Transmural Myocardial Infarction with Intramyocardial Hemorrhage, Apical Thrombus, and Ventricular Dysfunction Secondary to recurrent Coronary Vasospasm

Presenting Author(s)

• 

  Maria Camila Bartolome Roca, MD

  Trainee fellow (Cardiovascular Imaging)
  Hospital Italiano de Buenos Aires
  Ciudad Autonomam de Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina

Primary Author(s)

• 

  Maria Camila Bartolome Roca, MD

  Trainee fellow (Cardiovascular Imaging)
  Hospital Italiano de Buenos Aires
  Ciudad Autonomam de Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina

Co-Author(s)

• 

  Santiago del castillo, MD

  Cardiologist
  Hospital Italiano de Buenos Aires
  Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina
• RB

  Rodrigo Bagnatti, MD

  Cardiologist
  Hospital Italiano de Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina
• GC

  Giuliana Corna, MD

  Cardiologist
  Hospital Italiano de Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina
• 

  Sebastian Tonso, MD

  Medical associated
  Hospital Italiano de Buenos Aires
  Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina

Description of Clinical Presentation: We present a 66-year-old female, with a history of hypertension, dyslipidemia, and two prior episodes of STEMI. In the first episode, she received thrombolytics without coronary angiography. In the second, inferior wall ST-elevation prompted emergency catheterization, which showed no significant coronary obstructions. CMR revealed apical infarction with transmural LGE enhancement, suggesting coronary vasospasm. Treatment with calcium channel blockers (CCB) was initiated.



She now presents to the emergency department with oppressive, angina-like chest pain lasting for three hours.



Upon admission to our center, the patient continued to experience precordial pain. She was hypertensive, normocardic, and showed no signs of heart failure. ECG showed ST-segment elevation in the inferior, anterior, and lateral leads. Emergency coronary angiography was performed after dual antiplatelet therapy and intravenous nitroglycerin were administered. At the time of the study, the patient was asymptomatic, ECG changes had resolved, and no significant stenoses were found.



Laboratory tests confirmed elevated high-sensitivity troponin T (999 pg/ml). Transthoracic echocardiography demonstrated new anterior, anterolateral medial, and apical segments hypokinesia. Troponin rose (peak 3400 pg/ml), and considering the wall motion abnormalities, and the transient ST-elevation on ECG, the condition was interpreted as MINOCA, likely due to a third episode of coronary vasospasm.

CMR was performed and revealed dyskinesia of the apical segments, inferolateral basal and inferomedial hypokinesia, inferolateral medial akinesia, and moderately reduced LVEF (45%). An apical aneurysmal expansion containing thrombus was present. Transmural LGE was observed in multiple apical and inferolateral segments. Microvascular obstruction was noted, and T2* mapping indicated intra-infarct hemorrhage.



The patient had a favorable outcome with declining biomarkers and improved LVEF (55%) on follow-up echocardiography, and remains asymptomatic in NYHA class I. Due to the finding of intracardiac thrombus and microvascular obstruction, anticoagulation was initiated, and CCB therapy was optimized.

Diagnostic Techniques and Their Most Important Findings: CMR revealed moderately reduced LV function (LVEF 45%) with inferior and inferolateral wall motion abnormalities, apical aneurysm, and thrombus. Initial angiography showed no significant stenosis. Elevated T1/T2 mapping values indicated myocardial edema and transmural LGE pattern confirmed acute infarction. T2* mapping revealed intramyocardial hemorrhage, a marker of adverse remodeling and poor prognosis

Learning Points from this Case: CMR plays a critical role in MINOCA, for accurate diagnosis and management, as well as for ruling out other etiological causes, such as myocarditis or Takotsubo syndrome. It allows precise characterization of microvascular obstruction and intramyocardial hemorrhage, which are key prognostic determinants for recurrence of cardiovascular events and ventricular function integrity.

Figure 1. ECG on admission, showing ST-segment elevation in the inferior and anterolateral leads.
Figure 2. Coronary angiography showed no obstructive coronary lesions.
Figure 3. CMR findings: apical aneurysm, microvascular obstruction, and mural thrombus in four-chamber view (LGE). Lateral wall edema (T2 mapping) and intra-infarct hemorrhage (T2* mapping) in short axis at mid-ventricular level and three-chamber view.