Amano Y, Suzuki Y, Iso K, Ando C, Amano M. Diagnostic usefulness and limitation of cardiac magnetic resonance for identifying myocardial damage in survivors of cardiac arrest in midtown. World J Radiol 2025; 17(6): 104473 [DOI: 10.4329/wjr.v17.i6.104473]
Corresponding Author of This Article
Yasuo Amano, MD, Department of Radiology, Nihon University Hospital, 1-6 Kanda-Surugadai, Chiyoda-ku, Tokyo 1018309, Japan. yas-amano@nifty.com
Research Domain of This Article
Radiology, Nuclear Medicine & Medical Imaging
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Author contributions: Amano Y conceived and designed the study; Amano Y, Suzuki Y, Iso K, Ando C collected and assembled the data; Amano Y, Suzuki Y and Amano M analyzed and interpreted the data. All authors have read and approved the final manuscript.
Institutional review board statement: The study was reviewed and approved by Nihon University Hospital (approval No. 20241101).
Informed consent statement: Patients gave informed consent before cardiac magnetic resonance and no additional consent was needed for this retrospective analysis.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Data sharing statement: Patients gave informed consent before cardiac magnetic resonance and no additional consent was needed for this retrospective analysis.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yasuo Amano, MD, Department of Radiology, Nihon University Hospital, 1-6 Kanda-Surugadai, Chiyoda-ku, Tokyo 1018309, Japan. yas-amano@nifty.com
Received: December 23, 2024 Revised: March 24, 2025 Accepted: May 28, 2025 Published online: June 28, 2025 Processing time: 187 Days and 4.9 Hours
Abstract
BACKGROUND
Cardiac magnetic resonance (CMR) has been reported to identify myocardial damage inducing out-of-hospital cardiac arrest (OHCA). However, the usefulness of CMR may be affected by the medical institutions, patients’ ages, and myocardial diseases.
AIM
To clarify the clinical usefulness and limitation of CMR for identifying myocardial damage in the survivors of OHCA in midtown.
METHODS
Nineteen patients underwent CMR to detect myocardial damage related to OHCA in the midtown of a capital city. Cine, T1 and T2 mapping, T2-weighted, and late gadolinium enhancement (LGE) imaging were acquired using a 1.5 T scanner. We described the clinical characteristics of the survivors of OHCA and evaluated usefulness of CMR for identifying myocardial damage related to OHCA.
RESULTS
Among 19 patients experiencing OHCA, 7 experienced it in trains or on railway platforms, 4 while practicing sports, and 4 during their daily work. Ten of the 19 survivors were diagnosed with coronary vasospasm (CVS), in whom CMR failed to depict its characteristic findings. CMR was useful for identifying myocardial damage associated with hypertrophic cardiomyopathy (HCM) or myocardial infarction (MI). LGE was related to serious ventricular arrhythmias after implantable cardioverter defibrillator (ICD) installation in 3 patients (CVS, 2; HCM, 1).
CONCLUSION
CMR is useful for identifying myocardial damage of HCM or MI inducing OHCA and predicting ventricular arrhythmias after ICD implantation but has limited capability for detecting myocardial damage of CVS.
Core Tip: Cardiac magnetic resonance (CMR) may be useful for identifying the myocardial damage associated with hypertrophic cardiomyopathy or myocardial infarction and predicting ventricular arrhythmias after installation of implantable cardioverter defibrillator in the survivors of out-of-hospital cardiac arrest, whereas CMR has limited capability for detecting any findings characteristic of coronary vasospasm.
Citation: Amano Y, Suzuki Y, Iso K, Ando C, Amano M. Diagnostic usefulness and limitation of cardiac magnetic resonance for identifying myocardial damage in survivors of cardiac arrest in midtown. World J Radiol 2025; 17(6): 104473
Cardiac magnetic resonance (CMR) is the best imaging tool to measure cardiac function and visualize myocardial damage including myocardial fibrosis, and edema[1-3]. In particular, late gadolinium enhancement (LGE) CMR visualizes myocardial scar significantly related to the prognosis of various myocardial diseases[3-6]. Therefore, CMR is expected to identify myocardial damage inducing cardiac arrest or serious ventricular arrhythmias and contribute to the prevention of sudden cardiac death by device implantation[4-9]. When estimating the risk of cardiac arrest, CMR allows for the identification of the myocardial damage to provide incremental value over using left ventricular ejection fraction (LVEF) < 35% in isolation[8,10].
