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Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCA) is an increasingly recognised condition and accounts for 5% to 9% of all MI cases.[[1,2]] Recent study has shown that MINOCA has a higher rate of all-cause mortality than age and sex-matched population without cardiovascular disease (CVD) and the predominant contributor to mortality is non-CVD death.[[3]] This suggests the predisposing factors for MINOCA remain a potent risk factor for non-CVD death. Thus, recent American and European expert consensus documents have defined MINOCA as a “working diagnosis” that should prompt further investigations to ascertain the aetiology of the condition.[[1,2]]

Cardiac magnetic resonance (CMR) is not only accurate in the assessment of cardiac anatomy and function but is also superior in myocardial tissue characterization. Late gadolinium enhancement (LGE) and T2-weighted imaging allow assessment of myocardial scar, focal fibrosis, and myocardial oedema, respectively, thereby enhancing the capacity to delineate causes of suspected MINOCA. Advanced CMR imaging myocardial tissue characterisation methods such as T1 and T2 mapping techniques further improve the diagnosis of myocarditis and Takotsubo syndrome.

Novel T1 mapping techniques allow quantitative CMR assessment of myocardial fibrosis, with the two most common measures being native T1 and extracellular volume (ECV) fraction. Native T1 differentiates normal from infarcted myocardium, is abnormal in hypertrophic cardiomyopathy, and is useful in the diagnosis of Anderson–Fabry disease and amyloidosis.[[4]] In acute MI, native T1 mapping can differentiate microvascular obstruction (MVO) in infarcted myocardium; it is characterised by T1 values higher compared to those of remote myocardium but lower compared to those of infarcted myocardium.[[5,6]] Native myocardial T1 relaxation time was significantly higher in patients with acute myocarditis which is attributed to cellular oedema, increased extracellular space and water, inflammation, and myocyte necrosis, all of which commonly occur in the acute stage of myocarditis.[[7]]

ECV is a surrogate measure of the extracellular space and is equivalent to the myocardial volume of distribution of the gadolinium-based contrast medium. It is reproducible and correlates well with fibrosis on histology. ECV is abnormal in patients with cardiac failure and aortic stenosis, and is associated with functional impairment in these groups.[[8]]

T2 mapping has emerged as a valuable tool in the CMR assessment of myocardial oedema in ischaemic and non-ischaemic cardiomyopathies.[[9,10]] A high T2 value reliably identifies acute myocardial oedema in acute MI without the limitations associated with T2-weighted imaging.[[9]] whereas in chronic MI, T2 value is normal as myocardial oedema resolves within six months after an acute insult. T2 value is also significantly elevated in patients with acute myocarditis indicating myocardial inflammation.[[10]]

We describe three cases in which CMR ensures the correct diagnosis for optimal management and treatment of patients with MINOCA.

Case 1

A 57-year-old woman with hypertension, hyperlipidaemia, and family history of premature coronary artery disease presented with chest pain, elevated high-sensitive troponin (hs-TnT), and dynamic ST-segment changes in the anterior leads on electrocardiogram (ECG). Coronary angiography showed trivial coronary artery disease and transthoracic echocardiogram demonstrated hypokinesis of anteroseptal and inferoseptal, apical inferior and lateral walls. The diagnosis of Takotsubo syndrome was initially made based on these findings. Subsequent echocardiograms continued to show persistent hypokinesis of the septum. CMR (Figure 1A–1C) demonstrated myocardial fibrosis involving the septal wall, a pattern in keeping with previous left anterior descending (LAD) territory infarction. Further review of her angiography revealed paucity of the septal branches arising from the LAD (Figure 1D, Supplementary Video 1), raising the possibility of an occluded vessel.

Figure 1: A. Pre-contrast T1 mapping showed an abnormally increased T1 signal (black arrows) involving the anteroseptal wall, suggestive of myocardial fibrosis. B & C. On LGE imaging, there was near transmural enhancement (red arrows) involving the anteroseptal wall, a finding in keeping with myocardial infarction. D. Coronary angiography revealed paucity of sepal branches arising from the LAD (yellow circle) raising the possibility of an occluded vessel.

