ST Elevation MI

Answer 1

-Atherosclerosis
-Vulnerable plaque formation
-Plaque rupture or erosion event
-Coronary thrombosis (inflammatory cascade)
-Complete and sustained coronary occlusion
-Myocardial damage (size of area at risk/ duration of occlusion)

Question 2

STEMI symptoms

Answer 2

ACUTE AND SEVERE

-Chest pain- radiate?
-Shortness of breath
-Collapse/ cardiac arrest
-Associated autonomic features- pallor, sweating, nausea, vomiting

Question 3

Describe STEMI chest pain

Answer 3

-Acute retrosternal pain
-Typically described as tight pressure/ heavy feeling
-Commonly radiates to the shoulders, arms, jaw and neck

Question 4

Describe associated autonomic features of STEMI

Answer 4

-Pallor
-Diaphoresis or sweating
-Nausea and vomiting
-Light-headedness
-Feeling of anxiety

Question 5

Clinical signs of STEMI

Answer 5

-Inspection: unwell, pallor, sweating, breathless, in pain
-Palpation: tachycardia/ bradycardia, clammy, cold to touch, hyper/hypotension (cardiogenic shock)
-Auscultation: occasional new heart murmur (mitral valve dysfunction, VSD), signs of heart failure including pulmonary oedema

Question 6

STEMI investigations

Answer 6

-Coronary angiogram and percutaneous coronary intervention
-ECG= lesion location, duration of damage
-Troponin

Question 7

Definition of STEMI ECG

Answer 7

-ST elevation in 2 contiguous leads:
=≥ 2.5mm in V2-V3 in men <40 years old
=≥ 2mm in V2-V3 in men ≥40 years old
=≥ 1.5mm in V2-V3 in women
=≥ 1mm in all other leads
=New LBBB

Question 8

Describe STEMI ECG

Answer 8

-ST elevation in II, III and aVF with reciprocal changes (ST depression in I and aVL) -> inferior Myocardial infarction (RCA)
-Anterior-spetal= V1-4= LAD (left anterior descending)
-Lateral= 1, aVL, V5, V6= LCx

Question 9

Aims of STEMI treatment

Answer 9

-Restore adequate coronary blood flow ASAP

-Promote reperfusion
-Pain relief
-Supportive care
-Reduce mortality

Question 10

STEMI care treatment

Answer 10

-Activate primary percutaneous coronary intervention (PPCI) pathway or coronary reperfusion therapy

=Oxygen therapy if evidence of hypoxia (<94%)
=Morphine for pain and anxiety management (+ antiemetic)
=Nitrates (GTN spray) for ischaemic pain management (sublingual/IV caution if hypotensive)
=Anti-platelet (aspirin 300mg +clopidogrel/prasugrel if PCI/ticagrelor) loading dose.

MONA

-PCI
=Should be offered if the presentation is within 12 hours of symptoms AND PCI can be delivered within minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
=If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
=Drug-eluting stents are now used. Previously ‘bare-metal’ stents were sometimes used but have higher rates of restenosis
=Radial access is preferred to femoral access
=DAPT: if the patient is not taking an oral anticoagulant: prasugrel, if taking an oral anticoagulant: clopidogrel. Unfractionated heparin with bailout glycoprotein 2b/3a inhibitor

-Fibrinolysis
=Should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
=A practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient’s ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI
=tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile
=An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation
if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis
for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Question 11

Glycaemic control in DM patients with ACS

Answer 11

it recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l
intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as ‘DIGAMI’) regimes are not recommended routinely

Question 12

Post-STEMI care

Answer 12

-Monitoring and initial management in a Coronary Care Unit
-Echocardiogram to determine effect on cardiac function and need for further medical therapy
-Establish appropriate medical therapy
=Beta blocker
=ACEi/ARB
=DAPT (aspirin and clopidogrel)
-Identify and address cardiovascular risk factors
=Hypercholesterolemia management (statin)
=Hypertension management
=Diabetes management
=Smoking cessation

=post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months
=post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months
=this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events

-diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish
exercise: advise 20-30 mins a day until patients are ‘slightly breathless’
sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil

patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

Question 13

DAPT

Answer 13

post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months
post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months
this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events

Question 14

STEMI medication

Answer 14

-Beta blocker
-ACE inhibitor/ ARB
-Dual antiplatelet therapy (aspirin + clopidogrel/ prasugrel/ ticagrelor)

Question 15

Prognosis and long-term care of STEMI

Answer 15

-Cardiac rehabilitation
-Follow up
-Secondary prevention and lifestyle changes to manage risk factors of cardiovascular disease
-Future prognosis using echocardiography and risk assessment scores

-GRACE (Global Registry of Acute Coronary Events)
=age
=development (or history) of heart failure
=peripheral vascular disease
=reduced systolic blood pressure
=Killip class (1: no signs of HF, 2: lung crackles S3, 3: frank pulmonary oedema, 4: cardiogenic shock)
=initial serum creatinine concentration
=elevated initial cardiac markers
=cardiac arrest on admission
=ST segment deviation

Question 16

Complications of MI

Answer 16

-Cardiac arrest
=Patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.

-Cardiogenic shock
=If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture. Patients may require inotropic support and/or an intra-aortic balloon pump.

-Chronic heart failure
=If the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.

-Tachyarrhythmias
=Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.

-Bradyarrhythmias
=Atrioventricular block is more common following inferior myocardial infarctions.

-Pericarditis
=Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.
=Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

-Left ventricular aneurysm
=The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

-Left ventricular free wall rupture
=This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds, hypotension, muffled HS). Urgent pericardiocentesis and thoracotomy are required.

-Ventricular septal defect
=Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. Left to right shunt. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.

-Acute mitral regurgitation
=More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. ECH shows regurgitation across valve. Patients are treated with vasodilator therapy but often require emergency surgical repair.