masterclass on emerging priorities in cvd treatment of ... · - sap: episodes of reversible...
TRANSCRIPT
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www.epccs.eu
Masterclass on emerging priorities in CVD
Treatment of angina pectoris: The role of primary care
Dr Frans Rutten
Utrecht, The Netherlands
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Diagnosis: because it guides therapy
DEPTh
• Diagnosis What kind of disease has the patient?
• Etiology What is the cause of disease?
• Prognosis How does the disease progress (with/without treatment)
• Therapy What happens when treated?
Does therapy change prognosis?
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Diagnosing can be difficult…
• Patient A
• Woman, 53 yrs
• Diffuse chest pain, duration
20 minutes. A few times. Last
time gardening
• No radiation, no sweating or
nausea
• No cardiovascular risk factors
• Recently dad suddenly died
• Recently divorced
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Sometimes easy…
• Patient B
• Man, 65 yrs
• Tightening chest pain, 5
minutes, radiation to the left
arm
• Nausea, sweating, pale, ‘fear
in his eyes’
• Dyspnoea, slightly
tachypnoeic
• Hypertension
hypercholesterolemia
smoking (40 pack years)
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Time is crucial (also FU time)
• When at patient-specific moments and lasting months:
stable angina (all three characteristics)
• Progressive in time, at an ever lower level of exercise, and poor
relieve with rest:
progressive, unstable angina
• In rest
(especially with vasovagal symptoms & signs, and sustaining):
ACS (STEMI, NSTEMI, UAP in rest)
Caveat: at night!
differential diagnosis: GIRD
tachypnoea ≠ hyperventilation
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Differential diagnosis chest pain
Erhardt et al. Task force on the management of chest pain. Eur Heart J 2002
Primary care Hospital (ED)
Cardiac 20 45
Muscular/skeletal 43 14
Lung 4 5
Gastro-intestinal 5 6
Psychiatric 11 8
Others 16 26
Pre-test probability in PC is lower than at ED !
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Diagnosis can be difficult…
• Patient A
• ‘common’ situations
stable, atypical angina
or
non-cardiac chest pain/ GIRD?
• In rest
ACS
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Sometimes easy…
• Patient B
• ‘common’:
stable, typical angina
• In rest:
ACS
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SAP ≠ ACS
SAP: is ‘another disease’ than ACS
(both coronary arteriosclerosis)
- SAP: episodes of reversible myocardial
demand/supply mismatch related to ischaemia
in SAP episodes of insufficient coronary flow
in ACS plaque rupture or plaque erosion
typically in those with 30-40% stenosis
WITH THROMBOSIS (RED CLOT)
This impacts diagnosis & therapy
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Stable and ≥ 50% stenosis in one or more coronary
arteries with CAG (2260 personen; 39-76% CAD)
typical
Men
atypical
non-anginal
typical
Women
atypical
Non-anginal
30-39 59 29 18 28 10 5
40-49 69 38 25 37 14 8
50-59 77 49 34 47 20 12
60-69 84 59 44 58 28 17
70-79 89 69 54 68 37 24
>80 93 78 65 76 47 32
Genders et al. Eur Heart J 2011, ESC guidelines SCAD 2013
Diamond and Forrester 1979 revised
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New 2013 ESC guideline SCAD
(who is the GP involved?)
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New 2013 ESC guideline SCAD: SAP, stable
post-ACS, and pre-symptomatic coronary arteriosclerosis
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New 2013 ESC guideline SCAD
Ischaemia is what counts
NOT obstruction
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New 2013 ESC guideline SCAD
Remember:
diagnosis
should
guide
treatment
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Ain’t history taking enough?
What is added value of……
against what reference standard?
1. Exercise test
2. Coronary CTA
3. Stress imaging
SPECT
echo
MRI
PET
What does it measure?
Do the results change treatment?
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Is history taking enough? Back to cases
What is your next step in stable Patient A
(pre-test risk 12-20%) with the wrong reference test
• wait and see (diary, lab, maybe aspirin, ..)
• try PPI (GIRD?)
• resting ECG and exercise test
• to cardiologist for ‘whatshowever’
• to cardiologist for coronary CT angiography
(coronary calcium score)
• to cardiologist for stress testing
• to cardiologist for invasive coronary angiography
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Is history taking enough?
What is your next step in stable Patient B
(pre-test risk 84%) with the wrong reference test
• treat with aspirin, statin, beta-blocker
• first further diagnostic testing by cardiologist
• aspirin and statin and cardiologist for risk assessment
• treat and also to cardiologist for ‘whatshowever’
In letter to cardiologist:
being directive or
the cardiologists turn?
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Before going further...
Ischaemia (functional, macro or micro)
≠
Obstruction of coronary artery (on CAG) (anatomy)
≠
‘Atherosclerotic load’ (Coronary Calcium Score)
Impact on added value of additional testing
Suspicion of ACS:
ECG plus troponin ‘gold standard’ and CAG for locating
the culprit laesion)
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How much is seen of the coronary arteries?
• 15%
• 30%
• 50%
• 70%
• 90%
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ESC guideline SCAD
What about no stenosis but ischaemia (visa versa)?
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New 2013 ESC guideline SCAD
Risk assessment for prognostication
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New 2013 ESC guideline SCAD
what evidence?
What is the
impact on
patient
outcome?
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New 2013 ESC guideline SCAD
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New 2013 ESC guideline SCAD
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Important points to consider
- statines: plaque stabilisation
Higher dosage better effect , but …. more adverse effects
simvastatin 60 mg = rosuvastatin 10 mg = as effective
ezetemibe: not yet
- aspirin 80 to 100 mg: prevention of thrombus formation
PPIs reduce efficiency aspirin (and clopidogrel)!
H2-antagonists NOT
- beta-blockers: improve demand/supply mismatch
possibly prognostic benefits
- nitrates short/long acting: coronary vasodilator (also other arteries !)
take care for sildenafil and other PE5 inhibitors
- calcium channel blockers;diltiazem /verapamil , non-dihydropines
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Don’t forget lifestyle
- increase exercise
- stop smoking
- loose weight
- healthy diet
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Meta-analysis (11RCTs PCI vs medication, 2950 patients)
Katritsis et al, Circulation 2005;111:2906-12
Boden et al NEJM 2007;356:1503-16
Recently in Archives Internal Medicine
In stable angina:
PCI no advantage over OMT regarding
- mortality
- (re) infarction
- need for revascularisation
Stable angina: ‘NO’ PCI
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Conclusions
• History taking is key (and for free)
• Time is your friend when the patient is stable
• Ischaemia and microvasculature are key concepts
• Stable angina is ‘another disease’ than ACS
pathophysiology (no clots vs clots)
diagnostic assessment (history, stress imaging vs CAG)
treatment (no PCI vs (rescue) PCI
• Lack of diagnostic research, including comparison of strategies
• Lack of evidence for PCI when plaques are stable
• Treatment:
– Atherosclerosis/plaque stability statins
– thrombosis (‘white clots’) aspirin
– Supply/demand balance beta-blocker/CCB/nitrates
– ‘all 3’ improving lifestyle
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Good luck with your next patient with stable angina !