Fluctuation of thrombin-antithrombin III complex in patients with acute myocardial infarction: influence of low-dose heparin administration.

The haemostatic parameters were studied within 14 days of acute myocardial infarction (AMI) in 103 patients randomly allocated into a group receiving low-dose heparin or into a group treated without anticoagulants. Patients with isotopic evidence of deep vein thrombosis were excluded from the analysis. An important formation of thrombin-antithrombin III complex (TAT) in the plasma was detected in the early stage of the disease. It was accompanied by an activation of plasma intrinsic fibrinolysis (IF), an elevation of fibrinogen and its degradation products (FDP) and a reduction of extrinsic plasma fibrinolytic activity (EF) together with normal levels of factor X, antithrombin III (AT III), protein C and alpha-2-antiplasmin. Sequentially studies periods of the disease revealed a diminution of TAT complex concentration in the plasma on the seventh day of AMI together with a rise of the both plasma fibrinolytic activities (IF, EF) as well as an elevation of fibrinogen and its degradation products, returning to the initial values on the 14 day of AMI. In the patients treated with heparin the augmentation of TAT complex in the plasma was prolonged until the fifth day of AMI. Moreover, heparin administration was connected with significantly higher levels of AT III and protein C along with a lower concentration of factor X and FDP on the seventh day of the disease. The fluctuation of fibrinolytic activities (IF, EF) in the plasma was heparin-independent. The present results indicate that low-dose heparin treatment modulates the plasmatic fluctuation of TAT complex as well as factor X, AT III and protein C levels in patients with acute myocardial infarction.     

尿微量蛋白联合血凝在冠心病诊断中的检测价值

目的:探讨尿微量蛋白联合血清纤维蛋白原在冠心病的诊断价值。方法:选取同期在我院治疗的24例稳定型心绞痛的患者,36例诊断为不稳定型心绞痛的患者和30例诊断为急性心肌梗死的患者,并选择同期30例来我院体检健康志愿者为对照组。分析以上4组患者发病时尿微量蛋白及血清纤维蛋白原的变化情况。结果:与对照组比,3个冠心病组的尿微量蛋白及血清纤维蛋白原的含量显著升高(P<0.05),与稳定型心绞痛组比,不稳定型心绞痛组的尿微量蛋白及血清纤维蛋白原的含量显著升高(P<0.05);与不稳定型心绞痛组比,急性心梗的尿微量蛋白及血清纤维蛋白原的含量显著升高(P<0.05)。3组病患的尿微量蛋白及血清纤维蛋白原之间呈正相关关系(r=0.852,P<0.05)。结论:心肌梗死和心绞痛患者尿微量蛋白及血清纤维蛋白原含量较健康成人含量高,提示尿微量蛋白及血清纤维蛋白原的含量有助于对心肌梗死和心绞痛的诊断,对急性心肌梗死的诊断价值较高。     

冠心病患者血清尿酸、高敏C 反应蛋白、纤维蛋白原水平变化 的临床研究

目的:观察冠心病患者血清中尿酸、高敏C反应蛋白、纤维蛋白原水平的变化.方法:选取2010年11月至2011年11月于我院就诊的68例冠心病患者(稳定型心绞痛21例,不稳定型心绞痛24例,急性心肌梗死13例)作为研究对象,并选取同期于我院体检中心体检的62例健康人为对照组,检测受试者血清中尿酸、高敏C反应蛋白、纤维蛋白原的水平.结果:研究组患者血清中UA、CRP和FBG水平显著高于对照组(P＜0.05).与稳定型心绞痛组比,不稳定型心绞痛的CRP水平增高(5.34±1.98 mg/L vs.11.36±2.73 mg/L,P＜0.05),急性心肌梗死组的UA (345.63±86.4 μmol/L vs.493.76±101.2 μmol/L,P＜0.05)、CRP (5.34±1.98mg/L vs.21.3±2.24 mg/L,P＜0.05)和FBG(3.86±1.34 g/L vs.6.85±2.36 g/L,P＜0.05)水平显著增高,与不稳定型心绞痛组比,急性心肌梗死组的UA(378.91±89.7 μmol/L vs.493.76±101.2 μmol/L,P＜0.05)、CRP(11.36±2.73 mg/L vs.21.3±2.24 mg/L,P＜0.05)和FBG(4.27±2.08 g/L vs.6.85±2.36 g/L,P＜0.05)水平显著增高(P＜0.05).结论:冠心病患者血清中尿酸、高敏C反应蛋白和纤维蛋白原的水平升高,3个指标可用于评估治疗效果和预后.     

