Lipoprotein(a) is related to the extent of lesions in the coronary vasculature and to unstable coronary syndromes

BACKGROUND: Lp(a) is a highly atherogenic particle with a prothrombotic effect. Until now its relation to the extent and severity of the atheromatic lesions had not been established by standard procedures. HYPOTHESIS: This study examined the correlation of Lp(a) to the extent and severity of coronary artery disease (CAD) and its relation to unstable clinical events (not including sudden death). METHODS: In 202 patients undergoing coronary angiography, plasma lipids were measured with the usual procedures and Lp(a) with the enzyme-linked immunosorbent assay. The extent of CAD was expressed in the number of diseased vessels and its severity in terms of the severity coefficient and the obstruction coefficient. RESULTS: A very strong relationship between LP(a) and the number of diseased vessels (p = 0.0007) signifying diffuse atherosclerosis, but no relation with the severity of the lesions. was found. However, it was the only lipid that correlated significantly with the number of totally occluded vessels (p = 0.0003). The thrombogenic ability of Lp(a) was manifested by increased incidence of myocardial infarction and unstable angina episodes in patients with elevated Lp(a) (p = 0.0157). CONCLUSION: Elevated Lp(a) predisposes to the extent of CAD and total occlusions but not to the severity of lesions. Patients with increased Lp(a) levels and unstable angina are at increased danger of suffering myocardial infarction. Thus, Lp(a) may predispose to plaque destabilization and thrombosis of noncritical lesions.     

Identification of patients at high risk for adverse coronary events while awaiting routine coronary angioplasty.

BACKGROUND--Identification of patients at risk for progression of coronary stenosis and adverse clinical events while awaiting coronary angioplasty is desirable. OBJECTIVE--To determine the standard clinical or angiographic variables, or both, present at initial angiography associated with the development of adverse coronary events (unstable angina, myocardial infarction, and angiographic total coronary occlusion) in patients awaiting routine percutaneous transluminal coronary angioplasty (PTCA). PATIENTS AND METHODS--Consecutive male patients on a waiting list for routine PTCA. Routine clinical details were obtained at initial angiography. Stenosis severity was measured using computerised angiography. OUTCOME MEASURES--Development of one or more of myocardial infarction, unstable angina, or angiographic total coronary occlusion while awaiting PTCA were recorded as an adverse event. RESULTS--Some 214 of 219 patients underwent a second angiogram. One had a fatal myocardial infarction and four (2%) were lost to follow up. Fifty patients (23%) developed one or more adverse events (myocardial infarction five, unstable angina 35, total coronary occlusion 23) at a median (range) interval of 8 (3-25) months. Twenty (57%) of the 35 patients with unstable angina developed adverse events compared with 30 (17%) of the 180 with stable angina (P = 0.0001). Plasma triglyceride concentration was 2.6 (1.2) mmol/l in patients with adverse coronary events compared with 2.2 (1.1) mmol/l in those without such events (P < 0.05). Patients with adverse events were younger than those without (54 (9) years v 58 (9) years, P < 0.01). The relative risk of an adverse event in patients with unstable angina and increased plasma triglyceride concentrations was 6.9 compared with those presenting with stable angina and a normal triglyceride concentration (P < 0.02). CONCLUSIONS--The study shows that adverse events are not uncommon in patients awaiting PTCA. Patients at high risk for adverse events may be predicted by the presence of acute coronary syndrome, increased concentration of plasma triglyceride, and younger age at the time of the first angiogram.     

老年急性冠状动脉综合征患者UAER、LP（a）的检测及其与冠状动脉病变严重程度的关系

目的通过测定老年急性冠状动脉综合征（ACS）患者的脂蛋白（a）[LP（a）]、尿蛋白排泄率（UAER）水平,探讨其与冠状动脉病变严重程度的相关性。方法 ACS患者87例,其中不稳型心绞痛（UA）组48例,急性心肌梗死（AMI）组39例;正常对照组37例。所有病例入院后测定LP（a）、UAER水平;对患者进行冠状动脉造影,采用Gensini积分系统对各支冠状动脉狭窄程度进行定量分析。结果与对照组比较,UA组和AMI组LP（a）、UAER水升高（P〈0.05）;LP（a）、UAER均与冠状动脉积分正相关（P〈0.05）,前两者间亦呈正相关（P〈0.01）。结论 LP（a）和UAER可能参与了老年ACS的发生和发展,且与冠状动脉病变严重程度相关。     

Angiographic coronary artery lesion morphology and pathogenetic mechanisms of myocardial ischemia in stable and unstable coronary artery disease syndromes.

