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The prognostic value of dobutamine stress echocardiography amongst British Indian Asian and Afro-Caribbean patients: a comparison with European white patients

  • Jamie M. O’Driscoll1,
  • Claire Rossato1,
  • Paula Gargallo-Fernandez1,
  • Marco Araco1,
  • Dimitrios Giannoglou1,
  • Sanjay Sharma1, 2 and
  • Rajan Sharma1Email author
Cardiovascular Ultrasound201513:36

https://doi.org/10.1186/s12947-015-0028-1

Received: 15 May 2015

Accepted: 20 July 2015

Published: 6 August 2015

Abstract

Background

The incidence of cardiovascular disease is considerably disparate among different racial and ethnic populations. While dobutamine stress echocardiography (DSE) has been shown to be useful in Caucasian patients, its role among ethnic minority groups remains unclear. This study aimed to investigate the prognostic importance of DSE in three ethnic groups in the UK.

Methods

DSE was performed on 6231 consecutive patients. After exclusions, 5329 patients formed the study (2676 [50.2 %] Indian Asian, 2219 [41.6 %] European white and 434 [8.1 %] Afro-Caribbean). Study outcome measures were non-fatal cardiac events (NFCE) and all-cause mortality.

Results

There were 849 (15.9 %) NFCE and 1365 (25.6 %) deaths over a median follow-up period of 4.6 years. In total 1174 (22 %) patients had inducible myocardial ischaemia during DSE, 859 (16.1 %) had fixed wall motion abnormalities and 3645 (68.4 %) patients had a normal study. Ethnicity did not predict events. Among the three ethnic groups, ischaemia on DSE was associated with 2 to 2.5 times the risk of non-fatal cardiac events and 1.2 to 1.4 times the risk of all-cause mortality. Peak wall motion score index was the strongest independent predictor of non-fatal cardiac events and all-cause mortality in all groups. The C statistic for the prediction of NFCE and all-cause mortality were significantly higher when DSE parameters were added to the standard risk factors for all ethnic groups.

Conclusions

DSE is a strong predictor of NFCE and all-cause mortality and provides predictive information beyond that provided by standard risk factors in three major racial and ethnic groups. No major differences among racial and ethnic groups in the predictive value of DSE was detected.

Keywords

Dobutamine stress echocardiography Ethnicity Ischaemia Transthoracic echocardiography

Background

The UK has become more ethnically diverse with an increase in both the number and proportion of Afro-Caribbean and Asian minority ethnic groups. In 2011, all Afro-Caribbean and Asian minority groups accounted for 13% of the population in England and Wales [1]. The incidence of cardiovascular disease (CVD) is considerably disparate among different racial and ethnic populations [2]. CVD mortality is 40 % higher in Indian Asians compared with European white groups [3] and is significantly greater among Afro-Caribbeans compared with European whites [2, 4]. Coronary artery disease (CAD) is the leading cause of premature CVD death in European whites and Asians; however, in Afro-Caribbean populations death from stroke is the leading cause [5]. Although conventional risk factors contribute to the differences in CVD, they do not adequately explain the excess risk noted in Afro-Caribbean and Indian Asian populations [2]. However, there may be certain ethnic specific CVD risk factors [3, 6].

Afro-Caribbean and Indian Asian populations are under represented in epidemiological and cardiovascular research trials [7]. As a result, minority ethnic groups may be at risk of significant disadvantage across a range of health indicators. Reporting racial information is important since findings from European white populations may not necessarily be extrapolated to other ethnic groups, given the observed differences in CVD mortality.

Prior research has demonstrated a survival difference between white, black, and Hispanic ethnic groups undergoing exercise treadmill testing, even after adjustment for patient demographics, baseline electrocardiography abnormalities, CVD co-morbidities and risk factors, and exercise test findings [8]. Dobutamine stress echocardiography (DSE) is a widely accepted and useful non-invasive test for the diagnosis, risk stratification and prognosis of CAD [912], as well as having greater specificity and sensitivity for CAD diagnosis compared to exercise treadmill testing. In addition, DSE has provided important prognostic information among different age groups [13], in men and women [14], as well as in patients with diabetes [15] and renal disease [16]. However, despite the available evidence, no study has investigated the role of DSE in predicting outcome amongst Afro-Caribbean, Caucasian and Indian Asian patients or determined whether myocardial ischaemia and ischaemic burden have the same prognostic power in these different ethnic populations. Therefore the aim of this prospective cohort study was to evaluate the role of DSE in the prediction of non-fatal cardiac events (NFCE) and all cause mortality by ethnic group. We studied a large cohort of consecutive patients referred for DSE and evaluated outcomes in UK Afro-Caribbean, European whites and Indian Asian patients.

Methods

Study design and patients

The study population consisted of 6231 consecutive patients undergoing DSE for the evaluation of angina pectoris or shortness of breath on exertion between June 2006 to September 2011 in the outpatient setting. All patients were required to provide informed consent before testing and the local research ethics committee approved the study. Ethnicity was obtained through self-report using the 2001 UK Census categorisation for classifying ethnicity. Exclusion criteria included mixed ethnic groups, Chinese ethnicity, patients referred for viability assessment only, asymptomatic patients awaiting non-cardiac surgery, patients with severe valve disease, and patients who did not provide signed informed consent.

