[Cross sectional study of familial hypercholesterolemia in dyslipidemia patients receiving lipid-lowering therapy: DYSIS-China subgroup analysis].

Objectives: To analyze the incidence, blood lipid levels and cardiovascular disease of familial hypercholesterolemia (FH) in dyslipidemia patients receiving lipid-lowing therapy from the DYSIS-China. Methods: Dyslipidemia International Study-China (DYSIS-China) database was re-analyzed according to the criteria of "Chinese guidelines for prevention and treatment of dyslipidemia in adults-2016 version". DYSIS-China database included 25 317 dyslipidemia out-patients who received at least one lipid-lowering drug for at least three months. All the patients were divided into three groups: unlikely HF, possible FH and definite FH according to the Dutch Lipid Clinic Network diagnostic criteria. Age, gender, lipids levels, drug use and complications were compared among the three groups. Factors were compared between Possible FH group and definite FH group in terms of age stratification. Results: A total of 23 973 patients with dyslipidemia were included. The average age was (64.8±9.9) years, 11 757 patients were females (49.0%). The proportion of unlikely FH in the total population was 20 561 (85.7%), possible FH was 3294 (13.7%), and the definite FH was 118(0.5%). Patients in the definite FH group (58.3±8.5 years) was younger than in unlikely HF(65.3±9.8 years) and possible FH(61.8±9.9 years) group. LDL-C ((5.6±1.9) mmol/L) levels were significantly higher in definite FH group than in unlikely HF ((2.5±0.9) mmol/L) and possible FH ((4.3±1.0) mmol/L) group. TC ((7.4±1.8) mmol/L) levels were also significantly higher in definite FH group than in unlikely HF ((4.3±1.0) mmol/L) and possible FH ((6.0±1.0) mmol/L) group. Percent of female sex, sedentary lifestyle and systolic blood pressure value were significantly higher in definite FH group than in other two groups (all P<0.05). Statin use was similar among the 3 groups. Prevalence of ischemic cardiomyopathy (70(59.3%)) was significantly higher in the definite FH group than in unlikely FH group7519 (36.6%) and possible FH group1149 (34.9%). The rate of hypertension (82 (69.5%)) was also significantly higher in the definite FH group than in unlikely FH group (2 063 (62.6%) and in possible FH group (13 928 (67.7%)). The possible FH group had the highest proportion of patients aged 55-64 years (1 146 (34.8%)), and the prevalence of hypertension 358 (76.8%), diabetes 189 (40.6%), ischemic heart disease 186 (39.9%), cerebrovascular disease 149 (32.0%) and heart failure 28 (6.0%) was the highest in patients over 75 years old. The definite FH group had the highest proportion of patients aged 55-64 years (49 (41.52%)), and the prevalence of ischemic heart disease (70 (59.3%)) was the highest in patients aged 45-54 years old group, there was no significant difference in the prevalence of diabetes,hypertension,heart failure,peripheral artery disease and cerebrovascular disease among different age groups. Conclusion: The detection rate of FH in Chinese patients with dyslipidemia is not low, the blood lipid level is poorly controlled, and the risk of cardiovascular disease is high in Chinses FH patients.

[Efficacy and safety analysis of ivabradine hydrochloride treatment of Chinese patients with chronic heart failure: subgroup analysis of Chinese patients in the SHIFT study].

