Increased level of advanced oxidation products (AOPP) as a marker of oxidative stress in patients with acute coronary syndrome

Oxidative stress impairs endothelial function and may play an important role in the pathogenesis of acute cardiovascular diseases. Advanced oxidation protein products (AOPP) were proposed as one of the possible markers of oxidative injury, which originates under oxidative and carbonyl stress and increase global inflammatory activity. The present study was undertaken to compare AOPP concentrations in a control group of healthy individuals without ICHS (I), patients with stable angina pectoris (II), patients with acute coronary syndrome over 48 hours without ST elevations (III), and patients with ST elevation myocardial infarction (IV). Coronaronary angiography, risk factors and anamnestic data were analyzed. We examined 73 probands with signs of myocardial ischemia, mean age of 61.5 years (64% males) subjected to coronarography and 21 healthy individuals. No significant difference was found between venous blood and coronary samples, or between infarction and non-infarction arteries in the group IV. AOPP concentrations in healthy individuals in the group I (82.9 +/- 29.3 mmol/l) did not differ significantly from patients in group II (89.6 +/- 26.7 mmol/l) and group III (112.3 +/- 54.6 mmol/l). A significant difference in AOPP values was found between the groups I and IV, and between the groups II and IV (82.9 +/- 29.3 mmol/l vs. 125.8 +/- 101 mmol/l, p = 0.02, and 89.6 +/- 26.7 mmol/l vs. 125.8 +/- 101 mmol/l, p = 0.02). No correlations were found between AOPP and body mass index (BMI), nicotinism, left ventricular ejection fraction, parameters of glucose and lipid metabolism. ROC analysis revealed that AOPP concentrations of 89 mmol/l had 64% sensitivity and 71% specificity for revealing an acute coronary syndrome (AUC 0.65, 95% CI 0.55-0.80). AOPP are significantly increased in patients with acute coronary syndromes with ST segment elevation, but also tend to increase in patients with non-ST elevation myocardial infarction. Our observations suggest that AOPP may be used as a marker of oxidative stress and as a prognostic factor for severe forms of cardiovascular disease. A cut-off value of 89 mmol/l can be used with 64% sensitivity and 71% specificity for revealing acute coronary syndrome.     

Use of glycogen phosphorylase BB measurement with POCT in the diagnosis of acute coronary syndromes. A comparison with the ELISA method

Background: Glycogen Phosphorylase BB (GPBB) is considered an early and specific marker of myocardial necrosis and ischemia. A POCT kit GPBB for diagnostic use has recently been approved. Aim: an evaluation of the correspondence of qualitative POCT GBPP measurements with ELISA test results. Material and methodology: 20 individuals with non-ST elevation myocardial infarction (non-STEMI) and 20 probands without acute coronary syndrome (ACS) were tested. GPBB (POCT, ELISA) in venous plasma (lithium-heparin) was assayed in all probands. Results: individuals with non-STEMI had significantly higher GPBB ELISA values (32.3 vs. 6.1 mug/l; p < 0.01). GPBB sensitivity and specificity for non-STEMI presence 6 hours after chest pain generation were 100 %. No proband was classified in a different subgroup with POCT of GPBB (positive/negative). GPBB POCT correlate with a non- STEMI diagnosis (chi(2) 36.1; p <0.01). Conclusion: GPBB POCT measurement is comparable with ELISA test results. GPBB analysis could expand the diagnostic palette in the first hours after the onset of acute coronary syndrome.     

Initial Heparin Therapy in Acute Myocardial Infarction

The administration of heparin during the first 48 hours following acute myocardial infarction is widely practised. Heparin treatment is also recommended for acute coronary insufficiency on the grounds that it may prevent development of an impending myocardial infarction. These measures had been accepted without support of a controlled clinical trial. By random selection, 101 patients hospitalized with a provisional diagnosis of acute myocardial infarction received heparin (100 mg. intravenously every eight hours for 48 hours) and 105 patients were assigned to a control group. Both groups of patients received bishydroxycoumarin (Dicumarol). The mortality in the heparin series was 30% and in the control group, 28%. A significantly large number of the heparin-treated patients developed clinical and laboratory proof of recent myocardial infarction. It is concluded that early intermittent intravenous heparin treatment does not lower the mortality in patients with acute myocardial infarction nor does it prevent impending myocardial infarction in patients with acute coronary insufficiency.     