Nevertheless, the usefulness of CMR for identifying myocardial damage inducing out-of-hospital cardiac arrest (OHCA) is varied in the previous reports[7,11-13]. This may be attributed to the possibility that the usefulness of CMR is affected by the medical institutions, patients’ ages, and myocardial diseases. For example, in institutions specialized in hypertrophic cardiomyopathy (HCM), cardiac arrest or serious ventricular arrhythmia associated with HCM may be experienced much more frequently[5,14,15]. The territorial hospitals may receive cases of cardiac arrest with various clinical backgrounds and the bystanders who perform cardiopulmonary resuscitation on railway platforms of large cities may modify the OHCA patients’ prognosis[16-19]. Therefore, the purposes of this study were to evaluate the clinical usefulness and diagnostic limitation of CMR for identifying myocardial damage in the survivors of OHCA in the midtown of a capital city of more than 14 million people.
MATERIALS AND METHODS
Patients
The institutional review board approved this single-center retrospective observational study. Patients gave informed consent for CMR examinations, and the consent was waived for this retrospective analysis. Six hundred thirty-six CMR studies were performed from April 2016 to March 2024 in our institution, located in the midtown of the capital city of more than 14 million people. Among them, 20 patients underwent CMR to determine myocardial damage leading to OHCA.
CMR protocol
All CMR examinations were conducted using a 1.5 T imager (Ingenia Achieva, Philips Healthcare, Best, The Netherlands). The interval between the onset of OHCA and CMR examinations was 5-23 days (mean, 12.3 days). Cine steady-state free precession (SSFP) imaging was performed in the long- and short-axes 2-chamber and 4-chamber views. The typical imaging parameters of cine imaging were as follows: Repetition time (TR), 3.2 ms; echo time (TE), 1.6 ms; flip angle, 60°; in-plane resolution, 1.82 × 1.94 mm2; and slice thickness, 8 mm. Short-axis T1 mapping was acquired by a 5 s (3 s) 3 s modified Look-Locker inversion recovery (IR). This sequence used a single-shot balanced SSFP readout with an inversion time (TI) of 159.5 ms after the first inversion IR pulse; the 5-s data acquisition was done. Thereafter, a 3-s interval was set, and the 3-s data acquisition was done following a TI of 350.0 ms after the second IR pulse. The imaging parameters of single-shot balanced SSFP were: TR, 2.8 ms; TE, 1.3 ms; flip angle, 35°; in-plane resolution, 2.00 × 1.97 mm2; and slice thickness, 10 mm. Short-axis T2 mapping was acquired by multi-echo gradient- and spin-echo imaging with the typical parameters as follows: TR, RR; effective TE, 7.7-69.2 ms with 9 echos and an echo-planar imaging factor of 5; flip angle, 90°; in-plane resolution, 1.97 × 2.07 mm2; and slice thickness, 10 mm. T2-weighted short inversion time inversion recovery (STIR) was performed in the short-axis view with the typical parameters as follows: TR, 2 cardiac cycles; effective TE, 80 ms; flip angle 90°, TI, 165 ms; in-plane resolution, 1.45 × 2.32 mm2, and slice thickness, 10 mm. LGE was performed in the identical imaging planes to those of cine imaging. The imaging parameters of LGE were as follows: TR, 6.1 ms; effective TE, 3 ms; flip angle 25°, in-plane resolution, 1.59 × 1.96 mm2; and slice thickness, 10 mm. In the LGE imaging, TI nulling the normal myocardium was determined using Look-Locker IR imaging. Cine, T2-weighted STIR, and LGE imaging covered the entire left ventricle, while T1 and T2 mapping were done at the midventricular level[20]. Breath-holding, electrocardiogram (ECG) gating, and parallel imaging techniques (i.e., sensitivity encoding) were used for all sequences. Black-blood IR technique was used to suppress the blood signals within the cardiac chambers in T2 mapping and T2-weighted STIR. Chemical-shift fat-suppression was used in T2 mapping, and phase-sensitive IR was used in LGE.
Image analysis
LVEF, left ventricular myocardial mass (LVM), and end-diastolic left ventricular volume (LVEDV) were measured by a cardiologist with 25 years’ experience in cardiac imaging. The LVM index, LVEDV index (LVMi and LVEDVi, respectively), and LVM/LVEDV were calculated. Radiological technologists measured myocardial T1 and T2 values at the mid-septum under the supervision of the cardiologist and radiologist[20]. A radiologist with 27 years’ experience in CMR assessed high intensity on T2-weighted STIR (i.e., T2-high) and myocardial LGE visually, and the presence of LGE was confirmed using the 5 SD method[21].
