Objective To analyze the relationship between polymorphism at the Apolipoprotein AI (Apo AI) gene and the risk for coronary artery disease. Methods A total of 107 patients (mean age 56 ± 11 years) diagnosed as having stable angina pectoris (SAP) (23 cases), unstable angina pectoris (UAP)(23 cases) or myocardial infarction (MI) (61 cases)were prospectively evaluated. DNA was obtained from the 107 patients and 50 controls. In order to determine the Apo AI genotypes at two polymorphic sites (G/A at -75 bp, and C/T at +83 bp), DNA was PCR amplified and digested with MspI. Results The frequency of carriers of the rare allele at the - 75 bp site (M1-) was 0.49 in cases and 0.30 in controls ( P＜ 0.05). The frequencies of the M 1 - allele among patients with SAP, UAP, MI and controls were 0. 37 (vs. Controls, P ＞ 0.05), 0. 54 (vs. Controls, P ＜0.05), 0.52 (vs. Controls, P＜ 0.05) and 0.30, respectively. The frequencies for carriers of the rare allele at the + 83bp polymorphism (M2) were observed among patients with SAP (0.09, vs. Controls, P ＞0.05), UAP (0. 11, vs. Controls, P ＞ 0.05) or MI (0.12, vs. Controls, P ＞ 0.05) and controls (0. 12).There was an slightly increase in the frequency of the M1 - allele in patients with SAP to UAP or MI (0.37vs. 0.54 vs. 0.52; all P ＞ 0.05) and M1 polymorphism as a risk factor for CAD (OR=3.74, P ＜0.05). In the + 83bp polymorphism there was no difference in the allelelic frequencies in cases and controls (0. 11 vs. 0. 12; P ＞ 0.05). There was no significant difference in the frequency of the M2- allele in patients with SAP to UAP or MI (0.09 vs. 0.11 vs.0. 12; all P ＞ 0. 05) and M2 polymorphism not as a factor for CAD ( OR = 0. 80, P ＞ 0. 05) Plasma lipoprotein values in patients with the allele M1 - and M2 - had no different levels than those homozygous for the M1+ andM2+ (P＞ 0.05). Conclusion M1polymorphism (M1 - ) may be as a risk factor for CAD and M2 polymorphism (M2 - ) not as a factor for CAD in Chinese Xinjiang Uygur and Han population.

Objective The coronary anatomic feature and development after thrombolysis in acute myocardial infarction (AMI) were studied.Mehtods 100 patients with AMI received urokinase and strepokinase. Coronary angiography (CAG) was performed at 90 minuts and again at 3 to 4 weeks.Results Successful thrombolysis occurred in 60 cases,but failed in 40. The ratio of reperfusion was 60％.CAG showed there were residual thrombi in 84 patients (84％) and complete coronary occlusion in 40(40％ ).Angiography at 3 to 4 weeks after thrombolysis showed the stenosis worsened in 8 patients and improved in 10.Conclusion AMI is caused by sudden coronary thrombotic occlusion and can be repeffused by using thrombolytic agent or mechanical methods. Thrombolytic agents usually can not resolve thrombi completely. So percutaneous transluminal coronary angiography (PTCA) is recommended as an important method to improve serious residual stenosis.

Ojbective To find the independent predictors for restenosis after coronary stenting.Methods Quantitative angiography was performed on 60 cases (67 successfully dilated lesions) after angioplasty over 6-months follow-up, and both univariate and multivariate logistic regression analysis were done to identify the correlations of restenosis with clinical factors. Results The total restenosis rate was 31.3％(21 of 67 lesions), and according to univariate analysis the patients who underwent coronary stenting ≥3.5mm had a lower rate of restenosis ( P ＜ 0. 01).Collateral circulation to the obstruction site, high maximal inflation pressure, smoking and the less minimal lumen diameter after PTCA made the rate of restenosis higherower ( P ＜ 0.05) . Multivariate logistic regression analysis showed that coronary stenting ≥ 3.5mm had a low rate of restenosis, but high maximal inflation pressure and smoking made the restenosis rate higher. Conclusion Coronary stent size, maximal inflation pressure and. smoking were independent predictors for restenosis.

6 371 cases of acute myocardial infarction from 1984 to 1992 in Guangdong Province are reported in this article. The results show that the prevalence rate of acute myocardial infarction (AMI)has been increasing. The anterior walls are involved more often than the inferior ones are. The first symptom in 87.4％ of cases is pectoral pain. The most common complications are arrhythmia, heart failure and cardiac shock successively occurring in order. The mortality rate is 19.9％. The predominant causes of death is pump failure.

Object Diastolic function' s assessment is vital in order to produce information relevant to patients' functional class, management and prognosis. We sought to investigate diastolic dysfunction in essential hypertension (EH) with or without coronary heart disease (CAD) using color M- mode Doppler echocardiography and to study the relation between diastolic dysfunction and left ventricular mass index (LVMI) and geometry of LV, and to demonstrate partly the cause of increased cardiovascular risk of an echocardiographic pattern of LV geometry. Methods 36 normal subjects (Group Ⅰ) and 107 patients with essential hypertension (Group Ⅱ) were studied using color M- mode Doppler echocardiography. Four different LV anatomic adaptation to hypertension were identified by categorizing patients according to values of end-diastolic relative wall thickness (RWT) and LVMI. We measured the rate of propagation of peak early filling flow velocity (Vp), time delay (TD) of the peak early filling flow velocity from mitral tips to the apex and Vp/E. Results The geometry of LV was classified into four types according to the LVMI and RWT. The normal limits of LVMI and RWT were obtained from the upper limits of the 95 % confidence interval from mean of LVMI and RWT in healthy control group respectively, which were 115.2 g/m2 and 0.44. The definition of each type was as follows: Type Ⅰ (normal group): LVMI ≤ 115.2 g/m2 and RWT ≤0.44; Type Ⅱ (concentric remodeling): LVMI ≤115.2 g/m2 and RWT ＞ 0.44; Type Ⅲ (eccentric hypertrophy): LVMI＞ 115.2 g/m2 and RWT ≤0.44; Type Ⅳ (concentric hypertrophy): LVMI ＞115.2 g/m2 and RWT ＞ 0.44. Most parameters of diastolic function in each geometry type differed significantly from those in the control group, but the dif ference among each geometry type was not significant.When compared with type Ⅰ, there was a tendency thatTD was longer and Vp/E smaller in Type Ⅱ, Ⅲ and Ⅳgroups. The correlation between LVMI and Vp and TD had statistical significance (P ＜ 0. 01); the correlation coefficients were - 0. 21 and 0. 29, respectively.Conclusions There is diastolic dysfunction in different LV geometry in patients with essential hypertension, even in patients with LV normal geometry there is diastolic dysfunction. LVMI has negative correlation to Vp, and positive correlation to TD. It may indicate that the greater the LVMI is, the worse the LV diastolic function.

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.