急性心肌梗死伴先前性心绞痛患者临床分析

目的 :探讨急性心肌梗死 (AMI)伴先前性心绞痛 (AP)患者的冠状动脉 (冠脉 )病变特点及临床预后。方法 :在连续急诊冠脉造影的 385例AMI患者中分析伴有AP(AP组 ,2 0 2例 )及无AP者 (Non AP组 ,183例 )的临床资料与冠脉病变特征 ,并平均随访 (2 8.7± 8.2 )个月主要心血管事件 (包括反复心绞痛发作、非致命性心肌梗死、非致命性心力衰竭、靶血管血运重建及心脏性死亡 )和复合终点事件的发生率。结果 :与Non AP组比较 ,AP组肌酸激酶 (CK)及其同工酶 (CK MB)峰值均显著降低 [(196 5± 14 2 2 )∶(312 6± 2 10 8) ;(81± 4 6 )∶(118± 5 6 )IU/L ,均P <0 .0 1],但其三支病变及伴左主干病变者较多 (33.2 %∶16 .9% ;8.9%∶3.6 % ,均P <0 .0 5 ) ,随访期间AMI后反复心绞痛发作与心脏性死亡率较高 (36 .2 %∶2 3.6 % ,P <0 .0 1;10 .2 %∶3.6 % ,P <0 .0 5 ) ,复合终点事件明显增加 (4 8.0 %∶30 .0 % ,P <0 .0 1)。多元Logistic回归分析示AP与AMI患者死亡危险 (OR值 :3.96 ,95 %CI :2 .2 5～ 7.34,P <0 .0 5 )及复合终点事件 (OR值 :3.2 2 ,95 %CI:1.82～ 8.74 ,P <0 .0 1)增加独立相关。结论 :AMI有AP者 ,其冠脉病变多较重 ,且临床预后较差     

Comparison of plasma serotonin levels in patients with variant angina pectoris versus healed myocardial infarction

Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina pectoris also had greater levels of nitrite and nitrate plasma levels than did control subjects or patients with healed myocardial infarction, partly, perhaps, as a compensatory mechanism.     

B-type natriuretic peptide levels in patients in the emergency department with possible heart failure and previous stable angina pectoris and/or healed myocardial infarction

We examined the relation between B-type natriuretic peptide (BNP) levels and a history of stable angina pectoris and/or healed myocardial infarction in 1,240 patients who were evaluated in the emergency department for possible heart failure. In patients who had heart failure, there was no relation between BNP levels and previous stable angina pectoris and/or healed myocardial infarction. However, in patients who did not have heart failure, there was a relation between BNP levels and previous stable angina pectoris and/or healed myocardial infarction but no significant independent relation in multiple regression analysis.     

Prognostic significance of an early rise to peak creatine kinase after acute myocardial infarction

Because an early rise to peak creatine kinase (CK) is regarded as a noninvasive marker of early coronary reperfusion, the short- and long-term significance of this phenomenon was studied. In a series of consecutive patients admitted between 1974 and 1976 with acute myocardial infarction (AMI), 2 hourly CK estimations were performed. Complete CK curves were obtained in 102 patients, all of whom have been followed for 10 years. Without reference to their clinical course or follow-up, patients were divided into those with CK curves peaking less than or equal to 15 hours (mean 11 hours; n = 41) and those with curves peaking greater than 15 hours (mean 21 hours; n = 61). There were no differences in age, Norris index, location of AMI or past history of coronary artery disease between the groups; however, the mean peak CK was higher in the late peak group (p less than 0.05) and there were more non-Q-wave infarcts in the early peak group (p less than 0.01). In the first 9 months of follow-up there were fewer cardiac deaths in the early peak group (5 vs 13%), but this difference was not significant, and at 12 months the survival curves crossed. At 10 years, survival was 42% in the early peak group and 65% in the late peak group (p less than 0.05). Cox regression analysis showed that early peaking of the CK curve was an independent marker for cardiac death overall (relative risk 2.3, p less than 0.02). In 1-year survivors the relative risk increased to 3.8 (p less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of brain natriuretic peptide levels to discriminate patients with stable angina pectoris without and with electrocardiographic myocardial ischemia and patients with healed myocardial infarction

Brain natriuretic peptide (BNP) levels were measured in 100 patients with coronary heart disease (CHD) who underwent myocardial stress thallium-201 single-photon emission computed tomography (30 with stable angina without basal electrocardiographic ischemia and no perfusion defects, 31 with angina with electrocardiographic ischemia and reversible perfusion defects, and 39 with myocardial infarction and irreversible defects) and in 42 controls. BNP levels progressively increased in patients with CHD and were significantly greater in patients with ischemia (p <0.01) and infarction (p <0.001) compared with controls and subjects with angina. BNP concentration was correlated positively (r = 0.923, p <0.001) with perfusion defect extent and inversely (r = -0.690, p <0.001) with the left ventricle ejection fraction (not different in the subjects examined).     

