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CLINICAL STUDY

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

Kazufumi Tsuchihashi, MD, PhD^a, Kenji Ueshima, MD, PhD, Tatsuro Uchida, MD, PhD, Nobuhiro Oh-mura, MD, PhD, Kazuo Kimura, MD, PhD^||, Mafumi Owa, MD, PhD^¶, Minoru Yoshiyama, MD, PhD^#, Shunichi Miyazaki, MD, PhD^**, Kazuo Haze, MD, PhD, Hisao Ogawa, MD, PhD, Takashi Honda, MD, PhD, Mamoru Hase, MD^a, Ryu-ichi Kai, MD, PhD, Isao Morii, MD, PhD^** for the Angina Pectoris-Myocardial Infarction Investigations in Japan

^a Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
Second Department of Internal Medicine and Cardiology, Memorial Heart Center, Iwate Medical University School of Medicine, Morioka, Iwate, Japan
Division of Cardiovascular Medicine, Sendai Cardiovascular Center, Sendai, Japan
Department of Cardiovascular Medicine, Omiya Medical Center, Jichi Medical School, Omiya, Saitama, Japan
^|| Department of Cardiology, Yokohama City University Medical Center, Yokohama, Japan
^¶ First Department of Internal Medicine, Shinsyu University School of Medicine, Matsumoto, Nagano, Japan
^# Division of Cardiology, Osaka City University School of Medicine, Osaka, Japan
^** Division of Cardiology, National Cardiovascular Center, Suita, Osaka, Japan
Department of Cardiology, Osaka City General Hospital, Osaka, Japan
Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto, Japan
Cardiovascular Center, Saiseikai Kumamoto Hospital, Kumamoto, Japan

Manuscript received November 15, 2000; revised manuscript received March 8, 2001, accepted March 26, 2001.

Reprint requests and correspondence: Dr. Kazufumi Tsuchihashi, Second Department of Internal Medicine, Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo 060-0061, Japan
tsuchiha{at}sapmed.ac.jp

	Abstract

Top Abstract Subjects and methods Results Discussion Appendix References

 
OBJECTIVES

To determine the clinical features of a novel heart syndrome with transient left ventricular (LV) apical ballooning, but without coronary artery stenosis, that mimics acute myocardial infarction, we performed a multicenter retrospective enrollment study.

BACKGROUND

Only several case presentations have been reported with regard to this syndrome.

METHODS

We analyzed 88 patients (12 men and 76 women), aged 67 ± 13 years, who fulfilled the following criteria: 1) transient LV apical ballooning, 2) no significant angiographic stenosis, and 3) no known cardiomyopathies.

RESULTS

Thirty-eight (43%) patients had preceding aggravation of underlying disorders (cerebrovascular accident [n = 3], epilepsy [n = 3], exacerbated bronchial asthma [n = 3], acute abdomen [n = 7]) and noncardiac surgery or medical procedure (n = 11) at the onset. Twenty-four (27%) patients had emotional and physical problems (sudden accident [n = 2], death/funeral of a family member [n = 7], inexperience with exercise [n = 6], quarreling or excessive alcohol consumption [n = 5] and vigorous excitation [n = 4]). Chest symptoms (67%), electrocardiographic changes (ST elevation [90%], Q-wave formation [27%] and T-wave inversion [97%]) and elevated creatine kinase (56%) were found. After treatment of pulmonary edema (22%), cardiogenic shock (15%) and ventricular tachycardia/fibrillation (9%), 85 patients had class I New York Heart Association function on discharge. The LV ejection fraction improved from 41 ± 11% to 64 ± 10%. Transient intraventricular pressure gradient and provocative vasospasm were documented in 13/72 (18%) and 10/48 (21%) of the patients, respectively. During follow-up for 13 ± 14 months, two patients showed recurrence, and one died suddenly.

CONCLUSIONS

A novel cardiomyopathy with transient apical ballooning was reported. Emotional or physical stress might play a key role in this cardiomyopathy, but the precise etiologic basis still remains unclear.

