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. 2017 Mar 6;15(4):136–140. doi: 10.1016/j.jccase.2016.12.006

Role of 99mTc-sestamibi gated SPECT/CT myocardial perfusion imaging in the management of patients with myocardial bridging and its correlation with coronary angiography

Deepa Singh a, Shelvin K Vadi a, Madan Parmar a, Ashwani Sood a,, Saurabh Mehrotra b, Bhagwant R Mittal a
PMCID: PMC6135039  PMID: 30279761

Abstract

Myocardial bridging (MB)—a congenital coronary abnormality in its severe form leads to myocardial edema, fibrosis, and ischemia due to coronary artery compression during systole and early part of the diastole. This study evaluated the hemodynamic significance of MB by detecting severity and extent of perfusion abnormality using 99mTc-sestamibi (MIBI) gated single photon emission computed tomography (SPECT)/CT myocardial perfusion imaging (MPI), its correlation with coronary angiography and role in patient’s management. Five patients with complaints of atypical chest pain, exertional angina, or dyspnea underwent stress/rest 99mTc-MIBI SPECT/CT MPI. The gated stress and rest SPECT/CT images on 17 segment model using quantitative gated-SPECT (QGS) softwarewere analyzed and compared with coronary angiography. Four out of five patients showed reversible perfusion defect in the left anterior descending (LAD) territory segments involved with myocardial bridging (3 patients had already proven MB; while MB was detected in 1 patient after MPI). The fifth patient with MB in the distal LAD revealed normal myocardial perfusion. All the patients were conservatively managed either due to small reversible perfusion defects or normal study except one patient. The gated SPECT/CT MPI of five patients with MB in the present study revealed their perfusion status, information on myocardial wall thickening, contractility, and ejection fraction.

<Learning objective: Myocardial bridging may be one of the underlying causes for angina or sudden death even in absence of cardiovascular risk factors. The proven or clinical suspicious myocardial bridging in patients with typical/atypical chest pain and low probability of atherosclerosis should be evaluated with gated SPECT/CTMPI. It helps in detection of coronary artery disease along with severity and extent of myocardial ischemia for their further management.>

Keywords: Myocardial bridging, Gated SPECT/CT, Tc-99m sestamibi, Myocardial perfusion imaging, Coronary angiography

Introduction

Myocardial bridging (MB) is a congenital variant of coronary artery where part of an epicardial coronary artery traverses intramuscularly within the myocardium. The muscle overlying the intra-myocardial coronary artery is termed as myocardial bridge and artery itself is known as tunneled artery. This tunneled artery can be compressed with each systole by overlying contracting myocardium resulting in characteristic angiographic finding the “milking effect” or “step down-step up” phenomenon. As only 15% of coronary flow occurs during systole and myocardial bridge is a systolic event, its clinical relevance occurs only in exertional conditions such as tachycardia. Tachycardia causes diastole shortening with increased systolic blood flow requirement leading to myocardial edema, fibrosis, and ultimately provokes ischemia. The provocative tests such as exercise or some drugs can enhance sympathetic drive (increased chronotropic and inotropic stimulation) and cause increased systolic/diastolic time ratio at the expense of diastolic flow. This leads to reduced perfusion time in myocardium supplied by tunneled vessel, and thus aggravates ischemia. Although MB is a benign condition and patients remain asymptomatic, studies have demonstrated the rare but dangerous complications such as myocardial ischemia, acute coronary syndromes, or chronic coronary vasospasm [1], [2].

The individuals with MB may have the presentation of angina and/or dyspnea and need thorough evaluation. Although MB is defined by coronary angiography, its functional significance is assessable with MPI (myocardial perfusion imaging). This study was to evaluate the hemodynamic significance of MB by detecting severity and extent of perfusion abnormality using stress/rest 99mTc-MIBI gated single photon emission computed tomography (SPECT)/CT MPI, its correlation with coronary angiography and impact in patients’ management.

Description of cases

We evaluated stress/rest 99mTc-MIBI SPECT/CT MPI images with 17 segment model and quantitative gated-SPECT (QGS) software acquiredunder SPECT/CT dual head gamma camera (Brightview XCT, Philips, Amsterdam, the Netherlands) in five patients with complaints of chest pain found to have MB on coronary angiography. Stress modality during MPI was exercise treadmill test (TMT) with Bruce protocol in 4 patients and pharmacological stress with adenosine in 1 patient (Case 4). All five patients’ detail characteristics, echocardiography, coronary angiography, and myocardial perfusion imaging are mentioned in Table 1 (Fig. 1, Fig. 2). The quantitative gated-SPECT (QGS) data of all the five patients was also evaluated for dyssynchrony and no cardiac dyssynchrony was found in any of our patients.

Table 1.

Patients’ detail characteristics.

