We cannot observe the LV thrombus even the patients with depressed LV function; however, we can observe the LV thrombus even the LV function was more improved in follow up echocardiography. The patient did not be followed by echocardiography during 10 days, so we cannot clarify when the LV thrombus was developed. The physicians have to keep in mind that frequent echocardiographic follow up should be needed in the cases with stress-induced selleck kinase inhibitor cardiomyopathy not only a period of markedly reduced LV function but also after clinically improvement. Although no specific data exist regarding the role of anticoagulation
in stress-induced cardiomyopathy, short-term Inhibitors,research,lifescience,medical anticoagulation therapy has been indicated as a treatment for patients with LV thrombus. Further
research is needed to determine the true incidence of LV thrombus and the role of short-term anticoagulant therapy in patients with stress-induced cardiomyopathy with LV thrombus.
A 42-year-old male visited our hospital with refractory hypertension. In the past, he has taken antihypertensive drugs for Inhibitors,research,lifescience,medical 2 months in spite of the hypertension diagnosed 16 years ago. He had taken hydrochlorthiazide 50 mg, carvedilol 25 mg, diltiazem 180 mg, and losartan 100 mg per day. He was Inhibitors,research,lifescience,medical alert and did not have an acute ill appearance. There were normal breathing sound in both lung fields and regular heart beats without murmur. We could not Inhibitors,research,lifescience,medical hear bruit on abdomen. The pulsation of the dorsalis pedis artery was weaker than that of the upper limb. His blood pressure (BP) was 208/122 mmHg at the upper extremities and 153/107 mmHg at the lower extremities. A simple chest X-ray showed cardiomegaly. An electrocardiography showed normal sinus rhythm with left ventricular hypertrophy. Inhibitors,research,lifescience,medical He was first diagnosed as dyslipidemia and type 2 diabetes in our hospital by laboratory exam. The results of erythrocyte sedimentation rate and C-reactive protein were 35 mm/hr and 3.3
mg/L. In the 2-D echocardiography, the left ventricular ejection fraction (LVEF) was 39% with global hypokinesia. LV mass index was 139.1 g/m2 and E/E’ was elevated to 24.11. The LV end-diastolic dimension PAK6 was 63 mm (Fig. 1A and D). There was accelerated abdominal aortic Doppler flow velocity with mosaic patterns in subcostal view, with a pressure gradient of 50 mmHg. A chest computed tomography (CT) angiography was checked to rule out the COA and revealed a stenosis of lower thoracic aorta at a diaphragmatic level (Fig. 2D). We also performed examination of other causes of secondary hypertension, but could not find other causes of high BP. The cardiac catheterization and stent implantation were planned. In the coronary angiogram, there was a significant stenosis in the proximal left coronary artery (LAD), the distal left circumflex artery (LCx) and chronic total occlusion in the distal right coronary artery (Fig. 3A and B).