ST-Elevation Myocardial Infarction (STEMI)
Definition
ST-Elevation Myocardial Infarction (STEMI) is the most acute manifestation of coronary artery disease, characterized by ischaemic chest pain in conjunction with new ST-segment elevation in at least two contiguous electrocardiogram (ECG) leads or a new left bundle branch block (LBBB), which is subsequently confirmed by a rise and fall in cardiac biomarkers (7). It represents a life-threatening medical emergency caused by the total occlusion of a coronary artery (392).
Epidemiology
In Malaysia, ischaemic heart disease is the principal cause of death, with STEMI being a major contributor to this burden (393). According to the National Cardiovascular Disease Database (NCVD-ACS) Registry for 2020-2021, STEMI accounted for 50.3% of all Acute Coronary Syndrome (ACS) admissions, with 7,627 reported cases (398). A defining feature of the Malaysian STEMI population is the young age of presentation; the mean age was 56.0 years, and a significant 31.4% of patients were under 50 (408, 409). The condition disproportionately affects males (86.5%) (411). By ethnicity, Malays constitute the largest group of patients at 57.9%, followed by Chinese (15.9%) and Indian (14.8%) populations (412). The patient profile is further characterized by a high prevalence of modifiable risk factors, including hypertension (62.1% of all ACS), diabetes mellitus (43.7% of STEMI patients), and current smoking (37.0% of all ACS) (416, 419, 422). Globally, while STEMI is a major health issue, the Malaysian patient profile is notably "younger and sicker" compared to many Western nations (405, 409).
Pathophysiology
The underlying mechanism of STEMI is the rupture or erosion of an atherosclerotic plaque within a coronary artery (550). This event triggers the coagulation cascade and platelet aggregation, leading to the formation of an occlusive thrombus (550). The complete blockage of the artery interrupts blood flow to the downstream myocardium, causing transmural ischaemia. If not resolved rapidly, this leads to irreversible myocardial cell death (necrosis), manifesting as the clinical syndrome of STEMI (441).
Clinical Presentation
The classic presentation is sudden-onset, crushing central chest pain, often radiating to the left arm or jaw, and associated with diaphoresis, nausea, and dyspnoea (473).
Diagnostic Clues: The key diagnostic feature is the characteristic chest pain combined with persistent ST-segment elevation on a 12-lead ECG (473).
Common Symptoms (>50%):
Chest pain (Ischaemic-type)
Diaphoresis (sweating)
Dyspnoea (shortness of breath)
Less Common/Atypical Symptoms (10-50%): Atypical presentations are more common in women, the elderly, and patients with diabetes (451, 622, 624). These can include:
Epigastric pain or indigestion
Isolated fatigue or weakness
Jaw, neck, or back pain
Syncope or pre-syncope
⚠️ Red Flag Signs & Symptoms:
Persistent chest pain despite initial treatment
Signs of cardiogenic shock (hypotension, tachycardia, cool peripheries, altered mental state)
Acute pulmonary oedema
New cardiac murmurs, suggesting a mechanical complication
Complications
Cardiovascular:
Cardiogenic Shock: A state of severe end-organ hypoperfusion due to profound left ventricular dysfunction, complicating about 10.6% of STEMI cases in Malaysia and carrying a very high mortality rate (579, 580).
Heart Failure: Graded by the Killip classification; a higher class indicates more severe failure and a worse prognosis (435).
Arrhythmias: Ventricular fibrillation and ventricular tachycardia are common life-threatening arrhythmias in the acute phase (576).
Mechanical Complications: Including ventricular septal rupture, free wall rupture, and papillary muscle rupture leading to acute mitral regurgitation (586).
Right Ventricular Infarction: Occurs in the context of an inferior wall MI (586).
Thromboembolic:
Left ventricular thrombus formation with risk of systemic embolization (e.g., stroke).
Prognosis
Despite advances in therapy, STEMI in Malaysia carries a significant mortality burden. The NCVD 2020-2021 report indicates an in-hospital mortality rate of 9.4%, a 30-day mortality of 12.1%, and a 1-year mortality of 18.0% (428, 429). These rates are considerably higher than in developed Asia-Pacific nations (430). Key predictors of poor prognosis include a higher Killip class, a high TIMI risk score, and the absence of timely reperfusion therapy (435). For patients who do not receive any form of reperfusion, the 1-year mortality is a staggering 27.9% (538). Conversely, for those who undergo Primary Percutaneous Coronary Intervention (PPCI), the 1-year mortality is significantly lower at 9.1% (537).
