Stenting in acute coronary syndromes

The aim of this study was to assess Early and long-term outcome of intracoronary stent implantation for the treatment of acute coronary syndromes. Stenting has historically been contraindicated in thrombus containing lesion because of the risk of subacute thrombosis. With advance in stent implantation technique, and the recognition of the importance of adequate platelet inhibition, the incidence of subacute thrombosis has progressively fallen despite stenting in increasingly complex subset, inducing acute coronary syndromes and thrombus lader lesions. 50 patients with acute coronary syndromes who underwent coronary stenting where included in the study. According to medical history, resting 12 leads ECG, and serum cardiac enzymes, they were divided into 3 groups; the Q-wave Ml group, the non Q-Wave MI group, and the unstable angina group. All patients were treated with Aspirin, Ticlopidine and Heparin regimen. Through out the study period, 60 stents were successfully implanted in 50 patients [100%] success rate], with TIMI grade 3 restored in the whole study population. During hospitalization and at I month follow-up, there was no death, Q-wave MI or emergency CABG in the 3 groups. There was no major vascular complication but minor bleeding occurred in 16%. Late clinical follow up at a mean follow-up period of 6.3 +/- 1.02 months post coronary stenting showed that there was no death but there was 6% rate of Q-MI, 8% of elective bypass surgery and 8% repeated PCI for stented segments and 6%for non stented segment follow-up angiogram at a mean follow-up time of 6.1 +/- 0.5 stent restenosis rate was 19%. Stent implantation in acute coronary syndromes is associated with excellent early clinical outcome and good long-term results

Normalization of left ventricular systolic and diastolic asynchrony after valve replacement for aortic stenosis

The aim of the present study was to evaluate left ventricular wall thickness, systolic and diastolic asynchrony in pressure overload hypertrophy due to aortic stenosis. Twenty five patients were included in the present study. 15 patients with severe aortic stenosis were studied preoperatively as well as early [6 +/- 2 months] and late [36 +/- 12 months] after aortic valve replacement [AVR] using left ventricular biplane angiogram, high-fidelity pressure measurements and echocardiography. Ten normal subjects served as controls. LV systolic function was assessed from biplame ejection fraction and M-Mode echocardiography and diastolic function from the time constant of relaxation, the peak filling rate and the constant of myocardial stiffness. Non uniformity was evaluated. from the coefficient of variation of the time to end-systole [systolic asynchrony] and peak filling rate [diastolic asynchrony] of 12 regions in right and left anterior oblique projections. Ejection fraction was comparable in patients with aortic stenosis and in control, whereas preoperatively diastolic dysfunction with prolonged relaxation by cardiac catheterization and reversed E/A ratio as evidenced by echo-Doppler study was present in patients with aortic stenosis and was normalized late after AYR. Left ventricular hypertrophy also normalized late after AYR [36 months]. L Y systolic asynchrony was present [>2 SD of control] in ten patients and diastolic asynchrony in all patients [15] with aortic stenosis. Systolic asynchrony was normalized in most of our patients [14 of 15 patients] early as well as late after AYR. On the other hand, diastolic asynchrony was present early after AYR in all patients, although there was a significant improvement in comparison to the preoperative evaluation Late after AYR, there was a normalization of diastolic asynchrony in 14 out of 15 patients with aortic stenosis. Systolic asynchrony is normalized early after AYR probably due to reduction of file after load, whereas, diastolic asynchrony persists probably due to residual LV hypertrophy with myocardial stiffness and interstitial fibrosis. Late after AYR, diastolic asynchrony is normalized due to structural remodeling with regression of both myocardial hypertrophy and interstitial fibrosis