Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore an understanding of factors that influence platelet performance is important. This study was undertaken (1) to characterize during evolving myocardial infarction platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving myocardial infarction were studied. Twenty-two patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 min. In 15 patients with anterior myocardial infarction, transcardiac platelet function and response to PGI2 were studied. Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, were elevated three- and 10-fold. 6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets circulating during evolving myocardial infarction ("ischemic platelets") were hyperaggregable in response to ADP and relatively resistant to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic AMP and the cyclic AMP response to PGI2 were diminished. The platelet hyperreactivity, expressed by plasma beta-TG, platelet aggregation, and PGI2-induced inhibition of aggregation, was most intense early during infarct evolution and decreased with time. The increased platelet performance resulted in "platelet fatigue," indicated by decreased contents of beta-TG of the ischemic platelet and decreased TxA2 production in response to collagen. However, the ischemic platelet produced twice normal TxA2 in response to arachidonic acid (stimulus and substrate), demonstrating a heightened metabolic capacity. TxA2 was produced across the ischemic/infarcting compartment in 10 of 15 patients with anterior myocardial infarction. The antiplatelet effect of PGI2 was greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving myocardial infarction, characterized by a proaggregatory environment, heightened platelet reactivity in both the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequences of the data are that the patient in the acute phase of myocardial infarction may benefit from suppression of platelet function and requires significantly greater doses of PGI2 than normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)     

Prostaglandin I2 half-life regulated by high density lipoprotein is decreased in acute myocardial infarction and unstable angina pectoris

To investigate the prostaglandin I2 (PGI2) half-life regulated by high density lipoprotein (HDL) in patients with coronary artery disease (CAD), we determined the stability of PGI2 and serum apolipoprotein A-I (Apo A-I) and apolipoprotein A-II (Apo A-II) levels in four age-matched groups of patients: controls (n = 17), angina pectoris (n = 18), unstable angina pectoris (n = 17), myocardial infarction (n = 19) (acute phase, 3.6 +/- 1.7 hours from onset; subacute phase, 75 +/- 15 hours from onset in the same patients). Serum PGI2 half-life and total serum Apo A-I levels were lower in the CAD group than in the control group. PGI2 was least stable in patients with unstable angina and the acute phase of myocardial infarction. In these patients, the molar ratio of Apo A-I to Apo A-II and HDL-associated Apo A-I levels were decreased, and free Apo A-I levels were increased. After in vitro incubation of HDL with increasing amounts of Apo A-II, Apo A-I in HDL was displaced by Apo A-II, with the parallel decrease in stability of PGI2. Free Apo A-I cannot stabilize PGI2. HDL-associated Apo A-I, whose amount is affected by Apo A-II, stabilized PGI2 and correlated well with stability of PGI2 in patients with CAD and control patients. Decreased PGI2 half-life may play an important role in the pathogenesis of atherosclerosis and thrombus formation in the coronary arteries, especially thrombus formation during an acute coronary event.     

Endogenous digitalis-like factor in patients with acute myocardial infarction.

The authors examined endogenous digitalis-like factor (DLF) concentrations in the serum and urine in 65 patients with acute myocardial infarction. Radioimmunoassay was used for the examination and patients' data were analyzed in detail in relation to sex, risk factors and acute myocardial infarction complications. The concentrations of digitalis-like factor found in the serum of men (0.317 +/- 0.026 micrograms/l) and women (0.256 +/- 0.057 micrograms/l) with acute myocardial infarction were much higher compared with values of healthy men (0.009 +/- 0.004 micrograms/l) and women (0.015 +/- 0.012 micrograms/l). This finding is in agreement with data published by others and suggests a role of DLF in the pathogenesis of myocardial infarction.     

Predictors of coronary bypass grafting in a population of middle-aged men.