Case 1 Case 2 Case 3 Case 4 Case 5
Age (Years)/sex 38/Male 56/Male 64/Male 74/Male 42/Male
Complaints Atypical chest pain Atypical chest pain, exertional dyspnoea Atypical chest pain Exertional angina and dyspnoea Exertional angina and dyspnoea
Cardiac markers Not done CPKMB (high normal), Troponin I- positive Not done Not done Negative
Risk factors Obesity, hyperlipidemia Hypertension, hyperlipidemia Hypertension, diabetic, chronic alcoholic, hyperlipidemia Hypertension, heavy smoker, chronic alcoholism, hyperlipidemia Hypertension, obesity, chronic alcoholism, hyperlipidemia
ECHO Mild hypokinesia in RCA territory RWMA in LAD territory Normal NA Concentric left ventricular hypertrophy
Tc-99m MIBI Gated SPECT/CT MPI Qualitative data Reversible mild to moderate perfusion defects in parts of apical & mid inferior segment of LV myocardium
(∼4–6%)
Reversible mild perfusion defect in part of apical anterior segment of LV myocardium
(<5%)
Partially reversible mild perfusion defect in the parts of apex and apical antero-septum of LV myocardium
(∼4–6%)
Reversible mild perfusion defect in part of apex and apical antero-septum (∼6%); moderate reversible defect in apical & mid inferior and adjacent infero-septal (∼16–18%). Fixed severe perfusion defect in basal inferior and basal infero-septal segments (∼10–12%) of LV myocardium Normal
Quantitative data SSS-1, SRS-0, SDS-1; EDV-53 ml, ESV-9 ml, LVEF >65%; TPFR-180 ms; PFR-3.78 EDV/s SSS-2, SRS-0, SDS-2; EDV-60 ml, ESV-13 ml, LVEF >65%; TPFR-181 ms; PFR-4.07 EDV/s SSS-1, SRS-0, SDS-1; EDV-56 ml, ESV-12 ml, LVEF >65%; TPFR-154 ms; PFR-2.84 EDV/s SSS-12, SRS-9, SDS-3; EDV-63 ml, ESV-36 ml, LVEF ∼43%; TPFR-231 ms; PFR-2.33 EDV/s SSS-0, SRS-0, SDS-0; EDV-76 ml, ESV-14 ml, LVEF >65%; TPFR-220 ms; PFR-5.18 EDV/s
Coronary angiography 60% stenosis in OM1 and MB in mid LAD territory Mid LAD MB MB in LAD territory just after D2 origin LAD type III vessel with proximal plaque & mid MB. RCA proximal cut off followed by retrograde filling 60% plaque in proximal LAD and MB in distal LAD

MPI—myocardial perfusion imaging; MB—myocardial bridge; LAD—left anterior descending artery; LV—left ventricle; OM—obtuse marginal artery; SSS—summed stress score; SRS—summed rest score; SDS—summed difference score; EDV—end diastolic volume; ESV—end systolic volume; LVEF—left ventricular ejection fraction; TPFR—time to peak filling rate; PFR—peak filling rate; NA—not available.

Fig. 1.

Fig. 1

(Case 2) Coronary angiography showing large area of myocardial bridging in the mid-left anterior descending artery with near complete lumen obliteration during systole (arrow) (a), resolved during diastole (arrow) (b). Stress/rest 99mTc-sestamibi gated single photon emission computed tomography (SPECT)/CT: short axis (first four rows), vertical long axis (middle four rows), horizontal long axis (lower four rows). Non-attenuated corrected stress and rest images followed by attenuated corrected stress and rest images showing reversible mild perfusion defect in the part of apical anterior segment (arrow) involving <5% of left ventricular myocardium (c). Stress and rest polar map images showing the perfusion defect as mentioned above (d & e).

Fig. 2.

Fig. 2

(Case 4) Coronary angiography demonstrating left anterior descending artery type III vessel with proximal plaque and mid myocardial bridge and right coronary artery with proximal cut-off followed by retrograde filling (arrow) (a), which resolved during diastole (arrow) (b). Stress/rest 99mTc-sestamibi gated single photon emission computed tomography (SPECT)/CT images as described in Fig. 1, showing reversible perfusion defect of mild intensity in the part of apex and apical antero-septum involving ∼6% of left ventricular (LV) myocardium (arrow), reversible perfusion defect of moderate intensity in the apical and mid inferior and adjacent infero-septal segments involving ∼16–18% of LV myocardium. Scan also showing fixed perfusion defect of severe intensity in the basal inferior and basal infero-septal segments involving 10–12% of LV myocardium (c). Stress and rest polar map images showing the perfusion defects as mentioned above (d & e).

