Objective To retrospectively study clinical features and diagnostic imaging of vasculogeneic pulsatile tin-nitus, and the feasibility and efficacy of transvascular interventional treatment for this condition. Methods Data from 82 cases of arterial or venous pulsatile tinnitus were reviewed. DSA characteristics and possible pathophysiological mechanisms of pulsatile tinnitus in these cases were studied. Diagnoses in this group in-cluded intracranial arterovenous fistula (AVF) (n=3), spontaneous skull base dural AVF (n=16), traumatic ca-rotid-cavernous sinus fistula (n=5), subclavian artery stenosis (n=2), internal carotid artery stenosis (n=3), in-tracranial arterial stenosis (n=1), kinked and/or elongated vertebrobasilar artery (n=2), venous sinus divertic-ulum (n=2), venous sinus stenosis on the dominant drainage side (n=46) and occipital sinus stenosis (n=2). Treatments included embolization and stenting using coils, NBCA glue, Balt balloons, self-expansion stents and intracranial micro-stents via either the femoral artery or femoral vein. Results Procedures were suc-cessful in all cases with no surgery-related complications. Tinnitus disappeared within 2 days after the pro-cedure in all cases. Follow up duration was 5-36 months. Recurrence occurred in 4 cases of arterial tinnitus within 3 months following the initial procedure, which improved after revision embolization or symptom management. There was no recurrence in venous tinnitus cases following stent plastic or stent-coiling embo-lization treatments. Conclusions Endovascular intervention provides a new approach to the diagnosis and treatment of intractable pulsatile tinnitus. It is also effective in differentiating and studying other types of tinnitus.

Objective To observe the relationship between serum creatine kinase isoenzyme MM sub-bands (CKMM3/MM1 ratio) and the gradation of coronary stenosis and provide a simple, reliable, and economical method for identifying high-risk unstable angina pectoris (UAP). Mehtods Blood samples were drawn at different time after onset of chest pain in 21 patients with UAP and only once in 20 each volunteers for control. CKMM3/MM1 ratio was detected by nonserial buffer agarose gel electrophoresis. CKMB and CK were observed by velocity method. An emergent coronary arteriography was performed as soon as patients were admitted into hospital. Results Patients with UAP were divided into two subgroups:patients with elevated serum enzyme [P( + )] and patients with normal serum enzyme [P( - ) ] according to CKMM3/MM1 ratio ＜ 0.5. Patients with UAP(+)had higher serum CKMM3/MM1 ratios from 0.5 to 12hrs and serum CKMB from 2 to 12 hrs than those with UAP( - ) and control ( P ＜ 0.05) . Serum enzyme concentrations of patients with UAP whose coronary lumen had 90％ or more than 90％ stenosis were significantly higher than those whose coronary lumen had less than 90％ stenosis (P＜0.01) . AnyCKMM3/MM1 ratio was less than 1.0 and CK within the normal range in patients with UAP( + ) group. Conclusions CKMM3/MM1 ratios in patients with UAP can reflect severity of myocardial ischemia. Serum CKMM3/MM1 ratio provides a simple, reliable, and economical method for identifying high-risk UAP.

Objective To determine whether successful valvuloplasty causes an increase of mitral valve area reserve in patients with mitral stenosis, isoproterenol stress echocardiography was used to compare mitral valve area and hemodynamic changes between pre- and post- valvuloplasty under conditions of increased cardiac work. Methods Thirtyeight patients with pure rheumatic mitral stenosis who had received successful percutaneous balloon valvulo plasty underwent isoproterenol stress echocardiography pre- and post- valvuloplasty. Mitral valve area (by direct planimetry of two- dimensional echocardiography), mean transmitral pressure gradient (by continuous-wave Doppler echocardiography), and cardiac output (by M -mode echocardiography) were measured at rest and under isoproterenol stress to achieve heart rate of different stages. Results Mitral valve area (0. 91± 0. 28 to 1. 87±0.23cm2, P ＜0.01), mean transmitral pressure gradient ( 12.5 ± 6. 3 to 3.9 ± 1.9mmHg, P ＜ 0.01 ) and cardiac output (3.93 ± 1.44to 4. 73 ± 1.01 L/min, P ＜ 0.05) at rest between pre - and post -valvuloplasty were significantly different.Pre-valvuloplasty, as heart rate increased under stress, mean transmitral pressure gradient increased significantly ( P ＜ 0.01 ), but there were no significant differences in the measurements of mitral valve area and cardiac output (both P ＞ 0.05). In contrast, as heart rate increased post- valvuloplasty, there was a significant increase in mean transmitral pressure gradient (P ＜ 0.01), but both mitral valve area and cardiac output further increased significantly (both P ＜ 0. 01) . Moreover, valvuloplasty decreased mean transmitral pressure gradient at peak heart rate from 23.0 ± 4. 5 to 7.75 ± 2.30 mmHg ( P ＜ 0.01 ) under submaximal stress. Conclusions Successful percu taneous balloon valvuloplasty soon causes a significant increase of mitral valve area reserve in patients with mitral stenosis, which is markedly manifested under conditions of hemodynamic stress. Stress echocardiography provides a safe, feasible and non-invasive means of assessing this reserve capacity.