Stress cardiomyopathy pathophysiology: Difference between revisions
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It may be that the pathophysiology is multifactorial. | It may be that the pathophysiology is multifactorial. | ||
==References== | ==References== | ||
Revision as of 06:22, 28 August 2012
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Stress cardiomyopathy Microchapters |
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Diagnosis |
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Treatment |
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Unstable angina/non ST elevation myocardial infarction in Stress (Takotsubo) Cardiomyopathy |
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Stress cardiomyopathy pathophysiology On the Web |
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Risk calculators and risk factors for Stress cardiomyopathy pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The etiology of stress cardiomyopathy appears to involve the response of the myocardium to a hyperadrenergic state. The syndrome is often preceded by significant emotional and physical stress. Serum catecholamines may be markedly elevated in patients with stress cardiomyopathy with levels greater than seen in patients with thrombotic ST elevation myocardial infarction or congestive heart failure, though this is not always present. Thus, it has been postulated that catecholamine excess contributes at least in part to the pathophysiology, and that catecholamines may cause direct myonecrosis. [1]
Several other pathophysiologic mechanisms have been proposed. Lyon et al have hypothesized that the syndrome is a form of myocardial stunning that is mediated by epinephrine. [2] These authors hypothesize that high levels of circulating epinephrine observed in the syndrome trigger a switch in intracellular signal trafficking.
In particular, they hypothesize that ventricular cardiomyocytes (particularly those at the apex), switch from G(s) protein to G(i) protein signaling via the beta(2)-adrenoceptor. One potential benefit of this switch to beta(2)-adrenoceptor-G(i) protein signaling is that this may afford protection against the proapoptotic effects of intense activation of beta(1)-adrenoceptors. On the other hand, this switch is also negatively inotropic. Because beta-adrenoceptor density is greatest at the apex of the left ventricle (455 vs 341 fmol/mg),[3] the mechanical impact of the switch is also greatest at the apical myocardium. [2]
Patients who develop stress cardiomyopathy appear to have a higher prevalence of anxiety disorders preceding the event which suggests that psychosocial stress may be a predisposing factor [4].
While some of the original researchers of apical ballooning suggested that spasm in multiple coronary arteries could reduce epicardial blood flow to cause transient stunning of the myocardium (Kurisu et al. American Heart Journal 2002), other researchers have shown that vasospasm is much less common than initially thought (Tsuchuhashi K et al. JACC 2001, Kawai et al. JPJ 2000, Desmet et al. Heart 2003). It has also been noted that when there is epicardial artery vasospasm, even in multiple arteries, that they do not correlate with the areas of myocardium that are hypokinetic (Abe et al. JACC 2003).
One final hypothesis is that the syndrome is due to microvascular dysfunction.
It may be that the pathophysiology is multifactorial.
References
- ↑ Wittstein IS, Thiemann DR, Lima JA; et al. (2005). "Neurohumoral features of myocardial stunning due to sudden emotional stress". N. Engl. J. Med. 352 (6): 539–48. doi:10.1056/NEJMoa043046. PMID 15703419.
- ↑ 2.0 2.1 Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE (2008). "Stress (Takotsubo) cardiomyopathy--a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning". Nat Clin Pract Cardiovasc Med. 5 (1): 22–9. doi:10.1038/ncpcardio1066. PMID 18094670.
- ↑ Mori H, Ishikawa S, Kojima S; et al. (1993). "Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli". Cardiovasc. Res. 27 (2): 192–8. PMID 8386061.
- ↑ Summers et al. JACC 2010