Search
Close
Search
Advanced Search
Search Menu
AI Discovery Assistant

Abstract

Aims

Myocardial work (MW) is a novel parameter that can be used in a clinical setting to assess left ventricular (LV) pressures and deformation. We sought to distinguish patterns of global MW index in hypertensive vs. non-hypertensive patients and to look at differences between categories of hypertension.

Methods and results

Sixty-five hypertensive patients (mean age 65 ± 13 years; 30 male) and 15 controls (mean age 38 ± 12 years; 7 male) underwent transthoracic echocardiography at rest. Hypertensive patients were subdivided into Stage 1 (n = 32) and Stage 2 (n = 33) hypertension based on 2017 American College of Cardiology guidelines. Exclusion criteria were suboptimal image quality for myocardial deformation analysis, reduced ejection fraction, valvular heart disease, intracardiac shunt, and arrhythmia. Global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency were estimated from LV pressure–strain loops utilizing proprietary software from speckle-tracking echocardiography. LV systolic and diastolic pressures were estimated using non-invasive brachial artery cuff pressure. Global longitudinal strain and LV ejection fraction were preserved between the groups with no statistically significant difference, whereas there was a statically significant difference between the control and two hypertension groups in GWI (P = 0.01), GCW (P < 0.001), and GWW (P < 0.001).

Conclusion

Non-invasive MW analysis allows better understanding of LV response under conditions of increased afterload. MW is an advanced assessment of LV systolic function in hypertension patients, giving a closer look at the relationship between LV pressure and contractility in settings of increased load dependency than LV ejection fraction and global longitudinal strain.

myocardial work, hypertension, speckle-tracking echocardiography, transthoracic echocardiography

Introduction

Myocardial work (MW) is a novel parameter that is used as an advanced assessment of left ventricular (LV) function. It is calculated through interpretation of global longitudinal strain (GLS) by speckle-tracking echocardiography and a non-invasive estimate of LV systolic pressure. MW refers to the amount of work performed by the LV during mechanical systole and includes afterload.1–3 A recent study4 showed that LV pressure–strain loops (PSL) provide a unique method of quantifying MW with advantages over conventional ejection fraction and GLS assessment. MW accounts for myocardial deformation and overcomes the load dependency limitation of ejection fraction and GLS by the incorporation of LV pressure estimated by arterial cuff blood pressure.5,6

Recent advances in echocardiography make it possible to better understand the mechanical performance of the LV in patients with hypertension and how PSLs might give insight into the effect of different antihypertensive drugs on myocardial function.7,8 In this study, a rapidly emerging technique that incorporates GLS by speckle-tracking echocardiography and LV pressure curves was used to assess MW indices observed in subcategories of hypertensive patients.

Methods

Patient population

This single-centre, retrospective study assessed patients with a history of hypertension who presented to our institution for routine echocardiography. The study was approved by our institution’s Human Research and Ethics Committee. Informed consent was not obtained as this was a retrospective study. The data used in this article will be shared upon reasonable request to the corresponding author. Using the 2017 American College of Cardiology guidelines,9 the hypertensive population was sub-categorized into Stage 1 hypertension (systolic blood pressure 130–139 mmHg) and Stage 2 hypertension (systolic blood pressure ≥140). A total of 65 patients (32 Stage 1 and 33 Stage 2) with a history of hypertension who were hypertensive at the time of the echocardiogram were included in this study. Fifteen healthy controls who were screened in the hospital and had no history of hypertension, a normal ejection fraction, and no history of heart disease were included. Our control individuals had screening echocardiograms for indications such as palpitations or pre-syncopal episodes. Exclusion criteria were suboptimal image quality for myocardial deformation analysis, reduced ejection fraction, any valvular heart disease, intracardiac shunt, and arrhythmia.

Echocardiographic examination

Subjects received a transthoracic echocardiogram as part of their routine clinical care. All echocardiographic images were obtained utilizing a GE Vivid E95 platform (GE Healthcare, Wauwatosa, WI, USA). Patients were imaged at rest in the left lateral decubitus position. Blood pressure was acquired at the time of the exam in the imaging position. Standard imaging windows and measurements were obtained based on the American Society of Echocardiography and European Association of Cardiovascular Imaging guidelines.10,11 Echocardiographic parameters included LV end-diastolic dimension, interventricular septum dimension, posterior wall dimension, LV mass, LV mass index, LV ejection fraction, stroke volume utilizing Simpson’s biplane method, LV end-systolic volume, E′ average, E/e′ average, LA volume index, and deceleration time.

Two-dimensional MW analysis

Global MW analysis was performed on commercially available proprietary software (EchoPac 202, General Electric Vingmed Ultrasound, Horten, Norway). This innovative and non-invasive method utilizes brachial cuff blood pressure, which is assumed to be equivalent to LV systolic pressure, in conjunction with GLS by speckle-tracking echocardiography. GLS was obtained utilizing the three standard imaging windows—apical four-chamber, two-chamber, and long-axis—with a frame rate between 40 and 80 frames per second. Once GLS analysis was complete, MW was calculated by entering the subject’s brachial cuff blood pressure into the measurement tool as well as setting valvular event timing.12 Valvular event times include mitral valve closure, aortic valve opening, aortic valve closure, and mitral valve opening. These were set using pulsed-wave Doppler and then confirmed by aligning the event time by 2D image in the apical long-axis view. The software produces a non-invasive PSL based on valvular event times. MW indices that were calculated were global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE).