Case 2

A 57-year-old woman presented with fever, chest pain, elevated hs-TnT, and C-reactive protein (CRP). Coronary angiography demonstrated near normal coronaries. CMR was performed as part of the workup of suspected myocarditis. T2-weighted short-tau inversion recovery (T2-STIR) imaging and T2 mapping (Figure 2A and 2B) showed an oedematous area in the inferolateral wall. Native T1 mapping (Figure 2C) and LGE imaging (Figure 2D and 2E) revealed transmural myocardial fibrosis with MVO in the inferolateral wall, a pattern in keeping with circumflex artery territory infarction. Further review of her angiography (Figure 2F, Supplementary Video 2) demonstrated occlusion of the distal circumflex artery due to spontaneous coronary artery dissection (SCAD).

Figure 2: A. There was a hyperintense signal (yellow arrows) in the inferolateral wall, suggestive of myocardial oedema on T2-STIR imaging. B. Compared to the anterolateral wall (mean T2 value 35 msec, normal range <50 msec), T2 value was significantly higher in the inferolateral wall (mean T2 value 60 msec) indicating acute myocardial oedema. C. Pre-contrast T1 mapping showed an abnormally increased T1 signal involving the inferolateral wall. There was a dark region (red arrows) within the bright myocardium in keeping with microvascular obstruction (MVO). D & E. On LGE imaging, there was transmural myocardial enhancement in the inferolateral wall. MVO is observed as hypo-enhanced region within hyper-enhanced infarcted myocardium (yellow arrows). F. Coronary angiography revealed occlusion of a large circumflex artery (yellow arrow) secondary to spontaneous coronary artery dissection.

Case 3

A 75-year-old woman with hypertension, hyperlipidaemia, and previous transient ischaemic attack presented with chest pain and elevated hs-TnT. She was competing in an art competition a few hours prior to admission. Transthoracic echocardiogram demonstrated hypokinesis of the anteroseptal and anterior walls. Coronary angiography showed moderate disease in mid LAD (Figure 3A). Fractional flow reserve (FFR) was performed to the LAD as the vessel is large and does wrap around the apex and it suggested non-obstructive disease (FFR 0.87). The appearance of the left ventriculogram raises the possibility of Takotsubo syndrome (Figure 3B). CMR was subsequently performed to clarify the diagnosis. Native T1 mapping (myocardium T1 value 1201 msec, normal range 1225–1275 msec) and LGE imaging showed no evidence of myocardial fibrosis (Figure 3C and 3D). The regionality previously noted on transthoracic echocardiogram had resolved and this is in keeping with the diagnosis of Takotsubo syndrome.

Figure 3: A. Coronary angiography revealed moderate disease in mid LAD (yellow arrows). B. Left ventriculogram demonstrated apical akinesis and basal hypercontractility raised the possibility of Takotsubo syndrome. C & D. There was no myocardial fibrosis on LGE imaging. This is in keeping with the diagnosis of Takotsubo syndrome.

Supplementary material

Supplementary Video 1: Angiography showing paucity of the septal branches arising from the LAD, raising the possibility of an occluded vessel. View Supplementary Video 1.

Supplementary Video 2: Angiography showing occlusion of the distal circumflex artery due to spontaneous coronary artery dissection. View Supplementary Video 2.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Danting Wei: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand. Mansi Turaga: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand. Peter Barr: Department of Cardiology, Middlemore Hospital, New Zealand. Ruvin Gabriel: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand Jen-Li Looi: Department of Cardiology, Middlemore Hospital, POtahuhu, Auckland, New Zealand.

Acknowledgements

Correspondence

Jen-Li Looi, Department of Cardiology, Middlemore Hospital, Private Bag 93311, Otahuhu, Auckland 1640, New Zealand, +649 276 0061 (phone), +649 2709746 (fax)

Correspondence Email

JenLi.Looi@middlemore.co.nz

Competing Interests

Nil.

