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Masterclass on emerging priorities in CVD

Treatment of angina pectoris: The role of primary care

Dr Frans Rutten

Utrecht, The Netherlands

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?

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

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)

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

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 !

Diagnosis can be difficult…

• Patient A

• ‘common’ situations

stable, atypical angina

or

non-cardiac chest pain/ GIRD?

• In rest

ACS

Sometimes easy…

• Patient B

• ‘common’:

stable, typical angina

• In rest:

ACS

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

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

New 2013 ESC guideline SCAD

(who is the GP involved?)

New 2013 ESC guideline SCAD: SAP, stable

post-ACS, and pre-symptomatic coronary arteriosclerosis

New 2013 ESC guideline SCAD

Ischaemia is what counts

NOT obstruction

New 2013 ESC guideline SCAD

Remember:

diagnosis

should

guide

treatment

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?

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

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?

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)

How much is seen of the coronary arteries?

• 15%

• 30%

• 50%

• 70%

• 90%

ESC guideline SCAD

What about no stenosis but ischaemia (visa versa)?

New 2013 ESC guideline SCAD

Risk assessment for prognostication

New 2013 ESC guideline SCAD

what evidence?

What is the

impact on

patient

outcome?

New 2013 ESC guideline SCAD

New 2013 ESC guideline SCAD

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

Don’t forget lifestyle

- increase exercise

- stop smoking

- loose weight

- healthy diet

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

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

Good luck with your next patient with stable angina !