Article, Cardiology

Troponin elevation in aortic dissection patients may be due to takotsubo cardiomyopathy

Unlabelled imageTroponin elevation in aortic dissection “>Correspondence

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American Journal of Emergency Medicine

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Troponin elevation in aortic dissection patients may be due to takotsubo cardiomyopathy? Aortic dissection vs takotsubo cardiomyopathy

To the Editor,

Acute myocardial infarction (AMI) and acute aortic dissection (AoD) are important differential diagnoses because they share essential risk factors (eg, Arterial hypertension, male sex, psychical and/or emotional stress) [1] as well as essential features in clinical presentation (eg, strong chest pain, syncope). Acute myocardial infarction is far more common (750-800 times) than AoD [2,3].

Consequently, it is not clever to perform extensive, time-consum- ing imaging (eg, computed tomography) to exclude AoD in each patient with (suspected) AMI [4]. This would rarely be fruitful but will lead to prolongation of time to reperfusion, which is crucial in AMI [1,5-7]. Instead, both looking for some discriminative findings (such as migrating and back pain, differences in pulse presence/strength and in blood pressure between arms, aortic regurgitant murmur) as well as quick bedside transthoracic echocardiogram have been advised [1,6]. Moreover, AMI and AoD can be causally related–there are at least

5 recognized mechanisms how AoD may cause AMI directly (mechanically) [8]. It is believed that most AoD-induced AMIs is caused indirectly, via hemodynamic stresses and instability [9]. The prevalence of AMI among 988 AoD patients was 7% [1]. Myocardial ischemia is present in up to 19% of patients with acute AoD [1]. It may be different in various nations because Hirata et al [9] reported that almost 50% of AoD patients had acute electrocardiographic signs of injury or ischemia [9,10]. Coronary arteries are involved in 10% to 15% of AoD [7]. Up to 23.5% AoD patients had elevated troponin levels, with a 4-fold higher risk of death [9]. Moreover, the prevalence of ST-segment elevation myocardial infarction is 3% in AoD patients, according to report from the large International Registry of Aortic Dissection [4]. Besides, AoD-induced AMI is dominantly type 2 AMI [2].

Not recognizing that STEMI in particular patient is induced by AoD has several bad consequences, for example, administration of antiplatelet, anticoagulant, and even Fibrinolytic therapy [1]. This increases aortic medial dissecting hematomas; chances for aortic rupture; and already very high mortality (believed to be as high as 1% per hour in the first 2 days–if left untreated) as well as time to surgical treatment, which is the treatment of choice for proximal AoD. Inadvertent administration of thrombolysis to patients with AoD- induced STEMI may be expected to become even more frequent in the times to come. Namely, expansion of prehospital fibrinolysis has been

? This work has been supported by the Serbian Ministry of Education and Science, grant number III41018.

0735-6757/$ – see front matter (C) 2013

occurring, due to accumulated positive evidences and availability of “user-friendly” (practical) thrombolytic–in the form of intravenous injection. The price to pay would be an increase in the absolute number of patients receiving fibrinolytic for “STEMI-like” conditions (such as acute perimyocarditis) as well as for AoD-induced STEMI. Additional education and increase of awareness on the problem, which is potentially catastrophic for patients, might optimize the effects of prehospital fibrinolysis [8].

Takotsubo (stress-related) cardiomyopathy (TTs-CMP) is a revers- ible left ventricular dysfunction, possibly due to a catecholamine- mediated Myocardial stunning, which usually (?90%) occurs in Postmenopausal women and is associated with emotional or physical stress [11-13]. Takotsubo (stress-related) cardiomyopathy is an unclassified, nonfamilial cardiomyopathy [13,14]. The concept of TTs-CMP was introduced by Hiauru Sato in 1990, and it became important differential diagnosis of AMI [6]. Takotsubo (stress-related) cardiomyopathy is now considered to account for 1% to 2% or 1% to 3% of patients with suspected AMI [12,13]. Initially, apical wall motion abnormalities (“apical ballooning”) were considered typical, since the name tako-tsubo. It is a fisherman’s pot with a round bottom and narrow neck (used for trapping octopuses in Japan), which resembles the left ventriculogram during systole in TTs-CMP [12].