1) Agewall S, Beltrame JF, Reynolds HR, Niessner A, Rosano G, Caforio AL, et al. ESC working group position paper on myocardial infarction with non-obstructive coronary arteries. Eur Heart J. 2016;38:143-53.

2) Tamis-Holland JE, Jneid H, Reynolds HR, Agewall S, Brilakis ES, Brown TM, et al. Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease: a scientific statement from the American Heart Association. Circulation. 2019;139: e891-–908.

3) Everett RJ, Stirrat CG, Semple SI, Newby DE, Dweck MR, Mirsadraee S. Assessment of myocardial fibrosis with T1 mapping MRI. Clin Radiol. 2016 Aug;71(8):768-78.

4) Williams MJA, Barr PR, Lee M, Poppe KK, Kerr AJ. Outcome after myocardial infarction without obstructive coronary artery disease. Heart. 2019 Apr;105(7):524-30.

5) Dall'Armellina E, Piechnik SK, Ferreira VM, Si QL, Robson MD, Francis JM, et al. Cardiovascular magnetic resonance by non contrast T1-mapping allows assessment of severity of injury in acute myocardial infarction. J Cardiovasc Magn Reson. 2012;14:15.

6) Messroghli DR, Walters K, Plein S, Sparrow P, Friedrich MG, Ridgway JP, et al. Myocardial T1 mapping: application to patients with acute and chronic myocardial infarction. Magn Reson Med. 2007;58:34–40.

7) Jia Z, Wang L, Jia Y, Liu J, Zhao H, Huo L, et al. Detection of acute myocarditis using T1 and T2 mapping cardiovascular magnetic resonance: A systematic review and meta-analysis. J Appl Clin Med Phys. 2021 Oct;22(10):239-48.

8) Azevedo CF, Nigri M, Higuchi ML, Pomerantzeff PM, Spina GS, Sampaio RO, et al. Prognostic significance of myocardial fibrosis quantification by histopathology and magnetic resonance imaging in patients with severe aortic valve disease. J Am Coll Cardiol. 2010 Jul 20;56(4):278-87.

9) Verhaert D, Thavendiranathan P, Giri S, Mihai G, Rajagopalan S, Simonetti OP et al. Direct T2 quantification of myocardial edema in acute ischemic injury. JACC Cardiovasc Imaging. 2011;4:269-78.

10) Thavendiranathan P, Walls M, Giri S, Verhaert D, Rajagopalan S, Moore S et al. Improved detection of myocardial involvement in acute inflammatory cardiomyopathies using T2 mapping. Circ Cardiovasc Imaging. 2012; 5:102-10.

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contact nzmj@nzma.org.nz

View Article PDF

Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCA) is an increasingly recognised condition and accounts for 5% to 9% of all MI cases.[[1,2]] Recent study has shown that MINOCA has a higher rate of all-cause mortality than age and sex-matched population without cardiovascular disease (CVD) and the predominant contributor to mortality is non-CVD death.[[3]] This suggests the predisposing factors for MINOCA remain a potent risk factor for non-CVD death. Thus, recent American and European expert consensus documents have defined MINOCA as a “working diagnosis” that should prompt further investigations to ascertain the aetiology of the condition.[[1,2]]

Cardiac magnetic resonance (CMR) is not only accurate in the assessment of cardiac anatomy and function but is also superior in myocardial tissue characterization. Late gadolinium enhancement (LGE) and T2-weighted imaging allow assessment of myocardial scar, focal fibrosis, and myocardial oedema, respectively, thereby enhancing the capacity to delineate causes of suspected MINOCA. Advanced CMR imaging myocardial tissue characterisation methods such as T1 and T2 mapping techniques further improve the diagnosis of myocarditis and Takotsubo syndrome.