Before DSE, a structured history and medical record review was performed to document symptoms, medical history, medication use, cardiac risk factors, and previous cardiac events and procedures. The estimation of the pre-test probability of CAD was determined using previously described criteria, which included the presence and characteristics of chest pain, age, gender, and presence of greater than or equal to three CAD risk factors [17]. Patients were categorised into low, intermediate or high pre-test probability. For patients who underwent multiple DSE tests during this period, only the first DSE was considered in the analysis.

Follow-up data was obtained by investigators blinded to the DSE result and information was collated by contacting patients or a family member, general practitioners, and reviewing hospital records to inquire about interim hospital admissions, outpatient diagnosis of cardiovascular events, and deaths. The date of the last review or consultation was used to calculate the duration of follow-up through to June 2013.

Dobutamine stress echocardiography

All patients recruited underwent DSE. The image quality obtained was interpretable in all patients (1296 [24.3 %] requiring contrast) and the entire cohort was used in data analysis. DSE was performed according to a standard protocol [18] with images acquired in the standard parasternal long- and short-axis and apical 2-, 3-, and 4-chamber views. The left ventricle (LV) was divided into a 17-segment model for qualitative analysis [19] and wall motion was scored on a 4-point scale (1, normal wall motion; 2, hypokinesis; 3, akinetic; and 4, dyskinetic) as is standard [18]. In patients with resting akinetic segments a biphasic response was used to indicate ischaemia. LV ejection fraction was calculated using biplane Simpson’s technique. LV mass was derived from two-dimensional motion-mode and indexed to height [20]. Results were classified as a normal response with an overall increase in wall motion or abnormal response. An abnormal response was described as the occurrence under stress of hypokinesia, akinesia or dyskinesia in one or more resting normal segments and/or worsening of wall motion in one or more resting hypokinetic segments [21]. In this way patients were categorised as non-ischaemic or ischaemic. The extent and location of inducible ischaemia were evaluated and a wall motion score index (WMSI) was calculated, both at rest and during stress. Patients were further categorised with low (1–3 ischaemic LV segments) or high (>3 ischaemic LV segments) ischaemic burden. Non-viable myocardium was defined as severely dysfunctional myocardium without change during DSE [22] and referred to as fixed wall motion abnormalities (WMA). The territory of myocardial ischaemia was described according to an overlap model as previously described [23]: Left anterior descending artery (LAD) – anterior wall, anteroseptum, mid and apical inferoseptum; Circumflex artery (Cx) – mid inferolateral wall, basal and mid lateral wall; Right coronary artery (RCA)/Cx artery – inferior wall, basal inferolateral wall, basal inferoseptum.

End point definition

The principal end-point of interest for this analysis was non-fatal cardiac events (NFCE) and secondarily death from any cause, with patients censored at the time of the last follow-up. A NFCE was defined as hospitalisation for myocardial infarction, unstable angina, and time to coronary revascularisation procedures, defined either as coronary artery bypass graft surgery or percutaneous coronary intervention. Hospitalisations were identified by means of the principle discharge diagnosis. For patients with multiple events, only the first event was considered.

Data analysis

Continuous variables are expressed as mean ± SD and categorical variables as n (%). We used chi-square tests for discrete variables and one-way analysis of variance tests for continuous variables to test for differences in demographics, risk factors and DSE test results between ethnic groups and between participants with and without end point events. To describe the frequency of NFCE and all-cause mortality according to time since DSE, Kaplan-Meier cumulative event curves were constructed and compared using the log-rank test with a P value <0.05 considered statistically significant. The data were stratified according to A) ischaemic and non-ischaemic patients and B) non-ischaemic (0 segments), low ischaemic burden (1–3 ischaemic LV segments) and high ischaemic burden (>3 ischaemic LV segments) patients for NFCE and all-cause mortality. Event rates were calculated and expressed as percent per year. We used Cox proportional-hazards regression to estimate hazard ratios and corresponding 95 % confidence intervals (CI) for NFCE and all-cause mortality for each individual ethnic group and computed the C statistic (area under the receiver operator curve) as a measure of the incremental value of DSE beyond that provided by standard risk factors.

All models were adjusted for age, gender, smoking history, diabetes, hypercholesterolemia, hypertension, prior myocardial infarction, prior revascularization and use of lipid lowering or anti-hypertensive medication. All analyses were conducted using the statistical package for social sciences (SPSS 21 release version of SPSS for Windows; SPSS Inc., Chicago IL, USA).

