Imaging and clinical characteristics of patients with coronary artery stenosis located proximally to myocardial bridging / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the imaging and clinical characteristics and related risk factors of patients with coronary artery stenosis located proximally to myocardial bridging.</p><p><b>METHODS</b>This study enrolled 603 patients with angiography evidenced myocardial bridging-mural coronary artery between May 2004 to May 2009. Angiographic and clinic data were collected according to uniform protocol and standard questionnaires were used to obtain patients' demographic and clinical information. Univariate and multivariate analysis were performed to explore related risk factors.</p><p><b>RESULTS</b>Chest pain was present in 247 cases (41.0%). Dynamic ST-T changes were found in 229 cases (38%). A total of 644 myocardial bridging-mural coronary arteries were detected including 382 (62.4%) segments located proximally to myocardial bridging. Diastolic vessel diameters in the myocardial bridging segment were significantly smaller than reference segments (all P < 0.01). Stepwise multiple regression analysis suggested that vascular bifurcation lesions, the degree of narrowing and the number of diseased coronary vessels of non- myocardial bridging-mural coronary arteries, age, LDL-C/HDL-C, male gender, diabetes, and systolic narrow rate of myocardial bridging-mural coronary arteries were positively related with the narrowing degree of the first coronary artery stenosis located proximally to myocardial bridging (P < 0.05 or P < 0.01). Vascular bifurcation lesions, the degree of narrowing and the number of diseased coronary vessels of non- myocardial bridging-mural coronary arteries, age, LDL-C/HDL-C, male, diabetes and dyslipidemia were positively related with the narrowing degree of the most severe coronary artery stenosis located proximally to myocardial bridging (P < 0.05 or P < 0.01).</p><p><b>CONCLUSIONS</b>Myocardial ischemia is common in patients with myocardial bridging and the artery segments located proximally to myocardial bridging are prone to stenosis. Systolic narrow rate of myocardial bridging-mural coronary arteries is one of major determinants of coronary artery stenosis located proximally to myocardial bridging. Whereas the other coronary heart disease risk factors are likely to play more important roles.</p>

Control rate of increased low-density lipoprotein cholesterol levels in cardiology outpatients with coronary heart disease in Beijing / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the low-density lipoprotein cholesterol (LDL-C) levels in outpatients with coronary heart disease (CHD) visiting cardiology outpatient clinics of 8 hospitals in Beijing.</p><p><b>METHODS</b>A total of 903 outpatients with CHD were enrolled from 4 three-tier hospitals and 4 two-tier hospitals in Beijing. All patients were asked to finish the questionnaire including demographic data, CHD history, the knowledge on cholesterol, and the use of statins. Blood lipid was examined and the LDL-C control rate and related factors were then analyzed.</p><p><b>RESULTS</b>Questionnaire was obtained from 876 patients [619 male: 70.7%, mean age: (64.9 ± 10.7) years old] and blood lipid data were available in 709 patients. The general LDL-C control rate was 36.9% (262/709) and was 13.5% (27/173) in very high risk CHD patients, and lower in patients treated in two-tier hospitals than patients treated in three-tier hospitals[31.3% (121/386) vs. 43.7% (141/323), P < 0.01], in female patients than in male patients [27.1% (60/261) vs. 41.3% (201/496), P < 0.01] and in diabetic patients than in non-diabetic patients [13.5% (27/200) vs. 44.7% (197/441), P < 0.01]. The LDL-C control rate was lower in patients less than 60 years old and patients over 80 years old than that in 60-70 years old patients and 70 - 80 years old patients (P < 0.05). LDL-C control rate was not affected by the history of hypertension, percutaneous coronary intervention or coronary artery bypass grafting, smoking, lipid examination frequency, knowledge on goal level of LDL-C, diet control and regularly physical exercising (all P > 0.05). There were 18.2% (129/709) patients not taking statins or not aware if they were taking statin or not. The main reason for not taking statin [47.9% (23/48)] was statin was no prescribed by doctors, followed by withdrawal by patients due to various reasons [27.1% (13/48)].</p><p><b>CONCLUSIONS</b>LDL-C control rate was low in patients with CHD visiting cardiology outpatient clinics in Beijing. The CHD patients and cardiologists should be encouraged to achieve better LDL-C control by following lipid lowering guidelines and it is also important to improve the drug compliance among CHD patients.</p>

