Takotsubo Cardiomyopathy Triggered by a Fatal Subarachnoid Hemorrhage
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The autopsy showed that death was related to a SAH and confirmed the diagnosis of a takotsubo cardiomyopathy.
Stress-induced or takotsubo cardiomyopathy (TTC) is a recognized disease that was firstly described in Japan in 1991 in patients presenting signs of an acute coronary syndrome with transient left ventricular (LV) failure [1, 2, 3]. TTC is typically associated with sudden emotional stress, accompanied by a catecholamine surge. Triggering events may also include physical stressors such as major surgery medical procedures and illnesses [1, 2, 3, 4, 5]. This hypersympathetic state can be seen in SAH which is no longer considered as an exclusion criterion for takotsubo diagnosis according to the recent consensus document updating the Mayo Clinic guidelines and the InterTAK Diagnostic Criteria [2, 3, 4, 6].
In fact, intracerebral high pressure usually observed in cases of SAH can lead to an upregulation of the sympathetic system to assure brain perfusion. Therefore, it has been reported that 61.9% of patients with SAH will present with an abnormal ECG and that 20 to 30% of patients will develop secondary cardiomyopathy . Furthermore, transitory adrenergic activation can explain the occurrence of TTC which is a known complication of SAH.
The prevalence of TTC in SAH ranges between 1.2 and 26% . SAH patients with a high Hunt–Hess score (HHS) or low Glasgow Coma Scale (GCS) are more likely to develop TTC than those with low HHS or high GCS like our case .
The recent diagnostic criteria for TTC include transient hypokinesis, akinesis, or dyskinesis in the LV mid-wall segments with or without apical involvement; new ECG abnormalities or modest elevation in cardiac troponin; and the absence of myocarditis [2, 3, 6, 9].
TTC affects mainly the mid-wall and apical segments of the LV. However, when TTC is triggered by SAH, the most common abnormal myocardial segments are the basal and midventricular portions [4, 9] as seen in our case.
TTC affects predominantly postmenopausal women with a mean age of 68 years [3, 5]. Nevertheless, similar to our case, cases with an inverted pattern of TTC associated with SAH described in the literature tend to be younger and were most often associated with severe neurological pathologies and related to “neurologic stress” [3, 4, 7, 10].
The diagnosis of TTC is based on ultrasounds. In fact, some reported cases were diagnosed on the basis of echocardiographic signs without performing a cardiac angiogram. In these cases, patients presented cerebral lesions, ECG changes, high cardiac enzyme levels, and sometimes chest pain [4, 11].
In our case, TTC was suspected on the basis of clinical data (ECG changes, elevation of the cardiac enzyme, and akinesis of the basal walls of the LV). In the absence of cardiac angiogram, autopsy findings showed neither a coronary lesion nor any other anatomical abnormalities, and the histological examination did not reveal any myocarditis.
Most myocardial biopsies in TTC have shown interstitial infiltrates consisting primarily of mononuclear lymphocytes and macrophages; myocardial fibrosis; and contraction bands with or without myocardial necrosis . These abnormalities may be reversible .
In our case, no cellular lesion was noted in different histological sections. This allowed us to exclude any other myocardial damage as myocarditis, thus retaining the diagnosis of TTC and confirming the complete histological reconstitution.
The original point in this case is that the TTC is inverted, described in a male patient associated with a SAH with a fatal outcome.
Compliance with Ethical Standards
All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
Conflict of Interest
The authors declare that they have no conflict of interest.