Is Metabolic Syndrome Predictive of Prevalence,Extent, and Risk of Coronary Artery Disease beyond Its Components? Results from the Multinational Coronary CT Angiography Evaluation for Clinical Outcome: An International Multicenter Registry (CONFIRM)

Although metabolic syndrome is associated with increased risk of cardiovascular disease and events, its added prognostic value beyond its components remains unknown. This study compared the prevalence, severity of coronary artery disease (CAD), and prognosis of patients with metabolic syndrome to those with individual metabolic syndrome components. The study cohort consisted of 27125 consecutive individuals who underwent ≥64-detector row coronary CT angiography (CCTA) at 12 centers from 2003 to 2009. Metabolic syndrome was defined as per NCEP/ATP III criteria. Metabolic syndrome patients (n=690) were matched 1:1:1 to those with 1 component (n=690) and 2 components (n=690) of metabolic syndrome for age, sex, smoking status, and family history of premature CAD using propensity scoring. Major adverse cardiac events (MACE) were defined by a composite of myocardial infarction (MI), acute coronary syndrome, mortality and late target vessel revascularization. Patients with 1 component of metabolic syndrome manifested lower rates of obstructive 1-, 2-, and 3-vessel/left main disease compared to metabolic syndrome patients (9.4% vs 13.8%, 2.6% vs 4.5%, and 1.0% vs 2.3%, respectively; p<0.05), while those with 2 components did not (10.5% vs 13.8%, 2.8% vs 4.5% and 1.3% vs 2.3%, respectively; p>0.05). At 2.5 years, metabolic syndrome patients experienced a higher rate of MACE compared to patients with 1 component (4.4% vs 1.6%; p=0.002), while no difference observed compared to individuals with 2 components (4.4% vs 3.2% p=0.25) of metabolic syndrome. In conclusion, Metabolic syndrome patients have significantly greater prevalence, severity, and prognosis of CAD compared to patients with 1 but not 2 components of metabolic syndrome.     

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.     

斑点追踪技术对非ST 段抬高急性冠脉综合征的研究进展

非ST段抬高急性冠脉综合征(Non-ST segment elevation acute coronary syndrome,NSTE-ACS)是不稳定斑块基础上急性血栓形成,冠脉狭窄程度骤然加剧,冠脉血流减少导致心肌氧供应的直接减少为病理基础的一组临床综合征,好发于老年人,常累及多支血管,由于其心电图及常规超声心动图表现不典型,容易给临床带来困扰,斑点追踪成像(speckle tracking imaging,STI)无角度依赖性分别评价左室纵向、圆周、径向、扭转功能,为敏感评价左室功能早期改变提供了新的方法,本文对非ST段抬高急性冠脉综合征患者的临床特点以及斑点追踪技术的临床应用研究进展进行了综述。     

Disappearing signs of acute myocardial infarction in a patient with viral myocarditis

A case of acute viral myocarditis with the rapid appearance and disappearance of clinical, laboratory, electrocardiographic, and vectorcardiographic signs of acute myocardial infarction is described in this report. Although segmentary alterations in contractility were demonstrated by ventriculography, coronary angiography revealed normal coronary arteries.     

Interaction between left ventricular wall motion and intraventricular flow propagation in acute and chronic ischemia

Myocardial ischemia has been associated with left ventricular (LV) postsystolic shortening. The combination of tissue Doppler imaging and high frame-rate acquisition of two-dimensional color flow makes it possible to study the interaction between LV wall motion and intraventricular flow propagation. The aim of this study was to examine in a clinical model the impact that acute myocardial ischemia and prior myocardial infarct might have on LV flow patterns and to explain the underlying mechanisms from the tissue Doppler data. LV flow propagation and tissue velocities during early diastole were studied in 18 healthy individuals, 17 patients with prior anterior myocardial infarct, and 16 patients before and during percutaneous coronary intervention (PCI) of the left anterior descending artery. Normal individuals had intraventricular flow propagation toward the apex during isovolumic relaxation. During this early diastolic time phase, myocardial velocities measured at mid- and apical septal segment were directed away from the apex. Before PCI, patients without myocardial infarction had similar findings as in normal individuals. In contrast, each patient with either prior myocardial infarction or PCI-induced acute ischemia had flow propagation opposite to normal individuals, and tissue velocities reversed toward the apex during early diastole. Reversal of early diastolic LV flow propagation in acute and chronic anterior myocardial ischemia reflects postsystolic shortening in the dyskinetic apical and septal myocardial segments.     

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.     

