- Clinical science
Acute coronary syndrome (ACS) is characterized by acute chest pain due to partial or complete occlusion of a coronary artery that results from an unstable (often ruptured) plaque in the setting of advanced coronary heart disease. There are three clinical entities grouped under ACS: unstable angina pectoris (AP), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). These conditions are often difficult to distinguish from one another based on clinical symptoms. Chest pain typically radiates to the neck, epigastrium, upper back, and/or left arm. Additionally, autonomic symptoms such as diaphoresis, nausea, and vomiting are common. Myocardial infarction can also occur without prior angina pectoris and is often the first manifestation of coronary heart disease (see and ). ECG and laboratory tests are important diagnostic tools. In contrast to angina pectoris, NSTEMI and STEMI are characterized by the destruction of cardiac muscle tissue, which results in elevated cardiac enzymes in the blood (i.e., troponin T after 3–4 hours). Unlike unstable AP and NSTEMI, STEMI results in specific ECG changes (e.g., ST-segment elevation), which help to determine the location and acute stage of the infarct. ACS is initially managed with a standard algorithm consisting of blood thinners, analgesics, antiarrhythmic drugs, and O2 administration. Further management depends on diagnostic results, which should be quickly evaluated to ensure the best prognosis. Cardiac catheterization should be performed as soon as possible in STEMI and electively within (2–72 h) in NSTEMI. Other interventions should be carried out as soon as possible ("time is muscle"). Unstable AP may stabilize, in which case it can be understood as a temporary ischemic event, or may progress to myocardial infarction. Regardless, unstable AP should initially be managed in the same way as myocardial infarction, except for fibrinolysis. The decision to conduct early catheterization for unstable AP primarily depends on whether the patient's prognosis and whether he/she responds to medical therapy.
Acute coronary syndrome may manifest either as sudden cardiac death (SCD) or as one of the following conditions:
Symptoms typical of myocardial infarction (persisting ≥ 20 min)
- Unlike stable angina, symptoms occur at rest or on minimal exertion.
- Angina pectoris occurring for the first time ( ) or that worsens over time (crescendo angina)
- Angina pectoris occurring in a patient with a history of myocardial infarction
- Negative troponin T
- The sudden death of myocardial cells when they are critically undersupplied with blood due to obstruction of the coronary arteries
- Symptoms typical of myocardial infarction (persisting ≥ 20 min)
- Normal or nonspecific ECG findings
- Positive troponin T (mildly increased)
- Symptoms typical of myocardial infarction (persisting ≥ 20 min)
- ST elevation lasting ≥ 20 min or a new-onset left bundle branch block
- Positive troponin T (dramatically increased)
- ∼ 1.5 million cases of myocardial infarction in the US per year
- Approximately 40% of all myocardial infarctions occur in the early morning hours.
- ♂ > ♀ (3:1)
- Only 70% of all patients with myocardial infarction reach the emergency room alive; around 50% of all infarct patients die within the first 4 weeks.
- 5–10% of all infarct patients die within 2 years of being discharged from the hospital because of sudden cardiac death.
Epidemiological data refers to the US, unless otherwise specified.
Unstable plaque development
- Coronary artery disease leads to plaque formation (see and/or ).
- Both unstable and stable plaques normally increase in size in the outward direction (away from the lumen) and do not lead to stenosis.
- Unstable plaques are lipid-rich and covered by thin fibrous caps → These plaques rupture easily.
Development of coronary occlusion
Risk factors for coronary heart disease (CHD) → atherosclerosis → unstable plaque formation → plaque rupture → acts as a nidus for the formation of thrombus and/or thromboembolus → coronary occlusion → acute coronary syndrome → myocardial infarction and necrosis
- Stable AP: A stable, stenosing plaque slowly develops → symptomatic only during exertion, when there is an increased demand for oxygen
- Unstable AP: An unstable plaque ruptures, leading to thrombus formation that partially occludes the coronary vessel → A decrease in blood supply leads to symptoms regardless of demand (also during rest).
- NSTEMI = inner wall infarction: : Small emboli form from the unstable plaque and are carried to smaller vessels before completely occluding small branches affecting the inner layer of the heart.
- STEMI = transmural infarction: complete occlusion of a main coronary artery occurs due to thrombus formation directly at the ruptured plaque or thromboembolus directly after
- Stenosis ≥ 90% (mostly due to thrombus formation) → infarction followed by coagulation necrosis (see "Pathology" below)
General symptoms: See also .
