Acute Coronary Syndromes Flashcards
2nd most common cause of death in Scotland
Heart disease
What is ACS
A sudden collection of symptoms suspected or proven to be related to a problem with the coronary arteries which supply the myocardium, causes myocardial ischemia
What is MI
Cell death in heart muscle due to prolonged ischemia
What is cardiac arrest
Abnormal heart rhythm not compatible with life eg ventricular fibrillation, ventricular tachycardia, asystole
Can occur during acute MI or after due to scar
Or be unrelated
What is a heart attack
Doctors usually mean MI
Chronic ischemic heart disease
Stable angina
Acute coronary syndromes
Unstable angina (MI stemi or non-stemi)
ECG of complete coronary occlusion MI
Initial ST elevation then Q waves after 3 days
STEMI (full thickness damage)
Transmural
ECG of partial coronary occlusion MI
No st initially and no q wave after 3 days
Non STEMI
Subendocardial
Diagnosis of MI
Detection cardiac cell death/injury with positive cardiac biomarkers
And one of
Ischaemia symptoms
New ECG changes
Evidence of coronary problem on angiogram or autopsy
Evidence of new cardiac damage on another test
Cardiac biomarkers
Troponin-B1 large infarction eg STEMI B2 Small infarction but could be from arrythmias, PR, cardiac contusion, sepsis, renal failure
Myoglobin
CK-MB
Types of MI
1-spontaneous and due to primary coronary event eg rupture
2- due to imbalance in oxygen supply/demand
3- sudden cardiac death with new ST elevation or LBBB. Coronary thrombus but death
4a- from percutaneous coronary intervention, increased biomarkers
4b- from verified stent thrombosis via angiography or autopsy
5- associated with CABG, new Q waves
Coronary causes of MI other than atherosclerosis
Coronary vasospasm from drugs
Coronary dissection often in young healthy females
Embolism
Inflammation (vasculitis)
Symptoms of acs
Chest pain, may radiate
A discomfort
Not agony
Maybe nausea, sweating, breathlessness
Things to examine and investigations
HR and BP
Murmurs and crackles
ECG
Full bloods
ECG at 3 days for stemi and non-stemi
Stemi- full occlusion and Q waves
Non-stemi- partial occlusion and no Q waves
May have st depression, t wave inversion or be normal
Which artery is the problem
Inferior MI- right coronary artery
Anterior MI- left anterior descending coronary artery
Posterior MI- circumflex coronary artery (may be little ECG change like ST elevation, put leads on back of chest)
Treatments of STEMI
Reperfusion therapy
Mechanical in cath lab for primary PCI
Or pharmacological eg tenecteplase for thrombus if no time, risk of bleeding
Non-stemi patients
Older, more likely to have history, may not be as clear
Unstable angina
Convincing anginal symptoms, rapidly worsening. No cell deaths so no raised troponin
Risks of PCI and angiography
Bleeding Damage mI Coronary perforation Stroke Dye affecting kidney
When CABG instead of pci
Three vessels
Left main stem
Goal of Pharmacotherapy
Goal of therapy is to: Increase myocardial oxygen supply through coronary vasodilation. Decrease myocardial oxygen demand Decrease in heart rate, Decrease blood pressure, Decrease preload or myocardial contractility
Thrombolysis indication
STEMI usually occurs as a result of coronary artery occlusion due to formation of thrombus overlying an atheromatous plaque.
If no PCI within 2 hours then thrombolysis is indicated.
how thrombolytic agents work
Thrombolytic agents available today are serine proteases that work by converting plasminogen to the natural fibrinolytic agent plasmin.
Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot
types of thrombolytic agents
Fibrinolytics are divided into two categories.
1: Fibrin-specific agents such as
alteplase,
reteplase,
tenecteplase
All catalyse conversion of plasminogen to plasmin in the absence of fibrin.