Novel T1 mapping techniques allow quantitative CMR assessment of myocardial fibrosis, with the two most common measures being native T1 and extracellular volume (ECV) fraction. Native T1 differentiates normal from infarcted myocardium, is abnormal in hypertrophic cardiomyopathy, and is useful in the diagnosis of Anderson–Fabry disease and amyloidosis.[[4]] In acute MI, native T1 mapping can differentiate microvascular obstruction (MVO) in infarcted myocardium; it is characterised by T1 values higher compared to those of remote myocardium but lower compared to those of infarcted myocardium.[[5,6]] Native myocardial T1 relaxation time was significantly higher in patients with acute myocarditis which is attributed to cellular oedema, increased extracellular space and water, inflammation, and myocyte necrosis, all of which commonly occur in the acute stage of myocarditis.[[7]]

ECV is a surrogate measure of the extracellular space and is equivalent to the myocardial volume of distribution of the gadolinium-based contrast medium. It is reproducible and correlates well with fibrosis on histology. ECV is abnormal in patients with cardiac failure and aortic stenosis, and is associated with functional impairment in these groups.[[8]]

T2 mapping has emerged as a valuable tool in the CMR assessment of myocardial oedema in ischaemic and non-ischaemic cardiomyopathies.[[9,10]] A high T2 value reliably identifies acute myocardial oedema in acute MI without the limitations associated with T2-weighted imaging.[[9]] whereas in chronic MI, T2 value is normal as myocardial oedema resolves within six months after an acute insult. T2 value is also significantly elevated in patients with acute myocarditis indicating myocardial inflammation.[[10]]

We describe three cases in which CMR ensures the correct diagnosis for optimal management and treatment of patients with MINOCA.

Case 1

A 57-year-old woman with hypertension, hyperlipidaemia, and family history of premature coronary artery disease presented with chest pain, elevated high-sensitive troponin (hs-TnT), and dynamic ST-segment changes in the anterior leads on electrocardiogram (ECG). Coronary angiography showed trivial coronary artery disease and transthoracic echocardiogram demonstrated hypokinesis of anteroseptal and inferoseptal, apical inferior and lateral walls. The diagnosis of Takotsubo syndrome was initially made based on these findings. Subsequent echocardiograms continued to show persistent hypokinesis of the septum. CMR (Figure 1A–1C) demonstrated myocardial fibrosis involving the septal wall, a pattern in keeping with previous left anterior descending (LAD) territory infarction. Further review of her angiography revealed paucity of the septal branches arising from the LAD (Figure 1D, Supplementary Video 1), raising the possibility of an occluded vessel.

Figure 1: A. Pre-contrast T1 mapping showed an abnormally increased T1 signal (black arrows) involving the anteroseptal wall, suggestive of myocardial fibrosis. B & C. On LGE imaging, there was near transmural enhancement (red arrows) involving the anteroseptal wall, a finding in keeping with myocardial infarction. D. Coronary angiography revealed paucity of sepal branches arising from the LAD (yellow circle) raising the possibility of an occluded vessel.

Case 2

A 57-year-old woman presented with fever, chest pain, elevated hs-TnT, and C-reactive protein (CRP). Coronary angiography demonstrated near normal coronaries. CMR was performed as part of the workup of suspected myocarditis. T2-weighted short-tau inversion recovery (T2-STIR) imaging and T2 mapping (Figure 2A and 2B) showed an oedematous area in the inferolateral wall. Native T1 mapping (Figure 2C) and LGE imaging (Figure 2D and 2E) revealed transmural myocardial fibrosis with MVO in the inferolateral wall, a pattern in keeping with circumflex artery territory infarction. Further review of her angiography (Figure 2F, Supplementary Video 2) demonstrated occlusion of the distal circumflex artery due to spontaneous coronary artery dissection (SCAD).