Similar to GLS bull’s-eye plots, MW plots also can be analysed numerically and by colour shading. On a GWI bull’s-eye plot, red indicates areas of high work, green demonstrates normal work, and blue shows negative work.13 In analysing the GWI bull’s-eye plots, colour transitioned from a predominantly green plot in the control group to increased areas of red in the hypertension groups. An increase in areas of red shading directly corresponds to an increase in GWI values. The progression of increased red demonstrates worsening hypertension, indicating higher amounts of work being performed in those segments (Figure 1). The bull’s-eye plots in this study represent the median GWI values of each respective subgroup. Figure 2 illustrates the direct correlation between systolic blood pressure and GWI by showing an extreme scenario of a very elevated blood pressure with normal GLS and unaffected GWE.

(A) Control group. A normal global work index bull’s-eye (1770 mmHg%) represented by a predominantly green-coloured shaded plot. (B) Hypertension Stage 1. An elevated global work index bull’s-eye (2044 mmHg%) with a small area of red shading in the plot indicates a higher amount of work in those segments. (C) Hypertension Stage 2. An even more elevated global work index (2187 mmHg%) with an increase in the area of red-coloured segments depicting a higher amount of work. Global longitudinal strain and global work efficiency are relatively unaffected amongst the three subgroups.
Figure 1

(A) Control group. A normal global work index bull’s-eye (1770 mmHg%) represented by a predominantly green-coloured shaded plot. (B) Hypertension Stage 1. An elevated global work index bull’s-eye (2044 mmHg%) with a small area of red shading in the plot indicates a higher amount of work in those segments. (C) Hypertension Stage 2. An even more elevated global work index (2187 mmHg%) with an increase in the area of red-coloured segments depicting a higher amount of work. Global longitudinal strain and global work efficiency are relatively unaffected amongst the three subgroups.

Open in new tabDownload slide
An extreme hypertension scenario of a patient with significantly elevated blood pressure (182/80 mmHg). Global longitudinal strain is normal (−21%) (A), global work index is significantly elevated (3105 mmHg%) with a very predominantly red-shaded bull’s-eye (B), and global work efficiency is unaffected (96%) (C).
Figure 2

An extreme hypertension scenario of a patient with significantly elevated blood pressure (182/80 mmHg). Global longitudinal strain is normal (−21%) (A), global work index is significantly elevated (3105 mmHg%) with a very predominantly red-shaded bull’s-eye (B), and global work efficiency is unaffected (96%) (C).

Open in new tabDownload slide

Non-invasive PSL

The area inside the PSL represents GWI, which is the work performed by the LV. MW starts at mitral valve closure, goes in a counterclockwise rotation, and ends with mitral valve opening.13 There is a direct correlation between the area inside the PSL and the GWI. As GWI value increases, the area inside the PSL increases. The height or peak of the PSL increases with a rise in systolic blood pressure. Figure 3 illustrates an extreme scenario to highlight the difference in PSLs between a subject from the control group and a subject from our Stage 2 hypertension cohort.

Extreme comparison between a control subject with a normal blood pressure (110/70 mmHg) demonstrating a normal global work index (1770 mmHg%) (A), and a subject from the Stage 2 hypertension group with a significantly elevated blood pressure (182/80 mmHg) and greatly increased global work index (3105 mmHg%) (B). The area inside the pressure–strain loop increases as global work index increases, and the height of the PSL increases with an increase in systolic blood pressure.
Figure 3

Extreme comparison between a control subject with a normal blood pressure (110/70 mmHg) demonstrating a normal global work index (1770 mmHg%) (A), and a subject from the Stage 2 hypertension group with a significantly elevated blood pressure (182/80 mmHg) and greatly increased global work index (3105 mmHg%) (B). The area inside the pressure–strain loop increases as global work index increases, and the height of the PSL increases with an increase in systolic blood pressure.

Open in new tabDownload slide

Statistical analysis

The study sample included 65 patients. Descriptive data are displayed in tables. One-way analysis of variance (ANOVA) test was utilized to examine the differences of the mean measurements in the different blood pressure groups. The chi-square test was used for categorical variables. All P-values are reported as two-tailed, with <0.05 considered statistically significant. Analyses were performed using SPSS (IBM SPSS Statistics, Chicago, IL, USA) or SAS (SAS Institute, Cary, NC, USA) software.

Results

Sixty-five patients fulfilled the inclusion criteria (Table 1). The control group was significantly younger than the hypertension group. Systolic blood pressure was significantly higher in both hypertension groups. Heart rate, body mass index, and body surface area were consistent across the two groups. In the overall hypertension group, 11 patients had a history of cardiovascular disease, including myocardial infarction (4) and coronary artery disease (9), and 32 of the patients had hyperlipidaemia. The hypertension group had more history of chronic kidney disease and diabetes mellitus. Calcium channel blockers were the most common antihypertensive medications (46%) used to treat the patients.