The angiographic morphology of coronary artery stenoses was studied in 160 patients referred for diagnostic coronary arteriography. Three groups of patients were studied: 60 patients with stable angina, 78 patients with unstable angina and 22 patients with a recent myocardial infarction. Complex lesions were more frequently observed in patients with unstable angina (59%, p less than 0.001) and in patients with a recent myocardial infarction (54%, p less than 0.05) then in patients with stable angina (25%). Angiographic signs suggestive for the presence of intravascular thrombi were almost exclusively observed in the patients with unstable angina (34%, p less than 0.001) and in the patients with a recent myocardial infarction (27%, P less than 0.001) and were almost completely absent in the patients with stable angina (1.5%). The high prevalence of complex coronary artery lesion morphology and of intravascular thrombi observed in patients with unstable angina or with a recent myocardial infarction emphasizes the important role of intima disruption and of subsequent thrombosis in the pathogenesis of myocardial ischemia in those unstable syndromes of ischemic heart disease.     

Activated clotting times in acute coronary syndromes and percutaneous transluminal coronary angioplasty

A discrete fall in the ACT (activated coagulation time) has been observed in patients with known activation of the coagulation cascade. Injury to the coronary artery resulting in thrombin activation, whether spontaneous as in the case of acute myocardial infarction or planned as with percutaneous transluminal coronary angioplasty (PTCA), may there-fore be reflected in a change in ACT values. We reviewed the records of patients under-going PTCA at St. Luke's Episcopal Hospital/Texas Heart Institute from January 1990 through December 1992 for information regarding ACT values and clinical events. A total of 469 patients, whose record contained adequate information for study inclusion, were divided into four separate groups: acute myocardial infarction (group I, n = 62), unstable angina with heparin therapy that was withdrawn at least 4 hr prior to PTCA (group II, n = 102), unstable angina with heparin therapy continued until the time of PTCA (group III, n = 154), and stable angina undergoing elective PTCA (group IV, n = 151). Heparin was discontinued 12–15 hr after the procedure in all but group I where anticoagulation was often maintained up to 72 hr. ACT values were measured prior to the PTCA procedure (baseline), after the initial heparin bolus of 10,000 U (postheparin) and ～ 12–18 hr after the procedure (heparin withdrawal). The “baseline” ACT was significantly lower in patients with unstable angina (93 ± 13 sec) or acute myocardial infarction (78 ± 9 sec) who had their baseline value obtained off of heparin therapy than in patients with stable angina (136 ± 21 sec) or those receiving heparin at the time of baseline measurement (135 ± 14 sec, P < 0.001). All patients with unstable coronary syndromes had a blunted response to heparin (group 1–189 sec, group II-221 sec, group III-248 sec). Although groups I-III were not significantly different compared to one another, each was significantly lower than group IV whose past heparin ACT was 279 sec. Heparin withdrawal ACT values fell within the ranges seen in patients with unstable coronary syndromes untreated with heparin in all but group I (whose heparin therapy was continued through the time of the 12–18-hr postprocedure measurement time). Recurrent ischemic events were seen with increased frequency (16.6%) only in patients with unstable angina whose heparin therapy was interrupted prior to PTCA. In conclusion, low baseline ACT values and a blunted ACT response to heparin are associated with clinical syndromes known to result from thrombus formation. The possibility that the ACT may be of value in reflecting thrombus activity requires prospective evaluation.     

冠心病患者同型半胱氨酸、脑钠肽与冠脉病变的相关性

目的：探讨冠心病（CHD）患者同型半胱氨酸（Hcy）、脑钠肽（BNP）与冠状动脉病变程度的关系及临床意义。方法：选择CHD患者80例,根据临床表现,心电图变化及心肌损伤标志物水平分为急性心肌梗死组（AMI组）,不稳定型心绞痛组（UAP组）和稳定型心绞痛组（SAP组）,并设正常对照组58例,测定所有研究对象血浆Hcy、BNP水平,并进行组间对比。结果：AMI、UAP组及SAP组血浆Hcy[（26.72±4.62）μmol/L比（20.28±4.05）μmol/L比（15.34±3.93）μmol/L]、BNP[（480.27±70.84）pg/ml比（312.25±62.54）pg/ml比（215.78±68.27）pg/ml]水平均明显高于正常对照组的[（11.27±3.58）μmol/L,（35.14±17.12）pg/ml],各组间比较差异均有显著性（P均〈0.05）;随着冠状动脉病变Gensini评分的增加,Hcy、BNP浓度明显升高（P〈0.05）。结论：冠心病患者血浆同型半胱氨酸、脑钠肽水平明显升高,与冠状动脉病变程度有关。     

