Original Article
Differential relationships of systolic and diastolic blood pressure with components of left ventricular diastolic dysfunction Carlos D. Libhaber, Angela J. Woodiwiss, Hendrik L. Booysen, Muzi J. Maseko, Olebogeng H.I. Majane, Pinhas Sareli, and Gavin R. Norton
Aims: To determine whether SBP or DBP is best associated with different components of left ventricular diastolic dysfunction. Methods: In 241 randomly selected participants, echocardiographic left ventricular diastolic function was assessed from early-to-atrial (E/A) transmitral velocity and E/e0 where e0 represents myocardial tissue lengthening velocity in early diastole as measured at the mitral annulus. Relationships between diastolic function and blood pressure (BP) were assessed from brachial and central aortic (radial applanation tonometry and SphygmoCor software) measurements. Results: Independent of confounders, brachial DBP (partial r ¼ –0.21, P < 0.002), but not SBP (partial r ¼ –0.09, P ¼ 0.18), was associated with E/A and the relationship between brachial DBP and E/A persisted with adjustments for brachial (P < 0.002) or aortic (P < 0.05) SBP. Although aortic SBP was independently associated with E/A, this relationship did not persist with adjustments for DBP (partial r ¼ –0.05, P ¼ 0.44). In contrast, both brachial (partial r ¼ 0.34, P < 0.0001) and aortic (partial r ¼ 0.34, P < 0.0001) SBP were independently associated with E/e0 , effects that persisted with adjustments for DBP (P < 0.0001), although independent relationships between DBP and E/e0 did not persist with adjustments for brachial or aortic SBP (P ¼ 0.17–0.57). In quartiles of DBP or SBP within normal-to-high normal ranges, multivariate adjusted E/A was decreased and E/e0 increased as compared with those with optimal BP values (P < 0.05 to P < 0.005). Conclusion: Both SBP and DBP are important determinants of separate components of left ventricular diastolic dysfunction and these effects are noted even within normotensive BP ranges. DBP may be as important as SBP in the transition to diastolic dysfunction. Keywords: ambulatory blood pressure, aortic blood pressure, DBP, left ventricular diastolic dysfunction, SBP Abbreviations: baPWV, brachial-ankle pulse wave velocity; BP, blood pressure; cfPWV, carotid-femoral pulse wave velocity; CI, confidence interval; E/A, early-to-atrial transmitral velocity; E/e0 , E/velocity of myocardial tissue lengthening at the mitral annulus; HbA1C, glycated haemoglobin; LVH, left ventricular hypertrophy; LVM, left
ventricular mass; LVMI, left ventricular mass index; MAP, mean arterial pressure; TDI, tissue Doppler indices
INTRODUCTION
L
eft ventricular diastolic dysfunction (LVDD) is largely identified from abnormalities of the ratios of transmitral early-to-late (atrial) blood flow velocity (E/A) and E/velocity of myocardial tissue lengthening at the mitral annulus (Ea or e0 ) (E/e0 ), an index of filling pressures. These components of LVDD are either separately or together independently associated with mortality, cardiovascular outcomes or the development of heart failure with a normal ejection fraction [1–8]. At a community level, a number of comorbid conditions are associated with LVDD, including hypertension, obesity and diabetes mellitus [4,9–13]. As these conditions often coexist, it is difficult to segregate the underlying cause of LVDD in order to plan appropriate therapy. With respect to the impact of blood pressure (BP), the role of SBP versus DBP in contributing towards LVDD is unclear. The impact of vascular–ventricular interaction on LVDD has been emphasized as an important mechanism in the transition to heart failure with a preserved ejection fraction [14]. Indeed, a number of studies have demonstrated that increases in aortic stiffness, which are thought to mediate vascular–ventricular interactions, are associated with LVDD [15–28]. It is therefore possible that increases in SBP, which more closely reflect aortic stiffness changes, are more important in mediating LVDD than increases in DBP.