In-hospital mortality from TTs-CMP is low (b 2%), but pulmonary edema, cardiogenic shock, and arrhythmias are not rare [15]. There is a dramatic surge in recognition of TTs-CMP, more than 1000 reports were published (increasing to 300 per year) [16]. Takotsubo (stress- related) cardiomyopathy is frequently clinically indistinguishable from an acute coronary syndrome [17]. The onset may include chest pain (53%-71%), with similar characteristics and irradiation [17]. Stress has been recognized as important cause/trigger for both diseases [12,13]. Moreover, ECG changes are alike [12,13]. Thus, TTs- CMP is accepted as a differential diagnosis for AMI for good reasons, and it should automatically become differential diagnosis for AoD.

Similarities between AoD-induced STEMI and TTs-CMP are also numerous and important: stress is important for the etiopathogenesis of both conditions [1,12,13]. Chest pain is the leading symptom in both diseases [1,17]. Electrocardiogram is also similar. The most common abnormality on the initial ECG in TTs-CMP is ST-segment elevation (30%-50%, but up to 90%) or negative T wave [12,15,17]. Prevalence of TTs-CMP is reported to be as high as 7.6% among patients with ST elevation and Myocardial necrosis [15]. troponin values are increased commonly in TTs-CMP and are necessary for STEMI [12,15]. In addition, even computed tomographic findings may be similar. TTs- CMP can occasionally result in cardiogenic shock, which may cause abnormal aortic contrast medium distribution, due to functional rather

than to anatomical changes [11]. Furthermore, AoD-induced STEMI will have harm from thrombolysis. The same is true for TTs-CMP [12]. In patients with chest pain, findings of both raised troponin and ST- segment elevation narrow the differential diagnosis toward STEMI. Importantly, both AoD and TTs-CMP should remain as possibilities for differential diagnosis.

PubMed search (performed on December 20, 2012) for “aortic dissection takotsubo” had no more than 5 articles. Only 1 of them described AoD and TTs-CMP as differential diagnoses [11], but the patient described had no ST elevation. Recently, 2012 STEMI guidelines recommend differentiation of STEMI from both AoD and TTs-CMP [6]. To the contrary, current AoD guidelines do not mention TTs-CMP [1]. Acute aortic dissection-induced STEMI is suggested by the following findings (among others): pulse deficit [1], pseudohypotension (falsely low blood pressure either in the left or right arm, due to compromisED flow to the subclavian artery) [18], aortic regurgitant murmur [1], and others. To the contrary, TTs-CMP is more probable diagnosis in postmenopausal women with extraordinary stress, without prior

arterial hypertension [12,13]. Bedside echo may help [1,3].

In conclusion, AoD-induced STEMI has an additional important differential diagnosis–takotsubo cardiomyopathy because they have many similarities (eg, they are caused/triggered by stress, chest pain is the leading symptom, ST-segment elevation is present, etc). This important differential diagnosis is largely unrecognized, even in the best current guidelines. Moreover, PubMed search revealed not a single article about differential diagnosis between AoD-induced STEMI and takotsubo cardiomyopathy. It seems very likely that takotsubo cardiomyopathy (being increasingly recognized in prac- tice) is going to become even more important differential diagnosis for STEMI, including AoD-induced STEMI. It is probable that, in some AoD patients, increased troponin values were ascribed to AMI but were actually caused by takotsubo cardiomyopathy.

Goran P. Koracevic MD, PhD

Department of Cardiology, Clinical Centre and Medical Faculty

University of Nis, Nis, Serbia E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2012.12.034

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