Discussion

Reyman was the first to describe MB on autopsy finding in 1737 [3]. The overall prevalence of MB was found to be 5–86% (mean of 25%) in autopsy series and 0.5–12% in coronary angiography findings. The variation in prevalence may be due to presence of superficial intramuscular segments not getting compressed during systole. However, detection of MB can increase up to 40% with provocative tests using exercise or pharmacological agents. MB is most frequently localized to mid left anterior descending (LAD) artery. However, some of the autopsy series have also shown involvement of right coronary artery (RCA), left circumflex artery, diagonal and marginal branches.The usual depth of myocardial bridge is 1­10 mm and length of tunneled artery is 10­30 mm [4]. Ferreira et al. characterized pathological bridges in LAD artery as “superficial” (approximately 75% cases) or “deep” variant [1].

In the present study, the first four patients with atypical chest pain had reversible perfusion defects in the myocardial segments of LAD involved with myocardial bridge. However, the patient (case 5) with distal LAD MB had normal perfusion study. The reason for this discrepancy might be due to difference in extent of systolic narrowing of coronary artery, as systolic narrowing of more than 80% showed higher perfusion abnormality compared to 50–70% [5].

The presence of MB is revealed by anatomical imaging modalities, however its functional significance in the form of perfusion defects is feasible with stress MPI. The majority of the patients with MB had undergone thallium-201 (Tl-201) MPI, however few studies have been done either with 99mTc-MIBIor 99mTc-tetrofosmin. Stress/rest 99mTc-MIBI was used in the present study. Huang et al. in their retrospective study recruited 17 patients with mid LAD MB and positive TMT for stress (physical or pharmacological) Tl-201 MPI. A total 16 out of 17 patients showed partial reversible perfusion defects or significant reverse redistribution in anterior or inferior walls of left ventricle and 8 of them had additional reversible perfusion defects. They concluded that patients with MB having abnormal stress electrocardiograms should be evaluated with Tl-201 SPECT study [6].

Lee et al. in their study evaluated 12 MB patients and controls of 118 patients with fixed LAD disease using dipyridamole stress Tl-201 MPI. The study showed that patients with MB having 50–70% systolic narrowing showed reversible perfusion defects in 3/6 sites versus 7/8 sites in patients with more than 80% systolic narrowing. Five patients with septal branch bridging revealed isolated perfusion defects in mid antero-septal with no apical defect, however none of the patients in the control group had any defect in those areas (5/12 in MB group vs 0/118 of control group; p < 0.001). The septal branch bridging rather than fixed coronary artery disease may be the underlying pathology leading to isolated perfusion defect [5].

In a case report by Vijayvergiya and Mittal [7], a 32 ­year male with exertional angina having both positive exercise TMT and stress TI­201 MPI revealed MB in distal LAD artery on angiography. He had been managed on beta-blockers with continuous favorable outcome for 9 years of follow-up [7].

The treatment options for MB in symptomatic patients are beta-blockers, calcium channel blockers, surgical interventions such as myotomy, minimally invasive coronary artery bypass grafting, or stent placement in tunneled segments. The preferred treatment modality is beta-blockers as they decrease frequency of systolic narrowing and increase diastolic time along with decrease in cardiac contractility and compression of tunneled artery [8]. The normal cut-off quantitative values taken in our study were based on the study by Matsuo et al. [9]. In the present study, all the patients were followed with modified medical management due to presence of small sized perfusion defect and adequately contracted myocardium supplied by tunneled artery with good left ventricular ejection fraction. Although, the patient (case 4) was planned for intervention for the medium-large size moderate reversible defect in the RCA territory, but MB in LAD artery was managed conservatively.

The stress gated SPECT images were also evaluated for myocardial thickening, contractility, and left ventricular ejection fraction estimation in the present study. The gated SPECT MPI helps in guiding the treatment plan and response evaluation of therapy during follow up. Gawor et al. in a retrospective analysis of 42 patients with MB, using exercise gated SPECT 99mTc-MIBI MPI showed mild reversible perfusion abnormalities in 40% of patients with critical (≥50%) narrowing of artery affected by bridging. The CT for attenuation correction was not employed with SPECT in their study [10]. Whereas gated 99mTc-MIBI SPECT/CT study was undertaken with CT for attenuation correction in patients with MB in the present study. Attenuation correction reduces the artifacts caused by surrounding structures (diaphragmatic and breast attenuation) in myocardial perfusion images and helps in reducing the false positive perfusion defects.

MB can be the cause of angina or sudden death even in the absence of cardiovascular risk factors. MB should be considered as underlying etiology in the symptomatic patients even with low probability of atherosclerosis. 99mTc-MIBI gated SPECT/CT MPI has shown its utility in detection of CAD along with severity and extent of myocardial ischemia in patients with MB and in their management.

Conflict of interest disclosure

All the authors declare that they have no financial interest and there is no conflict of interest.

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