摘要:

BackgroundWhether and to what extent complement is activated in acute myocardial infarction (AMI) and how it contributes to inflammation of the ischemic area are not yet clear. Fibrinolytic agents used for thrombolysis are known to activate complement in vitro and may contribute to its activation in vivo. The aim of this study was to measure the extent of complement activation in AMI patients, some treated and some not treated with streptokinase. In addition, because abrupt complement activation in vivo is usually associated with leukocyte margination, plugging of cells in the microcirculation, and hypotension, we correlated complement activation with leukocyte numbers and mean arterial pressure.Methods and ResultsForty AMI patients were studied: 20 were treated with streptokinase (1.5 million IU IV over 60 minutes), and 20 were not given any fibrinolytic agent. The extent and severity of AMI were not significantly different in both groups. Blood samples were drawn on arrival at the hospital, during streptokinase infusion, and then daily for 1 week. Timematched samples were also drawn from patients not treated with streptokinase. We measured plasma levels of anaphylatoxin C4a, C3a, and C5a by radioimmunoassay and membrane attack com-plexes SC5b-9 by enzyme immunoassay. Leukocytes and arterial pressure also were measured when samples were obtained. C4a, C3a, and SC5b-9 levels increased about 10-fold (P< .0001) during infusion of streptokinase. There were no significant increases in complement catabolic products in AMI patients not treated with streptokinase. There was a significant transient leukopenia (mean±SEM, −29.5±7.0%;P= .001) and decreases in systolic and diastolic pressures (systolic, −29.3±3.2%,P< .0001; diastolic, −27.5±3.4%,P< .0001) after 15 minutes of streptokinase infusion in coincidence with the peak of anaphylatoxins in plasma.ConclusionsStreptokinase treatment of AMI causes abrupt activation of the complement system, whereas no significant complement activation can be detected in plasma of AMI patients not treated with fibrinolytic agents. Complement activation causes a transient leukopenia, as reported for such other clinical conditions as dialysis and cardiopulmonary bypass, and possibly contributes to the hypotension observed during streptokinase treatment.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundThe purpose of this study was to compare combination antithrombotic therapy with aspirin plus anticoagulation versus aspirin alone, when added to conventional antianginal therapy in patients with unstable rest angina or non-Q-wave myocardial infarction who were nonprior aspirin users.Methods and ResultsTwo hundred fourteen patients were randomized; 109 were randomized to receive aspirin alone (162.5 mg daily) and 105 to receive a combination of aspirin plus anticoagulation, ie, aspirin 162.5 mg daily plus heparin (activated partial thromboplastin time, two times control) followed by aspirin 162.5 mg daily plus warfarin (international normalized ratio, 2 to 3). Trial therapy was begun by 9.5±8.8 hours of qualifying pain and was continued for 12 weeks. Primary end points were recurrent angina with ECG changes, myocardial infarction, and/or death. Analysis by intention to treat of primary events at 12 weeks was performed. At 14 days, there was a significant reduction in total ischemic events in the combination group versus aspirin alone (10.5% versus 27%,P= .004). An efficacy analysis of primary events at 12 weeks also revealed a large reduction in total ischemic events in the combination group versus aspirin alone (13% versus 25%,P= .06). Bleeding complications were slightly more common with combination therapy.ConclusionsIn nonprior aspirin users, combination antithrombotic therapy with aspirin plus anticoagulation significantly reduces recurrent ischemic events in the early phase of unstable angina.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundSeveral studies indicate that endogenous hormones play a role in the etiology of coronary artery disease, either as independent risk factors or indirectly, via an effect on lipids, lipoproteins, or other heart disease risk factors.Methods and ResultsThe relation between endogenous hormone levels and premature (<56-year-old patients) myocardial infarction was assessed in a retrospective study involving 49 male survivors of premature myocardial infarction and 49 age-matched, volunteer male controls. Serum samples were obtained for each subject the morning after a a ≥12-hour fast and frozen at −70°C for subsequent hormonal analysis. Among the male patients, the average duration between the most recent myocardial infarction and blood sampling was 3.4 years (range, 0.7 to 19.2 years). Individuals reporting the use of any medications with the potential to alter lipid, lipoprotein, or hormone levels were excluded from these analyses. Dehydroepiandrosterone sulfate levels were significantly lower in the patients than in the control subjects. This association remained statistically significant even after accounting for the effects of total cholesterol, triglycerides, the ratio of total to high-density lipoprotein (HDL) cholesterol, HDL, apolipoprotein A-I, apolipoprotein A-II, apolipoprotein B, and body mass index. There were no significant differences in the levels of estradiol, testosterone, or free testosterone or the ratio of estradiol to testosterone between patients and control subjects.ConclusionsOur conclusions are limited by the retrospective nature of this study. However, these data indicate that serum dehydroepiandrosterone