Inosine and hypoxanthine as novel biomarkers for cardiac ischemia: From bench to point-of-care

Cardiac ischemia associated with acute coronary syndrome and myocardial infarction is a leading cause of mortality and morbidity in the world. A rapid detection of the ischemic events is critically important for achieving timely diagnosis, treatment and improving the patient''s survival and functional recovery. This minireview provides an overview on the current biomarker research for detection of acute cardiac ischemia. We primarily focus on inosine and hypoxanthine, two by-products of ATP catabolism. Based on our published findings of elevated plasma concentrations of inosine/hypoxanthine in animal laboratory and clinical settings, since 2006 we have originally proposed that these two purine molecules can be used as rapid and sensitive biomarkers for acute cardiac ischemia at its very early onset (within 15 min), hours prior to the release of heart tissue necrosis biomarkers such as cardiac troponins. We further developed a chemiluminescence technology, one of the most affordable and sensitive analytical techniques, and we were able to reproducibly quantify and differentiate total hypoxanthine concentrations in the plasma samples from healthy individuals versus patients suffering from ischemic heart disease. Additional rigorous clinical studies are needed to validate the plasma inosine/hypoxanthine concentrations, in conjunction with other current cardiac biomarkers, for a better revelation of their diagnostic potentials for early detection of acute cardiac ischemia.     

ACS,myocardial bridging,Tako-tsubo syndrome and mitral regurgitation

Isolated systolic compression of the mid portion of the left anterior descending artery (LAD) by a bridge of overlying cardiac muscle is an infrequent but well-recognised angiographic anomaly that is often considered harmless. The long-term prognosis appears to be excellent, but occasional reports of patients with angina pectoris, myocardial infarction and sudden death indicate that this is not always true. The prevalence of the anomaly in the normal population is unknown, but the incidence is low and ischaemic events are rare.Tako-tsubo-like left ventricular dysfunction syndrome (TTS) is characterised by ischaemia, anterior ST-segment elevation, no significant coronary artery disease and reversible ampulla-like left ventricular ballooning in postmenopausal females after emotional or physical stress. Dynamic left ventricular outflow tract (LVOT) obstruction is a rare but potentially fatal complication of acute anterior wall infarction.We present a patient with an acute coronary syndrome (ACS) with ST-segment elevation in the anterior leads, transient TTS and transient LVOT obstruction with systolic anterior motion (SAM) of the mitral valve and severe mitral regurgitation. This is the first report of myocardial bridging associated with TTS, and the first report of TTS associated with dynamic LVOT obstruction with SAM and mitral regurgitation.     

Growth differentiation factor 11 attenuates cardiac ischemia reperfusion injury via enhancing mitochondrial biogenesis and telomerase activity

It has been reported that growth differentiation factor 11 (GDF11) protects against myocardial ischemia/reperfusion (IR) injury, but the underlying mechanisms have not been fully clarified. Considering that GDF11 plays a role in the aging/rejuvenation process and that aging is associated with telomere shortening and cardiac dysfunction, we hypothesized that GDF11 might protect against IR injury by activating telomerase. Human plasma GDF11 levels were significantly lower in acute coronary syndrome patients than in chronic coronary syndrome patients. IR mice with myocardial overexpression GDF11 (oe-GDF11) exhibited a significantly smaller myocardial infarct size, less cardiac remodeling and dysfunction, fewer apoptotic cardiomyocytes, higher telomerase activity, longer telomeres, and higher ATP generation than IR mice treated with an adenovirus carrying a negative control plasmid. Furthermore, mitochondrial biogenesis-related proteins and some antiapoptotic proteins were significantly upregulated by oe-GDF11. These cardioprotective effects of oe-GDF11 were significantly antagonized by BIBR1532, a specific telomerase inhibitor. Similar effects of oe-GDF11 on apoptosis and mitochondrial energy biogenesis were observed in cultured neonatal rat cardiomyocytes, whereas GDF11 silencing elicited the opposite effects to oe-GDF11 in mice. We concluded that telomerase activation by GDF11 contributes to the alleviation of myocardial IR injury through enhancing mitochondrial biogenesis and suppressing cardiomyocyte apoptosis.Subject terms: Apoptosis, Heart failure     