The creatine kinase curve area and peak creatine kinase after acute myocardial infarction: Usefulness and limitations

We determined creatine kinase (CK) curve areas in 112 patients with acute myocardial infarction. Two-hour sampling was performed for the first 24 hours or until peak CK was reached, and a gamma density function was used to calculate curve areas from all available samples. Attempts to predict CK curve area by means of the portion of the curve prior to peak CK proved to be inaccurate; not until values 2 hours or more beyond peak CK were utilized did predicted and actual CK areas agree well. A good correlation (r = 0.93) was found between CK area and peak CK. To establish an approach for detecting peak CK in the clinical setting, a range of sampling intervals (4 to 24 hours) was assessed; 4-and 6-hour sampling intervals for 48 hours produced maximum CK values at or above 85% of true peak CK in 90% and 89% of patients, respectively, and average maximum CK at both sampling intervals exceeded 94% of that obtained with 2-hour samplings. We conclude that this simplified approach can provide a basis for estimating infarct severity in the individual patient.     

Effects of left ventricular dysfunction on left atrial performance in previous myocardial infarction and during pacing-induced myocardial ischemia in angina pectoris

This study aimed to evaluate acute and chronic response of left atrial function to left ventricular dysfunction in patients with coronary artery disease. We studied simultaneous measurements of left atrial volume by biplane cineangiography and left ventricular pressure at rest and after pacing in 59 patients with coronary artery disease and 11 normal subjects. At rest, 35 patients with previous myocardial infarction (MI group) had low left ventricular filling rate of the first third in diastolic time, large left atrial volume before contraction (LA pre-ACV) and large left atrial ejection volume (LAEV), compared with control group. Left atrial ejection fraction (LAEF), the ratio of LAEV to LA pre-ACV, was similar between both groups. LAEF was maintained within a wide range of values in accordance with left ventricular peak A pressure, except for 3 patients who had high values of left ventricular peak A pressure and low values of LAEF. After a right atrial pacing stress test, time constant was prolonged and mean emptying rate of left atrial volume during early diastole decreased in 11 patients with angina pectoris who had an increase greater than 5 mmHg in left ventricular end-diastolic pressure after pacing. In these group, LA pre-ACV increased, LAEF decreased and LAEV was unchanged. These results suggest that left atrial performance responds differently to acute and chronic left ventricular dysfunction in patients with coronary artery disease.     

Relation of ischemia-modified albumin (IMA) levels following elective angioplasty for stable angina pectoris to duration of balloon-induced myocardial ischemia

The results in this study confirm and expand previous reports that ischemia-modified albumin (IMA) is an early marker of ischemia in the setting of percutaneous coronary intervention (PCI). We observed that IMA levels are related to the number of inflations, inflation pressure, and duration of inflations. It is therefore likely that IMA reflects the magnitude and duration of ischemia induced during PCI.     

Prognosis of patients with different peak serum creatine kinase levels after first myocardial infarction

The extent to which patients with low peak serum creatine kinase(CK) at their first myocardial infarction differ from patientswith high CK levels in terms of risk for subsequent ischaemicevents was investigated in 266 patients who survived the first48 h from the onset of infarction. All patients were followedup for one year. Four groups were formed based on peak CK200,201–400, 401–800 and >800 IU l^-1. During follow-upthe incidence of mortality was 15% (N=39), non-fatal re-infarction9% (N=23), and angina 53% (N=140). Hospital mortality was significantlyhigher (P<0.02) in the highest CK-group (16%), but the incidenceof non-fatal re-infarction, angina pectoris and late mortalitywas similar in the four groups. In hospital survivors, ischaemicST-changes during pre-discharge symptom limited bicycle stresstest and multiple vessel disease were equally distributed inall four groups. We conclude that while hospital mortality is directly relatedto peak CK, there is no relationship between peak CK and latemortality, non-fatal re-infarctions, or recurrent angina. Accordingly,diagnostic and therapeutic procedures in the individual patientsare notinfluenced by the amount of serum CK released duringacute infarction.     

