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Systematic Review: Transient Left Ventricular Apical Ballooning: A Syndrome That Mimics ST-Segment Elevation Myocardial Infarction

Kevin A. Bybee, MD; Tomas Kara, MD, PhD; Abhiram Prasad, MD, MRCP; Amir Lerman, MD; Greg W. Barsness, MD; R. Scott Wright, MD; and Charanjit S. Rihal, MD
[+] Article and Author Information

From Mayo Clinic College of Medicine, Rochester, Minnesota.


Potential Financial Conflicts of Interest:Consultancies: R.S. Wright (Bayer); Grants received: R.S. Wright (Centocor, Merck, Bayer, Bristol-Myers Squibb).

Requests for Single Reprints: Charanjit S. Rihal, MD, Cardiac Catheterization Laboratory, Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905; e-mail, Rihal@mayo.edu.

Current Author Addresses: Drs. Bybee, Kara, Prasad, Lerman, Barsness, Wright, and Rihal: Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905.


Ann Intern Med. 2004;141(11):858-865. doi:10.7326/0003-4819-141-11-200412070-00010
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The transient left ventricular apical ballooning syndrome, also known as takotsubo cardiomyopathy, is characterized by transient wall-motion abnormalities involving the left ventricular apex and mid-ventricle in the absence of obstructive epicardial coronary disease. In this paper, we review case series that report on patients with the transient left ventricular apical ballooning syndrome to better characterize patients presenting with the syndrome.We identified 7 case series that reported on at least 5 consecutive patients with the transient left ventricular apical ballooning syndrome. The syndrome more often affects postmenopausal women (82% to 100%) (mean age, 62 to 75 years). Patients commonly present with ST-segment elevation in the precordial leads, chest pain, relatively minor elevation of cardiac enzyme and biomarker levels, and transient apical systolic left ventricular dysfunction despite the absence of obstructive epicardial coronary disease. An episode of emotional or physiologic stress frequently precedes presentation with the syndrome. The in-hospital mortality rate seems to be low, as does the risk for recurrence.

Figures

Grahic Jump Location
Figure 1.
Left ventriculograms (end-systole) of 2 patients with the transient left ventricular apical ballooning syndrome and examples of a tako-tsubo.

A. Note the characteristic appearance with “apical ballooning.” B and C. A tako-tsubo; note the similarities in appearance with the morphologic appearance of the left ventricle during systole. D and E. Left ventriculograms of another patient with the syndrome were obtained by cardiac catheterization during systole (D) and diastole (E). The photograph taken during systole demonstrates the characteristic left ventricular “apical ballooning” seen with the syndrome. Coronary angiography revealed no evidence of coronary artery disease. An echocardiogram obtained 30 days after presentation showed complete resolution of the left ventricular wall-motion abnormalities. Part A is adapted from and parts B and C are reprinted from American Heart Journal, volume 143, Kurisu S, Sato H, Kawagoe T, Ishihara M, Shimatani Y, Nishioka K, et al., Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction, pages 448-455, 2002, with permission from Elsevier.

Grahic Jump Location

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Transient left ventricular apical ballooning: is acute coronary syndrome exclusion correct?
Posted on December 14, 2004
Borja Ibanez
Fundacion Jimenez Diaz, Madrid, Spain.
Conflict of Interest: None Declared

We read with interest the review article by Bybee et al on transient left ventricular (LV) apical ballooning(1). On March 2004 our group published a series of 11 patients with tako-tsubo syndrome(2). While this paper was originally published in Spanish, its English version is available online (pubmed, www.revespcardiol.org). Beyond claiming the publication of one of the largest single centre series, our work provides new findings that may serve to understand better this syndrome. As mentioned by Bybee et al tako-tsubo patients meet the diagnose criteria of acute myocardial infarction (AMI)(3). However, AMI has been said to be ruled out for 2 reasons: the absence of luminal coronary stenosis, and the wide akinetic area not complying with the perfusion territory of a single coronary artery(4). In our initial work we described that patients with apical ballooning have a well developed left anterior descending coronary artery (LAD) with a long distal recurrent segment supplying a significant area of the inferior segments of the LV. Patients with a transmural anterior AMI due to an isolated LAD occlusion show a LV motion indistinguishable from that of tako-tsubo patients if the LAD has a well developed recurrent segment(2). Because of these findings we hypothesised that tako-tsubo transient LV apical ballooning could be due to an acute occlusion of the LAD followed by an early and complete spontaneous reperfusion occurring in patients with a well developed LAD. To test this hypothesis, we prospectively performed in five consecutive patients with this syndrome an intravascular ultrasound study on the LAD [Ibanez B, Navarro F, Cordoba M, Marcos- Alberca P, Farre J. "Tako-tsubo transient left ventricular apical ballooning: is IVUS the key to resolve the enigma?" Heart 2005; vol 91 (number 1) In Press]. In all these 5 patients, and in 2 more cases added after our submission to Heart, we found in the middle LAD a single complicated eccentric atherosclerotic plaque, not visible on angiography. The plaque features include disruption of the intimal layer with cavities inside the plaque or intimal dissection. Our findings highly support that this syndrome could be, at least in some cases, an AMI with early resolution of the coronary occlusion, either atherothrombotic or spastic. The rapid reperfusion could explain the minimal enzymatic release and the LV recovery within a few days (myocardial stunning rather than necrosis). These novel findings are of practical importance and we advocate managing these patients as an acute coronary syndrome.