急性冠脉综合征患者发生冠脉血管完全闭塞病变的影响因素分析

目的:探讨急性冠脉综合征(acute coronary syndrome,ACS)患者发生冠脉血管完全闭塞病变的影响因素。方法:从2013年在我院诊断为ACS且行冠状动脉造影检查患者中随机筛选出120例患者为研究对象,记录其基线及临床资料,回顾其造影图像,计算SYNTAX积分,根据是否存在完全闭塞病变分组,分析慢性完全闭塞病变的影响因素。结果:与不完全闭塞病变组相比,完全闭塞病变组吸烟(61.1%,P=0.041)、糖尿病(35.2%,P=0.025)、高脂血症(55.6%,P=0.033)发生率高,入院静息心率(77.07±11.99,P=0.023)高,中性粒细胞/淋巴细胞比值(Neutrophil-to-Lymphocyte Ratio,NLR)水平(8.69±9.46,P0.001)显著升高,左室射血分数(left ventricular ejection fraction,LVEF)(50.39±8.36,P=0.001)显著降低。多因素分析显示年龄(P=0.043)、急性心梗(acute myocardial infarction,AMI)的发生(P=0.003)、LVEF(P=0.002)、NLR(P=0.002)、脂蛋白(a)(P=0.039)、SYNTAX积分(P=0.002)和完全闭塞病变独立正相关。结论:ACS患者发生慢性完全闭塞病变与年龄、静息心率、吸烟史、高脂血症相关,与冠脉病变复杂程度、左室功能下降密切相关。NLR作为新型炎症标志之一,可预测ACS患者完全闭塞病变。     

Statin therapy for prevention and treatment of acute and chronic cardiovascular disease: update on recent trials and metaanalyses

PURPOSE OF REVIEW: To summarize the evidence from recent clinical trials and metaanalyses on the efficacy of statin therapy to reduce death, myocardial infarction and stroke, and to review the effects of statins in patients with low LDL cholesterol, diabetes, end-stage renal disease, and acute coronary syndrome. RECENT FINDINGS: In large metaanalyses of randomized controlled trials relative risk reductions from statins compared with placebo for patients with manifest or with risk factors for coronary artery disease were 13% for overall mortality, 26% for fatal and nonfatal myocardial infarction, and 18% for fatal and nonfatal stroke. Evidence from large trials suggests that patients with type II diabetes compared with patients without diabetes have similar risk reductions from statins for cardiovascular events, but this benefit is not seen in patients with diabetes and end-stage renal disease. In patients with acute coronary syndrome, early treatment with high-dose atorvastatin reduces cardiovascular morbidity after the first 4 months following the event, but the impact on mortality endpoints remains less clear. Results from recent trials in patients with stable coronary artery disease or type II diabetes suggest that statins provide benefit at considerable low LDL cholesterol levels. Therefore, target values for LDL cholesterol of less than 1.8 mmol/l (<70 mg/dl) should be considered for all patients with coronary artery disease or equivalent coronary risk. SUMMARY: For patients at high risk of coronary artery disease there is growing evidence for the concept of 'the lower, the better' regarding LDL cholesterol levels. Ongoing trials are further investigating the safety of lower target values in patients at various risk of coronary artery disease.     

Troponin elevation in patients with various tachycardias and normal epicardial coronaries

Troponin elevation is usually synonymous with acute coronary syndrome (ACS). Although sensitive for ACS, the elevation of serum troponin, in the absence of clinical evidence of ischemia, should prompt a search for other etiologies of myocardial necrosis. In fact, elevated values of troponin are correlated with myocardial necrosis even though it does not discriminate the mechanism involved. We report a series of seven patients (age range 18-67 years), who presented with complaints of chest discomfort and were found to have regular supraventricular tachycardia (5 patients) and one patient each with atrial fibrillation and ventricular tachycardia. All these patients had elevated troponin I and underwent coronary angiography that revealed normal epicardial coronary arteries. This is first case series in which all patients underwent coronary angiography and none of the patients was hemodynamically unstable at the time of presentation. Patients with elevated troponin due to conditions other than ACS can receive inappropriate and delayed definitive diagnosis and treatment.     

Antithrombotic therapy

Coronary heart disease is the leading cause of death in the US and the industrialized world. Ever since DeWood in 1980 demonstrated that a thrombus was the primary event leading to acute myocardial infarction and that they may subsequently lyse, the mainstay of therapy for the past 25 years has been antithrombotic therapy aimed at coronary thrombosis. There have been numerous advances in the treatment of acute coronary syndrome with antiplatelet, antithrombotic, and fibrinolytic agents that have significantly reduced morbidity and mortality. The role of various pharmaceutical agents in the different phases of acute coronary syndrome is a complex and ever changing field.7.     

Management of acute coronary occlusion during percutaneous transluminal coronary angioplasty: experience of complications in a hospital without on site facilities for cardiac surgery.

