Title : The alive “Cardiac Voodoo”: The heart-brain syndrome beyond stroke
Abstract:
Aim: To discuss life-threatening brain-heart comorbid syndrome in acute cerebral stress conditions.
Methods/Design: Case Reports and related literature update. Case1: A 72-year-old female with acute confusion, amnesia, and generalized fatigue was admitted for acute neurological evaluation. MRI brain showed no acute pathology, and the diagnosis of transient global amnesia (TGA) was made. Transthoracic echocardiography (TTE) found 20% LVEF and hypokinesia. Case 2: A 48-year-old female was brought to the hospital after a reported generalized tonic-clonic (GTC) seizure activity >30 minutes at home. A recurring GTC seizure was witnessed in the ED while the patient remained unconscious. Status epilepticus (SE) treatment and intubation were initiated. Brain MRI was diagnostic of posterior reversible encephalopathy syndrome (PRES) and a small, ill-defined left parietal cortical mass. TTE revealed LVEF of 10-15%, LV apical thrombus, and hypokinesia. In both cases, a diagnosis of Takotsubo cardiomyopathy (TC) was made. Beyond acute neurological care, both patients underwent acute anticoagulation and cardiomyopathy treatment and were discharged home with follow-up care.
Results: The life-threatening brain-heart comorbid syndrome with the maximal form of stress TC was first reported in 1944 as sudden death, later proved in association with cerebral edema, brain neoplasms, and acute strokes. Henceforth, it has also been recognized as concomitant with other acute cerebral stress conditions like TGA, SE, and PRES.
Discussion/Conclusions: Highlight the importance of recalling the “cardiac voodoo” heart-brain syndrome in acute cerebral stress conditions. The “cardiac voodoo is a condition with high morbidity and mortality due mostly to catecholamine surge and cardiac failure, stressing the early need for EKG and TTE evaluation in acute neurological conditions. This is even more apparent in the presence of hypotension and tachycardia and absence of other typical cardiac symptoms. The comorbid TC with acute neurological conditions has major consequent therapeutic decisions, from preventing or limiting the catecholamine surge and “stunt” organ damage to intensive care treatment, continuous Holter monitoring, preferred use of beta and calcium-channel blockers while avoiding drugs that prolong QT interval, and eventually cardiac pacing, to mitigate the high-risk morbidity and mortality of such complex potentially fatal cases.