References

(1) Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141:858-65.

(2) Ibanez B, Navarro F, Farre J, Marcos-Alberca P, Orejas M, Rabago R et al. Tako-tsubo syndrome associated with a long course of the left anterior descending coronary artery along the apical diaphragmatic surface of the left ventricle. Rev Esp Cardiol. 2004;57:209-16.

(3) Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000;36:959-69.

(4) Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart. 2003;89:1027-31.

Conflict of Interest:

None declared

Transient left ventricular dysfunction
Posted on January 3, 2005
Junya Ako
Stanford University
Conflict of Interest: None Declared

In their systematic review of transient left ventricular apical ballooning, Dr. Bybee et al. rightly describe this unusual disorder(1). They propose their criteria for the clinical diagnosis of this phenomenon in their article. We, however, disagree about the proposal to exclude patients with head trauma and intracranial bleeding.

Left ventricular dysfunction is known to occur in patients with acute brain injury. This left ventricular dysfunction is usually reversible within weeks(2), and the dysfunction pattern is reasonably similar to the transient disorder described in their article. In view of the resemblance of clinical pictures, we believe the left ventricular dysfunction after acute insult to the brain is of similar pathogenesis(3), and not a totally different clinical entity. Furthermore, we believe such types of reversible ventricular dysfunction, presumably mediated by the nervous system, should also be encompassed within the definition of this syndrome. Therefore, broader inclusion criteria would be suggested for this novel disease concept.

Nonetheless, the authors should be commended for their extensive research and excellent publication. Increased awareness and an interdisciplinary approach involving neurologists, neurosurgeons, psychologists, and cardiologists should further help us understand the nature of this disorder.

References

1. Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141(11):858-65.

2. Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol. 1994;24(3):636-40.

3. Ako J, Honda Y, Fitzgerald J. Tako-tsubo-like left ventricular dysfunction. Circulation. 2003;108(23):e158.

Conflict of Interest:

None declared

The "Mayo Criteria" for the diagnosis of transient left ventricular apical ballooning
Posted on January 6, 2005
Reza Alizadeh Dehnavi
Leiden University Medical Center
Conflict of Interest: None Declared

The "Mayo Criteria" for the diagnosis of transient left ventricular apical ballooning

R.Alizadeh Dehnavi MD.¹, E.E.van der Wall MD. Ph.D.²

¹ Vascular Medicine, Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands

² Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands

Dear Editor,

We have read the article by Bybee and collegues [1] on transient left ventricular apical ballooning with great interest. In their report, they propose the "Mayo Criteria" for the clinical diagnosis of this syndrome. Some adjustments have been made in comparison to the previously proposed criteria by Abe and Kondo. [2] In our opinion the addition of tachycardia induced cardiomyopathy as an exclusion criterion to the "Mayo Criteria" would be appropriate, if the primary form of the syndrome is to be diagnosed.

Reversible left ventricular dysfunction after an episode of ventricular tachycardia has been reported. [3] Rapid ventricular pacing in animal models has also been shown to result in a transient dysfunction of the left ventricle. [4] Although the specific apical ballooning has not been mentioned in these reports, the reversible character of the ventricular dysfunction is a sufficient argument for the addition of this entity to the exclusion criteria.

References

[1] Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004 Dec 7;141(11):858-65.

[2] Abe Y, Kondo M. Apical ballooning of the left ventricle: a distinct entity? Heart. 2003 Sep;89(9):974-6.

[3] Iga K, Hori K, Matsumura T. Reversible left ventricular dysfunction induced by recurrent ventricular tachycardia. Chest. 1992 Dec;102(6):1897-8.

[4] Howard RJ, Stopps TP, Moe GW, Gotlieb A, Armstrong PW. Recovery from heart failure: structural and functional analysis in a canine model. Can J Physiol Pharmacol. 1988 Dec;66(12):1505-12.

