- Email: [email protected]
Myocardial Infarction Caused by Accelerated Plaque Formation Related to Myocardial Bridge in a Young Man
Accepted Manuscript Myocardial Infarction Caused by Accelerated Plaque Formation Related to Myocardial Bridge in Very Young Male Shinnosuke Kikuchi, MD, Kozo Okada, MD, Kiyoshi Hibi, MD, Nobuhiko Maejima, MD, Yasushi Matsuzawa, MD, Masaaki Konishi, MD, Yuichiro Kimura, MD, Masami Kosuge, MD, Noriaki Iwahashi, MD, Toshiaki Ebina, MD, Kouichi Tamura, MD, Kazuo Kimura, MD PII:
S0828-282X(18)31059-6
DOI:
10.1016/j.cjca.2018.08.023
Reference:
CJCA 3023
To appear in:
Canadian Journal of Cardiology
Received Date: 7 June 2018 Revised Date:
1 August 2018
Accepted Date: 12 August 2018
Please cite this article as: Kikuchi S, Okada K, Hibi K, Maejima N, Matsuzawa Y, Konishi M, Kimura Y, Kosuge M, Iwahashi N, Ebina T, Tamura K, Kimura K, Myocardial Infarction Caused by Accelerated Plaque Formation Related to Myocardial Bridge in Very Young Male, Canadian Journal of Cardiology (2018), doi: 10.1016/j.cjca.2018.08.023. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Myocardial Infarction Caused by Accelerated Plaque Formation Related to
1
Myocardial Bridge in Very Young Male
2 3
Shinnosuke Kikuchi, MD1, Kozo Okada, MD1, Kiyoshi Hibi, MD1,
5
Nobuhiko Maejima, MD1, Yasushi Matsuzawa, MD1, Masaaki Konishi, MD1,
6
Yuichiro Kimura, MD1, Masami Kosuge, MD1, Noriaki Iwahashi, MD1,
7
Toshiaki Ebina, MD1, Kouichi Tamura, MD2, Kazuo Kimura, MD1
SC
RI PT
4
8 9
1
10
2
11
Graduate School of Medicine, Yokohama, Japan
M AN U
Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan,
Department of Medical Science and Cardiorenal Medicine, Yokohama City University
12
Short title: myocardial bridge and acute coronary syndromes
TE D
13 14 15
Word count: 1200 words with 1 Figure and 1 supplementary Figure
EP
16
Address for Correspondence
18
Kozo Okada, MD
19
Division of Cardiology, Yokohama City University Medical Center
20
4-57 Urafune-cho, Minami-ku, Yokohama, Japan 232-0024
21
Phone: +81-45-261-5656
22
E-mail: [email protected]
AC C
17
FAX: +81-45-261-9162
23
1
ACCEPTED MANUSCRIPT
Brief Summary
2
We reported the case of 28-year old male without coronary risk factors who admitted
3
with acute coronary syndromes (ACS) due to the acceleration of proximal plaque
4
formation potentially caused by myocardial bridge (MB) located distal to the plaque.
5
The present case highlights the importance of MB as a possible cause of ACS even in
6
younger patients with low cardiovascular risk.
8
SC
7
RI PT
1
Abstract
A 28-year old male without coronary risk factors was admitted with acute
10
coronary syndromes (ACS). The angiogram and intravascular ultrasound revealed
11
myocardial bridge (MB) in the mid left anterior descending artery and flow-limiting
12
plaque located 15.4 mm proximal to MB. The culprit lesion was treated only with drug-
13
coated balloon, considering patient’s extremely young age. The present case suggests
14
that an accelerated plaque formation caused by MB appeared to contribute to the
15
development of ACS, thus MB should be considered as an important cause of ACS in
16
younger patients with low cardiovascular risk.