Table 1
Open in new tab

Patient demographics and medications

Control n = 15Hypertension Stage 1 n = 32Hypertension Stage 2 n = 33Total hypertension n = 65P-value (total hypertension)P-value (overall)
Sex
 Male7 (47)11 (34%)19 (58%)30 (46%)0.060.17
Age (years)37.8 ± 12.059.8 ± 13.463.1 ± 130064.5 ± 13.20.33<0.001
SBP (mmHg)113.5 ± 11.9134.5 ± 3.6156.2 ± 8.8145.5 ± 12.8<0.001<0.001
DBP (mmHg)72.6 ± 11.673.5 ± 10.180.2 ± 12.076.9 ± 11.5<0.0010.03
Heart rate75.9 ± 12.172.1 ± 17.169.3 ± 11.270.7 ± 14.40.430.32
Body mass index (kg/m2)26.1 (22.1–31.7)27.45 (25.45–33.15)28.6 (26.46–32.9)27.8 (25.5–32.9)0.500.21
Hx of CVD0 (0)7 (22%)5 (16%)12 (19%)0.520.15
Hx of MI0 (0)2 (6%)3 (9%)5 (8%)0.670.48
PAD0 (0)4 (13%)1 (3%)5 (8%)0.150.16
Hx of HF0 (0)1 (3%)3 (9%)4 (6%)0.320.33
CAD0 (0)6 (19%)4 (12%)10 (15%)0.460.19
Diabetes mellitus1 (7)7 (22%)14 (42%)21 (32%)0.080.02
HLD2 (13)21 (66%)20 (61%)41 (63%)0.68<0.01
Nitrates0 (0)0 (0)1 (3%)1 (2%)0.320.49
β-Blockers0 (0)11 (34%)16 (48%)27 (42%)0.25<0.001
Ca blocker0 (0)6 (19%)23 (70%)29 (45%)<0.001<0.001
ACE0 (0)5 (16%)11 (33%)16 (25%)0.100.02
ARB0 (0)9 (28%)8 (24%)17 (26%)0.720.08
Diuretic0 (0)10 (31%)10 (30%)20 (31%)0.930.05
OSA1 (7)4 (13%)4 (12%)8 (12%)0.960.85
Obese3 (20)10 (31%)12 (36%)22 (34%)0.660.53
CKD0 (0)6 (19%)12 (36%)18 (28%)0.110.02
Control n = 15Hypertension Stage 1 n = 32Hypertension Stage 2 n = 33Total hypertension n = 65P-value (total hypertension)P-value (overall)
Sex
 Male7 (47)11 (34%)19 (58%)30 (46%)0.060.17
Age (years)37.8 ± 12.059.8 ± 13.463.1 ± 130064.5 ± 13.20.33<0.001
SBP (mmHg)113.5 ± 11.9134.5 ± 3.6156.2 ± 8.8145.5 ± 12.8<0.001<0.001
DBP (mmHg)72.6 ± 11.673.5 ± 10.180.2 ± 12.076.9 ± 11.5<0.0010.03
Heart rate75.9 ± 12.172.1 ± 17.169.3 ± 11.270.7 ± 14.40.430.32
Body mass index (kg/m2)26.1 (22.1–31.7)27.45 (25.45–33.15)28.6 (26.46–32.9)27.8 (25.5–32.9)0.500.21
Hx of CVD0 (0)7 (22%)5 (16%)12 (19%)0.520.15
Hx of MI0 (0)2 (6%)3 (9%)5 (8%)0.670.48
PAD0 (0)4 (13%)1 (3%)5 (8%)0.150.16
Hx of HF0 (0)1 (3%)3 (9%)4 (6%)0.320.33
CAD0 (0)6 (19%)4 (12%)10 (15%)0.460.19
Diabetes mellitus1 (7)7 (22%)14 (42%)21 (32%)0.080.02
HLD2 (13)21 (66%)20 (61%)41 (63%)0.68<0.01
Nitrates0 (0)0 (0)1 (3%)1 (2%)0.320.49
β-Blockers0 (0)11 (34%)16 (48%)27 (42%)0.25<0.001
Ca blocker0 (0)6 (19%)23 (70%)29 (45%)<0.001<0.001
ACE0 (0)5 (16%)11 (33%)16 (25%)0.100.02
ARB0 (0)9 (28%)8 (24%)17 (26%)0.720.08
Diuretic0 (0)10 (31%)10 (30%)20 (31%)0.930.05
OSA1 (7)4 (13%)4 (12%)8 (12%)0.960.85
Obese3 (20)10 (31%)12 (36%)22 (34%)0.660.53
CKD0 (0)6 (19%)12 (36%)18 (28%)0.110.02

Data are presented as n (%), mean±standard deviation, or median (inter-quartile range).

ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; Ca, calcium; CAD, coronary artery disease; CKD, chronic kidney disease; CVD, cardiovascular disease; DBP, diastolic blood pressure; HF, heart failure; HLD, hyperlipidaemia; HTN, hypertension; Hx, history; MI, myocardial infarction; OSA, obstructive sleep apnoea; PAD, peripheral artery disease; SBP, systolic blood pressure.

