The sound of silence
Case Study 2, part III:
The first EKG shows atrial fibrillation and ST elevations in the inferior leads (II, III, aVF) with reciprocal ST-depression in lead I and aVL. ST elevations with reciprocal depressions must prompt considerations of acute myocardial infarction, though there are other reasons for ST elevations such as ventricular aneurysm or acute pericarditis. A thorough history taking and medical examination did not reveal any other signs of ongoing myocardial ischemia. Blood tests did not show raised cardiac biomarkers.
First EKG:
The second EKG does not show signs of myocardial ischemia (there are no ST elevations). This suggest intermittent myocardial ischemia most likely due to a coronary artery spasm.
Second EKG:
Taken into consideration the recent onset of chest pain on exertion a coronary angiography was carried out. The angiography revealed a severe ulcerated plaque in the proximal right coronary artery (see picture below). The patient was treated with percutaneous coronary intervention.
Coronary angiography:
What can we learn from this? Patients with unstable angina (and stable angina) exhibit episodes of ischemia that are not associated with chest pain or chest discomfort. This is referred to as “silent myocardial ischemia”. This is the most common form of silent myocardial ischemia (the other being totally asymptomatic patients with coronary artery disease that may be severe). Ischemia that presents as intermittent ST elevation in a patient with an ulcerated plaque in a coronary vessel is due to local vasoconstrictors (serotonin and thromboxane A2) released from activated platelets as well as others factors including thrombin.
– Troels
Related content
Sound of silence – part I
Sound of silence – part II
Sound of silence – part III
{ 2 comments… read them below or add one }
Excellent case, certainly highlights the importance of early 12-Leads and serial acquisition.
I would add that the reciprocal changes in I and aVL effectively “rule out” pericarditis in the field. Focal myocarditis is a possibility, but with changes so frank I would imagine this would only be discovered after an emergent cath revealed no culprit lesions.
Interesting case! I think that the hallmark sign/symptom was the exertional chest pain. Clearly local vasoconstriction secondary to those mediators listed played a major role. It is just remarkable that the physical stress only induced flow related ischemia that manifested itself with transient ST elevation. The ulcerated area appears markedly unstable and on the verge of total occlusion. Thankfully his anticoagulation therapy averted a potentially lethal event. The vessel appears to be a dominant one. It would be interesting to see the size and distribution of the circumflex. I suspect it to be a rather small vessel by comparison.
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