17
19
Case
AC C
18
EP
TE D
M AN U
9
A 28-year old male who had no significant coronary risk factors presented to
20
our hospital with chest pain on effort and was admitted with a diagnosis of acute
21
coronary syndromes (ACS) based on electrocardiographic abnormalities (T-wave
22
inversion in leads V2-V4 and ST depression in leads V5-V6) and an increased troponin
23
I level (0.225 ng/ml). The patient was very young with low cardiovascular risk and
24
relatively stable during the hospital course. Therefore, we firstly performed non-
2
ACCEPTED MANUSCRIPT
invasive tests (treadmill test, coronary computed tomography angiography (CTA)) and
2
confirmed myocardial ischemia. Then, coronary angiogram was performed 10 days after
3
admission, which revealed severe stenosis in the proximal segment of the left anterior
4
descending artery (LAD), without any other significant stenosis. There was also arterial
5
compression in the mid LAD segment, suggesting the presence of myocardial bridge
6
(MB) (Figure S in supplementary materials). No dissection nor thrombus, suggesting
7
spontaneous coronary artery dissection (SCAD) and coronary artery embolism (CAE),
8
was observed on the angiogram. After excluding the other non-atherosclerotic diseases
9
(i.e., aortitis and autoimmune diseases) by additional non-invasive tests, percutaneous
10
coronary intervention (PCI) was performed at 17 days post-admission with intravascular
11
imaging guidance. Intravascular ultrasound (IVUS) identified significant flow-limiting
12
plaque with positive vessel remodeling in the proximal LAD segment, as well as MB
13
which was located 15.4 mm distal to the plaque, measured 39.1 mm in length, had
14
systolic arterial compression of 24.8%, and had halo of 0.51 mm (Figure). Optical
15
coherence tomography (OCT) also demonstrated severe stenosis with mixed plaque,
16
whereas plaque fissure or thrombus was not apparent. The culprit lesion was treated
17
only with drug-coated balloon (DCB), considering the patient’s extremely young age.
18
The patient was discharged on statin and minimum 3-month dual antiplatelet therapy
19
followed by single antiplatelet therapy. At 6-month follow-up, coronary CTA and
20
treadmill test showed no restenosis.
AC C
EP
TE D
M AN U
SC
RI PT
1
21 22
Discussion
23
MB is a common anatomic variant and predominantly involves the mid to
24
distal LAD segments.1,2 The prevalence of MB varies considerably, depending on the
3
ACCEPTED MANUSCRIPT
diagnostic methods (0.5-2.5% by angiography, 23% by IVUS, and up to 85% in autopsy
2
series).3 Although MB is generally considered benign, several studies have shown that
3
MB can predispose to ischemia, due to both anatomical and functional abnormalities,
4
including accelerated proximal plaque formation, endothelial dysfunction and severe
5
mechanical compression by MB1,3, even in cases of low-risk patients. In the present
6
case, the patient was extremely young with low cardiovascular risk. There were also no
7
episodes to suggest vasospastic angina, SCAD, or CAE (i.e., chest pain at rest and
8
arrhythmia), indicating that an accelerated plaque formation by MB appeared to play an
9
important role in the development of ACS.
M AN U
SC
RI PT
1
Multiple studies have shown the association between MB and subclinical
11
atherosclerosis.1,4 Based on these investigations, plaque formation related to MB is
12
typically seen up to 20 mm proximal to MB, which is consistent with our results (15.4
13
mm proximal to MB). It has also been reported that greater amounts of proximal
14
atherosclerotic plaque is associated with more abnormal anatomic properties of MB,
15
such as greater arterial compression and halo thickness, and longer MB length.1,4
16
Interestingly, these associations appeared to be prominent when the analysis was limited
17
to younger patients with ≤1 coronary risk factors,4 suggesting that MB itself may
18
contribute to coronary atherosclerosis. Although the exact mechanisms for the unique
19
characteristics of proximal plaque formation by MB remain a matter of speculation, it
20
may, in part, be explained by abnormal distributions of wall shear stress and abnormal
21
blood flow profiles at the segment proximal to MB,2-4 both of which have been
22
postulated to predispose enhanced lipid transfer augmentation across the endothelium
23
and plaque progression with subsequent plaque rupture. The present case did not show
24
apparent thrombus (suggesting plaque rupture) around the culprit lesion, primarily
AC C
EP
TE D
10
4
ACCEPTED MANUSCRIPT
attributable to delayed-angiography performed at 10 and 17 days after admission. Perl et
2
al.3 reported cases of patients with MBs who presented with ACS caused by plaque
3
rupture despite having low cardiovascular risk, potentially supporting the explanations
4
above.
RI PT
1
Treatment options for flow-limiting plaque caused by MB remain limited,
6
especially in younger patients. Generally, coronary stenting with drug-eluting stents
7
(DES) is the gold standard for treatments of coronary atherosclerosis; however, the
8
cumulative incidence of stent thrombosis over time after stent implantation may be of
9
concern in younger patients. Relatively high-rates of target lesion revascularization,
10
even with DES, has also been reported in previous MB studies.2 On the other hand,
11
several studies have shown that DCB has the potential to be an alternative treatment of
12
lesions where durable metallic-stent implantation is not desirable.5 Thus, in the present
13
case, the culprit lesion was treated only with DCB; the patient showed no restenosis for
14
at least 6 months. However, MB still exists in the same artery (LAD) and there may
15
remain an unavoidable risk of future recurrence of plaque progression caused by MB.
