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Are at-risk New Zealand women receiving recommended
cardiovascular preventive therapy?
Olivia Bupha-Intr, Sally B Rose, Beverley A Lawton, C Raina
Elley,
Simon A Moyes, Anthony C Dowell
Cardiovascular disease (CVD) is the leading cause of
premature death and disability in New Zealand for both men and women, accounting
for 40% of all deaths.1 Although
age-standardised deaths from coronary heart disease (CHD) are higher among men
than women, deaths from all CVD (including CHD, hypertensive disease and
cerebrovascular disease) are higher among women than deaths from all forms of
cancer.1 The New Zealand cardiovascular risk
guidelines were developed with the intent to systematically assess and manage
the population at risk for CVD.2
Absolute risk-based approaches to CVD event prediction have
been shown to be better than the traditional, single risk factor
approach.3 The guideline recommendation is that
any individual identified with a five-year cardiovascular risk of greater than
or equal to 15% should be offered pharmacological intervention consisting of low
dose aspirin, blood pressure-lowering medication and a lipid-lowering medication
(sometimes referred to as combination or ‘triple
therapy’).4 Use of triple therapy has
been shown to halve the absolute risk of having a cardiovascular
event.5–7
Despite the considerable potential for risk reduction, past
research suggests that those at highest risk of cardiovascular disease are not
receiving treatment recommended by the CVD
guidelines.8
9-12 For example, analysis of primary care
visits by men aged 45 and older, and women aged 55 and older in 2000 showed that
only 28% of those with cardiovascular disease were taking a combination of blood
pressure and lipid-lowering medication.8 Among
a cohort of 29,000 patients with type 2 diabetes, two thirds of patients with
cardiovascular disease and 44% of those at high risk were taking appropriate CVD
treatment.10
A recent audit of data collected for 621 patients undergoing
CVD risk assessment at a nurse clinic showed that 59% of patients with previous
cardiovascular disease were taking triple therapy when first assessed, and this
increased to 71% (51/72) at a follow-up
assessment.12
Medication use in relation to cardiovascular risk has not
been reported separately for men and women in past New Zealand research, so it
is not clear to what extent, if at all, the treatment gap exists for women.
There is also some controversy about the use of cholesterol
lowering medication (particularly statins) for
cardiovascular risk reduction in women,13 with
evidence from secondary prevention (but not primary prevention) trials showing
that statins reduce the risk of cardiovascular events in
women.6
Primary prevention trials have been limited to men, and it
has been argued that women respond differently to men and may not therefore
benefit from statin use to the same extent.14
15 Despite the different levels of evidence for the efficacy of
cardiovascular treatment for men and women, the cardiovascular treatment
guidelines do not differentiate between men and women (except as a marker for
absolute risk). The present study was therefore conducted to determine whether
women with a 5-year cardiovascular risk of greater than or equal to 15% are
being treated with triple therapy in line with guideline recommendations. Given
the debate surrounding the use of statins for cardiovascular risk reduction in
women, we also sought to investigate uptake of lipid-lowering agents for
secondary disease prevention.
MethodsParticipants—1089 women aged
40-74 years recruited through 17 general practices in the greater Wellington
region for the Women’s Lifestyle Study between 2004 and
2005.16 17 Women were identified through
General Practice registers and invited to attend a screening interview for a
‘lifestyle study’. Women were eligible for randomisation to an
intervention (enhanced Green Prescription) or control (Usual care) if deemed
physically inactive (self-reported undertaking less than 150 minutes of at least
moderate intensity physical activity per week), and medically able to increase
their activity levels.
Data collection—Data were
collected in face to face interviews with a research nurse and included:
demographics (age, ethnicity, NZ Deprivation
score,18 highest education level),
cardiovascular risk factor information (blood pressure and cholesterol
measurements, diabetes and smoking status), family history of coronary heart
disease or ischaemic stroke, past history of cardiovascular disease and current
use of cardiovascular medications (aspirin, blood pressure-lowering and
lipid-lowering medications). Participants attended a baseline visit (Time 1) and
2 subsequent annual visits (Time 2 and Time 3).
