Heart Views

: 2023  |  Volume : 24  |  Issue : 1  |  Page : 6--10

Myocardial bridging in cases of sudden death and its association with clinicopathologic characteristics

Mary Theresa Sylvia, R Soundharia, Ramachandra V Bhat, Fremingston Marak 
 Department of Pathology, Indira Gandhi Medical College and Research Institute, Puducherry, India

Correspondence Address:
Dr. Fremingston Marak
Department of Pathology, Indira Gandhi Medical College and Research Institute, Kadirkammam, Puducherry - 605 009


Background: Myocardial bridging (MB) is the course of the epicardial segment of a coronary artery within the myocardium. The systolic compression of this segment called the tunneled segment may lead to alterations in blood flow to the heart. We have studied the gross and microscopic features of MB in cases of sudden cardiac death and analyzed its characteristics and whether there is any association with other clinicopathological characteristics which may help us to understand the pathogenesis and risk stratification. Materials and Methods: This is a retrospective descriptive study of 132 postmortem heart specimens of sudden cardiac death. The coronary arteries were dissected, and MB and its characteristics were studied. Statistical analysis was performed using the Chi-square and Fisher's exact tests (P < 0.05 significant). Results: MB was present in 28 cases (21.2%), with a mean age of 49.5 years and male:female ratio of 27:1. MB was seen in the left anterior descending artery in 86.2% of cases, the right coronary artery in 10%, and left circumflex artery in 3.5% of cases. Atherosclerosis was seen in the segment proximal to the tunneling in 89.2% of cases leading to infarction in four cases. Left ventricular hypertrophy (LVH) was significantly associated with MB cases (19/68%) (P < 0.05). Conclusion: MB causes turbulence of blood in the proximal segment leading to coronary atherosclerosis, thereby predisposing the heart to ischemic changes and LVH and may lead to infarction in a few cases.

How to cite this article:
Sylvia MT, Soundharia R, Bhat RV, Marak F. Myocardial bridging in cases of sudden death and its association with clinicopathologic characteristics.Heart Views 2023;24:6-10

How to cite this URL:
Sylvia MT, Soundharia R, Bhat RV, Marak F. Myocardial bridging in cases of sudden death and its association with clinicopathologic characteristics. Heart Views [serial online] 2023 [cited 2023 Apr 1 ];24:6-10
Available from: https://www.heartviews.org/text.asp?2023/24/1/6/370264

Full Text


Sudden unexpected death is defined as death that occurs within an hour of manifestations of symptoms or 1 day without being monitored.[1] Myocardial bridging (MB) is the presence of a normal epicardial segment of a coronary artery within the myocardium.[2],[3] The left anterior descending (LAD) artery is most commonly documented to be tunneled.

Literature and case studies state that systolic compression of the tunneled segment causes alterations in blood flow which may lead to angina, myocardial ischemia, acute coronary syndrome, left ventricular dysfunction, arrhythmias, and sudden cardiac death.[2],[3] We have conducted this study to find the presence of MB; its gross, and microscopic features, and whether there is any association with other clinicopathological characteristics.

 Materials and Methods

This retrospective descriptive study was conducted in the department of pathology of our institute after getting approval from the Institute Research and Ethics Committees. The postmortem specimens of hearts of sudden death cases received for the histopathological analysis were included in the study. The sample size was calculated to be 132 using a simple random sampling method. Autolyzed specimens and cases with other direct causes of death involving other organs were excluded from the study. The clinicopathological characteristics were retrieved from the archives. Grossing of the heart was done using the inflow-outflow method, and the standard protocol was followed.

The coronary arteries were dissected throughout their course to identify MB. The segment and the branch involved the length of the tunneled segment and the presence of atherosclerosis in and around the tunneled segment were observed. Representative sections were taken from the tunneled segment, pre-and post-tunneling, and other routine sections from the ventricles and aorta. The microscopic sections were evaluated for the type of tunneling: (1) The tunneled segment with muscle roof and (2) Tunneled segment with a fibrous roof. The histopathological changes in the pre − post and tunneled segments were studied. Statistical Analysis: Data collected were analyzed using the professional Statistics Package SPSS Version 21. (International Business Machines corporation, Chicago Delaware, US). Student version. Descriptive data were represented as mean for the numerical variables, percentages, and proportions for the categorical variables. The Chi-square test and Fisher's exact test were used to find the association between the variables. P <0.05 was considered statistically significant.