Effect of early high-loading-dose tirofiban on platelet activity in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effect of early high-loading-dose tirofiban on platelet activity for patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention.</p><p><b>METHODS</b>A total of 120 acute STEMI patients were treated with 300 mg aspirin and 600 mg loading dose clopidogrel and randomized to high-dose tirofiban (25 µg/kg bolus followed by 0.15 µg×kg(-1)×min(-1) infusion for 36 hours, n = 40), standard-dose tirofiban (10 µg/kg bolus followed by 0.15 µg×kg(-1)×min(-1) infusion for 36 hours, n = 40) or control (no tirofiban, n = 40) before angiography. Inhibition of platelet aggregation (IPA) was assessed before angiography, at 10 min and 24 hours after tirofiban infusion, and at 12 and 24 hours after stopping tirofiban infusion by the thrombelastography assay.</p><p><b>RESULTS</b>There was no significant difference in baseline of IPA between the 3 groups (P > 0.05). IPA was significantly higher in high-dose tirofiban group compared with standard-dose tirofiban and no tirofiban group at 10 minutes after tirofiban infusion [(84.2 ± 12.0)% vs. (67.8 ± 26.8)% and (31.5 ± 21.9)%, all P < 0.01]. At 24 hours after tirofiban infusion, the IPA of high-dose and standard-dose tirofiban was similar [(93.0 ± 9.8)% vs. (88.5 ± 18.1)%, P > 0.05] and was significantly higher than no tirofiban group [(40.4 ± 22.8)%, all P < 0.01]. IPA was similar at 12 and 24 hours after stopping tirofiban use among the 3 groups (all P > 0.05). The maximum amplitude of high-dose tirofiban and standard-dose tirofiban groups at different time points was similar (all P > 0.05), and maximum amplitude in both tirofiban groups was significantly lower than in no tirofiban group at 10 min [(47.2 ± 7.6) mm and (50.0 ± 9.8) mm vs. (57.7 ± 6.5) mm, all P < 0.01] and at 24 hours after stopping tirofiban infusion [(54.6 ± 5.6) mm and (54.3 ± 9.0) mm vs. (59.6 ± 4.0) mm, all P < 0.01].</p><p><b>CONCLUSION</b>Early use of high-loading-dose of tirofiban on top of 600 mg loading dose clopidogrel is more efficient on inhibiting platelet activity than standard dose of tirofiban in patients with acute STEMI undergoing primary primary percutaneous coronary intervention.</p>

Predictive value of serum uric acid on cardiovascular disease and all-cause mortality in urban Chinese patients / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The association between increased serum uric acid (SUA) levels and cardiovascular risk has been debated for decades. Several large studies have provided conflicting results regarding the clinical significance of elevated SUA levels in cardiovascular disease (CVD) or cerebrovascular disease. The aim of this study was to investigate the relationship between SUA and CVD and all-cause mortality and their potential diagnostic value.</p><p><b>METHODS</b>A total of 3570 in-patients ranging in age from 56 to 95 years (mean (67.36 +/- 11.36) years) were selected from 20 hospitals in Beijing and Shanghai. A carefully designed questionnaire was used to gather baseline data of each patient. All patients were divided into two main groups according to their SUA levels: high SUA and normal SUA groups. Serum indices and other important parameters were measured.</p><p><b>RESULTS</b>Compared with normal SUA group, high SUA group had significant difference in systolic blood pressure (SBP), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), body mass index (BMI), and age (P < 0.05 or P < 0.01). High SUA prevailed in female and patients with history of essential hypertension, while history of smoking and diabetes showed no significant difference between two groups. All-cause and CVD mortality occurred more frequently in high SUA group than in normal SUA group. In the accumulative survival analysis, high SUA group had lower survival rate than normal SUA group both in CVD and all-cause mortality. COX regression analysis indicated that the history of smoking, age and high SUA were independent risk factors for the development of CVD.</p><p><b>CONCLUSIONS</b>These preliminary observations suggest that patients with high SUA levels would face higher risk of mortality. SUA measurement may be applied as a routine predictor for clinical assessment.</p>

