to carotid artery hypertrophy and extent of atherosclerosis (plaque score) are presented in Table 2. The strengths of relations were significantly higher for pulse pressure than for systolic pressure (with the exception of central pressures and vascular mass) and significantly higher for central aortic as opposed to brachial pressures. In addition, the arterial stiffness index was strongly related to intimal-medial thickness, vascular mass, and plaque score, all P<0.001. Furthermore, arterial stiffness was more strongly related to carotid hypertrophy and plaque than was brachial systolic pressure and to extent of atherosclerosis than was brachial pulse pressure.

TABLE 2. Relations of Central and Brachial Blood Pressures and Arterial Stiffness to Carotid Hypertrophy and Extent of Atherosclerosis*

VariableIntimal-Medial ThicknessVascular MassPlaque Score
SBP indicates systolic blood pressure; PP, pulse pressure; ns, not significant.
*All correlations P<0.001.
†Correlations compared by Z statistics.
Brachial SBP0.1960.2640.221
Central SBP0.2570.3170.288
Brachial PP0.2490.2890.309
Central PP0.2930.3200.364
Arterial stiffness index0.2520.3290.353
P value, brachial PP vs brachial SBP<0.001<0.02<0.001
P value, central PP vs central SBP<0.001ns<0.001
P value, central vs brachial SBP<0.001<0.001<0.001
P value, central vs brachial PP<0.002<0.05<0.001
P value, arterial stiffness vs brachial SBP<0.005<0.001<0.001
P value, arterial stiffness vs brachial PPnsns<0.02

Relations of Central Aortic and Brachial Blood Pressures and Arterial Stiffness to Clinical Outcome

The 2403 participants who were free of overt cardiovascular disease at the third examination were followed for a mean of 4.8±1.3 years during which time 319 suffered incident cardiovascular events, including 67 fatal and 252 nonfatal events (58 myocardial infarction, 54 stroke, 64 congestive heart failure, 120 coronary heart disease, 23 sudden and other cardiovascular deaths). Demographic and cardiovascular disease risk factors in those who did and did not suffer events are compared in Table 3. The 2 groups differed significantly in all variables other than gender, body mass index, and prevalence of current smoking.

TABLE 3. Comparison of Demographic Variables and Cardiovascular Disease Risk Factors in Participants Free of Prevalent Cardiovascular Disease at Baseline Subdivided According to Incident Cardiovascular Events During Follow-Up

VariableNo Events (n=2084)Events (n=319)P Value
SBP indicates systolic blood pressure; PP, pulse pressure; HDL, high density lipoprotein.
Age, years62.5±7.565.6±7.4<0.001
Male gender, %34.836.10.672
Body mass index, kg/m231.4±6.630.8±6.40.128
Hypertension, %50.363.0<0.001
Diabetes mellitus, %44.167.5<0.001
Current smoking, %27.528.30.777
Brachial SBP, mm Hg131±19135±23<0.001
Brachial PP, mm Hg56±1662±20<0.001
Central SBP, mm Hg121±17127±22<0.001
Central PP, mm Hg41±1548±18<0.001
Heart rate, bpm69±1171±12<0.001
Total cholesterol/HDL cholesterol4.7±1.55.0±1.7<0.003
Creatinine, mg/dL0.93±0.911.33±1.65<0.001
Fibrinogen, mg/dL380±119413±143<0.001

