Kyu Seop Kim

Prevalence and Patterns of Left Ventricular Dysfunction in Patients with Pheochromocytoma.

Background Excessive catecholamine release in pheochromocytoma is known to cause transient reversible left ventricular (LV) dysfunction, such as in the case of pheochromocytoma-associated catecholamine cardiomyopathy. We investigated patterns of clinical presentation and incidence of LV dysfunction in patients with pheochromocytoma. Methods From January 2004 to April 2011, consecutive patients with pheochromocytoma were retrospectively studied with clinical symptoms, serum catecholamine profiles, and radiologic findings. Patterns of electrocardiography and echocardiography were also analyzed. Results During the study period, a total of 36 patients (21 males, 49.8 ± 15.8 years, range 14-81 years) with pheochromocytoma were included. In the electrocardiographic examinations, normal findings were the most common findings (19, 52.8%). LV hypertrophy in 12 cases (33.3%), sinus tachycardia in 3 (8.3%), ischemic pattern in 1 (2.8%) and supraventricular tachycardia in 1 (2.8%). Echocardiographic exam was done in 29 patients (80.6%). Eighteen patients (62.1%) showed normal finding, 8 (27.6%) revealed concentric LV hypertrophy with normal LV systolic function, and 3 (10.3%) demonstrate LV systolic dysfunction (LV ejection fraction < 50%). Three showed transient LV dysfunction (2 with inverted Takotsubo-type cardiomyopathy and 1 with a diffuse hypokinesia pattern). Common presenting symptoms in the 3 cases were new onset chest discomfort and dyspnea which were not common in the other patients. Their echocardiographic abnormalities were normalized with conventional treatment within 3 days. Conclusion Out of total 36 patients with pheochromocytoma, 3 showed transient LV systolic dysfunction (catecholamine cardiomyopathy). Pheochromocytoma should be included as one of possible causes of transient LV systolic dysfunction.

Is Endoscopic Mucosal Resection a Sufficient Treatment for Low-Grade Gastric Epithelial Dysplasia?

Background/Aims The rate of diagnosis of gastric adenoma has increased because esophagogastroduodenoscopy is being performed at an increasingly greater frequency. However, there are no treatment guidelines for low-grade dysplasia (LGD). To determine the appropriate treatment for LGD, we evaluated the risk factors associated with the categorical upgrade from LGD to high grade dysplasia (HGD)/early gastric cancer (EGC) and the risk factors for recurrence after endoscopic treatment. Methods We compared the complication rates, recurrence rates, and remnant lesions in 196 and 56 patients treated with endoscopic submucosal dissection (ESD) and endoscopic mucosal resection (EMR), respectively, by histologically confi rming low-grade gastric epithelial dysplasia. Results The en bloc resection rate was significantly lower in the EMR group (31.1%) compared with the ESD group (75.0%) (p<0.001). However, no significant difference was observed in the prevalence of remnant lesions or recurrence rate (p=0.911) of gastric adenoma. The progression of LGD to HGD or EGC caused an increase in the incidence of tumor lesions >1 cm with surface redness and depressions. Conclusions For the treatment of LGD, EMR resulted in a higher incidence of uncertain resection margins and a lower en bloc resection rate than ESD. However, there was no signifi cant difference in recurrence rate.

Thrombotic occlusion of the radial artery as a complication of the transradial coronary intervention.

Transradial approach is known as a convenient method for percutaneous coronary intervention with lesser bleeding complication and improved patients comfort. However, thrombotic occlusion of the radial artery can be occurred as a complication of this procedure. Though there are few symptoms according to the radial artery occlusion due to dual blood supplies of the hand, thrombotic occlusion can be a problem especially in the patients with receiving coronary artery bypass graft surgery. To avoid this complication, we should keep in mind adequate anticoagulation, using smaller sheath as possible and meticulous handling during hemostasis. A 59-year-old man admitted for receiving coronary angiography. The patient was medicated with antihypertensive drug for five years and felt chest discomfort during modest exercise for five to seven days. After confirmation of his Allen test was normal, the patient was underwent coronary angiography via right radial artery with 6 Fr sheath (Fig. 1A). Because the coronary angiogram revealed significant stenosis of the first diagonal artery, the patient was treated with antianginal medications. The day after the procedure, his radial pulse was disappeared. The ultrasonographic exam demonstrated decreased flow of the radial artery distal to the puncture site and thrombus in it (Fig. 1B and video clip 1). Because there was no symptom related to that and his ulnar artery was normal, he was discharged with antiplatelet agent. After one month, the thrombus was disappeared in the follow up ultrasonogram of the radial artery. Fig. 1 A 6 Fr sheath is inserted to the right radial artery (A). The ultrasonogram taken one day after the transradial coronary angiography shows decreased flow and thrombus in the lumen (B).