Abbreviations and Acronyms   AMI = acute myocardial infarction   AP-MI = Angina Pectoris-Myocardial Infarction investigations   CAG = coronary angiogram or coronary angiographic   CK = creatine kinase   ECG = electrocardiogram or electrocardiographic   LV = left ventricle or left ventricular   LVG = left ventriculography or left ventriculographic

To determine the clinical characteristics of transient apical ballooning, the members of Angina Pectoris-Myocardial Infarction (AP-MI) investigations in Japan have retrospectively registered and analyzed patients.

	Subjects and methods

Top Abstract Subjects and methods Results Discussion Appendix References

 
Registration criteria.   From December 1991 to June 2000, a total of 125 patients with transient LV apical wall motion abnormalities without stenosis on CAG were retrospectively enrolled from cardiovascular institutes of AP-MI investigations in Japan (see Appendix). In this study, data from 88 patients were selected for analysis based on the following criteria: 1) patients with suspected AMI based on chest symptoms or ECG changes (ST-T changes, abnormal Q-wave formation); 2) transient LV ballooning confirmed by left ventriculography (LVG) or echocardiography; and 3) CAG-confirmed normal epicardial artery (luminal narrowing of <50% in all three coronary arteries) within 48 h of the onset.

In these selected patients, LV apical ballooning was confirmed by LVG in 77 patients (88%) in the acute phase (8 ± 9 h after onset; range, 1 to 48 h) and by echocardiography in all the subjects immediately after the onset. Patients with idiopathic cardiomyopathy, febrile disorders, pheochromocytoma or prior history of myocardial infarction and those receiving coronary revascularization therapy were excluded from this study. Thirty-seven of the 125 patients were excluded from this study due to a lack of coronary angiographic evaluation in the acute period (n = 35) or due to an underlying disorder (pheochromocytoma, n = 2). For analyses of 12-lead ECG findings and quantitative LV wall motion, patients with atrial fibrillation, intraventricular conduction abnormalities and frequent premature ventricular contractions were also excluded.

Methods.   Clinical characteristics (age, gender, onset, coronary risk factors) and the condition that preceded onset as a possible triggering factor were analyzed. Major coronary risk factors were determined by the Sixth Report of the Joint National Committee (1997) in hypertension and by the American Diabetes Association (1998) in diabetes. Hyperlipidemia was defined as hypercholesterolemia of 220 mg/dl or hypertriglycemia of 150 mg/dl. Cardiac enzyme release (creatine kinase [CK] release measured every 3 or 4 h [n = 88] and troponin T release measured once a day [n = 43]) for determining peak values and 12-lead ECG findings (ST shifts, T-wave changes and Q-wave formation in all leads) were examined in each registered center.

In the acute period, LV end-diastolic pressure and intraventricular pressure gradient, in which >30 mm Hg is defined as significant, were measured in 72 patients. Left ventricular wall motion was analyzed using contrast LVG. In the subacute period (24 ± 11 days; range: 13 to 53 days), vasospasm was assessed in 48 (55%) of the patients by a previously validated method using intracoronary acetylcholine administration (14). The functional change in LV wall motion was studied by LVG in 56 (64%) of the patients, and intraventricular pressure gradient was also examined.

Complications (arrhythmias, pulmonary edema and cardiogenic shock) and the use of intravenous catecholamine and assist devices (intra-aortic balloon pumping, percutaneous cardiopulmonary support system) were examined by review of medical records. In-hospital death and late follow-up of recurrences were also investigated by direct interviews with patients and by reviewing medical records.

Statistical analysis.   All of the data are expressed as mean ± 1 SD. The differences between cardiac functions on LVG in the acute and subacute periods were compared using paired Student t tests. The differences between incidences in two groups were analyzed by the chi-square test. A p value < 0.05 was considered to be statistically significant.