Journal of Hypertension 2014, 32:912–920 Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Correspondence to Angela J. Woodiwiss, PhD, Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand Medical School, 7 York Road, Parktown, 2193 Johannesburg, South Africa. Tel: +27 11 717 2363; fax: +27 11 717 2153; e-mail: [email protected] Received 22 May 2013 Revised 2 December 2013 Accepted 2 December 2013 J Hypertens 32:912–920 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins. DOI:10.1097/HJH.0000000000000100
912
www.jhypertension.com
Volume 32 Number 4 April 2014
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Blood pressure and left ventricular diastolic dysfunction
However, the relationships between indices of aortic stiffness and mild diastolic dysfunction, as defined by abnormalities in E/A (relaxation abnormalities), are less clear, with associations noted in some [15,23,26], but not other studies [19,21,27,29,30]. Moreover, the BP most strongly related to E/A or LVDD in some large studies is DBP rather than SBP [12,13,31,32]. As relaxation abnormalities (grade I LVDD) are as commonly noted at a community level as more severe forms of LVDD [12], and predict the progression to heart failure [7], it is possible that a focus on SBP alone will exclude a significant proportion of those with LVDD at risk of progressing to heart failure with a preserved ejection fraction. The uncertainty as to whether SBP or DBP, best identify that person with BP-related decreases in LVDD, and hence whom is most likely to progress to heart failure with a preserved ejection fraction, prompted us to evaluate which of these brachial or central aortic BP values best relate to the individual components of LVDD.
MATERIALS AND METHODS The study protocol was approved by the University of the Witwatersrand Committee for Research in Human Subjects (approval numbers: M02-04-72 renewed as M07-04-69 and M12-04-108). Participants gave informed, written consent. The study design has previously been described [13,33,34]. Briefly, nuclear families of black African ancestry consisting of siblings with a minimum age of 16 years were randomly recruited from the South West Township (SOWETO) of Johannesburg, South Africa. In a substudy, 241 participants had both transmitral velocity and myocardial tissue Doppler assessments for the current analysis.
Clinical, demographic and anthropometric measurements A standardized questionnaire was administered to obtain demographic data and information on each participant’s medical history, smoking habits, intake of alcohol and use of medication [13,33,34]. Participants were identified as being overweight if their BMI was at least 25 kg/m2 and obese if their BMI was at least 30 kg/m2. Laboratory blood tests of renal function, liver function, blood glucose, haematological parameters, lipid profiles and percentage glycated haemoglobin (HbA1C) (Roche Diagnostics, Mannheim, Germany) were performed. Diabetes mellitus was defined as the use of insulin or oral hypoglycaemic agents or an HbA1C greater than 6.1%.
Brachial blood pressures High-quality conventional BP measurements were obtained by a trained nurse-technician according to the European Society of Hypertension guidelines [35] as previously described [33]. BP was recorded to the nearest 2 mmHg. Korotkov phases I and V were employed to identify SBP and DBP, respectively, and care was taken to avoid auscultatory gaps. BP was measured five times consecutively using appropriate sized cuffs after the individuals had rested for 5–10 min in the sitting position. The BP measurements were obtained between 0900 and 1400 h. The average of the five recordings was taken as the Journal of Hypertension
conventional BP. The frequency of identical consecutive conventional recordings was 0% for SBP and 0% for DBP. No conventional BP values were recorded as an odd number. Of the conventional SBP and DBP readings, 32% ended on a zero (expected ¼ 20%). Hypertension was defined as the presence of antihypertensive treatment or a mean conventional BP of at least 140/90 mmHg.
Aortic blood pressures To determine central aortic BP, pulse wave analysis was conducted using techniques previously described [34]. After participants had rested for 15 min in the supine position, arterial waveforms at the radial (dominant arm) pulse were recorded by applanation tonometry during an 8-s period using a high-fidelity SPC-301 micromanometer (Millar Instrument, Inc., Houston, Texas, USA) interfaced with a computer employing SphygmoCor, version 6.21 software (AtCor Medical Pty. Ltd., West Ryde, New South Wales, Australia). Recordings wherein the systolic or diastolic variability of consecutive waveforms exceeded 5% or the amplitude of the pulse wave signal was less than 80 mV were discarded. All measurements were made by a single experienced trained technician unaware of the clinical history of the participants. To determine aortic BP, the pulse wave was calibrated by manual measurement (auscultation) of brachial BP taken immediately before the recordings. From an inbuilt generalized transfer function, an aortic waveform was generated from which aortic SBP, pulse pressure (PP) and DBP were derived. Mean arterial pressure (MAP) was calculated as DBP þ (SBP – DBP/3).