MB was present in 28 (21.2%) of the 132 cases studied. The clinicopathological features of cases with and without MB are summarized in [Table 1].{Table 1}

Pathological findings in hearts of cases without myocardial bridging

Of the 132 cases of sudden death, 104 cases did not have MB. The weight of the heart specimens ranged from 146 to 613 g. The autopsy specimens of the heart showed coronary atherosclerosis in 68 cases (65%), left ventricular hypertrophy (LVH) in two cases, myocardial infarction in two cases, myocarditis in three cases (2.8%), old infarct in twelve cases (9.1%), and calcified valves in two cases (1.5%). Gross and microscopic features were completely normal in 13 hearts (10%).

Pathological findings in hearts of cases with myocardial bridging

MB was seen in 28 cases. The weight of the heart in this group varied from 220 to 462 g. Histopathological features of the heart showed myocardial infarction in four cases (14%), LVH in 19 (68%) [[Table 2] shows the grading of LVH], coronary atherosclerosis in 11 (39%), old myocardial infarction in one (3.5%) myocarditis in one case (3.5%), and normal in eight cases (28%). [Table 3] shows the pathological findings in the heart.{Table 2}{Table 3}

Tunneling was seen in the LAD coronary artery in 86.2% of cases (25/28) [Figure 1]; right coronary in three cases (10%) and left circumflex artery in one case (3.5%). A single coronary artery showed tunneling in 27 hearts (96.4%) and one heart showed tunneling in two coronary arteries (3.5%) – one in the LAD artery and the other in the right coronary artery. The length of the tunneled segment varied from 0.2 to 4 cm (average length 2.03 cm). Histopathological sections of the tunneled segment showed a coronary artery surrounded by muscle bundles in 20 cases [Figure 2] and a connective tissue bed with adipose tissue in eight cases [Figure 3]. Atherosclerosis was seen proximal to the tunneled segment in 89.2% (25/28 cases), in the tunneled segment in 3 (10%), and in one case (3.5%) in the distal segment [Figure 4] and [Figure 5]. One case showed atherosclerosis proximal and distal to the tunneling. All four cases of myocardial infarction in this group showed tunneling of the LAD with atherosclerotic thrombus in the pretunneled segment.{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}

Statistical analysis

The clinicopathological factors did not show a statistically significant association with MB cases. The presence of LVH had a significant association with MB cases (P < 0.05).


The percentage of cases with MB in our study was 21.21% (28/132). The incidence of MB varies in the literature based on the mode of evaluation either angiography or autopsy studies. The incidence varies from 1.5% to 16% in angiographic studies and as high as 80% in autopsy series.[4],[5] Indian studies have reported an incidence of 1.23% to 4.22 % based on angiography.[6],[7]

Our incidence is similar to the study results conducted by Sujatha et al.,[6] Monika et al.,[8] Saidi et al.,[9] in which the prevalence rates were 36.7%, 29%, and 20.6%, respectively. Bandyopadhyay et al. found 90.4% of cadaveric specimens to have MB.[10] Cessy Job et al.,[11] reported an incidence of 56.7% of cadaveric specimens having MB. The variation in the prevalence may be due to regional variation, sampling method, or interobserver variation. Bridges with only fibrous roofs may also be easily damaged during dissection.

The tunneling was predominantly seen in the LAD artery (86.2%) in our study which is similar to the previous studies.[6],[8],[10],[11],[12],[13] The middle segment of the LAD artery was predominantly involved in our study (76%) which is higher compared to previous reports by Bandyopadhyay et al.[10] (45%) and Monika et al.[8] (33.3%). We did not find any double MB in a single artery as reported by Sujatha et al.[6] and Saidi et al.[13] The average length of the tunneled segment was 2.03 cm in our study and the range varied from 0.2 to 4 cm. The study conducted by Torii et al. showed similar results of length 1.99 cm ± 1.08 cm.[14]

Histopathology showed direct apposition of muscle bundles on the coronary artery in 20 of the cases. A layer of connective tissue was seen in eight cases. Previous studies have not mentioned this layer. Even though there was a cushion layer of adipose tissue in these eight cases, they also had atherosclerosis in the proximal segment. Hence, the presence of a connective tissue cushion did not prevent its compression.