Calculating cardiovascular
risk—A 5-year cardiovascular risk score was calculated using the
adjusted Framingham risk equation for individuals with no previous
cardiovascular history.19 The risk score
estimates the probability of having a cardiovascular event (including ischaemic
heart disease, cerebrovascular disease or peripheral arterial disease) in the
next 5 years. Variables required for the equation are sex, age, systolic blood
pressure, smoking, total cholesterol, HDL, diabetes, and ECG left ventricular
hypertrophy (LVH). For the purposes of this study the ECG LVH was set at zero.
Individuals with a cardiovascular history were classified as greater than 20%
cardiovascular risk over the next 5 years as per the
guidelines.2 At the time of the study, the New
Zealand CVD guidelines recommended a 5% upward adjustment of risk level for any
individual with:
Cardiovascular risk scores were
calculated as described above and scores moved up one risk category (5%) as per
the guidelines. Our study was limited in risk adjustment due to lack of data for
some of the adjustment criteria:
Cardiovascular
medications—Cardiovascular medications were grouped as
follows:
Participants were asked if they were
currently taking any medications in each of the above categories. Individuals
with a risk score of 15% or higher were assessed to determine whether they were
taking medications as per the guidelines.
Outcome measures—Cardiovascular
risk scores (grouped into the following categories: <10%, 10-14% and
≥15%, and ≥20%) and use of cardiovascular medications ascertained in
relation to guideline recommendations.
Analyses— Proportions with high
cardiovascular risk, and on medications in each risk category, were calculated
for ethnic and socioeconomic subgroups. Odds ratios and p-values were calculated
by constructing logistic regression models containing age, ethnicity and
deprivation (socioeconomic status) using SAS 9.1.3.
ResultsTable 1 displays the demographic and risk factor
characteristics of the sample when first assessed (Time 1). The majority of
women in the sample were aged between 50-64 years (mean age 58.9, SD 6.9). This
was not a population based sample, but purposive recruitment of Māori and
Pacific women resulted in the proportion of women in these ethnic groups being
comparable to that of the census for women in the 50–65 year
age-band.20
Cardiovascular risk profile—Not all
participants attended all three study visits, and some of those who attended did
not have their fasting blood test carried out, so full data were not available
on all participants at all time points. Five-year cardiovascular risk scores
were calculated for 1050 women (97% of the 1089 participants) at enrolment into
the Women's Lifestyle Study (Time 1). Risk scores were calculated for 974 women
(89%) at 12 months (Time 2) and 946 women (87%) at 24 months (Time 3). Table 2
presents the adjusted Framingham CVD risk scores stratified by age, ethnicity
and deprivation for 1050 women at Time 1.
Table 1. Demographic and risk factor profile of
1089 participants in the Women’s Lifestyle Study (figures are n (%) unless
otherwise denoted)
* Previous CVD includes: Heart attack (n=21), Angina
(n=43), CABG (n=14), Stroke (n=21).
The majority of women were low-risk with scores less than
10% (80%), and 33 women (3%) had calculated CVD risk scores of ≥15% (no
previous CVD). Seven percent of women (76/1050) self-reported previous
cardiovascular disease. Ten percent of women overall were classed as high-risk
including those with established CVD and a risk score ≥15% (109/1050).
Nineteen percent of Māori women were at high risk compared with 9% of
European women in the study (p<0.001). Māori women in the study were
significantly more likely to be at high risk than non-Māori women (odds
ratio: 4.0 (95% CI: 2.05 to 7.8)), after adjusting for age and socioeconomic
status.
While 7.5% of the women in the least deprived category were
at high risk, 14.4% and 12.7% were at high risk among women in the moderate and
high deprived categories, respectively (p=0.01).
When including only those participants for whom data were
available at all three assessment periods (n=902), the proportion of women at
high risk for cardiovascular disease (calculated score ≥15% or established
CVD) increased over time.