纤维蛋白原与冠心病PCI介入治疗围术期心肌梗死的相关性

目的:探讨纤维蛋白原与冠心病介入治疗围术期心肌梗死的相关性。方法:2013年1月到2015年1月,选择在我院进行诊治的冠心病患者92例,都给予PCI介入手术治疗,在手术前后进行纤维蛋白原与心功能的测定,对围术期心肌梗死发生情况与临床资料进行调查与分析。结果:所有患者都介入手术治疗成功,术后LVESVI与LVEDVI值都明显低于术前(P0.05),而术后LVEF值明显高于术前(P0.05);术后患者的血浆纤维蛋白原值为3.66±0.42 g/L,明显低于术前的7.45±0.56 g/L(P0.05)。围手术期发生心肌梗死8例,发生率为8.7%。Spearman秩相关分析法结果显示心肌梗死发病与血浆纤维蛋白原、LVESVI、LVEDVI、LVEF值都存在明显相关性(P0.05),多元Logistic回归分析结果显示纤维蛋白原、LVESVI、LVEDVI、LVEF、年龄为导致冠心病围术期心肌梗死的主要危险因素(P0.05)。结论:介入手术治疗冠心病具有很好的效果,但是围术期心肌梗死的发生率比较高,纤维蛋白原能有效反应病变状况,在心肌梗死的发生发展中起着关键性作用。     

Alterations of antithrombin III after acute myocardial infarction

The antithrombin III (AT III) activity and the AT III concentration were investigated in 62 consecutive patients with acute myocardial infarction (AMI). To identify the reactant pattern of AT III in postaggressive situations, we also determined labile and acute phase proteins. Firstly, 29 patients were nourished orally and then 33 patients were fed by i.v. hyperalimentation (additional caloric intake of approximately 1,000 cal). AT III activities and concentrations as well as prealbumin and retinol-binding protein decreased concomittantly and significantly whereas haptoglobin, C-reactive protein and fibrinogen increased significantly after AMI. The changes cannot be interpreted as being alterations of the haematocrit. The alterations of AT III correlated significantly with the changes of labile proteins but not with the acute phase reactant proteins. The AT III decrease in the postinfarctional phase may promote a prethrombotic state. In In addition it can be concluded from our results that AT III reacts as (nutritive-dependent) labile protein, which is lowered in postaggressive situation and does not increase as an acute phase reactant. This is in accordance with results from recent animal experiments.     

Thrombolysis with tissue plasminogen activator in patients with acute myocardial infarction

Thrombolytic agents are being employed clinically in increasing numbers of patients in the attempt to eliminate occlusive coronary thrombi in patients with evolving myocardial infarction. When administered by the intracoronary route, streptokinase lyses is successful in coronary thrombi in more than two-thirds of patients, but when administered intravenously is successful in only one-third. Since streptokinase is a nonselective plasminogen activator, it induces fibrinogenolysis when administered selectively or systematically with an attendant marked reduction in plasma fibrinogen levels and significant bleeding complications. In contrast, the action of tissue plasminogen activator (t-Pa) is relatively selective for fibrinolysis (as opposed to fibrinogenolysis). It induces coronary thrombolysis in at least 60% of patients when administered either into a coronary ostium or a peripheral vein without producing substantial reductions in circulating fibrinogen. Bleeding complications are modest and usually related to high administered doses and concomitant heparinization, and occur primarily at sites of vascular access. Thus, t-Pa appears to be a promising agent for thrombolytic treatment of patients with evolving acute myocardial infarction.     