2: Non–fibrin-specific agents such as streptokinase catalyse systemic fibrinolysis.
contraindications for thrombolysis
Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head trauma or facial trauma within 3 months
benefits of thromolysis
Timely thrombolysis associated with:
23% reduction in mortality
39% when used with aspirin
If no evidence of a STEMI ACS Medical Treatment Protocol
Aspirin Tigagrelor/Clopidogrel (blood thinners) Fondaparinux/LMW heparin Intravenous nitrate ( like GTN for lowering bp) Analgesia Beta Blockers
Management to reduce risk from NSTEMI
PCI or CABG Aspirin Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol Heparin (LMWH) Fondaparinux GIIb/IIIa receptor blockers Statins B blockers
Antiplatelet Agents
Low dose ASPIRIN (75-150 mg)
The formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI
Aspirin is a potent inhibitor of platelet thromboxane A2 production
Thromboxane stimulates platelet aggregation and vasoconstriction
The regular daily use of aspirin can In acute MI reduce mortality by 23% in combination with thrombolysis reduce mortality by 42% and reinfarction by 52% In unstable angina reduce MI and death by 50% In secondary prevention reduce reinfarction by 32% and combined vascular events by 25%
but no difference between high and low dose
Clopidogrel and issues with it
Clopidogrel is a prodrug
Inhibits ADP receptor activated platelet aggregation.
Specifically and irreversibly inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross-linking by fibrin
The blockade of this receptor inhibits platelet aggregation by blocking activation of the GP IIb/IIIa pathway.
The IIb/IIIa complex is a receptor for fibrinogen, fibronectin and von WF. Activation of this receptor complex is the “final common pathway” for platelet aggregation and cross-linking of platelets by fibrin.
Always used in combination with aspirin
Relative risk reduction of 21% when used together with aspirin.
Claimed lower incidence of GI bleeding.
However GI bleeding very common
Possible interaction with PPI with a reduction in effect
Evidence for clinical importance of this interaction very poor
Clopidogrel activated by Cyp 2C19
14% of population have low CYP2C19 levels and demonstrate resistance to clopidogrel
Prasugrel
Member of the thienopyridine class of ADP receptor inhibitors, like clopidogrel Compared to clopidogrel prasugrel inhibits ADP–induced platelet aggregation more rapidly, more consistently,
Low Molecular Weight Heparin
Low molecular weight heparin is an integral component of the ACS protocol
Several different products, probably all similar in effect:
Enoxaparin
Dalteparin
Tinzeparin
Fondaparinux
Fondaparinux
A Selective Inhibitor of Factor Xa Single chemical entity Synthetic pentasaccaride Highly selective for antithrombin Once-daily administration No need for platelet monitoring
Glycoprotein IIb/IIIa Receptor Inhibitors
GPIIb/IIIa is an integrin complex found on platelets
receptor for fibrinogen aids in platelet activation.
Platelet activation by ADP(blocked by clopidogrel) leads to a conformational change in platelet GPIIb/IIIa receptor that induces binding to fibrinogen.
The GPIIb/IIIa receptor is a target of several drugs including abciximab, tirofiban
Intravenous GPIIb/IIIa inhibitors block platelet aggregation by inhibiting fibrinogen binding to a conformationally activated form of the GPIIb/IIIa receptor on two adjacent platelets.
A meta-analysis involving 29570 showed a 9% RRR in death or non-fatal MI with GPIIb/IIIa inhibitors
major adverse effect in GPIIb/IIIa inhibitors
The major adverse effect is bleeding:
major bleeding occurrs in 1.4% of patients
minor bleeding in 10.5%.
Blood transfusion required to terminate bleeding and to improve bleeding-related anaemia in 4.0% of all patients.
Beta blockers post MI
for secondary prevention in the survivors of an acute MI.
I.V.atenolol or metoprolol reduce mortality following an acute MI
Oral beta blockade started weeks or months post MI reduce cardiac death
Beta-blockers competitively inhibit the myocardial effects of circulating catecholamines (stress hormones adrenaline and noradrenaline) and reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility.
Evidence for benefitshowing that beta-blocker was associated with a significant (RRR) of mortality
In patients at risk of developing cardiogenic shock (i.e. age >70 years, heart rate >110 beats/min, systolic blood pressure < 120 mmHg) the observed shock or death rate was significantly increased in patients receiving beta-blockers within 24 h of hospital admission.
Avoid in these and patients with symptoms possibly related to coronary vasospasm or cocaine use.