Echocardiography Echocardiographic measurements were performed using a Sonosite M-Turbo ultrasound (SonoSite Inc., Bothell, Washington, USA) device with the patient in the partial left decubitus position. All participants were assessed for mitral valve abnormalities as determined using two-dimensional and colour Doppler imaging. The left ventricular dimensions were determined using two-dimensional directed Mmode echocardiography in the short axis view and these recordings analysed according to the American Society of Echocardiography convention [36]. The left ventricular dimensions were measured only when appropriate visualization of both the right and the left septal surfaces occurred and where the endocardial surfaces of both the septal and posterior wall were clearly visible. Left ventricular end diastolic and systolic volumes were determined using the Teichholz method [37]. Left ventricular ejection fraction was calculated as [(LV end diastolic volume – LV end systolic volume)/LV end diastolic volume] 100. Left ventricular mass (LVM) was derived according to an anatomically validated formula [38] and indexed to height2.7 (LVM index, LVMI). Left ventricular diastolic function was assessed from a pulsed wave Doppler examination of the mitral inflow at rest and using tissue Doppler indices (TDIs) [39]. Pulse wave Doppler recordings of transmitral velocity were obtained with the sample volume at the tip of the mitral valve in the apical four-chamber view. Transmitral velocity measurements were obtained during the early (E) and late (atrial-A) period of left ventricular diastolic inflow and www.jhypertension.com
913
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Libhaber et al.
expressed as the E/A ratio. To perform TDI, the velocity of myocardial tissue lengthening at the level of the mitral annulus was recorded in the apical four-chamber view. The sample volume was positioned at the septal and lateral corners of the mitral annulus. To determine diastolic function using TDI, peak velocities during early (e0 ) and late (atrial) (a0 ) diastole were measured. Data were expressed as the E/e0 ratio (an index of LV filling pressures). Left ventricular diastolic dysfunction was evaluated as mild (impaired relaxation when E/A 0.75), moderate (pseudonormal, where E/A >0.75 51 g/m2.7) and LVH was more prevalent in those with a decreased E/A (0.75) (29.2%) or increased E/e0 (10) (23.1%) than in those without either a decreased E/A or increased E/e0 (11.5 or 11.4%, P < 0.05 for both).
Data analysis Database management and statistical analyses were performed with SAS software, version 9.1 (The SAS Institute Inc., Cary, North Carolina, USA). Data were expressed as mean SD or SEM as indicated. Relationships were evaluated from univariate or multivariate linear regression analysis and correlation coefficients compared using Z statistics. To determine probability values, further adjustments for nonindependence of family members were performed using nonlinear regression analysis (mixed procedure as defined in the SAS package). To ensure that results were not influenced by the presence of antihypertensive therapy, sensitivity analysis was conducted in 180 participants never treated for hypertension. Moreover, to ensure that colinearity between confounders did not influence the results, sensitivity analysis was performed with only age and sex included as confounders together with BP.
Factors associated with left ventricular diastolic function or left ventricular diastolic dysfunction
RESULTS
Are SBP, pulse pressure or DBP independently associated with impaired left ventricular relaxation?
Participant characteristics Table 1 shows the characteristics of the echocardiographic study sample with and without TDI measures. In general, a high proportion of participants had uncontrolled TABLE 1. Characteristics of the study sample with and without measures of tissue Doppler indices of left ventricular diastolic function
Sample number (% female) Age (years) BMI (kg/m2) % overweight/obese Regular tobacco (% individuals) Regular alcohol (% individuals) % diabetes mellitus or an HbA1C >6.1% % hypertensive Brachial SBP/DBP (mmHg) Brachial pulse pressure (mmHg) Mean arterial pressure (mmHg) Central aortic SBP (mmHg) Central aortic pulse pressure (mmHg) E/A E/e0
With TDI
Without TDI
241 (64.7) 42.3 17.9 28.9 8.0 22/42 17 17 27