Conflict of Interest:

None declared

Expanded diagnostic criteria for transient left ventricular apical ballooning
Posted on January 6, 2005
Mori J Krantz
Denver Health
Conflict of Interest: None Declared

Bybee and colleagues propose novel diagnostic criteria for transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction (1). While the absence of epicardial coronary artery disease is central to this unusual diagnosis, an expanded list of conditions associated with reversible myocardial dysfunction should be added to their exclusion criteria. For instance, transient dysfunction of the apical myocardium and normal coronary anatomy has been described with critical illness, acute respiratory distress syndrome, and toxic-metabolic derangements (2). Coronary arterial air embolus following penetrating trauma, if visualized and promptly aspirated may also result in reversible myocardial dysfunction (3). Similarly, migration of a venous thrombus through a patent foramen ovale (paradoxical embolus) fulfills all of their proposed diagnostic criteria: normal coronary anatomy, transient left ventricular dysfunction, ST-segment changes, and elevated cardiac biomarkers. Moreover, regional wall motion abnormalities may extend beyond a single epicardial vascular distribution if the embolus enters the left main coronary artery (4). Therefore, a simplified exclusionary criterion for this syndrome might be the absence of any established cause of reversible myocardial dysfunction.

1. Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858-65.

2. Bailen MR. Reversible myocardial dysfunction in critically ill, noncardiac patients: a review. Critical Care Medicine 2002;30:1280-90.

3. Graham JM, Beall AC, Mattox KL, Vaughan GD. Systemic air embolism following penetrating trauma to the lung. Chest 1977;72:449-54.

4. Meir-Ewert HK, Labib SB, Shick EC, Gossman DE, Stix MS, Williamson CA. Paradoxical embolism in the left main coronary artery: diagnosis by transesophageal echocardiography. Mayo Clin Proc 2003;78:103-6.

Conflict of Interest:

None declared

Author response to comments
Posted on January 17, 2005
Charanjit S. Rihal
Mayo Clinic College of Medicine
Conflict of Interest: None Declared

We appreciate Dr. Ibanez's interest in our review of the Transient Left Ventricular Apical Ballooning Syndrome (TLVABS) (1) and commend Dr. Ibanez and his colleagues on their investigative efforts into possible pathophysiologic mechanisms responsible for the syndrome. Ibanez and colleagues report rupture of mid left anterior descending (LAD) coronary artery plaque detected by intravascular ultrasound examination in 5 patients presenting with the TLVABS (2). These patients had angiographically normal appearing coronary arteries with a large recurrent distal LAD segment supplying the diaphragmatic segment. These findings are interesting, but seem an unlikely pathophysiologic explanation for most cases of TLVABS for several reasons. One would expect to more commonly observe residual, angiographically detectable intracoronary LAD thrombus if this were truly the cause of the syndrome in most cases. Second, abnormal coronary blood flow has been documented in all three major epicardial coronary arteries using TIMI frame count and coronary flow reserve techniques during the acute presentation phase of the syndrome (3-5). Third, it would be hard to explain the female gender predominance of those presenting with the syndrome based on the proposed plaque rupture mechanism. Fourth, in our experience, patients presenting with TLVABS do not consistently have long recurrent distal LAD coronary arteries, yet these patients consistently demonstrate regional wall motion abnormalities beyond the distribution of a single epicardial coronary artery. Lastly, we have observed acute transient right ventricular systolic dysfunction in many of the patients presenting to our medical center with TLVABS, which could not be explained by isolated transient LAD occlusion.

The pathophysiologic mechanisms responsible for TLVABS remain ill- defined and further research is needed. The diffuse nature of the left ventricular dysfunction, and in some cases right ventricular dysfunction, suggests that widespread transient myocardial ischemia or neurogenically- mediated metabolic myocardial injury may underlie the syndrome. As Dr. Ibanez rightly points out, TLVABS may very well represent an acute coronary syndrome and further investigation to this end is needed. However, we feel that the syndrome should be classified as an acute "cardiac" syndrome until further investigative data evaluating the pathophysiologic mechanisms underlying the syndrome become available. The findings of Dr. Ibanez and colleagues emphasize the need for additional physiologic and anatomic investigation of the syndrome utilizing intracoronary ultrasound and other techniques. Collaborative investigative efforts, including the development of a TLVABS registry, would likely expedite our understanding of this fascinating syndrome.