负荷量阿托伐他汀对稳定型冠心病患者非心脏手术围手术期保护作用的研究

目的:探讨负荷量阿托伐他汀对稳定型冠心病患者非心脏的择期外科手术围手术期主要不良心脏事件的保护作用。方法:将拟行非心脏外科手术的60名稳定型冠心病患者随机分为负荷量阿托伐他汀组(n=30)和对照组(n=30),其中负荷量阿托伐他汀治疗组在术前12小时给予阿托伐他汀80 mg顿服,术前2小时阿托伐他汀40 mg顿服,且每晚服用阿托伐他汀40 mg,对照组术前每晚服用阿托伐他汀20 mg,而后进行非心脏的外科手术(主要病种为慢性胆囊结石胆囊炎、慢性阑尾炎、消化性溃疡、疝气),术后负荷量组给予每晚服用阿托伐他汀40 mg,对照组每晚服用阿托伐他汀20 mg。比较两组围手术期主要不良心脏事件(包括心脏性猝死,急性心肌梗死,非计划性血运重建)的发生情况。结果:对照组出现1例急性前壁ST段抬高型心肌梗死并行急诊前降支介入再灌注治疗和7例无症状型心肌梗死,负荷量阿托伐他汀组出现1例无症状型心肌梗死,围手术期心肌梗死发生率较对照组明显降低(P0.05)。结论:负荷量阿托伐他汀可显著降低稳定型冠心病患者非心脏的择期外科手术围手术期主要不良心脏事件如心肌梗死,特别是无症状型心肌梗死的发生率,但该结果尚需大样本多中心随机对照临床试验进一步证实。     

Perforin expression after acute myocardial infarction--a pilot study

Perforin is an important mediator of inflammatory reactions. It is a quick-action cytotoxic mediator accumulated in the cytoplasmic granules of effector immunity cells (T lymphocytes, NK and NKT cells) which provide death signal in infected or transformed cells. Perforin-positive cells were previously detected in myocardial tissue during Trypanosoma cruzi infection and viral myocarditis while its role in chronic and progressive cardiovascular inflammatory disease such as atherosclerosis is almost completely unexplored. The perforin activity is also untested during acute coronary events that represent unexpected atherosclerotic complications due to the inflammatory destabilisation and atherosclerotic plaque rupture. The aim of this study was to investigate the presence of perforin, an important immunological inflammatory molecule in peripheral blood lymphocytes during the early period after acute myocardial infarction. We analyzed three subject groups: women with ST-segment elevation acute myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI), conservatively treated women with acute myocardial infarction without ST-segment elevation (NSTEMI) and a control group of healthy volunteers. The STEMI and NSTEMI groups did not basically differ in medication neither in levels of routine laboratory tests, while troponin I were significantly higher in the STEMI group. In the study, we detected an early decrease of perforin-positive lymphocytes in STEMI patients that were in contrast with their persisting elevation among NSTEMI patients. Despite greater myocardial necrosis in the STEMI group, results of this pilot-study indicated the prolonged perforin-mediated inflammatory response in patients with NSTEMI. This perforin down-regulation that follows the coronary interventional reperfusion in STEMI emphasized the possible anti-inflammatory role of primary PCI among patients with acute myocardial infarction. Given that the issue of routine primary PCI in NSTEMI is nowadays highly topical, the results we expect in the wake of this pilot study could demonstrate a significant impact on clinical practice. Further research is needed to confirm these results, compare the perforin-mediated activity to other inflammatory mediators in acute coronary events and to examine their impact on the long-term outcome.     

Circadian variation in onset of acute cardiogenic pulmonary edema is independent of patients' features and underlying pathophysiological causes

BACKGROUND: The present study aimed to confirm the existence of a circadian pattern in the onset of acute pulmonary edema (APE) and to verify whether sex, age, preexisting diseases, and clinical causes determining the event may influence it. SUBJECTS AND METHODS: The study considered all consecutive cases of APE observed at the St. Anna General Hospital of Ferrara, Italy, during a 7-year period from January 1, 1992, to December 31, 1998. The sample population was divided into subgroups by sex, age (<75 and > or =75 years), presence or absence of diabetes and hypertension, clinical causes determining the event (i.e., acute myocardial infarction (AMI), pulmonary embolism, arrhythmias). The most important associated or concomitant diseases were also considered (i.e., coronary heart disease and angina, previous myocardial infarction, chronic cardiac failure, dilatative cardiopathy, chronic atrial fibrillation, valvular disease, chronic obstructive pulmonary disease, chronic cor pulmonale, malignancy, chronic renal failure). Time of symptom onset of each event was recorded accurately, then tabulated into 24 increments of 1h (e.g., 06:00 to 06:59 was reported as 6 A.M.). For statistical chronobiological analysis, partial Fourier series were used. RESULTS: During the 7-year period, 1321 consecutive cases of APE in 1014 different subjects were observed. The majority of events occurred at night, and statistical analysis showed a 24h rhythmicity both in the total sample population and in all considered subgroups, with the only exception being patients with pulmonary embolism and arrhythmias, for which the small number of cases made the study of rhythms in APE impossible. CONCLUSIONS: The nighttime preference in the occurrence of APE appears to be quite independent of all demographic features or underlying pathophysiological causes.     

