Which diagnostic method is recommended to determine whether left ventricular hypertrophy has occured?

Journal Article

Pedro Blanch,

Cardiovascular Disease Area Department, Hospital Moisès Broggi, Barcelona, Spain

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Revision received:

18 June 2018

Published:

01 August 2018

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  Pedro Blanch, Pedro Armario, Anna Oliveras, Patricia Fernández-Llama, Susana Vázquez, Julia Pareja, Empar Álvarez, Francesca Calero, Cristina Sierra, Alejandro de la Sierra, Association of Either Left Ventricular Hypertrophy or Diastolic Dysfunction With 24-Hour Central and Peripheral Blood Pressure, American Journal of Hypertension, Volume 31, Issue 12, December 2018, Pages 1293–1299, https://doi.org/10.1093/ajh/hpy123

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Abstract

Left ventricular hypertrophy (LVH) is considered an important marker of hypertension-derived target organ damage, as it predicts cardiovascular events,1 and its regression with antihypertensive treatment improves hypertension-related outcomes.2 In addition to LVH, other cardiac alterations, such as left atrial size, or Doppler-guided tissue velocities are also predictive of cardiovascular events in hypertensive subjects.3,4

Central blood pressure (BP) measured by noninvasive methods has been found to be more closely related with LVH and left ventricular diastolic function in comparison with peripheral (brachial) BP,5–7 and most, but not all longitudinal studies, have shown a stronger predictive value of future cardiovascular events and mortality in hypertensive subjects.8–11

Noninvasive measurement of central BP throughout 24 hours has recently become possible due to technological advances.12 This has brought the possibility to directly compare 24-hour central vs. peripheral BP. Two previous reports found that 24-hour central BP was better correlated with left ventricular mass index (LVMI)13 and diastolic dysfunction (DD).14 More recently, a prospective multicenter study did not show statistically significant differences between 24-hour central and peripheral BP correlation coefficients with LVMI,15 although the association with LVH was reported to be greater with 24-hour central systolic BP (SBP).

We have previously reported that 24-hour central BP did not show superiority over 24-hour peripheral BP in their association with a combination of target organ damage.16 However, such endpoint included a mixture of alterations at different levels (LVH, microalbuminuria, reduced estimated glomerular filtration rate, and increased aortic stiffness). In the present analysis, we specifically assessed the associations of 24-hour ambulatory BP monitoring (ABPM)-derived both central and peripheral BP with hypertension-related cardiac alterations, including LVH and DD.

PATIENTS AND METHODS

Study design

This is a cross-sectional study, which included 208 patients aged >18 years, with a diagnosis of essential hypertension, mean age 57 ± 12 years, 34% women, who were consecutively enrolled from 5 hypertension units at corresponding university hospitals in the metropolitan area of Barcelona, Spain. Details regarding recruitment, as well as demographic and clinical characteristics, have been previously reported.16 The local Institutional Ethics Committees approved the study protocol. Written informed consent was obtained from all participants. The investigation conforms to the principles outlined in the declaration of Helsinki.

BP measurements

All BP measurements were performed by means of a noninvasive automated oscillometric device (Mobil-O-Graph PWV, IEM, Stolberg, Germany), validated for brachial BP measurement.17 The monitor was placed on a working day, starting between 08:00 am and 10:00 am. After 5 minutes of rest, BP was measured 4 times consecutively at 1-minute intervals. The mean of these measurements was settled as office BP. Thereafter, BP was measured automatically at 20-minute intervals throughout both the awake and asleep periods. All subjects included had recordings of good technical quality (at least 80% of valid readings). Otherwise, ABPM was repeated in 1 week.

Central (aortic) BP was determined from brachial waveforms and calculated at each BP measurement. The method of calibration used SBP/diastolic BP (DBP), which provides values of aortic SBP usually lower than brachial SBP. However, as recently recommended,18 the alternative calibration using mean BP (MBP)/DBP was also computed, and all the performed analyses were repeated based on this calibration method.

Echocardiography

Transthoracic echocardiography was performed by experienced operators blinded regarding clinical data and ambulatory BP of the patient. The examinations were carried out with the patients in the partial left decubitus position. The measurements were obtained in accordance with the recommendation of the European Association of Echocardiography.19 LVM was calculated according to the method devised by Devereux et al.20 LVMI was obtained by dividing LVM by the body surface area. LVH was defined as a LVMI ≥115 g/m2 in men or ≥95 g/m2 in women.