Efficacy and safety of early coronary stenting for unstable angina

To determine the efficacy and safety of early coronary stenting for unstable angina, we studied 91 consecutive patients with unstable angina. Thirty-one patients underwent stenting 72 h or more after admission, and another 60 patients underwent stenting within 72 h of admission. The clinical and angiographic follow-up had been done for 6 mo. There were no differences between the baseline clinical and angiographic characteristics of both groups. The maximum balloon pressure was higher (14.1 ± 1.2 vs. 12.6 ± 0.9, P < 0.01) and the hospital stay was shorter (9.7 ± 2.7 vs. 18.7 ± 5.8 d, P < 0.0001) in the early stenting group. These two groups were similar in the clinical success rate (90.0% vs. 93.5%), without any abrupt closure, subacute thrombosis, death, myocardial infarction, or coronary bypass surgery. These findings indicate that early stenting can be useful in patients with unstable angina. Cathet. Cardiovasc. Diagn. 43:381–385, 1998. © 1998 Wiley-Liss, Inc.     

Serum lipoprotein(a) level in relation to severity of coronary artery disease and coronary artery patency in acute myocardial infarction

Lipoprotein(a) (Lp(a)) is a low-density lipoprotein (LDL)-like particle that may accelerate atherogenesis and promote thrombosis. In the present study, relationships between serum Lp(a) levels and the severity of coronary artery disease and infarct artery patency were studied in 14 patients with acute myocardial infarction. Lp(a) was measured by enzyme-linked immunosorbent assay and the timing of reperfusion was evaluated using the creatine kinase myosin-brain fraction and myoglobin release curves. Thrombolysis in Myocardial Infarction (TIMI) flow grade and severity of coronary artery disease were assessed using a scoring system based on coronary angiography performed during hospitalization and 6 months thereafter. The median Lp(a) level on admission was 127 (range 11–2 513) mg/l. The overall coronary score was higher in patients with Lp(a) levels greater than 127 mg/l than in those with Lp(a) less than 127 mg/l (P < 0.01). Lp(a) level correlated with the coronary score measured during hospitalization (r = 0.80, P < 0.01) and 6 months later (r = 0.79, P < 0.01). The timing of reperfusion and infarct artery patency were not dependent on the serum Lp(a) level. The results show that the serum Lp(a) level is associated with the angiographic severity of coronary artery disease postmyocardial infarction but does not determine the patency of the infarct-related artery. Received: May 14, 2001 / Accepted: September 22, 2001     

Repeat percutaneous coronary angioplasty; clinical and angiographic follow-up in patients with stable or unstable angina pectoris

This study analyses the immediate outcome and the risk of recurrentrestenosis in patients who, at the time of repeat coronary angioplastyfor a first restenosis, had unstable (n = 50), 19%) or stable(n = 218, 81%) angina. Successful angioplasty was accomplishedin 250 (93%) patients, 222 (89%) of whom hadfollow-up angiography.Mean time from initial to repeat angioplasty was shorter (P= 0.0002) and angiographic evidence of thrombus was commoner(P = 0.0001) in the unstable group. Major complications (coronaryartery bypass grafting or myocardial infarction) were morefrequent(P <0.01) in the unstable group (6% vs 0.5%); no procedure-relateddeaths occurred. The angiographic rate of restenosis was significantlyhigher in the unstable group (61% vs 43%, P <0.05). Despitethis high rate of recurrent restenosis, most of the patientsin both groups were either asymptomatic or had atypical chestpain at follow-up. Repeat coronary angioplasty, in patients with unstable angina,has a high primary success rate but a higher risk of acute complicationsthan in patients with stable angina. The angiographic rate ofrestenosis was significantly higher in unstable than in stablepatients, however, the clinical status of most patients wasimproved at follow-up.     