The relations of central aortic and brachial systolic and pulse pressures to outcome were examined in separate models, including age, gender, body mass index, current smoking, total:HDL cholesterol ratio, creatinine, fibrinogen, diabetes status, and heart rate (Table 4). All variables other than gender, body mass index, and total:HDL cholesterol ratio were significant predictors of outcome. Age, diabetes, and plasma creatinine were very strongly related to outcome. Pulse pressures strengthened the models in comparison to systolic pressures for both central and brachial pressures. Central pulse pressure was more strongly predictive of cardiovascular events than was brachial pulse pressure both before (hazards ratio [HR]=1.15 per 10 mm Hg, χ2=13.4, P<0.001 versus HR=1.10, χ2=6.9, P=0.008) and after (HR=1.14, χ2=11.7, P=0.001 versus HR=1.09, χ2=5.8, P=0.016) additional adjustment for the presence of carotid atherosclerosis. Furthermore, when both central and brachial pulse pressures were included in the model, brachial pulse pressure ceased to be significant. The arterial stiffness index was also independently related to outcome (χ2=6.1, P=0.014), even after inclusion of carotid atherosclerosis as a covariate (χ2=5.6, P=0.018).

TABLE 4. Multivariable Cox Models of Relation of Traditional Risk Factors and Central and Brachial Blood Pressures to Cardiovascular Outcome

VariableHR (95% CIs)HR (95% CIs)HR (95% CIs)HR (95% CIs)HR (95% CIs)
All blood pressures per 10 mm Hg.
BMI indicates body mass index; SBP, systolic blood pressure; PP, pulse pressure.
*P<0.001;
P<0.01;
P<0.05;
§P<0.005.
Age, year1.06 (1.04–1.07)*1.05 (1.04–1.07)*1.06 (1.04–1.07)*1.05 (1.03–1.07)*1.05 (1.04–1.07)*
Male gender1.13 (0.87–1.45)1.17 (0.91–1.52)1.13 (0.88–1.46)1.22 (0.94–1.58)1.10 (0.83–1.45)
BMI, kg/m20.99 (0.97–1.01)0.99 (0.97–1.01)0.99 (0.97–1.01)0.99 (0.97–1.01)0.99 (0.97–1.01)
Smoking1.45 (1.10–1.91)1.44 (1.09–1.89)1.42 (1.08–1.87)1.39 (1.06–1.83)1.37 (1.01–1.85)
Cholesterol:HDL1.05 (0.98–1.13)1.06 (0.99–1.13)1.05 (0.98–1.13)1.05 (0.98–1.13)1.09 (1.01–1.18)
Creatinine, mg/dL1.20 (1.12–1.28)*1.18 (1.11–1.27)*1.20 (1.12–1.28)*1.18 (1.10–1.26)*1.13 (1.03–1.23)
Fibrinogen, mg/dL1.001 (1.000–1.002)1.001 (1.000–1.002)1.001 (1.000–1.002)1.001 (1.000–1.002)§1.001 (1.000–1.002)
Diabetes mellitus2.48 (1.91–3.22)*2.44 (1.88–3.17)*2.47 (1.91–3.21)*2.41 (1.86–3.13)*2.42 (1.838–3.22)*
Heart rate, bpm1.012 (1.001–1.022)1.013 (1.002–1.023)1.013 (1.008–1.143)1.012 (1.001–1.022)1.013 (1.001–1.025)
Brachial SBP1.08 (1.02–1.14)
Brachial PP1.10 (1.03–1.18)
Central SBP1.07 (1.01–1.14)
Central PP1.15 (1.07–1.24)*
Arterial stiffness1.06 (1.01–1.11)

Because aging lessens pulse pressure amplification and might diminish the predictive advantage of central compared with brachial pulse pressure, we repeated analyses in the younger (<62 years) and older (≥62 years) halves of the population. Aortic pulse pressure (HR=1.12, [CI 1.04 to 1.22], P=0.005), but not brachial pulse pressure (HR=1.06, [CI 0.98 to 1.14], P=0.145), remained predictive of outcome in the older half of the population with diminutions in both hazard ratios compared with the entire group. Hazards ratios for all blood pressures and arterial stiffness were uniformly increased in the younger half of the population compared with the entire group. Additional subgroup analyses based on gender did not substantially alter the findings.