Results

Study cohort

Of the 6231 patients referred for DSE, 814 did not meet inclusion criteria and 88 patients were lost at follow-up and therefore excluded from the final analysis. The remaining 5329 patients of which 434 (8.1 %) were Afro-Caribbean, 2219 (41.6 %) were European white and 2676 (50.2 %) were Indian Asian comprised the final study cohort (Fig. 1). Afro-Caribbean and Indian Asian patients had been resident in the UK for 38 ± 15 and 41 ± 17, respectively, and European whites were born in the UK. The majority of DSE requests were due to suspected angina pectoris (79.7 %) and the remainder were due to shortness of breath on exertion (20.3 %). The baseline characteristics of the study cohort varied significantly among the three ethnic groups, as shown in Table 1. Briefly, European white patients were significantly older than both Afro-Caribbean and Indian Asian patients. The presence of hypertension, diabetes mellitus, hypercholesterolemia and previous percutaneous coronary intervention was significantly greater in Indian Asians compared to Afro-Caribbeans and European whites. Family history of cardiovascular disease and smoking history was significantly greater in European whites compared to Afro-Caribbeans and Indian Asians. The low, intermediate and high pre-test probability of CAD did not significantly (p = 0.415) differ between ethnic groups (Table 1).
Fig 1

Study flow diagram

Table 1

Baseline demographic characteristics, risk factors and echocardiography measures according to ethnic group

Characteristics

Afro-Caribbean (n = 434)

European White (n = 2219)

Indian Asian (n = 2676)

P Value

Demographics

    
 

Age (yrs)

63.1 ± 12.6

66.8 ± 12.9

64 ± 11.5

<0.001

 

Male gender

196 (45.2)

1144 (51.6)

1395 (52.1)

0.079

 

Height (cm)

169.8 ± 8.7

170.4 ± 8.9

166.6 ± 9.8

<0.001

 

Weight (kg)

83.4 ± 16.5

81.4 ± 15.8

79 ± 14.5

<0.001

 

Body mass index (kg · m2)

29 ± 6

28 ± 5.2

28.5 ± 4.9

<0.001

 

Body surface area (m2)

1.94 ± 0.2

1.93 ± 0.2

1.87 ± 0.2

<0.001

History

    
 

Hypertension

247 (56.9)

1228 (55.3)

1624 (60.7)

0.001

 

Diabetes mellitus

102 (23.5)

451 (20.3)

880 (32.9)

<0.001

 

Hypercholesterolemia

203 (46.8)

967 (43.6)

1441 (53.8)

<0.001

 

Family history of CVD

91 (21)

586 (26.4)

644 (24.1)

0.026

 

Prior myocardial infarction

30 (6.9)

204 (9.2)

256 (9.6)

0.204

 

Prior PCI

75 (17.3)

450 (20.3)

732 (27.4)

0.009

 

Prior CABGS

46 (10.6)

237 (10.7)

359 (13.4)

0.958

 

Smoking history

   

<0.001

 

Never smoked

350 (80.6)

1411 (63.6)

2337 (87.3)

 
 

Ex-smoker

61 (14.1)

553 (24)

220 (8.2)

 
 

Current smoker

23 (5.3)

255 (11.1)

119 (4.4)

 

Pre-test probability of coronary artery disease

   

0.415

 

Low

137 (31.6)

616 (27.8)

723 (27)

 
 

Intermediate

164 (37.8)

872 (39.3)

1064 (39.8)

 
 

High

133 (30.6)

731 (32.9)

889 (33.2)

 

NYHA functional class symptom status

   

<0.001

 

NYHA functional class II

411 (94.7)

1962 (88.4)

2317 (86.6)

 
 

NYHA functional class III

23 (5.3)

257 (11.6)

359 (13.4)

 

Canadian Cardiovascular Society angina classification

   

0.001

 

Class I

255 (58.8)

1096 (49.4)

1338 (50)

 
 

Class II

153 (35.3)

874 (39.4)

1046 (39.1)

 
 

Class III

26 (6)

249 (11.2)

292 (10.9)

 

Long term cardiac medication

    
 

ACE inhibitor

155 (35.7)

817 (36.8)

959 (35.8)

0.759

 

Angiotensin II receptor antagonist

79 (18.2)

410 (18.5)

545 (20.4)

0.202

 

Aspirin

244 (56.2)

1211 (54.6)

1529 (57.1)

0.194

 

Beta blockers

187 (43.1)

962 (43.4)

1136 (42.5)

0.815

 

Calcium antagonists

140 (32.3)

662 (29.8)

847 (31.7)

0.319

 

Diuretic

104 (24)

491 (22.1)

605 (22.6)

0.707

 

Lipid-lowering agents

273 (62.9)

1478 (66.6)

1812 (67.7)

0.139

 

Nitrates

61 (14.1)

323 (14.6)

403 (15.1)

0.806

 

Warfarin

20 (4.6)

157 (7.1)

159 (5.9)

0.085

 

At least 1 anti-anginal medication

285 (65.7)

1404 (63.3)

1721 (64.3)

0.563

Baseline Echocardiography Data

    
 

LVESD (cm)

2.9 ± 0.7

3.2 ± 0.6

3.1 ± 0.6

0.009

 

LVEDD (cm)

4.48 ± 0.6

4.5 ± 0.5

4.38 ± 0.4

<0.001

 

LV ejection fraction (%)

56.6 ± 8.9

56.2 ± 8.9

56.9 ± 7.9

0.023

 

Maximal LVEDD Wall Thickness (cm)

1.19 ± 0.33

1.11 ± 0.21

1.12 ± 0.24

<0.001

 