OBJECTIVE--To determine whether percutaneous transluminal coronary angioplasty may be safely performed in cardiology centres in the United Kingdom without immediate on site cardiac surgical cover for complications arising at angioplasty. DESIGN--Retrospective review of coronary angioplasties and complications in a hospital without on site cardiac surgical cover. SETTING--All angioplasties were performed in the catheterisation laboratory of the Belfast City Hospital. Revascularisation surgery for complicated coronary angioplasty was performed in the cardiac surgical unit of the Royal Victoria Hospital, 2.4 km away from the catheterisation laboratory. PATIENTS--540 Coronary angioplasties were performed on 512 patients between late 1982 and November 1988. Indications included stable angina, unstable rest angina, and suitable coronary disease at coronary arteriography after myocardial infarction. MAIN OUTCOME MEASURES--In hospital mortality after complicated coronary angioplasty and delay to surgical revascularisation after acute coronary occlusion at angioplasty. RESULTS--Coronary angioplasty was successful in 444 cases (82%). Acute coronary occlusion occurred in 35 cases (6.5%). Twelve patients required urgent revascularisation surgery and were transferred safely to the surgical unit; none of these patients died. A mean delay of 268 minutes (range 180-390 minutes) occurred before revascularisation compared with 273 minutes (range 108-420 minutes) in the Royal Victoria Hospital, where on site surgical cover was available. The principal cause of delay was the wait for a cardiac operating theatre to become available and not the transfer time between hospitals. Five deaths occurred after coronary angioplasty, a mortality of 0.9%. Three deaths were related to acute coronary occlusion. The absence of immediate surgical help did not influence the outcome in any patient. CONCLUSION--With careful selection of patients coronary angioplasty may be safely performed in a hospital without on site cardiac surgical facilities, provided that these are available at a nearby centre.     

Fragmented QRS: What Is The Meaning?

Fragmented QRS (fQRS) is a convenient marker of myocardial scar evaluated by 12-lead electrocardiogram (ECG) recording. fQRS is defined as additional spikes within the QRS complex. In patients with CAD, fQRS was associated with myocardial scar detected by single photon emission tomography and was a predictor of cardiac events. fQRS was also a predictor of mortality and arrhythmic events in patients with reduced left ventricular function. The usefulness of fQRS for detecting myocardial scar and for identifying high-risk patients has been expanded to various cardiac diseases, such as cardiac sarcoidosis, arrhythmogenic right ventricular cardiomyopathy, acute coronary syndrome, Brugada syndrome, and acquired long QT syndrome. fQRS can be applied to patients with wide QRS complexes and is associated with myocardial scar and prognosis. Myocardial scar detected by fQRS is associated with subsequent ventricular dysfunction and heart failure and is a substrate for reentrant ventricular tachyarrhythmias.     

Interpretation of elevated plasma visfatin concentrations in patients with ST-elevation myocardial infarction

Visfatin is a cytokine that is expressed in many tissues, including the heart, and has been proposed to play a role in plaque destabilization leading to acute myocardial injury. The present study evaluates plasma levels of visfatin in acute ST-elevation myocardial infarction (STEMI) patients and examines the temporal changes in visfatin levels from the acute period to the subacute period to determine a correlation with the degree of myocardial ischemia. We evaluated 54 patients with STEMI. Circulating levels of visfatin and brain natriuretic peptide (BNP) were measured by ELISA. In addition, local expression of visfatin and BNP were detected by quantitative real-time polymerase chain reaction and immunohistochemical (IHC) analysis of left ventricular myocytes in a mouse model of myocardial infarction (MI). Plasma levels of visfatin were significantly increased in patients with STEMI on admission, relative to controls (effort angina patients and individuals without coronary artery disease). The visfatin levels reached a peak 24 h after percutaneous coronary intervention (PCI) and then decreased toward the control range during the first week after PCI. The basal plasma visfatin levels were found to correlate with peak troponin-I, peak creatine kinase-MB, total white blood cell count, and BNP levels. Trend analyses confirmed that visfatin levels correlated with the number of diseased coronary arteries. Further, in MI mice, mRNA levels of visfatin and BNP were found to be higher than in sham-treated mice. IHC analysis showed that visfatin and BNP immunoreactivity was diffusely observable in left ventricular myocytes of the MI mice. This study indicates that plasma visfatin levels are significantly higher in STEMI patients and that these higher visfatin levels correlate with elevated levels of cardiac enzymes, suggesting that increased plasma visfatin may be closely related to the degree of myocardial damage.