Effects of quinidine on pinacidil-induced transmural dispersion of repolarization in canine right ventricular wall / 中华心血管病杂志

<p><b>OBJECTIVE</b>On the basis that pinacidil can produce an "all or none" repolarization in right ventricular wall of canine, to observe the effects of quinidine on the marked transmural dispersion of repolarization. Recent studies have shown that ventricular myocardium is composed of at least 3 electrophysiological distinct cell types: epicardial, endocardial, and midcardial cells. Differences in the response of the 3 cell types to pharmacologic agents and/or pathophysiological states often result in amplification of intrinsic electrical heterogeneities, thus providing a substrate as well as a trigger for the development of arrhythmias. The study was designed to observe the right ventricular transmural heterogeneity in vitro canine heart tissue preparation level.</p><p><b>METHODS</b>The strips were isolated from the anterior wall of the right ventricular of canine. The preparations perfused with oxygenated (95%O(2)/5%CO(2)) Tyrode's solution. The tissues were stimulated at basic cycle lengths of 1000 ms. Standard microelectrode techniques were used. Transmembrane action potentials were recorded from epicardial, midcardial and endocardial cells respectively from right ventricular free wall of canine on different conditions [perusing with Tyrode's solution (Control), pinacidil (2.5 micromol/L), and quinidine (5 micromol/L) in turn].</p><p><b>RESULTS</b>Compared with that of endocardial cells, the action potentials of canine ventricular epicardial and midcardial cells had more obvious spike and dome morphology. Pinacidil (2.5 micromol/L) caused a loss of the dome of transmembrane action potentials and a marked abbreviation of the action potential duration (APD) in right ventricular epicardial and midcardial cells, especially in epicardial cells, but not in endocardial cells (n = 10). With pinacidil (2.5 micromol/L), in epicardial cells, phase 2 amplitude of action potentials decreased from (117.7 +/- 9.3) mV to (71.3 +/- 6.4) mV (P < 0.01), and 90% of the APD(90) decreased from (198.2 +/- 20.8) ms to (103.9 +/- 13.5) ms (P < 0.01). The transmural dispersion of action potential duration increased from (48.5 +/- 9.2) ms to (128.7 +/- 13.5) ms (P < 0.01). Quinidine (5 micromol/L) effectively prolonged the APD abbreviated by pinacidil, restored or partly restored the dome of transmembrane action potentials of epicardial and midcardial cells but not of endocardial cells (n = 10). In epicardial cells phase 2 amplitude increased from (71.3 +/- 6.4) mV to (106.6 +/- 7.7) mV (P < 0.01), and 90% of the APD(90) increased from (103.9 +/- 13.5) ms to (185.9 +/- 15.7) ms (P < 0.01). The transmural dispersion of action potential duration significantly decreased from (128.7 +/- 13.5) ms to (54.3 +/- 10.8) ms (P < 0.01). Quinidine reduced pinacidil-induced transmural dispersion of phase 2 amplitude and the APD in right ventricular wall of canine.</p><p><b>CONCLUSION</b>By restoring the dome and the APD of the epicardial and midcardial cells action potentials, quinidine (5 micromol/L) could reduce the marked transmural dispersion of repolarization caused by pinacidil.</p>