European heart journal. Case reports · 2026
Association of cardiac sarcoidosis with coronary slow flow: a case report unraveling the enigma.
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Hussein Hossameldin, Radhakrishnan Ashwin, Gul Uzma, Dhanjal Tarvinder
Аннотация
BACKGROUND: The exact mechanism of slow coronary flow (SCF) is still not well understood. SCF can manifest as acute coronary syndrome, or in rare scenarios, sudden cardiac death (SCD). Regional microvascular dysfunction (MVD) has been reported in inflammatory cardiomyopathies with a correlation between coronary flow reserve and active myocardial inflammation.
CASE SUMMARY: A 52-year-old gentleman presented with refractory ventricular tachycardia (VT) following an aborted out-of-hospital cardiac arrest. Apart from one prior episode of uninvestigated syncope, there was no history of prior cardiac symptoms or comorbidities. Initial blood tests were unremarkable with a normal troponin level. Coronary angiography identified no obstructive epicardial coronary artery disease but demonstrated SCF that was marked in the right coronary artery (RCA). Subsequent cardiac magnetic resonance imaging demonstrated transmural late gadolinium enhancement in the RCA territory, which correlated to VT origin on the surface electrocardiogram. With no reversible cause of VT identified, an implantable cardioverter defibrillator was implanted for secondary prevention. Following discharge, an out-patient 18F-fluorodeoxyglucose positron emission tomography/computed tomography scan revealed increased metabolic activity suggestive of active inflammatory myocardial involvement, most likely due to cardiac sarcoidosis (CS).
DISCUSSION: This case highlights the importance of SCF as a surrogate marker for underlying MVD in relation to active myocardial inflammation. Studies are required to understand the role of MVD as a causal link between SCF and CS. Whether MVD should be considered in risk stratification for primary prevention of SCD in CS patients is to be explored.
CASE SUMMARY: A 52-year-old gentleman presented with refractory ventricular tachycardia (VT) following an aborted out-of-hospital cardiac arrest. Apart from one prior episode of uninvestigated syncope, there was no history of prior cardiac symptoms or comorbidities. Initial blood tests were unremarkable with a normal troponin level. Coronary angiography identified no obstructive epicardial coronary artery disease but demonstrated SCF that was marked in the right coronary artery (RCA). Subsequent cardiac magnetic resonance imaging demonstrated transmural late gadolinium enhancement in the RCA territory, which correlated to VT origin on the surface electrocardiogram. With no reversible cause of VT identified, an implantable cardioverter defibrillator was implanted for secondary prevention. Following discharge, an out-patient 18F-fluorodeoxyglucose positron emission tomography/computed tomography scan revealed increased metabolic activity suggestive of active inflammatory myocardial involvement, most likely due to cardiac sarcoidosis (CS).
DISCUSSION: This case highlights the importance of SCF as a surrogate marker for underlying MVD in relation to active myocardial inflammation. Studies are required to understand the role of MVD as a causal link between SCF and CS. Whether MVD should be considered in risk stratification for primary prevention of SCD in CS patients is to be explored.