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

Patrick Meimoun, Jerome Clerc, Charles Vincent, Florent Flahaut, Anne Laure Germain, Frederic Elmkies, Hamdane Zemir, Anne Luycx-Bore
DOI: http://dx.doi.org/10.1093/ehjci/jes192 464-470 First published online: 22 September 2012


Aims Typical tako-tsubo cardiomyopathy (TTC) mimics acute anterior myocardial infarction (AMI) and the differential diagnosis is challenging before coronary angiography (CA) is performed; it demonstrates reduced or absent antegrade flow in the left anterior descending artery (LAD) in AMI, whereas there is no such flow limiting in TTC. At the acute phase, we tested the usefulness of the distal LAD flow visualization by transthoracic Doppler echocardiography (TDE) to distinguish between these two diseases. For this purpose, we prospectively enrolled 28 consecutive patients with TTC (75 ± 10 years, 93% females) who were compared with 28 consecutive patients with AMI treated successfully by primary angioplasty (66 ± 12 years, 79% females). All the patients underwent the assessment of the distal LAD flow just before CA, using colour and pulsed-wave TDE. In addition, the symmetric involvement of wall motion abnormalities (WMAs) based on the extent of the disease far beyond one coronary territory in TTC was searched by TDE. Non-invasive coronary flow reserve (CFR) by TDE, in the distal LAD, was also performed within 1 day after admission.

Results Before CA, the distal LAD flow was visible in 38 of 56 cases (68%) in the whole population, in all cases with TTC and in 10 cases with AMI (36%). The sensitivity (Se) and specificity (Sp) of the LAD flow visualization for the diagnosis of TTC were 100 and 64%, respectively, with a diagnostic accuracy of 82%. In comparison, the pattern of WMA yielded a Se of 75% and Sp of 86%, and a diagnostic accuracy of 80%. With the combination of both tools, the Se and Sp to detect TTC were 75 and 96% respectively, with a diagnostic accuracy of 86%. After CA, the acute CFR was less severely impaired in the TTC group when compared with the AMI group (2.2 ± 0.5 vs. 1.7 ± 0.6, P < 0.01) despite a worse LV systolic dysfunction.

Conclusion Non-invasive evaluation of the distal LAD flow could be helpful to differentiate TTC from AMI, and its combination with the pattern of WMA improved slightly its diagnostic accuracy. Furthermore, the acute CFR is less severely impaired in TTC compared with AMI despite poorer LV systolic dysfunction, suggesting that other mechanisms than direct microcirculatory damage are also involved in the pathogenesis of WMAs in TTC.

  • Tako-tsubo
  • Myocardial infarction
  • Coronary flow
  • Doppler


The differential diagnosis between typical tako-tsubo cardiomyopathy (TTC)14 and acute coronary syndrome involving the left anterior descending coronary artery (LAD) is challenging before coronary angiography (CA); however, the therapeutic implications are of paramount importance in this setting. The assessment of coronary flow velocity (CFV) and coronary flow reserve (CFR) by transthoracic Doppler echocardiography (TDE) allows the non-invasive evaluation of the coronary circulation in various settings, with a high feasibility in the LAD territory.3,5 Furthermore, in a stable haemodynamic condition and in the absence of epicardial coronary artery stenosis, the non-invasive CFR is a valuable surrogate for the evaluation of the coronary microcirculation.5 Acute anterior ST-segment elevation myocardial infarction (AMI) is characterized by reduced or absent antegrade flow in the LAD, whereas in TTC, by definition, there is no such underlying flow limiting in the LAD. Consequently, we hypothesize that the visualization of the antegrade distal LAD flow by TDE before angiography could be helpful to distinguish between these two diseases. Furthermore, the CFR is impaired after primary angioplasty in patients with AMI, reflecting the injury of the coronary microcirculation, and is ascribed as a determinant of prognosis.6,7 The non-invasive CFR is also transiently impaired in TTC.3,8,9 However, it is unknown whether the CFR impairment in TTC is as important as what is seen in AMI. In other words, does TTC mimic AMI also at the microcirculatory level? Therefore, our objective was to test the usefulness of the non-invasive assessment of the CFV at admission and the acute CFR in the distal part of the LAD for the discrimination between patients with typical TTC and AMI.


