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      Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: A novel cardiac syndrome mimicking acute myocardial infarction

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          Abstract

          Peculiar asynergy, which consists of hypokinesis or akinesis from the mid portion to the apical area and hyperkinesis of the basal area on contrast left ventriculogram, is rare. Because the end-systolic left ventriculogram looks like a "tako-tsubo," which was used for trapping octopuses in Japan, we proposed the term "tako-tsubo-like left ventricular dysfunction." Our aim was to evaluate its clinical features and causes. We studied 30 patients with tako-tsubo-like left ventricular dysfunction without significant coronary artery disease. We assessed its pathophysiologic mechanisms by coronary spasm provocation test, endomyocardial biopsy, measurement of virus titer, and measurement of circulating catecholamine levels. Patient age ranged from 55 to 83 years. Twenty-eight were women and 2 were men. Tako-tsubo-like left ventricular dysfunction was dramatically resolved on predischarge left ventriculogram at 11.3 +/- 4.3 days. Acute coronary angiography revealed spontaneous multivessel coronary spasm in 3 patients. Among 14 patients, ergonovine or acetylcholine induced epicardial single coronary spasm in 4 patients and multivessel coronary spasm in 6 patients. Spontaneous microvascular spasm occurred at predischarge in 1 patient. An endomyocardial biopsy specimen in 3 patients and measurement of virus titer in 7 patients did not show evidence of acute myocarditis. Circulating norepinephrine was normal or slightly elevated in 6 patients. We showed clinical features of a novel cardiac syndrome with tako-tsubo-like left ventricular dysfunction. Although the precise cause remains unclear, simultaneous multivessel coronary spasm at the epicardial artery or microvascular levels may contribute to the onset of tako-tsubo-like left ventricular dysfunction.

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          Most cited references25

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          Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction

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            Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium.

            The purpose of this study was to determine whether a relation exists between electrocardiographic (ECG) abnormalities and left ventricular wall motion in patients with subarachnoid hemorrhage. Although ECG changes simulating acute myocardial infarction are frequently seen in patients with subarachnoid hemorrhage, their relation to left ventricular wall motion has not been established. Twelve patients with subarachnoid hemorrhage were classified according to the presence of ST segment elevation in at least two consecutive leads on admission: seven patients with ST segment elevation (group I) and five patients without ST segment elevation (group II). No patients had a previous history of heart disease. Left ventricular regional wall motion was evaluated by the centerline method. The mean (+/- SEM) duration from onset of subarachnoid hemorrhage to left ventriculography was 9 +/- 3 h in group I and 10 +/- 1 h in group II. Coronary angiography was performed to rule out wall motion abnormalities due to coronary artery disease while the ST segment was still elevated. Two-dimensional echocardiography was used to evaluate wall motion thereafter. All patients in group I showed ST segment elevation in ECG leads V4 to V6. Wall motion of the left ventricular apex was significantly reduced in group I compared with group II (-2.48 +/- 0.41 vs. -0.45 +/- 0.72, p < 0.02). No patients showed organic stenosis or vasospasm, or both, of epicardial coronary arteries. Wall motion abnormalities decreased echocardiographically in all patients, but one patient in group I died in hospital at 2 or 3 weeks after the onset of subarachnoid hemorrhage, when the T wave was inverted in leads V4 to V6. These findings suggest that patients with subarachnoid hemorrhage and ST segment elevation may demonstrate transient corresponding regional wall motion abnormalities. The mechanism of neurogenic stunned myocardium was not clearly elucidated in the present study.
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              Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm.

              We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.
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                Author and article information

                Journal
                American Heart Journal
                American Heart Journal
                Elsevier BV
                00028703
                March 2002
                March 2002
                : 143
                : 3
                : 448-455
                Article
                10.1067/mhj.2002.120403
                11868050
                29bd64dc-a8b1-42a1-bde9-359fb48f8bd7
                © 2002

                https://www.elsevier.com/tdm/userlicense/1.0/

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