Endothelial Dysfunction in the Smokers Can Be Improved with Oral Cilostazol Treatment

Background Smoking is one of well known environmental factors causing endothelial dysfunction and plays important role in the atherosclerosis. We investigated the effect of cilostazol could improve the endothelial dysfunction in smokers with the measurement of flow-mediated dilatation (FMD). Methods We enrolled 10 normal healthy male persons and 20 male smokers without any known cardiovascular diseases. After measurement of baseline FMD, the participants were medicated with oral cilostazol 100 mg bid for two weeks. We checked the follow up FMD after two weeks and compared these values between two groups. Results There was no statistical difference of baseline characteristics including age, body mass index, serum cholesterol profiles, serum glucose and high sensitive C-reactive protein between two groups. However, the control group showed significantly higher baseline endothelium-dependent dilatation (EDD) after reactive hyperemia (12.0 ± 4.5% in the control group vs. 8.0 ± 2.1% in the smoker group, p = 0.001). However, endothelium-independent dilatation (EID) after sublingual administration of nitroglycerin was similar between the two groups (13.6 ± 4.5% in the control group vs. 11.9 ± 4.9% in the smoker group, p = 0.681). Two of the smoker group were dropped out due to severe headache. After two weeks of cilostazol therapy, follow-up EDD were significantly increased in two groups (12.0 ± 4.5% to 16.1 ± 3.7%, p = 0.034 in the control group and 8.0 ± 2.1% to 12.2 ± 5.1%, p = 0.003 in the smoker group, respectively). However, follow up EID value was not significantly increased compared with baseline value in both groups (13.6 ± 4.5% to 16.1 ± 3.7%, p = 0.182 in the control group and 11.9 ± 4.9% to 13.7 ± 4.3%, p = 0.430 in the smoker group, respectively). Conclusion Oral cilostazol treatment significantly increased the vasodilatory response to reactive hyperemia in two groups. It can be used to improve endothelial function in the patients with endothelial dysfunction caused by cigarette smoking.

Significant left main coronary artery disease from iatrogenic dissection during coronary angiography

Though atherosclerotic obstruction is the major cause of the obstructive left main coronary artery (LMCA) disease, it can be associated with iatrogenic dissection during coronary angiography. Here we report a case with severe LMCA stenosis due to catheter induced dissection in a 77-year-old man which was detected 9 months later. By careful review of the angiogram had taken at 9 months ago, the LMCA was injured by the diagnostic left Judkins catheter during the first coronary angiography. The initial lesion was neglected and the dissection got worse with time. The patient was successfully treated with two drug-eluting stents by crushing technique and discharged without further complication.

Aortic intramural hematoma after thrombolysis in a patient with acute massive pulmonary embolism