Tissue factor, tissue factor pathway inhibitor and cytoadhesive molecules in patients with an acute coronary syndrome

The tissue factor plays a crucial role in initiating blood coagulation after plaque rupture in patients with acute coronary syndrome. It is abundant in atherosclerotic plaques. Moreover, P-selectin, some cytokines, endotoxin and immune complexes can stimulate monocytes and induce the tissue factor expression on their surface. The aim of the study was to compare plasma levels of the tissue factor, tissue factor pathway inhibitor, P-selectin, E-selectin and ICAM-1 in patients with acute myocardial infarction, unstable angina pectoris, stable coronary artery disease and normal control subjects. In addition, plasma levels of the tissue factor, tissue factor pathway inhibitor, P-selectin, E-selectin and ICAM-1 were measured in the blood withdrawn from the coronary sinus in a subgroup of patients with unstable angina pectoris and stable coronary artery disease in which the difference between concentrations in the coronary sinus and systemic blood was calculated. A significant increase in tissue factor pathway inhibitor plasma levels was detected in patients with acute myocardial infarction (373.3+/-135.1 ng/ml, p<0.01) and unstable angina pectoris (119.6+/-86.9 ng/ml, p<0.05) in contrast to the patients with stable coronary artery disease (46.3+/-37.5 ng/ml) and normal subjects (45.1+/-14.3 ng/ml). The plasma levels of tissue factor pathway inhibitor were significantly increased both in the coronary sinus and systemic blood in the patients with unstable angina pectoris. There was only a non-significant trend to higher plasma levels of the tissue factor in patients with acute myocardial infarction and unstable angina pectoris as compared to the patients with stable coronary artery disease and normal subjects, the values being 129.1+/-30.2 pg/ml, 130.5+/-57.8 pg/ml, 120.2+/-45.1 pg/ml and 124.9+/-31.8 pg/ml, respectively. Plasma levels of soluble P-selectin was only slightly, but non-significantly higher in patients with unstable angina pectoris and stable coronary artery disease (184.2+/-85.4 ng/ml and 201.6+/-67.9 ng/ml, respectively) than in patients with the acute myocardial infarction (157.4+/-88.4 ng/ml) or normal subjects (151.4+/-47.1 ng/ml). The difference in plasma levels of soluble ICAM-1 between the blood withdrawn from the coronary sinus and systemic circulation correlated significantly with the corresponding difference in plasma levels of soluble P-selectin and E-selectin. In conclusion, the tissue factor and the tissue factor pathway inhibitor play a crucial role in the initiation of arterial thrombosis. The tissue factor pathway inhibitor levels are increased both in the systemic blood and in the coronary sinus of patients with the acute coronary syndrome.     

Association between dental health and acute myocardial infarction.

Known risk factors for coronary heart disease do not explain all of the clinical and epidemiological features of the disease. To examine the role of chronic bacterial infections as risk factors for the disease the association between poor dental health and acute myocardial infarction was investigated in two separate case-control studies of a total of 100 patients with acute myocardial infarction and 102 controls selected from the community at random. Dental health was graded by using two indexes, one of which was assessed blind. Based on these indexes dental health was significantly worse in patients with acute myocardial infarction than in controls. The association remained valid after adjustment for age, social class, smoking, serum lipid concentrations, and the presence of diabetes. Further prospective studies are required in different populations to confirm the association and to elucidate its nature.     

Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise electrocardiography and coronary angiography.