16
Although further studies will need to investigate optimal treatment for this unique
17
pathology (i.e., MB), surgical unroofing, in addition to coronary bypass grafting of the
18
LAD, may also be a treatment option, especially in MB patients who are refractory to
19
maximal medical treatment and PCI.
M AN U
TE D
EP
AC C
20
SC
5
21
Disclosures
22
The authors have nothing to disclose.
23 24
Acknowledgments
25
The authors appreciate Heidi N. Bonneau, RN, MS, CCA for her expert review and 5
ACCEPTED MANUSCRIPT
1
editing advice.
2 3
References
4
1.
2.
J Investig Med High Impact Case Rep. 2016;4(4):2324709616680227.
Compression on Proximal Atherosclerotic Plaque. J Am Heart Assoc. 2016;5(4):e001735.
13
16
5.
Nishiyama N, Komatsu T, Kuroyanagi T, et al. Clinical value of drug-coated balloon angioplasty for de novo lesions in patients with coronary artery disease. Int J Cardiol. 2016;222:113-118.
17
TE D
12
15
Yamada R, Tremmel JA, Tanaka S, et al. Functional Versus Anatomic Assessment of Myocardial Bridging by Intravascular Ultrasound: Impact of Arterial
M AN U
4.
11
14
Perl L, Daniels D, Schwartz J, et al. Myocardial Bridge and Acute Plaque Rupture.
SC
3.
9 10
Möhlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation. 2002;106(20):2616-2622.
7 8
RI PT
predisposing to myocardial infarction. Circulation. 2009;120(5):376-383.
5 6
Ishikawa Y, Akasaka Y, Suzuki K, et al. Anatomic properties of myocardial bridge
Figure Legend
19
Figure. Myocardial bridge and proximal plaque formation
20
A. proximal reference site. B. culprit lesion site. C. distal reference site. D. site with
21
maximal halo thickness. E. site with maximal arterial compression. F. longitudinal
22
IVUS view. MB was identified by IVUS as an echolucent-band “halo” (green arrow
23
heads, D/E). IVUS and OCT showed flow-limiting plaque located 15.4 mm proximal to
24
MB (B/F).
AC C
EP
18
25 26
Figure S (in supplementary materials). Coronary angiogram
27
There was severe stenosis in the proximal LAD segment and arterial compression in the
6
ACCEPTED MANUSCRIPT
1
mid LAD segment.
2
AC C
EP
TE D
M AN U
SC
RI PT
3
7
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
S0828-282X(18)31059-6
DOI:
10.1016/j.cjca.2018.08.023
Reference:
CJCA 3023
To appear in:
Canadian Journal of Cardiology
Received Date: 7 June 2018 Revised Date:
1 August 2018
Accepted Date: 12 August 2018
Please cite this article as: Kikuchi S, Okada K, Hibi K, Maejima N, Matsuzawa Y, Konishi M, Kimura Y, Kosuge M, Iwahashi N, Ebina T, Tamura K, Kimura K, Myocardial Infarction Caused by Accelerated Plaque Formation Related to Myocardial Bridge in Very Young Male, Canadian Journal of Cardiology (2018), doi: 10.1016/j.cjca.2018.08.023. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Myocardial Infarction Caused by Accelerated Plaque Formation Related to
1
Myocardial Bridge in Very Young Male
2 3
Shinnosuke Kikuchi, MD1, Kozo Okada, MD1, Kiyoshi Hibi, MD1,
5
Nobuhiko Maejima, MD1, Yasushi Matsuzawa, MD1, Masaaki Konishi, MD1,
6
Yuichiro Kimura, MD1, Masami Kosuge, MD1, Noriaki Iwahashi, MD1,
7
Toshiaki Ebina, MD1, Kouichi Tamura, MD2, Kazuo Kimura, MD1
SC
RI PT
4
8 9
1
10
2
11
Graduate School of Medicine, Yokohama, Japan
M AN U
Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan,
Department of Medical Science and Cardiorenal Medicine, Yokohama City University
12
Short title: myocardial bridge and acute coronary syndromes
TE D
13 14 15
Word count: 1200 words with 1 Figure and 1 supplementary Figure
EP
16
Address for Correspondence
18
Kozo Okada, MD
19
Division of Cardiology, Yokohama City University Medical Center
20
4-57 Urafune-cho, Minami-ku, Yokohama, Japan 232-0024
21
Phone: +81-45-261-5656
22
E-mail: [email protected]
AC C
17
FAX: +81-45-261-9162
23
1
ACCEPTED MANUSCRIPT
Brief Summary
2
We reported the case of 28-year old male without coronary risk factors who admitted
3
with acute coronary syndromes (ACS) due to the acceleration of proximal plaque
4
formation potentially caused by myocardial bridge (MB) located distal to the plaque.