Objective: To evaluate the efficacy and safety of ivabradine for the treatment of Chinese patients with chronic heart failure based on the Chinese subgroup data of the systolic heart failure treatment with the I(f) inhibitor ivabradine trial (SHIFT). Method: A total of 6 558 stable outpatients who presented symptoms of heart failure, with a left ventricular ejection fraction (LVEF) ≤35%, sinus rhythms with a heart rate ≥70 bpm participated in the randomized, double-blind, placebo-controlled, international multicenter clinical study.The subset of Chinese patients with heart rate ≥75 bpm was enrolled in the post-hoc subgroup analyses.Patients were randomly allocated by computer-generated assignment through a telephone interactive voice response system to ivabradine group (starting dose 5 mg bid, which was then uptitrated to the maximum 7.5 mg bid) or matched placebo group.The clinical baseline characteristics of participants were obtained and analyzed.The primary outcome endpoint was a composite endpoint of cardiovascular death or hospitalization resulting from worsening HF.The primary safety endpoint included total incidence of adverse events during the study, bradycardia, and adverse visual reaction (phosphenes). Results: A total of 49 Chinese centers enrolled a total of 225 patients with chronic heart failure, of whom, 106 patients were randomized to the ivabradine group and the other 119 patients to the placebo group, and the mean follow-up time was (15.6±5.1) months.By the end of the study, mean heart rate (71.0 bpm vs. 80.3 bpm, P<0.05) and incidence of the primary endpoint events (18.9% (20/106) vs. 31.9%(38/119), HR=0.56, 95%CI 0.33-0.97, P=0.039) were significantly lower, while the percentage of patients with improvement in heart functional class NYHA (53.8% (56/106) vs. 34.5% (41/119), P=0.006 1) was significantly higher in the ivabradine group than in the placebo group.The total number of adverse events (129 events, 49.6% PY) in the ivabradine group was lower than that in the placebo group (203 events, 50.8% PY). In the ivabradine group and the placebo group, there were respectively 2 patients (1.9%) and 0 patients experienced bradycardia, 3 patients (2.9%) and 1 patient (0.8%) experienced adverse visual reaction (phosphenes). Conclusions: Ivabradine significantly reduced heart rate and improved the clinical outcomes and NYHA function class in Chinese patients with chronic heart failure, these beneficial effects are achieved without inducing remarkable adverse reactions.The results of Chinese subgroup analysis were thus consistent with the overall results of the SHIFT study. Clinical Trial Registry: International standard randomized controlled trials registry, ISRCTN 70429960.

[Status of cholesterol goal attainment for the primary and secondary prevention of atherosclerotic cardiovascular disease in dyslipidemia patients receiving lipid-lowering therapy: DYSIS-China subgroup analysis].

OBJECTIVE: To analyze the current status of cholesterol goal attainment for the primary and secondary prevention of cardiovascular disease in dyslipidemia patients using data from the DYSIS-China study. METHODS: Based on criteria defined in the 2014 China Cholesterol Education Program (CCEP) and the 2007 Chinese guidelines for the prevention and treatment of dyslipidemia in adults, 25 317 dyslipidemia patients enrolled in the DYSIS-China study (from March 2012 to October 2012) were stratified to the atherosclerotic cardiovascular disease(ASCVD) primary prevention and secondary prevention groups. The total cholesterol (TC) target goals were <3.11, 4.14, 5.18, and 6.22 mmol/L, respectively, and the low-density lipoprotein cholesterol (LDL-C) therapeutic goals were less than 1.8, 2.6, 3.4, and 4.1 mmol/L, respectively, for the very high-risk, high-risk, moderate-risk, and low-risk patients in the primary prevention group. The TC targets for the very high-risk and high-risk patients were <3.11 and <4.14 mmol/L, respectively, and the LDL-C targets were <1.8 and <2.6 mmol/L, respectively, in the secondary prevention group. The TC and LDL-C goal attainment rates were calculated for the different risk groups according to the targets values. RESULTS: Totally, 71.09% (n=18 000) of the dyslipidemia patients were grouped into very high and high risk groups, 51.76% (n=13 104) and 48.24% (n=12 213) patients were stratified to primary and secondary prevention of ASCVD. The LDL-C and TC goal attainment rates for the secondary prevention group were 33.09%(4 041 cases) and 21.05% (2 571 cases), respectively. The LDL-C and TC goal attainment rates for the primary prevention group were 52.40% (6 866 cases) and 42.06% (5 511 cases), respectively. Multivariate logistic regression analysis showed that diabetes mellitus(OR=5.75, 4.15, P<0.05), coronary heart disease(OR=5.70, 3.58, P<0.001), and peripheral arterial disease(OR=2.42, 1.49, P<0.05) were risk factors for failure to achieve TC and LDL-C goals, respectively. CONCLUSIONS: Despite the widespread application of the 2014 CCEP and 2007 Chinese dyslipidemia guidelines, LDL-C goal attainment among secondary and primary prevention patients remains suboptimal in China. More rigorous guideline adherence is therefore required to increase the LDL-C and TC goal attainment rates and improve the long-term cardiovascular outcomes in Chinese dyslipidemia patients.