Relation of Chlamydia pneumoniae infection in Taiwan to angiographically demonstrated coronary artery disease and to the presence of acute myocardial infarction or unstable angina pectoris.

Reports of the association of Chlamydia pneumoniae (C. pneumoniae) infection with coronary artery disease (CAD) are scarce in the Oriental population. We therefore conducted a case-control study to explore this issue in Taiwan. There were 242 consecutive subjects (166 men and 76 women) who underwent cardiac catheterization at the National Taiwan University Hospital Cardiac Catheterization Laboratory. Patients with CAD (n = 156) had > or = 1 coronary artery lesion of > 50% diameter stenosis on angiography. Controls (n = 86) had no demonstrable CAD angiographically. Antibodies to C. pneumoniae were tested by using an enzyme-linked immunosorbent assay. The prevalence of antibodies to C. pneumoniae was as follows: immunoglobulin-G (IgG), 50% (122 of 242 patients); immunoglobulin-A (IgA), 72% (176 of 242 patients); and either IgG or IgA, 79% (192 of 242 patients ). The odds ratio (OR) for CAD with either IgG or IgA was 1.4 (95% confidence interval [CI] 0.7 to 2.7, p = 0.31). After adjusting for the known CAD risk factors, the OR decreased to 0.8 (95% CI 0.3 to 2.1, p = 0.60). The OR for unstable angina or acute myocardial infarction with the presence of either IgG or IgA was 0.5 (95% CI 0.2 to 1.1, p = 0.08) and 0.4 ( 95% CI 0.1 to 1.0, p = 0.049) after adjusting for other risk factors. These results suggest a high prevalence of C. pneumoniae infection in Taiwan. However, C. pneumoniae infection is not associated with angiographically documented CAD, and, in contrast, is a negative predictor for the development of acute coronary syndromes.     

Prognostic significance of a low peak serum creatine kinase level in acute myocardial infarction

To assess the prognostic significance of a low peak creatine kinase (CK) level, 723 consecutive patients admitted with acute myocardial infarction (AMI) within 16 hours after onset of symptoms were studied. Thrombolytic therapy was not attempted during the study. Patients were dichotomized according to their peak CK levels, determined from a cluster analysis of peak CK distribution among the population of patients who died within 3 years after hospital discharge. The 139 patients with low peak CK (less than or equal to 650 IU/liter) (group 1) were compared to the 584 patients with high peak CK (greater than 650 IU/liter) (group 2). Patients in group 1 were older and had a higher incidence of previous AMI, angina pectoris before AMI and non-Q-wave AMI. Despite a lower incidence of in-hospital complications and a nonsignificantly lower hospital mortality rate (4 vs 9%) the group 1 three-year posthospital mortality rate was higher (26 vs 17%; p less than 0.02), especially in the subgroup of patients with a Q-wave infarct (mortality 31% in group 1 vs 16% in group 2; p less than 0.001). Among the 491 patients who had a first Q-wave AMI, 55 had a peak CK less than or equal to 650 IU/liter. Compared to the 436 patients with a higher peak CK, these 55 patients had a higher incidence of early postinfarction angina (31 vs 14%; p less than 0.01), a similar hospital mortality (4 vs 7%) but a higher 3-year posthospital mortality (23 vs 12%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Myoglobin and creatine kinase rates of release during acute myocardial infarction

The release of cardiac enzymes as an index of infarct size (IS) development was studied in patients with acute myocardial infarction (AMI) treated at a coronary care unit. Serial determinations of serum myoglobin (MG) and creatine kinase (CK) were made on 34 consecutive patients with duration of symptoms less than 6 h at admission and with initial CK values below the upper reference limit. Computer-calculated CK-IS was determined on the basis of the log-normal algorithm. This was compared to discretely calculated CK and MG release. The correlation between computer- and discretely calculated cumulated CK release was 0.995 with a regression close to the line of equivalence. Computer-calculated CK rates of release showed a one-peak development, while, when discretely calculated, mostly three or four peaks were observed, as found also for MG rates of release. The occurrence of MG and CK peaks was related as indicated by a correlation coefficient of 0.75. The initial CK rate of release was slower when computer-calculated. In the group studied, CK release began about 3 h post onset of symptoms, at which time 56% had an MG value above the upper reference limit. The CK and MG releases were finished about 31 and 36 h post onset of symptoms, respectively, with MG peaks at 6, 11, 19, and 22 h with corresponding CK peaks delayed 2, 3, 3, and 9 h. The first MG and CK peaks represented between 30 and 40% of the total release while the following three peaks represented between 20 and 30% each. Cumulative MG release was correlated to the time of AMI development. No such correlation was found for CK. The results indicate that the development of AMI is a wavelike process not sufficiently described by the log-normal algorithm, on the basis of which, however, an index of total release might be obtained.     