Discussion

Our population-based study demonstrates stronger relations of central aortic than brachial blood pressure with the extent of carotid hypertrophy and atherosclerosis, thereby lending support to the hypothesis that central pressures more accurately reflect the loading conditions on the cerebral vasculature than do brachial pressures. More importantly, central aortic pulse pressure more strongly predicted cardiovascular outcome than did brachial pressures. Our study provides additional support for the greater importance of pulse pressure over systolic pressure6–8,11–14 in predicting cardiovascular outcome over a broad age range, although the size of the population and number of events do not permit subgroup analyses in different age ranges. In addition, arterial stiffness was as strongly related to carotid hypertrophy and extent of atherosclerosis as was central aortic pulse pressure.

Many studies have examined the importance of brachial blood pressure in relation to target organ damage and clinical outcome. Far fewer studies have examined the relation of central blood pressure and arterial stiffness to preclinical and clinical disease, and very few studies have examined the relative importance of central and brachial blood pressures in their relations to cardiovascular target organ damage or events. Boutouyrie et al found a stronger relation of carotid pulse pressure (r=0.42, P<0.001) than brachial pulse pressure (r=0.27, P<0.001) to carotid intimal-medial thickness in 167 normotensive and hypertensive volunteers,42 although statistical significance of differences in the strengths of relation was not tested. In a study of 114 men with documented coronary artery disease, the severity of coronary stenosis was independently related to carotid but not brachial systolic and pulse pressures.43 In a small substudy of the pREterax in regression of Arterial Stiffness in a contrOlled double-bliNd (REASON) Project involving 52 hypertensive subjects in whom central blood pressure was determined using applanation tonometry, change in carotid pulse pressure but not brachial pulse pressure was associated with the greater reduction in left ventricular mass detected in the perindopril+indapamide arm as compared with the atenolol treatment arm.44 Finally, carotid pulse pressure and aortofemoral pulse wave velocity, but not brachial pulse pressure, were independently related to all-cause mortality in patients with end-stage renal disease.45

In contrast, brachial pulse pressure but not central pulse pressure was independently related to cardiovascular events in 484 elderly (65 to 84 years old) female hypertensives participating in the Second Australian National Blood Pressure Study.46 This finding is somewhat surprising given the similarity between brachial and central pulse pressures at baseline (85±17 versus 84±26 mm Hg, respectively), consistent with minimal pulse wave amplification in this elderly population. Likewise, systemic arterial compliance and the augmentation index were not related to outcome; more direct measures of arterial stiffness such as pulse wave velocity and the arterial stiffness index were not examined in the study.

The most important study to date to examine the relative importance of central and brachial blood pressures has been the Conduit Artery Function Evaluation (CAFE) study of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) hypertension trial.26 Although brachial blood pressure was reduced to a similar extent in both the atenolol±thiazide and amlodipine±perinopril arms of the CAFE study, central systolic and pulse pressures were reduced to a significantly greater extent by amlodipine-based treatment. Furthermore, both brachial and central pulse pressures were similarly related (χ2=4.1 for both) to a post hoc-defined composite outcome (new cardiovascular events, cardiovascular procedures, renal impairment) independent of other risk factors. However, it is uncertain whether the more favorable outcome associated with the amlodipine-based arm in the overall ASCOT trial was related to the greater central blood pressure lowering with this regimen.

The findings of the present study, a longitudinal observational study, complement those of the CAFE study, a treatment trial of high-risk hypertensive patients. The number of subjects and mean age are comparable, whereas duration of follow-up was slightly longer in the present study. Similarly, the SHS cohort is high-risk given the high prevalence of diabetes. Fewer events occurred in the CAFE study than in the current study (225 in hypertensives without prevalent cardiovascular disease at baseline versus 319 in the SHS cohort). It is possible that fewer events in the CAFE study explain the comparability of central and brachial pulse pressures in predicting outcome, whereas in the present study, central aortic pulse pressure was a stronger predictor of outcome than was brachial pulse pressure. Alternatively, this difference in findings may relate to inherent differences in the designs and populations of the two studies. Interestingly, mean brachial pulse pressure in the current study (55 mm Hg) is comparable to that of the 2 arms in the CAFE study (55.3 mm Hg in the atenolol arm and 56.2 mm Hg in the amlodipine arm), whereas central pulse pressure was lower in the present study (41 mm Hg versus 46.4 mm Hg in the atenolol arm and 43.4 mm Hg in the amlodipine arm of the CAFE study), indicating a stronger separation between central and brachial pressures in the SHS cohort.

