Cairo University – Faculty of Medicine

Cardiology Department

Examination of the MD degree in Cardiology

May 26,  2002. Paper III (Commentary).

Please read the following case presentation and respond to the questions given below:

- A 59-year old male with a history of hypertension presented to the emergency department complaining of persistent chest pain lasting about two hours. He was slightly tachypneic. Heart rate was 92/min and blood pressure 110/70 mmHg. Heart sounds were normal and a soft systolic murmur was audible at the apex. Crackles were detected over the bases of the lungs.
On admission the ECG showed marked ST-segment elevation in leads V1-5 and mild repolarization abnormalities in the inferior leads. The echocardiogram revealed end-diastolic and end-systolic dimensions of 51 and 40 mm, respectively. There was akinesis involving the anterior wall, anterior septum and apex. the ejection fraction was 38% and there was a mild mitral regurgitation.
- The patient was commenced on intravenous infusion of heparin and eptifibatide and promptly transferred to the catheterization laboratory for emergency coronary angiography and primary percutaneous coronary intervention (PCI) if suitable. Coronary angiography revealed occlusion of the mid portion of the left anterior descending (LAD) coronary artery after the first diagonal branch. A myocardial contrast echocardiography (MCE) was performed by injecting 3 ml hand-agitated iopamidol during coronary occlusion that revealed the absence of contrast effect in the middle segment of the septum and apex. a successful angioplasty (TIMI flow grade 3 and residual stenosis < 30%) and stenting of the LAD were performed. Repeat MCE shortly after infarct-related artery recanalization showed an homogenous contrast enhancement of the risk area.
After primary PCI, the patient remained asymptomatic and was transferred to the coronary care unit where intravenous infusion of eptifibatide and low-dose heparin was continued for 12 hours and oral aspirin 150 mg/day, ticlopidin 500 mg/day and ACE inhibitor therapy was instituted. Creatine phosphokinase peaked at 2575 IU/L from onset of chest pain.
- During the first 48 hours after the primary PCI, the patient recovered quickly. There were neither recurrent ischemic episodes nor significant arrhythmias, no sings of congestion were seen on the chest X-ray, and the ECG showed progressive disappearance of the ST-segment shift with T waves becoming negative in the infarct leads. Repeat MCE at 48 hours showed the absence of contrast enhancement in the risk area, but persistent brisk (TIMI 3) epicardial flow. Predischarge echocardiogram sowed a mild segmental and global functional recovery and the calculated ejection fraction was 45%.
- Four weeks after discharge the patient started to complain of progressive exertional dyspnea. Repeat coronary arteriography revealed persistence of LAD patency but the echocardiogram showed a dilated poorly contractile left ventricle and the ejection fraction was 25%.
Discuss the diagnosis of the condition and the potential underlying pathophysiological disturbances.