From 1 May 2009 to 1 May 2012, 28 consecutive patients with typical TTC were included in this prospective study. During the same period, 28 consecutive patients with first AMI, who underwent successful primary coronary angioplasty within 12 h of symptom onset and a comprehensive TDE at the acute phase, were compared with TTC patients. The distal LAD flow was searched at admission, while awaiting the CA which was performed in all cases regardless of the echocardiographic data, in an emergency in patients with ECG ST-segment elevation, and within 12 to 24 h in patients without ST-segment deviation. The CFR was performed within 24 h after admission or angioplasty (in cases of AMI). Patients with shock, more than mild valvular disease, or with poor echocardiographic window were exclusion criteria. All patients gave inform consent to the protocol. TTC was diagnosed according to the following criteria: acute chest pain or dyspnoea, a stressful event when present, transient LV wall motion abnormalities (WMA) at the apex of the LV, ECG changes, no luminal narrowing >50% and no evidence of plaque rupture in all epicardial coronary arteries on angiography, and a minimal troponine release despite extensive WMA.14 Furthermore, no patient had a history of coronary artery disease, or a febrile or acute neurological disorder. Selective CA was performed using standard techniques, and demonstrated no significant coronary artery disease in all patients. Left ventriculography demonstrated the typical pattern like an octopus pot.14 in all. The diagnosis of AMI was based on chest pain lasting > 30 min, ST-segment elevation >2 mm in at least two contiguous precordial ECG leads, and increase in serum troponin T (normal <0.05 µg/L in our hospital). Diagnostic CA was performed using the radial or femoral approach and coronary angioplasty by standard techniques. Successful angioplasty, required for inclusion to the study, was defined as a final angiographic TIMI 3 flow with a residual stenosis <30% of the LAD. After the procedure all patients received medical therapy according to current guidelines for ST-elevation myocardial infarction.10

CFV and CFR assessment

A comprehensive TDE was performed using a commercially available machine (Vivid E9 system, GE). Distal LAD flow was searched as previously described.6 Briefly, the distal part of the LAD was studied using the M5S probe, and the artery was visualized by colour Doppler flow-mapping guidance, in the modified parasternal view with a velocity range defined from 12 to 19 cm/s. The blood flow velocity was measured by pulsed-wave Doppler echocardiography, using a sample volume of 3–4 mm, placed on the colour signal in the distal LAD. The ultrasound beam direction was aligned as closely as possible with the distal LAD flow. No angle correction was performed for the study. However, the angle was kept as small as possible. When the distal LAD flow was not visualized within 5 min, or retrograde flow was obtained, antegrade LAD flow was considered to be absent and the test was discontinued. The CFR was performed using i.v. adenosine infusion (140 µg/kg/min over 2 min). The CFR was calculated as the ratio of the hyperaemic to basal peak diastolic flow velocity. A no-reflow pattern of the baseline flow velocity was defined as previously described.11 Blood flow velocity measurements were performed offline by an experienced investigator blinded to patient data, by contouring the spectral Doppler signals, using the integrated software package of the ultrasound system. Final values of flow velocity represented an average of three cardiac cycles. The inter-observer and intra-observer variability for CFR measurements in our experience have been previously reported (∼5 and 4%, respectively).6,9

Transthoracic Doppler echocardiography (TDE)

A comprehensive TDE was performed at admission or within 24 h after angiography, and all echocardiograms were digitized online and stored on a workstation (Echo PAC 7 version 108 for PC, GE, USA) for subsequent offline analysis by two observers blinded to patient data. The symmetric involvement of WMAs was carefully searched as previously described.12,13 Briefly, from the four-, two-, and three-apical chamber views, a symmetric pattern of WMAs of the opposite LV wall was searched, this pattern being strongly suggestive of TTC instead of AMI, because in TTC the WMAs extend far beyond one coronary artery territory.13 For example, in typical TTC, in the four-apical chamber view, the proportion of WMAs in the lateral LV wall is ∼50%, whereas in AMI, this proportion does not exceed one-third of the wall. In comparison, the WMA of the opposite septal LV wall is also ∼50% in TTC and more variable in AMI.12,13 Two cardiologists blinded to patient's data assessed qualitatively the pattern of WMA among three possibilities: a typical symmetric pattern suggestive of TTC, typical asymmetric pattern suggestive of AMI, or inconclusive pattern. The pattern retained for the final analysis was a consensus of the two observers. In the case of disagreement between observers, a third observer served as a referee. Left ventricular end-diastolic (EDV) and end-systolic volume (ESV) were measured from the apical four- and two-chamber view and left ventricular ejection fraction (LVEF) calculated from the modified biplane Simpson's rule. The wall motion score index (WMSI) was measured using the 16-segment model. Right ventricular (RV) WMA was evaluated by the visual assessment of multiple apical- and short-axis views. TDE was serially performed at 1 month in TTC patients, and at 3 months in the AMI group.


