In Japan there have been a number of reports of reversible left ventricular dysfunction with symptoms similar to those of acute myocardial infarction but without coronary artery stenosis/occlusion even during the acute phase with ST segment elevation. This transient left ventricular apical wall motion abnormality, so-called "Takotsubo cardiomyopathy", was first described by Satoh (3) in 1990. In case studies reported since, this cardiac syndrome was shown to have the following characteristics: 1) emotional and somatic background (4), 2) onset symptoms resembling those of acute myocardial infarction, 3) apical akinesis and basal hyperkinesis, 4) T wave inversion (giant negative T wave) and QT prolongation following myocardial infarction-like ST elevation, 5) minimal myocardial enzyme release, 6) no angiographical stenosis in the epicardial coronary artery, 7) dissociation of findings between 201Tl myocardial scintigram and 123I-BMIPP myocardial scintigram, and 8) reversible left ventricular dysfunction (5) . As of this writing 250 cases have been reported in Japan, rather many compared to the numbers reported in Europe and the United States (5). Mental and/or physical stress are suspected as causal factors leading to the appearance of this cardiac syndrome (6).
The following features of our patient are consistent with typical "Takotsubo cardiomyopathy": 1) the presence of a trigger such as rapid alcohol withdrawal, ventricular fibrillation, and/or cardiopulmonary resuscitation; 2) ECG changes resembling acute myocardial infarction; 3) minimal myocardial enzyme release; 4) an absence of organic coronary artery lesions, including coronary spasms; 5) reversible ECG changes, left ventricular dysfunction, and myocardial enzyme release; and 6) dissociation of findings between 201Tl myocardial scintigram and 123I-BMIPP myocardial scintigram. However, the degree of eminent ST elevation and the focal anterior wall motion abnormalities were not typical of "Takotsubo cardiomyopathy".
A balloon-like asynergy in the apical regions and excessive contraction in the basal regions of the left ventricle have been demonstrated in "Takotsubo cardiomyopathy". However, it remains unknown why the left ventricle assumes this specific shape. The numbers of sympathetic nerve endings and their receptors on the myocardium differ in the left vetricle of the dog (7). The number of sympathetic nervous endings in the apical region of the left ventricle is decreased, whereas the number of receptors is increased. The opposite is true in the basal region of the left ventricle. These disturbances might be related to the balloon-like asynergy in the apical regions and the hyperkinesis in the basal regions of the bilateral ventricles. However, the distribution of the sympathetic nerve endings and their receptors remains to be clarified in humans.
Akashi et al from our institute previously hypothesized that excessive activation of cardiac catecholamine receptors may have either the result or the origin of this cardiomyopathy (8). The excessive activation of cardiac catecholamine receptors in the left ventricle and the discrepancy in the distribution of sympathetic nerve endings and their receptors could explain the strong appearance of wall motion abnormalities in the anterior wall.
The precise pathophysiological basis is still not fully clarified. The mechanism of left ventricular dysfunction in "Takotsubo cardiomyopathy" has generally been reported as coronary vasospasm (9), microvascular disturbance in the myocardium (10), or acute myocarditis (11).
We diagnosed this case as "Takotsubo cardiomyopathy" with ischemic event-like ST elevation and no significant coronary lesion. In view of the sustained ST segment elevation during coronary angiogram in the absence of any apparent coronary vasospasm, we determined that coronary artery vasospasm, one of the etiologies in "Takotsubo cardiomyopathy", did not occur in our case.
The latter, microvascular disturbance in the myocardium, is speculated to result from myocardial ischemia due to coronary microvascular spasm, which results in the focal stunned myocardium. In the present case, we could confirm the absence of epicardial coronary spasm in the left anterior descending artery. Regarding the presence of acute myocarditis, there was no evidence of early infection or any significant elevation of viral antibody titer.
Our institute previously reported high levels of circulating catecholamine in patients with this type of "Takotsubo cardiomyopathy" (12). We did not recognize any elevation of circulating catecholamine level in the present case, but the blood samples were taken at 24 hours after the onset of the ventricular fibrillation. Thus, it remains unclear whether there was any elevation in catecholamine at onset in our case.
Other diseases that have been reported to show ST segment elevation include Brugada syndrome (13) (idiopathic ventricular fibrillation), subarachnoidal hemorrhage (14), tension pneumothorax (15), commotio cordis (16) after strong chest compression, and others.
We could not completely exclude idiopathic ventricular fibrillation from the history of sudden onset of ventricular fibrillation and ST segment elevation in our patient. On the other hand, we consider Brugada syndrome fairly unlikely, as there was no evidence of typical right bundle branch block or pilsicainide-induced ST elevation when we tested the patient 28 days after the onset of the ventricular fibrillation. Further, subarachnoidal hemorrhage was excluded by computed tomography at the onset of the ventricular fibrillation. Commotio cordis following the strong chest compression was also not completely ruled out. Although commotio cordis is thought to be related to chest wall compliance and shock impact to the heart, the condition has never been reported to result directly from cardiopulmonary resuscitation. All of the above mentioned diseases were unlikely in this case.
Prior to the patient's cardiopulmonary arrest, the ECG showed only a mild QT prolongation. Moreover, there is no evidence that alcohol withdrawal triggered the disease onset. However, we cannot rule out the acute stress induced by the alcohol withdrawal during the hospitalization as a causal factor.