5
The present case highlights the importance of MB as a possible cause of ACS even in
6
younger patients with low cardiovascular risk.
8
SC
7
RI PT
1
Abstract
A 28-year old male without coronary risk factors was admitted with acute
10
coronary syndromes (ACS). The angiogram and intravascular ultrasound revealed
11
myocardial bridge (MB) in the mid left anterior descending artery and flow-limiting
12
plaque located 15.4 mm proximal to MB. The culprit lesion was treated only with drug-
13
coated balloon, considering patient’s extremely young age. The present case suggests
14
that an accelerated plaque formation caused by MB appeared to contribute to the
15
development of ACS, thus MB should be considered as an important cause of ACS in
16
younger patients with low cardiovascular risk.
17
19
Case
AC C
18
EP
TE D
M AN U
9
A 28-year old male who had no significant coronary risk factors presented to
20
our hospital with chest pain on effort and was admitted with a diagnosis of acute
21
coronary syndromes (ACS) based on electrocardiographic abnormalities (T-wave
22
inversion in leads V2-V4 and ST depression in leads V5-V6) and an increased troponin
23
I level (0.225 ng/ml). The patient was very young with low cardiovascular risk and
24
relatively stable during the hospital course. Therefore, we firstly performed non-
2
ACCEPTED MANUSCRIPT
invasive tests (treadmill test, coronary computed tomography angiography (CTA)) and
2
confirmed myocardial ischemia. Then, coronary angiogram was performed 10 days after
3
admission, which revealed severe stenosis in the proximal segment of the left anterior
4
descending artery (LAD), without any other significant stenosis. There was also arterial
5
compression in the mid LAD segment, suggesting the presence of myocardial bridge
6
(MB) (Figure S in supplementary materials). No dissection nor thrombus, suggesting
7
spontaneous coronary artery dissection (SCAD) and coronary artery embolism (CAE),
8
was observed on the angiogram. After excluding the other non-atherosclerotic diseases
9
(i.e., aortitis and autoimmune diseases) by additional non-invasive tests, percutaneous
10
coronary intervention (PCI) was performed at 17 days post-admission with intravascular
11
imaging guidance. Intravascular ultrasound (IVUS) identified significant flow-limiting
12
plaque with positive vessel remodeling in the proximal LAD segment, as well as MB
13
which was located 15.4 mm distal to the plaque, measured 39.1 mm in length, had
14
systolic arterial compression of 24.8%, and had halo of 0.51 mm (Figure). Optical
15
coherence tomography (OCT) also demonstrated severe stenosis with mixed plaque,
16
whereas plaque fissure or thrombus was not apparent. The culprit lesion was treated
17
only with drug-coated balloon (DCB), considering the patient’s extremely young age.
18
The patient was discharged on statin and minimum 3-month dual antiplatelet therapy
19
followed by single antiplatelet therapy. At 6-month follow-up, coronary CTA and
20
treadmill test showed no restenosis.
AC C
EP
TE D
M AN U
SC
RI PT
1
21 22
Discussion
23
MB is a common anatomic variant and predominantly involves the mid to
24
distal LAD segments.1,2 The prevalence of MB varies considerably, depending on the
3
ACCEPTED MANUSCRIPT
diagnostic methods (0.5-2.5% by angiography, 23% by IVUS, and up to 85% in autopsy
2
series).3 Although MB is generally considered benign, several studies have shown that
3
MB can predispose to ischemia, due to both anatomical and functional abnormalities,
4
including accelerated proximal plaque formation, endothelial dysfunction and severe
5
mechanical compression by MB1,3, even in cases of low-risk patients. In the present
6
case, the patient was extremely young with low cardiovascular risk. There were also no
7
episodes to suggest vasospastic angina, SCAD, or CAE (i.e., chest pain at rest and
8
arrhythmia), indicating that an accelerated plaque formation by MB appeared to play an
9
important role in the development of ACS.
