冠心病患者血小板功能在精神应激后的变化

目的观察冠心病（CAD）患者血小板功能在精神应激前后的变化。方法用流式细胞术测定冠状动脉造影证实的22例CAD患者精神应激（心算10min）前、结束后即刻、休息10min后外周血血小板膜糖蛋白ⅡbⅢa复合物的α亚单位（CD41）、P选择素（CD62p）的变化。结果精神应激后CAD患者外周血中CD41阳性率由（75±20）%增加到（89±10）%（P<0.05）;CD62p阳性百分率由（2.5±0.9）%增加到（3.5±0.8）%（P<0.05）;休息10min后则降至应激前水平。结论精神应激可以激活CAD患者血小板功能。     

Comparison of platelet function during exercise in normal subjects and coronary artery disease patients: Potential role of platelet activation in myocardial ischemia

Platelet function parameters as influenced by exercise stress were evaluated in 22 patients with coronary artery disease (CAD) and in 13 normal subjects. Upon exercise stress, 14 CAD patients exhibited positive tests and eight exhibited negative tests. Platelet counts during exercise increased similarly in normal and CAD patients. Platelet aggregation response to ADP was unaffected by exercise both in normal and CAD patients. Platelets from 7 of the 14 CAD patients with positive stress tests had increased sensitivity to endoperoxide analog (U-46619) defined as less than 200 ng/ml U-46619 required for 50% platelet aggregation. Resting plasma beta-thromboglobulin (B-TG) levels, an index of in vivo platelet activation, were significantly higher in CAD patients compared to normal subjects (74 +/- 7 and 41 +/- 5 ng/ml, respectively; p less than 0.02). During exercise plasma B-TG levels increased in normal subjects to 60 +/- 5 ng/ml. In contrast, B-TG levels increased to 102 +/- 14 ng/ml in CAD patients (p less than 0.01 compared to normal subjects). These increases were transient and B-TG declined to preexercise values soon after exercise. Eleven of the 12 CAD patients with positive exercise stress tests had increases in plasma B-TG levels, whereas only three of the eight CAD patients with negative stress tests had any increase. These observations of increased platelet activation in certain CAD patients during exercise may be related to exercise-induced myocardial ischemia.     

The effect of atorvastatin on platelet function in patients with coronary artery disease

BACKGROUND: Lipid-lowering therapy was shown to have several beneficial effects in patients with coronary artery disease (CAD). AIM: The objective of this study was to investigate the effect of atorvastatin on platelet aggregation in patients with CAD. METHODS: Twenty-five hypercholesterolaemic patients who had angiographically proven CAD and 16 normal subjects were enrolled. All patients received 10 mg/day atorvastatin for two months. Anti-platelet agents were discontinued 15 days prior to blood sampling at the beginning and at the end of the atorvastatin therapy. Aggregometric curves of the platelets in response to ADP, collagen and epinephrine were obtained using the aggregometry (turbidimetric) technique. RESULTS: In patients with CAD, total cholesterol (TC) and LDL cholesterol (LDL-C) basal levels were measured (230 +/- 49 mg/dl, 140 +/- 41 mg/dl, respectively). Following lipid-lowering therapy, TC and LDL-C decreased significantly (p < 0.05). The activation measurements of aggregometric curves decreased significantly compared with basal parameters in response to ADP but not in response to collagen and epinephrine. CONCLUSION: Lipid-lowering therapy with the HMG-CoA reductase inhibitor, atorvastatin, had a marked reduction effect on platelet aggregation.     

Effect of aging on Doppler echocardiographic filling parameters in normal subjects and in patients with coronary artery disease

This study was performed investigate and to investigate the influence of age on left ventricular diastolic filling parameters, as assessed by pulsed Doppler echocardiography. The study population consisted of 67 normal healthy subjects (Group I, age 15-66 years) and 117 patients (Group II, age 24-79 years), with angiographically proven coronary artery disease. Transmitral flow velocities were obtained by pulsed Doppler measurements at the level of the mitral annulus. Peak early and late diastolic filling velocities as well as integrated velocities during early and late filling phases were investigated for their relation to aging and a possible alteration with coronary artery disease. In normal subjects, a reduction of early filling velocities and a compensatory increase in late filling velocities were found with increasing age. In patients with coronary artery disease, however, there was no significant correlation of filling parameters with age. In addition, a comparison of filling parameters between age-matched normals and patients with coronary artery disease showed a further reduction of the contribution of early filling in patients with coronary artery disease. Thus, factors other than age may influence left ventricular diastolic filling behavior in patients with coronary artery disease. This can be demonstrated noninvasively using pulsed Doppler technique.     