[Decline of ATP-binding cassette transporter G1 expressions with a liver X receptor-independent pathway in patients with type 2 diabetes].

OBJECTIVE: To examine the cholesterol efflux and the expressions of ATP-binding cassette transporter G1 (ABCG1) in macrophages of diabetic patients and the roles of liver-X receptor (LXR) in regulation of ABCG1 expressions. METHODS: Blood was collected from patients with type 2 diabetes mellitus and healthy controls. The peripheral blood monocytes were differentiated into macrophages with macrophage colony stimulating factor (M-CSF). The cells were radio labeled with [(3)H] cholesterol and were performed with cholesterol efflux assays. Quantitative real-time PCR (qRT PCR) and Western blot were performed to measure the mRNA and protein expressions of ABCA1 and ABCG1. To test the effects of LXR on ABCG1 expressions, inhibition of LXRα and LXRß by siRNA were performed. The DNA-protein complex of LXR and LXR element (LXRE) located in the promoter region of ABCG1 gene were detected with electrophery mobility supershift assay (EMSA). RESULTS: Macrophage ABCG1 expressions and high-density lipoprotein (HDL) induced cholesterol efflux were significantly reduced (19.0%±1.2% vs. 12.8%±3.6%, t=2.532, P=0.016) in the diabetic subjects whereas ABCA1 expressions and apolipoprotein A1 (ApoA1) induced cholesterol efflux were comparable (12.0%±1.2% vs. 10.2%±2.3%, t=1.771, P=0.109) between the diabetic patients and healthy subjects. The mRNA expressions of LXRα and LXRß had no changes between the diabetes subjects and healthy controls (t=1.025, P=0.315; t=-0.531, P=0.600). The LXR-LXRE DNA-protein complex detected by EMSA were also similar between the diabetes subjects and healthy controls (t=1.483, P=0.164). Moreover, ABCG1 expressions were not altered by inhibition of LXRα/ß siRNA (t=2.143, P=0.061). CONCLUSION: Our data indicated that expression of ABCG1 and HDL induced cholesterol efflux were reduced in type 2 diabetic patients. However, the LXR mRNA expression and binding complex of LXR and ABCG1 promoter were not changed. The impairment of cholesterol efflux and ABCG1 gene expressions might be regulated via an LXR-independent pathway.

The clinical characteristics and outcome of intracardiac thrombus and aortic valvular involvement in Behçet's disease: an analysis of 20 cases.

OBJECTIVES: To assess the clinical characteristics and outcome of patients with cardiac Behçet's disease(BD). METHODS: Medical charts of 20 cardiac BD patients admitted in Peking Union Medical College Hospital from June 1996 to June 2011 were systematically reviewed, including demographic data, clinical features, laboratory and histopathology findings and outcome. RESULTS: Patients age ranged 19~57 yrs[mean (35±10) yrs], included 17 males and 3 females. Six (30%) of them did not fulfill the ISG criteria at cardiac onset, and fourteen (70%) of them experienced heart failure. Echocardiography findings included intracardiac thrombus (n=7), and aortic valve involvement with left ventricular enlargement and severe aortic regurgitation (n=13). Eight patients underwent surgery before efficient immunosuppressant treatment, and five (62.5%) underwent re-operation due to recurrence of thrombus or valvular dehiscence and severe paravalvular leakage. Histopathology findings revealed predominantly inflammatory cells infiltration, thrombus and fibrous tissue formation. After initiation of prednisone plus immunosuppressant, patients were followed up for 6~42 months (mean 14.8±9.9 months), the intracardiac thrombus disappeared or decreased in size in five cases, remained stable after surgery in the other two cases, and the heart failure disappeared in all patients with aortic involvement. CONCLUSIONS: Cardiac BD affects males more than females, and is prone to delayed diagnosis because some patients do not have typical clinical manifestations at cardiac onset; Corticosteroids plus immunosuppressants reduce the thrombus and improve aortic regurgitation and heart failure in cardiac BD, whereas surgery alone does not lead to complete resolution.

Study of ATP-binding cassette transporter A1 (ABCA1)-mediated cellular cholesterol efflux in diabetic golden hamsters.