Potential limitations of the current study include the fact that 70% of hypertensive participants (33% of the entire population) were taking antihypertensive medications at the time of study. If anything, such use might be expected to dilute the impact of findings insofar as antihypertensive therapy lowers blood pressure, thereby lessening the significance of bivariate correlations, and improves outcome. Furthermore when antihypertensive medication use was added to the Cox regression models including atherosclerosis, only central aortic pulse pressure remained an independent predictor of outcome (P=0.004). Although not necessarily a limitation, our study was not a randomized treatment trial but rather a longitudinal observational study, including normotensive and hypertensive individuals, examining the relative prognostic importance of central and brachial blood pressures. The greater importance of central aortic pulse pressure and arterial stiffness in relation to target organ damage and outcome noted in the present study may not apply to blood pressure lowering trials, although similarity of data from the CAFE study suggest this might be the case. While our study population is limited to American Indians and results may not be applicable to other populations, the increasing prevalences of obesity and diabetes in the general US population suggest that our findings may be highly applicable to US public health.

In conclusion, noninvasively determined central aortic pulse pressure and arterial stiffness are more strongly related to vascular hypertrophy and extent of carotid atherosclerosis than is brachial pressure. Furthermore central pulse pressure better predicts outcome than does brachial pressure. These findings support the recent call for prospective examination of use of arterial stiffness and central blood pressure as treatment targets in future trials.47

Perspectives

Although central blood pressure more directly reflects the load on the heart and coronary and cerebral arteries than does brachial blood pressure and thereby should more directly relate to target organ damage and clinical cardiovascular disease, data to support this hypothesis have been lacking. The recently acquired ability to accurately measure central pressure using noninvasive techniques in population-based samples allows this theory to be tested. The present study provides direct support for the hypothesis that central pressure is more important than brachial pressure in predicting outcome in the Strong Heart Study, an observational study of prevalent and incident cardiovascular disease and their risk factors in American Indians. Whether treatment based on central as opposed to brachial blood pressure favorably alters cardiovascular risk remains to be determined.

The views expressed in this manuscript are those of the authors and do not necessarily represent those of the Indian Health Service.

Sources of Funding

This work was supported by grants HL41642, HL41652, HL41654, HL65521 from the National Heart, Lung, and Blood Institute.

Disclosures

None.

Footnotes

Correspondence to Mary J. Roman, MD, Division of Cardiology, 525 East 68th Street, New York, NY 10021. E-mail