Table 2. Adjusted CVD risk scores for 1050
women at Time 1 stratified by age, ethnicity and NZ Deprivation
band
* Individuals with a calculated 5yr CVD risk ≥15%
(without established CVD)
** Individuals considered as high risk as per NZGG
guidelines (includes those with previous CVD, and those with a calculated 5-year
CVD risk ≥15%)
Use of cardiovascular medications—At
the first study visit (Time 1), 9% of women (96/1089) were taking aspirin, 25%
(269/1089) were taking blood pressure-lowering medication, 13% (138/1089) were
taking lipid-lowering medication and only 3% (29/1089) were taking all three
medications. Figure 1 depicts the use of cardiovascular medications by women in
relation to CVD risk scores at Time 1. Of 109 women at high risk (established
cardiovascular disease or a calculated 5-year CVD risk score greater than 15%),
the proportion taking the recommended medications was low; 36% (39/109) were
taking aspirin, 55% (60/109) were taking blood pressure-lowering medication, 45%
(49/109) were taking a lipid-lowering agent and 17% (19/109) were taking all
three medications.
At Time 1, women with established CVD clearly had the
highest uptake of cardiovascular medication, with 55% taking blood pressure
medications (42/76), 47% taking lipid-lowering medication (36/76), 42% taking
aspirin (32/76) and only 20% taking all three therapies (15/76). Those women
without established CVD but with a calculated risk score greater than 15% had
relatively low uptake of the recommended medications, with only 12% taking all
three therapies (4/33). The proportions taking cardiovascular medications were
similar across different ethnic groups after adjusting for age and socioeconomic
status (p=0.5).
Figure 1. Use of cardiovascular medications by
1050 women at Time 1 in relation to CVD risk scores
![]() Use of lipid-modifying
medications—109 women were classified as high risk at Time 1 (76
had established CVD, 33 had a calculated score of at least 15%), with 45% taking
lipid-lowering medication (49/109). The remaining 55% (60/109) of those who met
the guideline criteria were not taking lipid-lowering medication for secondary
prevention at the time of the interview, representing a ‘treatment
gap’. The proportions of women in the high-risk category taking
lipid-lowering medications were similar across ethnic groups at Time 1 after
adjusting for age and socioeconomic status (p=0.9), with 44% of Māori women
at high risk taking lipid-lowering medications and 45% of New Zealand European
women.
Table 3 shows use of cardiovascular medications by women at
high risk for CVD stratified by ethnic group over time. Use of aspirin was not
recorded at Time 2 and 3, so use of triple therapy could not be determined
beyond Time 1. The proportion of women taking blood pressure and lipid-lowering
medications did not differ significantly over time. Our results suggested that
Māori women at high cardiovascular risk (>15% or previous CVD) in the
study were more likely to be on triple cardiovascular treatment than
non-Māori women at high risk (odds ratio: 2.28 (95% CI: 0.6 to 9.2) after
adjusting for age and socioeconomic status, although this result did not reach
statistical significance, possibly due to the small numbers involved.
Table 3. Medications taken by women at high
risk for CVD (5-year risk ≥15%, and established CVD) over time presented
by Ethnic Group
* Includes only those for whom complete data were
available at each assessment.
** Ethnic groups other than NZ European and Māori
were collated due to the small sample size (includes Pacific, Asian and Other
ethnicities).
*** Data on aspirin were not collected at Times 2 and
3.
DiscussionThis research suggests that there is a significant treatment
gap between the New Zealand cardiovascular risk guideline recommendations and
clinical practice for women at risk for cardiovascular disease. Over 80% of
women meeting the cardiovascular guideline criteria for combined cardiovascular
treatment (aspirin, BP-lowering and lipid modifying medications) were not taking
all three. Of particular concern was the proportion of women with established
cardiovascular disease (80%) who were not receiving the recommended triple
therapy (61/76).
