Transcript Neurologists, Cardiologists and GPs working together

Stroke Prevention
Neurologists, Cardiologists
and GPs working together
Southern Neurology
Stroke – Australian facts 1

Incidence: 40,000 strokes per year
(73% first episode)
 Prevalence (1995):116,500 (0.6% of
population) had a stroke
 Hospitalisation (1998-1999):
52,439, (0.9% of all hospitalisations)
 Second greatest single killer after CHD
11,982 death (1998)
Stroke – Australian facts 2
Risk of Stroke:
1 in 4 men and 1 in 5 women over age 45 yrs will
have a stroke before age 85 yrs.
Leading cause of long-term disability in adults:
63,530 Australians with a disability whose main
condition was stroke (1998).
Stroke –Australian facts 3
 Stroke Type
23%
14%
63%
IS
ICH
TIA
AIHW 2001
Stroke and stroke risk factor
statistics in Australia
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Perth Community Stroke Study 1989-1990 : 370
cases of first-ever stroke – only 42% still alive at 5
years.
 ASAP general practice audit: 70% of patients
presenting to GP had 1 or more stroke risk factors
and 34% had 2 or more stroke risk factors.
Prevalence of hypertension 44%,  cholesterol
43% and current smoking 17%.
 START retrospective audit of acute strokes – risk
factors: hypertension 71%, hyperlipidaemia 41%,
AF 30%, diabetes 26%, current smoking 25%
Stroke and myocardial infarct
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After stroke, 5-10% of patients per year suffer MI;
after TIA 3% of patients per year suffer MI.
After MI, ? stroke risk. LIPID – 350/9014 patients
(4%) with previous MI and total cholesterol 4-7
mmol/L suffered an ischaemic stroke during 6 year
follow-up.
CAPRIE: Stroke subgroup: 13% had previous MI;
17% angina pectoris. MI subgroup: 2% had history of
previous ischaemic stroke, 3% TIA. First outcome
event in stroke subgroup was most commonly a
stroke. First outcome event in MI subgroup was most
commonly an MI.
Hypertension as stroke risk
factor

Estimated relative risk 3-5.
 Risk of recurrent stroke  by 28% for every 10
mmHg increment in systolic BP from 130-160
mmHg (UKTIA).
 WHO/ISH (1999) guidelines – 130/85 mmHg in
patients under age 60 years or patients with
diabetes mellitus; 140/90 in patients aged > 60
years.
 Average 24 hr or home BP values of 125/80 mm
Hg correspond to office BP of 140/90 mmHg.
Prevalence of isolated clinic hypertension ?10%
Anti-hypertensive therapy
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NHF of Australia (1999) recommended diuretics or betablockers as first line agents for patients with mild
hypertension and no co-morbidities.
1,223,000 Australians received anti-hypertensive
medication through the PBS scheme in 1998, almost 60%
prescribed a single drug. RAS > CCB > thiazides >
betablockers.
Population studies indicate that only 10-40% of patients
receiving antihypertensive therapy are optimally treated. In
PROGRESS, 50% of patients recruited were not on antihypertensives and 64% were either on treatment or had
SBP>160 or DBP>95. Mean baseline BP for all patients
recruited in PROGRESS was 147/86 mmHg
Anti-hypertensive drug use in
Australia
Diuretics
700000
600000
Beta Blockers
500000
400000
300000
Calcium Channel
Blockers
200000
ACE Inhibitors
100000
1998
1997
1996
1995
1994
0
1993
Patient numbers (Hypertension)
Hypertension Patient Numbers 1993-98
Angiotensin II
Antagonists
Selected trial results
UKPDS (1998) – tight control of BP in HT patients with
DM <150/85 (vs less tight control < 180/105), 32% 
deaths related to DM, 44%  strokes. No difference b/w
captopril or beta-blocker. 29% in tight group on  3 drugs.
 HOT study (2001)– target DBP 80 or 85 or 90
achieved in 92%. Felodipine first drug chosen but patients
commonly on 2 or 3 drugs. Event rates lower than
expected from meta-analysis data.
 HOPE (2000) and PROGRESS (2001) – benefits of ACE
inhibitors ramipril and perindopril in stroke prevention. In
PROGRESS, average patient took  3 drugs.
 LIFE – losartan > atenolol (including 25% stroke) in
HT/LVH patients despite similar  BP