BACKGROUND: Coronary bypass grafting is a procedure which is usually undertaken because of extensive coronary heart disease, whereas acute myocardial infarction may occur with patients with moderate or even minimal disease. Having undergone coronary bypass grafting may thus serve as a marker for extensive coronary atherosclerosis. The aim of this study was to assess risk factors for future coronary bypass grafting as a first coronary event, and to compare them with risk factors for a first acute myocardial infarction. DESIGN: This was a prospective cohort study. METHOD: In the Multifactor Primary Prevention Study, 7388 men aged 47-55 years and free of previous acute myocardial infarction or stroke were investigated between 1970 and 1973. During 28 years of follow-up 1664 men (22%) had an acute myocardial infarction or died from coronary disease. One hundred and forty six men (2%) underwent coronary bypass grafting with no prior acute infarction. RESULTS: Serum cholesterol was a stronger predictor of coronary bypass grafting than of acute myocardial infarction. Compared to men with serum cholesterol of 5.0 or lower, men with serum cholesterol 5.1-6.4, 6.5-7.4 and over 7.4 mmol/l had age-adjusted hazard ratios for acute myocardial infarction of 1.22 (1.00-1.49), 1.66 (1.35-2.03) and 2.04 (1.65-2.51). Corresponding hazard ratios for coronary bypass grafting were 1.57 (0.66-3.70), 3.44 (1.47-8.03) and 5.21 (2.20-12.31) (95% confidence interval). In contrast, smoking was a weaker risk factor for coronary bypass grafting than for acute myocardial infarction with no discernible increase in risk except in very heavy smokers (25 g/day or more; n=193); hazard ratio 2.19 (1.02-4.66). Elevated blood pressure predicted coronary bypass grafting and acute myocardial infarction equally well. In multivariate analysis an increase in serum cholesterol of 1 mmol/l was associated with an odds ratio of 1.56 (1.38-1.76) for coronary bypass grafting but only 1.30 (1.24-1.36) for AMI (P for difference in odds ratio 0.004). CONCLUSION: Elevated serum cholesterol is a stronger predictor for future coronary bypass grafting than for acute myocardial infarction. Moderate smoking was not associated with coronary bypass grafting. Different manifestations of coronary disease have different risk factor patterns, suggesting that secular changes in risk factor pattern could potentially influence the clinical expression of the disease.     

Increased Risk of Acute Myocardial Infarction in Systemic Sclerosis: A Nationwide Population-based Study

Purpose

Systemic sclerosis is a life-threatening autoimmune disease characterized by vasculopathy, which results in myocardial involvement in an extremely high percentage of patients. Nevertheless, there have been no large-scale epidemiological studies about the risk of acute myocardial infarction in patients with systemic sclerosis. The aims of this study were to evaluate the hazard ratio (HR) and risk factors of acute myocardial infarction in patients with systemic sclerosis, as well as to compare the risks of acute myocardial infarction among systemic sclerosis patients taking different immunosuppressors.

Methods

The study cohort included 1344 patients with systemic sclerosis and 13,440 (1:10) age-, sex-, and comorbidity-matched controls during the period between 1997 and 2006, from the National Health Insurance Research Database. We compared the risk of acute myocardial infarction between patients with systemic sclerosis and controls and calculated the adjusted HRs for acute myocardial infarction in systemic sclerosis patients taking immunosuppressors and not taking immunosuppressors.

Results

The incidence rates of acute myocardial infarction were 535 and 313 cases per 100,000 person-years for systemic sclerosis cohort and reference cohort, respectively (P <.001, unadjusted). After adjusting for age, sex, and underlying medical diseases on Cox proportional hazards model, systemic sclerosis was found to be an independent risk factor for acute myocardial infarction (HR 2.45). Other risk factors included hypertension (HR 2.08) and diabetes (HR 2.14). The multivariate adjusted HR for acute myocardial infarction did not decrease among the systemic sclerosis patients taking systemic steroids, penicillamine, cyclophosphamide, azathioprine, methotrexate, or cyclosporine.

Conclusion

Systemic sclerosis is independently associated with an increased risk of acute myocardial infarction. Immunosuppressors do not lower the risk of acute myocardial infarction in our study.     