To the Editor, Aortic intramural hematoma (AIH) is an acute aortic syndrome with no communication between the AIH and the aortic lumen [1]. One possible pathogenic mechanism is rupture of the vasa vasorum and hemorrhage into it. In this case report, we present a patient with acute massive pulmonary embolism (PE) who developed an AIH after thrombolytic therapy. In this patient, the AIH may have been a complication associated with thrombolysis. A 78-year-old woman was admitted to our emergency department complaining of dyspnea lasting 20 days. She had been medicated with oral antihypertensive drugs for 5 years. On admission, her blood pressure was 88/50 mmHg, and bilateral jugular venous engorgements were noted. An electrocardiogram revealed right bundle branch block, and the chest X-ray was normal. The echocardiogram taken in the emergency room showed a dilated right ventricle (RV) and marked RV dysfunction, with a D-shaped left ventricle. Spiral computed tomography (CT) of the chest demonstrated multifocal intraluminal filling defects in the distal main pulmonary artery, the truncus anterior, and proximal vascular dilatation in the lobar and interlobar arteries (Fig. 1). Figure 1 (A, B) Chest computed tomography reveals extensive intraluminal filling defects in the right main pulmonary artery. The lobar, interlobar, and segmental branches are consistent with acute pulmonary embolism (arrows). The patient was diagnosed with massive PE and was treated with intravenous recombinant tissue plasminogen activator (rt-PA, 100 mg for 2 hours). After thrombolysis, anticoagulation therapy with intravenous unfractionated heparin was continued. Her blood pressure increased with the treatment. However, the patient complained of severe epigastric pain about 10 hours after thrombolytic therapy. A follow-up CT scan revealed newly developed high-attenuation areas indicating eccentric mural thickening of the descending aorta, and she was diagnosed with acute Stanford type B AIH (Fig. 2). The CT scan also showed newly developed soft tissue swelling with high-attenuation nodular lesions in the left breast and axilla, consistent with subcutaneous hematomas. Figure 2 (A) Computed tomography (CT) performed on admission showed a normal descending thoracic aorta. However, newly noted eccentric mural thickening of the descending thoracic aorta was noted on the CT taken a day after thrombolytic therapy. (B) The thickening ... To avoid expansion of the AIH and hematoma, anticoagulation therapy was discontinued immediately, and a vena cava filter was inserted into the inferior vena cava. The patient was treated with intravenous labetalol followed by oral antihypertensives. The hematoma had nearly resolved on the follow-up CT scans taken 10 days after stabilization. We restarted anticoagulation after confirming that the AIH had improved. The patient was discharged without other complications. Thrombolysis or embolectomy is the treatment of choice in patients with RV dysfunction and shock associated with acute PE. In 2003, the Management Strategies and Prognosis of Pulmonary Embolism-3 Trial (MAPPET-3) group compared treatment with rt-PA plus heparin and heparin alone in a double-blind trial of 256 PE patients with RV dysfunction but without hypotension or shock. The MAPPET-3 trial found that rt-PA given with heparin improved the clinical course of these patients [2]. However, thrombolysis is also associated with a significant increase in the risk of fatal or disabling hemorrhagic complications [2]. In the International Cooperative Pulmonary Embolism Registry, in 2,454 consecutive patients with acute PE, the incidence of intracranial hemorrhage after thrombolytic therapy was about 3% [3]. However, there is no case report of AIH as a complication of thrombolytic therapy. Compared with classic aortic dissection, AIH is believed to involve hemorrhage into the medial layer of the aortic wall, in the absence of an intimal tear. There is some debate about the pathogenesis of AIH, although rupture of the vasa vasorum in the aorta is considered the most likely mechanism [1]. However, sporadic cases show accidental development of a typical AIH associated with percutaneous intervention, supporting the presence of a primary intimal-medial tear in AIH [4]. In this patient, the AIH developed after thrombolytic and anticoagulation therapy without aortic manipulation, suggesting that the pathogenic mechanism was rupture of the vasa vasorum. Treatment of an AIH in patients requiring anticoagulation therapy remains problematic, and there are no definitive data regarding the use of anticoagulants in these patients. Discontinuation of anticoagulants is common practice. In one report, by Canadas et al. [5], the continued use of anticoagulants was not associated with progression of AIH. However, only three patients were included, and one of them had been treated with stenting for the newly developed aortic dissection. We decided to discontinue the anticoagulant and insert a vena cava filter into the inferior vena cava. Because the AIH was confined to the descending aorta (Stanford type B), she was treated with antihypertensives. After medical stabilization, the maximal diameter of the AIH thickness decreased from 6.0 to 1.7 mm. Anticoagulation therapy was restarted after resolution of the AIH. In our case, Stanford type B AIH developed after use of a thrombolytic agent and anticoagulation therapy for the massive PE. The patient was treated successfully with medical stabilization, which included discontinuation of the anticoagulant therapy, insertion of a vena cava filter, and strict blood pressure control.