Figure 2: A. There was a hyperintense signal (yellow arrows) in the inferolateral wall, suggestive of myocardial oedema on T2-STIR imaging. B. Compared to the anterolateral wall (mean T2 value 35 msec, normal range <50 msec), T2 value was significantly higher in the inferolateral wall (mean T2 value 60 msec) indicating acute myocardial oedema. C. Pre-contrast T1 mapping showed an abnormally increased T1 signal involving the inferolateral wall. There was a dark region (red arrows) within the bright myocardium in keeping with microvascular obstruction (MVO). D & E. On LGE imaging, there was transmural myocardial enhancement in the inferolateral wall. MVO is observed as hypo-enhanced region within hyper-enhanced infarcted myocardium (yellow arrows). F. Coronary angiography revealed occlusion of a large circumflex artery (yellow arrow) secondary to spontaneous coronary artery dissection.

Case 3

A 75-year-old woman with hypertension, hyperlipidaemia, and previous transient ischaemic attack presented with chest pain and elevated hs-TnT. She was competing in an art competition a few hours prior to admission. Transthoracic echocardiogram demonstrated hypokinesis of the anteroseptal and anterior walls. Coronary angiography showed moderate disease in mid LAD (Figure 3A). Fractional flow reserve (FFR) was performed to the LAD as the vessel is large and does wrap around the apex and it suggested non-obstructive disease (FFR 0.87). The appearance of the left ventriculogram raises the possibility of Takotsubo syndrome (Figure 3B). CMR was subsequently performed to clarify the diagnosis. Native T1 mapping (myocardium T1 value 1201 msec, normal range 1225–1275 msec) and LGE imaging showed no evidence of myocardial fibrosis (Figure 3C and 3D). The regionality previously noted on transthoracic echocardiogram had resolved and this is in keeping with the diagnosis of Takotsubo syndrome.

Figure 3: A. Coronary angiography revealed moderate disease in mid LAD (yellow arrows). B. Left ventriculogram demonstrated apical akinesis and basal hypercontractility raised the possibility of Takotsubo syndrome. C & D. There was no myocardial fibrosis on LGE imaging. This is in keeping with the diagnosis of Takotsubo syndrome.

Supplementary material

Supplementary Video 1: Angiography showing paucity of the septal branches arising from the LAD, raising the possibility of an occluded vessel. View Supplementary Video 1.

Supplementary Video 2: Angiography showing occlusion of the distal circumflex artery due to spontaneous coronary artery dissection. View Supplementary Video 2.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Danting Wei: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand. Mansi Turaga: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand. Peter Barr: Department of Cardiology, Middlemore Hospital, New Zealand. Ruvin Gabriel: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand Jen-Li Looi: Department of Cardiology, Middlemore Hospital, POtahuhu, Auckland, New Zealand.

Acknowledgements

Correspondence

Jen-Li Looi, Department of Cardiology, Middlemore Hospital, Private Bag 93311, Otahuhu, Auckland 1640, New Zealand, +649 276 0061 (phone), +649 2709746 (fax)

Correspondence Email

JenLi.Looi@middlemore.co.nz

Competing Interests

Nil.

1) Agewall S, Beltrame JF, Reynolds HR, Niessner A, Rosano G, Caforio AL, et al. ESC working group position paper on myocardial infarction with non-obstructive coronary arteries. Eur Heart J. 2016;38:143-53.

2) Tamis-Holland JE, Jneid H, Reynolds HR, Agewall S, Brilakis ES, Brown TM, et al. Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease: a scientific statement from the American Heart Association. Circulation. 2019;139: e891-–908.

3) Everett RJ, Stirrat CG, Semple SI, Newby DE, Dweck MR, Mirsadraee S. Assessment of myocardial fibrosis with T1 mapping MRI. Clin Radiol. 2016 Aug;71(8):768-78.

4) Williams MJA, Barr PR, Lee M, Poppe KK, Kerr AJ. Outcome after myocardial infarction without obstructive coronary artery disease. Heart. 2019 Apr;105(7):524-30.

5) Dall'Armellina E, Piechnik SK, Ferreira VM, Si QL, Robson MD, Francis JM, et al. Cardiovascular magnetic resonance by non contrast T1-mapping allows assessment of severity of injury in acute myocardial infarction. J Cardiovasc Magn Reson. 2012;14:15.