First, we described the clinical characteristics, treatments, and outcomes of the OHCA survivors. Second, we assessed the myocardial damage, including elevated T1 or T2 values of the myocardium, T2-high, and LGE, by comparing clinical characteristics, invasive coronary angiography (CAG), and patients’ outcomes. The locations and patterns of LGE were defined according to the left ventricular segmentation recommended by the American Heart Association (AHA) and intramural pattern (ischemic or non-ischemic LGE)[3,22,23]. Third, the interval between OHCA and CMR examinations were compared in coronary vasospasm (CVS) patients between with and without the myocardial damage using Wilcoxon signed-ranked test. A P < 0.05 indicated a statistical significance. Fourth, LVEF and the other functional parameters acquired by cine imaging were assessed in each myocardial disease. The continuous data were expressed as mean ± SD, while the counting data were expressed as cases or percentages.
RESULTS
Participants and their clinical characteristics
Because of the low image quality of T2-weighted STIR and LGE, an 80-year-old male patient was excluded from further analysis. Therefore, 19 survivors of OHCA were analyzed. The mean age of the group was 54.5 years and males were prevalent (n = 17, 89.5%). All patients presented with ventricular fibrillation (VF) on an automated external defibrillator (AED) or ECG immediately after the onset. Their clinical diagnoses were CVS in 10 patients (52.6%), HCM in 2, idiopathic VF in 2, and Brugada syndrome, long QT syndrome, acute myocardial infarction (MI), chronic MI, and multi-vessel coronary artery disease in each of the other patient. Among the 10 patients with CVS, the right coronary artery (RCA) showed vasospasm in 5 patients, the left anterior descending artery (LAD) in 4, and the left main trunk in 1 by the CAG under acetylcholine provocation or during cannulation. The left circumferential artery (LCX) was involved in the patient with acute MI, while the RCA was stenosed in the patient with chronic MI. Among 19 patients, 7 (36.7%) experienced cardiac arrest in trains or on railway platforms, 4 (21.1%) while practicing sports including 3 during running, and 4 (21.1%) during their daily work. The other 4 presented with cardiac arrest in a bathtub, a toilet, and a hotel room, and when smoking. Nine of the 19 patients (47.4%) had obesity, which was defined as a body mass index (BMI) ≥ 25 kg/m2, 5 (26.3%) had hypertension, 2 had hyperlipidemia, and 2 had diabetes mellitus. Except for one patient with HCM, none had a family history possibly related to cardiac arrest.
Implantable cardioverter defibrillator (ICD) was installed in 15 of the 19 patients (78.9%). Two patients, the one with CVS of LAD and the other with chronic MI, underwent both ICD and percutaneous coronary intervention (PCI). One patient with CVS of RCA and another with long QT syndrome received medication for heart failure. The patient with acute MI received PCI alone, while the patient with multi-vessel coronary artery disease underwent coronary artery bypass graft.
Sixteen of the 19 survivors (84.2%) were followed up after OHCA in our institution. The mean follow-up was 4 years and 4 months ± 2 years and 6 months (range, 9 months to 7 years and 10 months). Ten of the 16 patients (62.5%) did well, while 2 showed neurological impairment, 2 experienced non-sustained ventricular tachycardia (NSVT), 1 experienced VF, and 1 died. NSVT occurred 9 times from 2 years and 8 months to 4 years and 3 months after ICD implantation in the CVS patient. One HCM patient experienced NSVT and syncope simultaneously 9 months after ICD installation. Another patient with CVS experienced VF 8 months after the ICD implantation and ICD discharged appropriately. The patient with long QT syndrome, who had experienced cardiac arrest in the bathtub and received medication for heart failure, died in the bathtub 1 year and 1 month after the first OHCA. Three patients with neurological impairment had been diagnosed with CVS, 2 of whom were followed up in our hospital and the other in another institution. Table 1 described the complications of OHCA.
Table 1 The complications of out-of-hospital cardiac arrest.
