Reversible Stress Cardiomyopathy in Guillain-Barré Syndrome

A Case Report

A. Gravos; A. Destounis; K. Katsifa; P. Tselioti; K. Sakellaridis; V. Grammatikopoulou; C. Tsapas; A. Nodarou; P. Batiani; A. Prekates

Disclosures

J Med Case Reports. 2019;13(150) 

In This Article

Discussion

We present a case of a woman diagnosed with GBS who developed reversible stress cardiomyopathy. Massive catecholamine release due to the stressful event of rapid respiratory deterioration and hemodynamic instability after induction of anesthesia most likely caused the development of cardiomyopathy. In addition, norepinephrine infusion could have aggravated catecholamine excess, which might have contributed to the myocardial dysfunction. Takotsubo cardiomyopathy has been described in patients with GBS;[5–12] however, our patient presented with a type of stress cardiomyopathy (severe diffuse hypokinesis of the left ventricle) without the classical characteristics of takotsubo cardiomyopathy (transient hypokinesis, akinesis, or dyskinesis in the middle/apical segments of the left ventricular wall, with basal hyperkinesis).

Stress cardiomyopathy can be difficult to distinguish from the more common cardiovascular complications in GBS, owing to autonomic dysfunction such as tachyarrhythmias and bradyarrhythmias, blood pressure fluctuations, acute coronary syndromes, and myocarditis.[4] Coronary angiography and cardiac MRI are needed in order to exclude coronary artery disease and myocarditis.

The name "takotsubo" refers to a Japanese jar used by fishermen to catch octopuses. The round bottom but tight neck resemble a picture often seen by echocardiography of the left ventricular wall, called "apical ballooning".[14] As more reports were published, it became clear that wall movement disorders were not restricted to the apex but could involve multiple segments of the left ventricular wall, as in our patient.[15,16]

The exact pathogenic mechanism of takotsubo cardiomyopathy is still controversial. The catecholamine hypothesis, which is that takotsubo cardiomyopathy is commonly induced by physical and/or emotional stress, seems the best explanation.[16] Sympathetic excitation of the brain triggers the release of the catecholamines norepinephrine and epinephrine, resulting in hyperdynamic basal contraction and apical systolic dysfunction. Takotsubo cardiomyopathy is a specific type of a broad spectrum of reversible cardiomyopathies, often stress-related.[14,17,18] In subarachnoid hemorrhage, pheochromocytoma, traumatic brain injury, and other neurological emergencies, excessive catecholamine release secondary to the primary insult has been reported, causing what is known as neurogenic stress cardiomyopathy/neurogenic stunned myocardium.[19–24]

Transient cardiac dysfunction in GBS could also be attributed to aberrant immune responses directed against myocardial cells and peripheral nerves.[8] Alternatively, abnormal myocardial blood flow due to sympathetically mediated microvascular dysfunction has been suggested and is supported by decreased coronary flow reserve during the acute phase.[25] Furthermore, myocardial necrosis could result from increased sympathetic tone, and catecholamines could be the pathologic substrate of this transient cardiac dysfunction.[25] This is supported by the observation that plasma catecholamine levels are markedly elevated in acute stress cardiomyopathy compared with acute myocardial infarction.[25] An alternative explanation is the direct effect of catecholamines on cardiac myocytes. High levels of circulating epinephrine trigger a switch in intracellular signal trafficking. This change in signaling might be negatively inotropic. Despite these reports, a causal link between catecholamine exposure and stress cardiomyopathy has not been convincingly demonstrated.[18]

On the basis of this background, the use of β-receptor-stimulating agents in patients with stress cardiomyopathy and GBS who have severe hypotension seems inappropriate. Non-β-receptor-stimulating agents such as vasopressin or terlipressin might be beneficial.[26,27]

Few cases associating GBS with reversible stress cardiomyopathy have been reported in the literature. In most of them, cardiomyopathy presented within the first week of hospital admission and completely resolved on discharge, after days or weeks.[5–12] Complications include heart failure (17.7%), recurrence (3.5%), and mortality (2.7%).[28] Treatment consists of angiotensin-converting enzyme inhibitors, β-blockers, and diuretics in hemodynamically stable patients. β-blockers are believed to reduce sympathetic tone and improve the myocardial work/oxygen consumption ratio.[28] In hemodynamically unstable patients, the use of norepinephrine may be counterproductive, and treatment must be individualized for each patient. Treatments used in this setting include enoximone, a phosphodiesterase inhibitor that has positive inotropic as well as vasodilating properties and therefore reduces afterload; levosimendan; dobutamine; and intra-aortic balloon pump.[29–31]

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