Diastolic mitral annular motion in normal subjects and patients with coronary artery disease

The purpose of this study was to evaluate the characteristicsof mitral annular motion during diastole in 28 normal subjects,40 patients with prior myocardial infarction (MI), and 23 patientswith coronary artery disease but without prior MI. Mitral annularmotion during diastole was obtained from the apex by M-modeechocardiography at the posterior wall of the left ventricle.Determinants of mitral annular excursion during early (MAE-E)and late diastole (MAE-L) were investigated in all subjects.Differences in the MAE-E, MAE-L, and the MAE-L.MAE-E ratio werecompared among the three patient groups. The Doppler-derivedtransmitral flow velocity-time integral during early (El) andlate (AI) diastole and mitral annular excursions during diastolewere obtained in 55 other patients with a prior MI and in 29healthy volunteers. The relationships between the MAE-L: MAE-Eratio and AI: EI ratio in these two groups were studied. The MAE-E was determined mainly by heart rate and left ventricularejection fraction (LVEF). The MAE-L was determined only by age.The magnitude of MAE-E was significantly less in patients witha prior MI than in normal subjects (P<0.01). However, theMAE-L did not differ among the three groups. The MAE-L.MAE-Ewas higher in patients with a prior MI than in normal subjects(P<0.05), and was significantly correlated with AI: EI inhealthy volunteers (r=0.65, P<0.001) and in patients witha prior MI (r=0.50, P<0.001). The MAE-E in patients with a prior MI decreases in proportionto the deterioration in LVEF. The relative at rial contributionto left ventricular longitudinal distension is increased inpatients with a prior MI and diastolic mitral annular motionhas a significant relationship to the transmitral flow. Thesefindings suggest that mitral annular motion during late diastoleplays an important role in maintaining left ventricular fillingin patients whose left ventricular systolic function has deteriorated.     

Effect of loading conditions on Doppler-derived transmitral flow indices in normal subjects and patients with coronary artery disease

The influence of alterations in preload and afterload on left ventricular diastolic filling using echocardiography was examined in nine normal volunteers (NLS) and nine patients (PTS) with coronary artery disease. The sequential interventions used were handgrip to increase afterload, nitroglycerin to decrease preload, and nifedipine to decrease afterload. Transmitral flow was measured using pulsed-Doppler echocardiography. Measurements were made pre- and post interventions. With increase in afterload using handgrip, the A and E wave velocities and the A/E ratio increased in both groups: 0.62 +/- 0.14 versus 0.86 +/- 0.17 in NLS; 0.75 +/- 0.45 versus 0.84 +/- 0.50 in PTS (P less than 0.05). Following administration of nitroglycerin to reduce preload, the A wave velocities increased, the E wave velocity decreased in both groups, and the A/E ratio increased 0.57 +/- 0.11 versus 0.67 +/- 0.13 in NLS; 0.78 +/- 0.40 versus 0.91 +/- 0.44 in PTS (P less than 0.05). Following use of nifedipine, the A and E wave velocities decreased in both groups with an increase in the A/E ratio in the patient group 0.83 +/- 0.13 versus 0.89 +/- 0.11 (P = NS). Thus, both normal subjects and patients with coronary artery disease had similar changes in Doppler-derived indices of left ventricular filling following interventions that changed left ventricular preload and afterload.     

Myocardial blood-flow response during mental stress in patients with coronary artery disease

Positron emission tomography was used to quantify changes in myocardial blood flow during mental stress in patients with and without coronary artery disease. Blunted augmentation of myocardial blood flow during mental stress was observed in regions without significant epicardial stenosis.     

