Published online before print May 25, 2006, doi: 10.1161/01.STR.0000226576.83902.2e
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2006;37:1635.)
© 2006 American Heart Association, Inc.
Editorials |
Adrenoreceptor Polymorphisms and Subarachnoid Hemorrhage
From the Davee Department of Neurology and Anesthesiology (Section of Critical Care), Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Correspondence to Andrew M. Naidech, Davee Department of Neurology, Northwestern University Feinberg School of Medicine, 710 N Lake Shore Dr, Chicago, IL, 60611 USA. E-mail a-naidech@northwestern.edu
Key Words: subarachnoid hemorrhage
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
See related article, pages 1680–1685.
Neurogenic stunned myocardium (NSM) is reversible cardiac dysfunction, typically after subarachnoid hemorrhage (SAH).1,2 The most likely pathophysiology of NSM is a catecholamine surge that leads to transient ventricular dysfunction. The pathophysiology is probably similar to Tako-Tsubo cardiomyopathy3 and cardiac dysfunction caused by fright.4 SAH presents a different and acute clinical scenario, however, because these patients often require hyperdynamic therapy for symptomatic or radiographic vasospasm.5 Both increasing cardiac output and blood pressure increase cerebral perfusion,6 but hyperdynamic therapy with a failing left ventricle can quickly lead to pulmonary edema, hypoxia, hypotension and cerebral infarction.7
Methods to predict which patients will develop NSM would be very helpful. Serum catecholamine levels might reasonably be expected to coincide with the catecholamine surge and NSM; however, the available data have not borne this out.8 Cardiac troponin I (cTI) has emerged as a fast, cheap and prognostic test for predicting NSM, as well as poor outcome and death.9 Although cTI is helpful, it does not answer several important questions: Why do some patients have an elevation in cTI and others do not? What are the underlying mechanisms that lead to NSM? Do they offer further insights into diagnosis than measuring cTI?
An article in this issue of Stroke10 offers some insights. Genotyping was done for catecholamine receptor subtypes. Several genetic receptor subtypes were associated with both cTI release and depressed ejection fraction on echocardiography. This implicates the genetic code of receptor subtypes, and probably receptor function, in cTI release and
Related Article:
Stroke 2006 37: 1680-1685.