	Results

Top Abstract Subjects and methods Results Discussion Appendix References

 
Representative patients.   Case 1
A 72-year-old woman was admitted to Sapporo Medical University (Sapporo, Japan) on September 17, 1997 due to exacerbation of bronchial asthma and was transferred from another hospital. Ten days later, she felt chest pain at rest. A 12-lead ECG showed ST elevation in I, aVL and V₁ to V₅ (max +4.5 mm in V₃), reciprocating ST depression II, III, aVF and V₆ and abnormal Q-wave in leads V₁ to V₄ (Fig. 1). One hour later, LVG revealed LV apical ballooning (Fig. 1), but no significant stenosis on CAG was confirmed. Intracardiac pressure recording (Fig. 2) showed intraventricular pressure gradient estimated at 75 mm Hg. Maximally released CK was 242 IU/l. After 14 days, the ECG had no ST elevation or abnormal Q-wave but showed a typical coronary T-wave in leads aVL and V₁ to V₄. The LVG demonstrated remarkable functional recovery with an ejection fraction of 72% (Fig. 1), and the intraventricular pressure gradient disappeared (Fig. 2).

View larger version (75K): [in this window] [in a new window]   Figure 1 Representative electrocardiographic changes and left ventriculogram of transient left ventricular (LV) apical ballooning (Case 1). (Left) 12-lead electrocardiogram during chest pain (B) demonstrated ST elevation in leads I, aVL, V1 to V5 and reciprocating ST depression in leads II, III and aVF compared with control (A). Fourteen days after onset (C), a coronary T-wave was confirmed. (Right) Left ventriculogram demonstrated LV apical ballooning. After 15 days, almost all of the contracted LV configuration recovered to normal.

View larger version (80K): [in this window] [in a new window]   Figure 2 Changes in intracardiac pressure recording (Case 1). Intraventricular pressure recording immediately after onset revealed a significant intraventricular pressure gradient (PG), estimated to be 75 mm Hg, with a systolic ejection murmur (Levine III/VI). In the subacute period, no significant pressure gradient was recorded.

View larger version (48K): [in this window] [in a new window]   Figure 3 Electrocardiography and left ventriculographic findings of a representative case (Case 2). (Left) 12-lead electrocardiogram showed ST elevation in leads II, III, aVF and V3 to V6. In the subacute period, the electrocardiogram exhibited a negative T-wave. (Right) Initial left ventriculogram revealed apical ballooning only in the acute period.

View larger version (67K): [in this window] [in a new window]   Figure 4 Scintigraphic and positron emission computed tomographic (PET) findings (Case 2). Nuclear cardiographic evaluations showed marked perfusion (Tc-99m sestamibi [MIBI]) metabolic (I-123 beta-methyl-p-iodophenyl pentadecanoic acid [BMIPP] or I-123 metaiodobenzyl-guanitidine [MIBG]) mismatches mainly at the left ventricular apex. However, in the subacute period, this perfusion metabolic mismatch decreased after the functional recovery (three-dimensional left ventriculography by Tc-99m MIBI). After five months, PET by N-13 ammonia showed improvement in the coronary flow reserve (CFR) assessed by dipyridamole administration. EDV = end-diastolic volume; EF = ejection fraction; ESV = end-systolic volume; MBF = myocardial blood flow; SPECT = single photon emission computed tomography.

As shown in Table 1, 38 patients had a wide spectrum of onset and aggravation of systemic disease including acute-phase cerebrovascular accidents (n = 3), attacks of epilepsy (n = 3), exacerbation of bronchial asthma (n = 3), commencement of dialysis therapy (n = 4) and acute abdomen with pain (n = 7). Moreover, 11 patients exhibited this syndrome during noncardiac surgery or during a procedure (intubation, tracheotomy, transbronchial lung biopsy, delivery, general anesthesia for orthopedic surgery, cholecystectomy, subtotal gastrectomy and colonectomy). The remaining 23 patients had no such specific conditions.

Hemodynamics and LV function.   The results of LVG in the acute and in subacute periods are summarized in Table 4. All of the patients exhibited characteristic apical ballooning with mean ejection fraction of 41 ± 11% (range: 10% to 62%). However, in the subacute period, the mean ejection fraction significantly increased to 64 ± 10% (ranging from 44% to 88%, p < 0.0001). In the acute period, 12 of 72 (18%) patients had a significant intraventricular pressure gradient >30 mm Hg. However, no patients exhibited residual pressure gradient in the subacute period. In an acetylcholine provocative test, coronary spasm was provoked in 10 of the 48 (21%) patients.