sulfate levels are inversely related to premature myocardial infarction in males and that this association is independent of the effects of several known risk factors for premature myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundConcern thattrans-fatty acids formed in the partial hydrogenation of vegetable oils may increase the risk of coronary disease has existed for several decades, but direct evidence on this relation in humans is limited.Methods and ResultsWith a case-control design, we studied the association between intake oftrans-fatty acids and a first acute myocardial infarction among 239 patients admitted to one of six hospitals in the Boston area and 282 population control subjects. Intake of trans-fatty acids was estimated using a previously validated food frequency questionnaire. After adjustment for age, sex, and energy intake, intake of trans-fatty acids was directly related to risk of myocardial infarction (relative risk for highest compared with lowest quintile, 2.44; 95% confidence interval, 1.42, 4.19; for trendP< .0001). This relation remained highly significant after adjustment for established coronary risk factors, multivitamin use, and intake of saturated fat, monounsaturated fat, linoleic acid, dietary cholesterol, vitamins E and C, carotene, and fiber. Intake of margarine-–the major source oftrans-isomers– was significantly associated with risk of myocardial infarction.ConclusionsThese data support the hypothesis that intake of partially hydrogenated vegetable oils may contribute to the risk of myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundIn a recent Finnish study, ferritin was suggested to be an independent risk factor for acute myocardial infarction. This study suggested that high levels of iron stores might thus be atherogenic and possibly explain partly the sex difference in the incidence of ischemic heart disease.Methods and ResultsA randomly selected group (n=2036), men and women aged 25 to 74 years, were examined between June and September 1983. All classic risk factors for coronary artery disease were measured as well as basic hematologic parameters and the parameters of iron metabolism, ie, iron, total iron-binding capacity (TIBC), and ferritin. During the follow-up for 8.5 years, 81 subjects experienced acute myocardial infarction (63 men and 18 women). The differences in the iron parameters between men and women were almost exclusively seen in ferritin values (198 μg/L in men and 91 μg/L in women), whereas small differences were seen in TIBC. The Cox proportional hazards model was used to estimate the contribution of independent variables to the risk of myocardial infarction. TIBC was found to be a strong independent negative risk factor in men (RR=0.95; 95% CI, 0.92 to 0.98), whereas ferritin (RR=0.999; 95% CI, 0.997 to 1.001) or other iron parameters had no significant predictive power. Each increase in TIBC of 1 μmol/L was associated with a 5.1% decrease in the risk of myocardial infarction. The classic major risk factors, ie, blood pressure, smoking, total cholesterol, and high-density lipoprotein, had significant independent correlation with myocardial infarction. When Cox multivariate analysis was carried out on both sexes combined, TIBC was still an independent negative risk factor, and the logarithmic transform of ferritin had a weak negative correlation but was not statistically significant. Sex was in this group still a very strong risk factor after taking into account all classic risk factors as well as the parameters of iron metabolism.ConclusionsThis study suggests that transferrin, measured as TIBC, is an independent negative risk factor for myocardial infarction. Other parameters of iron metabolism, including ferritin, were not found to contribute to the risk.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundBy national statistics, Japanese ischemic heart disease (IHD) mortality is one of the lowest of all industrialized countries, and the proportion of deaths due to heart failure in heart disease is the highest. There may be a difference in diagnostic preference between Japan and other industrialized countries.Methods and ResultsIHD deaths according to the death certificates were reevaluated with World Health Organization MONICA criteria for those 25 to 74 years old by use of clinical and police records in a Japanese city with a population of 347 000. Their cause of death was given on the death certificates as IHD (International Classification of Diseases [ICD], ninth revision, codes 410-414), heart failure (428), or other heart diseases (393-405, 415-427, 429) in 1984 through 1986. Some deaths in 1985 through 1986 from stroke (430-438) or other diseases (250, 272, 278, 440-448, 797-799) were added. Of 409 subjects, 397 (97%) could be examined. Reevaluation of the 106 deaths originally diagnosed as IHD yielded 73 IHDs and 11 sudden deaths of unknown origin (SD), and reevaluation of 160 deaths originally called heart failure yielded 26 IHDs and 50 SDs. In total, reevaluation of all 397 deaths yielded 101 IHDs and 69 SDs. Some 88% of SD cases were originally certified as heart failure (72%) or IHD (16%). Only two SDs were originally certified as stroke.ConclusionsAssuming that 30% of SDs were due to IHD, the number of IHD deaths would be 122, which is 11% larger than the number of IHD deaths according to the death certificates. After reevaluation, the IHD mortality in this study area still was the lowest in the industrialized countries.