Consistent with existing knowledge, we found Māori
women in the study to have higher rates of established cardiovascular disease
compared with non- Māori.9
11 Encouragingly, there was no evidence of
disadvantage in use of medication by ethnicity, with both Māori and non-
Māori having the same rate of cardiovascular medication use, which is
consistent with past research.9 11
Comparison with other studies—This
cardiovascular treatment gap has been identified in past research that has
included, but not separately reported on, the use of cardiovascular medication
by women at risk.8
10 9
11 The proportion of at-risk women in our study
receiving triple therapies was lower than found for males and females in
previous studies (17.4% of all high-risk women, and 20% for secondary prevention
at Time 1). Riddell et al reported use of triple therapy by 48% of Māori
and 44% of non- Māori for secondary
prevention9 and Peiris et al found that 50% of
high-risk patients were receiving all three recommended
therapies.11
Rafter et al found that 28% of patients were taking blood
pressure and lipid-lowering medications for secondary prevention but their
sample included both men and women.8 These
cardiovascular ‘treatment gaps’ are not limited to New Zealand,
research in the USA and United Kingdom has demonstrated similar findings for
statin use for secondary prevention, with up to 88% of patients with coronary
artery disease not taking statins in a US
study,21 and only 13% of men and 8% of women
with ischemic heart disease prescribed statins in a UK
study.22
Although New Zealand has been a world leader in absolute
risk based guidelines,23 uptake has been
variable within primary care. The reasons for this are likely to be multiple and
complex, involving a range of barriers to assessment and management of CVD risk
at the health system, doctor and patient level. For example, surveys of family
physicians in the United States suggest that cost of medications, side effects,
knowledge and skills to recommend lifestyle changes and to facilitate patient
adherence, time for counselling, and adherence to medications are significant
barriers to CVD risk management.24 25
Furthermore, divided clinical opinion about the
appropriateness of cholesterol lowering medication for
women26 27 is likely to play a contributing
role. Likewise the ongoing debate over whether aspirin reduces coronary heart
disease events in women may also have contributed to the lack of uptake of the
guidelines.28 Since this study was completed, a
meta-analysis of primary prevention trials involving aspirin has been published
and the results suggest that routine aspirin is not justified for primary
prevention of coronary heart disease.29
Strengths and limitations—This is one
of the first studies to describe cardiovascular medication use in relation to
cardiovascular risk among a large sample of New Zealand women that includes good
participation by both Māori and Pacific participants. Although not a
representative sample, eligibility criteria for the Women’s Lifestyle
Study was being ‘physical inactive’, therefore women in the present
study might be expected to have higher overall risk profiles than women of this
age group in the general population. Limitations of this study are that we are
unable to determine the reasons for the ‘treatment gap’.
Medication data were based on self-report, and not checked
against prescriptions, and it is unclear whether individuals had been offered
the medication but declined to take it, or if there was a contraindication or
previous adverse reaction to the medication. If so our treatment gap may have
been overestimated. Likewise, previous cardiovascular events were self-reported
not based on medical records, so the number of women with established
cardiovascular disease may be over or under-reported here.
ConclusionsThe low uptake of recommended medications by women who are
at high risk of cardiovascular disease indicates there are still substantial
gaps in the use of evidence based guidelines in clinical practice. Modifiable
barriers to the successful management of women at risk for cardiovascular
disease need to be identified and addressed to reduce cardiovascular related
morbidity and mortality.
Competing interests: None known.
Author information: Olivia
Bupha-Intr, 4th Year Medical
Student, Department of Primary Health Care & General Practice, University of
Otago, Wellington; Sally B Rose, Senior Research Fellow, Women’s Health
Research Centre, Department of Primary Health Care & General Practice,
University of Otago, Wellington; Beverley A Lawton, Director, Women’s
Health Research Centre, University of Otago, Wellington, Department of Primary
Health Care & General Practice; C. Raina Elley, Senior
Lecturer, Department of General Practice & Primary Health Care, School of
Population Health, University of Auckland, Auckland; Simon A
Moyes, Statistician, Department of General Practice &
Primary Health Care, School of Population Health University of
Auckland, Auckland; Anthony C Dowell, Professor, Department of Primary Health
Care & General Practice University of Otago, Wellington
Acknowledgement: We thank the National
Heart Foundation of New Zealand for funding this summer studentship
project.
Correspondence: Beverley Lawton, Women's
Health Research Centre, Department of Primary Health Care and General Practice,
University of Otago, P O Box 7343 Wellington South, New Zealand. Fax: 04 385
5473; email: bev.lawton@otago.ac.nz
References:
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