Symptomatic myocardial bridging or cardiac Whipple's Diseas

Abstract

patient suffered from progressive dyspnea, palpitations, and precordial pain. In fact, he was admitted to the hospital with a diagnosis of coronary disease and atrial flutter. Serum cardiac enzymes and routine laboratory tests were considered normal, except for mild, microcytic anemia. He underwent electrical cardioversion, and amiodarone was started. Echocardiography revealed mild antero-lateral wall hypokinesis, a moderate left ventricular dilatation with preserved ejection fraction, thickening of the mitral and tricuspid cusps, aortic and mitral regurgitation, and moderate pericardial effusion. Electrocardiographic monitoring showed supraventricular tachycardia, and cardiac catheterization demonstrated normal coronary arteries and myocardial bridging in the left anterior descending coronary artery. He remained asymptomatic for a long period, although repeated echocardiography was consistent with the previous findings.He was readmitted to the hospital because of a 10-month history of liquid, diarrhea, malnutrition, and anorexia. Previously he had undergone a colonoscopy with rectum biopsy, showing a nonspecific chronic colitis that was treated with sulfasalazine and corticosteroids without any clinical improvement. His blood pressure was 90/60mmHg, and nonthrombocytopenic purpura was noted on both legs. On cardiac auscultation, a grade II pansystolic murmur was detected at the apex. Laboratory examination showed a hemoglobin of 8.8 g/dL, mean corpuscular volume of 65fL, normal ferritin level, an erythrocyte sedimentation rate (ESR) of 59 mm/h, platelet count of 480,000 mm³ , and serum albumin of 29 g/L. A barium transit of the small bowel was normal, colonoscopy detected hyperemia in the left colon, and the biopsy showed a normal colonic mucosa. Abdominal computed tomography (CT) demonstrated thickened intestinal walls. At upper gastrointestinal endoscopy, duodenal mucosa appeared hyperemic with petechiae. Histopathological examination detected infiltration of the lamina propria by PAS-positive and Ziehl-Neelsen-negative macrophages. Oral therapy with trimethoprim-sulfamethoxazole and folate were started and continued for 18 months. All clinical signs of malabsorption disappeared, previous

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