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundPressure recovery is the variable increase in lateral pressure downstream from a stenotic orifice. The magnitude and clinical significance of pressure recovery in aortic valve stenosis are poorly defined.Methods and ResultsWe obtained high-fidelity pressure and velocity recordings in 11 patients with isolated significant aortic valve stenosis at the time of diagnostic cardiac catheterization. Systematic catheter pullback from the left ventricular cavity revealed a consistent although variable subvalvular gradient. Further pullback across and distal to the region of the stenosed aortic valve revealed a consistent and progressive increase in the ascending aortic pressure. This increase in lateral pressure occurred pari passu with a diminution in amplitude of the velocity pulse. The extent of pressure recovery was directly related to systemic blood flow and transvalvular flow but inversely related to the Gorlin-derived aortic valve area.ConclusionsThese findings have potentially important implications for the hemodynamic evaluation of mild to moderately severe aortic valve stenosis. The extent of pressure recovery may be of additional utility in the assessment of aortic valve stenosis under varying physiological states.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundIn hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo.Methods and ResultsTagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142±41 g/m) and normal ejection fraction (mean, 64±9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall longaxis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29±6% at the endocardium in hypertensive subjects versus 44±6% in normal subjects (P= .0001); 20±6% at the midwall versus 30±6% (P= .0001); and 13±5% at the epicardium versus 21±5% (P= .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10±9% at the base versus 21±6% in normal subjects (P= .0001); 14±8% at the midventricle versus 18±3% (P= .03); and 14±8% at the apex versus 18±4% (P= .04).ConclusionsIn hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundStandard mitral valve replacement (MVR) in patients with chronic mitral regurgitation results in consistent reductions in resting postoperative ejection fraction. This has been attributed to removal of the low-impedance ejection pathway into the left atrium or to disruption of the chordal apparatus. Mitral valve repair (MVP) does not reduce ejection fraction at rest. However, whether MVP confers any advantages with regard to dynamic left ventricular performance has not been investigated. The aim of this study was to directly compare standard MVR with MVP and to determine their respective influences on ventricular ejection performance during bicycle exercise.Methods and ResultsTen consecutive patients with pure chronic mitral regurgitation who underwent MVP and 10 patients matched for age, sex, and preoperative ejection fraction who underwent standard MVR for pure chronic mitral regurgitation performed symptom-limited, graded upright bicycle exercise with simultaneous Doppler and quantitative two-dimensional echocardiography. Patients with MVP had significantly greater rest (55 ± 12%) and exercise 63±11%) ejection fractions than matched patients with MVR 40±13% [P< .0001] and 42±17% [P< .005], respectively). End-systolic circumferential wall stress was significantly lower at rest (190±36 versus 244±46;P< .03) and at peak exercise 231±46 versus 300±52;P< .02) in patients with MVP. At peak exercise, left ventricular shape was significantly more spherical in patients with MVR than those with MVP 1.84±0.31 versus 2.45±0.59;P< .02).ConclusionsMVR with chordal transection resulted in significant reductions in rest and exercise ejection fraction. This was caused in part by a significant increase in end-systolic circumferential wall stress. MVP resulted in improved rest and exercise ejection indexes, primarily due to a marked reduction in end-systolic stress and maintenance of a more ellipsoidal chamber geometry.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

BackgroundConsidering the controversial results published in the literature concerning associations between human leukocyte antigens (HLA) and rheumatic fever (RF), the purpose of the present study was to investigate by means of cosegregation analysis the participation of HLA genes in susceptibility to RF.Methods and ResultsThe sample reported here was composed of 51 affected and 66 healthy individuals belonging to 22 genetically informative families. The comparison (χ2goodness- of-fit test) of the observed numbers of identical-bydescent (IBD) HLA haplotypes among all affected individuals siblings, cousins, and uncle/nephew and grandparent/grandchild type of pairs) with the expected ones under the assumption of independent segregation of HLA alleles and the presumptive RF susceptibility gene gave a value ofP= .088. Since the number of subjects studied was relatively small and the rejection level obtained was near the usual .05 significance level, we calculated the expected HLA IBD scores in the 13 pairs of affected sibs of our sample for all possible frequencies of the presumptive RF susceptibility gene. This analysis allowed clear rejection of a recessive mode, considering susceptibility gene frequencies lower than 20%, whereas the observed values fitted very well a dominant mode of inheritance, with penetrance (K) values varying between 0.5 and 0.9 and a frequency of the susceptibility gene of at least 1%.ConclusionsThe present data support the hypothesis of an RF susceptibility gene within or very near the HLA complex.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID