International Journal of Cardiovascular ResearchISSN: 2324-8602

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Letter to Editor, Int J Cardiovas Res Vol: 6 Issue: 3

Takotsubo Cardiomyopathy ? Acute Myocarditis ? or Both? Not so Easy to Diagnose in Certain Settings

Kenan Yalta*, Mustafa Yılmaztepe, Fatih Ucar and Cafer Zorkun

Trakya University Cardiology Department, Edirne, Turkey

*Corresponding Author : Kenan Yalta
Trakya University Cardiology Department, Edirne, Turkey
E-mail: [email protected]

Received: March 31, 2017 Accepted: April 12, 2017 Published: April 19, 2017

Citation: Yalta K, Yılmaztepe M, Ucar F, Zorkun C (2017) Takotsubo Cardiomyopathy ? Acute Myocarditis ? or Both ? Not so Easy to Diagnose in Certain Settings. Int J Cardiovasc Res 6:3. doi: 10.4172/2324-8602.1000310


In clinical practice, there exists a significant clinical overlap between takotsubo cardiomyopathy (TTC) and myocarditis potentially creating a diagnostic challenge particularly in the setting of forme-fruste manifestations. Moreover, these two conditions may occasionally co-exist possibly rendering the ultimate diagnosis even more complicated. On the other hand, since TTC and myocarditis have different prognostic and therapeutic implications, clinicians should make every effort to reach a definitive diagnosis. The present paper primarily aims to discuss differential features of these two conditions along with the diagnostic value of certain sophisticated tools including cardiac magnetic resonance imaging (MRI), etc. in this setting.

Keywords: Takotsubo cardiomyopathy; Myocarditis; Forme-fruste presentation and Magnetic resonance imaging

Takotsubo cardiomyopathy (TTC) has been regarded as a spesific form of cardiomyopathy with a transient nature and a particular predilection for post-menopausal females [1-5]. Currently,central to the pathogenesis of this phenomenon, as widely accepted, is well known to be a state of sympathetic hyperstimulation associated with a variety of internal or external stressors [1-5]. In particular, TTC needs to be differentiated from acute coronary syndromes (ACS) in a proper manner as these two clinical conditions potentially harbor a striking analogy in terms of their clinical presentations including signs, symptoms as well as electrocardiographic (ECG) findings [2,4]. On the other hand, patients with TTC may also present with signs and symptoms of acute heart failure in certain settings potentially indicating a variety of predictors (an existing physical trigger, senility etc.) for the evolution of clinical heart failure in these patients [4,6]. Therefore, besides ACSs, TTC should also be differentiated from a variety of acute heart failure syndromes (AHFS) including acute viral myocarditis primarily regarded as an inflammatory process involving the myocardium (viral, idiopathic, etc in origin) without a gender predilection [7].

In clinical practice, acute myocarditis may potentially mimick TTC, particularly in terms of its clinical manifestations including symptomatology (dyspnea, chest pain, etc.), presence of insignificant stenoses on coronary angiography (thus ruling out ACS), histopathological findings (to some extent), and ECG changes (ST-T segment alterations, pathological Q waves, reduction in R wave amplitute, etc.) and elevation of myocardial enzymes (though disproportionately much lower in the setting of TTC) in certain settings [7]. On the other hand, transthoracic echocardiogram (TTE) demonstrates a typical apical ballooning pattern with a segmentary basal hyperkinesis of the left ventricle (LV) in the majority of TTC patients [7]. In contrast, TTE findings of myocarditis generally appear to be quite non-spesific and may be characterized by a variety of regional or global wall thickening and contractile dysfunction of the LV with or without pericardial effusion [7]. More importantly, it is well known that certain forms of AHFS including acute myocarditis, in comparison to TTC, may have a particular predisposition to a variety of acute complications including bradyarrhythmias, etc [7]. Regarding myocardial impairment, acute myocarditis , unlike TTC,may not always manifest as a completely reversible pathology suggesting variable degrees of persistent myocardial damage (even after full recovery) as measured with a variety of sophisticated imaging modalities including cardiac magnetic resonance imaging (MRI) [8] gradually leading to a form of dilated cardiomyopathy, (D-CMP) [9] largely associated with myocardial remodelling in the long-term. Futhermore, management strategies including medication and follow-up may significantly vary between TTC and myocarditis in the hospital setting as well as in the postdisharge period. Therefore, absolute differentiation between these two conditions in the hospital setting appears to be mandatory owing to a variety of prognostic [8,9] as well as therapeutic implications both in the short and long terms.

In the current literature, borderline cases with ambiguous features (in favor of both myocarditis and TTC) have been reported: in their recently published article [10], Oh PC et al. reported a case of recurrent TTC with signs and symptoms of acute heart failure on admission who completely recovered on follow-up. The same patient was previously reported to suffer another TTC attack also manifesting as an AHFS 1 year before her latest admission with TTC [11]. In our opinion, even though previous presentation of the patient totally confirrmed to the features of a typical TTC in isolation complicated by acute heart failure (with an emotional trigger and reversible segmentary wall motion abnormalities on echocardiogram (TTE), etc) [9], in her latest presentation with a reportedly TTC recurrence appeared to have a variety of ambigiuous findings that might also be suggestive of an emerging viral myocarditis (in isolation or in combination with TTC) rather than a definitive recurrent TTC attack in isolation (largely based on findings potentially supporting myocarditis including preceding flu-like symptoms [8], presence of reversible global hypokinesia on TTE and no mention of any emotional or physical trigger) [10]. Similarly, Jorge C et al. previously reported a case strongly suggestive of a TTC attack with mid-apical LV involvement that finally turned out to be a case of myocarditis through evaluation of cardiac MRI [9].