Short and long term outcome of percutaneous transluminal coronary angioplasty in unstable versus stable angina pectoris: A report of the 1985–1986 nhlbi ptca registry

In a cohort of 1,720 consecutive patients from the National Heart, Lung, and Blood Institute, Percutaneous Transluminal Coronary Angioplasty (PTCA) Registry (August 1985–May 1986), we compared 768 patients (45%) with stable angina and 952 patients (55%) with unstable angina pectoris. Unstable angina patients exhibited at least one of the following characteristics: new onset angina, rapidly progressing angina, angina at rest, angina refractory to medication, variant angina, acute coronary insufficiency, or angina recurring shortly after an acute myocardial infarct. The distribution of single- and multi-vessel disease was similar among stable and unstable angina patients; multi-vessel disease predominated. Average severity of stenosis and incidence of tubular and diffuse stenosis morphology were higher among patients with unstable angina (both p<0.001). Patient success rates were similar in stable and unstable patients. However, on a per lesion basis, overall angiographic success rate and average reduction of severity of stenosis in successfully dilated lesions were significantly higher among patients with unstable angina (both p<0.001). Incidence of major patient complications (p<0.01) and of emergency coronary bypass surgery (p<0.05) were also higher in patients with unstable angina but consistent with their more precarious clinical condition and stenosis morphology. During a two year follow-up, the cumulative distributions of death, myocardial infarct, repeat PTCA, and coronary bypass surgery were not significantly different in patients with stable angina compared to patients with unstable angina. Comparison of the current PTCA Registry cohort with the cases reported in the 1979–1982 Registry revealed a 19% higher success rate for both stable and unstable angina patients. Major complication rates decreased between time periods for stable but not for unstable angina patients. Incidence of emergency bypass surgery decreased more for stable than for unstable angina patients. Coronary angioplasty is indicated in properly selected patients with unstable angina and both single-and-multi-vessel coronary disease.     

N-terminal pro-brain natriuretic peptide but not highsensitivity C-reactive protein is related to severity of coronary artery stenosis in patients with acute coronary syndrome

Objective Biochemical indicators such as N-terminal pro-brain type natriuretic peptide（NT pro-BNP）and high-sensitivity Creactive protein（hsCRP）predict mortality in acute coronary syndrome（ACS）.However,little is known about the relationship of these factors with severity of coronary artery stenosis in patients with.Methods Three hundred and thirty-one subjects including 246 unstable angina pectoris patients and 85 myocardial infarction patients were recruited and classified into two groups：single-vessel disease group（1-vessel disease,n=93）and multiple-vessel disease group（≥2-vessels disease,n=238）according to selective coronary angiography.Plasma levels of NT pro-BNP and hsCRP were measured and severity of coronary stenosis was determined by Gensini score.Results NT pro-BNP but not hsCRP level was higher in patients with myocardial infarction than in patients with unstable angina pectoris.The patients with multiple-vessel disease had significantly higher NT pro-BNP level but not hsCRP compared with those with single-vessel disease.NT pro-BNP levels increased significantly as left ventricle（LV）function decreased,and only NT proBNP but not hsCRP level was related to Gensini score of severity of coronary stenosis in ACS.Conclusion NT proBNP but not hsCRP level is related to severity of coronary artery stenosis in patients in ACS.     

氟伐他汀对冠心病患者PAPP-A和ox-LDL水平的影响

目的观察氟伐他汀治疗对冠心病患者妊娠相关血浆蛋白-A（PAPP-A）和氧化型低密度脂蛋白（ox-LDL）水平的影响。方法选择冠心病组患者75例,包括急性心肌梗死（AMI）患者32例,不稳定型心绞痛（UAP）患者22例和稳定型心绞痛（SAP）患者21例。正常对照组60例。采用双抗体夹心酶联免疫吸附试验检测冠心病患者PAPP-A和ox-LDL水平。结果PAPP-A在急性冠脉综合征组（ACS,包括AMI、UAP）浓度较SAP及正常对照组均明显偏高（P<0.05）;ox-LDL在冠心病组中的浓度较正常对照组高（P<0.05）,且在AMI、UAP、SAP各组组间比较均有显著性差异（P<0.05）;氟伐他汀治疗后冠心病患者PAPP-A和ox-LDL浓度均显著下降（P<0.01）;PAPP-A与ox-LDL水平呈正相关（P<0.01）。结论氟伐他汀治疗后冠心病患者PAPP-A和ox-LDL浓度降低,氟伐他汀可能通过抑制炎症反应,减少氧化应激来发挥心血管的保护作用。     

