We read with great interest the article ‘Transient left ventricular apical ballooning syndrome: a 4-year experience’ recently published by Spedicato et al. [1]. Our interest on this subject dates back to 1998, when we studied our first case of transient left ventricular (LV) dysfunction in a 74-year-old woman, who presented with minor stroke as a consequence of apical thrombus formation. At that time, our knowledge about this ‘freak of nature’ was so poor. During the last decade, a series of patients showing equivalent, but not identical, clinical features have been encountered as consecutive frameworks of a polyhedric group of cardiac diseases, firstly recognized as ‘unspecific myocardial diseases’, then ‘ischemic-like ventricular dysfunctions’ and finally ‘stress cardiomyopathies’ [2]. We had to wait a few years to learn about the Takotsubo- like cardiomyopathy or apical ballooning syndrome, thanks to the number of single case reports, original studies – mainly consisting of single-centre cohorts from tertiary-care hospitals [1] – and systematic reviews [2,3]. Despite this great body of literature that allowed us to know such peculiar aspects of the disease, some variants have been described. For instance, apical-sparing wall motion abnormalities were also reported in Takotsubo- like cardiomyopathy patients [2]. Thus, there is a general consensus about the need of a large, centralized, pro- spective registry to improve our clinical knowledge. One important question to be answered is whether neuro- genic stress cardiomyopathy (NSC) [2] and Takotsubo- like cardiomyopathy should no longer be considered as different clinical entities. Differently than in their previous topical review [3], the Mayo Clinic group has recently outlined [2] several similarities in pathophysiology, clinical features and prognosis, with only a few differ- ences (namely, the patterns of ECG presentation and wall motion abnormalities distribution) between the two con- ditions, which would support the need for a common nomenclature. Although questions about the pathogenesis are still open and controversial, a catecholamine-mediated cardio- toxicity has been roughly established [4]. With this regard, we recently observed two (unpublished) cases of transient LV dysfunction complicating a sub- arachnoid haemorrhage that matched all the diagnostic criteria for typical Takotsubo-like cardiomyopathy syn- drome, likely confirming this clinical overlap. Of note, the ECG obtained early after admission showed in both cases a mild ST segment elevation in the anterior leads. Besides, patients with either NSC or Takotsubo-like cardiomyopathy need specialized cardiology assistance, with serial ECG and echocardiographic examinations, as well as laboratory testing. At times, they require intravenous inotropic agents, Swan-Ganz catheter or life- support procedures, which usually indicate admission to intensive cardiology care unit, yet without significant differences in terms of in-hospital complications and prognosis [1]. For all these aforementioned reasons, the common nomenclature of ‘stress-related cardiomyopathy syndromes’ as suggested by the Mayo Clinic group [2], or simply ‘stress-related LV dysfunction’, is encouraged for both these cardiac disorders. Though unspecified, the microvascular dysfunction that has been hypothesized to accompany the transient LV dysfunction is likely to indicate less empiric therapeutic strategies. Together with b-blockade, in our opinion, patients should be given antithrombotic and/or anti- coagulants routinely, not only to prevent the possible, although rare, LV thrombus formation [5], but also to contrast microvascular thrombosis. Obviously, the inherent contraindications in patients with severe intra- cranial haemorrhage make this one of the real differences between the two clinical conditions.

Stress-related left ventricular dysfunction: a common terminology for both Takotsubo-like and neurogenic stress syndromes?

DE GREGORIO, Cesare
Writing – Review & Editing
;
ANDO', Giuseppe
Validation
;
TRIO, OLIMPIA
Visualization
2009-01-01

Abstract

We read with great interest the article ‘Transient left ventricular apical ballooning syndrome: a 4-year experience’ recently published by Spedicato et al. [1]. Our interest on this subject dates back to 1998, when we studied our first case of transient left ventricular (LV) dysfunction in a 74-year-old woman, who presented with minor stroke as a consequence of apical thrombus formation. At that time, our knowledge about this ‘freak of nature’ was so poor. During the last decade, a series of patients showing equivalent, but not identical, clinical features have been encountered as consecutive frameworks of a polyhedric group of cardiac diseases, firstly recognized as ‘unspecific myocardial diseases’, then ‘ischemic-like ventricular dysfunctions’ and finally ‘stress cardiomyopathies’ [2]. We had to wait a few years to learn about the Takotsubo- like cardiomyopathy or apical ballooning syndrome, thanks to the number of single case reports, original studies – mainly consisting of single-centre cohorts from tertiary-care hospitals [1] – and systematic reviews [2,3]. Despite this great body of literature that allowed us to know such peculiar aspects of the disease, some variants have been described. For instance, apical-sparing wall motion abnormalities were also reported in Takotsubo- like cardiomyopathy patients [2]. Thus, there is a general consensus about the need of a large, centralized, pro- spective registry to improve our clinical knowledge. One important question to be answered is whether neuro- genic stress cardiomyopathy (NSC) [2] and Takotsubo- like cardiomyopathy should no longer be considered as different clinical entities. Differently than in their previous topical review [3], the Mayo Clinic group has recently outlined [2] several similarities in pathophysiology, clinical features and prognosis, with only a few differ- ences (namely, the patterns of ECG presentation and wall motion abnormalities distribution) between the two con- ditions, which would support the need for a common nomenclature. Although questions about the pathogenesis are still open and controversial, a catecholamine-mediated cardio- toxicity has been roughly established [4]. With this regard, we recently observed two (unpublished) cases of transient LV dysfunction complicating a sub- arachnoid haemorrhage that matched all the diagnostic criteria for typical Takotsubo-like cardiomyopathy syn- drome, likely confirming this clinical overlap. Of note, the ECG obtained early after admission showed in both cases a mild ST segment elevation in the anterior leads. Besides, patients with either NSC or Takotsubo-like cardiomyopathy need specialized cardiology assistance, with serial ECG and echocardiographic examinations, as well as laboratory testing. At times, they require intravenous inotropic agents, Swan-Ganz catheter or life- support procedures, which usually indicate admission to intensive cardiology care unit, yet without significant differences in terms of in-hospital complications and prognosis [1]. For all these aforementioned reasons, the common nomenclature of ‘stress-related cardiomyopathy syndromes’ as suggested by the Mayo Clinic group [2], or simply ‘stress-related LV dysfunction’, is encouraged for both these cardiac disorders. Though unspecified, the microvascular dysfunction that has been hypothesized to accompany the transient LV dysfunction is likely to indicate less empiric therapeutic strategies. Together with b-blockade, in our opinion, patients should be given antithrombotic and/or anti- coagulants routinely, not only to prevent the possible, although rare, LV thrombus formation [5], but also to contrast microvascular thrombosis. Obviously, the inherent contraindications in patients with severe intra- cranial haemorrhage make this one of the real differences between the two clinical conditions.
2009
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/1890767
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