Reversibility of severe left ventricular dysfunction in patients with subarachnoid hemorrhage

Neuromediated stunned myocardium is a well-known complication of subarachnoid hemorrhage but has rarely been reported in association with other central nervous system disorders. The pathophysiology of this entity remains unclear, but a catecholamine-induced neurocardiogenic injury has been proposed as a causal factor. Typically, patients have rapid full cardiovascular recovery within a few days. We report a case of ischemic stroke, coexisting with ischemic electrocardiographic changes, increased cardiac-specific necrosis biomarkers, regional wall motion abnormalities and a cardiac SPECT consistent with inferior myocardial infarction despite normal coronary arteries. Interestingly, left-ventricular dysfunction in this case persisted longer than usually described despite full neurologic recovery. This case also illustrates the diagnostic challenges posed by this entity which frequently mimics acute myocardial infarction and emphasizes the investigation needed in this area.

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“…It has been described that cardiac abnormalities are typically transient and limited to the acute phase of the neurologic event [3, 4]. …”

Section: Discussionmentioning

confidence: 99%

Stunned Myocardium following Ischemic Stroke

Dias

Cabral²,

Meireles³

et al. 2009

Cardiology

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“…And, of the SAH survivors, approximately one-third remain dependent and 50% remain permanently disabled because of cognitive dysfunction [36,37]. Cardiac dysfunction that occurs following an SAH may normalize over time based on a few case reports and small studies [38][39][40]. The onset of LV dysfunction occurs early in the course of SAH [15,23].…”

Section: Natural Historymentioning

confidence: 99%

Neurogenic cardiac injury

Banki

Zaroff

2003

Curr Treat Options Cardio Med

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Cardiac injury may occur following many types of brain injury, although the most widely investigated form of neurocardiogenic injury is subarachnoid hemorrhage (SAH). Echocardiography may help prognosticate and aid in the treatment of SAH if left ventricular (LV) dysfunction is suspected or if troponin levels are elevated. Cardiac catheterization, however, is not routinely recommended in SAH patients with LV dysfunction and elevated troponin. The priority should be treatment of the underlying neurological condition, even in the setting of LV dysfunction. Cardiac injury that occurs following an SAH appears to be reversible. For patients that develop brain death cardiac evaluation under optimal conditions may help increase the donor pool.

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“…[1][2][3][4][5][6] Sometimes the clinical findings mimic acute myocardial infarction, which may make an exact diagnosis difficult. We describe here an unusual case of transient ventricular aneurysm that showed torsades de pointes (TdP) and ischemic changes on electrocardiogram (ECG) despite angiographically normal coronary arteries.…”

Section: Transient Left Ventricular Aneurysm and Hypertrophy Accompanmentioning

confidence: 99%

“…The initial ECG ( Figure 1A) showed sinus bradycardia, QT prolongation (QTc = 0.63), negative T waves in leads I, aVL and V [2][3][4][5][6] , and repeated VT that was compatible with TdP ( Figure 1B). She was treated with intravenous lidocaine, which was not effective on the TdP.…”

Section: Case Reportmentioning

confidence: 99%

“…Other case reports describe the pathogenesis of reversible left ventricular systolic dysfunction, either presented during a crisis of pheochromocytoma, 3) or associated with subarachnoid hemorrhage. 4) These reports suggest that an intense sympathetic nervous system or catecholamine may mediate myocardial injury.…”

Section: Considering Prominent Negative T Waves With Qt Prolongation Andmentioning

confidence: 99%

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Transient Left Ventricular Aneurysm and Hypertrophy Accompanied by Polymorphic Ventricular Tachycardia in a Patient Suspected of Acute Myocarditis.

et al. 2000

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EVERSIBLE causes of myocardial dysfunction have a wide spectrum of pathophysiologies: coronary vasospasm, coronary thromboembolism, myocardial stunning, neurohumoral abnormalities, acute myocarditis, severe prolonged anemia, tachycardia-induced cardiomyopathy, and other causes.1-6) Sometimes the clinical findings mimic acute myocardial infarction, which may make an exact diagnosis difficult. We describe here an unusual case of transient ventricular aneurysm that showed torsades de pointes (TdP) and ischemic changes on SUMMARYA 75-year-old woman presented with recurrent ventricular tachycardia (VT) compatible with torsades de pointes (TdP) based on sinus bradycardia and QT prolongation. Previously she had received pirmenol, at a serum concentration within therapeutic range, for her paroxysmal atrial fibrillation. Emergent cardiac catheterization identified a ventricular aneurysm of the anteroapical and inferior wall along with angiographically normal coronary arteries. A right ventricular endomyocardial biopsy revealed postmyocarditic change. The left ventricular contraction improved after 5 weeks of conservative treatment. A follow-up echocardiogram revealed transient thickening of partial left ventricular wall consistent with the segment of the aneurysm. Several months later, almost all abnormal findings had improved except for sustained deep negative T waves in precordial leads. Acute myocarditis was primarily suspected as the cause of her clinical presentation. (Jpn Heart J 2000; 41: 97-102)

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Reversibility of severe left ventricular dysfunction in patients with subarachnoid hemorrhage

Cited by 13 publications

References 5 publications

Stunned Myocardium following Ischemic Stroke

Stunned Myocardium following Ischemic Stroke

Neurogenic cardiac injury

Transient Left Ventricular Aneurysm and Hypertrophy Accompanied by Polymorphic Ventricular Tachycardia in a Patient Suspected of Acute Myocarditis.

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