The effects of cyclic adenosine monophosphate (cAMP) and atorvastatin on macrophage adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux were investigated in a diabetic animal model. Golden hamsters were fed a high-fat diet which resulted in insulin resistance. Diabetes was induced by a single intraperitoneal injection of streptozotocin (30 mg/kg). Normal golden hamsters were used as controls. Peritoneal macrophages were incubated with apolipoprotein A-1 (apoA-1), 8-bromoadenosine-3',5'-cyclic monophosphate (8-br-cAMP), and atorvastatin in vitro. Intracellular cholesterol accumulation was greater in the diabetic animals than in the insulin-resistant animals. Expression of ABCA1 mRNA in macrophages from diabetic animals was upregulated by 8-br-cAMP and atorvastatin. ApoA-1 caused a time-dependent cellular cholesterol efflux. Both atorvastatin and 8-br-cAMP significantly facilitated ABCA1-mediated cellular cholesterol efflux, with the maximal cholesterol efflux rate observed in the macrophages from diabetic animals. Accumulation of cholesterol in the macrophages of diabetic animals can be significantly alleviated by atorvastatin or 8-br-cAMP through improving ABCA1-mediated cellular cholesterol efflux.

Effects of high-volume continuous hemofiltration on experimental pancreatitis associated lung injury in pigs.

OBJECTIVE: To investigate the effect of high-volume continuous hemofiltration on experimental pancreatitis associated lung injury (PALI) in pigs. METHODS: Animals had severe acute pancreatitis (SAP) induced by intraductal injection of sodium taurocholate and trypsin and were randomly assigned to three groups: 1) Controls, 2) Low-volume (LV) (20 ml/kg/h) continuous venovenous hemofiltration (CVVH) and 3) High-volume (HV) (100 ml/kg/h) CVVH at the onset of the induction of SAP. Systemic and pulmonary hemodynamic index were monitored intermittently. At the same time, arterial oxygen tension (PaO 2 ), cytokines and activated NF- ê B levels of peripheral blood mononuclear cell were measured. After the animals died, the degree of microscopic lung injury was judged and scored. RESULTS: The median survival times of control, low-volume and high-volume groups were respectively 41 h, 50 h and 65 h. Temperatures in high-volume CVVH group were more steady than in control and LV CVVH groups (p<0.01). MPAP was significantly decreased by 4-5 mmHg in the HV CVVH group after 12 h of treatment. PaO(2) was significantly higher in HV group than in LV group at 6 h , 12 h, 24 h and 48 h (p<0.01). HV CVVH resulted in significant reductions not only in interstitial edema and atelectasis but also hemorrhages, hyaline membranes, microthrombi and total lung injury histology score. Plasma cytokines in the high-volume group were significantly lower than in the LV and control groups. In the HV group, the expression of NF- ê B activation at 6 h, 12 h and 24 h was lower than in the control and LV groups respectively. CONCLUSION: CVVH can reduce pulmonary edema and the severity of PALI in pigs with high-volume CVVH being significantly better than low-volume CVVH. The beneficial effects of CVVH on arterial oxygenation and pulmonary function may be connected with improvements in systemic hemodynamics, reduction in plasma cytokine concentration and decreased activity of NF- ê B in peripheral blood mononuclear cells.

Isradipine improves endothelium-dependent vasodilation in normotensive coronary artery disease patients with hypercholesterolemia.