Left atrial size (mm)

38 ± 15

37 ± 11

37 ± 17

0.781

 

Left ventricular mass (g)

182.8 ± 35.2

169.7 ± 38.6

153.3 ± 34.8

<0.001

 

Left ventricular mass index (g · m−1)

103.8 ± 21.2

94.1 ± 23.5

89.9 ± 19.4

<0.001

 

Mitral E/A

1.21 ± 0.4

1.22 ± 0.3

1.22 ± 0.4

0.72

 

Mitral E Deceleration (ms)

202 ± 55

209 ± 69

203 ± 63

0.623

 

Mitral E/Ea

9.6 ± 3.9

9.5 ± 4.3

9.6 ± 4.1

0.875

 

Mitral Annular Calcification

14 (3.2)

73 (3.3)

130 (4.9)

0.014

 

Mitral Regurgitation

54 (12.4)

315 (14.2)

384 (14.3)

0.564

 

Aortic Stenosis

15 (3.5)

71 (3.2)

48 (1.8)

0.003

 

Aortic Regurgitation

14 (3.2)

66 (3)

62 (2.3)

0.274

Dobutamine stress echocardiography test

    
 

Baseline heart rate (b · min−1)

69.6 ± 16.1

69.3 ± 18.8

71.1 ± 15.1

0.001

 

Peak heart rate (b · min−1)

137.1 ± 21.7

131.8 ± 22.7

136.3 ± 19.1

<0.001

 

Target heart rate achieved

358 (82.5)

1842 (83)

2231 (83.4)

0.943

 

Baseline sBP (mmHg)

133.3 ± 24.1

131.2 ± 24.8

132.9 ± 24.5

0.039

 

Peak sBP (mmHg)

160.3 ± 83

147.8 ± 31.5

151.1 ± 31.9

<0.001

 

Baseline dBP (mmHg)

71.7 ± 18.3

71.3 ± 22.9

70.7 ± 19.6

0.498

 

Peak dBP (mmHg)

75.1 ± 18.7

72.5 ± 17.6

74.5 ± 18.1

<0.001

 

Resting wall motion score index

1.03 ± 0.1

1.05 ± 0.13

1.04 ± 0.11

0.006

 

Peak wall motion score index

1.06 ± 0.13

1.09 ± 0.16

1.08 ± 0.15

0.001

 

Fixed wall motion abnormality

55 (12.7)

377 (17)

427 (16)

0.078

 

New wall motion abnormality

69 (15.9)

485 (21.9)

620 (23.2)

0.003

Number of ischaemic LV segments

   

<0.001

 

0 LV segments

365 (84.1)

1734 (78.1)

2056 (76.8)

 
 

1-3 LV segments

61 (14.1)

398 (17.9)

555 (20.7)

 
 

>3 LV segments

8 (1.8)

87 (3.9)

65 (2.4)

 

Outcome

    
 

Non-fatal cardiac event

55 (12.7)

363 (16.4)

431 (16.1)

0.149

 

All-cause mortality

108 (24.9)

564 (25.4)

693 (25.9)

0.870

Note: CVD Cardiovascular disease, PCI Percutaneous coronary intervention, CABGS Coronary artery bypass graft surgery, NYHA New York Heart Association, ACE Angiotensin converting enzyme, LVESD Left ventricular end systolic dimension, LVEDD Left ventricular end diastolic dimension, LV Left ventricle, sBP systolic blood pressure, dBP diastolic blood pressure

Baseline atrial fibrillation was present in 82 (1.5 %) patients, and 116 (2.2 %) had left bundle branch block. Atrial fibrillation induced by DSE occurred in 27 (0.5 %) patients, and non-sustained ventricular tachycardia in 2 (0.04 %) patients. None of the patients required intravenous beta-blocker to reverse the effects of dobutamine or treat arrhythmias. Long-term cardiac medication was similar among all groups and the proportion of patients prescribed anti-anginal (defined as any treatment alone or in combination of beta-blockers, calcium antagonists, or nitrates) medication was similar between groups (Table 1). The Canadian Cardiovascular Society angina classification was similar between European white and Indian Asians, but significantly different from Afro-Caribbeans.

Importantly, there were significant differences in baseline cardiac function, structure and geometry between ethnic groups. Afro-Caribbean patients had a significantly lower LV end systolic diameter and significantly greater LV end diastolic diameter (LVEDD) maximal wall thickness, LV mass, and LV mass index compared to European white and Indian Asian patients (Table 1). Indian Asian patients had a significantly smaller LVEDD compared to Afro-Caribbean and European white patients and a significantly greater LV ejection fraction compared to European white patients (Table 1). The cardiovascular risk profile was less favourable in patients whom went onto have a NFCE and among those who died during follow-up, as shown in Table 2.
Table 2

Baseline demographic characteristics and risk factors according to non-fatal cardiac events and all-cause mortality in all patients

Parameter

No non-fatal cardiac event (n = 4480)

Non-fatal cardiac event (n = 849)

P Value

Survived (n = 3964)

All-cause mortality (n = 1365)

P Value

Demographics

      
 

Age (yrs)