Continuous variables were expressed as mean ± SD and categorical variables as percentages. When a variable was not normally distributed, a logarithmic transformation was performed for analysis (NT-proBNP and troponin peak). The Unpaired or paired student's t-test, the χ² test (or Fisher's exact test as appropriate) were performed according to the variables tested. A diagnostic test was performed to assess the sensitivity (Se) and specificity (Sp) of the LAD flow visualization for the differentiation of TTC and AMI. The diagnostic accuracy of this parameter was compared with the symmetric involvement of WMAs as discussed above. Furthermore, a receiver operating characteristic (ROC) curve was established to assess the best cut-off of the CFR to differentiate TTC from AMI, and an ANOVA test to assess an eventual interaction between vascular risk factors, CFR, and the underlying disease (TTC vs. AMI). Intra-observer and inter-observer variability of the pattern of the WMA was tested with Kappa inter-rater agreement in 30 random cases from both groups, using video clips stored on the workstation 1 month apart. Kappa showing intra-observer and inter-observer agreement were 0.80 ± 0.1 and 0.70 ± 0.1, respectively. Statistical analysis was performed using MedCalc for Windows, version (Mariakerke, Belgium). A P-value <0.05 was considered as statistically significant.


Baseline characteristics are summarized in Table 1. Gender and the distribution of vascular risk factors were not significantly different between groups, but TTC patients were older (P < 0.01). The AMI involved the proximal LAD in 50% of the cases, and the artery was not always occluded at the time of angiography (11% of patients with an initial angiographic TIMI 3 flow). Single vessel disease was found in 24 of 28 (86%) patients and two-vessel disease in 4 of 28 (14%) patients on angiography. In the TTC group, a stressful event was found in 22 cases (79%), chest pain was the presenting symptom in 21 (75%), dyspnoea in 7 (25%), ECG showed ST-segment elevation in 15 (54%), and negative T-waves in 13 (46%), whereas in the AMI group, as expected ST-segment elevation was present in all patients (P < 0.01 vs. TTC). Table 2 summarizes TDE data. Transmitral E-wave, e′, and TAPSE were significantly higher in the AMI group compared with the TTC group, whereas the WMSI was higher in the latter group (all, P < 0.05).

View this table:
Table 1


Tako-tsubo (n = 28)Myocardial infarction (n = 28)
Age, years75 ± 1066 ± 12*
Females, n (%)26 (93)22 (79)
Hypertension, n (%)16 (57)14 (50)
Diabetes, n (%)6 (21)7 (25)
Dyslipidaemia, n (%)9 (32)13 (46)
Smoking, n (%)3 (11)8 (29)
Body surface area, m²1.69 ± 0.221.84 ± 0.18*
Troponin peak, µg/L (median, IQ range)0.34 (0.06–0.79)4.9 (2.5–10.3)*
NT-pro BNP, pg/mL (median, IQ range)5027 (2921–12 048)2809 (1217–5351)*
LAD proximal/mid, n (%)14 (50%)/14 (50%)
Antiplatelet agent, n (%)24 (86)28 (100)
Beta-blocker, n (%)21 (75)28 (100)*
ACE inhibitor or ARA II, n (%)19 (68)28 (100)*
Statin, n (%)17 (61)28 (100)*
Antialdosteron, n (%)4 (14)9 (32)
  • *P≤ 0.01 vs. tako-tsubo; ACE, angiotensin-converting enzyme; ARA II, angiotensin II receptor antagonist.