Thirteen of the 19 patients underwent T1 and T2 mapping, whereas the remaining 6 did not in the early phase of this study. Site-specific upper reference limits of the mid-septal myocardium were determined based on the 20 volunteers’ study: 1111.0 ms for T1 and 52.0 ms for T2. Two patients with CVS showed elevated T1, while each with CVS, HCM, and Burugada syndrome showed elevated T2. The one patient with CVS involving RCA had both elevated T1 and T2 values at the mid-septal region (Figure 1A). Three of the 19 patients showed T2-high. Each of them had CVS, HCM, and acute MI. In the patients with CVS and acute MI, the T2-high locations were consistent with the distributions of the involved coronary arteries. The HCM patient with T2-high presented with extensive LGE. Myocardial LGE was identified in 6 of the 19 patients (31.6%). There were 2 CVS patients who showed LGE. Of note, one patient with CVS involving the RCA showed non-ischemic LGE in the basal septum (Figure 1B), while the other with CVS of LAD showed ischemic LGE in the basal lateral myocardium, indicating chronic MI of the LCX territory; these 2 patients with CVS presented with ventricular tachyarrhythmias after ICD implantation. The 3 CVS patients associated with neurological impairment did not exhibit any myocardial damage except decreased LVEF of 33.3% and 41.5% (Figure 2). Both patients with HCM showed LGE: The one with a suspicious family history of HCM, obesity, and T2-high had extensive non-ischemic LGE (i.e., 5 AHA segments), while the other showed focal non-ischemic LGE. The latter experienced an NSVT and associated syncope after ICD implantation (Figure 3A). The distributions of LGE were consistent with those of involved coronary arteries in the patients with acute or chronic MI. The patient with acute MI of the LCX territory also presented with ischemic LGE of the RCA territory, which was considered chronic MI because T2-high was not associated (Table 1).
Figure 1 A 59-year-old man experiencing cardiac arrest during running is diagnosed with coronary vasospasm.
A: T1 mapping shows an elevated T1 value of 1127 ms at the midventricular septum; B: Non-ischemic late gadolinium enhancement is observed at the basal septum (arrows). This patient has experienced non-sustained ventricular tachycardia 9 times after the installation of an implantable cardioverter defibrillator.
Figure 2 A 50-year-old man experiencing cardiac arrest during daily work is diagnosed with coronary vasospasm.
His body mass index is 33.3 kg/m2. A: Late gadolinium enhancement is not found in this patient; B and C: Cine images at end-diastolic and end-systolic phases are shown, and the left ventricular ejection fraction is decreased to 33.3%. The out-of-hospital cardiac arrest is associated with neurological impairment in this patient.
Figure 3 An 80-year-old man experiencing cardiac arrest at the railway station is diagnosed with hypertrophic cardiomyopathy.
A: Focal, non-ischemic late gadolinium enhancement is observed at the mid-inferior segment (arrow); B: Asymmetrical septal hypertrophy and hypertrophied papillary muscle are shown. This patient has experienced non-sustained ventricular tachycardia and associated syncope 9 months after the installation of an implantable cardioverter defibrillator.
Four of the 10 patients with CVS exhibited myocardial damage on CMR, whereas the remaining 6 did not. The interval between the onset of OHCA and CMR examinations did not differ in CVS patients between with (14.5 ± 7.0 days) and without myocardial damage (13.3 ± 5.2) (P = 0.77).
Eight of the 19 survivors of OHCA (42.1%) presented with LVEF < 50%, and 3 showed LVEF < 35.0%: 2 were patients with CVS (Figure 2B and C) and the other with acute MI. Compared to the mean + SD of cine functional parameters, HCM showed higher LVM, LVMi, and LVM/LVEDV (Figure 3B). The LVEDV and LVEDVi were increased in the patient with chronic MI.
DISCUSSION
Cardiac arrest and consequent sudden cardiac death affect 0.05%-0.09% of the general population and account for 15%-20% of all death[16,19]. The main etiology of cardiac arrest is coronary artery diseases[13,16,19]. CAG should be performed immediately after suspecting or diagnosing acute coronary syndrome (ACS). After that, CMR can be recommended to make an accurate diagnosis of myocardial diseases leading to cardiac arrest[8,13,24]. This study described clinical usefulness of CMR for diagnosing HCM and MI in the survivors of OHCA in the midtown of a large capital city and for identifying the myocardial damage related to ventricular arrhythmias that occurred after ICD installation. However, CMR had diagnostic limitations for detecting myocardial damage associated with CVS.
As reported previously, the survivors of OHCA in the midtown of our capital city were male predominant, and more than half of them experienced the cardiac arrest in trains, on a railway platforms, while practicing sports, or during daily work[7,11,16,25,26]. Their mean age of 54.5 years and early bystanders’ intervention, such as the use of AED, may have saved their lives[6,17]. Although the etiologies of OHCA have varied, the mean ages of our patients were similar to those of the previous reports[8,26]. Obesity was often observed in our study population. Kim et al[25] have reported an indirect association between cardiac arrest and obesity. One patient with HCM and OHCA had a family history of HCM and extensive LGE as well as obesity of BMI > 30.0 kg/m2. In HCM, however, obesity is reported to increase the likelihood of atrial fibrillation but not ventricular arrhythmias[27].