- Retrosternal pain (often a squeezing type), acute in onset and continuous in nature
- Location of pain (in decreasing order of frequency): retrosternal, left side of the chest, left arm, left shoulder, neck, lower jaw, back, epigastrium
- Orthopnea, dyspnea
- Cyanosis, pallor
- Autonomic symptoms: diaphoresis, syncope, palpitations, nausea, and vomiting
- If MI: Symptoms of CHF (pulmonary edema) or cardiogenic shock (↓ BP, ↑ HR, pallor) may occur.
- Possibly a new murmur (typically systolic) and/or heart sound
Specific to inferior wall infarction
- Epigastric pain
- Often associated with bradycardia
- Atypical presentation: little to no chest pain
- Best initial test
- Unstable angina pectoris and NSTEMI: no specific ECG changes
- STEMI: specific ECG changes caused by myocardial infarction
- Acute stage
- Absence of R wave
- Terminal T-wave inversion
- Pathological Q-wave formation
Chronic stage (lifelong)
- Persistent, broad, and deep Q wave
- Often incomplete recovery of the R wave
- Permanent T-wave inversion may occur.
Localization of the infarct with the help of ECG changes
|Affected part - i.e., level of the stenosis||Localization of the infarct||ECG changes in myocardial infarction|
|Left coronary artery (LCA)||Left anterior descending artery (LAD)||Proximal LAD||Large anterior wall infarction||I, aVL, V1-6|
|Peripheral LAD + anterior interventricular branch||Anteroseptal infarction||I, aVL, V1-4|
|Peripheral LAD||Apical infarction||I, aVL, V3-5|
|Diagonal branch||Lateral wall infarction (anterolateral wall infarction)||I, aVL, V5-6/7|
|Left circumflex coronary artery (LCX)||Proximal circumflex coronary artery||Posterior wall infarction||III, aVF, V7-9|
|Posterolateral artery||Lateral wall infarction (posterolateral wall infarction)||II, III, aVF, ∼ (sometimes I and aVL are also affected )|
|Right coronary artery (RCA)||Proximal RCA||Inferior wall infarction||II, III, aVF|
|In approximately 20% of cases, inferior wall infarction is associated with infarction of the right ventricle.||V1 and V3r-6r also|
|Posterior interventricular branch||Posterior wall infarction||V7-9, inverse in V1-2|
An easy rule of thumb: "Infarction of the anterior wall" is caused by obstruction of the LAD or its branches. Depending on the extent of anterior wall infarction, it results in ECG changes in I, aVL, and/or anterior wall leads (V1-6). Infarction of the posterior wall is caused by obstruction of the LCX or RCA or their branches, and ECG changes are seen in leads II, III, and aVF."
Laboratory diagnostics (cardiac enzymes)
|Troponin T/I|| |
∼ 3 h
∼ 2–4 h
|Creatine kinase (creatine phosphokinase)||Total CK||∼ 3–12 h||12–24 h||2–6 days|| |
|CK-MB||∼ 3–12 h||12–24 h|| |
|SGOT (AST)||∼ 6–12 h||18–36 h||3–6 days|| |
|LDH1 and LDH2 (HBDH )|| |
∼ 6–12 h
|2–7 days|| |
|* The values rise, reach a certain maximum, and normalize in the span of hours or days following the onset of myocardial infarction or its symptoms.|
Troponin T is the most important cardiac-specific marker and may be measured 3–4 hours after the onset of myocardial infarction. CK-MB values correlate with the size of the infarct, reach a maximum after approximately 12–24 h, and normalize after only 2–3 days, making CK-MB a good marker for evaluating reinfarction.
Instrumental diagnostic procedures
- Cardiac CT to visualize the coronary arteries
- Coronary angiography (see "Treatment" below)
- Obstruction of a coronary artery branch with over 90% stenosis or embolization results in coagulation necrosis of the post-stenotic zone.
- Microscopically, it proceeds according to the following phases:
|Interval post-MI||Histopathological findings|
|0–24 hrs|| |
Early coagulative necrosis (> 4 hrs) → release of content from necrotic cells → release of inflammatory cytokines → recruitment of neutrophils (granulocytes). Hypercontraction of myofibrils and wavy fibers (1–4 hrs), coagulative necrosis (4–72 hrs).
|No gross changes (0–12 hrs), dark mottling (12–24 hrs)|
Coagulative necrosis (4–72 hrs), neutrophilic infiltrate (1–3 days)
|Hyperemia, yellow pallor|
|3–14 days||Hyperemic border, central yellow pallor (yellowest at ∼ 10 days), softening|
|2 weeks to several months|| |
Granulation tissue becomes denser and forms a collagenous scar.
Cellular swelling during the ischemia: secondary to more free water entering the cell to maintain osmotic balance in the setting of an increase in ion concentration (↑ intracellular Na+ + Ca2+)
- Ischemic cardiac muscle depletes its ATP during anaerobic respiration, which leads to:
- Cell death: ↑ intracellular Ca2+ → ↑ activation of cellular proteases → ↑ breakdown of cellular proteins → irreversible cell damage → cell death
- Reperfusion injury: due to free radical formation after the introduction of oxygen into a previously ischemic environment.
- See .
The differential diagnoses listed here are not exhaustive.
Initial management of suspected ACS
- IV access
- Evaluate 12-lead ECG and continue cardiac monitoring (BP, pulse, Spo2, ECG)
Administer symptomatic treatment ASAP
- Delivery of oxygen; via mask or nasal prongs (4–8 liters) if oxygen saturation is < 90% or if the patient has dyspnea.
- Place the patient in a sitting position to reduce volume load.
- Sublingual or intravenous nitrate (nitroglycerin or ISDN)
- Analgesic: morphine IV or SC (3–5 mg), if the patient has severe, persistent chest pain, or anxiety related to the myocardial event
- Consider a sedative (diazepam)
- Consider a loop diuretic (e.g., furosemide), if the patient has flash pulmonary edema or features of heart failure
Give blood thinners
- Platelet aggregation inhibitors
An anticoagulant: low molecular weight heparin (superior to unfractionated heparin)
- Consider fondaparinux
- Beta-blocker (IV or PO)
- Early initiation of high-intensity HMG-CoA reductase inhibitors () such as atorvastatin 80 mg, regardless of baseline cholesterol, LDL, and HDL levels
- Immediate transportation of the patient to a center equipped with a cardiac catheterization lab
Intramuscular injections during the pre-hospital phase are contraindicated because they may lead to a nonspecific rise in CK.
Treatment algorithm based on ECG findings
- STEMI: PTCA is performed as quickly as possible (balloon dilatation with stent implantation if necessary).
- NSTEMI: PTCA is performed rapidly within 2–72 h
- The appearance of typical symptoms without any ECG changes or elevation of cardiac enzymes in the blood
- Secondary prophylaxis: See , ; , and .
- See .
Early complications (within 48 hours of MI)
- Sudden cardiac death
- Acute left heart failure → pulmonary edema
- Cardiogenic shock
Late complications (medium and long-term complications)
- Left ventricular free wall rupture → cardiac tamponade
- Ventricular septal rupture → right heart failure
- Papillary muscle rupture → rupture of chordae tendinae → mitral regurgitation (occurs 2-7 days after myocardial infarction)
Atrial and s
- Affects 10–20% patients
- True ventricular aneurysm or ventricular pseudoaneurysm
- Diagnostic clue: persistent ST elevation and T-wave inversion
- Diagnostic procedures: echocardiography
- Treatment: Anticoagulation is key; surgery may be performed if required.
- Arterial thromboembolism with an associated risk of a cerebral insult or stroke
- Early infarct-associated pericarditis (postinfarction fibrinous pericarditis): occurs within the first week of a large infarct close to the pericardium
Dressler syndrome (postmyocardial infarction syndrome): pericarditis occurring 2–10 weeks post-MI without an infective cause (pleuritis may also occur)
- Circulating antibodies against cardiac muscle cells can be detected (autoimmune etiology).
- Presents with features of fever, stabbing chest pain; , dry cough; , friction rub
- Laboratory findings include leukocytosis; serum troponin levels are often elevated, ECG shows diffuse ST elevations
- NSAIDS and glucocorticoids (if needed) are used as painkillers and anti-inflammatory therapy is also indicated.
- Rare complication: hemopericardium/pericardial tamponade
- Congestive heart failure
We list the most important complications. The selection is not exhaustive.
Tertiary prevention for post-MI patients
- Generally, lifelong therapy with aspirin, an ACE inhibitor, a statin, and likely a beta-blocker, are recommended.
- Platelet aggregation inhibitors
- LDL cholesterol should normally be brought below 100 mg/dL; in high-risk patients, it should be below 70 mg/dL.
- Should be administered irrespective of the lipid profile
- : prevent unfavorable remodeling of the infarct area
- without → antiarrhythmic effect, reduced cardiac workload (anti-ischemic effect)
- Counseling: to minimize risk factors ; patients may be introduced to a rehabilitation program and/or secondary prevention program
- See coronary heart disease. for general recommendations regarding