Author + information
- Jeffrey J. Goldberger, MD∗ ( and )
- Daniel C. Lee, MD
- Division of Cardiology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
- ↵∗Reprint requests and correspondence:
Dr. Jeffrey Goldberger, Division of Cardiology, Department of Medicine, Feinberg School of Medicine, Northwestern University, 251 East Huron, Feinberg Pavilion, Suite 8-542, Chicago, Illinois 60611.
Sudden cardiac arrest (SCA) is one of the most striking clinical presentations of cardiovascular disease. An estimated 234,000 to 326,000 SCAs occur in the United States each year (1). Unfortunately, mortality for out-of-hospital SCA remains high, with only 10.6% of patients surviving to hospital discharge. In patients who reach the hospital, a rapid multidisciplinary approach is initiated to preserve neurological function, identify and treat the underlying cause of SCA, and prevent future occurrences.
Approximately 38% of these patients will have obvious noncardiac causes of SCA, such as pulmonary embolism, primary respiratory failure, drug/medication intoxication, acidemia, or aneurysmal subarachnoid hemorrhage. In the remaining patients, up to 48% may have coronary artery occlusion (2). The electrocardiogram (ECG) is one of the first tests performed in these patients; however, 26% of patients without chest pain or ST-segment elevation can have an acute coronary artery occlusion. Because of the high prevalence of acute coronary artery occlusions in resuscitated patients with SCA and the suboptimal detection by ECG, the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend immediate angiography and percutaneous coronary intervention as a component of post–cardiac arrest protocols (3).
After patient stabilization, initiation of cooling to protect neurological function, and coronary angiography to identify and treat acute coronary occlusion, the evaluation turns to more chronic cardiac conditions that may have set the stage for SCA. These can be divided into abnormalities that are mainly structural (e.g., idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy [HCM], arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis, cardiac amyloidosis, myocarditis) or primary electrical abnormalities (e.g., long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, rarely Wolff-Parkinson-White syndrome).
Echocardiography remains the most commonly used imaging modality to identify structural abnormalities due to its wide availability, lower cost relative to cardiac magnetic resonance (CMR) and cardiac computed tomography, and ability to accurately diagnose many of the common cardiac abnormalities contributing to SCA. However, the cause of SCA remains uncertain in many patients even after echocardiography and coronary angiography.
In this issue of iJACC, Neilan et al. (4) present a 2-center experience of CMR in patients with SCA etiology that was uncertain after such a workup. They retrospectively identified 137 patients who presented with SCA over a 6-year period and underwent CMR to better elucidate the cause of SCA after a workup that included clinical history, ECG, echocardiography, and coronary angiography did not reveal a clear etiology for SCA. The CMR protocol consisted of cine images for cardiac function and late gadolinium enhancement (LGE) for identification and quantification of myocardial fibrosis. The investigators also characterized the pattern of LGE, which could be used to infer the etiology of myocardial fibrosis. Indeed, in the current study, CMR identified a potential arrhythmic substrate in 104 of 137 patients (76%). The diagnoses were based upon LGE in a pattern of myocardial infarction (MI), non-MI LGE, myocarditis, HCM, sarcoidosis, and arrhythmogenic right ventricular cardiomyopathy. Over a median follow up of 29 months (range 18 to 43 months), 16 patients (12%) died and 47 patients (34%) experienced appropriate implantable cardioverter-defibrillator shock. On multivariable analysis, the strongest predictor of events was the presence of LGE and the extent of LGE.
The retrospective nature of this study somewhat limits the generalizability of these findings, as noted by the researchers. Patients with SCA at the 2 centers were treated according to clinical routine, not a standardized protocol. The total number of patients experiencing SCA during the study time frame was not reported; thus, the proportion of all patients with SCA who did not undergo CMR either because the etiology for SCA was clear or it was not ordered for other reasons is unknown. In these patients, the results of the diagnostic workup and prognosis were also not described. Nevertheless, the results of this study are useful in establishing the diagnostic abilities of CMR in patients with a routine clinical workup that is unrevealing. The American Heart Association Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death give CMR a Class IIa recommendation for “when echocardiography does not provide accurate assessment of LV and RV function, and/or evaluation of structural changes.”
LGE in a pattern of MI was found in 49 of 137 patients (36%) who had an unrevealing coronary angiogram and echocardiogram. An apparent ischemic LGE pattern, even after severe coronary artery disease was excluded by coronary angiography, has also been reported in patients with a clinical diagnosis of idiopathic dilated cardiomyopathy (5). Establishing this etiology has both diagnostic and therapeutic significance. An additional 26 of 137 patients (19%) had LGE in a noninfarct pattern that could sometimes be attributed to myocarditis, HCM, or sarcoidosis. Again, delineation of these etiologies has both diagnostic and therapeutic significance. Furthermore, the presence of LGE, irrespective of its origin, has reliably been shown in multiple studies to confer a higher risk of ventricular arrhythmia and adverse cardiovascular events (6). With the further refinement and application of new techniques such as T2 mapping to quantify myocardial edema and T1 mapping to quantify diffuse myocardial fibrosis, the ability of CMR to interrogate the myocardial substrate for ventricular arrhythmia is likely to be further enhanced.
Given the observational nature of this study, it is unknown what impact CMR had on patient management. Although all of these patients received implantable cardioverter-defibrillators, an appropriate measure by guidelines and in light of the high rate of subsequent cardiac events, medical management targeted toward specific diagnoses would likely differ based on the CMR results. For example, in those with LGE in a pattern of MI, secondary prevention of coronary heart disease would be initiated. Identification of systemic diseases such as sarcoidosis and amyloidosis would lead to disease-specific therapy. Screening of family members in patients diagnosed with HCM may lead to earlier diagnosis and preventive strategies. In patients with preserved left ventricular function and normal echocardiograms, electrophysiology studies may potentially have been avoided in patients with CMR-based diagnoses that are known substrates for SCA who would otherwise have been labeled as SCA in a structurally normal heart.
In patients with new-onset heart failure who were free of angina, LGE-CMR has been evaluated as a gatekeeper to invasive coronary angiography, enabling accurate characterization of the underlying cause of heart failure (7). Figure 2 of Assomull et al. (7) illustrates how myocardial tissue characterization by CMR complements coronary anatomic information from angiography to provide a more nuanced understanding of heart failure etiology in each patient. Whether CMR could be employed earlier in the diagnostic workup of SCA—instead of echocardiography after exclusion of significant coronary artery disease by coronary angiography—remains unanswered. If a large proportion of patients had both an echocardiogram and CMR, a CMR-only strategy could be cost effective. However, it is difficult to speculate without knowing more about the patients who did not undergo CMR. There may also be some limitations to more widespread CMR use. Local expertise in CMR may be lacking and CMR may be difficult to perform in some post-SCA patients due to clinical instability and/or residual neurological impairment.
In summary, CMR provides an exquisitely detailed evaluation of the myocardial substrate for ventricular arrhythmia. In patients surviving SCA, this information can be critical for further management. If feasible, the use of CMR in the early part of the diagnostic workup for patients with aborted SCA should be strongly considered, particularly when the etiology of SCA has not been identified by the intercurrent workup. Further studies are needed to determine the most cost-effective strategy for imaging survivors of SCA.
↵∗ Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.
Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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