References

  • 1 Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of different blood-pressure-lowering regimens on major cardiovascular events: results of prospectively-designed overviews of randomised trials. Lancet. 2003; 362: 1527–1535.CrossrefMedlineGoogle Scholar
  • 2 Wang J-G, Staessen JA, Franklin SS, Fagard R, Gueyffier F. Systolic and diastolic blood pressure lowering as determinants of cardiovascular outcome. Hypertension. 2005; 45: 907–913.LinkGoogle Scholar
  • 3 Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Farmingham Heart Study. Ann Intern Med. 2003; 138: 10–16.CrossrefMedlineGoogle Scholar
  • 4 Madhavan S, Ooi WL, Cohen H, Alderman MH. Relation of pulse pressure and blood pressure reduction to the incidence of myocardial infarction. Hypertension. 1994; 23: 395–401.LinkGoogle Scholar
  • 5 Benetos A, Safar M, Rudnichi A, Smulyan H, Richard J-L, Ducimetière P, Guize L. Pulse pressure: a predictor of long-term cardiovascular mortality in a French male population. Hypertension. 1999; 30: 1410–1415.Google Scholar
  • 6 Franklin SS, Khan SA, Wong NA, Larson MG, Levy D. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham Heart Study. Circulation. 1999; 100: 354–360.CrossrefMedlineGoogle Scholar
  • 7 Glynn RJ, Chae CU, Guralnik JM, Taylor JO, Hennekens CH. Pulse pressure and mortality in older people. Arch Intern Med. 2000; 160: 2765–2772.CrossrefMedlineGoogle Scholar
  • 8 Vaccarino V, Holford TR, Krumholz HM. Pulse pressure and risk for myocardial infarction and heart failure in the elderly. J Am Coll Cardiol. 2000; 36: 130–138.CrossrefMedlineGoogle Scholar
  • 9 Domanski M, Norman J, Wolz M, Mitchell G, Pfeffer M. Cardiovascular risk assessment using pulse pressure in the First National Health and Nutrition Examination Survey (NHANES I). Hypertension. 2001; 38: 793–797.CrossrefMedlineGoogle Scholar
  • 10 Palmieri V, Devereux RB, Holloywood J, Bella JN, Liu JE, Lee ET, Best LG, Howard BV, Roman MJ. Association of pulse pressure with cardiovascular outcome is independent of left ventricular hypertrophy and systolic dysfunction: The Strong Heart Study. J Hypertens. 2006; 19: 601–607.Google Scholar
  • 11 Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension. 1998; 32: 560–564.CrossrefMedlineGoogle Scholar
  • 12 Sesso HD, Stampfer MJ, Rosner B, Hennekens CH, Gaziano JM, Manson JE, Glynn RJ. Systolic and diastolic blood pressure, pulse pressure and mean arterial pressure as predictors of cardiovascular disease in men. Hypertension. 2000; 36: 801–807.CrossrefMedlineGoogle Scholar
  • 13 Pastor-Barriuso R, Banegas JR, Damián J, Appel LJ, Guallar E. Systolic blood pressure, diastolic blood pressure and pulse pressure: an evaluation of their joint effect on mortality. Ann Intern Med. 2003; 139: 731–739.CrossrefMedlineGoogle Scholar
  • 14 Franklin SS, Larson MG, Khan SA, Wong NA, Leip EP, Kannel WB, Levy D. Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham Heart Study. Circulation. 2001; 103: 1245–1249.CrossrefMedlineGoogle Scholar
  • 15 Cushman WC, Materson BJ, Williams DW, Reda DJ, for the Veterans Affairs Cooperative Study Group on Antihypertensive Agents. Pulse pressure changes with six classes of antihypertensive agents in a randomized, controlled trial. Hypertension. 2001; 38: 953–957.CrossrefMedlineGoogle Scholar
  • 16 Millar JA, Lever AF, Burhe V. Pulse pressure as a risk factor for cardiovascular events in the MRC Mild Hypertension Trial. J Hypertens. 1999; 17: 1065–1072.CrossrefMedlineGoogle Scholar
  • 17 Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L, Ducimetiere P, Benetos A. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001; 37: 1236–1241.CrossrefMedlineGoogle Scholar