453 (65.2) 43.5 17.8 29.8 7.7 24/44 13 22 24
45 127 23/83 14 44.1 17.2 98 16 117 22 32.9 15.4
42 130 22/84 12 46.2 14.7 100 15 121 22 37.6 15.2
1.39 0.55 6.90 3.44
1.24 0.44 –
E/A, ratio of transmitral early-to-atrial (late) blood flow velocity; E/e0 , E/velocity of the mean value of lateral and septal wall myocardial tissue lengthening in early diastole at the mitral annulus. P
Differential relationships of systolic and diastolic blood pressure with components of left ventricular diastolic dysfunction Carlos D. Libhaber, Angela J. Woodiwiss, Hendrik L. Booysen, Muzi J. Maseko, Olebogeng H.I. Majane, Pinhas Sareli, and Gavin R. Norton
Aims: To determine whether SBP or DBP is best associated with different components of left ventricular diastolic dysfunction. Methods: In 241 randomly selected participants, echocardiographic left ventricular diastolic function was assessed from early-to-atrial (E/A) transmitral velocity and E/e0 where e0 represents myocardial tissue lengthening velocity in early diastole as measured at the mitral annulus. Relationships between diastolic function and blood pressure (BP) were assessed from brachial and central aortic (radial applanation tonometry and SphygmoCor software) measurements. Results: Independent of confounders, brachial DBP (partial r ¼ –0.21, P < 0.002), but not SBP (partial r ¼ –0.09, P ¼ 0.18), was associated with E/A and the relationship between brachial DBP and E/A persisted with adjustments for brachial (P < 0.002) or aortic (P < 0.05) SBP. Although aortic SBP was independently associated with E/A, this relationship did not persist with adjustments for DBP (partial r ¼ –0.05, P ¼ 0.44). In contrast, both brachial (partial r ¼ 0.34, P < 0.0001) and aortic (partial r ¼ 0.34, P < 0.0001) SBP were independently associated with E/e0 , effects that persisted with adjustments for DBP (P < 0.0001), although independent relationships between DBP and E/e0 did not persist with adjustments for brachial or aortic SBP (P ¼ 0.17–0.57). In quartiles of DBP or SBP within normal-to-high normal ranges, multivariate adjusted E/A was decreased and E/e0 increased as compared with those with optimal BP values (P < 0.05 to P < 0.005). Conclusion: Both SBP and DBP are important determinants of separate components of left ventricular diastolic dysfunction and these effects are noted even within normotensive BP ranges. DBP may be as important as SBP in the transition to diastolic dysfunction. Keywords: ambulatory blood pressure, aortic blood pressure, DBP, left ventricular diastolic dysfunction, SBP Abbreviations: baPWV, brachial-ankle pulse wave velocity; BP, blood pressure; cfPWV, carotid-femoral pulse wave velocity; CI, confidence interval; E/A, early-to-atrial transmitral velocity; E/e0 , E/velocity of myocardial tissue lengthening at the mitral annulus; HbA1C, glycated haemoglobin; LVH, left ventricular hypertrophy; LVM, left
ventricular mass; LVMI, left ventricular mass index; MAP, mean arterial pressure; TDI, tissue Doppler indices
INTRODUCTION
L
eft ventricular diastolic dysfunction (LVDD) is largely identified from abnormalities of the ratios of transmitral early-to-late (atrial) blood flow velocity (E/A) and E/velocity of myocardial tissue lengthening at the mitral annulus (Ea or e0 ) (E/e0 ), an index of filling pressures. These components of LVDD are either separately or together independently associated with mortality, cardiovascular outcomes or the development of heart failure with a normal ejection fraction [1–8]. At a community level, a number of comorbid conditions are associated with LVDD, including hypertension, obesity and diabetes mellitus [4,9–13]. As these conditions often coexist, it is difficult to segregate the underlying cause of LVDD in order to plan appropriate therapy. With respect to the impact of blood pressure (BP), the role of SBP versus DBP in contributing towards LVDD is unclear. The impact of vascular–ventricular interaction on LVDD has been emphasized as an important mechanism in the transition to heart failure with a preserved ejection fraction [14]. Indeed, a number of studies have demonstrated that increases in aortic stiffness, which are thought to mediate vascular–ventricular interactions, are associated with LVDD [15–28]. It is therefore possible that increases in SBP, which more closely reflect aortic stiffness changes, are more important in mediating LVDD than increases in DBP.