The pulsed-wave Doppler was performed in an apical 4-chamber view to obtain mitral inflow velocities to assess left ventricular filling. Pulsed-wave Doppler tissue imaging was also performed in apical views to acquire mitral annulus velocities. Doppler tissue imaging myocardial velocities were obtained at the septal and lateral mitral annulus from the apical 4-chamber view. All reported echocardiographic measurements represent the average of 3 consecutive cardiac cycles. DD was defined if the patient had 1 of the following: left atrium volume (estimated using the apical 4- and 2-chamber views with biplane method) ≥34 ml/m2, septal e′ velocity <8 cm/s, or lateral e′ velocity <10 cm/s, as suggested in the European Society of Hypertension/European Society of Cardiology guidelines.21 Only 187 patients from the entire group of 208 had the DD estimated.

Statistical analysis

Data are presented as mean ± SD for normally distributed variables, median [interquartile range] for continuous variables that deviated from the normal distribution, or frequencies (%) for qualitative variables. Differences in clinical parameters and BP values between patients with and without LVH or between those with and without DD were estimated by means of Student’s t-test, Mann–Whitney U-test, or Pearson’s chi-squared test, when appropriate. The association of each BP estimate with the presence of defined cardiac alterations was assessed by means of logistic regression analyses, with odds ratio calculation adjusted for age, gender (only for DD associations), and the use of antihypertensive treatment. The assessment of the relative impact of central vs. peripheral BP estimates on defined cardiac alterations was carried out in 3 different analyses. First, multiple logistic regression analyses with LVH or DD as dependent variables were repeated entering each pair of BP estimates (peripheral and central) in the same model and calculating multivariate odds ratio (also adjusted for confounders). Second, by calculating the area under the curve (AUC) of receiver-operating curves (ROCs) and comparing AUC from each pair of BP estimates (peripheral vs. central).22 Third, by calculating correlation coefficients between BP estimates and LVMI and comparing each pair of such estimates (peripheral vs. central).23 All such comparisons were done with both ways of estimating central BP (calibration using SBP/DBP and calibration using MBP/DBP). The SPSS for Windows version 18.0 software (SPSS, Chicago, IL) and MedCalc software (Ostende, Belgium) were used for statistical analysis.

RESULTS

A total of 77 patients (37%) had LVH, whereas 110 (58%) had DD. Table 1 shows differences in clinical parameters between patients with and without LVH or between those with and without DD. Patients with either LVH or DD were older, with a higher proportion of women, more frequently treated with antihypertensive drugs, and had increased values of urinary albumin excretion. Patients with LVH also had lower values of estimated glomerular filtration rate compared with those without LVH. The prevalence of LVH among patients with DD was higher in comparison with those with normal diastolic function (50.0% vs. 22.1%, respectively; P < 0.001).

Table 1.

Clinical characteristics of patients studied according to the presence or absence of LVH or DD

Abbreviations: BMI, body mass index; CV, cardiovascular; DD, diastolic dysfunction; eGFR, estimated glomerular filtration rate; LVH, left ventricular hypertrophy; LVMI, left ventricular mass index. *P value < 0.05, **P value < 0.01, ***P value < 0.001.

Table 1.

Clinical characteristics of patients studied according to the presence or absence of LVH or DD

Abbreviations: BMI, body mass index; CV, cardiovascular; DD, diastolic dysfunction; eGFR, estimated glomerular filtration rate; LVH, left ventricular hypertrophy; LVMI, left ventricular mass index. *P value < 0.05, **P value < 0.01, ***P value < 0.001.

Relationship between peripheral and central BP and LVH

Patients with LVH had significantly higher values of all SBP and pulse pressure (PP) estimates, both peripheral and central, including office, 24-hour, daytime, and nighttime values, compared with those without LVH (Supplementary Table S1). DBP was not significantly different between patients with or without LVH, with the exception of nocturnal central DBP, which was higher in LVH (P = 0.014). Values of central BP using MBP/DBP calibration were numerically higher than both central BP obtained with SBP/DBP calibration and peripheral BP. When patients with or without LVH were compared, results were almost identical (higher values for SBP and PP in LVH patients and similar values of DBP) with the exception of nocturnal central DBP (Supplementary Table S2).

SBP and PP, both central and peripheral, were associated with the presence of LVH, after adjustments for age and the use of antihypertensive treatment (Table 2). Odds ratios were similar for peripheral and central BP and generally higher for 24-hour BP with respect to other BP estimates (day, night, or office), When each pair of BP values (peripheral and central) were put together in the same regression model, central BP estimates were not independently associated with LVH.