The clinical relevance of reciprocal changes in the ST segment occurring at the time of acute myocardial infarction was studied prospectively in 85 consecutive uncomplicated cases. Reciprocal depression of the ST segment was defined as depression of 1 mm or more in electrocardiogram leads other than those reflecting the infarct. All patients underwent maximal, symptom limited treadmill stress testing two weeks after the infarct and coronary angiography six weeks after infarction. Forty six patients had inferior, 34 anterior, and five true posterior infarction. Of the 51 patients with reciprocal changes, 45 (88%) developed exercise induced ST segment depression in areas remote from the infarction zone. At angiography all 45 patients were shown to have stenoses greater than 70% in at least two major vessels. Four patients had negative exercise electrocardiograms and were sequently shown to have single vessel disease subtending their infarct, and the remaining two patients had a false negative treadmill test result. Of the 27 patients without reciprocal changes, 21 (78%) had negative treadmill stress test results associated with single vessel coronary disease. Five had positive stress test results and multivessel coronary disease, and one had a false negative stress test result. The remaining seven patients had ST segment elevation without Q wave formation in the reciprocal areas and were assessed separately. Of these, six had positive stress test results and multivessel coronary disease and one had a negative stress test result and single vessel coronary disease to the infarct area. Twenty one patients with anterior infarcts (62%) and 27 with inferior infarcts (59%) had reciprocal changes. No differences emerged in the relation between infarct site, reciprocal change, and presence of additional coronary disease. At follow up of the 51 patients with reciprocal changes in the ST segment 36 had become symptomatic, of whom 29 had undergone coronary artery bypass surgery. By contrast, only four of the 27 patients without reciprocal changes in the ST segment had developed symptoms, and two of these had undergone coronary revascularisation. Reciprocal ST segment depression at the time of acute myocardial infarction may identify patients with severe coronary disease who are at risk of subsequent cardiac events and appears to be as reliable as results of early postinfarction treadmill stress testing in predicting the underlying coronary anatomy. When the electrocardiogram does not show reciprocal changes treadmill testing provides valuable additional information.     

MYOCARDIAL INFARCTION FOLLOWING CAROTID ENDARTERECTOMY

Myocardial infarction has been the major cause of mortality following operation for cerebrovascular insufficiency. In our institution, a clinical diagnosis of coronary artery disease was made in 37 of 125 (29.6%) consecutive male patients having carotid endarterectomy. Six of these 37 patients developed postoperative myocardial infarction. In contrast, none of the 88 patients without coronary artery disease developed myocardial infarction. A more recently treated group of 20 patients who had undergone carotid artery surgery and had previously undergone coronary artery bypass for angina did not develop postoperative myocardial infarction. These data suggest that in patients with both coronary artery and carotid artery disease, prior or concomitant coronary artery bypass should be considered. Myocardial infarction has been the leading cause of early and late death following operation for cerebrovascular insufficiency.(1) DeBakey(2) found operative mortality in patients having surgery for cerebrovascular insufficiency directly related to the incidence of coronary artery disease. An increased operative mortality due to reinfarction has been found in patients recovering from recent myocardial infarction.(3) Cooley(4) found that in patients having aortocoronary bypass there was no increased operative mortality 30 days after myocardial infarction and this may apply to patients having carotid endarterectomy. Subendocardial postoperative infarction associated with minor T wave changes and slight enzyme elevation had a better prognosis than did transmural infarction causing significant Q waves, sequential ST and T wave changes and marked enzyme elevations.(5) The purpose of this study was to document our experience with myocardial infarction in patients undergoing carotid artery operation for clinical coronary artery disease. Consideration of the role of saphenous vein bypass in those patients with coronary artery disease was the background for this review even though the evidence that myocardial infarction can be prevented with saphenous vein bypass operation is only preliminary at the present time.(6)     

Role of missense mutation (M235T) in the angiotensinogen gene in development of cerebral ischemia

Possible correlation of M/T polymorphism of angiotensinogen gene with risk of ischemic stroke and basic risk factors of cerebral pathology (levels of arterial pressure and blood cholesterol; presence of diabetes mellitus, coronary heart disease, or myocardial infarction in anamnesis; and stenosis of major cerebral arteries) was studied. It was shown that M/T polymorphic variants of angiotensinogen gene were factors determining neither clinical variant of cerebral ischemia development (acute ischemic stroke or chronic brain ischemia) nor formation of main risk factors of stroke.     