冠脉病变与血清同型半胱氨酸及脂蛋白（a）的相关性研究

目的:观察冠心病(CHD)患者冠状动脉病变程度与血清同型半胱氨酸(Hcy)和血清脂蛋白(a)[Lp(a)]水平间的相关性。方法:选择经冠状动脉造影确诊的CHD患者108例为CHD组,其中亚组:稳定型心绞痛(SAP)37例,不稳定型心绞痛(UAP)36例,急性心肌梗死(AMI)35例,另选择82例健康体检者为健康对照组,比较两组及CHD组内各亚组血清Hcy和Lp(a)水平,分析冠状动脉病变程度与血清Hcy、Lp (a)水平的相关性。结果:与健康对照组比较,CHD组血清Hcy[(7.1±2.1)μmol/L比(15.6±5.0)μmol/L]和Lp(a)[(122.6±20.4)mg/L比(220.2±42.6)mg/L]水平均显著升高(P均=0.001);且与SAP组比较,UAP组和AMI组血清Hcy[(12.5±4.0)μmol/L比(18.1±5.9)μmol/L、(20.1±6.0)μmol/L]和Lp(a)[(150.8±30.8)mg/L比(272.8±50.3)mg/L、(280.6±52.9)mg/L]水平及Gensini评分[(15.5±8.5)分比(50.6±11.2)分、(54.3±12.8)分]均显著升高(P均=0.001);Pearson相关分析显示,CHD患者冠状动脉病变程度与血清Hcy及Lp(a)水平呈显著正相关(r=0.582、0.663,P均=0.001)。结论:血清Hcy和Lp(a)水平与CHD冠状动脉病变程度呈正相关,联合检测之有助于了解病情,并指导治疗。     

血清脂蛋白(a)在冠心病的意义

目的探讨血清脂蛋白(a)与冠心病类型、病变、预后的关系。方法冠心病95例分为3组:急性心肌梗死组30例,不稳定型心绞痛组35例及稳定型心绞痛组30例。正常对照组30例。比较冠心病各组与对照组脂蛋白(a)。观察冠心病患者在住院期间及出院1个月内心脏性死亡等心脏事件。结果冠心病各组脂蛋白(a)均高于对照组,差异有统计学意义(P<0.05),脂蛋白(a)高于300mg/L患者心脏事件发生率55%(11/20),脂蛋白(a)小于或等于300mg/L患者心脏事件发生率19%(14/75),差异有统计学意义(χ2=5.439,P=0.02)。结论脂蛋白(a)是冠心病独立危险因素,与冠心病严重程度及预后相关。     

Change of plasma leukotriene c4 during myocardial ischemia in humans

Changes in leukotriene C4 levels during different degrees of myocardial ischemia in humans were examined by comparing radioimmunoassay measures of leukotriene C4 plasma levels obtained during transient and prolonged myocardial ischemia. Leukotriene C4 levels in systemic arterial and coronary sinus blood were determined in patients with chronic stable angina before and after myocardial ischemia induced either by exercise (supine bicycle ergometer exercise stress testing; n = 14; age, 52 ± 8 years) or by coronary occlusion during angioplasty (n = 14; age 53 ± 7 years). Temporal changes of leukotriene C4 were also followed in arterial and pulmonary artery blood within 24 h after the onset of chest pain (acute phase), and 1 day, 1 week, and 1 month later in 22 patients with acute myocardial infarction (AMI) (12 patients with thrombolytic therapy, age 61 ± 10 years; 10 patients without thrombolytic therapy, age 60 ± 11 years). Clinical characteristics, including coronary risk factors and the severity of coronary artery disease, were not significantly different among the groups. Exercise-induced myocardial ischemia and coronary occlusion did not induce any significant leukotriene C4 changes in the chronic stable angina patients, whereas AMI patients had significantly higher plasma leukotriene C4 levels in both arterial and pulmonary artery blood in the acute phase compared with those of chronic stable angina patients (arterial blood, 471 ± 164 pg/ml and 477 ±235 pg/ml vs. 275 ± 254 pg/ml or 240 ± 66 pg/ml, p< 0.05; pulmonary artery blood in AMI, 543 ± 162 pg/ml vs. 234 ± 125 pg/ml or 225 ±64 pg/ml, coronary sinus blood in chronic stable angina, p < 0.05). These results suggest that leukotriene C4 is involved more in prolonged myocardial ischemia than in transient myocardial is chemia, and that leukocyte function might play a significant role in the pathogenesis of patients with AMI.     