Prescribed medications were calcium channel antagonist in 47% of the patients, beta- blockers in 18%, angiotensin-converting enzyme inhibitor in 15%, long-acting nitrate in 47% and diuretics in 19%. Exercise capacities on discharge were New York Heart Association class I in 85 (97%) of the patients, but the remaining two patients had a functional limitation due to advanced age. During a follow-up period of 13 ± 14 months, two of the 72 patients (2.7%) exhibited recurrence due to other emotional stress, and one patient, in whom multivessel spasms had been provoked by an intracoronary acetylcholine test, died suddenly.

	Discussion

Top Abstract Subjects and methods Results Discussion Appendix References

 
Several case studies on transient LV apical ballooning without stenosis on CAG have been reported in Japan (1–6), but this is the first report of a multicenter study on a novel heart syndrome. A total of 88 patients with transient LV apical ballooning were retrospectively analyzed. The main results of this study were: 1) acute onset and aggravation of various systemic disorders (cerebrovascular accidents, epileptic attacks, exacerbation of bronchial asthma, acute abdomen), noncardiac surgery/procedure and emotional/physical problems (sudden accidents, death/funeral of a family member, inexperienced exercise, quarreling or excessive alcohol consumption, vigorous excitation) were found to be possible triggering factors; 2) there were no differences between clinical characteristics of patients with and without the above mentioned factors except for gender likelihood and chest pain/discomfort as an initial symptom; and 3) transient intraventricular pressure gradient and provocative coronary vasospasm were observed in some cases.

Pathophysiologic basis of transient LV apical ballooning.   The precise etiologic basis of transient LV apical wall motion abnormalities could not be determined from the results of this study. Stunned myocardium is generally defined as a prolonged postischemic LV dysfunction after brief myocardial ischemia (16). The results of CAG performed immediately after onset showed no definite evidence of myocardial ischemia originating from epicardial obstruction in any of the subjects. Therefore, we could not confirm reversible wall motion abnormality as in apical stunned myocardium and, instead, named this clinical syndrome "transient LV apical ballooning."

Transient wall motion abnormality after multiple vasospastic angina has also been postulated to be a cause of stunned myocardium (2,7–12,17–19). In our series of cases, provocative vasospasm was confirmed only in limited cases (10/48, 21%). Therefore, multiple vasospasm is not thought to be a main cause. Another possible mechanism is myocardial ischemia due to microvascular spasm. Recently, Mohri et al. (17) indicated that microvascular spasm is one type of myocardial ischemia without significant stenosis in an epicardial artery. Of course, we cannot exclude the possibility of microvascular spasm and the watershed infarction, such that occurs in a cerebrovascular accident, because we could not examine microvascular function.

Several possible triggering conditions that preceded onset were documented in this study. Exposure to internal (emotional) and external stresses (physical, exacerbated disorder, procedural and perioperative) was confirmed. As has been shown in the neurogenic stunned myocardium (7–9) during acute cerebrovascular accidents and catecholamine cardiomyopathy during the endocrine crisis of pheochromocytoma (11,12), enhanced sympathetic activities might be a cause of similar types of myocardial damages. In our retrospective registered cases, we did not measure neurohumoral factors such as the endogenous norepinephrine level, which would have been helpful in confirming this possibility. Triggering factors such as emotional exposure, physical stress and preceding disorders are more important clinical information as the pathophysiologic basis of this heart syndrome. The histologic finding in the syndrome by Kawai et al. (6) in this heart syndrome revealed similar myocardial damage in catecholamine-induced cardiomyopathy. This novel heart syndrome might be one of the clinical models of stress-related sudden death (20–22). However, we found various heterogeneous disorders and procedures as possible triggering factors. All of these conditions might be stressors for patients, but we cannot rule out the possibility of coincident conditions.

Regional apical ballooning and intraventricular pressure gradient.   It was also not evident why the LV apex is selectively vulnerable and subsequently forms balloons. Several anatomic and physiologic factors might contribute to LV apical wall motion abnormalities: 1) the fact that the LV apex does not have a three-layered myocardial structure; 2) the easy loss of elasticity of LV apex after excessive expansion; 3) the fact that the LV apex is the border zone (locus minoris) of the perfusion area of major coronary arteries; and 4) the delay of functional recovery from global dysfunction.