Table 1
Open in new tab

Patient demographics and medications

Control n = 15Hypertension Stage 1 n = 32Hypertension Stage 2 n = 33Total hypertension n = 65P-value (total hypertension)P-value (overall)
Sex
 Male7 (47)11 (34%)19 (58%)30 (46%)0.060.17
Age (years)37.8 ± 12.059.8 ± 13.463.1 ± 130064.5 ± 13.20.33<0.001
SBP (mmHg)113.5 ± 11.9134.5 ± 3.6156.2 ± 8.8145.5 ± 12.8<0.001<0.001
DBP (mmHg)72.6 ± 11.673.5 ± 10.180.2 ± 12.076.9 ± 11.5<0.0010.03
Heart rate75.9 ± 12.172.1 ± 17.169.3 ± 11.270.7 ± 14.40.430.32
Body mass index (kg/m2)26.1 (22.1–31.7)27.45 (25.45–33.15)28.6 (26.46–32.9)27.8 (25.5–32.9)0.500.21
Hx of CVD0 (0)7 (22%)5 (16%)12 (19%)0.520.15
Hx of MI0 (0)2 (6%)3 (9%)5 (8%)0.670.48
PAD0 (0)4 (13%)1 (3%)5 (8%)0.150.16
Hx of HF0 (0)1 (3%)3 (9%)4 (6%)0.320.33
CAD0 (0)6 (19%)4 (12%)10 (15%)0.460.19
Diabetes mellitus1 (7)7 (22%)14 (42%)21 (32%)0.080.02
HLD2 (13)21 (66%)20 (61%)41 (63%)0.68<0.01
Nitrates0 (0)0 (0)1 (3%)1 (2%)0.320.49
β-Blockers0 (0)11 (34%)16 (48%)27 (42%)0.25<0.001
Ca blocker0 (0)6 (19%)23 (70%)29 (45%)<0.001<0.001
ACE0 (0)5 (16%)11 (33%)16 (25%)0.100.02
ARB0 (0)9 (28%)8 (24%)17 (26%)0.720.08
Diuretic0 (0)10 (31%)10 (30%)20 (31%)0.930.05
OSA1 (7)4 (13%)4 (12%)8 (12%)0.960.85
Obese3 (20)10 (31%)12 (36%)22 (34%)0.660.53
CKD0 (0)6 (19%)12 (36%)18 (28%)0.110.02
Control n = 15Hypertension Stage 1 n = 32Hypertension Stage 2 n = 33Total hypertension n = 65P-value (total hypertension)P-value (overall)
Sex
 Male7 (47)11 (34%)19 (58%)30 (46%)0.060.17
Age (years)37.8 ± 12.059.8 ± 13.463.1 ± 130064.5 ± 13.20.33<0.001
SBP (mmHg)113.5 ± 11.9134.5 ± 3.6156.2 ± 8.8145.5 ± 12.8<0.001<0.001
DBP (mmHg)72.6 ± 11.673.5 ± 10.180.2 ± 12.076.9 ± 11.5<0.0010.03
Heart rate75.9 ± 12.172.1 ± 17.169.3 ± 11.270.7 ± 14.40.430.32
Body mass index (kg/m2)26.1 (22.1–31.7)27.45 (25.45–33.15)28.6 (26.46–32.9)27.8 (25.5–32.9)0.500.21
Hx of CVD0 (0)7 (22%)5 (16%)12 (19%)0.520.15
Hx of MI0 (0)2 (6%)3 (9%)5 (8%)0.670.48
PAD0 (0)4 (13%)1 (3%)5 (8%)0.150.16
Hx of HF0 (0)1 (3%)3 (9%)4 (6%)0.320.33
CAD0 (0)6 (19%)4 (12%)10 (15%)0.460.19
Diabetes mellitus1 (7)7 (22%)14 (42%)21 (32%)0.080.02
HLD2 (13)21 (66%)20 (61%)41 (63%)0.68<0.01
Nitrates0 (0)0 (0)1 (3%)1 (2%)0.320.49
β-Blockers0 (0)11 (34%)16 (48%)27 (42%)0.25<0.001
Ca blocker0 (0)6 (19%)23 (70%)29 (45%)<0.001<0.001
ACE0 (0)5 (16%)11 (33%)16 (25%)0.100.02
ARB0 (0)9 (28%)8 (24%)17 (26%)0.720.08
Diuretic0 (0)10 (31%)10 (30%)20 (31%)0.930.05
OSA1 (7)4 (13%)4 (12%)8 (12%)0.960.85
Obese3 (20)10 (31%)12 (36%)22 (34%)0.660.53
CKD0 (0)6 (19%)12 (36%)18 (28%)0.110.02

Data are presented as n (%), mean±standard deviation, or median (inter-quartile range).

ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; Ca, calcium; CAD, coronary artery disease; CKD, chronic kidney disease; CVD, cardiovascular disease; DBP, diastolic blood pressure; HF, heart failure; HLD, hyperlipidaemia; HTN, hypertension; Hx, history; MI, myocardial infarction; OSA, obstructive sleep apnoea; PAD, peripheral artery disease; SBP, systolic blood pressure.

GLS and LV ejection fraction in the control group were not significantly different than in the Stage 1 or Stage 2 hypertension groups (Table 2). LV mass, LV mass index, mitral annular early diastolic velocity (e′), ratio between early mitral inflow velocity and mitral annular early diastolic velocity (E/e′), and left atrial volume index were elevated echocardiographic parameters observed in both the Stage 1 and Stage 2 hypertension groups (Table 2).