Potential prevention of myocardial rupture resulting from acute myocardial infarction

The clinical characteristics of 30 cases of myocardial rupture resulting from acute myocardial infarction were analyzed. Predisposing factors of myocardial rupture appeared to be the following (1) age 60 years or older, (2) female, (3) no previous history of angina or myocardial infarction, (4) hypertension on admission, (5) persistent or recurrent chest pain, (6) physical activity and/or emotional unrest, (7) less than 10 days since the onset of myocardial infarction. From 1979 to 1982, we tried to eliminate these risk factors in the acute stage of myocardial infarction, of which hypertension appeared to be the most important and main correlating factor. The incidence of myocardial rupture before elimination of risk factors was 31.2% (26 of 84 patients) which was reduced to 8.8% after elimination. In the years 1981 and 1982, only two cases of myocardial rupture were found in each year, 4.3% and 5.6% of MI patients, respectively.     

Serum cholesterol and acute myocardial infarction: a case-control study from the GISSI-2 trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto-Epidemiologia dei Fattori di Rischio dell'Infarto Miocardico Investigators.

OBJECTIVE--To examine the role of serum cholesterol in acute myocardial infarction in a population of patients with no history of coronary heart disease and to establish the nature of this association, the degree of risk, and the possible interaction between serum cholesterol and other major risk factors for acute myocardial infarction. DESIGN--Case-control study. SETTING--90 hospitals in northern, central, and southern Italy. PATIENTS--916 consecutive cases of newly diagnosed acute myocardial infarction and 1106 hospital controls admitted to hospital with acute conditions not related to known or suspected risk factors for coronary heart disease. DATA COLLECTION--Data were collected with a structured questionnaire and blood samples were taken by venepuncture as soon as possible after admission to hospital from cases and controls. Blood cholesterol concentrations were available for 614 cases and 792 controls. RESULTS--After adjustment by logistic regression for sex, age, education, geographical area, smoking status, body mass index, history of diabetes and hypertension, and family history of coronary heart disease the estimated relative risks of acute myocardial infarction for quintiles of serum cholesterol (from lowest to highest) were 2.3 (95% confidence interval (CI) 1.6 to 3.4), 3.1 (95% CI 2.1 to 4.6), 4.1 (95% CI 2.8 to 6.0), and 5.2 (95% CI 3.5 to 7.7). The estimated relative risk across selected covariates increased from the lowest to the highest quintile of serum cholesterol particularly for men, patients under 55 years of age, and smokers. When the possible interaction of known risk factors with serum cholesterol was examined, smoking habits, diabetes, and hypertension had approximately multiplicative effects on relative risk. CONCLUSIONS--This study indicates that serum cholesterol was an independent risk factor for acute myocardial infarction. This association was linear, with no threshold level. Moreover, there was a multiplicative effect between cholesterol and other major risk factors on the relative risk of acute myocardial infarction.     

Platelet hyperactivity in acute myocardial infarction in man--effects of prostacyclin

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore, an understanding of factors which impact on platelet performance is important. The present study was undertaken 1. to characterize during evolving myocardial infarction (MI) platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and 2. to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving MI were studied. 22 patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 minutes. In 15 of these patients, who had an anterior MI, transcardiac platelet function and response to PGI2 were studied. The results are as follows: Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, are elevated three and ten fold. 6-keto-prostaglandin F1 alpha, the stable end product of PGI2, is less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets, circulating during evolving MI ("ischemic platelets") are hyperaggregable in response to adenosine diphosphate and relatively resistent to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic adenosine monophosphate and the cAMP response to PGI2 are diminished. The platelet hyper-reactivity is most intense early during infarct evolution and decreases with time. Transcardiac measurements indicate that thromboxane is produced across the ischemic/infarcting compartment in ten of 15 patients with anterior MI. The antiplatelet effect of PGI2 is greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving MI characterized by a pro-aggregatory environment, heightened platelet re-activity, both in the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequence of the data are that the infarct patient in the acute phase may benefit from platelet function suppression and requires significantly greater doses of prostacyclin than normal subjects. The data also suggest future directions for therapeutic manipulation of platelet hyper-reactivity in the setting of acute myocardial ischemia.     