Journal of Hypertension 2014, 32:912–920 Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Correspondence to Angela J. Woodiwiss, PhD, Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand Medical School, 7 York Road, Parktown, 2193 Johannesburg, South Africa. Tel: +27 11 717 2363; fax: +27 11 717 2153; e-mail: [email protected] Received 22 May 2013 Revised 2 December 2013 Accepted 2 December 2013 J Hypertens 32:912–920 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins. DOI:10.1097/HJH.0000000000000100
912
www.jhypertension.com
Volume 32 Number 4 April 2014
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Blood pressure and left ventricular diastolic dysfunction
However, the relationships between indices of aortic stiffness and mild diastolic dysfunction, as defined by abnormalities in E/A (relaxation abnormalities), are less clear, with associations noted in some [15,23,26], but not other studies [19,21,27,29,30]. Moreover, the BP most strongly related to E/A or LVDD in some large studies is DBP rather than SBP [12,13,31,32]. As relaxation abnormalities (grade I LVDD) are as commonly noted at a community level as more severe forms of LVDD [12], and predict the progression to heart failure [7], it is possible that a focus on SBP alone will exclude a significant proportion of those with LVDD at risk of progressing to heart failure with a preserved ejection fraction. The uncertainty as to whether SBP or DBP, best identify that person with BP-related decreases in LVDD, and hence whom is most likely to progress to heart failure with a preserved ejection fraction, prompted us to evaluate which of these brachial or central aortic BP values best relate to the individual components of LVDD.
MATERIALS AND METHODS The study protocol was approved by the University of the Witwatersrand Committee for Research in Human Subjects (approval numbers: M02-04-72 renewed as M07-04-69 and M12-04-108). Participants gave informed, written consent. The study design has previously been described [13,33,34]. Briefly, nuclear families of black African ancestry consisting of siblings with a minimum age of 16 years were randomly recruited from the South West Township (SOWETO) of Johannesburg, South Africa. In a substudy, 241 participants had both transmitral velocity and myocardial tissue Doppler assessments for the current analysis.
Clinical, demographic and anthropometric measurements A standardized questionnaire was administered to obtain demographic data and information on each participant’s medical history, smoking habits, intake of alcohol and use of medication [13,33,34]. Participants were identified as being overweight if their BMI was at least 25 kg/m2 and obese if their BMI was at least 30 kg/m2. Laboratory blood tests of renal function, liver function, blood glucose, haematological parameters, lipid profiles and percentage glycated haemoglobin (HbA1C) (Roche Diagnostics, Mannheim, Germany) were performed. Diabetes mellitus was defined as the use of insulin or oral hypoglycaemic agents or an HbA1C greater than 6.1%.
Brachial blood pressures High-quality conventional BP measurements were obtained by a trained nurse-technician according to the European Society of Hypertension guidelines [35] as previously described [33]. BP was recorded to the nearest 2 mmHg. Korotkov phases I and V were employed to identify SBP and DBP, respectively, and care was taken to avoid auscultatory gaps. BP was measured five times consecutively using appropriate sized cuffs after the individuals had rested for 5–10 min in the sitting position. The BP measurements were obtained between 0900 and 1400 h. The average of the five recordings was taken as the Journal of Hypertension
conventional BP. The frequency of identical consecutive conventional recordings was 0% for SBP and 0% for DBP. No conventional BP values were recorded as an odd number. Of the conventional SBP and DBP readings, 32% ended on a zero (expected ¼ 20%). Hypertension was defined as the presence of antihypertensive treatment or a mean conventional BP of at least 140/90 mmHg.
Aortic blood pressures To determine central aortic BP, pulse wave analysis was conducted using techniques previously described [34]. After participants had rested for 15 min in the supine position, arterial waveforms at the radial (dominant arm) pulse were recorded by applanation tonometry during an 8-s period using a high-fidelity SPC-301 micromanometer (Millar Instrument, Inc., Houston, Texas, USA) interfaced with a computer employing SphygmoCor, version 6.21 software (AtCor Medical Pty. Ltd., West Ryde, New South Wales, Australia). Recordings wherein the systolic or diastolic variability of consecutive waveforms exceeded 5% or the amplitude of the pulse wave signal was less than 80 mV were discarded. All measurements were made by a single experienced trained technician unaware of the clinical history of the participants. To determine aortic BP, the pulse wave was calibrated by manual measurement (auscultation) of brachial BP taken immediately before the recordings. From an inbuilt generalized transfer function, an aortic waveform was generated from which aortic SBP, pulse pressure (PP) and DBP were derived. Mean arterial pressure (MAP) was calculated as DBP þ (SBP – DBP/3).