Table 2.

Odds ratio for each mm Hg increase (95% confidence interval) of the association of each blood pressure value with the presence of LVH, without and with simultaneous adjustment for each pair of estimates (peripheral and central)

Adjusted for age and the use of antihypertensive treatment. Abbreviations: LVH, left ventricular hypertrophy; PP, pulse pressure; SBP, systolic blood pressure.

Table 2.

Odds ratio for each mm Hg increase (95% confidence interval) of the association of each blood pressure value with the presence of LVH, without and with simultaneous adjustment for each pair of estimates (peripheral and central)

Adjusted for age and the use of antihypertensive treatment. Abbreviations: LVH, left ventricular hypertrophy; PP, pulse pressure; SBP, systolic blood pressure.

These results were reproduced almost identically when central BP was obtained using MBP/DBP calibration. Supplementary Table S3 shows the association of each BP estimate with LVH. As it occurred with the SBP/DBP calibration method, all the odds ratios obtained after adjustment for age and antihypertensive treatment were significant, and again, such significance was lost after adjustment for peripheral BP.

Moreover, as shown in Supplementary Table S4, the assessment of the association of ABPM-derived BP estimates with LVH using the calculation of the AUC from ROCs revealed AUC values between 0.6 and 0.7 without significant differences when comparing peripheral vs. central BP (either with SBP/DBP or MBP/DBP calibration methods).

Table 3 shows the correlation coefficients of peripheral and central BP with LVMI. Most of such coefficients were in the range between 0.2 and 0.3. The comparison between peripheral and central correlation coefficients revealed significant differences for 24-hour, daytime, and nighttime PP, with higher values for peripheral BP. An alternative analysis of central BP obtained with MBP/DBP calibration produced slightly greater correlation coefficients (values between 0.3 and 0.4), but the comparison with peripheral coefficients using z-statistics revealed no significant differences (Table 3).

Table 3.

Correlation coefficients between each BP estimate and LVMI and comparison between peripheral and central obtained correlation coefficients

Abbreviations: BP, blood pressure; DBP, diastolic blood pressure; LVMI, left ventricular mass index; MBP, mean blood pressure; SBP, systolic blood pressure.

*All correlation coefficients significant at P < 0.01 level, except for central (SBP/DBP calibration) night pulse pressure (P < 0.05).

Table 3.

Correlation coefficients between each BP estimate and LVMI and comparison between peripheral and central obtained correlation coefficients

Abbreviations: BP, blood pressure; DBP, diastolic blood pressure; LVMI, left ventricular mass index; MBP, mean blood pressure; SBP, systolic blood pressure.

*All correlation coefficients significant at P < 0.01 level, except for central (SBP/DBP calibration) night pulse pressure (P < 0.05).

Relationship of peripheral and central BP with DD

Patients with DD had significantly higher values of all SBP estimates, both peripheral and central, including office, 24-hour, daytime, and nighttime values. These differences were also observed for PP, whereas DBP was similar in both groups, with the exception of night central DBP, which was found higher in patients with DD (Supplementary Table S5).

Similar to the results obtained in LVH, odds ratios of the association with the presence of DD for all SBP and PP estimates, peripheral and central, were significant after adjustment for age, gender, and antihypertensive treatment, but such significance was lost after simultaneous adjustment for each pair of peripheral and central BP estimates. The only exception was nocturnal peripheral PP, which maintained statistical significance. (Table 4).

Table 4.

Odds ratio for each mm Hg increase (95% confidence interval) of the association of each blood pressure value with the presence of diastolic dysfunction, without and with simultaneous adjustment for each pair of estimates (peripheral and central)

Adjusted for age, gender, and the use of antihypertensive treatment. Abbreviations: PP, pulse pressure; SBP, systolic blood pressure.

Table 4.

Odds ratio for each mm Hg increase (95% confidence interval) of the association of each blood pressure value with the presence of diastolic dysfunction, without and with simultaneous adjustment for each pair of estimates (peripheral and central)

Adjusted for age, gender, and the use of antihypertensive treatment. Abbreviations: PP, pulse pressure; SBP, systolic blood pressure.