OBJECTIVE: The dihydropyridine calcium antagonist isradipine has anti-atherosclerotic effects in animals and improves endothelium-mediated nitric oxide (NO)-dependent vasodilation in vitro. As improved endothelial function may be beneficial we investigated its effects in patients with a high likelihood of endothelial dysfunction. DESIGN: Thirty patients (two female, age 55.4 +/- 10.5 years) with known coronary artery disease and elevated (> 6 mmol/l) total cholesterol (cholesterol: mean 6.7 +/- 0.78 mmol/l) or a cholesterol/high density lipoproteins (HDL) ratio of > 5 not on lipid lowering therapy, participated in the study. Endothelial vasodilator function was assessed before and after double-blind, randomized administration of isradipine 5 mg/day or placebo for 3 months. METHODS: Endothelial function was assessed as forearm blood flow (FBF, venous occlusion plethysmography) responses to graded brachial artery infusions of acetylcholine (Ach), to the NO-synthase blocker NG-monomethyl-L-arginine (L-NMMA) and to the endothelium-independent vasodilator sodium nitroprusside (SNP). Blood pressure was measured either directly from the brachial arterial or by sphygmomanometer during clinic visits. RESULTS: Blood pressure was unchanged in both groups after 3 months (isradipine: 88.8 versus 92.1 mmHg; placebo: 81.0 versus 82.5 mmHg; NS) but cholesterol levels decreased similarly in both groups (isradipine: 6.7 versus 6.1 mmol/l, NS; placebo: 6.6 versus 5.9 mmol/l, P< 0.05). The vasodilator response to SNP and the decrease in FBF in response to blockade of NO synthesis by L-NMMA were unchanged in both groups. However, isradipine, but not placebo, enhanced the NO-dependent vasodilator response to Ach (P < 0.05). CONCLUSION: Isradipine improves acetylcholine-mediated vasodilation in hypercholesterolemic patients independent of changes in lipids or blood pressure.

Systemic, pulmonary, and renal hemodynamic effects of endothelin ET(A/B)-receptor blockade in patients with maintained left ventricular function.

Endothelin-1 (ET-1) regulates vascular tone in congestive heart failure and modulates renal function. Its role in patients with normal left ventricular (LV) function and its renal effects are unclear. Cardiac and renal hemodynamics were studied in 24 patients with normal LV function and coronary arteries after single-dose, double-blind, randomized administration of TAK-044 (25, 50, or 100 mg, i.v.), an ET(A/B)-receptor antagonist, or placebo. Hemodynamics were monitored using Swan-Ganz and arterial catheters, and ET levels were measured. Renal function was assessed by clearance techniques. In the absence of a dose-response relation, TAK-044 patients were analyzed as a single group. Most hemodynamic effects occurred during the first 4 h. TAK-044 reduced mean arterial (-9.3 mm Hg, p < 0.001), pulmonary (-1.8 mm Hg, p = 0.01), and pulmonary capillary wedge pressure (-1.6 mm Hg, p < 0.001) between 30 min and 4 h. Mean reduction in systemic vascular resistance was 279 dyne/s/cm2 (p < 0.001), whereas heart rate increased 6.1 beats/min (p < 0.001) and cardiac index by 0.37 L/m2 (p = 0.01). Stroke volume index, right atrial pressure, and pulmonary vascular resistance did not change. TAK-044 increased renal plasma flow in proportion to the increase in cardiac output (+119 ml/min, 4 h after TAK-044; p < 0.05) and ET-1 levels (2.5-fold; p < 0.05). No serious side effects were noted. In patients with normal cardiac function, ET-receptor blockade causes vasodilation and reduces systemic but not pulmonary vascular resistance and increases cardiac index and renal plasma flow.

Cyclosporine A and control of vascular tone in the human forearm: influence of post-transplant hypertension.

OBJECTIVE: The use of cyclosporine A after organ transplantation is associated with a high incidence of hypertension, but the underlying mechanisms for this process are not clear. We investigated the effects of blockade of basal release of endothelial nitric oxide and the effects of endothelium-independent and -dependent vasodilators and vasoconstrictors in patients treated with cyclosporine A after heart transplantation. DESIGN: We measured blood pressure and forearm blood flow responses to brachial artery infusions of NG-monomethyl-L-arginine (L-NMMA), sodium nitroprusside, acetylcholine, norepinephrine and vasodilating and vasoconstricting doses of endothelin-1 in eight patients early (< 3 months) and in 11 patients late (> 18 months) after transplantation. RESULTS: Diastolic blood pressure was higher late after transplantation, but calculated forearm vascular resistance was lower (P < 0.01). Thus, increased forearm vascular resistance does not contribute to the increase in blood pressure. The vasoconstrictor response to L-NMMA was similar in both groups but a reduced endothelium-dependent vasodilator response to acetylcholine was seen late after transplantation. However, impaired smooth muscle responsiveness to nitric oxide may have contributed to this finding, since the response to sodium nitroprusside tended to be reduced. Vasoconstrictor responses to norepinephrine and endothelin-1 were comparable but no vasodilation was seen with low doses of endothelin-1 late compared with early after transplantation (P < 0.05). CONCLUSIONS: The findings in the forearm circulation question the concept of generalized increases in vasoconstrictor responses or a disturbance of tonic, basal release nitric oxide in the pathogenesis of cyclosporine-A-induced hypertension. Although the forearm vasodilator responses to the stimulation of endothelial nitric oxide production and release by acetylcholine, and to low doses of endothelin-1, were impaired, these findings could be explained by the increase in blood pressure rather than cyclosporine A itself.