6) Messroghli DR, Walters K, Plein S, Sparrow P, Friedrich MG, Ridgway JP, et al. Myocardial T1 mapping: application to patients with acute and chronic myocardial infarction. Magn Reson Med. 2007;58:34–40.

7) Jia Z, Wang L, Jia Y, Liu J, Zhao H, Huo L, et al. Detection of acute myocarditis using T1 and T2 mapping cardiovascular magnetic resonance: A systematic review and meta-analysis. J Appl Clin Med Phys. 2021 Oct;22(10):239-48.

8) Azevedo CF, Nigri M, Higuchi ML, Pomerantzeff PM, Spina GS, Sampaio RO, et al. Prognostic significance of myocardial fibrosis quantification by histopathology and magnetic resonance imaging in patients with severe aortic valve disease. J Am Coll Cardiol. 2010 Jul 20;56(4):278-87.

9) Verhaert D, Thavendiranathan P, Giri S, Mihai G, Rajagopalan S, Simonetti OP et al. Direct T2 quantification of myocardial edema in acute ischemic injury. JACC Cardiovasc Imaging. 2011;4:269-78.

10) Thavendiranathan P, Walls M, Giri S, Verhaert D, Rajagopalan S, Moore S et al. Improved detection of myocardial involvement in acute inflammatory cardiomyopathies using T2 mapping. Circ Cardiovasc Imaging. 2012; 5:102-10.

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCA) is an increasingly recognised condition and accounts for 5% to 9% of all MI cases.[[1,2]] Recent study has shown that MINOCA has a higher rate of all-cause mortality than age and sex-matched population without cardiovascular disease (CVD) and the predominant contributor to mortality is non-CVD death.[[3]] This suggests the predisposing factors for MINOCA remain a potent risk factor for non-CVD death. Thus, recent American and European expert consensus documents have defined MINOCA as a “working diagnosis” that should prompt further investigations to ascertain the aetiology of the condition.[[1,2]]

Cardiac magnetic resonance (CMR) is not only accurate in the assessment of cardiac anatomy and function but is also superior in myocardial tissue characterization. Late gadolinium enhancement (LGE) and T2-weighted imaging allow assessment of myocardial scar, focal fibrosis, and myocardial oedema, respectively, thereby enhancing the capacity to delineate causes of suspected MINOCA. Advanced CMR imaging myocardial tissue characterisation methods such as T1 and T2 mapping techniques further improve the diagnosis of myocarditis and Takotsubo syndrome.

Novel T1 mapping techniques allow quantitative CMR assessment of myocardial fibrosis, with the two most common measures being native T1 and extracellular volume (ECV) fraction. Native T1 differentiates normal from infarcted myocardium, is abnormal in hypertrophic cardiomyopathy, and is useful in the diagnosis of Anderson–Fabry disease and amyloidosis.[[4]] In acute MI, native T1 mapping can differentiate microvascular obstruction (MVO) in infarcted myocardium; it is characterised by T1 values higher compared to those of remote myocardium but lower compared to those of infarcted myocardium.[[5,6]] Native myocardial T1 relaxation time was significantly higher in patients with acute myocarditis which is attributed to cellular oedema, increased extracellular space and water, inflammation, and myocyte necrosis, all of which commonly occur in the acute stage of myocarditis.[[7]]

ECV is a surrogate measure of the extracellular space and is equivalent to the myocardial volume of distribution of the gadolinium-based contrast medium. It is reproducible and correlates well with fibrosis on histology. ECV is abnormal in patients with cardiac failure and aortic stenosis, and is associated with functional impairment in these groups.[[8]]

T2 mapping has emerged as a valuable tool in the CMR assessment of myocardial oedema in ischaemic and non-ischaemic cardiomyopathies.[[9,10]] A high T2 value reliably identifies acute myocardial oedema in acute MI without the limitations associated with T2-weighted imaging.[[9]] whereas in chronic MI, T2 value is normal as myocardial oedema resolves within six months after an acute insult. T2 value is also significantly elevated in patients with acute myocarditis indicating myocardial inflammation.[[10]]

We describe three cases in which CMR ensures the correct diagnosis for optimal management and treatment of patients with MINOCA.