Intraventricular pressure gradients were documented in several cases in this study. It is unlikely that acute exacerbation of midventricular obstruction in hypertrophic cardiomyopathy is a main cause because no case exhibited ECG or echocardiographic myocardial hypertrophy. However, a similar mechanism in apical aneurysm formation in midventricular obstruction of hypertrophic cardiomyopathy might contribute to apical ballooning. Compensatory transient basal hypercontraction may produce midventricular obstruction and plays an important role in causing apical ballooning, which might contribute to secondary ischemia due to increased wall tension.

Clinical implications.   This novel clinical syndrome with chest symptoms and ECG changes mimicking AMI is of clinical importance even though its etiologic basis is not clear. First, we had difficulty in differentiating from stenotic AMI when considering intravenous thrombolysis therapy. Indeed, chest symptoms and ECG findings are similar to those in typical cases of AMI. Second, in many patients, this syndrome occurred in the clinical course of various systemic diseases in the absence of predisposing angina, making it difficult to predict the occurrence of attacks. In patients with a preceding disorder, there might be a diagnostic difficulty because of the absence of typical chest pain/discomfort and the higher incidence of pulmonary congestion. Therefore, careful ECG monitoring will be required. In-hospital prognosis is generally good after appropriate treatment of acute phase complications such as hypotension, pulmonary congestion and ventricular tachyarrhythmias.

Study limitations.   Our study was a retrospective investigation, and there are several limitations. First, the incidence of this syndrome is not clear, nor is it clear why there was a large percentage of women with this heart syndrome. The incidence in women is very high (approximately 6.3-fold higher than that in men), which is clearly different from the established male dominance in coronary artery diseases, including vasospastic angina. However, we could not obtain specific evidence of female dominance. Third, most previous case studies of this syndrome have been conducted in Japan (1–6). Only two case studies outside Japan have been reported (23,24). Therefore, further cases should be investigated to determine regional and racial differences. Fourth, CK was serially examined in these patients, but a more specific method, such as measurement of troponin T levels, would be helpful for precise determination of myocardial injury.

Conclusions.   Precise clinical features of a novel heart syndrome with transient LV ballooning mimicking AMI occurred and were related to various exacerbated systemic disorders; noncardiac surgical procedure and various types of psychotic exposure were shown, but the etiologic basis should be examined in future prospective studies.

	Appendix

Top Abstract Subjects and methods Results Discussion Appendix References

 
Cardiovascular institutes of AP-MI investigations.   Sapporo Medical University (A. Hashimoto, K. Uno, K. Shimamoto); Sapporo JR Hospital (D. Hotta); Iwate Medical University (T. Suzuki, K. Kikuchi); Sendai Cardiovascular Center (S. Tanizaki, Y. Hen); Omiya Medical Center, Jichi Medical University (M. Saito); Yokohama City University Medical Center (T. Saruwatari, I. Kobayashi, M. Shimizu, T. Saito); Shinsyu University (M. Sasamoto, H. Ichinose, M. Aizawa, N. Urasawa, K. Iwamura, S. Ikeda); Osaka City University (J. Yoshikawa); Izumi City Hospital (Y. Kawase); Wakakusa Daiichi Hospital (K. Misu, T. Hirooka); National Cardiovascular Center (S. Sakuragi, Y. Gotoh, H. Nonogi); Osaka City General Hospital (T. Naruko, A. Ito); Wakayama Medical College (M. Obana, K. Tomobuchi); Seiyu Memorial Hospital (N. Nakamura); Tsukazaki Memorial Hospital (H. Iida); Fukuyama Cardiovascular Hospital (M. Taniguchi, H. Kohno, S. Haruta); Kumamoto Central Hospital (F. Ishibashi); Kumamoto Saiseikai Hospital (Y. Takao); Kumamoto University (T. Sakamoto, H. Yasue).