Table 2
Open in new tab

Conventional echocardiographic parameters

Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
LVDd (mm)47.0 ± 6.145.4 ± 6.248.6 ± 7.347.1 ± 6.90.060.16
IVSd (mm)9.6 ± 1.611.6 ± 2.612.2 ± 2.511.9 ± 2.60.30<0.01
PWd (mm)8.8 ± 1.910.2 ± 2.611.3 ± 12.210.7 ± 2.60.08<0.01
LV mass (g)137 (126–189)166 (134.5–205.5)209 (160–242)187 (151–234)0.02<0.01
LV mass index (g/m2)77 (69–89)90.5 (72.5–113.5)97 (84–121)97 (76–118)0.08<0.01
Biplane ESV (mL)42.5 (33.5–60.3)38.05 (30.65–49.45)47.8 (28.7–65.7)43.2 (30.6–53.9)0.210.22
Biplane SV (mL)71.0 ± 23.069.35 (54.7–77.95)74 (54.7–90.7)71.2 (54.7–85.2)0.200.40
Biplane EF (%)60 (58–64)63.5 (60–66.5)60 (57–64)61 (59–66)0.030.03
GLS (%)−19.5 ± 1.3−18.5 ± 2.9−16.9 ± 3.4−17.7 ± 3.20.060.01
E′ (cm/s)12.6 ± 3.78.4 ± 3.27.0 ± 2.37.6 ± 2.70.04<0.001
E/e′6.6 ± 2.110.5 ± 4.312.6 ± 5.411.6 ± 5.00.10<0.001
 LAVi (mL/m2)28.6 ± 8.036.5 ± 9.839.0 ± 11.437.8 ± 10.60.36<0.01
DT (ms)182.9 (156.2–215.3)199.1 (166.7–233.8)224.5 (162–270.8)221.9 ± 71.40.310.06
Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
LVDd (mm)47.0 ± 6.145.4 ± 6.248.6 ± 7.347.1 ± 6.90.060.16
IVSd (mm)9.6 ± 1.611.6 ± 2.612.2 ± 2.511.9 ± 2.60.30<0.01
PWd (mm)8.8 ± 1.910.2 ± 2.611.3 ± 12.210.7 ± 2.60.08<0.01
LV mass (g)137 (126–189)166 (134.5–205.5)209 (160–242)187 (151–234)0.02<0.01
LV mass index (g/m2)77 (69–89)90.5 (72.5–113.5)97 (84–121)97 (76–118)0.08<0.01
Biplane ESV (mL)42.5 (33.5–60.3)38.05 (30.65–49.45)47.8 (28.7–65.7)43.2 (30.6–53.9)0.210.22
Biplane SV (mL)71.0 ± 23.069.35 (54.7–77.95)74 (54.7–90.7)71.2 (54.7–85.2)0.200.40
Biplane EF (%)60 (58–64)63.5 (60–66.5)60 (57–64)61 (59–66)0.030.03
GLS (%)−19.5 ± 1.3−18.5 ± 2.9−16.9 ± 3.4−17.7 ± 3.20.060.01
E′ (cm/s)12.6 ± 3.78.4 ± 3.27.0 ± 2.37.6 ± 2.70.04<0.001
E/e′6.6 ± 2.110.5 ± 4.312.6 ± 5.411.6 ± 5.00.10<0.001
 LAVi (mL/m2)28.6 ± 8.036.5 ± 9.839.0 ± 11.437.8 ± 10.60.36<0.01
DT (ms)182.9 (156.2–215.3)199.1 (166.7–233.8)224.5 (162–270.8)221.9 ± 71.40.310.06

Data are presented as mean ± standard deviation or median (inter-quartile range).

DT, deceleration time; E′, mitral annular early diastolic velocity; E/e′, ratio between early mitral inflow velocity and mitral annular early diastolic velocity; EF, ejection fraction; ESV, end-systolic volume; GLS, global longitudinal strain; IVSd, diastolic interventricular septal thickness; LAVi, left atrial volume index; LV, left ventricular; LVDd, left ventricular diameter diastole; PWd, diastolic posterior wall thickness; SV, systolic volume.

Table 2
Open in new tab

Conventional echocardiographic parameters

Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
LVDd (mm)47.0 ± 6.145.4 ± 6.248.6 ± 7.347.1 ± 6.90.060.16
IVSd (mm)9.6 ± 1.611.6 ± 2.612.2 ± 2.511.9 ± 2.60.30<0.01
PWd (mm)8.8 ± 1.910.2 ± 2.611.3 ± 12.210.7 ± 2.60.08<0.01
LV mass (g)137 (126–189)166 (134.5–205.5)209 (160–242)187 (151–234)0.02<0.01
LV mass index (g/m2)77 (69–89)90.5 (72.5–113.5)97 (84–121)97 (76–118)0.08<0.01
Biplane ESV (mL)42.5 (33.5–60.3)38.05 (30.65–49.45)47.8 (28.7–65.7)43.2 (30.6–53.9)0.210.22
Biplane SV (mL)71.0 ± 23.069.35 (54.7–77.95)74 (54.7–90.7)71.2 (54.7–85.2)0.200.40
Biplane EF (%)60 (58–64)63.5 (60–66.5)60 (57–64)61 (59–66)0.030.03
GLS (%)−19.5 ± 1.3−18.5 ± 2.9−16.9 ± 3.4−17.7 ± 3.20.060.01
E′ (cm/s)12.6 ± 3.78.4 ± 3.27.0 ± 2.37.6 ± 2.70.04<0.001
E/e′6.6 ± 2.110.5 ± 4.312.6 ± 5.411.6 ± 5.00.10<0.001
 LAVi (mL/m2)28.6 ± 8.036.5 ± 9.839.0 ± 11.437.8 ± 10.60.36<0.01
DT (ms)182.9 (156.2–215.3)199.1 (166.7–233.8)224.5 (162–270.8)221.9 ± 71.40.310.06
Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
LVDd (mm)47.0 ± 6.145.4 ± 6.248.6 ± 7.347.1 ± 6.90.060.16
IVSd (mm)9.6 ± 1.611.6 ± 2.612.2 ± 2.511.9 ± 2.60.30<0.01
PWd (mm)8.8 ± 1.910.2 ± 2.611.3 ± 12.210.7 ± 2.60.08<0.01
LV mass (g)137 (126–189)166 (134.5–205.5)209 (160–242)187 (151–234)0.02<0.01
LV mass index (g/m2)77 (69–89)90.5 (72.5–113.5)97 (84–121)97 (76–118)0.08<0.01
Biplane ESV (mL)42.5 (33.5–60.3)38.05 (30.65–49.45)47.8 (28.7–65.7)43.2 (30.6–53.9)0.210.22
Biplane SV (mL)71.0 ± 23.069.35 (54.7–77.95)74 (54.7–90.7)71.2 (54.7–85.2)0.200.40
Biplane EF (%)60 (58–64)63.5 (60–66.5)60 (57–64)61 (59–66)0.030.03
GLS (%)−19.5 ± 1.3−18.5 ± 2.9−16.9 ± 3.4−17.7 ± 3.20.060.01
E′ (cm/s)12.6 ± 3.78.4 ± 3.27.0 ± 2.37.6 ± 2.70.04<0.001
E/e′6.6 ± 2.110.5 ± 4.312.6 ± 5.411.6 ± 5.00.10<0.001
 LAVi (mL/m2)28.6 ± 8.036.5 ± 9.839.0 ± 11.437.8 ± 10.60.36<0.01
DT (ms)182.9 (156.2–215.3)199.1 (166.7–233.8)224.5 (162–270.8)221.9 ± 71.40.310.06

