Non-invasive detection of tako-tsubo cardiomyopathy vs. acute anterior myocardial infarction by transthoracic Doppler echocardiography

Meimoun, Patrick; Clerc, Jérôme; Charles, Vincent; Flahaut, F.; Germain, Anne Laure; Elmkies, F.; Zemir, H.; Luycx-Bore, A.

doi:10.1093/ehjci/jes192

Cited by 27 publications

(26 citation statements)

References 22 publications

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“…This suggests that mechanisms other than direct microcirculatory damage are also involved in the pathogenesis of SCM-associated wall motion abnormalities. 2,3 These magnetic resonance imaging data also suggest the existence of differences in myocardial contractility in LV apical regions in patients with acute-phase SCM and those with LAD-MI, even if apical akinesia appears visually similar. However, visual evaluation of ventricular wall motion is limited.…”

Section: To the Editormentioning

confidence: 71%

Letter by Dandel et al Regarding Article, “Systolic and Diastolic Mechanics in Stress Cardiomyopathy”

2015

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issue of Circulation. The differential diagnosis of stress cardiomyopathy (SCM) and acute left anterior descending coronary artery territory myocardial infarction (LAD-MI) before the mandatory coronary angiography is challenging but paramount given the important therapeutic implications. The potential life-threatening consequences of catecholamine use for emergency circulatory support if the underlying cause of acute left ventricular (LV) dysfunction is unrecognized SCM are only 1 of the problems that can derive from diagnostic errors. Clinically, electrocardiographically, and echocardiographically, SCM mimics acute apical MI, and the comprehensive study by Medeiros et al provides strong new evidence that alterations in LV global systolic and diastolic function in SMI and acute LAD-MI are also indistinguishable. Nevertheless, we believe that transthoracic echocardiography can be useful for early distinction between SCM and LAD-MI if attention is focused on regional myocardial function using the advantages of strain imaging. Magnetic resonance imaging data from patients with acute-phase SCM showed viable myocardium in visually akinetic apical regions, and coronary flow reserve assessed by color Doppler appeared less impaired in SCM than in acute LAD-MI, even with poorer systolic function in SCM patients. This suggests that mechanisms other than direct microcirculatory damage are also involved in the pathogenesis of SCM-associated wall motion abnormalities.2,3 These magnetic resonance imaging data also suggest the existence of differences in myocardial contractility in LV apical regions in patients with acute-phase SCM and those with LAD-MI, even if apical akinesia appears visually similar. However, visual evaluation of ventricular wall motion is limited. It assesses displacement and radial deformation but not longitudinal shortening. No (or no visible) inward wall movement in regions with high circumferential wall stress (σ c ), which opposes circumferential fiber shortening, does not exclude myocardial contraction with predominantly longitudinal shortening of fibers. In acute-phase SCM, the LV is subdivided into 2 functionally different chambers with an increase in σ c in the distal apical chamber resulting from the large transversal diameter and smaller wall thickness. 4,5 Thus, because of the increasing differences in transversal diameter and wall thickness between the apical and basal LV regions during the acute phases of SCM, the preejection and end-ejection σ c can reach values that are several times higher in the apex, resulting in wall motion impairment with severe LV dysfunction. 5 Nevertheless, even in patients with SCM with an LV ejection fraction drop below 25%, there was evidence of longitudinal myocardial shortening in the visually akinetic apical region.5 This is not surprising because longitudinal shortening depends more on meridional stress (σ m ), the force acting along the LV long axis, than on σ c . The longitudinal strain pattern usually shows asynchrony and dyssynergy in early systole and mi...

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Section: To the Editormentioning

confidence: 71%

Letter by Dandel et al Regarding Article, “Systolic and Diastolic Mechanics in Stress Cardiomyopathy”

2015

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“…Invasive studies (using TIMI frame counts, myocardial perfusion grading, intracoronary Doppler evaluation of vasomotor function, coronary flow reserve and thermodilution method to assess index of microvascular resistance) and noninvasive studies (using doppler echocardiography, myocardial contrast echocardiography, SPECT/PET metabolism/ perfusion and Cardiac MRI) have all demonstrated coronary microvascular dysfunction in the acute phase of takotsubo cardiomyopathy 5,7,[12][13][14][15][17][18][19][20][22][23][24][25][26][27][28]33 Of significance, all of these microvascular abnormalities demonstrated by both invasive and noninvasive testing usually are transient and reversible, with follow up testing indicating normalization of microvascular function, in parallel with recovery of LV function. The precise mechanism of this transient coronary microvascular dysfunction, although not completely understood, could involve adrenoreceptor overstimulation/sympathetic hyperactivity, resulting from a catecholamine surge secondary to physical or emotional stress and differences in the type and density of adrenoreceptors in the cardiac apex versus the base might partly explain the proclivity of transient apical dysfunction in TC.…”