64.4 ± 12.4

68.9 ± 11

<0.001

65.1 ± 11.8

65.1 ± 13.5

0.948

 

Male gender

2315 (51.7)

420 (49.5)

0.451

2124 (53.6)

611 (44.8)

<0.001

 

Ethnic group

  

0.149

  

0.870

 

Black

379 (8.5)

55 (6.5)

 

326 (8.2)

108 (7.9)

 
 

European White

1856 (41.4)

363 (42.8)

 

1655 (41.8)

564 (41.3)

 
 

Indian Asian

2245 (50.1)

431 (50.8)

 

1983 (50)

693 (50.8)

 
 

Weight (kg)

79.3 ± 15.3

80.6 ± 15.2

0.027

78.9 ± 15.2

80.9 ± 15.3

<0.001

 

Body mass index (kg · m2)

28.3 ± 5.1

28.3 ± 5.1

0.659

28 ± 5

28.4 ± 5.3

0.014

 

Body surface area (m2)

1.88 ± 0.2

1.9 ± 0.2

0.003

1.88 ± 0.2

1.91 ± 0.2

<0.001

 

Systolic blood pressure (mmHg)

132 ± 33

132 ± 39

0.934

131 ± 25

132 ± 25

0.356

 

Diastolic blood pressure (mmHg)

70 ± 18

76 ± 30

<0.001

70 ± 20

71 ± 21

0.381

 

LV ejection fraction (%)

56.9 ± 8.3

55.1 ± 9.2

<0.001

57.2 ± 7.8

54.9 ± 9.9

<0.001

History

      
 

Hypertension

2547 (56.9)

552 (65)

<0.001

2310 (58.3)

789 (57.8)

0.913

 

Diabetes mellitus

1154 (25.8)

279 (32.9)

<0.001

1043 (26.3)

390 (28.6)

0.104

 

Hypercholesterolemia

2098 (46.8)

513 (60.4)

<0.001

1886 (47.6)

725 (53.1)

<0.001

 

Family history of CVD

1072 (23.9)

249 (29.3)

0.001

926 (23.4)

395 (28.9)

<0.001

 

Prior myocardial infarction

394 (8.8)

96 (11.3)

0.020

356 (9)

134 (9.8)

0.346

 

Prior PCI

1034 (23.1)

223 (26.3)

0.124

940 (23.7)

317 (23.2)

0.784

 

Prior CABG

508 (11.3)

134 (15.8)

<0.001

431 (10.9)

211 (15.5)

<0.001

 

Smoking history

  

0.024

  

0.503

 

Non-smoker

3474 (77.5)

629 (74.1)

 

3047 (76.9)

1056 (77.4)

 
 

Ex-smoker

690 (15.4)

139 (16.4)

 

628 (15.8)

201 (14.7)

 
 

Current smoker

316 (7.1)

81 (9.5)

 

289 (7.3)

108 (7.9)

 

NYHA functional class symptom status

  

<0.001

  

<0.001

 

NYHA functional class II

4063 (90.7)

627 (73.9)

 

3665 (92.5)

1025 (75.1)

 
 

NYHA functional class III

417 (9.3)

222 (26.1)

 

299 (7.5)

340 (24.9)

 

CCS angina classification

  

<0.001

  

<0.001

 

Class I

2689 (60)

0 (0)

 

2202 (55.5)

487 (35.7)

 
 

Class II

1402 (31.3)

671 (79)

 

1524 (38.4)

549 (40.2)

 
 

Class III

389 (8.7)

178 (21)

 

238 (6)

329 (24.1)

 

Long term cardiac medication

      
 

ACE inhibitor

1632 (36.4)

299 (35.2)

0.551

1443 (36.4)

488 (35.8)

0.648

 

Angiotensin II receptor antagonist

861 (19.2)

173 (20.4)

0.404

753 (19)

281 (20.6)

0.206

 

Aspirin

2578 (57.5)

406 (47.8)

<0.001

2176 (54.9)

808 (59.2)

0.006

 

Beta blockers

1965 (43.9)

320 (37.7)

0.001

1674 (42.2)

611 (44.8)

0.109

 

Calcium antagonists

1389 (31)

260 (30.6)

0.880

1222 (30.8)

427 (31.3)

0.771

 

Diuretic

1005 (22.4)

195 (23)

0.714

857 (21.6)

343 (25.1)

0.007

 

Lipid-lowering agents

3027 (67.6)

536 (63.1)

0.017

2614 (65.9)

949 (69.5)

0.017

 

Nitrates

689 (15.4)

98 (11.5)

0.004

581 (14.7)

206 (15.1)

0.724

 

Warfarin

271 (6)

65 (7.7)

0.073

245 (6.2)

91 (6.7)

0.530

Note: CVD Cardiovascular disease, PCI Percutaneous coronary intervention, CABGS Coronary artery bypass graft surgery, NYHA New York Heart Association, ACE Angiotensin converting enzyme

Clinical outcomes

The mean follow-up time was 4.6 ± 1.3 years (Afro-Caribbean: 4.6 ± 1.2 years; European white 4.4 ± 1.4 years; Indian Asians 4.8 ± 1.2 years). NFCE occurred in 849 (15.9 %) patients overall and were noted in 12.7 % (55 events) Afro-Caribbean patients, 16.4 % (363 events) in European white patients and 16.1 % (431 events) in Indian Asians. All-cause mortality occurred in 1365 (25.6 %) of patients (24.9 % in Afro-Caribbean patients, 25.4 % in European white patients and 25.9 % in Indian Asians). There were no significant differences between ethnic groups regarding NFCE and all-cause mortality.

