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A 67-year-old woman was sent for a coronary angiography seven days after infarction. The patient presented with prolonged chest pain and was admitted to another hospital because of the diagnosis of acute myocardial infarction.  The first electrocardiogram (ECG) (performed on May 31, 2005 at 4:40 p.m.) revealed no alterations indicating infarction (Figure 1); however, the second ECG (performed on May 31, 2005 at 9:45 p.m.) when a new pain episode occurred revealed alterations indicating infarction.    Figure 1  ECG: sinus rhythm, likely electrically inactive area of the inferior wall.    The second ECG revealed sinus bradycardia, pathological Q waves in leads II, III, and aVF, with ST elevation and positive T waves in the same leads as well as ST depression in V1 and V2; these findings are compatible with an acute infarction in progress (Figure 2).    Figure 2  ECG: infarction in progress in the inferior wall, ST depression in V1, V2, and aVL.    The patient reported less pain and was in Killip Class I.  An ECG (performed on June 7, 2005) revealed pathological Q waves in leads II, III, and avF, with slight ST elevation and T waves that were still positive. The exam also revealed ST depression in V1 and V2 (Figure 3).    Figure 3  ECG: QRS complex parallel to the anatomic base-to-apex axis of the heart, QR waves (II, III, and aVF) with slight ST elevation and positive T waves, and ST depression in V1, V2, I, and aVL.    This same ECG showed that the aorta was 27 mm in diameter, left atrium was 39 mm in diameter, left ventricular diastole was 61 mm in diameter, ejection fraction was 45%, and septal and posterior wall thickness was 9 mm. The left ventricle exhibited apparent diffuse hypokenesis and impaired ventricular filling (E < A); the valves did not show any abnormalities.  On physical examination (performed on June 8, 2005) the patient was in a poor condition overall; she was pale and hypotensive, with cold limbs and increased pressure in the jugular vein. The results of pulmonary and cardiac auscultation were normal; there were no signs of deep vein thrombosis in the legs.  Laboratory tests (performed on June 8, 2005) revealed the following values: hemoglobin 10.8 g/dL, hematocrit 33%, MCV 70 µm3, leukocytes 9000/mm3, platelets 245000/mm3, urea 50 mg/dL, creatinine 1.7 mg/dL, troponin I 32.6 ng/mL (8:00 a.m.) and 27.1 ng/mL (4 p.m.), and CK-MB 3.70 ng/mL (8:00 a.m.) and 4.2 ng/mL (4:00 p.m.).  A coronary angiography performed on June 8, 2013 revealed proximal occlusion of the right coronary artery, left coronary trunk free of obstructive lesions, left circumflex artery free of lesions, and anterior interventricular artery with 70% obstruction in the mid segment. A right coronary angioplasty was performed and showed thrombi; many stents were inserted between the proximal and distal portions.  After the coronary angiography, the patient developed severe dyspnea and respiratory insufficiency. Orotracheal intubation was required for respiratory support, and the patient remained in shock.  The ECG (performed on June 8, 2005) revealed new ST elevation in the inferior wall, with negative T waves and ST depression in V2 and V3, aVL, and lead I (Figure 4).    Figure 4  ECG: ST re-elevation in the inferior wall and repeated ST depression in lead I, aVL, V1, and V2.    The patient remained in shock with the use of vasoactive drugs and went into cardiorespiratory arrest. She did not respond to resuscitation efforts and died a few hours later.

Case 02/2015 - A 67 Year-Old Woman with Sudden Cardiogenic Shock in the 7th Day after Acute Myocardial Infarction