Risks of discontinuing anticoagulant therapy in a selected group of patients with atherosclerotic heart disease: a prospective study

In 134 patients with coronary artery disease, long-term oral anticoagulant therapy (mean duration, 56 months) for acute myocardial infarction (98 patients), acute coronary insufficiency (25 patients) or severe chronic angina (11 patients) was terminated abruptly in 50 patients (group 1) and gradually in 84 (group 2). The 134 patients represented a homogeneous population of patients with coronary artery disease since most patients older than 75 years and those with conditions known to increase the risks of thromboembolic complications were excluded. The two groups were comparable in terms of sex, age, presence of risk factors, duration of anticoagulant therapy, and presence of angina and abnormal resting electrocardiograms during therapy. Patients were evaluated 6 months after cessation of anticoagulant therapy and, since abrupt withdrawal of therapy did not carry a higher risk than gradual discontinuation, data for groups 1 and 2 were tabulated together.Of the 84 patients with angina at the end of therapy 15 experienced an increase in its severity and this symptom appeared in another patient (relapse rate, 18%). Angina progressed to fatal acute myocardial infarction in four (mortality, 3%) and nonfatal infarction in two; however, all six had extensive coronary artery disease and poor left ventricular function. The results of this study suggest that neither abrupt nor gradual cessation of anticoagulant therapy is associated with an inordinate exacerbation of heart disease.     

Multivessel myocardial infarction

A 56-year-old female patient with hypertension, obesity and chronic intermittent cauda equina compression suffered an acute myocardial infarction five days after a lumbar hernia operation. The electrocardiogram (ECG) showed ST-segment elevation in multiple leads, consistent with an extensive acute apical and lateral myocardial infarction (figure 1, panel A). Acute coronary angiography revealed occlusion of the end-arteries of the left coronary artery in the absence of significant atherosclerotic disease (figure 1, panel B).     

The relationship between trace elements and cardiac markers in acute coronary syndromes

Previous studies have demonstrated increased serum copper and iron levels and decreased selenium and zinc levels in patients with myocardial infarction. Furthermore, the prognostic value of the levels of trace elements in myocardial infarction has been stressed. We examined serum levels of Cu, Fe, Zn and Se, as well as glutathione peroxidase (GPx), a selenoenzyme with antioxidant properties, and C-reactive protein (CRP), a marker of inflammation, in acute coronary syndromes (ACS) regarding their relationship to cardiac troponins and creatine kinase-MB mass (CK-MBm), important prognostic markers. Serum trace elements, GPx activity and CRP were determined in 70 patients with ACS who were admitted within 12 h after the onset. Differences in these parameters were evaluated in three groups of patients divided according to the levels of cardiac markers: group III consisted of patients with high increases in cTnT, cTnI and CK-MBm (> or =0.9 ng/mL, > or =1.0 ng/mL, > or =30 ng/mL, respectively), patients with milder increases in these markers were included in groups II and I consisted of patients with values just above the upper reference limits. Serum Fe levels increased significantly in group II and even more prominently in group III compared to group I (p = 0.04, 0.002, respectively). There was no significant difference between groups II and III. The increase in serum Cu was significant in group III compared to both groups II and I (p = 0.04, 0.001, respectively). There was no significant difference between groups I and II regarding Cu and Zn. The decrease in serum Se and GPx levels was significant only between groups III and I (p = 0.004 for Se and p = 0.0001 for GPx). CRP levels showed a significant increase in group III compared to groups II and I (p = 0.03 and 0.001). CRP showed a significant positive and GPx a significant negative correlation to the cardiac markers cTnT, cTnI and CK-MBm. Cu was positively correlated to all cardiac markers, while the positive correlation between Fe and cardiac markers was significant only for cTnI. Both Zn and Se were negatively correlated to cTnT, and Se was also to cTnI. In conclusion, the increase in serum levels of Cu and Fe and the decrease in serum levels of Zn and Se in patients with higher levels of troponins and CK-MBm imply that trace element levels are related to the degree of myocardial damage and thus may play a role in the pathogenesis of ischemic heart disease. The strong correlations between cardiac markers and both CRP and GPx suggest that these parameters are promising prognostic factors in acute coronary syndromes.     