Repeated analyses with central BP calculated using MBP/DBP calibration produced similar results, with mean values of SBP and PP significantly higher in patients with DD (Supplementary Table S6), and significant odds ratios after clinical adjustments, losing their significance after adjustment for peripheral BP (Supplementary Table S7). Furthermore, differences in BP were also present when patients were divided on the basis of having or not having each specific abnormality (left atrium volume ≥34 ml/m2, septal e′ velocity <8 cm/s, or lateral e′ velocity <10 cm/s) contained in the definition of DD (Supplementary Table S8). Alternative analyses by obtaining AUC of ROCs compared with z-statistics did not produce any significant advantage of central BP calculated either using SBP/DBP or MBP/DBP calibration methods. On the contrary, the AUC of ROC from nocturnal peripheral PP was significantly greater than those obtained from central PP (Supplementary Table S9).

DISCUSSION

This study shows an association of both peripheral and central BP with hypertension-related cardiac alterations, including LVH and DD. The relationship is present with SBP and PP, but not with DBP, and stronger with ABPM-derived estimates with respect to office BP. However, both peripheral and central BP was similarly associated with either LVH or DD, without a clear superiority of central BP over peripheral BP. As we have previously reported16 using a combined endpoint of target organ damage, which included cardiac, renal, and vascular alterations, these results do not suggest the routine use of 24-hour central BP monitoring for a better assessment of hypertensive patients with suspected hypertensive heart damage.

The role of central BP measurement in the evaluation of the hypertensive patient and its clinical utility is still a matter of debate. Whereas several, but not all, studies have shown that central BP has a better correlation with organ damage than peripheral BP5–7,16,24, the added value on clinical outcomes has been estimated as moderate.8–11 One of the possible reasons of such discrepancy is the fact that central BP has been measured at the office, even directly on the carotid artery or by pulse wave analysis of the peripheral waveform, and thus, it could be affected by the same confounders that affect office brachial BP measurement, the most important being the alert reaction.

It is clearly established that BP estimates obtained through ABPM are also better related with organ damage and prognosis than office BP.25 Thus, the possibility of measuring central BP also during 24 hours and obtaining 24-hour, day, and night estimates makes more feasible to clearly study whether such measurements have advantages and contain any added value over the traditional peripheral BP. Two previous studies have examined the relationship of 24-hour central BP with cardiac alterations. Protogerou et al.13 firstly reported that 24-hour central BP was better correlated with LVH than 24-hour peripheral BP. Zhang et al.14 reported in the same group of patients that 24-hour central BP was better associated with left ventricular DD in relation to peripheral BP. A more recent multicentre study has also reported a trend toward a better association of 24-hour central SBP with LVH.15

Our results are apparently in contrast with these previous observations. We were unable to detect a clear advantage of 24-hour central, over peripheral BP in the association with both LVH and DD. The analyses performed in the present paper examined such associations in 3 different ways. First, comparing AUC of ROC built in relation to LVH or DD for each pair of estimates (central vs. peripheral) did not reveal statistically significant better values for central BP. Second, the correlation coefficients calculated for LVMI, although quantitatively higher for central BP using MBP/DBP calibration, again not enough to exhibit statistical significance when compared with peripheral BP. Third, in multiple regression models, the significant odds ratios obtained for central SBP and PP estimates were no longer statistically significant when peripheral estimates were included in the model. We believe this last observation is of particular interest. Although central BP estimates are derived from the peripheral waveform and therefore they are highly correlated, from a practical point of view, the use of a new technology, which is more expensive and also less comfortable for the patients (each central BP measurement lasts longer than simple peripheral measurements), requires that it contains an added value, independently of the classical measurement. We think this particular goal is not accomplished by 24-hour central BP measurements.

It is also important trying to elucidate such discrepancies with previously published data. In fact, when examining crude values, these discrepancies are not as large as they appear. With respect to correlation coefficients with LVMI, Protogerou et al.13 found values of 0.511, 0.332, and 0.399, respectively for 24-hour central SBP with MBP/DBP calibration, 24-hour central SBP with SBP/DBP calibration, and peripheral SBP (statistically significant differences when comparing central SBP with MBP/DBP calibration and peripheral SBP). The correspondent values in the European multicentre study15 were respectively 0.47, 0.40, and 0.41 without significant differences comparing central (both types of calibration) vs. peripheral. In our study, correspondent values were 0.35, 0.24, and 0.29, again without statistically significant differences between central and peripheral estimates.