View this table:
Table 2

Echocardiography–Doppler data

Tako-tsubo Myocardial infarction
Acute phaseFollow-upAcute phaseFollow-up
LVEF, %43 ± 670 ± 6**45 ± 753 ± 12*,**
LV EDV, mL/m²52 ± 1145.5 ± 7**55 ± 1062 ± 14*,**
LV ESV, mL/m²30 ± 914 ± 4**31 ± 929 ± 14*
WMSI1.97 ± 0.221**1.85 ± 0.2*1.5 ± 0.38*
Left atrial volume, mL/m²26 ± 926 ± 1225 ± 730 ± 7*
E, cm/s62 ± 2169 ± 2077 ± 23*80 ± 28
A, cm/s77 ± 3078 ± 2787 ± 2276 ± 24
E/A0.92 ± 0.61.05 ± 0.90.94 ± 0.41.2 ± 0.8
DTE, ms211 ± 92225 ± 65172 ± 41*212 ± 71**
e′, cm/s5.3 ± 1.96.5 ± 26.6 ± 2*6.5 ± 1.5
a′, cm/s8.3 ± 2.58.5 ± 2.59.4 ± 2.38.1 ± 2.7
Sa, cm/s6.4 ± 1.27.5 ± 1.97 ± 1.96.7 ± 1.3
E/e′12.4 ± 4.511 ± 4.512.5 ± 412.6 ± 4.3
PASP, mmHg35 ± 933 ± 636 ± 1035 ± 10
TAPSE, mm19 ± 2.922 ± 4.5**21.5 ± 4.3*23 ± 4.8
  • *P < 0.05 vs. tako-tsubo, **P < 0.05 vs. acute phase; LV, left ventricle; EDV, end-diastolic volume; ESV, end-systolic volume; WMSI, wall motion score index; DTE, deceleration time of mitral E-wave; PASP, pulmonary artery systolic pressure; TAPSE, tricuspid annular plane systolic excursion; e′, a′, Sa, average of septal and lateral annular mitral tissue Doppler velocity.

Distal LAD flow and symmetric WMA

The visualization of the distal LAD flow was feasible without contrast enhancement, in all cases in the TTC group and in 10 cases (36%) in the AMI group. In AMI patients with an initial angiographic TIMI flow grade 0–1 (n = 12), the LAD flow was detectable in one patient who had an upstream homolateral collateral Rentrop grade 3, whereas it was visible in all patients with a TIMI 3 flow (n = 3), and in 6 of 13 patients with a TIMI 2 flow. Accordingly, the distal LAD flow was visible in 38 of 56 patients (68%) in the whole population, and therefore its Se, and Sp for the diagnosis of TTC were 100 and 64%, respectively, and the diagnostic accuracy was 82%. A no-reflow pattern was not detected in this very early evaluation. An example of LAD flow is depicted in Figure 1. In comparison, the symmetric pattern of the WMA yielded a Se of 75% and Sp of 86%, and a diagnostic accuracy of 80%, the evaluation of this pattern being inconclusive in 11 patients (20%) (seven TTC, four AMI). However, when combining the pattern of the WMA and LAD flow evaluation, the Se and Sp to detect TTC were 75% and 96%, respectively, with a diagnostic accuracy of 86%. The RV WMA and systolic anterior motion of the mitral valve (SAM), absent in AMI, were present in, respectively, five (18%) and three (11%) cases with TTC who had a typical symmetric pattern of WMA (all, P < 0.05).

Figure 1

Visualization of the distal LAD flow by colour Doppler and the corresponding CFV recorded with the pulsed-wave Doppler sampling.

Coronary flow reserve

The CFR was feasible in 51 cases (24 TTC including 15 with ECG ST-segment elevation at presentation, and 27 AMI) because two patients had contra-indication to adenosine, and four were not in an appropriately stable haemodynamic condition at the time of the test (Table 3). A contrast enhancement was used in eight patients (15%). The haemodynamic variables were not significantly different between groups (all, P = NS). At the time of the CFR, the main cardiac medications prescribed to the patients are summarized in Table 1, with a significant difference between groups for some drugs. Adenosine was well tolerated with no serious adverse event. Patients with AMI had a higher baseline CFV (P < 0.05) and lower hyperaemic CFV (P = 0.27) compared with TTC patients. Consequently, despite having received primary angioplasty, patients with AMI had a significantly lower CFR when compared to TTC patients (P < 0.01) (Table 3). Furthermore, a CFR ≥2 was seen in 17 of 24 cases (71%) in the TTC group vs. 4 of 27 cases (15%) in the AMI group (P < 0.01). In the TTC group, among the nine patients without ST-segment elevation at presentation, only one depicted a CFR <2. An example of the CFR is illustrated in Figure 2. A no-reflow pattern was seen in nine (32%) patients in the AMI group vs. none in the TTC group (P < 0.01) (example in Figure 3). Using an ROC curve analysis, a CFR >1.8 was the best cut-off to differentiate TTC and reperfused AMI, with a Se of 83% and a Sp of 74%, with an AUC of 0.81 (95% CI: 0.67–0.91); P < 0.001 (Figure 4). In comparison, a CFR ≥2 yielded a similar accuracy (78%), with an Se of 71% and Sp of 85%. No significant interaction was found between vascular risk factors and CFR, except for hypertension (ANOVA, P < 0.05).

