A MINOCA with complications as a bystander finding in a patient with cardiomyopathy

Presenting Author(s)

• 

  Paolo Costa, MD

  Honorary fellow CMR department Harefield Hospital
  University of Genoa
  Genova, Liguria, Italy

Primary Author(s)

• 

  Paolo Costa, MD

  Honorary fellow CMR department Harefield Hospital
  University of Genoa
  Genova, Liguria, Italy

Co-Author(s)

• 

  Chiara Bucciarelli-Ducci, MD, PhD

  Consultant cardiologist
  Royal Brompton & Harefield NHS Foundation Trust
  London , England, United Kingdom
• 

  Joyce Wong, MD, PhD, FSCMR

  Consultant Cardiologist in CMR
  Harefield Hospital, Guys' and St Thomas' NHS Foundation Trust.
  Chiswick, England, United Kingdom
• 

  Ana-Maria Poenar, MD

  Clinical and research CMR fellow
  Royal Brompton & Harefield NHS Foundation Trust
  Uxbridge, England, United Kingdom
• GB

  Giandomenico Bisaccia, MD, PhD, MSc

  CMR Fellow
  Royal Brompton and Harefield Hospitals
  CHIETI, Abruzzi, Italy
• 

  Jacopo Giulio Rizzi, MD

  Clinical and research fellow, CMR Unit, Harefield Hospital, London
  Royal Brompton & Harefield NHS Foundation Trust
  Senago, Lombardia, Italy
• AE

  Angela Elhyka, MD

  Resident in Cardiology università di Padova
  Royal Brompton & Harefield NHS Foundation Trust, Italy
• NM

  Nikolaos Miaris

  locum consultant, Cardiologist
  Royal Brompton & Harefield NHS Foundation Trust, Greece

Description of Clinical Presentation: A 46-year-old man with no prior cardiac history was admitted with acute chest pain and worsening dyspnea. His cardiovascular risk factors included overweight and mild alcohol consumption. On physical examination, a third heart sound was audible and mild bilateral pitting edema was present. A 12-lead ECG demonstrated sinus rhythm with T-wave inversion in V5–V6. Laboratory tests revealed elevated troponin concentration (Troponin I 11,590 ng/L; normal < 19.8 ng/L).


Bedside transthoracic echocardiography showed normal wall thickness, severe left ventricular systolic dysfunction (LVEF 20%) with global hypokinesia, though image quality was limited by the acoustic window. Subsequent coronary angiography revealed unobstructed coronary arteries. A cardiac magnetic resonance (CMR) was performed confirming severe biventricular systolic dysfunction (LVEF 20%, RVEF 20%), global LV hypokinesia, inferior wall akinesia and an apical LV thrombus. Additional findings included increased wall thickness (IVS 13 mm) and significant biatrial enlargement (LAVI 78 ml/m², RAVI 48 ml/m²). Tissue characterization demonstrated elevated T2 values in the mid-inferior wall (57 ms, normal 41–52 ms). LGE sequences revealed transmural enhancement of the mid-to-apical inferior wall with a hypointense core, suggesting microvascular obstruction (MVO). A separate non-specific mid-wall septal patch of enhancement was also noted.


Therapeutically, anticoagulation was initiated, leading to complete resolution of the LV thrombus at discharge. Guideline-directed medical therapy (GDMT) for heart failure was introduced and progressively up-titrated. At three-month follow-up, contrast-enhanced echocardiography showed marked improvement in biventricular systolic function (LVEF 50%, RVEF >35%) and confirmed the absence of LV thrombus.

Diagnostic Techniques and Their Most Important Findings:

1. A 1.5 Tesla CMR study was performed on the day of admission with a protocol including cine and tissue characterization with both T2 and LGE imaging. The findings were in keeping with a biventricular dilated cardiomyopathy with mid wall fibrosis and bystander focal infarction in the RCA territory (likely embolic), complicated by MVO and apical thrombus.

Learning Points from this Case: This case highlights the role of CMR both for the acute diagnosis and the clinical management of patients with working diagnosis MINOCA. First, by allowing detailed tissue characterization, it helps distinguishing ischemic from non-ischemic myocardial injury and identifying the extent of acute infarction as well as potential complications, such as MVO and LV apical thrombus, missed by beside echocardiography.Secondly, it holds clinical importance by differentiating ischemic injury from underlying cardiomyopathic, that might benefit from GDMT uptitration. Lastly, CMR is more sensitive than bedside echocardiography for detecting left ventricular thrombus, enabling timely initiation of anticoagulation.

Basal inferior MVO with peri-infarct haemorrage, likely secondary to embolic MI. T2 mapping (left panel), late gadolinium sequences (right panel).
Non ischemic late enhancement (left panel), apical thrombus in early gad sequences (right panel).
Transtoracic echocardiography (TTE) with contrast showing no residual LV thrombus, with 3D volume reconstruction.