Short-term oral endothelin-receptor antagonist therapy in conventionally treated patients with symptomatic severe chronic heart failure.

BACKGROUND: The vasoconstrictor peptide endothelin-1 (ET-1) is important for increased vascular tone in patients with chronic heart failure, but the effects of endothelin-receptor blockade in addition to conventional triple therapy are unknown. METHODS AND RESULTS: Thirty-six men (mean age+/-SD, 55+/-8 years) with symptomatic heart failure (NYHA class III; left ventricular ejection fraction, 22.4+/-4.5%) despite treatment with diuretics, digoxin, and ACE inhibitors received, in a double-blind and randomized fashion, either additional oral bosentan (1.0 g BID; n=24) or placebo (n=12) over 2 weeks. Hemodynamic and hormonal (plasma ET-1, norepinephrine, renin activity, and angiotensin II) measurements were obtained before and repeatedly for 24 hours after administration of bosentan on days 1 and 14. Bosentan was discontinued in 1 patient with symptomatic hypotension, and 2 patients (bosentan group) declined hemodynamic investigations on day 14. Compared with placebo, bosentan on day 1 significantly decreased mean arterial pressure (difference from baseline over 12 hours [95% CIs], -13.9% [-16.0% to -11.7%]), pulmonary artery mean (-12.9% [-17. 4% to -8.3%]) and capillary wedge (-14.5% [-20.5% to -8.5%]) pressures, and right atrial pressure (-20.2% [-29.4% to -11.0%]). Cardiac output increased (15.1% [10.7% to 19.7%]), but heart rate was unchanged. Both systemic (-24.2% [-28.1% to -20.3%]) and pulmonary (-19.9% [-28.4% to -11.4%]) vascular resistance were reduced. After 2 weeks, cardiac output had further increased (by 15. 2% [10.8% to 19.6%]) and systemic (-9.3% [-12.3% to -6.4%]) and pulmonary (-9.7% [-16.3% to -3.1%]) vascular resistances further decreased compared with day 1. Heart rate remained unchanged. Plasma ET-1 levels increased after bosentan, but baseline levels of the other hormones were unchanged. CONCLUSIONS: Additional short-term oral endothelin-receptor antagonist therapy improved systemic and pulmonary hemodynamics in heart failure patients who were symptomatic with standard triple-drug therapy. Further investigations are warranted to characterize the effects of long-term endothelin-receptor antagonist therapy on symptoms, morbidity, and mortality in such patients.

Acute cardiovascular effects of insulin-like growth factor I in patients with chronic heart failure.

Insulin-like growth factor I (IGF-I) enhances myofibrillar development in cardiomyocytes of rats in culture and in vivo. In addition, IGF-I has vasodilatory effects and improves cardiac function in healthy volunteers. This study was conducted to evaluate the acute hemodynamic effects of IGF-I in patients with chronic heart failure Eight patients with chronic heart failure were randomized to receive recombinant human IGF-I (60 micrograms/kg) or placebo, i.v., over 4 h in a cross-over, double blind study on 2 consecutive days. Electrocardiogram as well as systemic hemodynamics were continuously monitored over 7 h by flow-guided thermodilution and radial artery catheters. IGF-I was well tolerated by all patients, and no pathological changes on electrocardiogram were recorded. Compared with placebo, IGF-I increased the cardiac index by 27 +/- 3.7% (+/- SE; P < 0.0005) and the stroke volume index by 21 +/- 5.6% (P < 0.05), and decreased systemic vascular resistance by 28 +/- 4.4% (P < 0.0002), right atrial pressure by 33 +/- 9.0% (P < 0.003), and pulmonary artery wedge pressure by 25 +/- 6.1% (P < 0.03). Mean systemic and pulmonary artery pressure as well as heart rate and pulmonary vascular resistance were not significantly influenced by IGF-I treatment. Insulin and C peptide levels were decreased by IGF-I, whereas glucose and electrolyte levels remained unchanged. Urinary levels of norepinephrine decreased significantly (P < 0.05) during IGF-I infusion. Thus, acute administration of IGF-I in patients with chronic heart failure is safe and improves cardiac performance by afterload reduction and possibly by positive inotropic effects. Further investigations to establish whether the observed acute effects of IGF-I are maintained during chronic therapy appear to be warranted.

