Atypical case of acute coronary syndrome due to coronary-pulmonary steal syndrome secondary to pulmonary embolism

Abstract

on chronic oxygen therapy due to chronic obstructive pulmonary disease (COPD) in the setting of a bronchiectasic disease, referred to our hospital in September 2009 because of a micturition-nocturnal-syncope preceded by dizziness. The patient had neither a personal history of coronary artery disease nor known cardiovascular risk factors. In the emergency department (ED) the patient presented preserved consciousness and mild dyspnea despite low flows of inhalatory O 2 (2 l/min); chest examination was characterized by sibilant and sonorous rales in addition to bibasilar thin crackles; hemo-gas analysis (HGA) showed severe hypoxemic-hypercapnic acidosis (pH 7.18, pCO 2 85 mmHg, pO 2 58 mmHg, sO 2 84%, HCO 3 -23.5, 5); the ECG demonstrated sinus tachycardia, mild and non-specific ST segment elevation V1-V3; the chest X-ray study showed a COPD pattern, right-basal paracardiac radio-opacity, enlargement of the left cardiac chambers. Blood tests demonstrated a leukocytosis with a mild elevation of LDH and D-Dimer [WBC 19,860, Hb 13.4 g/dL, creatinine 0.85 mg/dL, troponin I (T I ) 0.02 ng/mL, CPK e CPK-MB ns, D-Dimer 678 mg/dL, BNP 37 pg/mL]. In the ED, the patient was started on inhalatory salbutamol, furosemide, steroids and empiric i.v.antibiotic-therapy with piperacillin/tazobactam. An HGA executed 2 h later, documented resolution of the acidosis and of the hypoxia, clear reduction of the pCO 2 (pH 7.4, pO 2 70 mmHg, pCO 2 55 mmHg, sO 2 95%). In the afternoon, the patient was transferred to the department of Internal Medicine. About 1 h after admission, he presented sudden, severe shortness of breath and diaphoresis, the ECG demonstrated sinus tachycardia, a new onset of mild ST segment elevation V3-V6; an HGA showed severe respiratory hypoxic-hypercapnic acidosis (pH 7.16 pCO 2 91 mmHg, pO 2 56 mmHg, sO 2 79%). IV steroids and inhaled salbutamol were again administered with subsequent resolution of the dyspnea and improvement of gas exchange. Blood tests revealed a mild, initial increase of T I (0.77 ng/mL at time 0 min, 0.17 ng/mL 6 h later) with persistently normal LDH, AST, and CK. The ECG presented giant and symmetrical negative T-waves in inferiorlateral derivations (D1-D3, V4-V6). Preliminary diagnosisDr. Squizzato, Prof. Ageno: After cardiologic consultation, on the basis of the ECG abnormalities and a positive marker for myocardial necrosis, therapy with ASA, nitrates and a therapeutic dose of low molecular weight heparin was started. The cardio-thoracic examination was unchanged. A trans-thoracic echocardiogram revealed a mild eccentric left ventricular hypertrophy; a wellpreserved global and segmentary wall-motion (ejection fraction 60%); an altered diastolic function with a pseudonormalized pattern at color-Doppler and tissue-Dopplerimaging; an absence of tricuspidal regurgitation and a normal systolic pulmonary artery pressure; a high-resistance Doppler flow pattern in the first tract of pulmonary