While our institution located in midtown received the survivors of OHCA with various myocardial diseases, more than half were diagnosed with CVS. This might contribute to the patients’ ages and limited capability of CMR for identifying myocardial damage related to OHCA[18,28]. We did not identify any CMR findings characteristic of CVS and channelopathy, including Brugada syndrome and long QT syndrome. Nevertheless, Tateishi et al[29] have suggested that CMR is useful for differentiating CVS from cardiac sarcoidosis and myocarditis that can exhibit vasospasm induced by intracoronary acetylcholine administration.
T2-weighted STIR and LGE were useful for identifying myocardial damage related to OHCA in several patients. T2-high may reflect myocardial edema that is probably transient arrhythmogenic substrate[7], whereas LGE has been established as a myocardial scar related to sudden cardiac death[5,6,8,9,24]. In our study, the 3 patients with LGE of 1 or 2 AHA segments experienced ventricular arrhythmias after ICD implantation. Neither HCM with extensive LGE nor MI was associated with the arrhythmias after ICD installation, while extensive or inhomogeneous LGE is reported to be the risk factors for serious ventricular arrhythmias[5,9,14,15,21,26,30]. We did not determine any reasons for this discrepancy. Our study indicated the relation of the absence of LGE to no arrhythmic events after ICD implantation. In clinical situations, close follow-up may be required to find recurrent events in the OHCA survivors with LGE regardless of its extent, because recurrent arrhythmia after the ICD installation may be related to the progression of myocardial damage, such as myocardial ischemia or cardiomyopathy[9,19,21,26]. There were only 3 patients with LVEF < 35% in our study. In some patients, the systolic function might recover at the interval between the onsets and CMR examinations. Waldmann et al[18] have reported that patients with CVS and associated cardiac arrest tend to have higher LVEF.
There were some limitations in this study. First, the study population was small, and the results were mainly descriptive. The OHCA survivors with ACS or under unstable conditions may not have undergone CMR. On the other hand, the clinical backgrounds and CMR features of our patients, who experienced OHCA in the midtown of a large capital city, were specified. Second, the mean interval between OHCA and CMR examinations was 12.3 days, which may affect CMR findings: Myocardial edema on T2-weihgted images or T2 mapping may disappear over time[13]. The interval of this study was almost equal to or shorter than those of previous studies, which indicates that CMR immediately after OHCA cannot be performed because of safety concerns[7,13]. The present study showed that the interval did not affect CMR findings in our 10 patients with CVS. In HCM, T2-high is reported to be lymph vessels dilatation but not ischemic myocardial edema that changes over time[31]. Third, we measured T1 and T2 values only at the mid-septal myocardium, because we used the mapping sequences to identify diffuse myocardial damage but not regional fibrosis and edema[20]. If we had performed T1 and T2 mapping covering the entire left ventricle, we could have investigated subtle myocardial damage that could not be identified with T2-weighted and LGE images. Fourth, the diagnostic capability of CMR was limited in the patients with CVS and possibly in those with VF. The 2 CVS patients showed non-ischemic LGE or unrecognized MI. These CMR findings of CVS have been indicated in a previous report[22], and non-ischemic septal LGE can be found in the patients with ischemic cardiomyopathy[9]. The six patients with CVS and OHCA did not show any particular myocardial damage on CMR. Previous studies have demonstrated that approximately 40% of MI without coronary artery stenosis, which may include CVS, does not LGE but probably edema of the myocardium[32,33]. Bergamaschi et al[33] have also revealed that LGE is related to major cardiac events in these patients. These results may be consistent with our results about the relationship between LGE and arrhythmic events before and after ICD installation in patients with CVS.
CONCLUSION
In conclusion, our institution, located in the midtown of a large capital city, has handled various myocardial diseases associated with OHCA. CMR may be useful for identifying the myocardial damage of HCM or MI, inducing OHCA. However, CMR fails to identify myocardial damage characteristic of CVS, which is seen in more than half of the survivors of OHCA. CMR is able to identify myocardial LGE related to serious ventricular arrhythmias after ICD implantation, which leads physicians to check more closely and add appropriate treatments to the OHCA survivors with LGE.
ACKNOWLEDGEMENTS
The authors thank Hitoshi Maeda RT, Naoki Shinoda RT and Yuna Kaneko RT for their technical support, including measurement of T1 and T2 values of the myocardium.
Footnotes
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Radiology, nuclear medicine and medical imaging
Country of origin: Japan
Peer-review report’s classification
Scientific Quality: Grade B, Grade B
Novelty: Grade A, Grade B
Creativity or Innovation: Grade B, Grade B
Scientific Significance: Grade B, Grade B
P-Reviewer: Chen L S-Editor: Qu XL L-Editor: A P-Editor: Zhao S
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