DSE was completed in all patients and the level of agreement; kappa between the two sonographers was 0.84. Consensus was obtained in discordant cases and 90,593 left ventricular segments were analysed. In total 3645 (68.4 %) patients had a normal study, 1174 (22 %) patients developed a new or worsening WMA (ischaemic response) during their DSE, and 859 (16.1 %) had fixed WMA’s. Of the patients with fixed WMA’s, 349 (40.6 %) developed a new or worsening WMA during DSE. The territory of myocardial ischaemia did not significantly differ between groups (LAD, p = 0.821; Cx, p = 0.748; RCA, p = 0.975).

During the follow-up period, 958 (18%) patients (85 [19.6 %] Afro-Caribbean, 366 [16.5 %] European white, 507 [18.9 %] Indian Asian) underwent coronary angiography within 29 ± 2.2 days of DSE. Of these patients, 561 (58.6 %) had inducible ischaemia during DSE. In total, 530 (9.9 %) patients had significant (defined as ≥70 % coronary lumen stenosis by visual determination in ≥1 coronary artery) CAD (47 [10.8 %] Afro-Caribbean, 213 [9.6 %] European white, 270 [10.1 %] Indian Asian patients). The resulting sensitivity, specificity, positive and negative predictive values for DSE in detecting significant CAD were 93.6, 84.8, 88.4 and 91.4 %, respectively. There were no significant differences between the ethnic groups in the proportion of patients who underwent coronary angiography (p = 0.181) or the proportion of patients who had significant coronary disease (p = 0.781).

The NFCE rate for all patients without ischaemia was 2.3 % per year, increasing to 4.8 % for patients with fixed WMA’s, 7.3 % per year for those with 1–3 ischaemic segments and highest among those with >3 ischaemic segments (10.1 % per year). Patients with any ischaemia during DSE had a cardiac event rate of 7.7 % per year, suggesting that a positive DSE was associated with 90 extra NFCE per 100 person years of follow-up.

The all-cause mortality event rate for all patients without ischaemia was 4 % per year, increasing to 7.9 % for those with fixed WMA’s, 10.5 % per year for those with 1–3 ischaemic segments and highest among those with >3 ischaemic segments (16 % per year). Patients with any ischaemia during DSE had a mortality event rate of 11.2 % per year, suggesting that a positive DSE was associated with 132 extra deaths per 100 person years of follow-up.

Dobutamine stress echocardiography as a predictor of outcome

Figure 2 and Fig. 3 show the unadjusted Kaplan-Meier cumulative event curves for NFCE and all-cause mortality, respectively, dichotomized according to myocardial ischaemia (a) and number of ischaemic LV segments (b). The differences amongst these curves were significant (P < 0.001) and illustrates that myocardial ischaemia and greater ischaemic burden translate into significantly worse outcome.
Fig 2

Kaplan-Meier hazard curves for the cumulative survival and freedom from non-fatal cardiac events in each ethnic group. Kaplan-Meier hazard curves dichotomized according to myocardial ischaemia (a) and number of ischaemic LV segments (b)

Fig 3

Kaplan-Meier hazard curves for the cumulative survival and freedom from all-cause mortality in each ethnic group. Kaplan-Meier hazard curves dichotomized according to myocardial ischaemia (a) and number of ischaemic LV segments (b)

Table 3 and Additional file 1: Table S1 show the risk of NFCE and all-cause mortality respectively in each of the three ethnic groups, adjusted for standard risk factors including age, gender, hypertension, diabetes mellitus, hypercholesterolemia, family history of CVD, smoking history, prior myocardial infarction, prior revascularization and use of lipid lowering or anti-hypertensive medication. Among the three ethnic groups, ischaemia on DSE was associated with 2 to 2.5 times the risk of NFCE and 1.2 to 1.4 times the risk for all-cause mortality. For each ethnic group, the risk associated with a NFCE and all-cause mortality increased as the burden of myocardial ischaemia increased. Importantly, peak WMSI was the strongest independent predictor in all-ethnic groups for both NFCE and all-cause mortality. All adjusted hazard ratios for DSE parameters are significant (P < 0.038), for NFCE and all-cause mortality.
Table 3

Risk of non-fatal cardiac events associated with dobutamine stress test result in three ethnic groups

 

Afro-Caribbean

European White

Indian Asian

Parameter

HR (95 % CI)

P

HR (95 % CI)

P

HR (95 % CI)

P

Age (yrs)

1.025 (1.000-1.051)

0.050

1.020 (1.009-1.031)

0.001

1.018 (1.008-1.027)

0.002

Male gender

1.366 (0.793-2.353)