Angiographic morphology of coronary lesions in various syndromes of ischemic cardiopathy

The angiographic morphology of coronary lesions is often completely ignored in the prognostic and decision-making process related to patients with coronary disease. We performed this study to evaluate the possibility of identifying complex or complicated atherosclerotic lesions by means of routine diagnostic coronary arteriography, and to assess their prevalence in the different syndromes of ischaemic heart disease. From an overall group of 200 successive cases studied using coronary angiography, 111 patients with significant coronary artery disease in whom a "culprit lesion" could be identified were retrospectively selected. The angiographic morphology of coronary lesions was defined according to an original classification as: 1) simple stenosis, 2) complex lesion, 3) thrombosis. Of the 111 patients, 36 had been studied for stable angina, 31 for unstable angina, 10 for a non-Q wave myocardial infarction, 34 for transmural infarction. The clinical groups did not show any significant differences when compared on the basis of number of vessels involved and degree of narrowing of the ischaemia-producing artery. Significant differences were found when angiographic morphology was analyzed. In stable angina 78% of ischaemia producing lesions appeared as simple stenoses, while 92% of the unstable or more severely ischaemic patients exhibited complicated lesions (p less than 0.001). In unstable angina and non-Q infarction a complex lesion was present respectively in 71% and 60% of the cases; clear-cut intraluminal thrombosis was demonstrated in 23% of unstable angina, in 30% of non-Q wave infarction and in 39% of transmural infarction (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain

Aims An increase in platelet aggregability is associated withunstable angina and myocardial infarction. Platelet size andactivity correlate and mean platelet volume was found to beincreased before acute myocardial infarction. We measured themean platelet volume and platelet count in patients with stableangina, unstable angina and non-cardiac chest pain. Methods and results We studied 981 patients (734 men; 247 women)defined clinically as stable angina (n=688), unstable angina(n=108) and unstable angina requiring immediate angioplasty(n=52). After coronary angiography the patients were subdividedinto single (n=269), double (n=304) and triple-vessel disease(n=311) and the control group of non-cardiac chest pain (n=97).There was no significant difference in platelet count betweenthe control group and patients with 1, 2, or 3-vessel disease.However, the platelet size in patients with coronary arterydisease was significantly larger (single: 8·7±1·19fl;double: 8·7±1·12fl; triple-vessel disease:8·8±1·18fl) than the control group (8·2±0·95fl)(P<0·01). Patients with stable angina similarly hadno significant difference in platelet count compared to thecontrol group but did have a significantly increased mean plateletvolume (8·7±1·13;P<0·01). Incontrast, patients with unstable angina had a decreased plateletcount (245±56x10/l) compared to either stable angina(262±62x10/l;P<0·05) or the control group (261±58x10/l;P<0·05);furthermore, the mean platelet volume (9·4±1·23fl)was significantly greater than for stable angina (P<0·01).Patients with unstable angina requiring immediate PTCA had aneven lower platelet count (231±55x10/l) and higher meanplatelet volume (10·4±1·03fl) (P<0·01)than the rest of the population with unstable angina. Conclusions In stable angina the platelet count is unchangedcompared to patients with normal coronary arteries but the plateletsize is increased. However, in unstable angina there is a decreasein platelet count and an even larger increase in platelet size.We interpret this as meaning that unstable angina might be associatedor preceded by an increase in platelet destruction rate thatis not completely compensated for by an increase in plateletproduction rate. The large, more reactive platelets might becausally related to an ongoing coronary artery obstruction inunstable angina.     