Changing axis deviation and elevation of prostate-specific antigen during acute myocardial infarction

Left bundle branch block with changing axis deviation also during acute myocardial infarction has been rarely reported. Changing axis deviation with changing bundle branch block during acute myocardial infarction has also been rarely reported. Prostate-specific antigen (PSA) is an established tool in detecting prostate cancer. Immediately after 15 min of exercise on a bicycle ergometer, serum PSA concentrations increased by as much as threefold. Apparently spurious result has been reported in a work about mean serum PSA concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. We present a case of changing axis deviation and elevation of serum PSA concentration in a 92-year-old Italian man with acute myocardial infarction. Our report confirms previous findings and extends the evaluation of PSA during acute myocardial infarction.     

Prostate-specific antigen and acute myocardial infarction: A possible new intriguing scenario

Prostate-specific antigen (PSA) has been identified as a member of the human kallikrein family of serine proteases and it is an established marker for detection of prostate cancer. Apparently spurious result has been reported in a work about mean serum PSA concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. Elevation of prostate-specific antigen has also been reported during acute myocardial infarction in three patients and in another one also after transurethral resection of the prostate (TURP) and without histological diagnosis of prostate cancer. In our report we present three cases of diminution of serum PSA concentration during acute myocardial infarction. Our report extends the evaluation of PSA during acute myocardial infarction. It seems that when elevation of prostate-specific antigen occurs during acute myocardial infarction, coronary lesions are frequent and often more severe than when diminution of prostate-specific antigen occurs during acute myocardial infarction. It opens a possible new intriguing scenario of the role of the prostate-specific antigen in acute myocardial infarction.     

Mid-term prognostic value of plasma heavy-chain myosin in thrombolysed myocardial infarction

Plasma myosin heavy chain assay, which can be easily performed during the acute phase of myocardial infarction, is a recent method allowing quantitative assessment of the extent of infarction. However, to our knowledge, its prognostic value has not been studied in contrast with serum myosin light chain assay. We monitored the state of health of 40 patients (including 37 men with a mean age of 56 years) for two years after a first myocardial infarction, thrombolized during the acute phase. Their survival (mortality) and the development of "cardiac events" (MI, angina, sudden death, etc.) were evaluated at 2 years. The results observed at 2 years were correlated with the initial plasma myosin assay results and other direct and indirect methods of assessment of the extent of infarction, performed during the acute phase of myocardial infarction (cardiac enzymes, contrast angiography). The main result of this study is the demonstration that an unusual plasma myosin release kinetic (complex appearance) is predictive for the medium-term development of heart failure (p = 0.04) and/or destabilization of coronary insufficiency (p = 0.02). These results need to be emphasized, as with only 5 serum myosin assays performed over a 10-day period, it seems possible to identify a group of patients at high risk of medium-term complications, who possess a complex release kinetic during the acute phase of myocardial infarction and a value for area under the curve greater than 10.470 microliters U/L (cut-off value, p = 0.043).     

Alpha 1-antitrypsin in acute myocardial infarction.

Alpha 1-antitrypsin serum levels were measured in 48 patients with acute myocardial infarction and in 19 control patients either with coronary heart disease without necrosis, or with neither coronary disease nor inflammation. Alpha 1-antitrypsin was significantly raised in the group of patients with acute myocardial infarction. As some patients individually showed no change in alpha 1-antitrypsin levels, however, they were divided into two groups according to the maximum serum levels attained. Patients with non-increasing levels of alpha 1-antitrypsin showed increased mortality and a higher incidence of cardiogenic shock, whereas reinfarction occurred more frequently in the group with high alpha 1-antitrypsin levels. Our findings may suggest that the course of a myocardial infarction is determined not only by the severity of the ischaemic event, but also by the response of the "acute" phase reaction" mechanism. We conclude that a failure of alpha 1-antitrypsin levels to increase after myocardial infarction may be associated with a worse clinical course.     

Paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of prostate-specific antigen during acute myocardial infarction

Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. Paroxysmal atrial fibrillation is a frequent complication of acute myocardial infarction. It has been reported that subclinical hyperthyroidism is not associated with coronary heart disease or mortality from cardiovascular causes but it is sufficient to induce arrhythmias including an increase in atrial fibrillation rate. It has also been reported that increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. Moreover chronic renal failure presents an increased arrhythmic risk. Apparently spurious result has been reported in a work about mean serum prostate-specific antigen (PSA) concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. We present a case of paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of serum PSA concentration in a 90-year-old Italian man during acute myocardial infarction. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism and of chronic renal failure. Moreover, our report also confirms previous findings and extends the evaluation of PSA during acute myocardial infarction.     

