IHD symposium Flashcards
Heart attack process
Heart disease develops over time as fatty deposits narrow coronary arteries, restricting blood flow to the heart
Coronary artery blocks – usually by a clot resulting from ruptured atherosclerotic plaque
Blood flow is restricted and a heart attack begins
If blockage continues, parts of the heart muscle start to die
Heart may stop beating, leading to cardiac arrest
Stopping a heart attack
Quick action and medical treatment
Dead muscle cannot be restored
Rapid treatment of STEMI
Antiplatelet agents (aspirin + clopidogrel)
AND
“Clot-busting” drug (thrombolysis): pharmacologically break up clots, restoring blood flow
‘Primary’ angioplasty (balloons, stents): artery is mechanically reopened, restoring blood flow
Revascularisation therapies - PCI
Clinical evidence to suggest the superiority of primary PCI over thrombolysis1
The NIAP* suggests that PPCI is most effective if delivered within 150mins of the patient’s call for help (‘call-to-balloon’ time)1
Revascularisation therapies - Thrombolysis
Treatment of choice in STEMI when primary PCI cannot be performed
Aim to initiate within 90mins of patient calling for help (‘call-to-needle’) or within 30mins of arrival at hospital (‘door-to-needle’)
Thrombolysis limitations
Despite therapeutic advances in thrombolytics only 50% restore normal coronary flow after 90 minutes
Increased bleeding risks with thrombolysis (haemorrhagic stroke)
Lack of reliable non-invasive methods for assessing patency of infarct related artery
Therapeutic goals in STEMI
restore epicardial vessel patency
limit myocardial necrosis
control symptoms
Anti-platelelet therapy
anti-ischaemic therapy
secondary prevention
IHD 2nd prevention
Antiplatelet therapy
aspirin
clopidogrel /prasugrel /ticagrelor
Statin ACE inhibitors Beta blockers Smoking cessation Lifestyle modification