Section: Resultsmentioning

confidence: 99%

“…19 In another study by the same author, distal LAD flow was assessed within 12-24 hours of admission in 28 patients admitted with TC and was compared to 28 patients with acute MI. 20 The blood flow velocity was assessed by pulse wave Doppler, and CFR (ratio of hyperemic to basal peak diastolic flow velocity) was evaluated after adenosine infusion over 2 minutes. The sensitivity and specificity of diagnosing TC were 100% and 64% respectively, with a high diagnostic accuracy of 82%.…”

Section: Noninvasive Methods Of Cmvd Assessmenttransthoracic Doppler mentioning

confidence: 99%

“…The higher CFR in the face of lower wall motion score index in TC patients implies that factors other than microcirculatory impairment also play a role in TC pathogenesis. 20 However, some studies have shown conflicting results. Sganzerla et al evaluated 5 patients with TC with no concomitant medical conditions by transthoracic pulse wave doppler echo to evaluate distal LAD perfusion in the acute phase of TC, and they were compared to five age, sex and ejection fraction matched controls.…”

Section: Noninvasive Methods Of Cmvd Assessmenttransthoracic Doppler mentioning

confidence: 99%

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Microvascular Dysfunction in Takotsubo Cardiomyopathy

Gowdar

Chhabra

2016

ICFJ

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<p>Takotsubo cardiomyopathy or stress-induced cardiomyopathy, is characterized by transient cardiac dysfunction, usually but not always triggered by physical or emotional stress. Takotsubo cardiomyopathy may mimic an acute coronary syndrome due to an overlapping presenting clinical spectrum. Typically, apical involvement with hypercontraction of basal left ventricle (apical type) is predominant, but atypical types involving basal, midventricular, and right ventricular myocardium have also been described. To date, the exact pathogenic mechanism of this disease remains unclear however sympathetic or catecholaminergic hyperactivity, mutivessel coronary vasospasm, microcirculatory disorder, and estrogen deficiency have been proposed to be the likely underlying pathogenic mechanisms. In this review, we specifically highlight the association of microcirculatory dysfunction in takotsubo cardiomyopathy which has been more recently recognized as an important pathogenetic contributor to this disease.</p>

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“…Takotsubo cardiomyopathy (TC), also known as stress-induced cardiomyopathy, is characterized by the abrupt onset of cardiac dysfunction, with transient apical and midventricular hypo-/akinesia with a compensatory hypercontractility of the remaining segments of the myocardium [1,2]. Typical electrocardiographic changes, which are seen in up to 84% of patients, are characterized by ST segment elevation, predominantly in the precordial leads, followed by T wave inversions [3,4].…”

Section: Introductionmentioning

confidence: 99%

Takotsubo Cardiomyopathy after Systemic Consolidation Therapy with High-Dose Intravenous Cytarabine in a Patient with Acute Myeloid Leukemia

et al. 2014

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Background: Takotsubo cardiomyopathy (TC) is characterized by the abrupt onset of cardiac dysfunction, with transient apical and midventricular hypo-/akinesia with a compensatory hypercontractility of the remaining segments. The clinical presentation appears to be similar to acute myocardial infarction (AMI). However, the myocardial dysfunction is reversible. Case Report: We report on the case of a 58-year-old man with acute myeloid leukemia (AML) who was admitted to our hospital to receive the second course of consolidation chemotherapy with intravenous cytarabine. Subsequently, the patient developed severe dyspnea at rest, with cardiogenic shock after the central venous catheter was removed. Echocardiography revealed severe dyskinesia of the mid and apical portions of both ventricles, accompanied by a highly reduced left ventricular function (LVF). 5 months later, 12-lead electrocardiography (ECG) did not show any evidence of repolar-ization disorders and echocardiographic evaluation revealed a normal LVF. We suppose that the underlying mechanism was TC. Conclusions: TC can occur in patients with AML under systemic chemotherapy, which possibly represents a triggering factor for TC development. Cardiogenic shock is a serious life-threatening complication of TC. Nevertheless, the prognosis of TC is favorable and a complete recovery of the LVF is possible.

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Non-invasive detection of tako-tsubo cardiomyopathy vs. acute anterior myocardial infarction by transthoracic Doppler echocardiography

Cited by 27 publications

References 22 publications

Letter by Dandel et al Regarding Article, “Systolic and Diastolic Mechanics in Stress Cardiomyopathy”

Letter by Dandel et al Regarding Article, “Systolic and Diastolic Mechanics in Stress Cardiomyopathy”

Microvascular Dysfunction in Takotsubo Cardiomyopathy

Takotsubo Cardiomyopathy after Systemic Consolidation Therapy with High-Dose Intravenous Cytarabine in a Patient with Acute Myeloid Leukemia

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