Data are presented as mean ± standard deviation or median (inter-quartile range).

DT, deceleration time; E′, mitral annular early diastolic velocity; E/e′, ratio between early mitral inflow velocity and mitral annular early diastolic velocity; EF, ejection fraction; ESV, end-systolic volume; GLS, global longitudinal strain; IVSd, diastolic interventricular septal thickness; LAVi, left atrial volume index; LV, left ventricular; LVDd, left ventricular diameter diastole; PWd, diastolic posterior wall thickness; SV, systolic volume.

Hypertension and MW

MW showed that GWI was elevated in the Stage 1 and Stage 2 hypertension groups compared with the control group, (reference range: 1896 ± 308 mmHg%)14 (P < 0.01) (Table 3). The median GWI of all hypertensive patients was 2108.4 mmHg%, which was also elevated. GCW and GWW were elevated in the Stage 1, Stage 2, and overall hypertension populations compared with the control group (Table 3). No difference was observed in GWE among the three groups (Table 3). There were no statistically significant differences in MW parameters between the two groups of hypertension patients, Stage 1 vs. Stage 2.

Table 3
Open in new tab

Calculated myocardial work indices across the three groups

Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
GWI (mmHg%)1770 (1613–1888)2040 (1769–2246.5)2052 (1732–2372)2043 (1758–2319)0.530.01
GCW (mmHg%)2035 (1918–2213)2360.5 (1988–2568.5)2446 (1934–2692)2363 (1972–2615)0.75<0.001
GWW (mmHg%)66 (31–92)111.5 (77–148)104 (74–142)108 (75–145)0.51<0.001
GWE (%)96 (95–98)94 (92–96)95 (93–96)95 (93–96)0.270.08
Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
GWI (mmHg%)1770 (1613–1888)2040 (1769–2246.5)2052 (1732–2372)2043 (1758–2319)0.530.01
GCW (mmHg%)2035 (1918–2213)2360.5 (1988–2568.5)2446 (1934–2692)2363 (1972–2615)0.75<0.001
GWW (mmHg%)66 (31–92)111.5 (77–148)104 (74–142)108 (75–145)0.51<0.001
GWE (%)96 (95–98)94 (92–96)95 (93–96)95 (93–96)0.270.08

Data are presented as median (interquartile range).

GCW, global constructive work; GWI, global work index; GWE, global work efficiency; GWW, global wasted work.

Table 3
Open in new tab

Calculated myocardial work indices across the three groups

Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
GWI (mmHg%)1770 (1613–1888)2040 (1769–2246.5)2052 (1732–2372)2043 (1758–2319)0.530.01
GCW (mmHg%)2035 (1918–2213)2360.5 (1988–2568.5)2446 (1934–2692)2363 (1972–2615)0.75<0.001
GWW (mmHg%)66 (31–92)111.5 (77–148)104 (74–142)108 (75–145)0.51<0.001
GWE (%)96 (95–98)94 (92–96)95 (93–96)95 (93–96)0.270.08
Control n = 15Hypertension Stage 1Hypertension Stage 2Total hypertensionP-value (total hypertension)P-value (overall)
GWI (mmHg%)1770 (1613–1888)2040 (1769–2246.5)2052 (1732–2372)2043 (1758–2319)0.530.01
GCW (mmHg%)2035 (1918–2213)2360.5 (1988–2568.5)2446 (1934–2692)2363 (1972–2615)0.75<0.001
GWW (mmHg%)66 (31–92)111.5 (77–148)104 (74–142)108 (75–145)0.51<0.001
GWE (%)96 (95–98)94 (92–96)95 (93–96)95 (93–96)0.270.08

Data are presented as median (interquartile range).

