Myocardial Infarction Rupert and Fergus rupert.larkin@warwick.ac.uk F.M.A.Liggins@warwick.ac.uk

What is Myocardial Infarction? MI is defined as..

What is Myocardial Infarction? MI is defined as.. ‘Myocardial cell death occurring due to a prolonged mismatch between perfusion and demand, usually caused by an occlusion in the coronary arteries.’ MI is a type of Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome (ACS) ACS refers to acute myocardial ischaemia caused by atherosclerotic coronary disease and includes: ST-elevation MI (STEMI) [Myocyte death] Non ST-elevation MI (NSTEMI)  [Myocyte death] Unstable angina These terms are used as a framework for guiding management.

Acute Coronary Syndrome (ACS) STEMI NSTEMI Unstable Angina Should be considered for immediate reperfusion therapy NSTEMI & UA patients do not benefit from immediate reperfusion therapy (note that reperfusion therapy may be chosen later, just not as first line treatment)

Signs and Symptoms of MI

Signs and Symptoms of MI Acute central chest pain (heavy/crushing, can radiate to jaw and left arm)  lasting >15 mins Nausea Sweatiness Dyspnoea Palpitations Signs;

Signs and Symptoms of MI Acute central chest pain (heavy/crushing, can radiate to jaw and left arm)  lasting >15 mins Nausea Sweatiness Dyspnoea Palpitations Signs; Distress Anxiety Pallor Tachycardia Raised BP Signs of heart failure – JVP, 3rd heart sounds, basal crepitation's (why crepitation's?) Pan-systolic murmur Why crepitation's? MII’s can cause the left side of the heart to stop functioning correctly if the infarct is in the left ventricular wall. Left sided heart failure results in reduced left ventricular stroke volume and therefore the left side of the heart is not able to pump out all the blood arriving from the pulmonary system. The consequence of this failure is pulmonary congestion due to a backup of blood. Pul. Congestion  Increased Pulmonary system pressure  Increased intravascular hydrostatic pressure  Leaky vessels  Pulmonary oedema  Basal crepitation's on auscultation.

Risk Factors Non-modifiable; Modifiable;

Risk Factors Non-modifiable; Age Male FHx of IHD Modifiable;

Risk Factors Non-modifiable; Modifiable; Age Male FHx of IHD Smoking Hypertension DM Hyperlipidaemia Obesity Sedentary lifestyle

Differential Diagnosis (think central chest pain!)

Differential Diagnosis (think central chest pain!) Angina Pneumothorax Pericarditis Myocarditis PE Costrochondritis Oesophageal reflux/spasm Aortic dissection (usually pain between shoulder blades) Anxiety/panic attack

Initial Management of ACS symptoms What do you do initially? Remember, you don’t know if its STEMI/NSTEMI/UA yet! 1st  2nd  3rd 

Initial Management of ACS symptoms What do you do initially? Remember, you don’t know if its STEMI/NSTEMI/UA yet! 1st 12-lead ECG 2nd  IV access: FBC, Glucose, lipids, U & E, Cardiac Enzymes 3rd  Stabilisation & symptomatic relief!

Initial Management of ACS symptoms Stabilisation & symptomatic relief Mechanism by which GTN relieves pain/discomfort from MI/Angina depends on the pathological mechanism causing the inadequate perfusion. GTN is metabolised to Nitric Oxide in endothelial cells which causes vasodilation. This has several pain relieving downstream effects: Reduces myocardial oxygen demand secondary to venous dilation (reduced preload) and arteriolar dilation (reduced afterload). The vasodilatory effect is much larger on veins. The effect of less preload and less afterload is reduced cardiac contractility and myocardial wall tension  decreased myocardial O2 demand and increased myocardial perfusion during systole. Increased myocardial perfusion, via dilation of the coronary arteries. Relief of coronary artery vasospasm (more useful for Angina relief, especially Prinzmetal’s vasospastic angina)

Initial Management of ACS symptoms Stabilisation & symptomatic relief  [MONA] Morphine  Pain relief  Reduced associated sympathetic activity  Decreased myocardial O2 demand Oxygen Nitrates  GTN – how does this work to relieve the pain? Aspirin Key question for subsequent management is whether there is STEMI or not Mechanism by which GTN relieves pain/discomfort from MI/Angina depends on the pathological mechanism causing the inadequate perfusion. GTN is metabolised to Nitric Oxide in endothelial cells which causes vasodilation. This has several pain relieving downstream effects: Reduces myocardial oxygen demand secondary to venous dilation (reduced preload) and arteriolar dilation (reduced afterload). The vasodilatory effect is much larger on veins. The effect of less preload and less afterload is reduced cardiac contractility and myocardial wall tension  decreased myocardial O2 demand and increased myocardial perfusion during systole. Increased myocardial perfusion, via dilation of the coronary arteries. Relief of coronary artery vasospasm (more useful for Angina relief, especially Prinzmetal’s vasospastic angina)