	Acknowledgments

 
The authors would like to express special thanks to each AP-MI investigator in Japan, especially Professor K. Hiramori (Morioka), Professor M. Saito (Omiya), Professor N. Kaneko (Shimotsuga) and the late Mr. K. Hayasaka (Kumamoto) for their suggestions and discussions regarding AP-MI investigations.

	References

Top Abstract Subjects and methods Results Discussion Appendix References

 

1. Satoh H, Tateishi H, Uchida T, et al. Takotsubo-type cardiomyopathy due to multivessel spasm. Kodama K, Haze K, Hon M. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure (in Japanese). Tokyo: Kagakuhyouronsya Co; 1990. p. 56–64
2. Dote K, Sato H, Tateishi H, et al. Myocardial stunning due to simultaneous multivessel spasms: a review of five cases. (in Japanese with English abstract)J Cardiol. 1991;21:203–214[Medline]
3. Dote K, Mitsuda H, Ninomiya M, et al. Tako-tsubo cardiomyopathy (acute reversible catecholamine cardiomyopathy). Okada R. Syndrome of Cardiovascular Disease, III. (in Japanese). Tokyo: Nihon Rinsyoh Co; 1996. p. 166–169
4. Ishihara M, Satoh H, Tateishi H, et al. "Tako-tsubo" type cardiomyopathy (in Japanese with English abstract). Kokyu-to-Junkan. 1997;45:879–885
5. Kawakami H, Matsuoka H, Koyama Y, et al. "Takotsubo" type cardiomyopathy due to acute myocarditis. (in Japanese with English abstract)Kokyu-to-Junkan. 1998;46:913–917
6. Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla cardiomyopathy ("Takotsubo" cardiomyopathy): reversible left ventricular dysfunction with ST segment elevation. Jpn Circ J. 2000;64:156–159[CrossRef][Medline]
7. Kono T, Morita H, Kuroiwa T, et al. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol. 1994;24:636–640[Abstract]
8. Sakomoto H, Nishimura H, Imataka K, et al. Abnormal Q wave, ST-segment elevation, T wave inversion and widespread focal myocytolysis associated with subarachnoid hemorrhage. Jpn Circ J. 1996;60:254–257[CrossRef][Medline]
9. Ohtsuka T, Hamada M, Kodama K, et al. Neurogenic stunned myocardium. Circulation. 2000;101:2122–2124[Free Full Text]
10. Yamanaka O, Yasumasa F, Nakamura T, et al. "Myocardial stunning-" like phenomenon during a crisis of pheochromocytoma. Jpn Circ J. 1994;58:737–742[Medline]
11. Shaw TRD, Bafferty P, Tait GW. Transient shock and myocardial impairment caused by pheochromocytoma crisis. Br Heart J. 1987;57:194–198[Abstract/Free Full Text]
12. Akutsu Y, Shinozuka A, Huang TY, et al. Hypertrophic cardiomyopathy with apical left ventricular aneurysm. Jpn Circ J. 1998;62:127–131[CrossRef][Medline]
13. Kuramoto K, Matsushita S, Murakami M. Acute reversible myocardial infarction after blood transfusion in the aged. Jpn Heart J. 1977;18:191–201[Medline]
14. Yasue H, Horio Y, Nakamura N, et al. 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. Circulation. 1986;84:955–963
15. WHO MONICA Project Principal InvestigatorsTunstall-Pedoe H. The World Heath Organization MONICA project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. J Clin Epidemiol. 1988;41:105–114[CrossRef][Medline]
16. Braunwald E, Kloner RA. The stunned myocardium: prolonged postischemic ventricular dysfunction. Circulation. 1982;66:1146–1149[Abstract/Free Full Text]
17. Mohri M, Koyanagi M, Egashira K, et al. Angina pectoris caused by coronary microvascular spasm. Lancet. 1998;351:1165–1169[CrossRef][Medline]
18. Mathias P, Kerin NZ, Belvins RD, et al. Coronary vasospasm as a cause of stunned myocardium. Am Heart J. 1987;113:383–385[CrossRef][Medline]
19. Fournier C, Boujon B, Herbert JL, et al. Stunned myocardium following coronary spasm. Am Heart J. 1991;121:593–595[CrossRef][Medline]
20. Earnest MP, Thomas GE, Eden RA, et al. The sudden unexplained death syndrome in epilepsy: demographic, clinical and postmortem features. Epilepsia. 1992;33:310–316[CrossRef][Medline]
21. Rockhold RW, Acuff CG, Clower BR. Excitotoxin-induced myocardial necrosis. Eur J Pharm. 1989;166:571–576[CrossRef][Medline]
22. Mittleman MA, Maclure M, Sherwood JB, et al. Triggering of acute myocardial infarction onset by episodes of anger. Circulation. 1995;92:1720–1725[Abstract/Free Full Text]
23. Scully RE, Mark EJ, McNeely BU. Case 16-1986: case records of Massachusetts General Hospital. N Engl J Med. 1986;314:1240–1247[Medline]
24. Villareal RP, Achari A, Wiansky S, Wilson JM. Anteroapical stunning and left ventricular outflow obstruction. Mayo Clin Proc. 2001;76:79–83[Medline]