GCW, global constructive work; GWI, global work index; GWE, global work efficiency; GWW, global wasted work.

Discussion

It is well known that LV ejection fraction is not a sensitive parameter for analysis of subclinical LV dysfunction, and in the past 10 years, LV GLS analysis has been proven to be a more sensitive marker.15,16 MW analysis is a rapidly emerging practice used for advanced assessment of LV function. Until recently, non-invasive measurements were not used to calculate MW, making it difficult to use MW in clinical practice.1 With the introduction of LV pressure curves derived from non-invasively acquired brachial artery cuff pressure, utilization of this analysis in everyday practice is more feasible.1 MW is becoming more commonly used to assess LV systolic function because it takes into account both cardiac afterload and deformation.

Hypertension is one of the most common chronic medical conditions, with a worldwide prevalence among adults of about 32% in 2010.17 Hypertension is a common cardiovascular risk factor that can lead to LV remodelling and dysfunction. This is due in part to accelerated stiffening of the LV and large arteries. In this study, we focused on subcategories of hypertension based on the 2017 American College of Cardiology guidelines.

MW and hypertension

This study showed that MW is an advanced assessment of LV systolic function as an incremental increase in GWI in the two hypertension groups compared with the control group was observed. This is attributed to the fact that with increased LV systolic pressure there is an increase in afterload and, therefore, more work is required by the LV to perform mechanical systole. There are statistically significant differences when the two hypertension populations are compared against the control group.

Hypertension has been studied once before with MW analysis. That study described the role of the LV PSL in hypertensive patients when compared with patients with cardiomyopathy and looked at 37 hypertensive patients using the international guidelines for hypertension, Grade 1–Grade 3, with regard to MW.4 The study found a statistically significant increase in MW in hypertensive patients compared with control groups,4 in line with our study. The average systolic blood pressure in that study was 158 vs. 145.5 mmHg in the current study. Thus, the average GWI was much more elevated and the bull’s-eye plot shown in the previous study’s figure had more red shading. We believe our study portrays a reliable and accurate scenario reflective of a true clinical setting, with corresponding bull’s-eye plots.

Our control patients, when compared with a larger-scale study looking at healthy volunteers, landed within 1 SD of all values of MW indices.14

Limitations

One limitation of MW is that it does not take into account wall stress, wall thickness, or wall curvature. The force exerted on the LV is more accurately reflected by wall stress than LV pressure exclusively. LV afterload is proportional to LV pressure as well as geometric changes in LV chamber dimensions but inversely related to wall thickness. An increase in wall thickness will cause the wall stress to be reduced.18 In conditions in which LV wall thickness is increased with eccentric curvature, there could be a scenario in which it would be appropriate for MW to include wall stress.

Another limitation was the small sample size. Exclusion criteria included heart failure, valvular disease, and known coronary artery disease; the prevalence of these co-morbidities is high in this patient population, limiting sample size.

A third limitation was the age difference between the control and hypertension groups. Because comorbidities become more common with age, it was difficult to find healthy elderly individuals who required echocardiograms.

Conclusion

MW is a novel tool that can be used to assess LV function through a non-invasive LV PSL. MW eliminates the load dependency limitations of GLS and LV ejection fraction analysis. We show that while ejection fraction and GLS do not show any statistically significant difference, MW is significantly elevated in both Stage 1 and Stage 2 hypertension.

Acknowledgements

The authors thank the following from Aurora Cardiovascular and Thoracic Services: Jennifer Pfaff and Susan Nord for editorial preparation of the manuscript and Brian Miller and Brian Schurrer for assistance with the figures.

Conflict of interest: none declared.

References

1

Russell
K
,
Eriksen
M
,
Aaberge
L
,
Wilhelmsen
N
,
Skulstad
H
,
Remme
EW
 et al.
A novel clinical method for quantification of regional left ventricular pressure-strain loop area: a non-invasive index of myocardial work
.
Eur Heart J
2012
;
33
:
724
–
33
.

Google Scholar

Crossref
Search ADS
PubMed

 
2

Boe
E
,
Russell
K
,
Eek
C
,
Eriksen
M
,
Remme
EW
,
Smiseth
OA
 et al.
Non-invasive myocardial work index identifies acute coronary occlusion in patients with non-ST-segment elevation-acute coronary syndrome
.
Eur Heart J Cardiovasc Imaging
2015
;
16
:
1247
–
55
.

Google Scholar

Crossref
Search ADS
PubMed

 
3

Hulshof
HG
,
van Dijk
AP
,
George
KP
,
Hopman
MTE
,
Thijssen
DHJ
,
Oxborough
DL.
Exploratory assessment of left ventricular strain-volume loops in severe aortic valve diseases
.
J Physiol
2017
;
595
:
3961
–
71
.

Google Scholar

Crossref
Search ADS
PubMed

 
4

Chan
J
,
Edwards
NFA
,
Khandheria
BK
,
Shiino
K
,
Sabapathy
S
,
Anderson
B
 et al.
A new approach to assess myocardial work by non-invasive left ventricular pressure-strain relations in hypertension and dilated cardiomyopathy
.
Eur Heart J Cardiovasc Imaging
2019
;
20
:
31
–
9
.

Google Scholar

Crossref
Search ADS
PubMed

 
5

Urheim
S
,
Abraham
TP
,
Korinek
J
,
Wang
J
,
Belohlavek
M.
Increased right ventricular afterload induces postsystolic thickening of the ventricular septum in nonischemic hearts
.
J Am Soc Echocardiogr
2005
;
18
:
839
–
43
.