[Changes in the clinical features of infective endocarditis in recent decade].

In order to know whether there are changes of the clinical features of infective endocarditis (IE) in recent decades, 66 cases of IE diagnosed from 1983 to 1992 were included in this study and compared with the IE patients of Beijing area from 1948 to 1963. The results showed the following changes in the recent decade: 1. Rheumatic heart diseases accounted for less and congenital heart diseases more of the proportion of IE cases when compared with materials of previous decades. Idiopathic mitral valve prolapse and valvular degeneration were found in some of the patients. 2. Cardiac operation and catheterization induced IE became more common, whereas oral infection incited IE less. 3. Skin lesion got much less so that the clinical manifestations of IE were atypical. 4. Hospital mortality decreased markedly.

[The evaluation of thrombolytic effect of snake venom antithrombus enzyme in treatment of acute myocardial infarction].

To evaluate the thrombolytic effect of Snake Venom Antithrombus Enzyme (SVATE) in the treatment of early acute myocardial infarction (AMI), 52 cases with AMI were randomly allocated to three groups, control (22 cases), SVATE (15 cases), and Urokinase (15 cases). The results show that SVATE can inhibit platelet aggregation, activate slightly fibrinolytic system and decrease markedly plasma fibrinogen level. However, the thrombolytic effect of SVATE in early treatment of AMI is not ideal, it can be used in combination with effective thrombolytic drugs to prevent reocclusion and reinfarction in AMI.

[The effect of low dose aspirin on the platelet function in patients with acute myocardial infarction].

To assess the appropriate dose of aspirin in the treatment of patients with acute myocardial infarction (AMI), 60 cases of AMI were randomized into 2 groups, 30 cases each; one with conventional therapy, another with conventional therapy combined with daily oral aspirin 100mg. The second group was further divided into subgroup I with serum peak CK < 1000 U/L and subgroup II with serum peak CK > 1000U/L. The parameters of platelet function including plasma TXB2, TXB2/6-keto-PGF1 alpha, platelet aggregation induced by 5-HT and epinephrine were studied on different days for 3 weeks. The results revealed that there was a successful inhibition of platelet function as assessed by significant decrease of plasma TXB2 and TXB2/6-keto-PGF1 alpha ratio and inhibition of platelet aggregation in the subgroup I, but little effect on subgroup II. It is shown that in the treatment of AMI, a daily dose of 100mg of aspirin is insufficient for severe cases, and according to the observation in ISIS-2 study, a daily dose of aspirin around 160mg may be appropriate.

[The effect of indapamide on plasma prostaglandins in hypertensive patients].

After two weeks' treatment of indapamide (2.5 mg/d) in 30 cases of mild to moderate hypertensive patients, there was a significant decline of systolic and diastolic blood pressure. And 8 weeks after indapamide administration, 2/3 of the total treated patients achieved complete control of hypertension. During the treatment period, there were no changes of serum cholesterol, triglyceride and renal function, except a slight, but still in the normal range, decrease of serum potassium and sodium. Concurrently, plasma vasoconstrictive prostaglandins TXB2 (metabolite of TXA2) and PGF2 alpha reduced significantly (P < 0.01 and P < 0.001 respectively), whereas plasma vasodilative prostaglandins 6-keto-PGF1 alpha (metabolite of PGI2) and PGE2 increased significantly (P < 0.02 and P < 0.05 respectively). The results support the theory that prostaglandins system may play an important role in the hypotensive process of indapamide. The influence of indapamide on prostaglandin system may favour the improvement of platelet function and the maintenance of the homeostasis.