Undoubtedly, both myocarditis and TTC, even in their isolated forms, might emerge with a variety of ‘forme fruste’ manifestations that might potentially hinder the definitive diagnosis [9,12-15] (for ins; myocarditis with an exclusively mid-apical involvement [14] following a respiratory infection or atypical TTC variants including inverted or reverse TTC (affecting mid-basal segments and sparing apex of the LV), etc. [16]. Therefore, clinicians should stand aloof from preconditionings regarding presentation patterns of AHFSs including TTC and myocarditis with a full awareness of possible intersecting zones,and should not feel strictly bound by categorical definitions of these conditions [12]. Within a deeper etiopathogenetic context, a potential casual association between TTC and myocarditis (or perimyocarditis) was also previously suggested beyond a simple coincidence indicating that one might have the potential to trigger the other without a mutual exclusion in clinical practice [12-15,17]. In the setting of myocarditis as the primary event,a variety of stressors including chest pain, etc., if above a certain threshold of intensity, might have the potential to trigger sympathetic discharge potentially eliciting a secondary TTC attack [13]. Conversely, TTC, as an index pathology, might per se account for myocarditis (or even perimyocarditis) typically manifesting as a subtle complication presumably associated with chemical and toxic effects of excessive catecholamine levels throughout the myocardial tissue [13,14].

In the setting of ambiguous cases where a definitive diagnosis of TTC or myocarditis can not be attained , certain non-invasive tools including cardiac MRI (with late gadolinium enhancement (LGE)) might be of utmost diagnostic value to evaluate the presence as well as the extent of ‘myocarditis component’ ( in isolation or accompanying TTC) [7,9,13-15]. Predilection sites and patterns of wall motion impairment , myocardial edema as well as the LGE enhancement were previously proposed as valuable measures of cardiac MRI for the differentiation of TTC and myocarditis [8]. Accordingly, TTC is generally characterized by wall motion impairment typically involving mid-apical regions of the left ventricle (LV) with a transmural and circumferential myocardial edema in the same regions whereas myocarditis is more likely to present with a global contractile dysfunction along with a basolateral and subepicardial edema pattern involving LV [8]. On the other hand , LGE is only encountered in a portion of cases (up to 40%) in patients with TTC manifesting as a low-intensity, transmural pattern in the mid-apical territory of the LV [8]. In contrast, LGE with a high or low intensity is generally observed in a great majority of subjects with myocarditis typically involving the subepicardial layer of the mid-myocardial regions [8]. Consistent with this, a typical case with an initial echocardiographic and clinical diagnosis of TTC was reported to be ultimately diagnosed as having myocarditis through the guidance of cardiac MRI demonstrating a subepicardial LGE enhancement in the lateral wall of the LV [9]. Moreover, in a series of consecutive patients undergoing coronary angiography (CAG), 8 out of 59 subjects (nearly 14%) with a presumptive diagnosis of TTC (having a pattern of LV apical ballooning on left ventriculography and normal coronary vasculature) were reported to have cardiac MRI findings consistent with myocarditis [18]. Taken together, cardiac MRI appears to be as of particular relevance to further demonstrate spesific characteristics of these two conditions beyond gross analysis,and hence to establish the final diagnosis [9,18].

Absolute identification of myocarditis in isolation or on top of TTC might have a variety of prognostic [8,9] and therapeutic implications in subjects with a presumptive diagnosis of TTC. As mentioned previously, patients with myocarditis (in isolation or accompanying TTC), as compared with subjects with an isolated TTC attack, might be more likely to incur a variety of arrhythmogenic complications including temporary or permanent heart blocks [7] etc. along with a well known predisposition to the evolution of D-CMP [9] and hence; chronic congestive heart failure in the long term even after complete or near-complete recovery of systolic functions following the acute phase. Accordingly, patients with a ‘myocarditis component’ may need to take medications including RAAS blockers [9] and beta blockers indefinitely in an effort to preclude or slow down the process of adverse myocardial remodelling. These patients also need to undergo a more frequent echocardiographic evaluation after discharge to closely supervise the temporal changes in left ventricular geometry, structure and functions (diameters,ejection fraction, etc.) with the goal to tailor individual therapeutic strategies.

In summary, there exists a continuous interest towards the particular challenges confronted in the differentiation of TTC and myocarditis as well as the potential etiopathogenetic association between these two conditions in clinical practice [7-9,12-15]. The current literature regarding borderline cases appears to be quite demonstrative and didactic and potentially suggests that TTC and myocarditis might have a significant overlap with regard to their presentation patterns particularly in the presence of atypical findings leading to a diagnostic challenge in certain settings [8-10,12]. In other terms,a portion of cases with myocarditis (alone or in combination with TTC) might appear to be misdiagnosed as having TTC in isolation in clinical practice [9,18] and vice versa. However,as these two conditions (despite full recovery in a portion of cases with myocarditis [8] and in all with TTC [1-5]) potentially confer different prognostic [9] and therapeutic implications in the hospital as well as post-discharge settings,every effort should be made to reach a definitive diagnosis. Accordingly, current literature (8,9,18) potentially suggests the need for more widespread use of non-invasive sophisticated tools including cardiac MRI etc. at least, in the setting of ambiguous cases with ‘forme fruste’findings where a final diagnosis cannot be established definitively through clinical evaluation and basic diagnostic modalities.


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