Google Scholar

Crossref
Search ADS
PubMed

 
6

Vecera
J
,
Penicka
M
,
Eriksen
M
,
Russell
K
,
Bartunek
J
,
Vanderheyden
M
 et al.
Wasted septal work in left ventricular dyssynchrony: a novel principle to predict response to cardiac resynchronization therapy
.
Eur Heart J Cardiovasc Imaging
2016
;
17
:
624
–
32
.

Google Scholar

Crossref
Search ADS
PubMed

 
7

Kuznetsova
T
,
D’hooge
J
,
Kloch-Badelek
M
,
Sakiewicz
W
,
Thijs
L
,
Staessen
JA.
Impact of hypertension on ventricular-arterial coupling and regional myocardial work at rest and during isometric exercise
.
J Am Soc Echocardiogr
2012
;
25
:
882
–
90
.

Google Scholar

Crossref
Search ADS
PubMed

 
8

Davidson
BP
,
Giraud
GD.
Left ventricular function and the systemic arterial vasculature: remembering what we have learned
.
J Am Soc Echocardiogr
2012
;
25
:
891
–
4
.

Google Scholar

Crossref
Search ADS
PubMed

 
9

Whelton
PK
,
Carey
RM
,
Aronow
WS
,
Casey
DE
Jr. ,
Collins
KJ
,
Dennison Himmelfarb
C.
2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines
.
J Am Coll Cardiol
2018
;
71
:
e127
–
e248
.

Google Scholar

Crossref
Search ADS
PubMed

 
10

Mor-Avi
V
,
Lang
RM
,
Badano
LP
,
Belohlavek
M
,
Cardim
NM
,
Derumeaux
G
, From the University of Chicago, Chicago, Illinois (V.M.-A., R.M.L.); the University of Padua, Padua, Italy (L.P.B.); Mayo Clinic, Scottsdale, Arizona (M.B.); Hospital da Luz, Lisbon, Portugal (N.M.C.); Universite Claude Bernard Lyon 1, Lyon, France (G.D.) et al.
Current and evolving echocardiographic techniques for the quantitative evaluation of cardiac mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of Echocardiography
.
Eur J Echocardiogr
2011
;
12
:
167
–
205
.

Google Scholar

Crossref
Search ADS
PubMed

 
11

Lang
RM
,
Badano
LP
,
Mor-Avi
V
,
Afilalo
J
,
Armstrong
A
,
Ernande
L
 et al.
Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging
.
Eur Heart J Cardiovasc Imaging
2015
;
16
:
233
–
70
.

Google Scholar

Crossref
Search ADS
PubMed

 
12

Russell
K
,
Eriksen
M
,
Aaberge
L
,
Wilhelmsen
N
,
Skulstad
H
,
Gjesdal
O
 et al.
Assessment of wasted myocardial work: a novel method to quantify energy loss due to uncoordinated left ventricular contractions
.
Am J Physiol Heart Circ Physiol
2013
;
305
:
H996
–
1003
.

Google Scholar

Crossref
Search ADS
PubMed

 
13

Samset
E.
Evaluation of Segmental Myocardial Work in the Left Ventricle. GE Healthcare, 2017. https://www.gehealthcare.com/-/media/8cab29682ace4ed7841505f813001e33.pdf (24 July 2020, date last accessed).

14

Manganaro
R
,
Marchetta
S
,
Dulgheru
R
,
Ilardi
F
,
Sugimoto
T
,
Robinet
S
 et al.
Echocardiographic reference ranges for normal non-invasive myocardial work indices: results from the EACVI NORRE study
.
Eur Heart J Cardiovasc Imaging
2019
;
20
:
582
–
90
.

Google Scholar

Crossref
Search ADS
PubMed

 
15

Fung
MJ
,
Thomas
L
,
Leung
DY.
Left ventricular function and contractile reserve in patients with hypertension
.
Eur Heart J Cardiovasc Imaging
2018
;
19
:
1253
–
9
.

Google Scholar

Crossref
Search ADS
PubMed

 
16

Zito
C
,
Longobardo
L
,
Citro
R
,
Galderisi
M
,
Oreto
L
,
Carerj
ML
 et al.
Ten years of 2D longitudinal strain for early myocardial dysfunction detection: a clinical overview
.
Biomed Res Int
2018
;
2018
:
1
–
14
.

Google Scholar

Crossref
Search ADS

 
17

Mills
KT
,
Bundy
JD
,
Kelly
TN
,
Reed
JE
,
Kearney
PM
,
Reynolds
K
 et al.
Global disparities of hypertension prevalence and control: a systematic analysis of population-based studies from 90 countries
.
Circulation
2016
;
134
:
441
–
50
.

Google Scholar

Crossref
Search ADS
PubMed

 
18

Cvijic
M
,
Duchenne
J
,
Ünlü
S
,
Michalski
B
,
Aarones
M
,
Winter
S
 et al.
Timing of myocardial shortening determines left ventricular regional myocardial work and regional remodelling in hearts with conduction delays
.
Eur Heart J Cardiovasc Imaging
2018
;
19
:
941
–
9
.

Google Scholar

Crossref
Search ADS
PubMed

 
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: [email protected].
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://dbpia.nl.go.kr/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
Topic:
Issue Section:
Original Article
Download all slides