Case 1

A 57-year-old woman with hypertension, hyperlipidaemia, and family history of premature coronary artery disease presented with chest pain, elevated high-sensitive troponin (hs-TnT), and dynamic ST-segment changes in the anterior leads on electrocardiogram (ECG). Coronary angiography showed trivial coronary artery disease and transthoracic echocardiogram demonstrated hypokinesis of anteroseptal and inferoseptal, apical inferior and lateral walls. The diagnosis of Takotsubo syndrome was initially made based on these findings. Subsequent echocardiograms continued to show persistent hypokinesis of the septum. CMR (Figure 1A–1C) demonstrated myocardial fibrosis involving the septal wall, a pattern in keeping with previous left anterior descending (LAD) territory infarction. Further review of her angiography revealed paucity of the septal branches arising from the LAD (Figure 1D, Supplementary Video 1), raising the possibility of an occluded vessel.

Figure 1: A. Pre-contrast T1 mapping showed an abnormally increased T1 signal (black arrows) involving the anteroseptal wall, suggestive of myocardial fibrosis. B & C. On LGE imaging, there was near transmural enhancement (red arrows) involving the anteroseptal wall, a finding in keeping with myocardial infarction. D. Coronary angiography revealed paucity of sepal branches arising from the LAD (yellow circle) raising the possibility of an occluded vessel.

Case 2

A 57-year-old woman presented with fever, chest pain, elevated hs-TnT, and C-reactive protein (CRP). Coronary angiography demonstrated near normal coronaries. CMR was performed as part of the workup of suspected myocarditis. T2-weighted short-tau inversion recovery (T2-STIR) imaging and T2 mapping (Figure 2A and 2B) showed an oedematous area in the inferolateral wall. Native T1 mapping (Figure 2C) and LGE imaging (Figure 2D and 2E) revealed transmural myocardial fibrosis with MVO in the inferolateral wall, a pattern in keeping with circumflex artery territory infarction. Further review of her angiography (Figure 2F, Supplementary Video 2) demonstrated occlusion of the distal circumflex artery due to spontaneous coronary artery dissection (SCAD).

Figure 2: A. There was a hyperintense signal (yellow arrows) in the inferolateral wall, suggestive of myocardial oedema on T2-STIR imaging. B. Compared to the anterolateral wall (mean T2 value 35 msec, normal range <50 msec), T2 value was significantly higher in the inferolateral wall (mean T2 value 60 msec) indicating acute myocardial oedema. C. Pre-contrast T1 mapping showed an abnormally increased T1 signal involving the inferolateral wall. There was a dark region (red arrows) within the bright myocardium in keeping with microvascular obstruction (MVO). D & E. On LGE imaging, there was transmural myocardial enhancement in the inferolateral wall. MVO is observed as hypo-enhanced region within hyper-enhanced infarcted myocardium (yellow arrows). F. Coronary angiography revealed occlusion of a large circumflex artery (yellow arrow) secondary to spontaneous coronary artery dissection.

Case 3

A 75-year-old woman with hypertension, hyperlipidaemia, and previous transient ischaemic attack presented with chest pain and elevated hs-TnT. She was competing in an art competition a few hours prior to admission. Transthoracic echocardiogram demonstrated hypokinesis of the anteroseptal and anterior walls. Coronary angiography showed moderate disease in mid LAD (Figure 3A). Fractional flow reserve (FFR) was performed to the LAD as the vessel is large and does wrap around the apex and it suggested non-obstructive disease (FFR 0.87). The appearance of the left ventriculogram raises the possibility of Takotsubo syndrome (Figure 3B). CMR was subsequently performed to clarify the diagnosis. Native T1 mapping (myocardium T1 value 1201 msec, normal range 1225–1275 msec) and LGE imaging showed no evidence of myocardial fibrosis (Figure 3C and 3D). The regionality previously noted on transthoracic echocardiogram had resolved and this is in keeping with the diagnosis of Takotsubo syndrome.