0.262

0.967 (0.534-1.752)

0.913

0.870 (0.720-1.052)

0.152

Hypertension

2.201 (1.089-4.449)

0.028

0.910 (0.721-1.149)

0.428

1.040 (0.823-1.315)

0.714

Diabetes mellitus

1.038 (0.549-1.963)

0.909

1.118 (0.865-1.445)

0.393

2.652 (2.538-2.790)

<0.001

Hypercholesterolemia

0.831 (0.434-1.590)

0.575

1.773 (1.624-1.959)

0.019

1.347 (1.073-1.691)

0.010

Family history of CVD

1.177 (0.582-2.380)

0.650

1.350 (1.078-1.691)

0.009

0.906 (0.717-1.145)

0.407

Prior myocardial infarction

1.311 (0.552-3.644)

0.164

1.126 (0.792-1.601)

0.509

1.028 (0.743-1.422)

0.868

Prior PCI

0.520 (0.223-1.211)

0.130

0.826 (0.631-1.081)

0.164

0.981 (0.793-1.214)

0.863

Prior CABG

2.496 (1.199-5.198)

0.015

1.043 (0.764-1.424)

0.790

0.781 (0.590-1.034)

0.085

Smoking history

 

0.565

 

0.252

 

0.658

 

Non-smoker

1 (reference)

 

1 (reference)

 

1 (reference)

 
 

Ex-smoker

0.738 (0.263-2.076)

 

0.871 (0.671-1.130)

 

1.028 (0.709-1.491)

 
 

Current smoker

1.260 (0.365-4.347)

 

1.375 (1.004-1.885)

 

1.326 (0.867-2.027)

 

ACE inhibitor

0.963 (0.507-1.830)

0.909

0.989 (0.780-1.253)

0.925

1.029 (0.833-1.272)

0.788

Angiotensin II receptor antagonist

1.090 (0.513-2.313)

0.823

1.099 (0.822-1.469)

0.524

1.158 (0.909-1.474)

0.236

Beta blockers

0.965 (0.532-1.751)

0.906

0.805 (0.644-1.008)

0.059

0.766 (0.625-0.939)

0.010

Calcium antagonists

1.532 (0.838-2.801)

0.166

0.871 (0.685-1.108)

0.261

0.985 (0.801-1.212)

0.888

Lipid-lowering agents

0.969 (0.509-1.843)

0.922

0.715 (0.579-0.883)

0.002

0.868 (0.701-1.073)

0.191

Fixed wall motion abnormality

0.879 (0.116-1.240)

0.109

0.933 (0.628-1.384)

0.729

0.827 (0.555-1.234)

0.353

Resting wall motion score index

0.749 (0.220-9.947)

0.304

1.489 (1.200-1.848)

0.008

1.991 (1.985-1.997)

0.003

Peak wall motion score index

2.273 (2.114-17.483)

0.038

3.092 (3.026-6.306)

<0.001

3.643 (3.254-12.033)

<0.001

New wall motion abnormality

2.026 (1.121-2.351)

<0.001

2.105 (1.166-2.251)

<0.001

2.490 (1.340-4.620)

<0.001

Number of Ischaemic LV Segments

 

<0.001

 

<0.001

 

<0.001

 

0 LV segments

1 (reference)

 

1 (reference)

 

1 (reference)

 
 

1-3 LV segments

1.092 (1.036-1.238)

 

1.171 (1.121-1.242)

 

1.62 (1.44-4.18)

 
 

>3 LV segments

2.192 (2.146-4.238)

 

2.803 (2.567-5.138)

 

3.040 (2.68-7.70)

 

Note: CVD Cardiovascular disease, PCI Percutaneous coronary intervention, CABGS Coronary artery bypass graft surgery, ACE Angiotensin converting enzyme

Table 4 shows the C-statistic for the prediction of NFCE and all-cause mortality according to ethnic group, calculated on the basis of the standard risk factors alone and on the basis of the standard risk factors in addition to DSE parameters. The C-statistic for the prediction of NFCE and all-cause mortality was greater when DSE parameters were added to standard risk factors. These increases were statistically significant for each ethnic group indicating an improvement in discrimination.
Table 4

C-statistic for risk factors alone and for risk factors plus dobutamine stress test results to predict non-fatal cardiac events and all-cause mortality

Ethnic Group

Non-fatal cardiac event

 

All-cause mortality

 
 

C-statistic for risk factors alone

C-statistic for risk factors plus DSE test results

P value

C-statistic for risk factors alone

C-statistic for risk factors plus DSE test results

P value

Afro-Caribbean

0.67

0.74

0.009

0.6

0.72

0.004

European White

0.68

0.76

<0.001

0.61

0.72

<0.001

Indian Asian

0.64

0.74

<0.001

0.57

0.69

<0.001

Total

0.64

0.74

<0.001

0.61

0.68

<0.001

Discussion

We examined the predictive value of DSE in a multiethnic UK population. We found that DSE is a strong and independent predictor of NFCE and all-cause mortality irrespective of ethnicity. The risk of NFCE and all-cause mortality was associated with the burden of myocardial ischaemia, as assessed by the peak WMSI and the number of ischaemic segments during DSE. The addition of DSE to standard risk factor models including age, gender, hypertension, diabetes mellitus, hypercholesterolemia, family history of CVD, smoking history, prior myocardial infarction, prior revascularization and use of lipid lowering or anti-hypertensive medication for the prediction of NFCE and all-cause mortality significantly increased the C statistic, an order of magnitude comparable to that observed with coronary calcium scoring in different ethnic populations [24, 25]. Importantly, DSE parameters contributed to the risk of both NFCE and all-cause mortality in three major ethnic groups independently of other risk factors.