  • 18 Boutuyrie P, Tropeano AI, Asmar R, Gautier I, Benetos A, Lacolley P, Laurent S. Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study. Hypertension. 2002; 39: 10–15.CrossrefMedlineGoogle Scholar
  • 19 Meaume S, Benetos A, Henry OF, Rudnichi A, Safar ME. Aortic pulse wave velocity predicts cardiovascular mortality in subjects >70 years of age. Arterioscler Thromb Vasc Biol. 2001; 21: 2046–2050.CrossrefMedlineGoogle Scholar
  • 20 Sutton-Tyrrell K, Najjar SS, Boudreau RM, Venkitachalam L, Kupelian V, Simonsick EM, Havlik R, Lakatt EG, Spurgeon H, Kritchevsky S, Pahor M, Bauer D, Newman A, for the Health ABC Study. Elevated aortic pulse wave velocity, a marker of arterial stiffness, predicts cardiovascular events in well-functioning older adults. Circulation. 2005; 111: 3384–3390.LinkGoogle Scholar
  • 21 Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM. Impact of aortic stiffness on survival in end-stage renal disease. Circulation. 1999; 99: 2434–2439.CrossrefMedlineGoogle Scholar
  • 22 Pannier B, Guerin AP, Marchais SJ, Safar ME, London GM. Stiffness of capacitive and conduit arteries: prognostic significance for end-stage renal disease patients. Hypertension. 2005; 45: 592–596.LinkGoogle Scholar
  • 23 Hansen TW, Staessen JA, Torp-Pedersen C, Rasmussen S, Thijs L, Ibsen H, Jeppesen J. Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population. Circulation. 2006; 113: 664–670.LinkGoogle Scholar
  • 24 Mattace-Raso FUS, van der Cammen TJM, Hofman A, van Popele NM, Bos ML, Schalekamp MADH, Asmar A, Reneman RS, Hoeks APG, Breteler MMB, Witteman JCM. Arterial stiffness and risk of coronary heart disease and stroke: The Rotterdam Study. Circulation. 2006; 113: 657–663.LinkGoogle Scholar
  • 25 Pauca AL, O’Rourke MF, Kon ND. Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform. Hypertension. 2001; 38: 932–937.CrossrefMedlineGoogle Scholar
  • 26 The CAFÉ Investigators, for the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) Investigators. Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes. Principal results of the Conduit Artery Function Evaluation (CAFÉ) Study. Circulation. 2006; 113: 1213–1225.LinkGoogle Scholar
  • 27 Hamilton WF, Dow P. An experimental study of the standing waves in the pulse propagated through the aorta. Am J Physiol. 1939; 125: 48–59.CrossrefGoogle Scholar
  • 28 Schnabel TG Jr, Fitzpatrick HF, Peterson LH, Rashkind WJ, Talley D, Raphael RL. A technique of vascular catheterization with small plastic catheters: its utilization to measure the arterial pulse wave velocity in man. Circulation. 1952; 5: 257–262.CrossrefMedlineGoogle Scholar
  • 29 Nichols WW, O’Rourke MF, eds. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. Fifth Edition. Oxford: Hodder Arnold; 2005: 193–213, 339–386.Google Scholar
  • 30 Lee ET, Welty TK, Fabsitz RR, Cowan LD, Lee N-A, Oopik AJ, Cucchiara AJ, Savage PJ, Howard BV. The Strong Heart Study: a study of cardiovascular disease in American Indians: design and methods. Am J Epidemiol. 1990; 132: 1141–1155.CrossrefMedlineGoogle Scholar
  • 31 North KE, Howard BV, Welty TK, Best LG, Lee ET, Yeh JL, Fabsitz RR, Roman MJ, MacCluer JW. Genetic and environmental contributions to cardiovascular disease risk in American Indians: The Strong Heart Family Study. Am J Epidemiol. 2002; 157: 303–314.Google Scholar
  • 32 The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: follow-up report on the diagnosis of diabetes mellitus. Diabetes Care. 2003; 26: 3160–3167.CrossrefMedlineGoogle Scholar
  • 33 Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ, the National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003; 42: 1206–1252.LinkGoogle Scholar