The glutathione peroxidase 1 (GPX1) single nucleotide polymorphism pro198Leu: association with life span and coronary artery disease

In this study we genotyped polymorphism in GPX1 Pro198Leu (C > T) rs 1050450 in four groups: patients with coronary artery disease, long-livers - above 90 years, early died peoples (before 55 years) from cardiovascular diseases and Russian population as control group. We have found significant higher allele T frequency in men with coronary artery disease -34.84% (Chi2 = 5.228, p = 0.022; OR = 1.46) and in early died men from cardiovascular diseases--38.16% (Chi2 = 6.461, p = 0.011; OR = 1.69) compared with control men--26.8%. Moreover, significantly higher genotype TT frequency has been shown in patients with coronary artery disease and myocardial infarction before age 50--19.44% in comparison with control group--7.28% (Chi2 = 9.55, p = 0.002). The TT frequency in long-livers (4.39%) was the lowest and significantly different from coronary artery disease group--12.79% (Chi2 = 8.07, p = 0.0045) and from coronary artery disease subgroup with myocardial infarction before 50--19.44% (Chi2 = 14.49, p = 0.0001). Thus our results indicate that allele T (Leu) of GPX1 Pro198Leu (C > T) polymorphism is unfavorable for successful ageing. It predisposes to coronary heart disease, earlier myocardial infarction (before age 50) and earlier death (before age 55).     

血清Trx1、FGL2与急性心肌梗死后心力衰竭患者预后的关系

摘要 目的：探讨血清硫氧还蛋白1（Trx1）、纤维蛋白原样蛋白2（FGL2）与急性心肌梗死后心力衰竭患者预后的关系。方法：选择2019年10月至2020年5月我院收治的158例急性心肌梗死后心力衰竭患者作为观察组,并根据心功能Killip分级分为Ⅱ级组54例、Ⅲ级组57例、Ⅳ级组47例。另选择同期我院收治的102例急性心肌梗死患者作为对照组。入院后采用酶联免疫吸附法（ELISA）检测所有患者血清Trx1、FGL2水平;观察组患者出院后随访2年,并根据是否出现主要不良心血管事件（MACE）将患者分为预后不良组和预后良好组。采用多因素Logistic回归分析影响急性心肌梗死后心力衰竭患者预后的相关因素,采用受试者工作特征（ROC）曲线评估血清Trx1、FGL2对急性心肌梗死后心力衰竭患者预后的预测价值。结果：观察组血清FGL2水平明显高于对照组,血清Trx1水平明显低于对照组（P<0.05）;心功能Killip分级Ⅳ级组患者血清Trx1水平明显低于Ⅱ级组、Ⅲ级组（P<0.05）,血清FGL2水平明显高于Ⅱ级组、Ⅲ级组（P<0.05）。预后不良组患者血清Trx1、LVEF均明显低于预后良好组,而年龄、血清FGL2及血尿酸、血肌酐、N末端B型利钠肽原（NT-proBNP）均明显高于预后良好组（P<0.05）,两组心功能Killip分级比例比较差异有统计学意义（P<0.05）。多因素Logistic回归分析显示,年龄（较高）、心功能Killip分级为Ⅳ级、Trx1下降、FGL2升高均是影响急性心肌梗死后心力衰竭患者预后的危险因素（P<0.05）。ROC曲线结果显示,血清Trx1、FGL2预测急性心肌梗死后心力衰竭患者预后的曲线下面积分别为0.807、0.811,两者联合检测预测急性心肌梗死后心力衰竭患者预后的曲线下面积为0.889。结论：急性心肌梗死后心力衰竭患者血清中Trx1水平降低,FGL2水平升高,且血清Trx1、FGL2水平与患者心功能分级及预后密切相关,可作为评估急性心肌梗死后心力衰竭患者预后的辅助性指标。     

The x-ray picture of pulmonary circulation in the course of acute myocardial infarct

A study was made of the time course of lesser circulation (LC) in 80 patients with acute transmural myocardial infarction and in 20 patients with chronic coronary heart disease with the help of chest x-ray. A possibility of preclinical detection of left ventricular insufficiency was confirmed. The capacity of roentgenography to reflect objectively the time course of LC disorder and its correlation with primary determination of a degree of changes, age, cardiac sizes, the expression of aortic atherosclerosis, pleurocardiac reactions and site of myocardial infarction were defined.