The effects of glucose on myocardial substrate utilization in acute myocardial infarction or angina pectoris

Infusion of glucose-insulin-potassium during acute myocardial infarction has favorable clinical and hemodynamic effects, presumably as a result of decreased myocardial utilization of free fatty acids. In 14 patients with coronary artery disease, hypertonic glucose (a bolus of 10 g followed by infusion of a 30% glucose solution at a constant rate of 10 mg/kg/min) was infused and arterial and coronary sinus levels of glucose, lactate and free fatty acids were measured before and after 15 and 30 minutes of infusion. Arterial glucose and lactate levels increased significantly after glucose infusion, whereas free fatty acid levels decreased significantly. Modest but significant correlations also existed between glucose arterial levels and the arterial-coronary sinus glucose difference (r = 0.53, p less than 0.001); arterial lactate and the arterial-coronary sinus lactate difference (r = 0.35, p less than 0.01); arterial free fatty acids; and the arterial-coronary sinus free fatty acid difference (r = 0.62, p less than 0.001). These results with a hypertonic glucose infusion are similar to those reported after infusion of glucose-insulin-potassium without the potential for harmful adverse effects from infusions of insulin or potassium. Therefore, infusion of hypertonic glucose may be beneficial in patients with coronary artery disease. Further work is necessary to study its effects in different subgroups of patients with coronary artery disease.     

急性心肌梗塞前有无心绞痛对梗塞后心肌损害的影响

目的　探讨心绞痛对急性心肌梗塞（ＡＭＩ）后心肌损害的影响。方法　将８２例急性心肌梗塞患者分成心绞痛组（４８例）和无心绞痛组（３４例）,测定心脏肌酸磷酸激酶（ＣＰＫ）及其同功酶（ＣＫ－ＭＢ）、血清肌钙蛋白（ＣＴｎＴ）、Ｃ反应蛋白（ＣＲＰ）和尿微白蛋白分泌率（ＡＥＲ）变化。结果　心肌梗塞前有心绞痛者的ＣＰＫ、ＣＫ－ＭＢ、ＣＴｎＴ、ＣＲＰ和ＡＥＲ增高水平均较低,与心肌梗塞前无心绞痛患者比较,均有显著性差异（Ｐ＜ ０．０５）。结论　心绞痛对ＡＭＩ的心肌损害有明显保护作用。     

Relation between previous lipid-lowering therapy and infarct size (creatine kinase-MB level) in patients presenting with acute myocardial infarction

Animal experimental data have shown that lipid-lowering agents reduce myocardial infarct size. This association has not been well studied in humans. We compared infarct size in 10,548 patients in the GUSTO IIb and PURSUIT trials who were (n = 1,028) or were not (n = 9,520) on lipid-lowering therapy before an enrolling myocardial infarction (MI). Patients using lipid-lowering agents before their index MI had smaller infarcts than those who were not using these agents (median peak creatine kinase [CK]-MB 4.2 vs 5.2 times the upper limit of normal [ULN]; p <0.0001). Similarly, in an unadjusted model, patients on previous lipid-lowering therapy were less likely to have a peak CK-MB >3 times the ULN (620 of 1,028 [60.3%] vs 6,486 of 9,520 patients [68.1%]; p <0.001; relative risk 0.88, 95% confidence interval 0.84 to 0.93, p <0.0001). In a covariate- and propensity-adjusted multivariable model, the association between pretreatment with lipid-lowering agents and smaller infarct size persisted (relative risk for CK-MB >3 times the ULN 0.94, 95% confidence interval 0.88 to 0.99, p = 0.04). In conclusion, patients on lipid-lowering agents before an MI had significantly smaller infarcts. These findings suggest that lipid-lowering therapy may exert additional salutary effects in the setting of acute coronary syndromes.