ANBP2 study -12% first events and 11%
 total CVS mortality with ACE-I
Hazard Ratio (95% CI) p
ACE better
0.2
Cardiovascular
0.88 (0.77,1.01) 0.07
Non-Fatal Cardiovascular
0.86 (0.74,0.99) 0.03
Cerebrovascular
0.90 (0.73,1.12) 0.35
Stroke
1.02 (0.78,1.33) 0.91
Coronary
0.86 (0.70,1.06) 0.16
Myocardial Infarction
0.68 (0.47,0.98) 0.04
Other Cardiovascular
0.90 (0.71,1.14) 0.36
Heart Failure
0.85 (0.62,1.18) 0.33
New Engl J Med, 2003;348:583-92.
1.0
Diuretic better
5.0
ANBP-2 study –fatal events
Hazard Ratio (95% CI)
p
ACE better
0.2
Cardiovascular
0.99 (0.72,1.35)
0.94
Non-Cardiovascular
0.84 (0.66,1.08)
0.18
Cancer
0.98 (0.73,1.32)
0.89
Trauma
2.87 (0.31,26.9)
0.36
Other Non-Cardiovascular
0.57 (0.37,0.90)
0.01
Stroke
1.91 (1.04,3.50)
0.04
Coronary
0.74 (0.49,1.11)
0.14
Myocardial Infarction
0.79 (0.31,1.99)
0.61
Other Cardiovascular
0.95 (0.46,1.96)
0.89
Heart Failure
0.24 (0.03,1.94)
0.18
1.0
Diuretic better
5.0
ALLHAT – favoured chlorthalidone over lisinopril as firststep treatment in high-risk patients with HT
Cholesterol as stroke risk
factor

Framingham and MRFIT studies –  CHD
progressively with an  in cholesterol.
 For every 20%  cholesterol,  CHD by 15% and
 mortality by 11%.
 ARIC (2003) –14,175 M and F followed-up 10
years, no correlation b/w serum cholesterol and
risk of stroke.
Selected cholesterol trials
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LIPID (1998) and CARE (1996) – 19% and 31% risk
reduction for stroke, respectively, with pravastatin in
patients with CHD.
ASCOT – HT patients with  3 other risk factors and
cholesterol < 6.5 show  stroke risk with atorvastatin 10
mg.
MRC/BHF Heart Protection Study (2002), simvastatin
40mg/day  incidence of first stroke by 25% and CHD
death rate by 18% in patients age < or > 70 years; patients
with cholesterol < 5 mmol/L, patients on aspirin or HT
therapy.
How hard is it to achieve
target cholesterol ?
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Lipid Treatment Assessment Project (2000), only 18%
of patients had LDL-cholesterol reduced to < 2.6
mmol/L.
ACCESS (2001)– in which drug dosage titrated as
needed, LDL-cholesterol fell to < 2.6 mmol/L in
<25% taking pravastatin, 30% taking fluvastatin, 44%
lovastatin, 51% simvastatin and 72% taking
atorvastatin.
Discontinuation – JAMA (2002) in patients aged > 66
years prescribed statin for ACS, chronic CHD and
primary health, 2 year adherence rates were 40%, 36%
and 25%, respectively.
Schedule of Pharmaceutical
Benefits November 2002
PBS guidelines may influence discontinuation rate in
stroke patients in Australia
Patients with existing
CHD
1 or more of following:
DM; Familial
hypercholesterolaemia;
Family Hx CHD; HT;
PVD
Cholesterol > 4 mmol/L
Cholesterol > 6.5 mmol/L
or
Cholesterol > 5.5 mmol/L
And HDL < 1 mmol/L
AF – rhythm or rate control?

