ESC guidelines for percutaneous coronary interventions.
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Biomedical subjects
Publications and source records attributed to Mona A Kholeif.
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The increasing usage of cephalosporins, to which the enterococci are resistant, has resulted in the rising number of enterococcal infections worldwide. Enterococci are a normal part of the flora of the human gastrointestinal tract, buccal cavity, perineal skin, vagina, urethra and gallbladder, but may occur as pathogens in a number of sites causing urinary tract infections, intra-abdominal infections, fatal bacteremia, meningitis and endocarditis. A Saudi male who developed enterococcal endocarditis with vegetations on both aortic and mitral valves required mitral and aortic valve replacement. The attention of physicians is drawn to the increasing frequency of enterococcus as a cause of nosocomial infections, the risk factors, and antibiotic resistance pattern including resistance to vancomycin as well as its potential for virulence.
A 70-year old man presented with retrosternal chest pain. His electrocardiogram showed nonspecific T wave changes. Cardiac-specific troponin I (cTnI) was elevated. His condition was managed as acute coronary syndrome, following which he had two minor episodes of hemoptysis. A CT pulmonary angiogram showed no evidence of pulmonary embolism, but a large mass lesion was seen in the mediastinum. Echocardiography and cardiac MRI demonstrated a large solid mass, arising from the right ventricular outflow tract and causing compression of the main pulmonary artery (MPA). The differential diagnosis included pericardial and myocardial tumors and clotted aneurysm of the MPA. At surgery, a clotted aneurysmal sac was identified originating from the MPA and the defect was healed. Aneurysms of the MPA are rare. They most commonly present with dyspnea and chest pain. Compression of surrounding structures produces protean manifestations. A high index of suspicion coupled with imaging modalities establishes the diagnosis. Blunt trauma to the chest, at the time of an accident 4 years previously, may explain this aneurysm. The patient's presentation with chest pain was probably due to compression and/or stretching of surrounding structures. Coronary artery compression simulating acute coronary syndrome has been documented in the literature. The rise in cTnI may have been due to right ventricular strain, as a result of right ventricular outflow obstruction by the aneurysm. This has not been reported previously in the literature. The saccular morphology and narrow neck of the aneurysm predisposed to stagnation leading to clotting of the lumen and healing of the tear, which caused the diagnostic difficulty.