M AN U
SC
RI PT
1
Multiple studies have shown the association between MB and subclinical
11
atherosclerosis.1,4 Based on these investigations, plaque formation related to MB is
12
typically seen up to 20 mm proximal to MB, which is consistent with our results (15.4
13
mm proximal to MB). It has also been reported that greater amounts of proximal
14
atherosclerotic plaque is associated with more abnormal anatomic properties of MB,
15
such as greater arterial compression and halo thickness, and longer MB length.1,4
16
Interestingly, these associations appeared to be prominent when the analysis was limited
17
to younger patients with ≤1 coronary risk factors,4 suggesting that MB itself may
18
contribute to coronary atherosclerosis. Although the exact mechanisms for the unique
19
characteristics of proximal plaque formation by MB remain a matter of speculation, it
20
may, in part, be explained by abnormal distributions of wall shear stress and abnormal
21
blood flow profiles at the segment proximal to MB,2-4 both of which have been
22
postulated to predispose enhanced lipid transfer augmentation across the endothelium
23
and plaque progression with subsequent plaque rupture. The present case did not show
24
apparent thrombus (suggesting plaque rupture) around the culprit lesion, primarily
AC C
EP
TE D
10
4
ACCEPTED MANUSCRIPT
attributable to delayed-angiography performed at 10 and 17 days after admission. Perl et
2
al.3 reported cases of patients with MBs who presented with ACS caused by plaque
3
rupture despite having low cardiovascular risk, potentially supporting the explanations
4
above.
RI PT
1
Treatment options for flow-limiting plaque caused by MB remain limited,
6
especially in younger patients. Generally, coronary stenting with drug-eluting stents
7
(DES) is the gold standard for treatments of coronary atherosclerosis; however, the
8
cumulative incidence of stent thrombosis over time after stent implantation may be of
9
concern in younger patients. Relatively high-rates of target lesion revascularization,
10
even with DES, has also been reported in previous MB studies.2 On the other hand,
11
several studies have shown that DCB has the potential to be an alternative treatment of
12
lesions where durable metallic-stent implantation is not desirable.5 Thus, in the present
13
case, the culprit lesion was treated only with DCB; the patient showed no restenosis for
14
at least 6 months. However, MB still exists in the same artery (LAD) and there may
15
remain an unavoidable risk of future recurrence of plaque progression caused by MB.
16
Although further studies will need to investigate optimal treatment for this unique
17
pathology (i.e., MB), surgical unroofing, in addition to coronary bypass grafting of the
18
LAD, may also be a treatment option, especially in MB patients who are refractory to
19
maximal medical treatment and PCI.
M AN U
TE D
EP
AC C
20
SC
5
21
Disclosures
22
The authors have nothing to disclose.
23 24
Acknowledgments
25
The authors appreciate Heidi N. Bonneau, RN, MS, CCA for her expert review and 5
ACCEPTED MANUSCRIPT
1
editing advice.
2 3
References
4
1.
2.
J Investig Med High Impact Case Rep. 2016;4(4):2324709616680227.
Compression on Proximal Atherosclerotic Plaque. J Am Heart Assoc. 2016;5(4):e001735.
13
16
5.
Nishiyama N, Komatsu T, Kuroyanagi T, et al. Clinical value of drug-coated balloon angioplasty for de novo lesions in patients with coronary artery disease. Int J Cardiol. 2016;222:113-118.
17
TE D
12
15
Yamada R, Tremmel JA, Tanaka S, et al. Functional Versus Anatomic Assessment of Myocardial Bridging by Intravascular Ultrasound: Impact of Arterial
M AN U
4.
11
14
Perl L, Daniels D, Schwartz J, et al. Myocardial Bridge and Acute Plaque Rupture.
SC
3.
9 10
Möhlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation. 2002;106(20):2616-2622.
7 8
RI PT
predisposing to myocardial infarction. Circulation. 2009;120(5):376-383.
5 6
Ishikawa Y, Akasaka Y, Suzuki K, et al. Anatomic properties of myocardial bridge
Figure Legend
19
Figure. Myocardial bridge and proximal plaque formation
20
A. proximal reference site. B. culprit lesion site. C. distal reference site. D. site with
21
maximal halo thickness. E. site with maximal arterial compression. F. longitudinal
22
IVUS view. MB was identified by IVUS as an echolucent-band “halo” (green arrow
23
heads, D/E). IVUS and OCT showed flow-limiting plaque located 15.4 mm proximal to
24
MB (B/F).
AC C
EP
18
25 26
Figure S (in supplementary materials). Coronary angiogram
27
There was severe stenosis in the proximal LAD segment and arterial compression in the
6
ACCEPTED MANUSCRIPT
1
mid LAD segment.
2
AC C
EP
TE D
M AN U
SC
RI PT
3
7
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT