Type 2 Myocardial Infarction

Type 2 myocardial infarction is myocardial necrosis caused by an imbalance between myocardial oxygen supply and demand, without acute atherothrombotic plaque disruption. It needs a rise or fall of cardiac troponin with at least one value over the 99th percentile, plus evidence of ischaemia and of a supply demand mismatch.

Evidence of ischaemia is symptoms, new ischaemic ECG change, new Q waves, or imaging showing new loss of viable myocardium or a regional wall motion abnormality.

It makes up about 5 to 30% of myocardial infarctions, depending on the series and troponin assay. Long term mortality is higher than in type 1 infarction, driven by comorbidity and the underlying illness.

Myocardial injury is different: troponin rises without evidence of ischaemia, in acute illness (sepsis, myocarditis, pulmonary embolism, takotsubo syndrome) and chronic disease (kidney failure, heart failure).

Triggers are tachyarrhythmia and bradyarrhythmia, anaemia and haemorrhage, hypoxaemia and respiratory failure, hypotension and shock, hypertensive crisis, severe aortic stenosis, hypertrophic cardiomyopathy, coronary spasm, microvascular dysfunction, coronary embolism, spontaneous coronary artery dissection, thyrotoxicosis, and stimulants.

In sub-Saharan Africa, severe anaemia from malaria, hookworm and sickle cell crisis is important.

Pathophysiology. Demand rises (heart rate, wall stress, contractility) or supply falls (oxygen content, perfusion pressure, diastolic time). Fixed obstructive disease of 50% or more is present in many patients and lowers the threshold. The subendocardium is hit first.

• Chest pain in under half. Dyspnoea, fatigue or no symptoms.
• Signs of the trigger: tachycardia, hypotension, pallor, fever, wheeze, hypertension, tremor.
• ECG: ST depression and T wave change are common. ST elevation is less common.

Red flags.

• ST elevation or ongoing ischaemic pain despite correction of the trigger
• Cardiogenic shock or ventricular arrhythmia
• Haemoglobin under 70 g/L, or active bleeding
• Severe hypoxaemia or respiratory failure
• Heart rate over 150/min, or sustained arrhythmia with hypotension

• High sensitivity troponin serially (0 and 1 to 3 hours) to show a rise or fall. In kidney disease, a change of over 20% from baseline matters more than the absolute value.
• ECG repeated, with comparison with old tracings.
• Echocardiography. Regional wall motion, ejection fraction, aortic stenosis, hypertrophic cardiomyopathy, tamponade, right ventricular strain.
• Trigger workup. Full blood count, ferritin, lactate, blood gas, creatinine, electrolytes, thyroid function, cultures, toxicology, malaria test in endemic regions, and CT pulmonary angiography when embolism is suspected.
• Coronary imaging. CT coronary angiography or stress imaging when stable and anatomy matters. Invasive angiography for ST elevation, ongoing ischaemia, or doubt over a type 1 event.

Differential diagnosis.

• Type 1 myocardial infarction
• Acute myocardial injury without ischaemia (myocarditis, takotsubo syndrome, sepsis, pulmonary embolism)
• Chronic myocardial injury (kidney disease, heart failure)
• Myocardial infarction with non-obstructive coronary arteries
• Aortic dissection
• Pericarditis
• Coronary embolism

Treat the cause. This is the treatment.

• Tachyarrhythmia. Atrial fibrillation with a rapid rate: metoprolol 2.5 to 5 mg intravenously over 2 minutes, repeated every 5 minutes to a maximum of 15 mg. Hold for heart rate under 50/min or systolic pressure under 100 mm Hg. Contraindicated in decompensated heart failure, shock and severe asthma. Unstable: synchronised cardioversion at 120 to 200 J biphasic under sedation. Amiodarone 300 mg intravenously over 1 hour (central line when possible), then 900 mg over 23 hours, maximum 1.2 g in 24 hours, for refractory cases.
• Anaemia and bleeding. Control the source and transfuse. A threshold of 80 g/L applies in cardiac disease, and up to 100 g/L is reasonable with ongoing ischaemia (evidence is mixed). Give one unit over 3 to 4 hours and reassess, with furosemide 20 to 40 mg intravenously between units in heart failure. Treat iron deficiency, malaria and hookworm.
• Hypoxaemia. Oxygen to a saturation of 94 to 98% (88 to 92% in hypercapnia), and treat pneumonia, pulmonary embolism or exacerbation.
• Hypotension or shock. Fluid in 250 mL boluses with reassessment, and noradrenaline 0.05 microgram/kg/min intravenously, titrated to a mean pressure of 65 mm Hg (usual maximum 0.5 microgram/kg/min). Avoid tachycardic inotropes unless output is low.
• Hypertensive emergency. Glyceryl trinitrate 10 to 20 microgram/min intravenously, increased by 5 to 10 microgram/min every 5 to 10 minutes, usual maximum 200 microgram/min (contraindicated with phosphodiesterase type 5 inhibitors and in hypotension). Lower mean arterial pressure by no more than 25% in the first hour.
• Sepsis. Early antibiotics, source control and fluids.
• Coronary spasm. Diltiazem 60 mg orally every 8 hours, maximum 360 mg daily, with isosorbide mononitrate modified release 30 mg once daily if needed.
• Stimulant toxicity. Diazepam 5 to 10 mg or lorazepam 1 to 2 mg intravenously. Avoid beta blockers in acute intoxication.
• Thyrotoxicosis. Propranolol 20 to 40 mg orally every 6 to 8 hours, to a heart rate under 90/min, maximum 320 mg daily, with antithyroid therapy.
• Valve and structural disease. Aortic stenosis: valve replacement by the usual indications. Hypertrophic cardiomyopathy: bisoprolol 2.5 mg once daily increased to 5 to 10 mg, avoid vasodilators and hypovolaemia.

Antithrombotic and secondary therapy.

• Dual antiplatelet therapy and full dose anticoagulation for the event are not routine. Aspirin 75 to 100 mg orally once daily and atorvastatin 40 to 80 mg once daily are started when coronary atherosclerosis is shown, whether obstructive or not (liver enzymes at baseline and 3 months).
• Revascularisation only for a flow limiting culprit lesion with persisting ischaemia after the trigger has been corrected, or for left main and proximal left anterior descending disease.
• Heart failure and reduced ejection fraction: ramipril 2.5 mg orally once daily increased every 2 to 4 weeks to 10 mg once daily (maximum 10 mg daily, 5 mg daily at creatinine clearance under 30 mL/min) and bisoprolol 1.25 mg once daily increased every 1 to 4 weeks to 10 mg once daily (maximum 10 mg daily in heart failure).
• After recovery, assess for coronary disease with CT angiography or stress imaging.

Special groups.

• Kidney impairment: interpret troponin by change, and adjust drug doses.
• Older adults: look for anaemia, atrial fibrillation and aortic stenosis as the usual triggers.
• Pregnancy: consider anaemia, spontaneous coronary artery dissection and peripartum cardiomyopathy.

Monitoring. Telemetry and serial troponin until the trigger is controlled and troponin is falling. Echocardiography at discharge and at 3 months when function was reduced. Haemoglobin, electrolytes and creatinine daily in acute illness.

Referral and escalation. Refer to cardiology for ST elevation, ongoing ischaemia, reduced ejection fraction or doubt over the type. Urgent for shock, arrhythmia or ischaemia that persists after the trigger is corrected.