Author: Dr Vaibhav Singh, King George’s Medical University
Reference: Harrison’s Principles of Internal Medicine, 21st Edition
Clinical Presentation
Precipitating Factors: Up to 50% of STEMI cases are preceded by factors like physical exercise, stress, or illness.
Timing: A higher incidence of STEMI occurs in the morning hours after waking up.
Main Symptom: Pain is the most common symptom, often deep and visceral, described as heavy, squeezing, or crushing. Pain radiates to the arm, neck and back but never goes below the umbilicus and above the mandible.
Pain Characteristics: Similar to angina but more severe, longer-lasting, and typically occurs at rest, affecting the chest and possibly radiating to arms, neck, or back.
Associated Symptoms: Includes weakness, sweating, nausea, vomiting, anxiety, and a sense of doom.
Differential Diagnosis: Pain can mimic conditions like Acute pericarditis, pulmonary embolism, acute aortic dissection or Costochondritis. In Pericarditis, pain often radiates to Trapezius.
Painless STEMI: More common in diabetic and elderly patients, presenting as breathlessness or pulmonary oedema.
Alternative Presentations: This may include loss of consciousness, confusion, weakness, arrhythmias, embolism, or a drop in blood pressure.
Physical Examination
Patient Behaviour: often anxious, restless, and try to ease pain by moving in bed.
Symptoms: Persistent substernal chest pain with sweating for over 30 minutes is indicative of STEMI.
Vital Signs: Anterior infarcts have tachycardia and/or hypertension; Inferior infarcts exhibit bradycardia and/or hypotension.
Physical Examination: Quiet precordium, apical impulse hard to palpate, and Abnormal systolic pulsation due to possible dyskinetic bulging in anterior wall infarction.
Heart Sounds: Signs of ventricular dysfunctions (3rd & 4th heart sounds, decreased intensity of 1st heart sound, and paradoxical splitting of 2nd heart sound) may be present.
Mitral Valve Dysfunction: systolic murmur may be present.
Pericardial Friction Rub: in transmural STEMI.
Carotid Pulse: Usually decreased, indicating lower stroke volume.
Temp. and BP: Mild fever up to 38°C and a 10–15 mmHg drop in systolic pressure are common post-STEMI.
Lab Tests
ECG:
ST-Segment Elevation: due to a completely blocked epicardial coronary artery.
Q Wave: Most STEMI patients develop Q waves, Some STEMI patients don’t develop Q waves if the blockage is partial, temporary, or if there’s good collateral circulation.
NSTEMI Diagnosis: Ischemic discomfort without ST-segment elevation plus serum cardiac biomarkers indicates NSTEMI.
MI Types: Traditional MI classifications [Q-wave(transmural) & non-Q-wave(non-transmural)] are now replaced by STEMI and NSTEMI as MRI studies suggest Q wave formation on ECG is more linked to infarct size rather than depth.
Biomarkers:
Serum Cardiac Biomarkers: Released from necrotic heart muscle & become detectable in blood when cardiac lymphatics’ capacity is exceeded, causing spillover into the venous circulation. Biomarkers are checked when ECG findings are unclear.
Cardiac Troponins: cTnT and cTnI are highly specific to cardiac muscle so preferred markers for MI diagnosis, remain elevated for 7–10 days after STEMI. may increase up to levels >20 times higher than the upper reference limit (the highest value seen in 99% of a reference population not suffering from MI),
Creatine Phosphokinase(CK): CK rises within 4-8 hours and returns to normal in 48-72 hours. CK is also elevated in skeletal muscle disease, and trauma(even after IM injection). CKMB is more specific to cardiac tissue but can be elevated due to cardiac surgery, myocarditis, & electrical cardioversion.
Effect of Recanalization: Early recanalization leads to quicker biomarker peaking due to rapid washout from the infarct zone.
Other Blood Count Changes: Post-STEMI, polymorphonuclear leukocytosis and elevated ESR are observed.
Imaging
2D Echo: reveals wall motion abnormalities in STEMI, useful for screening in emergencies.
– Can’t differentiate acute STEMI from old myocardial scars or severe ischemia.
– Assists in making treatment decisions, when ECG is non-diagnostic.
– Helps estimate left ventricular function, guiding therapies like RAAS inhibitors.
– also detect right ventricular infarction, ventricular aneurysm, pericardial effusion, and left ventricular thrombus.
Doppler Echocardiography: can detect complications of STEMI: VSD and MR.
Radionuclide Imaging: Less frequently used than echo; sensitive but not specific for acute MI diagnosis as can’t differentiate between acute infarct & chronic scars.