Differential Diagnosis
Aortic Dissection: This is a critical differential due to the shared feature of severe, sudden-onset chest pain. However, the pain in aortic dissection is often described as "tearing" or "ripping," may radiate to the back, and can be associated with unequal blood pressures in the arms or neurological deficits. A widened mediastinum on chest X-ray and a normal ECG would increase suspicion.
Pulmonary Embolism: Consider this diagnosis, especially if the patient presents with pleuritic chest pain, dyspnoea, and tachycardia. Points against STEMI include the absence of classic ECG changes (though right heart strain patterns can be seen) and a clinical context of immobility or hypercoagulability.
Pericarditis: This condition can present with central chest pain and ECG changes, including ST elevation. However, the pain is typically sharp, pleuritic, and relieved by sitting forward. The ST elevation in pericarditis is usually diffuse (widespread across many leads) and concave, unlike the localized, convex ST elevation seen in STEMI.
Investigations
Immediate & Bedside Tests
12-Lead ECG: This is the single most important immediate test, mandatory within 10 minutes of first medical contact (FMC) (473). Its purpose is to rapidly identify the characteristic ST-segment elevation or new LBBB (the rationale), which confirms the diagnosis and triggers the entire reperfusion pathway (the action).
Diagnostic Workup
First-Line Investigations:
Cardiac Biomarkers (e.g., Troponin T/I): While a rise and fall in these markers retrospectively confirms myocardial necrosis (the rationale), initial treatment decisions must not be delayed awaiting these results (the action) (473). Serial measurements are crucial for confirming the diagnosis and assessing infarct size.
Gold Standard:
Coronary Angiography: This is the definitive diagnostic test, as it directly visualizes the coronary anatomy and identifies the occluded vessel (the rationale), allowing for immediate therapeutic intervention via PCI (the action). It is performed emergently as part of a PPCI strategy (495).
Monitoring & Staging
Full Blood Count: An urgent Full Blood Count is essential to identify anaemia, which could exacerbate ischaemia, or thrombocytopenia (the rationale), which is critical for assessing bleeding risk before starting potent antithrombotic therapy (the action).
Renal Profile: Assessing baseline renal function is crucial as it influences the choice and dosing of certain medications (e.g., anticoagulants) and risk of contrast-induced nephropathy (the rationale), thereby guiding a safer therapeutic strategy (the action) (600, 601).
Echocardiogram: A bedside echocardiogram helps to assess left ventricular function, identify regional wall motion abnormalities confirming the territory of the infarct (the rationale), and rule out mechanical complications, which is vital for risk stratification and immediate management changes (the action) (568).
Management
Management Principles
The management of STEMI focuses on two urgent, parallel goals: immediate medical stabilisation to prevent arrhythmias and limit infarct size, and achieving rapid, complete, and sustained reperfusion of the occluded coronary artery (441, 547).
Acute Stabilisation (The First Hour)
Airway/Breathing: Administer supplemental oxygen via a nasal cannula or mask only if oxygen saturation is <90% (the action), to correct hypoxia without causing hyperoxic vasoconstriction that could worsen myocardial injury (the rationale) (482).
Circulation: Secure IV access (preferably two large-bore cannulas) and provide immediate pain relief (475). For pain and vasodilation, administer sublingual Glyceryl Trinitrate (GTN), provided the patient is not hypotensive (SBP <90 mmHg) or has suspected right ventricular infarction (the action), as GTN reduces preload and myocardial oxygen demand (the rationale) (479). For severe, persistent pain, intravenous Morphine can be given cautiously (the action) as it is a potent analgesic and anxiolytic (the rationale) (480).
Disability (Antiplatelet Therapy): Administer a loading dose of Aspirin 300 mg (chewable) and a loading dose of a P2Y12 inhibitor immediately upon diagnosis (477, 478). This dual antiplatelet therapy (DAPT) is crucial to inhibit platelet aggregation (the rationale), thereby preventing further thrombus propagation and re-occlusion (the action) (552).
Definitive Therapy
The choice of reperfusion is dictated by time and logistics. The goal is to open the artery as quickly as possible (491).
First-Line Treatment (Gold Standard): Primary Percutaneous Coronary Intervention (PPCI)
PPCI is the preferred strategy if it can be performed by an experienced team within specific timeframes (497).
Indication: All eligible STEMI patients presenting to a PCI-capable hospital or who can be transferred to one in a timely manner (497).
Timeline: The FMC-to-device (balloon inflation) time should be <90 minutes if at a PCI-capable hospital, or <120 minutes if requiring transfer from a non-PCI hospital (500, 501).
Second-Line (When PPCI is not timely): Fibrinolytic Therapy
This is the recommended strategy if the anticipated time from diagnosis to PPCI is >120 minutes (523).
Agent: Fibrin-specific agents like Tenecteplase are preferred, given as a single weight-adjusted IV bolus (521).