1. Bybee KA, Kara T, Prasad A, Lerman A, Barsness G, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858-865. 2. Ibanez B, Navarro F, Cordoba M, Marcos-Alberca P, Farre J. Tako-tsubo transient left ventricular apical ballooning: is intravascular ultrasound the key to resolve the enigma? Heart 2005;91:102-104. 3. Bybee KA, Prasad A, Barsness G, Lerman A, Murphy J, Jaffe A, Wright RS, et al. Clinical characteristics and TIMI frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343-346. 4. Kurisu S, Inoue I, Kawagoe T, Ishihara M, Shimatani Y, Nishioka K, et al. Myocardial perfusion and fatty acid metabolism in patients with tako- tsubo-like left ventricular dysfunction. J Am Coll Cardiol 2003;41:743- 748. 5. Ako J, Takenaka K, Uno K, Nakamura F, Shoji T, Iijima K, et al. Reversible left ventricular systolic dysfunction"”reversibility of coronary microvascular abnormalities. Jpn Heart J 2001;42:355-363.

Conflict of Interest:

None declared

Authors' Reply
Posted on January 27, 2005
Charanjit S. Rihal
Mayo Clinic College of Medicine
Conflict of Interest: None Declared

We thank Dr. Ibanez, Dr. Ako, as well as Drs. Dehnavi and van der Wall for their interest in our review of the Transient Left Ventricular Apical Ballooning Syndrome (TLVABS)(1). Ibanez and colleagues report LAD plaque rupture detected by intravascular ultrasound in 5 patients presenting with TLVABS(2). These patients had angiographically normal- appearing coronary arteries with a large recurrent distal LAD segment. These findings are interesting, but seem an unlikely pathophysiologic explanation for the majority of cases of TLVABS. First, angiographically detectable intracoronary LAD thrombus would be expected more frequently if plaque rupture were the primary mechanism of the syndrome. Second, abnormal coronary blood flow has been documented in all three major epicardial coronary arteries during the acute presentation phase of the syndrome (3,4). Third, patients presenting with TLVABS commonly do not have long recurrent distal LAD coronary arteries, and indeed manifest wall motion abnormalities beyond that of a single epicardial coronary artery distribution. Fourth, this mechanism would not explain the strong female gender predominance reported with TLVABS. Lastly, we have observed acute transient right ventricular systolic dysfunction in many patients presenting with TLVABS, which could not be explained by isolated transient LAD occlusion. It is our feeling that TLVABS should be considered an acute cardiac syndrome, rather than an acute coronary syndrome, until additional investigative data elucidating the pathophysiologic mechanisms underlying TLVABS are available.

In listing exclusion criteria as a part of the diagnostic criteria for TLVABS, our intent was to exclude distinct conditions that could potentially present in a similar manner as TLVABS. Tachycardia-mediated LV dysfunction rarely presents as an acute cardiac syndrome and lacks the characteristic distribution of wall motion abnormalities seen with TLVABS. Therefore, we do not feel it is necessary to include this entity as an exclusion critereon, as suggested by Drs. Dehnavi and van der Wall. Dr. Ako suggests that head trauma and intracranial bleeding should not be an exclusion critereon for the clinical diagnosis of TLVABS. Significant head trauma and intracranial bleeding may indeed be associated with reversible apical LV dysfunction, however the reported distribution of wall motion abnormalities in consecutive patients with brain injury differs. For example, one study suggests that basal hypokinesis with preservation of apical function is the most common finding in these patients (5). At this point, it is unclear if LV dysfunction associated with brain injury and TLVABS share similar pathophysiologic mechanisms.

The mechanisms responsible for TLVABS remain ill-defined and further research is needed. Collaborative investigative efforts, including the development of a TLVABS registry, would likely expedite our understanding of this under-recognized syndrome.

References:

1. Bybee KA, Kara T, Prasad A, Lerman A, Barsness G, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858-865.

2. Ibanez B, Navarro F, Cordoba M, Marcos-Alberca P, Farre J. Tako- tsubo transient left ventricular apical ballooning: is intravascular ultrasound the key to resolve the enigma? Heart 2005;91:102-104.

3. Bybee KA, Prasad A, Barsness G, Lerman A, Murphy J, Jaffe A, Wright RS, et al. Clinical characteristics and TIMI frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343-346.

4. Kurisu S, Inoue I, Kawagoe T, Ishihara M, Shimatani Y, Nishioka K, et al. Myocardial perfusion and fatty acid metabolism in patients with tako-tsubo-like left ventricular dysfunction. J Am Coll Cardiol 2003;41:743-748.

5. Dujardin K, McCully R, Wijdicks E, Tazelaar HD, Seward JB, McGregor CG, et al. Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features. J Heart Lung Transplant 2001;20:350-357.

Conflict of Interest:

None declared

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