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Table 3

Coronary flow velocity (CFV) and CFR data in the LAD at the acute phase

Tako-tsuboMyocardial infarction
Baseline CFV, cm/s31 ± 940 ± 16**
Hyperaemic CFV, cm/s68 ± 2164 ± 17
CFR2.2 ± 0.51.7 ± 0.6*
No reflow pattern, n (%)09 (32)*
Baseline heart rate, bpm80 ± 1776 ± 14
Baseline systolic/diastolic blood pressure, mmHg121 ± 18/63 ± 12123 ± 19/68 ± 16
LAD flow visualization before angiography, n (%)28 (100)10 (36)*
CFV before angiography, cm/s32 ± 937 ± 16
  • *P < 0.01 and **P < 0.05 vs. tako-tsubo.

Figure 2

An example of CFR in the distal LAD in a patient with TTC the baseline CFV is in the left and the hyperaemic CFV in the right of the figure. The CFR = 2.3.

Figure 3

An example of no-reflow pattern in a patient with AMI. The baseline coronary flow shows an early systolic retrograde flow, an absent systolic antegrade flow, and a rapid deceleration time of the diastolic component.

Figure 4

An ROC curve analysis showing the best cut-off of the CFR to differentiate TTC from AMI Se, sensitivity; Sp, specificity; AUC, area under the curve.


As expected, at follow-up a total recovery of LV systolic function was observed in all patients with TTC, in addition to a significant improvement of TAPSE, when compared with the acute phase (all, P < 0.01), whereas an incomplete recovery was found in the AMI group (Table 2).


This study shows that the visualization of the distal LAD flow by TDE in patients presenting as acute coronary syndrome could help to differentiate TTC from AMI, and the diagnostic accuracy improves when combined with careful examination of the WMA. The acute CFR is also useful for the differentiation. The differential diagnosis of TTC and AMI is challenging and otherwise of paramount importance given the important therapeutic implications.10 CA remains the cornerstone tool for this distinction. However, some particular therapy could be discussed upstream prior to angiography such as thrombolysis, particularly in centres where angiography is not available. Furthermore, some patients affected by TTC are very old and frail with several co-morbidities including renal insufficiency, and most physicians are reluctant to refer them for angiography in an emergency. Efficient antithrombotic regimens including dual antiplatelet therapy usually used in acute coronary syndrome could lead to an unnecessary risk of severe haemorrhage when given to frail TTC patients. On the other hand, avoiding these treatments could impair the prognosis in patients with AMI.10 That is' why upstream prior to angiography all valuable parameters easily available at bedside are welcome to allow the distinction between TTC and AMI. Some subtle ECG changes have been described but need confirmation in large prospective and comparative populations. The troponin peak is very helpful but it occurs too late and is unsuited with the urgent revascularization required in AMI. TDE could be a promising tool in this setting focusing on the evaluation of the regional WMA. One study including a few patients (n = 8) showed that when there is a symmetric WMA involving the lateral LV wall, there is a high likelihood of TTC instead of AMI.12 A recent study including more patients confirmed this particular pattern with an extent of the WMA far beyond one coronary territory in TTC.13 Furthermore, the RV is sometimes involved in TTC, in ∼25–30% of cases using MRI, adding to its diagnostic value in this setting.4 However, the evaluation of the WMA is subjective and may be affected by the tethering phenomenon, the lateral resolution is often poor, and the evaluation of the morphology and function of the RV is frequently challenging by echo. Furthermore, the recovery of the WMA is not uniform in TTC, the symmetric pattern becoming asymmetric when the patient is seen later on.14 Left ventricular obstruction with SAM is also seen in TTC, but is rarely present (∼20% of cases).15,16 and not specific. That's why additional tools easily available at bedside are also warranted in this setting. Apart from TTC, non-invasive CFR has been used with regard to several situations including the detection of functionally significant coronary stenosis, the follow-up after angioplasty, the evaluation of coronary bypass grafts, as well as the estimation of the coronary microcirculation in hypertension, several cardiomyopathies, and AMI.5 In AMI, the CFR predicts LV recovery and LV remodelling with good accuracy.6,7 However, the CFR was not performed at admission as a diagnostic tool for technical and pathophysiological reasons. This test requires the presence of a nurse for the adenosine injection. It is rarely possible at day night when several patients are admitted. Furthermore, for a proper interpretation, the CFR needs to be performed under stable haemodynamic condition, which is not always the case at admission. The search of the resting CFV is not limited by these factors. In one study involving 46 patients with a first AMI, non-invasive evaluation of the CFV in the distal LAD by TDE just before CA was useful to differentiate patients with a subsequent TIMI 3 from TIMI ≤2 coronary reperfusion, with an accuracy of 89% when the baseline LAD CFV was ≥25 cm/s.17 However, the baseline CFV is influenced by several factors apart from a coronary stenosis, including haemodynamic conditions, myocardial oxygen demand, vasomotor tone, vasoactive drugs, regional ventricular mass, ageing, the angle between the Doppler beam and the artery,5 as well as the post-ischaemic reactive hyperaemia. Therefore, it would be speculative to draw a differential diagnosis based solely on a cut-off from the CFV. That is' why we have chosen a simple qualitative factor: the presence or the absence of the antegrade distal LAD flow using TDE. However, although the Se was as high as 100%, the Sp was only 64% to differentiate TTC from AMI based on the detection of the distal LAD flow. One explanation is the inherent presence of spontaneous reperfusion in some patients with AMI or induced by antithrombotics given upstream prior to angiography. On the other hand, not visualizing the artery could be due to an intrinsic limitation of the technique. Despite its limitations cited above, the search of the symmetric pattern of WMA in addition to the distal LAD flow is helpful for detecting TTC. Interestingly, among the 11 patients with an inconclusive pattern of WMA, unlike the seven TTC patients, the LAD flow was never visible in the four AMI patients.