Figure 3: A. Coronary angiography revealed moderate disease in mid LAD (yellow arrows). B. Left ventriculogram demonstrated apical akinesis and basal hypercontractility raised the possibility of Takotsubo syndrome. C & D. There was no myocardial fibrosis on LGE imaging. This is in keeping with the diagnosis of Takotsubo syndrome.

Supplementary material

Supplementary Video 1: Angiography showing paucity of the septal branches arising from the LAD, raising the possibility of an occluded vessel. View Supplementary Video 1.

Supplementary Video 2: Angiography showing occlusion of the distal circumflex artery due to spontaneous coronary artery dissection. View Supplementary Video 2.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Danting Wei: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand. Mansi Turaga: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand. Peter Barr: Department of Cardiology, Middlemore Hospital, New Zealand. Ruvin Gabriel: Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand Jen-Li Looi: Department of Cardiology, Middlemore Hospital, POtahuhu, Auckland, New Zealand.

Acknowledgements

Correspondence

Jen-Li Looi, Department of Cardiology, Middlemore Hospital, Private Bag 93311, Otahuhu, Auckland 1640, New Zealand, +649 276 0061 (phone), +649 2709746 (fax)

Correspondence Email

JenLi.Looi@middlemore.co.nz

Competing Interests

Nil.

1) Agewall S, Beltrame JF, Reynolds HR, Niessner A, Rosano G, Caforio AL, et al. ESC working group position paper on myocardial infarction with non-obstructive coronary arteries. Eur Heart J. 2016;38:143-53.

2) Tamis-Holland JE, Jneid H, Reynolds HR, Agewall S, Brilakis ES, Brown TM, et al. Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease: a scientific statement from the American Heart Association. Circulation. 2019;139: e891-–908.

3) Everett RJ, Stirrat CG, Semple SI, Newby DE, Dweck MR, Mirsadraee S. Assessment of myocardial fibrosis with T1 mapping MRI. Clin Radiol. 2016 Aug;71(8):768-78.

4) Williams MJA, Barr PR, Lee M, Poppe KK, Kerr AJ. Outcome after myocardial infarction without obstructive coronary artery disease. Heart. 2019 Apr;105(7):524-30.

5) Dall'Armellina E, Piechnik SK, Ferreira VM, Si QL, Robson MD, Francis JM, et al. Cardiovascular magnetic resonance by non contrast T1-mapping allows assessment of severity of injury in acute myocardial infarction. J Cardiovasc Magn Reson. 2012;14:15.

6) Messroghli DR, Walters K, Plein S, Sparrow P, Friedrich MG, Ridgway JP, et al. Myocardial T1 mapping: application to patients with acute and chronic myocardial infarction. Magn Reson Med. 2007;58:34–40.

7) Jia Z, Wang L, Jia Y, Liu J, Zhao H, Huo L, et al. Detection of acute myocarditis using T1 and T2 mapping cardiovascular magnetic resonance: A systematic review and meta-analysis. J Appl Clin Med Phys. 2021 Oct;22(10):239-48.

8) Azevedo CF, Nigri M, Higuchi ML, Pomerantzeff PM, Spina GS, Sampaio RO, et al. Prognostic significance of myocardial fibrosis quantification by histopathology and magnetic resonance imaging in patients with severe aortic valve disease. J Am Coll Cardiol. 2010 Jul 20;56(4):278-87.

9) Verhaert D, Thavendiranathan P, Giri S, Mihai G, Rajagopalan S, Simonetti OP et al. Direct T2 quantification of myocardial edema in acute ischemic injury. JACC Cardiovasc Imaging. 2011;4:269-78.

10) Thavendiranathan P, Walls M, Giri S, Verhaert D, Rajagopalan S, Moore S et al. Improved detection of myocardial involvement in acute inflammatory cardiomyopathies using T2 mapping. Circ Cardiovasc Imaging. 2012; 5:102-10.

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