Echocardiography Echocardiographic measurements were performed using a Sonosite M-Turbo ultrasound (SonoSite Inc., Bothell, Washington, USA) device with the patient in the partial left decubitus position. All participants were assessed for mitral valve abnormalities as determined using two-dimensional and colour Doppler imaging. The left ventricular dimensions were determined using two-dimensional directed Mmode echocardiography in the short axis view and these recordings analysed according to the American Society of Echocardiography convention [36]. The left ventricular dimensions were measured only when appropriate visualization of both the right and the left septal surfaces occurred and where the endocardial surfaces of both the septal and posterior wall were clearly visible. Left ventricular end diastolic and systolic volumes were determined using the Teichholz method [37]. Left ventricular ejection fraction was calculated as [(LV end diastolic volume – LV end systolic volume)/LV end diastolic volume] 100. Left ventricular mass (LVM) was derived according to an anatomically validated formula [38] and indexed to height2.7 (LVM index, LVMI). Left ventricular diastolic function was assessed from a pulsed wave Doppler examination of the mitral inflow at rest and using tissue Doppler indices (TDIs) [39]. Pulse wave Doppler recordings of transmitral velocity were obtained with the sample volume at the tip of the mitral valve in the apical four-chamber view. Transmitral velocity measurements were obtained during the early (E) and late (atrial-A) period of left ventricular diastolic inflow and www.jhypertension.com
913
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Libhaber et al.
expressed as the E/A ratio. To perform TDI, the velocity of myocardial tissue lengthening at the level of the mitral annulus was recorded in the apical four-chamber view. The sample volume was positioned at the septal and lateral corners of the mitral annulus. To determine diastolic function using TDI, peak velocities during early (e0 ) and late (atrial) (a0 ) diastole were measured. Data were expressed as the E/e0 ratio (an index of LV filling pressures). Left ventricular diastolic dysfunction was evaluated as mild (impaired relaxation when E/A 0.75), moderate (pseudonormal, where E/A >0.75 51 g/m2.7) and LVH was more prevalent in those with a decreased E/A (0.75) (29.2%) or increased E/e0 (10) (23.1%) than in those without either a decreased E/A or increased E/e0 (11.5 or 11.4%, P < 0.05 for both).
Data analysis Database management and statistical analyses were performed with SAS software, version 9.1 (The SAS Institute Inc., Cary, North Carolina, USA). Data were expressed as mean SD or SEM as indicated. Relationships were evaluated from univariate or multivariate linear regression analysis and correlation coefficients compared using Z statistics. To determine probability values, further adjustments for nonindependence of family members were performed using nonlinear regression analysis (mixed procedure as defined in the SAS package). To ensure that results were not influenced by the presence of antihypertensive therapy, sensitivity analysis was conducted in 180 participants never treated for hypertension. Moreover, to ensure that colinearity between confounders did not influence the results, sensitivity analysis was performed with only age and sex included as confounders together with BP.
Factors associated with left ventricular diastolic function or left ventricular diastolic dysfunction
RESULTS
Are SBP, pulse pressure or DBP independently associated with impaired left ventricular relaxation?
Participant characteristics Table 1 shows the characteristics of the echocardiographic study sample with and without TDI measures. In general, a high proportion of participants had uncontrolled TABLE 1. Characteristics of the study sample with and without measures of tissue Doppler indices of left ventricular diastolic function
Sample number (% female) Age (years) BMI (kg/m2) % overweight/obese Regular tobacco (% individuals) Regular alcohol (% individuals) % diabetes mellitus or an HbA1C >6.1% % hypertensive Brachial SBP/DBP (mmHg) Brachial pulse pressure (mmHg) Mean arterial pressure (mmHg) Central aortic SBP (mmHg) Central aortic pulse pressure (mmHg) E/A E/e0
With TDI
Without TDI
241 (64.7) 42.3 17.9 28.9 8.0 22/42 17 17 27
453 (65.2) 43.5 17.8 29.8 7.7 24/44 13 22 24
45 127 23/83 14 44.1 17.2 98 16 117 22 32.9 15.4
42 130 22/84 12 46.2 14.7 100 15 121 22 37.6 15.2
1.39 0.55 6.90 3.44
1.24 0.44 –
E/A, ratio of transmitral early-to-atrial (late) blood flow velocity; E/e0 , E/velocity of the mean value of lateral and septal wall myocardial tissue lengthening in early diastole at the mitral annulus. P