ECG The ECG can tell you about the pattern of ischaemia/infarction e.g. STEMI, NSTEMI, UA Helps decide upon management Can diagnose arrhythmias Transmural infarction = one which traverses the full thickness of the myocardium

ECG - STEMI STEMI (classical presentation) Transmural infarction = one which traverses the full thickness of the myocardium

ECG - STEMI STEMI (classical presentation) Minutes-hours  Tall T waves, ST elevation Usually indicates a transmural infarction (full wall thickness) Transmural infarction = one which traverses the full thickness of the myocardium

ECG - NSTEMI NSTEMI

ECG - NSTEMI NSTEMI T wave depression Non-specific changes In 20% MI, ECG may be normal initially

CXR Why perform a CXR? Look for…

CXR Why perform a CXR? Look for… Do not delay treatment for CXR Help rule out differentials for chest pain/dyspnoea MI can cause heart failure and consequent pulmonary oedema – how? Look for… Cardiomegaly Pulmonary oedema Widened mediastinum  could indicate aortic rupture Do not delay treatment for CXR

Cardiac Enzymes Cardiac Troponin T and I - What is the normal role of these? Most sensitive and specific markers for myocardial necrosis Levels increase 3-12 hours from onset of chest pain Peak 24-48 hours Return to normal levels in 5-14 days Creatine Kinase 3 types of CK, CK-MB is variant used in diagnosis of acute MI. Levels begin to ↑ 3-12hrs after event, peak within 24hrs and return to normal after 48-72 hrs. MI sensitivity = 95% with high specificity - What are the definitions of these? Myoglobin - What is it? Levels rise within 1-4 hours. High sensitivity, low specificity Troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue. In a relaxed muscle, tropomyosin blocks the attachment site for the myosin crossbridge, thus preventing contraction. When the muscle cell is stimulated to contract by an action potential, calcium channels open in the sarcoplasmic membrane and release calcium into the sarcoplasm. Some of this calcium attaches to troponin, which causes it to change shape, exposing binding sites for myosin (active sites) on the actin filaments. Myosin's binding to actin causescrossbridge formation, and contraction of the muscle begins. Sensitivity = The proportion of people who have the disease that the test correctly identifies as disease positive Specificity = The proportion of people who do not have the disease that the test correctly identifies as disease negative Myoglobin is the muscle equivalent of Hb, i.e. an oxygen binding protein found in myocytes.

Diagnosis

Management of STEMI STEMI  Reperfusion therapy! Percutaneous Coronary Intervention (PCI) (stenting) if <90 mins since first medical contact Thrombolysis of PCI not available within first 90 mins of first medical contact Efficacy decreases with time from symptom onset – ideally initiate within 3 hours Check for contraindications e.g. previous intracranial haemorrhage E.g. Alteplase (Tissue Plasminogen Activator)

Management of NSTEMI Immediately Then Beta-blocker e.g. Atenolol P2Y12 inhibitor e.g. Clopidogrel (+ consider LMW Heparin) Assess risk of further CV events e.g. GRACE or TIMI score Then Decide whether the patient requires an invasive or non-invasive treatment approach  Assess risk of further CV events using GRACE or TIMI score + Coronary angiogram to help decide Invasive revascularisation (stenting) for high risk patients such as those with  Elevated cardiac biomarkers (troponin T or I) New or presumably new ST-segment depression High risk score or Diabetes PCI during previous 6 months Prior CABG Non-invasive treatment  Conservative, early medical management strategy for those without above high risk features and with a low risk score. Guidelines recommend that an invasive approach is appropriate if any of the following high-risk features are present: Recurrent angina or ischaemia at rest or with low-level activities despite intensive medical therapy Elevated cardiac biomarkers (troponin T or I) New or presumably new ST-segment depression Signs or symptoms of heart failure, or new or worsening mitral regurgitation High-risk findings from non-invasive testing Haemodynamic instability Sustained ventricular tachycardia PCI within 6 months Prior CABG High-risk score (i.e., TIMI, GRACE) Mild to moderate renal dysfunction Diabetes mellitus Reduced left ventricular function (ejection fraction <40%).