Cardiac MRI: High-resolution cardiac MRI with late enhancement technique using gadolinium effectively detects MI. Gd is administered and images are taken after a 10-min delay. little gadolinium enters normal myocardium(due to tightly packed myocytes), but percolates into the expanded intercellular region of the infarct zone(appears bright).
Management
The prognosis depends on two classes of complications: Electrical- Arrhythmias and mechanical- Pump Failure
Most out-of-hospital deaths from STEMI occur due to: Ventricular Fibrillation (occur within 1st 24 hours, ½ of which occur in 1st hour).
Drugs:
Aspirin- Chewed aspirin (160–325 mg), followed by oral 75–162 mg OD.
Supplemental O2: ineffective, not cost-effective for normal O2 saturation patients.
For hypoxemia, administer O2 (2–4 L/min) for 6–12 hours after MI, then reassess.
Sublingual nitroglycerin: up to three 0.4 mg doses at 5-minute intervals
– reduces chest discomfort, decreases myocardial oxygen demand, and increases oxygen supply by dilating coronary vessels, If chest discomfort continues, start IV NTG
Avoid nitroglycerin:
- low systolic pressure (<90 mmHg)
- suspected right ventricular infarction.
- recent PDE-5 inhibitor use (e.g., sildenafil)
Morphine: IV 2–4 mg every 5 minutes.
-may cause hemodynamic disturbances, treatable with leg elevation or intravenous saline.
-can also cause bradycardia or heart block, especially in inferior infarction, usually responsive to atropine (0.5 mg IV).
IV beta-blockers:
Prerequisite: HR>60, SBP>100, PR interval<0.24s
Metoprolol, 5 mg IV every 2–5 minutes (up to 3 doses), followed by oral dosing.
– controls pain and reduces reinfarction and ventricular fibrillation risks.
– Oral beta-blockers should start within 24 hours, avoided in heart failure, low-output state, cardiogenic shock, or beta-blocker contraindications(2nd / 3rd Degree Block or Asthma).
– Calcium antagonists are not effective in acute settings.
Reperfusion therapy(Fibrinolysis or PCI): For patients with ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads.
– In the absence of ST-segment elevation, fibrinolysis is not helpful.
Primary PCI:
– preferable over fibrinolysis for patients with contraindications to fibrinolytic therapy.
– more effective than fibrinolysis
– Primary PCI is done when diagnosis is uncertain, cardiogenic shock is present, increased bleeding risk, or if symptoms are present for 2-3 hours or when the clot is less easily lysed by fibrinolysis.
– Limitations: high cost and limited availability in hospitals.
Fibrinolysis: should ideally begin within 30 minutes of presentation.
Fibrinolytic agents promote the conversion of plasminogen to plasmin, lysing fibrin thrombi.
TIMI grading system: assesses flow in the infarct-related artery.
- Grade 0: Total occlusion
- Grade 1: some flow
- Grade 2: slow flow
- Grade 3: full perfusion(the goal of reperfusion therapy)
Benefits: reduced infarct size, limited LV dysfunction, fewer complications like septal rupture & cardiogenic shock.
Fibrinolysis remains beneficial up to 12 hours after infarction onset, especially with ongoing chest discomfort and elevated ST segments. Fibrinolysis is preferred in patients presenting within the first hour, logistical delays in PCI, or anticipated PCI delays.
Drugs used: tPA, streptokinase, Tenecteplase(TNK), and reteplase(rPA).
tPA, TNK, and rPA are more effective than streptokinase
- tPA regimen: a 15 mg bolus f/b 50 mg IV over 1st 30 min f/b 35 mg over next 60 min
- Streptokinase: 1.5 MU IV over an hour.
rPA and TNK are administered as bolus doses.
Avoid streptokinase if previously used between 5 days and 2 years ago to prevent allergic reactions.
Absolute C/I: cerebrovascular haemorrhage, recent stroke, SBP>180 & DBP>110, suspected aortic dissection, and active internal bleeding (except menses).
Relative C/I: recent anticoagulant use(INR>2), Prolonged CPR(>10 min) invasive procedures or surgery, bleeding diathesis, pregnancy, Diabetic retinopathy, active peptic ulcer, and controlled severe hypertension.
-The most frequent & serious complication is haemorrhage, particularly intracranial.
– After fibrinolytic therapy, consider cardiac catheterization and angiography in cases of reperfusion failure (i.e. Rescue PCI), and reocclusion/recurrent ischemia(urgent PCI).
