Myocardial Stunning

Myocardial stunning is reversible contractile dysfunction that persists after an episode of ischaemia has been relieved and blood flow has been restored, without irreversible myocyte injury. Function recovers over hours to weeks even though perfusion is normal.

It follows reperfusion in myocardial infarction (after primary intervention or fibrinolysis), exertional or vasospastic ischaemia, cardioplegic arrest and cardiopulmonary bypass, cardiac arrest with resuscitation, and sepsis related and catecholamine induced states. Takotsubo syndrome has a similar but distinct mechanism.

Duration depends on the ischaemic insult. After brief ischaemia, recovery takes hours to days, and after large infarction with reperfusion it may take weeks. After cardiac arrest, post-resuscitation dysfunction usually recovers within 48 to 72 hours.

It matters clinically because dysfunction can look like irreversible damage, and decisions on devices and surgery should wait for recovery.

Pathophysiology.

Oxygen free radicals generated at reperfusion, calcium overload, and degradation of contractile proteins, with reduced myofilament sensitivity to calcium, impair contraction without cell death.

Perfusion is normal, and the myocardium keeps its contractile reserve, so low dose dobutamine improves wall motion. This distinguishes stunning from necrosis (no response) and hibernation (reduced resting flow).

Repeated episodes of ischaemia can cause cumulative stunning. Stunned myocardium can generate arrhythmia.

Heart failure symptoms, hypotension or cardiogenic shock after reperfusion or surgery, with persisting regional or global wall motion abnormality despite a patent artery. Low cardiac output after cardiac surgery typically peaks 4 to 6 hours after bypass and improves over 24 to 48 hours.

• Echocardiography: regional or global hypokinesia in a territory with a patent artery. Repeat after 24 to 72 hours, then at 2 to 4 weeks and 3 months to document recovery.
• Low dose dobutamine echocardiography (5 to 10 microgram/kg/min) shows improved thickening of stunned segments (contractile reserve).
• Cardiac MRI: no or limited late gadolinium enhancement in the dysfunctional segments, with possible oedema on T2.
• Perfusion imaging by PET or SPECT shows preserved flow and viability.
• Troponin, lactate, mixed venous oxygen saturation, invasive haemodynamics in shock, and angiography to confirm a patent artery.

Differential diagnosis.

• Hibernating myocardium and established infarction.
• Takotsubo syndrome and acute myocarditis.
• Septic cardiomyopathy and tachycardia induced cardiomyopathy.
• Acute stent thrombosis and no reflow.

Management is supportive until function recovers.

Treat the cause and optimise filling. Confirm a patent artery and absence of mechanical complications. Correct acidosis, hypoxia, anaemia, electrolytes and arrhythmia. Maintain mean arterial pressure over 65 mmHg.

Low output or shock.

• Dobutamine 2.5 to 10 microgram/kg/min intravenously (maximum 20), titrated to cardiac index and perfusion. Use the lowest effective dose because excess inotropy increases oxygen demand and arrhythmia.
• Milrinone 0.25 to 0.75 microgram/kg/min, without a bolus when blood pressure is low (reduce to 0.2 to 0.33 microgram/kg/min at creatinine clearance under 30 mL/min).
• Levosimendan 0.05 to 0.2 microgram/kg/min over 24 hours (optional bolus 6 to 12 microgram/kg over 10 minutes, omitted when systolic blood pressure is under 90 mmHg), where licensed. Monitor blood pressure, heart rate, potassium and QTc. Effect lasts about a week.
• Noradrenaline 0.05 to 0.5 microgram/kg/min to support blood pressure.
• Intra-aortic balloon pump, percutaneous ventricular assist device or veno arterial extracorporeal membrane oxygenation for refractory shock, as a bridge to recovery.

After cardiac arrest. Maintain mean arterial pressure over 65 mmHg and oxygen saturation of 94 to 98%, control temperature (between 32 and 37.5 degrees Celsius, avoiding fever for 72 hours), and treat the cause of the arrest.

Heart failure therapy once stable.

• Ramipril 1.25 to 2.5 mg orally twice daily or once daily, titrated to 10 mg daily (or sacubitril/valsartan 24/26 mg twice daily, titrated every 2 to 4 weeks to 97/103 mg twice daily); potassium and creatinine at 1 to 2 weeks.
• Metoprolol succinate 12.5 to 25 mg daily, titrated every 2 weeks to 200 mg, or bisoprolol 1.25 mg titrated to 10 mg daily, once congestion has settled.
• Eplerenone 25 mg daily, increased to 50 mg after 4 weeks (potassium under 5.0 mmol/L, eGFR over 30; check at 1 week and 4 weeks).
• Dapagliflozin 10 mg or empagliflozin 10 mg once daily (eGFR 25 or over and 20 or over respectively).
• Furosemide 20 to 80 mg daily for congestion.

Device decisions. Defer a defibrillator for primary prevention until at least 40 days after infarction and 90 days after revascularisation, with repeat echocardiography. A wearable defibrillator may bridge high risk patients.

Monitoring. Echocardiography at 24 to 72 hours, 2 to 4 weeks and 3 months; troponin and lactate until stable; creatinine and potassium after each drug change; ambulatory ECG at 2 to 4 weeks.

Referral and escalation. Refer to a heart failure service when function has not recovered at 4 to 6 weeks. Urgent referral for shock, ventricular arrhythmia and need for mechanical support.

Special groups.

• Pregnancy: stop ACE inhibitors, sacubitril/valsartan, eplerenone and SGLT2 inhibitors; use metoprolol and diuretics.
• Older adults: low starting doses and slower titration.
• Kidney impairment: adjust milrinone, avoid eplerenone when eGFR is under 30.