Out-of-hospital cardiac arrest (OHCA) without ST-segment elevation represents a challenging diagnostic scenario, particularly in young patients with low pretest probability of atherosclerotic disease. We report the case of a 25-year-old man with cystic fibrosis who presented with ventricular fibrillation during a pulmonary exacerbation complicated by hemoptysis and hypoxemia. After successful resuscitation, electrocardiography showed anterolateral T-wave inversions and high-sensitivity troponin demonstrated a marked rise and fall. Transthoracic echocardiography revealed regional wall motion abnormalities with mildly reduced left ventricular ejection fraction. In the absence of ST-segment elevation, coronary computed tomography angiography was performed and excluded obstructive coronary artery disease and congenital anomalies. Early cardiac magnetic resonance demonstrated extensive transmural late gadolinium enhancement in a coronary distribution with microvascular obstruction, consistent with acute ischemic myocardial infarction despite normal epicardial coronaries, establishing a diagnosis of myocardial infarction with nonobstructive coronary arteries (MINOCA). This case illustrates a structured, stepwise, and entirely noninvasive multimodality imaging approach to OHCA without ST-elevation and highlights the central role of early cardiac magnetic resonance in mechanism clarification and clinical decision-making in suspected MINOCA.
A 25-year-old man with cystic fibrosis (F508del homozygous) with concomitant CF-related diabetes, chronic pulmonary infection due to Scedosporium spp. and recurrent hemoptysis, was admitted after out-of-hospital cardiac arrest (OHCA) secondary to ventricular fibrillation. The event occurred during a pulmonary exacerbation complicated by active hemoptysis and hypoxemia. After successful resuscitation, the electrocardiogram showed new anterolateral T-wave inversions without ST-segment elevation ( Figure 1 ). High-sensitivity troponin I demonstrated a marked rise and fall (peak 293,000 ng/L). Transthoracic echocardiography revealed hypokinesis of the antero-lateral, infero-lateral, and anterior midapical segments with mildly reduced left ventricular ejection fraction (LVEF 44%) and a small circumferential pericardial effusion ( Supplementary Video 1-3 ).
Upper Panel: Single ECG strip recorded during cardiopulmonary resuscitation documenting cardiac arrest due to ventricular fibrillation. Lower Panel: ECG performed after OHCA showing T-wave inversions in anterolateral leads without evidence of ST-segment elevation.
Question 1
In a young patient with ventricular fibrillation, a dynamic troponin rise and fall, and regional wall motion abnormalities without ST-segment elevation, what is the most appropriate next diagnostic-therapeutic step?
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A.
Immediate thrombolysis.
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B.
Immediate invasive coronary angiography.
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C.
Coronary computed tomography angiography (CCTA).
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D.
No coronary imaging if symptoms resolve postresuscitation.
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E.
Endomyocardial biopsy.
Correct Response: C. Coronary computed tomography angiography (CCTA)
In this clinical context, the key issue is to define the coronary anatomy in a young patient with a low pretest probability of atherosclerotic disease and no electrocardiographic evidence of ST-segment elevation mandating emergent catheterization. While 90% of STEMI cases involve an occluded artery, fewer than a third of NSTEMI cases show acute occlusion. In both the TOMAHAWK and COACT trials, immediate coronary angiography after OHCA without ST-segment elevation did not improve survival or major clinical outcomes compared with a delayed/selective strategy. , Accordingly, current guidelines support immediate invasive coronary angiography after out-of-hospital cardiac arrest primarily when postresuscitation electrocardiogram shows ST-segment elevation or when there is ongoing hemodynamic or electrical instability strongly suggestive of an acute culprit occlusion. In a clinically stabilized patient without ST-elevation, a selective approach is appropriate.
CCTA represents a robust noninvasive strategy to exclude obstructive coronary artery disease, congenital coronary anomalies, and myocardial bridging, all of which are relevant considerations in young individuals. In addition, the presence of active hemoptysis increases bleeding risk, further supporting an initial noninvasive anatomical evaluation.
Immediate thrombolysis is not indicated in the absence of ST-elevation and would expose the patient to unnecessary hemorrhagic risk. Forgoing coronary imaging would ignore clear evidence of myocardial injury, as demonstrated by dynamic troponin elevation and regional wall motion abnormalities. Endomyocardial biopsy is reserved for selected cases with high suspicion of inflammatory or infiltrative cardiomyopathy and is not part of first-line evaluation in this setting.
CCTA demonstrated normal coronary origins and course, a calcium score of 0, and no coronary stenoses (CAD-RADS 0). No anomalous vessels or myocardial bridging were identified ( Figure 2 , Supplementary Video 3 ).
CCTA showing no significant coronary artery disease in the LAD, LCx, and RCA territories.
Question 2
In the setting of OHCA without evidence of obstructive coronary artery disease, which diagnostic test is most appropriate to determine the underlying mechanism?
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A.
Repeat CCTA with delayed enhancement.
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B.
Cardiac magnetic resonance (CMR) during the acute phase
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C.
Perform exercise stress SPECT test before discharge.
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D.
Routine invasive acetylcholine testing in all patients.
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E.
Empirical corticosteroid therapy.
Correct Response: B. Cardiac magnetic resonance (CMR) during the acute phase
Once obstructive coronary artery disease has been excluded, the central clinical challenge becomes identification of the underlying mechanism. Early CMR (within 7-10 days) plays a pivotal role in this phase, as it allows comprehensive myocardial tissue characterization. Through assessment of late gadolinium enhancement patterns, myocardial edema, T1 and T2 mapping, and the presence of microvascular obstruction, CMR can differentiate ischemic myocardial injury from myocarditis, Takotsubo cardiomyopathy, or other nonischemic cardiomyopathies.
A wealth of recent studies has shown that early CMR reclassifies a substantial proportion of patients initially labeled as MINOCA—up to 60% to 70% in some series; meta-analyses show myocarditis accounts for approximately 31% to 33% of these cases and Takotsubo for approximately 10% to 18%. , Furthermore, the extent of late gadolinium enhancement (LGE) and T2 mapping values are independent predictors of major adverse cardiovascular events (MACE) . Repeat CCTA would not offer additional insight into myocardial tissue characteristics. Exercise stress SPECT test is inappropriate early after cardiac arrest and acute myocardial injury. Routine invasive vasospasm testing may be considered in selected stable patients after exclusion of alternative diagnoses, but it is not the first diagnostic step in the immediate evaluation. Empirical corticosteroid therapy would be inappropriate in the absence of confirmed inflammatory cardiomyopathy.
CMR confirmed the mild LV systolic disfunction (LVEF 42%) with hypokinesis of the anterolateral and inferolateral wall ( Supplementary Video 5 ). Tissue characterization showed extensive transmural late gadolinium enhancement involving the anterolateral and inferolateral walls from base to apex, the anterior midapical wall and all the other apical segments with involvement also of the papillary muscles in a coronary distribution. A large area of microvascular obstruction was present ( Figure 3 , Supplementary Video 6 ). Native T1 and extracellular volume were elevated within LGE areas, and T2 mapping showed increased values consistent with an acute process.
Upper Panel: CMR demonstrating extensive LGE involving the lateral wall and the anterior mid-apical segments, with areas of MVO. Lower panel: SAX PSIR CMR view demonstrating the infarcted area with MVO (left), corresponding elevated native T1 mapping values (center), and post-contrast T1 shortening within LGE areas but not within the region of MVO (right).