Timeline: The goal is a door-to-needle (or FMC-to-needle) time of <30 minutes (524).
Pharmaco-invasive Strategy: After successful fibrinolysis, all patients should be transferred to a PCI-capable centre for coronary angiography within 3 to 24 hours (a Class I, Level A recommendation) (the action), as this approach combines early pharmacological reperfusion with the superior long-term outcomes of definitive PCI (the rationale) (530). If fibrinolysis fails, immediate rescue PCI is indicated (532).
Supportive & Symptomatic Care
Anticoagulation: Administer parenteral anticoagulants (e.g., Enoxaparin or Unfractionated Heparin) alongside reperfusion therapy to prevent further thrombus formation (559).
Beta-blockers: Initiate oral beta-blocker therapy (e.g., Bisoprolol or Carvedilol) within the first 24 hours if there are no signs of heart failure or other contraindications (the action), as they reduce myocardial oxygen demand, arrhythmias, and long-term mortality (the rationale) (566, 567).
High-Intensity Statins: Start high-dose statin therapy (e.g., Atorvastatin 80 mg) as early as possible, regardless of baseline cholesterol levels (the action), for its pleiotropic effects including plaque stabilization and anti-inflammation, which improve outcomes (the rationale) (564, 565).
ACE Inhibitors/ARBs: Start an ACE inhibitor (e.g., Perindopril) or an ARB within 24 hours, especially in patients with anterior MI, heart failure, or LVEF ≤40% (the action), to prevent adverse ventricular remodelling and reduce the risk of death and heart failure (the rationale) (568, 569).
Key Nursing & Monitoring Instructions
Continuous cardiac monitoring for at least 24-48 hours to detect arrhythmias.
Strict hourly monitoring of vital signs (BP, HR, RR, SpO2) during the acute phase.
Monitor closely for signs of reperfusion (e.g., pain resolution, resolution of ST elevation) or failed fibrinolysis (persistent pain/ST elevation).
Inform medical staff immediately if SBP <90 mmHg, new arrhythmias occur, or patient develops chest pain or shortness of breath.
Long-Term Plan & Patient Education
Discharge planning involves comprehensive education on medication adherence, lifestyle changes, and follow-up (634).
Secondary Prevention: Lifelong adherence to Aspirin, a P2Y12 inhibitor for up to 12 months, a high-intensity statin, a beta-blocker, and an ACEI/ARB is crucial (637).
Lifestyle Modification: This is the single most impactful intervention. Counsel strongly on smoking cessation (referral to MQuit program), adopting a heart-healthy diet (e.g., Malaysian "Quarter Quarter Half" plate), and engaging in regular physical activity (30-60 minutes, most days of the week) (646, 648, 649, 652).
Cardiac Rehabilitation: All patients should be referred to a structured cardiac rehabilitation program, which is a Class I recommendation to optimize physical and psychological recovery (655).
When to Escalate
Call Your Senior (MO/Specialist) if:
The patient has persistent chest pain or haemodynamic instability (hypotension, tachycardia) despite initial therapy.
The ECG shows evidence of failed fibrinolysis 60-90 minutes post-administration (less than 50% ST-segment resolution).
The patient develops any new neurological signs (suggesting a stroke).
The patient develops acute pulmonary oedema or a new cardiac murmur.
Life-threatening arrhythmias (e.g., VT, VF) occur.
Referral Criteria:
Immediate discussion with the on-call Cardiologist upon diagnosis of STEMI to decide on reperfusion strategy.
Refer to the Nephrology team if the patient develops acute kidney injury.
All patients who receive fibrinolysis must be discussed with and transferred to a PCI-capable centre for a pharmaco-invasive approach (530).
References
(1) Ministry of Health Malaysia. (2019). Management of Acute ST-Elevation Myocardial Infarction (4th Edition). Putrajaya: MOH. https://www.moh.gov.my/moh/resources/penerbitan/CPG/CPG%20STEMI%202019.pdf
(2) National Heart Association of Malaysia. (2023). Annual Report of the NCVD-ACS Registry 2020-2021. http://www.acrm.org.my/ncvd/documents/report/ACS%20Report%202020-2021_Final.pdf
(3) Wan Ahmad, W. A., & Sim, K. H. (Eds.). (2024). A Clinical Review of ST-Elevation Myocardial Infarction (STEMI) in the Malaysian Context: From Guidelines to Real-World Practice. (Provided PDF document)
(Note: All numerical citations in the text refer to the page or finding number within the provided PDF document, "Malaysian STEMI Clinical Review.pdf", which synthesizes data from the primary Malaysian CPG and NCVD reports.)