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				A. Chockalingam, L. Tejwani, K. Aggarwal, and K. C. Dellsperger Dynamic Left Ventricular Outflow Tract Obstruction in Acute Myocardial Infarction With Shock: Cause, Effect, and Coincidence Circulation, July 31, 2007; 116(5): e110 - e113. [Full Text] [PDF]

				R. C. Ziegelstein Acute Emotional Stress and Cardiac Arrhythmias JAMA, July 18, 2007; 298(3): 324 - 329. [Abstract] [Full Text] [PDF]

				A. Lerman, D. R. Holmes, J. Herrmann, and B. J. Gersh Microcirculatory dysfunction in ST-elevation myocardial infarction: cause, consequence, or both? Eur. Heart J., April 1, 2007; 28(7): 788 - 797. [Abstract] [Full Text] [PDF]

				B. Teo A mimicry of an acute coronary syndrome Emerg. Med. J., April 1, 2007; 24(4): e25 - e25. [Abstract] [Full Text] [PDF]

				S. Buchholz and G. Rudan Tako-tsubo syndrome on the rise: a review of the current literature Postgrad. Med. J., April 1, 2007; 83(978): 261 - 264. [Abstract] [Full Text] [PDF]

				G. D. Lewis, C. B. Holmes, G. Holmvang, and J. R. Butterton Case 8-2007 -- A 48-Year-Old Man with Chest Pain Followed by Cardiac Arrest N. Engl. J. Med., March 15, 2007; 356(11): 1153 - 1162. [Full Text] [PDF]

				S. W. Sharkey, J. R. Lesser, M. S. Maron, and B. J. Maron Stress Cardiomyopathy J. Am. Coll. Cardiol., February 27, 2007; 49(8): 921 - 921. [Full Text] [PDF]

				A. Prasad Apical Ballooning Syndrome: An Important Differential Diagnosis of Acute Myocardial Infarction Circulation, February 6, 2007; 115(5): e56 - e59. [Full Text] [PDF]

				M. Berman, M. Saute, E. Porat, M. Vaturi, L. Paul-Kislin, B. A. Vidne, and A. Kogan Takotsubo Cardiomyopathy: Expanding the Differential Diagnosis in Cardiothoracic Surgery Ann. Thorac. Surg., January 1, 2007; 83(1): 295 - 298. [Abstract] [Full Text] [PDF]

				A L Baggish, R N Smith, I Palacios, G J Vlahakes, D M Yoerger, M H Picard, P A Lowry, I-k Jang, and M A Fifer Pathological effects of alcohol septal ablation for hypertrophic obstructive cardiomyopathy Heart, December 1, 2006; 92(12): 1773 - 1778. [Abstract] [Full Text] [PDF]

				M B. Iqbal, J. C Moon, O. P Guttmann, P. Shanahan, P. J Goadsby, and D. R Holdright Stress, emotion and the heart: tako-tsubo cardiomyopathy Postgrad. Med. J., December 1, 2006; 82(974): e29 - e29. [Abstract] [Full Text] [PDF]

R. T. Hurst, J. W. Askew, C. S. Reuss, R. W. Lee, J. P. Sweeney, F. D. Fortuin, J. K. O