Alpha 1-antitrypsin in acute myocardial infarction

Alpha 1-antitrypsin serum levels were measured in 48 patients with acute myocardial infarction and in 19 control patients either with coronary heart disease without necrosis, or with neither coronary disease nor inflammation. Alpha 1-antitrypsin was significantly raised in the group of patients with acute myocardial infarction. As some patients individually showed no change in alpha 1-antitrypsin levels, however, they were divided into two groups according to the maximum serum levels attained. Patients with non-increasing levels of alpha 1-antitrypsin showed increased mortality and a higher incidence of cardiogenic shock, whereas reinfarction occurred more frequently in the group with high alpha 1-antitrypsin levels. Our findings may suggest that the course of a myocardial infarction is determined not only by the severity of the ischaemic event, but also by the response of the "acute" phase reaction" mechanism. We conclude that a failure of alpha 1-antitrypsin levels to increase after myocardial infarction may be associated with a worse clinical course.     

Changing axis deviation, paroxysmal atrial fibrillation and elevation of prostate-specific antigen during acute myocardial infarction

It has been rarely reported left bundle branch block with changing axis deviation also during acute myocardial infarction. It has also been rarely reported changing axis deviation with changing bundle branch block during acute myocardial infarction. Prostate-specific antigen (PSA) is an established tool in detecting prostate cancer. Immediately after 15 min of exercise on a bicycle ergometer, serum PSA concentrations increased by as much as threefold. Apparently spurious result has been reported in a work about mean serum PSA concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. We present a case of changing axis deviation with onset of atrial fibrillation and elevation of serum PSA concentration in an 88-year-old Italian man during acute myocardial infarction. Our report confirms previous findings and extends the evaluation of PSA during acute myocardial infarction.     

冠状动脉粥样硬化斑块破裂的临床危险因素分析

目的　研究临床危险因素与冠状动脉粥样硬化斑块破裂的关系 ,探讨斑块破裂的危险因素。方法　选取 1992～ 1998年间的尸检病例 ,急性心肌梗死 (AMI) 2 0例 ,不稳定心绞痛 (UA) 10例 ,稳定心绞痛 (SA) 12例 ,对所有冠状动脉连续取材制片 ,常规及免疫组化染色 ,光镜观察斑块破裂的形态改变及血栓伴随情况 ,并调查 8个相应的临床危险因素。结果　 8个危险因素中 ,血浆甘油三酯水平与斑块破裂有关 (P <0 .0 5 )。结论　高血浆甘油三酯是国人急性冠状动脉综合征患者斑块破裂的一个重要危险因素。     

Alteration in risk factor accumulations of acute myocardial infarction during the last one decade: analysis of patients admitted in Coronary Care Unit

The present study was undertaken to determine accumulation of risk factors in acute myocardial infarction during two periods of 2002 and 1990-1991. We collected 173 and 153 patients with acute myocardial infarction in 2002 and 1990-1991, respectively, and analyzed the history of multiple risk factors, including diabetes mellitus, impaired glucose tolerance, hyperlipidemia, hypertension and obesity, and laboratory findings. The numbers and their percentages of all the risk factors increased in 2002 compared with 1990-1991. According to plasma glucose level, the patients who had type 2 diabetes mellitus, and impaired fasting glucose or impaired glucose tolerance had increased markedly from 41 to 65%. Multiple accumulation of risk factors had increased during the last one decade, and only one or no risk factor per se was not the case in the patients with acute myocardial infarction. Hyperlipidemia and hypertension became fairly controlled in the patients, but not hyperglycemia in type 2 diabetes mellitus in the period of 2002. These findings may indicate that increased multiple accumulation of risk factors accelerates the occurrence of acute myocardial infarction in 2002 as compared to 1990-1991.     

