Cardiogenic shock post-percutaneous coronary intervention for myocardial infarction.

in inferior leads (Fig. 1A). Cardiac enzymes showed an upward trend consistent with myocardial necrosis. Creatine kinase myocardial b (CKMB) fraction rose from 41.4 ug/L to 111.0 ug/L over 15 hours, while troponin I rose from undetectable levels on admission to >80.000 ug/L over the same period. He was treated as a non-ST elevation myocardial infarction with a thrombolysis in myocardial infarction (TIMI) risk score of 5. On the second day of admission, a coronary angiogram was performed in view of ongoing chest pain. Angiogram done 14 hours from onset of chest pain, showed native triple vessel disease and patent left internal mammary and saphenous vein grafts. The occluded right posterolateral artery was deemed the culprit lesion (Fig. 1B) and balloon angioplasty was performed with successful revascularisation, as well as symptom resolution (Fig. 1C). Eight hours after procedure, the patient developed acute pulmonary oedema and severe hypotension. He was in cardiogenic shock. A new holosystolic murmur was also heard loudest over the apex. However, there was no thrill palpable in the precordium. Cardiogenic Shock Post-Myocardial Infarction—Weiqin Lin et al Images in Medicine