Neurosurgery notes/Vascular/Haemorrhagic diseases/SAH/SAH complication/Neurogenic stress cardiomyopathy (NSC)

Neurogenic stress cardiomyopathy (NSC)

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SAH complication

General

  • Aka
    • Neurogenic stunned myocardium (NSM)
    • Reversible post-ischamic myocardial dysfunction
    • Takotsubo cardiomyopathy (“broken heart”)
      • Named after the Japanese octopus trap ‘Tako- tsubo’
      • A severe cardiomyopathy associated with such major life events or stresses as the death of a loved one or intense fear.
      • Mimics the apical left ventricular ballooning seen on echocardiography
  • Classically seen in patients following cardiac surgery, and attributed to a defect in troponin-I (TnI)

Numbers

  • Prevalence of NSC among aSAH patients range from 2.2% to 17%
    • Global or regional left ventricular systolic dysfunction on echocardiogram has been described after SAH with an approximate incidence of 10-28%.
  • Mortality rates
    • Very high cTnI (>1.0 ng/ml) levels 40%
    • Mild or low cTnI 11%

Pathophysiology

  • SAH → Hypothalamic ischaemic → Increased sympathetic tone → Catecholamine releases → Coronary artery spasm → Sub-endocardial ischaemic → Reduced myocardial contractility with relatively (to MI) low tropT → Decrease stroke volume → Decrease cardiac output → hypotension does not occur because reduced CO is offset by increase SVR
  • Reduced CO
    • May impair the ability to tolerate barbiturates administered for cerebral protection during early surgery due to their myocardial suppressant effect
    • Impede the use of hyperdynamic therapy for vasospasm

Risk factors

  • Higher Hunt Hess grade (> 3)
  • Female gender
  • Smoking status
  • Age

Natural history

  • Peak incidence 2 days -2 weeks post SAH
  • Condition reverse in 5 days
    • Normal myocardial cells replace those with defective TnI
  • 10% can progress to actual MI
  • Diastolic dysfunction is also common after SAH, is associated with the severity of neurologic injury, and may be the cause of pulmonary edema in these patients.

Clinical features

  • Hypertension (27%)
  • Hypotension (18%)
    • Hypotension does not always occur since the reduced cardiac output (CO) may be offset by an increase in SVR
  • Life-threatening arrhythmias (8%)
  • Myocardial ischaemia (6%)
  • Successful resuscitation from cardiac arrest (4%)

Investigations

  • Bloods
    • Troponin I elevation (20-68%)
  • Echo
    • Regional wall motion abnormalities (26%)
    • Stroke volume and cardiac output are reduced
    • May appear compatible with an MI on echocardiography, yet, troponin levels are typically lower (often < 2.8 ng/ml) than would be predicted given the level of myocardial impairment
  • EEG changes: 50%
      • ST segment changes (15-67%)
      • T-wave changes (12-92%)
      • Prominent U waves (4-52%)
      • QT prolongation (11-66%)
      • Conduction abnormalities (7.5%)
      • Sinus bradycardia (16%)
      • Sinus tachycardia (8.5%)
      A graph of a heart rate AI-generated content may be incorrect.
       

Treatment

  • Intraoperative TEE monitoring may be a useful guide for titrating pressors.
  • Dobutamine: when SBP<90 and low SVR
  • Milrinone:
    • When SBP>90 and normal SVR
    • When the patient is on chronic beta blockers
  • Other options: stellate ganglion block, magnesium

DDx

Coronary artery disease (CAD)
NSC
Myocardial necrosis typically follows a vascular distribution.
No myocardial necrosis or myofibrillar necrosis localizing near cardiac nerves
Occurs in a delayed fashion after progressive ischemia and muscle cell death.
Acute onset with surge in catecholamine
Unique, apical-sparing pattern of regional wall motion abnormality