Lipoprotein (a) blood levels in unstable angina pectoris, acute myocardial infarction, and after thrombolytic therapy

Lipoprotein (a) [Lp(a)] appears to be involved in atherogenesis and in vitro studies have suggested that it may interfere with thrombolysis. In this study, Lp(a) serum levels were determined by radioimmunoassay in 124 patients with ischemic heart disease. Of these, 47 had acute myocardial infarction, 13 had unstable angina, and 64 were age-matched patients with stable angina. Of the 60 patients with acute coronary artery disease, 34 received thrombolysis and 26 did not. In addition to Lp(a), serum plasminogen, alpha 2 antiplasmin, fibrinogen, and D-dimer (cross-linked fibrin degradation products) levels were measured. These tests were repeated after 6 hours in patients with myocardial infarction and unstable angina. No significant difference was found for admission Lp(a) levels among patients with myocardial infarction (0.324 +/- 0.047 g/liter), unstable angina (0.435 +/- 0.123 g/liter) and stable angina (0.431 +/- 0.023 g/liter), between patients with myocardial infarction with or without thrombolytic treatment, nor between late and early measurements in patients with unstable angina and acute myocardial infarction. Plasminogen, alpha 2 antiplasmin and fibrinogen values decreased significantly after thrombolytic treatment. The size of this decrease correlated positively with higher Lp(a) blood levels (p less than 0.05). Patients with Lp(a) greater than 0.25 g/liter had a 66% decrease in fibrinogen and a 53% decrease in anti-plasmin, compared with 35 and 32%, respectively, in patients with Lp(a) level less than or equal to 0.25 g/liter (p less than 0.05). Plasminogen levels revealed a similar trend, with a 61% decrease for the higher values and a 45% decrease for the lower values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circulating miR-214 is associated with the severity of coronary artery disease

Objective To study whether miR-214 is regulated in coronary artery disease (CAD) patients and whether placental growth factor (PLGF) is a possible target for miR-214 in atherosclerosis. Methods Circulating miR-214 was measured by quantitative PCR using RNA isolated from 40 patients with CAD, including 12 with stable angina pectoris, 16 with unstable angina pectoris and 12 with acute myocardial infarction, and 15 controls without CAD. Plasma level of PLGF was measured by ELISA. Results The miR-214 level was significantly lower in CAD patients compared with that in controls (P < 0.01). Compared to controls, patients with unstable angina pectoris (UAP, 38.6±9.1 pg/mL) and acute myocardial infarction (AMI, 46.3±13.4 pg/mL) had significantly higher level of plasma PLGF, but not those with stable angina pectoris (SAP; P = 0.012, UAP vs. Control; P = 0.005, AMI vs. Control). In patients with AMI, the plasma level of miR-214 was positively correlated to that of PLGF. Conclusions The results suggest that miR-214 is a beneficial microRNA for CAD patients. Loss of its protection may lead to increased PLGF levels and worsening atherosclerosis. Circulating miR-214 is a promising biomarker for alerting severe CAD.     

Elevated Plasma Lipoprotein(a) Is Associated With Coronary Artery Disease in Patients With Chronic Stable Angina Pectoris

Objectives. We sought to assess the relation between plasma lipoprotein(a) [Lp(a)] levels, clinical variables and angiographic coronary artery disease (CAD) in patients with chronic stable angina.Background. The relation between plasma Lp(a) levels and the severity and extent of angiographic CAD has not been studied in well characterized patients with stable angina pectoris.Methods. We investigated clinical variables, lipid variables and angiographic scores in 129 consecutive white patients (43 women) undergoing coronary angiography for chronic stable angina.Results. Plasma Lp(a) levels were significantly higher in patients with than in those without significant angiographic stenoses (≥70%) (372 mg/liter [interquartile range 87 to 884] vs. 105 mg/liter [interquartile range 56 to 366], respectively, p = 0.002). This difference remained significant when patients with mild or severe angiographic disease were compared with those with completely normal coronary arteries (312 mg/liter [interquartile range 64 to 864] vs. 116 mg/liter [interquartile range 63 to 366], respectively, p = 0.02). However, subset analysis indicated that this difference achieved statistical significance only in women. Multiple logistic regression analysis indicated that Lp(a) concentration was independently predictive of significant angiographic stenoses (adjusted odds ratio [OR] 9.1, 95% confidence interval [CI] 2.0 to 42.1, p = 0.006) and remained true even after exclusion of patients receiving lipid-lowering treatment (n = 27) (OR 10.4, 95% CI 1.1 to 102.9, p = 0.05). Lp(a) also had independent predictive value in a similar analysis using mild or severe angiographic disease as the outcome variable (OR 11.8, 95% CI 1.5 to 90.8, p = 0.02).Conclusions. Our results indicate that elevated plasma Lp(a) is an independent risk factor for angiographic CAD in chronic stable angina and may have particular significance in women.