Atherosclerosis was present predominantly proximal to the tunneled segment (89.2%) in our study which is similar to the findings by Yamada et al.[15] The four cases with myocardial infarction involved a stenotic atherosclerotic lesion in the proximal segment of the tunneled artery. This observation is similar to the findings of Yukio et al. who also found a longer segment of tunneling in cases of MB with infarction.[16] This shows that the turbulence created due to the compression of the tunneled segment predisposes the proximal segment to atherosclerosis and secondary thrombosis. However, the findings were not statistically significant due to the less number of cases. LVH was significantly associated with MB cases in our study. Analyzing and following up on normal general population angiographic results would help to clarify the etiological role of MB in the development of LVH. MB has been studied in literature as a frequent component in cases of hypertrophic cardiomyopathy,[17] but we could not find any literature on the etiological role of LVH.


MB was seen in 21% of autopsy cases of sudden death. The LAD coronary artery was involved predominantly with tunneled segments varying from 0.2 to 4 cm. The presence of a connective tissue interface did not prevent compression of the MB segment. The proximal segment of the tunneled artery showed the presence of atherosclerosis with infarction in a few cases. LVH was significantly associated with MB cases.


MB causes turbulence of blood in the proximal segment leading to coronary atherosclerosis, predisposing the heart to ischemic changes, LVH, and infarction. Hence, monitoring patients with additional risk factors for the proximal segment of the tunneled artery may help to prevent ischemic changes in the heart.


A pilot project of this study was done as a part of the short-term student project under the Indian Council of Medical Research and was selected and approved.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Chaturvedi M, Satoskar M, Khare MS, Kalgutkar AD. Sudden, unexpected and natural death in young adults of age between 18 and 35 years: A clinicopathological study. Indian J Pathol Microbiol 2011;54:47-50.
2Gow RM. Myocardial bridging: Does it cause sudden death? Card Electrophysiol Rev 2002;6:112-4.
3Lee MS, Chen CH. Myocardial bridging: An up-to-date review. J Invasive Cardiol 2015;27:521-8.
4Möhlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation 2002;106:2616-22.
5Alegria JR, Herrmann J, Holmes DR Jr., Lerman A, Rihal CS. Myocardial bridging. Eur Heart J 2005;26:1159-68.
6Sujatha M, Subhadra Devi V, Raju CS, Yugandhar B, Nagaraju. Angiographic aspects of myocardial bridges. Int J Anat Res 2015;3:1689-96.
7Karna SK, Chourasiya M, Parikh RP, Chaudhari T, Patel U. Prevalence of myocardial bridge in angiographic population—A study from rural part of western India. J Family Med Prim Care 2020;9:1963-6.
8Monika S, Asha D, Vandana S, Abijeet Y, Kumar SD. A study to find out the incidence of myocardial bridges in formalin-fixed hearts and its correlates. IOSR J Dent Med Sci 2014;13:66-9.
9Saidi HS, Olumbe AO, Kalebi A. Anatomy and pathology of coronary artery in adult black Kenyans. East Afr Med J 2002;79:323-7.
10Bandyopadhyay, M., Das, P., Baral, K. Chakraborthy P.. Morphological study of myocardial bridge on the coronary arteries. Indian J Thorac Cardiovasc Surg 2010;26:193-197. https://doi.org/10.1007/s12055-010-0044-6.
11Job C, Prasanna MB, Nandagopalan PA. A study of myocardial bridges on the coronary arteries. International Journal of Contemporary Medical Research 2016;3:1782-3.
12Polacek P, Kralove H. Relation of myocardial bridges and loops on the coronary arteries to coronary occulsions. Am Heart J 1961;61:44-52.
13Saidi H, Ongeti WK, Ogeng'o J. Morphology of human myocardial bridges and association with coronary artery disease. Afr Health Sci 2010;10:242-7.
14Torii S, Virmani R, Finn A. Myocardial bridge and the progression of atherosclerotic plaque in the proximal segment. Arterioscler Thromb Vasc Biol 2018;38:1250-1.
15Yamada R, Tremmel JA, Tanaka S, Lin S, Kobayashi Y, Hollak MB, et al. Functional versus anatomic assessment of myocardial bridging by intravascular ultrasound: Impact of arterial compression on proximal atherosclerotic plaque. J Am Heart Assoc 2016;5:e001735.
16Yukio I, Yoko K, Ehiichi K, Toshiharu I. (1) coronary events caused by myocardial bridge. Ann Vasc Dis 2009;2:79-94.
17Basso C, Thiene G, Mackey-Bojack S, Frigo AC, Corrado D, Maron BJ. Myocardial bridging, a frequent component of the hypertrophic cardiomyopathy phenotype, lacks systematic association with sudden cardiac death. Eur Heart J 2009;30:1627-34.