The prognostic value of DSE has been previously reported in large studies in patients with various pre-test probabilities [9, 13, 16, 2631]. Ischaemic burden and severe wall motion abnormalities during stress were independently associated with events in the present study, findings which previous research have recognised that indicate worse prognosis [9, 13]. However, previous analysis has not attempted to evaluate the predictive value of DSE in different ethnic groups. Importantly, in all three ethnic groups studied, the addition of DSE parameters to clinical data improved the predictive power. This finding contrasts prior research, which demonstrated ethnic differences in the survival of patients undergoing exercise treadmill testing [8].

This study also demonstrated ethnicity related differences in the function, structure and geometry of the left ventricle at rest. Afro-Caribbean patients demonstrated greater concentric cardiac remodelling with significantly greater maximal LV wall thickness and LV mass compared to European white and Indian Asian patients. A greater LV wall thickness has been shown previously in Afro-Caribbean populations compared to other ethnic groups and is associated with an increased mortality risk [32]. Furthermore, an increased LV mass has been shown to be a powerful independent predictor for CVD morbidity and mortality in individuals previously free of clinical cardiovascular disease [33]. Treatment to control modifiable risk factors in Afro-Caribbean populations may reduce cardiac remodelling [34]. Indian Asian patients had a significantly smaller LV cavity and the smallest LV mass compared to Afro-Caribbean and European white patients. Other studies support these findings [3436]. Indexing LV mass did not attenuate the observed difference. A decreased LV cavity and smaller LV mass may lead to an increase in LV wall stress and myocardial oxygen demand, which may increase the vulnerability to myocardial ischaemia [34]. This was a specific cohort of patients referred for DSE. These differences may contribute to the elevated CVD risk seen in Afro-Caribbean and Indian Asian ethnic groups. It is important to note that European white patients were significantly older than both Afro-Caribbean and Indian Asian patients. Therefore, for an age matched cohort the prevalence of CVD may be significantly different between ethnic groups.

Angiographic comparisons of CAD between Caucasians and Asians have reported similar findings to the present study. Dhawan and Bray [37] reported no difference in the severity or extent of CAD between Caucasians and Asians. As shown in our study, there was a significant difference in age between groups, with Asians being significantly younger than Caucasians. In a recent study including 279,256 patients, South Asians were younger, had more extensive coronary artery disease and greater prevalence of major risk factors, particularly diabetes compared to Caucasians [38]. However, as shown in our study, when correcting for these differences, outcome was similar between South Asians and Caucasians. Similar to our study, angiographic differences in CAD were minimal among African American compared to white patients, with a similar distribution of coronary vessel disease and mean stenosis score [39].

Disproportionate rates of heart disease are seen in racial and ethnic minority populations. The ability to reliably risk stratify populations at greater risk of adverse cardiac events is therefore of great importance. Recently, cardiovascular screening demonstrated the potential to reduce ethnic health inequalities [40]. In our study Indian Asians had a significantly greater prevalence of hypertension, diabetes mellitus, and hypercholesterolemia compared to Afro-Caribbeans and European whites. However, a significantly greater proportion of Indian Asians had previous coronary intervention compared to Afro-Caribbeans and European whites. In addition, Indian Asian and European whites had greater Canadian Cardiovascular Society angina classification compared to Afro-Caribbeans. Irrespective of differences in risk factors, the results of this study indicate that DSE adds incremental value in estimating the probability of cardiac events and all-cause mortality in three major ethnic groups and is therefore a valuable tool in the assessment of CAD.

Our study has limitations. This was a prospective observational study from a single centre. Patients recruited into our study were referred for a clinically indicated DSE and there is the potential for referral bias and high pre-test probability related to a higher prevalence of co-morbidities and symptoms. Only 18.9 % on the study populations underwent coronary angiography within 1-month of DSE, which may bias test sensitivity and specificity. Medication listed refers to treatment at time of DSE and changes in medication over the follow-up period were not taken into account. Due to difficulties in accurately determining the cause of death by reviewing death certificates or medical records, all-cause mortality was selected as a more objective and unbiased end point [41]. Notwithstanding these limitations, the present study is consistent with earlier work and extends our knowledge in different ethnic populations.

Conclusions

In a multiethnic UK cohort, DSE added incremental value to the prediction of NFCE and all-cause mortality over that of standard CVD risk factors in Afro-Caribbean, European white and Indian Asian patients.

Declarations

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Department of Cardiology, St George’s Healthcare NHS Trust
(2)
St George’s, University of London

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Copyright

© O’Driscoll et al. 2015

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