AFFIRM trial (NEJM 2002)
 5-year mortality 21.3% for rate control versus
23.8% for rhythm control (p=0.08). Sinus rhythm
present in 62.6% and patients taking warfarin >
70%. No reduction in stroke rates, other thromboembolic complications or haemorrhages for
rhythm versus rate control.
 In rhythm control group, 55% of ischaemic strokes
occurred after discontinuation of warfarin and
further 21% occurred during treatment but INR <
2.0. Only 31% had AF at time of stroke.
The concept of a stroke
prevention clinic
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Combined neurological and cardiac
assessment of patients with CHD, CVD
and/or vascular risk factors for both.
 Aim is to provide patient and general
practitioner with stroke prevention
treatment options to minimise risk and
further events (both neurological and nonneurological).
Ingredients of stroke
prevention clinic
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GP referred patients “at-risk” of stroke who, in the opinion
of the GP, would benefit from combined cardiac and
neurological assessments.
Agreement by neurologist and cardiologist that “urgent”
referrals can be seen through this clinic.
Patients see neurologist and cardiologist on same day.
Investigations arranged on individual patient requirements.
Clinical nurse co-ordinates investigations, follow-up and
liaises with neurologist and cardiologist to provide
combined report with unified treatment recommendations.
GP is responsible for the ongoing management of the
patient.
Limitations of this “model”
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Duration of time spent by patients undergoing
initial (same day) assessments.
Some patients referred already see a different
cardiologist and/or neurologist.
? Cost-benefit of ‘combined’ clinic to patient and
tax-payer.
? What if there isn’t ‘agreement’ on treatment
recommendations.
? Should there be follow-up to monitor treatment
response.
First 50 patients to Southern Neurology
Stroke Clinic–referral and patient details
Referral source – GPs (56%), ophthalmologists
(20%), cardiologists (18%), endocrinologists
(6%).
 Reason for referral – recent TIA (34%), recent
ischaemic stroke (20%), general vascular
assessment (18%), other (28%) – including
presyncope, gait disorder, cognitive decline
 24 M (mean age 75y), 26 F (mean age 77 y)
 Past history – hypertension (58%),  cholesterol
(46%), previous CVA/TIA (32%), IHD (28%),
DM (12%), AF (10%), current smoker (6%).

Hypertension
19 of 29 patients with HT were on  2drugs.
 RAS were most commonly prescribed (n=13
patients on ACE-I and n=5 ATIIRA) followed by
diuretics (n=13), beta blockers (n=9), CCA (n=7)
 14 of 29 patients with a history of HT had office
BPs > 140/90 mmHg. 11/14 had systolic BP 160.
 8 patients newly diagnosed with HT were
commenced treatment (7 given RAS drug and 1
given a diuretic).
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Lipid profile
Lipid profile – performed on 42 patients, of whom
only 6 patients had total cholesterol  4 mmol/L
and 5 had total cholesterol  6.5 mmol/L.
 12/23 patients with a history of  cholesterol were
already on a statin. 13 patients were commenced
statin therapy including 5 patients with a history of
IHD.
 6 new patients started on a statin did not qualify
for PBS subsidy.
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Anti-thrombotic therapy
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Post-clinic treatment – 16 patients on
asasantin (10 changed from aspirin to
asasantin and 4 de novo asasantin), 14
patients on aspirin monotherapy (including
9 de novo patients), 6 patients on
aspirin/clopidogrel (vs 1 pre-clinic), 5
patients on clopidogrel monotherapy, 4
patients on warfarin.
Patients undergoing surgery
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5 patients underwent surgery after stroke
prevention clinic assessment.
 2 patients had CEA for symptomatic carotid
stenosis, 1 underwent CABG, 1 underwent
IPPM and 1 patient had surgical repair of
atrial septal aneurysm.
Conclusions
Most patients with HT are ‘under-treated’ and
many will require  2 drugs if target is to be
reached.
 Most patients on lipid therapy do not achieve
target total or LDL-cholesterol levels. Many will
probably discontinue treatment after 2 years.
 Our combined cardiac/neurological stroke
prevention clinic resulted in a significant change
in medication in the majority of patients referred
to the clinic.
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