Something similar occurred when comparing ROC curves built with LVH as the outcome variable. AUC of 0.74 and 0.70 was reported by Protogereou et al.13 for central (MBP/DBP calibration) and peripheral 24-hour SBP, respectively (statistically significant differences when compared). Correspondent values from Weber et al.15 were 0.67, 0.63, and 0.64 for central SBP with MBP/DBP calibration, central SBP with SBP/DBP calibration, and peripheral SBP. The comparison of 24-hour central SBP (MBP/DBP calibration) with 24-hour peripheral SBP was statistically significant, but the comparison of the former with office peripheral BP (AUC: 0.62) was not. In our study, AUC for 24-hour SBP was respectively 0.66 (central SBP with MBP/DBP calibration), 0.65 (central SBP with SBP/DBP calibration), and 0.67 (peripheral SBP), without any significant differences when comparing central vs. peripheral.

Regarding DD, we found AUC from ROCs similar between 24-hour central and peripheral SBP and PP, whereas Zhang et al.14 found significant differences for 24-hour SBP (central: 0.69, peripheral: 0.63) but not for PP (0.77 vs. 0.74). Interestingly, the only statistically significant differences we found in our study favored peripheral PP, when nighttime AUC values were compared.

A critical view of all these studies show more similarities than discrepancies with only small differences in the parameters analyzed and statistical significance in some, but not all comparisons. As tests for comparing either correlation coefficients or AUC are highly dependent on the colinearity of related variables (central and peripheral BP), the statistical significance might be present or not with only small fluctuations in values obtained. In view of our results and also with this critical reappraisal of the previous studies,13–15 we think that the added value of 24-hour central BP measurement is relatively small with respect to 24-hour BP measurement.

We would also like to notice that 2 different ways of estimating central BP produced different values and associations. As also reported in previous studies,13–15 central BP obtained with MBP/DBP calibration showed correlation coefficients with LVMI and areas under ROC curves of LVH and DD numerically higher than central BP obtained with SBP/DBP calibration. The former measurement has been found to have advantages, as it better correlates with aortic BP obtained by invasive methods.18 However, values can be higher than peripheral BP, thus producing a negative amplification phenomenon, which is justified by an underestimation of brachial BP (as compared with invasive methods) during oscillometric measurements, and a more accurate central SBP estimation (as compared also with invasive methods) and measurement error, particularly in elders.18

Our study has several limitations. First, its cross-sectional nature allows only descriptive associations, but it does not explore the predictive value of central or peripheral BP in the development, progression, or regression of hypertension-related cardiac alterations. Second, most patients included were hypertensives of long duration currently on antihypertensive treatment (drug use is detailed in Supplementary Table S10) and often with other comorbid conditions which can influence the presence and severity of such alterations. This may lead to different results when assessed in untreated individuals. Third, in the comparison of the correlation coefficients for LVMI, central BP estimates (calibrated with MBP/DBP) produced quantitatively higher values than peripheral BP, which in some cases (24-hour estimates) were close to statistical significance (P < 0.1). These results cannot rule out a type 2 error, as the sample was originally calculated for the sum of cardiac and renal organ damage and thus underpowered when assessing only cardiac alterations (a secondary objective of the main study without a sample size calculation). However, the lack of statistical significance in the comparison of correlation coefficients was accompanied by similar results when assessing differences in AUC of ROC or when calculating OR for the association of BP estimates with either LVH or DD, thus suggesting that the added value of 24-hour central BP over peripheral BP is relatively small.

In conclusion, hypertensive patients with heart damage, either LVH or DD, exhibited higher SBP and PP values than those without such organ damage. The BP elevation was present independently of the method of assessment, office or ambulatory, peripheral, or central. Twenty-four–hour central BP was not found to be better associated with LVH or DD than peripheral BP, although such conclusion might be limited due to sample size and would require further confirmation. Only correlation coefficients of 24-h BP were numerically higher (without statistical significance) for central, compared with peripheral BP. Further studies focused on the ability of 24-hour central BP to predict cardiovascular outcomes would be necessary in order to possibly justify a routine central BP monitoring.

ACKNOWLEDGMENTS

The authors like to thank Erik Cobo, PhD, for his statistical advice. Funding was supported in part by the Instituto de Salud Carlos III (PI14/00592) and by Fundació de Recerca I Docència Mútua Terrassa.

DISCLOSURE

The authors declared no conflict of interest.

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© American Journal of Hypertension, Ltd 2018. All rights reserved. For Permissions, please email:

© American Journal of Hypertension, Ltd 2018. All rights reserved. For Permissions, please email:

Topic:

• antihypertensive agents
• hypertension
• heart failure, diastolic
• left ventricular hypertrophy
• blood pressure

Supplementary data

How is left ventricular hypertrophy diagnosed?

How do you detect left ventricular hypertrophy on ECG?

How do you diagnose hypertrophy?

What indicates left ventricular hypertrophy?