Radionuclide left ventricular function curve during atrial pacing in normal subjects and in patients with coronary artery disease

We used radionuclide angiography during right atrial pacing to assess left ventricular function in 7 normal subjects and 20 patients with coronary artery disease. A left ventricular function curve relating stroke volume to end-diastolic volume was plotted for each patient. The normal pacing ventricular function curve was a straight line passing through the origin of axes. The pacing ventricular function curve was abnormal in 18 of the 20 patients with coronary artery disease, and three different shaped curves were obtained, reflecting decreased contractile force for the same end-diastolic volume during ischemia. Cardiac output and blood pressure do not change during atrial pacing, thus the Frank-Starling relationship is evaluated by this method during almost experimentally controlled conditions. Relating stroke volume to end-diastolic volume, and not end-diastolic pressure, distinguishes between overall left ventricular systolic function and left ventricular compliance.     

Usefulness of laboratory mental stress test in patients with stable coronary artery disease

Background and hypothesis: Many episodes of ischemia in daily life are silent occurring during sedentary activities and may be related to mental stress. In 35 patients with stable angina and positive exercise test awaiting bypass surgery, we investigated whether laboratory mental stress tests would trigger ischemia of a comparable severity to that occurring in daily life and attempted to elucidate some of the underlying mechanisms. Methods: All patients underwent exercise testing, personality assessment, 2-day Holter monitoring, and laboratory mental stress tests while on their usual medications. Results: Only four patients (12%) had positive mental stress test (ST depression ≥0.1 mV). All episodes were silent and usually associated with fast heart rate (>90 beats/min). In contrast, ambulatory ischemia was common (average duration of 51 min per 24 h), and at least one episode was recorded in 27 patients (77%) including the 4 with positive test. Patients with positive mental stress test had a higher heart rate during testing (124 ± 24 vs. 86 ± 16 beats/min, p<0.01), and a shorter exercise time and time to 1 mm ST depression on cycle ergometry than those with negative mental stress test. None of the four patients were on beta blockers. There was no difference in personality inventory between the two groups. Comparisons between patients with and without positive mental stress test revealed no difference in the duration and frequency of ambulatory ischemia, or in the occurrence of silent ischemia. However, the heart rate at onset of ambulatory ischemia tended to be higher in the patients with positive mental stress test (96 ± 9 vs. 62 ± 43, p = 0.07). Further subgroup analysis in patients without beta blockers (4 mental stress test positive and 18 negative) showed similar results. Conclusions: Laboratory mental stress test is a weak inducer of ischemia detected by electrocardiographic monitoring in patients with frequent ambulatory ischemia. Wall motion evaluation during mental stress test may improve sensitivity. While larger scale studies may determine its clinical role, the present study illustrated that patients with heightened heart rate response to mental stress were identified in whom beta blockers could be the drug of choice.     

精神应激时冠心病患者冠状动脉的舒缩反应

目的　观察精神应激时冠心病患者冠状动脉的舒缩反应。方法　用定量冠状动脉造影观察 2 1例冠心病患者精神应激 (心算 10min)前后冠状动脉内径。结果　精神应激时心率由 ( 78± 16 )增加到 ( 91± 2 2 )次 /min(P <0 0 0 1) ;收缩压由 ( 14 4± 2 2 )上升到 ( 16 6± 2 9)mmHg( 1mmHg =0 133kPa) (P <0 0 0 1) ;舒张压由 ( 93± 8)上升到 ( 10 1± 11)mmHg(P <0 0 5 ) ;心率收缩压乘积由 ( 11 4±3 3)增加到 ( 15 6± 5 7)次 /min·mmHg·10 3 (P <0 0 0 1)。精神应激时冠状动脉病变 ( 2 2处 )段内径由应激前的 ( 1 97± 0 5 7)mm降至 ( 1 6 6± 0 5 2 )mm (P <0 0 1) ,休息 10min后为 ( 1 75± 0 6 2 )mm ,仍明显小于应激前的 ( 1 97± 0 5 7)mm(P <0 0 5 )。结论　精神应激使冠心病患者心率血压明显增高 ,病变段冠状动脉内径明显降低     

Effect of vitamin C on platelet adhesiveness and platelet aggregation in coronary artery disease patients