  • 34 Howard BV, Lee ET, Cowan LD, Devereux RB, Galloway JM, Go OT, Howard WJ, Rhoades ER, Robbins DC, Sievers ML, Welty TK. Rising tide of cardiovascular disease in American Indians: The Strong Heart Study. Circulation. 1999; 99: 2389–2395.CrossrefMedlineGoogle Scholar
  • 35 Lee ET, Cowan LD, Welty TK, Sievers M, Howard WJ, Oopik A, Wang W, Yeh J, Devereux RB, Rhoades ER, Fabsitz RR, Go O, Howard BV. All-cause mortality and cardiovascular disease mortality in three American Indian populations, aged 45–74 years, 1984–1988: The Strong Heart Study. Am J Epidemiol. 1998; 147: 995–1008.CrossrefMedlineGoogle Scholar
  • 36 Roman MJ, Naqvi TZ, Gardin JM, Gerhard-Herman M, Jaff M, Mohler E. Clinical application of noninvasive vascular ultrasound in cardiovascular risk stratification: a report from the American Society of Echocardiography and the Society of Vascular Medicine and Biology. J Am Soc Echocardiogr. 2006; 19: 943–954.CrossrefMedlineGoogle Scholar
  • 37 Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults. J Am Coll Cardiol. 1996; 28: 751–756.CrossrefMedlineGoogle Scholar
  • 38 Kelly R, Hayward C, Ganis J, Daley J, Avolio A, O’Rourke M. Noninvasive registration of the arterial pressure waveform using high-fidelity applanation tonometry. J Vasc Med Biol. 1989; 1: 142–149.Google Scholar
  • 39 Chen C-H, Ting CT, Nussbacher A, Nevo E, Kass DA, Pak P, Wang SP, Chang MS, Yin FCP. Validation of carotid artery tonometry as a means of estimating augmentation index of ascending aortic pressure. Hypertension. 1996; 27: 168–175.LinkGoogle Scholar
  • 40 Hayashi K, Handa H, Nagasawa S, Okumura A, Moritaki K. Stiffness and elastic behavior of human intracranial and extracranial arteries. J Biomechanics. 1980; 13: 175–184.CrossrefMedlineGoogle Scholar
  • 41 Hirai T, Sasayma S, Kawasaki T, Yagi S. Stiffness of systemic arteries in patients with myocardial infarction. A noninvasive method to predict severity of coronary atherosclerosis. Circulation. 1989; 80: 78–86.CrossrefMedlineGoogle Scholar
  • 42 Boutouyrie P, Bussy C, Lacolley P, Girerd X, Laloux B, Laurent S. Association between local pulse pressure, mean blood pressure, and large-artery remodelling. Circulation. 1999; 100: 1387–1393.CrossrefMedlineGoogle Scholar
  • 43 Waddell TK, Dart AM, Medley TL, Cameron JD, Kingwell BA. Carotid pressure is a better predictor of coronary artery disease severity than brachial pressure. Hypertension. 2001; 38: 927–931.CrossrefMedlineGoogle Scholar
  • 44 De Luca N, Asmar RG, London GM, O’Rourke MF, REASON Project Investigators. Selective reduction of cardiac mass on low-dose combination perindopril/indapamide in hypertensive subjects. J Hypertens. 2004; 22: 1623–1630.CrossrefMedlineGoogle Scholar
  • 45 Safar ME, Blacher J, Pannier B, Guerin AP, Marchais SJ, Guyonvarc’h P-M, London GM. Central pulse pressure and mortality in end-stage renal disease. Hypertension. 2002; 39: 735–738.CrossrefMedlineGoogle Scholar
  • 46 Dart AM, Gatzka CD, Kingwell BA, Willson K, Cameron JD, Liang Y-L, Berry KL, Wing LMH, Reid CM, Ryan P, Beilin LJ, Jennings GLR, Johnston CI, McNeil JJ, MacDonald GJ, Morgan TO, West MJ. Brachial blood pressure but not carotid arterial waveforms predict cardiovascular events in elderly female hypertensives. Hypertension. 2006; 47: 785–790.LinkGoogle Scholar
  • 47 Laurent S, Cockcroft J, Van Bortel L, Boutouyrie P, Giannattasio C, Hayoz D, Pannier B, Vlachopoulos C, Wilkinson I, Struijker-Boudier H, on behalf of the European Network for Non-Invasive Investigation of Large Arteries. Expert consensus document on arterial stiffness: methodologic issues and clinical applications. Eur Heart J. 2006; 27: 2588–2605.CrossrefMedlineGoogle Scholar

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