Serum myoglobin levels in patients with ischemic myocardial insult

Serum myoglobin levels were studied in 178 consecutive patients admitted for chest pain due to ischemic cardiac injury. Serum myoglobin level was compared with the clinical condition, electrocardiographic changes, and serum creatine kinase levels. Elevated serum myoglobin concentration was present in all patients with acute myocardial infarction, as defined by World Health Organization, Geneva, criteria, and, in addition, in about 50% of patients with so-called acute coronary insufficiency. On this basis we could define two different groups of patients with acute coronary insufficiency: cases exhibiting elevated serum myoglobin levels (group 1) and those with normal levels (group 2). In group 1 although creatine kinase levels were in the normal range, they were significantly higher than in group 2. Four patients from group 1 developed heart failure and another a typical acute myocardial infarction during hospitalization, whereas no patients of group 2 had such complications. In patients with acute myocardial infarction, the elevation of serum myoglobin preceded that of creatine kinase in most cases. Myoglobin release appears to be related to infarct size, the highest levels were found in extensive myocardial infarction and less marked elevations in cases of subendocardial infarction and in half of the cases with acute coronary insufficiency. It is proposed that serum myoglobin is a reliable measure of myocardial necrosis and serves to detect a hitherto undefined population of small-size acute myocardial infarction, with its attendant clinical and prognostic implications.     

Fibrinogen and other coronary risk factors

The association between plasma fibrinogen concentration and other coronary risk factors diverged in previous studies, and the impact from complex lipoprotein patterns has not been studied. Our research involved 24 healthy subjects without coronary heart disease (control) and 22 patients who had survived having acute myocardial infarction before the age of 41 years (cases), overall 40 men and 6 women with age range of 34 to 54 years. In multiple linear regression analyses concerning control subjects, family disposition, social class, a score based on serum triglyceride and high-density lipoprotein (HDL) cholesterol concentrations, and fasting capillary blood glucose concentration were significantly associated with plasma fibrinogen concentration (P < .00005, R2 = 0.81). For case subjects, the ratio between serum low-density lipoprotein cholesterol and high-density lipoprotein cholesterol concentrations was significantly associated with plasma fibrinogen concentration (P = .0018, R2 = 0.39). Thus, for healthy subjects, 4 coronary risk factors explained three quarters of the variation of plasma fibrinogen concentration, and for patients with a previous acute myocardial infarction, another coronary risk factor explained one third of the variation. In conclusion, the pattern of coronary risk factors associated with plasma fibrinogen concentration differed between those without coronary heart disease and those with a previous acute myocardial infarction.     

A decrease in plasma factor which stimulates prostaglandin I2 synthesis in patients with acute myocardial infarction

PG I2 stimulating plasma factor was measured in patients with ischemic heart disease and age-matched controls. The plasma factor measured by bioassay using rat aorta was 3.2 +/- 0.6 (n = 21), 2.7 +/- 0.8 (n = 7), 1.6 +/- 1.5*** (n = 18) and 2.2 +/- 0.06** (n = 3) PG I2 ng/mg rat aorta (mean +/- SD; * p less than 0.05, ** p less than 0.01, *** p less than 0.001) in control, angina pectoris, acute myocardial infarction and old myocardial infarction with angina pectoris groups, respectively. The plasma factor measured by radioimmunoassay was 43.5 +/- 19.5 (n = 11), 35.4 +/- 13.1 (n = 4), 38.5 +/- 18.0 (n = 9), 26.0 +/- 20.1* (n = 7) and 59.5 +/- 31.2 (n = 5) ng/mg rat aortic protein/15 min in control, variant angina, stable angina, acute myocardial infarction and old myocardial infarction groups, respectively. The factor in deproteinized plasma of the acute myocardial infarction group was also smaller than that of the control group. PG I2 synthesis by rat aortic ring was inhibited by mepacrine, which inhibits phospholipase A2. The plasma factor was not inactivated by heating. The results indicate that a heat-stable plasma factor which acts on phospholipase A2 or on its surrounding reaction systems is deficient in the early stage of acute myocardial infarction. A decrease in the factor may cause PG I2 deficiency, resulting in coronary thrombosis or vasospasm and consequently in acute myocardial infarction.