The effect of oral administration of vitamin C on platelet adhesive index (PAI), platelet aggregate ratio (PAg R) and serum ascorbic acid levels was studied. Feeding 75 g of butter to healthy males (group I, n = 10 cases), enhanced the tendency of platelet adhesiveness (PAd) and platelet aggregation (PAg) to a significant level at the end of 4 h. This was distinctly prevented when 1 g of vitamin C was added to the fatty meal. In coronary artery disease (CAD) patients (group II, n = 20 cases) 10 days of vitamin C administration at 1 g every 8 hours decreased the PAd (p less than 0.001) and PAg (p less than 0.05) significantly. There was also a significant (p less than 0.001) rise in the vitamin C levels. The study brings out a property of vitamin C which may be of considerable importance in prevention of chronic thromboatherosclerotic disease of the arteries.     

Heparin-releasable platelet factor 4 in patients with coronary artery disease.

Recently, platelet factor 4 (PF4) release by heparin (heparin-releasable PF4) has been examined as a useful marker of the interaction between the substances liberated from circulating platelets and the vascular endothelium. We compared the plasma levels of PF4 and beta-thromboglobulin (beta-TG) after intravenous heparin injection in patients with coronary artery disease (CAD) and normal control subjects. We also studied the effects of low-dose aspirin (81 mg/day) on the plasma level of heparin-releasable PF4 in the CAD patients. Blood samples were obtained before and 5 min after the intravenous injection of heparin (1,000 IU) from 23 patients with CAD and 15 normal control subjects. Although the plasma beta-TG level remained unchanged after heparin injection, the plasma PF4 level markedly increased in both groups. There was a significant difference in plasma PF4 levels at 5 min after heparin injection between the CAD group (100.1 +/- 38.1) and the control group (61.0 +/- 24.0) (p less than 0.01). The PF4/beta-TG ratio after heparin injection was also higher in the CAD group than in the control group (p less than 0.01). There was a correlation between the PF4/beta-TG ratio after heparin and the Gensini CAD score, which defines the severity of coronary atherosclerosis (r = 0.489, n = 23, p less than 0.01). Low-dose aspirin was administered to 11 CAD patients for 246.0 +/- 28.8 days. Blood samples for the assay of PF4 and beta-TG were obtained as stated above, and platelet aggregation, thromboxane B2 (TxB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) levels were also measured before and during aspirin administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cholinergic stimulation with pyridostigmine prevents the impairment in ventricular function during mental stress in coronary artery disease patients

Mental stress causes physiological autonomic adjustments that may trigger myocardial ischemia and ventricular dysfunction in patients with coronary artery disease. Thus, it was hypothetized that cholinergic stimulation may counteract the ventricular dysfunction provoked by mental stress in coronary disease. Six patients with coronary disease underwent a randomized, double-blind, cross-over, and placebo-controlled protocol in which they received placebo or a single dose of pyridostigmine bromide (45 mg p.o.), a reversible cholinesterase inhibitor, and thus, a cholinomimetic agent 2 h before a standard mental stress task (Stroop color-word test), while hemodynamic and echocardiographic variables were continuously monitored. There were no signs of myocardial ischemia on ECG during mental stress under PYR or placebo. Heart rate and blood pressure increased during mental stress (P<0.01) similarly with placebo and PYR (P>0.05). There were no ventricular wall motion abnormalities during mental stress with either placebo or PYR, but mental stress decreased ejection fraction (pre 63+/-2%, stress 57+/-2%; P=0.004) and impaired the indices of diastolic ventricular function. On the other hand, PYR prevented the fall in ejection fraction (pre 62+/-2%, stress 64+/-2%; P=0.13) and in the indices of diastolic function (P>0.05). In conclusion, cholinergic stimulation with pyridostigmine prevented the impairment in myocardial function during mental stress in patients with coronary artery disease.     

Comparative study of exercise-induced ventricular arrhythmias in normal subjects and patients with documented coronary artery disease.

The incidence, types and patterns of emergence of treadmill exercise induced ventricular arrhythmias were studied in 482 subjects with and without coronary heart disease. All subjects were free of premature ventricular complexes at rest and were classified into groups on the basis of their clinical status. In Group 1A were 141 patients with chest pain and normal coronary arteriograms and in Group IB 144 age-matched subjects free of clinical evidence of heart disease. Group II consisted of 197 patients with chest pain and arteriographically documented coronary artery disease. Patients in Group IA and II exercised to at least 85% of their predicted maximal heart rate or until chest pain occurred. Subjects in Group IB underwent maximal exercise testing. The total incidence of exercise-induced ventricular arrhythmias was 16% in Group IA, 44% in Group IB and 29% in Group II. However, when exercise heart rate at the time of appearance of ventricular arrhythmias was taken into account the incidence of exercise-induced ventricular arrhythmias up to a heart rate of 130/min was 27% in the patients with documented coronary artery disease (Group II) compared with rates of 9 and 6%, respectively, for Groups IA and IB (P less than 0.001). The incidence rates of multifocal ventricular premature complexes, ventricular tachycardia and ventricular premature complexes at a rate of more than 10/min were also significantly greater at submaximal heart rates in the patients with coronary disease. Patients with three vessel coronary artery disease and abnormal left ventricular wall motion had a significantly greater incidence of exercise-induced ventricular arrhythmias. The incidence of exercise-induced ventricular arrhythmias in patients with coronary disease and a positive S-T segment response was not significantly increased.     

肌氨肽苷对冠心病患者血管内皮功能的影响及其与血小板功能的关系

目的　评价肌氨肽苷注射液对冠心病患者血管内皮功能及血小板功能的影响及二者之间的相互关系。方法　将 14 6例冠心病患者分为肌氨酞苷治疗组与常规治疗组 ,各组又分别分为急性心肌梗死 (AMI)、陈旧性心肌梗死 (OMI)、不稳定型心绞痛 (UA)及稳定型心绞痛 (SA) 4个亚组。对照组 2 0例。分别测定各组治疗前后的血浆内皮素 (ET)、一氧化氮 (NO)及血小板最大聚集率 (PAGTmax)、血栓素B2 (TXB2 )的变化。结果　 1.治疗前 ,各AMI组与UA组的血浆ET、PAGTmax及TXB2 较对照组显著增高 ,NO与对照组比较显著降低 ;OMI及SA组各参数均无显著性差异。 2 .肌氨肽苷治疗后AMI组与UA组的血浆ET、PAGTmax及TXB2 较治疗前显著降低 ,NO呈显著性增高(P <0 .0 5 ,P <0 .0 1) ,与对照组比较差异无显著性 (P >0 .0 5 ) ;ET下降值分别与PAGTmax、TXB2 的变化呈显著性正相关关系。而常规治疗组治疗后各值与治疗前比较虽有变化 ,但均无显著性差异。结论　肌氨肽苷注射液可通过降低血浆ET水平和增加NO浓度来改善血管内皮功能及进一步发挥抑制血小板聚集及血栓形成的作用     

Influence of plasma triglycerides on lipoprotein patterns in normal subjects and in patients with coronary artery disease

This study examined the correlation of plasma triglyceride levels with concentrations of intermediate, low and high density lipoproteins (IDL, LDL, and HDL, respectively) and to particle sizes of LDL in 93 normal men and 106 men with coronary artery disease. Plasma triglyceride concentrations were in the normal range for all persons in both groups. Analysis of lipoproteins of density less than 1.063 g/ml was carried out by analytical ultracentrifugation. The analytical pattern gave the peak Sf for LDL as well as an indication of heterogeneity of particle sizes in the density range of LDL. In both normal subjects and patients with coronary artery disease, a positive correlation was found between peak Sf for LDL and concentrations of plasma triglycerides. Plasma triglyceride levels also were correlated positively with concentrations of Sf 20 to 60 lipoproteins and total IDL mass, and inversely with HDL cholesterol levels. Furthermore, the value for peak Sf for LDL correlated inversely with the IDL mass concentration and IDL/LDL mass ratio, and positively with the HDL cholesterol levels. The results indicate that the lipoprotein pattern, including lipoprotein concentrations and particle sizes, is sensitive to concentrations of plasma triglycerides even when the latter are within the normal range.