When the brain breaks your heart

davidI am more of a stroke guy myself. As an over-generalization, I see the heart as the organ responsible for maintaining adequate brain function. When the heart fails, the brain fails. But sometimes, we see the converse–where neurologic disease results in massive cardiovascular dysfunction. Several common examples of such a causal relationship include intracranial hypertension with systemic hypertension and bradycardia, insular infarcts with resultant autonomic instability, paroxysmal sympathetic hyperactivity, and neurogenic stress cardiomyopathy. In this BrainWaves interview, Dr. David Manly (right) discusses the pathogenesis and management of neurogenic stress cardiomyopathy syndromes.

What we know about stress cardiomyopathy is that it can follow significant neurologic and psychiatric illnesses, as well as emotional stressors. Reports of patients developing acute severe heart failure after spousal death, robbery, natural disasters, and even (unfortunately) following good news, abound in the literature. Many physicians have turned to recently published findings from a 2015 New England Journal of Medicine report by 26 centers in the US and Europe. Among the findings presented by this international consortium, the degree of systolic heart failure is 20% worse among patients with Takotsubo’s than with acute coronary syndrome (ejection fraction ~40% vs. ~50%). And while we believe this to be largely a reversible heart failure syndrome, it is accompanied by a high rate of morbidity and mortality (5.6% per patient-year).


The Japanese octopus traps after which this disease is named. Adapted from https://en.wikipedia.org/wiki/Takotsubo_cardiomyopathy#/media/File:Takotubo_akasi-si_PC012375.jpg. Public domain.

Octopus pot. The literal translation of Takotsubo is “octopus pot” or “octopus trap.” The name comes from the characteristic shape of the heart during the acute phase of the illness, which oddly resembles the Japanese fishing instrument (see image). In addition to reduced ejection fraction and elevated cardiac enzymes with characteristic chest pain, you will see apical ballooning and ventriculomegaly. But in other cases of neurogenic stress cardiomyopathy, you may see focal basal wall motion changes or even multi-segmental wall motion abnormalities. [Although we are by no means offering medical advice here] A cardiac catheterization is frequently required to rule out acute coronary thrombosis or vasospasm. Interestingly, although a prevailing notion is that Takotsubo’s is the result of a hyper-catecholaminergic state, beta blockade was not associated with improved outcomes in the Takotsubo registry. In fact, ACE-inhibitors seem to be protective–a finding that confirms the complexity of the pathophysiology underlying Takotsubo’s.

Sounds pretty scary, right? Well it can be. So prepare yourself for it in the hospital setting by checking out our podcast. But don’t stress over it. I’d hate to see you develop a cardiomyopathy.


[Jim Siegler]

The content in this episode was vetted and approved by Ramani Balu.


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