Although the clinical presentation of TTC is now well understood, its pathophysiology is not entirely clear.14 Several mechanisms are suggested,14,16 but a common finding is a sudden rush of catecholamine release secondary to a stressful event,1 leading to myocardial stunning, which is different from the scenario of ischemia-reperfusion at the molecular level, according to animal models of TTC.18 Interestingly, the no-reflow pattern, seen in AMI in ∼30% of cases, is induced by several mechanisms and portends a poorer prognosis.11 It has never been found in patients with TTC in our study. Several reports demonstrated that a transient impairment of the coronary microcirculation is also present at the acute phase of TTC3,8,9,1922 but whether it is a causative mechanism, a consequence, or an epiphenomenon is still unresolved. In the current study, the CFR was significantly higher in patients with TTC when compared with AMI despite poorer WMSI suggesting that other factors than the microcirculatory damage are also involved in the pathogenesis of WMA in TTC. Other parameters such as ageing, haemodynamic and vascular risk factors, as well as cardiac medications, which could also influence the CFR, did not favour TTC vs. AMI patients in the current study, and therefore are less likely to explain the difference of the CFR in patient groups.


Our study focused on typical TTC, and patients with AMI had mostly single-vessel disease. Therefore, our results cannot be extrapolated to patients with variant TTC and AMI with two- or three-vessel disease, which could influence the extent of WMA. This was a pilot single-centre study, where CFV and CFR assessment by TDE are routinely performed for various reasons. Furthermore, the small sample size is a limitation of our study. So, our results need confirmation in a larger multicentre study. Our results did not infringe the need for CA, which was performed regardless of the TDE data. However, TDE could be helpful upstream prior to angiography to screen these patients as mentioned above. In the TTC group, some patients had no ST-segment elevation at presentation. The main results did not differ even after excluding these patients from analysis (data not shown). All but one patient in this subgroup exhibited a CFR >2, whereas in most of the patients with a significant coronary stenosis a CFR <2 is expected.5 A less subjective and more sensitive tool than visual WMA analysis such as two-dimensional strain has recently been used to differentiate TTC and coronary artery disease with promising results.14,23,24 However, its additive diagnostic value remains to be established in prospective studies, in comparison with CFV assessment for instance.

In conclusion, non-invasive evaluation of the distal LAD flow by TDE could help to differentiate TTC from AMI patients upstream prior to angiography. In a proper setting, when the LAD flow is absent there is a high likelihood of AMI, and, when it is present the diagnosis of TTC is plausible when this assessment is combined with a careful visualization of WMA. Furthermore, although the CFR is transiently impaired in TTC, it is otherwise less severely decreased when compared with AMI despite a poorer WMSI, suggesting that other mechanisms than direct microcirculatory damage are also involved in the pathogenesis of WMA occurring in TTC.

Conflict of interest: none declared.


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