Cardiac hypertrophy in hypertension: relation to 24-h blood pressure profile and arterial stiffness

Lekakis, John; Zakopoulos, Nikos; Protogerou, Athanase D.; Kotsis, Vasilios; Papaioannou, Theodore G.; Stamatelopoulos, Kimon; Tsitsiricos, Marios D.; Pitiriga, Vassiliki; Papamichael, Christos; Toumanides, Savvas; Mavrikakis, Myron

doi:10.1016/j.ijcard.2003.06.011

Cited by 59 publications

(49 citation statements)

References 32 publications

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“…Cardiac hypertrophy correlated best with the week-4 average systolic pressure compared with other hemodynamic parameters such as diastolic pressure, MAP and ratepressure product, suggesting that systolic pressure is the most important determinant of the cardiac size. This finding is consistent with studies in hypertensive human subjects (Lekakis et al 2004, Libhaber et al 2005 that showed cardiac hypertrophy correlated with systolic pressure more significantly.…”

Section: Discussionsupporting

confidence: 92%

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

et al. 2007

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Pressure overload (POL) is a classical model for studying cardiac hypertrophy, but there has been no direct measure of hemodynamics in a conscious ambulatory mouse model of POL. We used abdominal aortic constriction to produce POL and radiotelemetry to measure the blood pressure and heart rate for three weeks. The cardiac size correlated with the systolic pressure in the last week is better than other hemodynamic parameters. Cardiac fibrosis was more correlated to the cardiac size than to the systolic pressure. The expression of the cardiac genes that are typically associated with cardiac hypertrophy was correlated with both cardiac size and systolic pressure. In conclusion, the systolic pressure is the major determinant of cardiac hypertrophy in the murine POL model. In contrast, cardiac fibrosis shows the influence of other factors besides systolic pressure. The combination of the POL model with continuous direct measurements of hemodynamics represents a significant technological advance and will lead to an extended usefulness of POL methodologically.

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Section: Discussionsupporting

confidence: 92%

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

et al. 2007

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“…The possible importance of brachial-aortic SBP difference on end organ damage was shown in patients with essential hypertension where central SBP outweighed 24 h ambulatory BP for predicting left ventricular (LV) mass. 22 However, a larger study of relatively healthy subjects with a low rate of hypertension (20%) and LV hypertrophy (5%) showed no significant difference in the prevalence of cardiac hypertrophy when subjects were stratified into quartiles of brachial-aortic SBP difference. 23 Others have shown central pressure waveform indices to be important predictors of LV and carotid artery structure.…”

Section: Pressure Amplification and Riskmentioning

confidence: 93%

Central blood pressure measurement may improve risk stratification

et al. 2008

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Central systolic blood pressure (SBP) may differ between individuals with similar brachial SBP, which may have implications for risk assessment. This study aimed to determine the variation and potential clinical value of central SBP between patients with similar brachial SBP. Brachial SBP was measured by sphygmomanometer and central SBP by radial tonometry in 675 people (430 men), comprising healthy individuals (n ¼ 222), patients with known or suspected coronary artery disease (n ¼ 229) and diabetes (n ¼ 224). Individuals were stratified by brachial SBP in accordance with European Society of Hypertension guidelines (optimal, normal, high-normal, grades 1, 2 and 3 hypertension). The potential clinical value of central SBP was determined from the percentage of patients re-classified into different brachial SBP groups due to the difference between brachial and aortic SBP (defined as brachial SBP-central SBP). Central SBP increased with each brachial SBP level (optimal to grade 3 hypertension; Po0.001 for all). However, large variation in brachialaortic SBP difference occurred within each brachial SBP group (range 2-33 mm Hg), resulting in sizeable overlap of central SBP between brachial SBP groups. For patients with normal brachial SBP, 96% had central SBP within the range of patients with high-normal brachial SBP, as well as 64% within the range of patients with grade 1 hypertension. We conclude that wide variation in brachial-aortic SBP difference occurs between patients with similar brachial SBP. This results in a significant overlap of central SBP scores between brachial SBP risk groups. This is likely to have treatment implications but remains to be tested.

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“…The augmentation of central aortic systolic pressure is typically quantified as the increase of pressure from the first systolic shoulder to the systolic pressure peak of the aortic pressure waveform and is expressed as a percentage of central aortic pulse pressure (augmentation index (AIx)) [11]. A greater AIx is an indicator of the additional load imposed on the left ventricle by the reflected wave and is correlated with left ventricular mass [12,13]. AIx has also been found to correlate with CHD risk factors [14][15][16][17][18], coronary atherosclerosis [19,20], and cardiovascular outcomes [21,22].…”

Section: Introductionmentioning

confidence: 99%

Aortic augmentation index is associated with the ankle-brachial index: A community-based study

Khaleghi

Kullo

2007

Atherosclerosis

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Background-Increased arterial stiffness has been associated with greater risk of cardiovascular events. We investigated whether aortic augmentation index (AIx), a measure of arterial stiffness and wave reflection, was associated with the ankle-brachial index (ABI), a measure of peripheral arterial disease (PAD).Method-AIx and ABI were measured in a community-based sample of 475 adults without prior history of heart attack or stroke (mean age 59.3 years, 46.5% men). Radial artery pulse waveforms were obtained by applanation tonometry and an ascending aortic pressure waveform derived by a transfer function. AIx is the difference between the first and second systolic peak of the ascending aortic pressure waveform indexed to the central pulse pressure. ABI was measured using a standard protocol, and subjects with non-compressible vessels (ABI >1.5) were excluded from the analyses. Multivariable linear and logistic generalized estimating equations (GEE) analyses were used to assess whether AIx was associated with ABI and ABI <1.00 respectively, independent of conventional risk factors.Results-Mean (± SD) values were: AIx, 29.3±11.6 %; ABI, 1.12±0.13; 59 (12.4%) participants had an ABI <1.00. Variables associated with a lower ABI (and ABI <1.00) included older age, shorter height, female sex, higher total cholesterol, hypertension medication use, history of smoking, and higher AIx. After adjustment for mean arterial pressure and the above variables, higher AIx remained associated with a lower ABI (P=0.015) and ABI <1.00 (P=0.002). A significant interaction (P=0.007) was present between AIx and age in the prediction of ABI; the (inverse) association of AIx with ABI was stronger in older subjects (>65 years).Conclusion-AIx, a measure of arterial stiffness and wave reflection, was independently associated with a lower ABI in asymptomatic subjects from the community, and this association was modified by age.

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Cardiac hypertrophy in hypertension: relation to 24-h blood pressure profile and arterial stiffness

Cited by 59 publications

References 32 publications

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

Central blood pressure measurement may improve risk stratification

Aortic augmentation index is associated with the ankle-brachial index: A community-based study

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