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Background: Recent studies show Silent Myocardial Infarction (SMI) as a quite frequent event. However, regarding severe tertiary care patients that frequently present consequences of Coronary Artery Disease (CAD) and Left Ventricular Dysfunction (LVD), the occurrence of this manifestation is unexpected and its associated factors aren't clear in the literature., Aim: To compare clinical, laboratorial, ventricular and angiographic factors between silent and classical presentation of MI in patients with CAD and LVD., Methods: Patients with multivessel CAD with over 70 % obstructive lesions and LVD with EF less than 35 % were evaluated for MASS VI trial and later included in the present study. The ventricular function and coronary assessment were measured by echocardiography and SYNTAX score, respectively. The population was stratified in a SMI group and Clinically Manifested Myocardial Infarction (CMMI) group based on MI presentation for a comparison of medical parameters., Results: From 132 patients, 47 (35.6 %) were classified as SMI and 85 (64.4 %) as CMMI. No differences were observed between groups regarding age, sex, diabetes mellitus, SYNTAX score, or collateral circulation. Higher proportion of NYHA II classification, inferior wall MI and lower creatinine clearance were found in SMI group. After multivariate analysis, peripheral diabetic neuropathy (OR = 4.6 [1.1‒12.7] p = 0.032) and inferior wall MI (OR = 4.1 [1.5‒11.4] p = 0.007) were significantly associated with SMI., Conclusion: Peripheral diabetic neuropathy and inferior wall MI were associated with SMI presentation. Overall, associated factors tend to be similar comparing SMI and CMMI, but in the specific population of diabetic patients with chronic neuropathy a special care should be taken., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2024 HCFMUSP. Published by Elsevier España, S.L.U. All rights reserved.)

Background: After the results of the ISCHEMIA Trial, the role of myocardial ischemia in the prognosis of coronary artery disease (CAD) was under debate. We sought to comparatively evaluate the long-term prognosis of patients with multivessel CAD with or without documented myocardial ischemia., Methods: This is a single-center, retrospective, observational cohort study that included patients with CAD obtained from the research protocols database of "The Medicine, Angioplasty or Surgery Study," the MASS Study Group. Patients were stratified according to the presence or absence of myocardial ischemia. Cardiovascular events (overall mortality and myocardial infarction) were tracked from the registry entry up to a median follow-up of 8.7 years. Myocardial ischemia was assessed at baseline by a functional test with or without imaging., Results: From 1995 to 2018, 2015 patients with multivessel CAD were included. Of these, 1001 presented with conclusive tests at registry entry, 790 (79%) presenting with ischemia and 211 (21%) without ischemia. The median follow-up was 8.7 years (IQR 4.04 to 10.07). The primary outcome occurred in 228 (28.9%) patients with ischemia and in 64 (30.3%) patients without ischemia (p log-rank =0.60). No significant interaction was observed with the presence of myocardial ischemia and treatment strategies in the occurrence of the combined primary outcome (p interation =0.14)., Conclusions: In this sample, myocardial ischemia was not associated with a worse prognosis compared with no ischemia in patients with multivessel CAD. These results refer to debates about the role of myocardial ischemia in the occurrence of cardiovascular events., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Introduction: Coronary atherosclerotic burden and SYNTAX Score (SS) are predictors of cardiovascular events., Objectives: To investigate the value of SYNTAX scores (SS, SYNTAX Score II (SSII) and residual SYNTAX Score (rSS)) for predicting cardiovascular events in patients with coronary artery disease (CAD)., Design: Retrospective cohort study., Setting: Single tertiary centre., Participants: Medicine, Angioplasty or Surgery Study database patients with stable multivessel CAD and preserved ejection fraction., Interventions: Patients with CAD undergoing coronary artery bypass graft (CABG), percutaneous coronary intervention (PCI) or medical treatment (MT) alone from January 2002 to December 2015., Primary and Secondary Outcomes: Primary: 5-year all-cause mortality. Secondary: composite of all-cause death, myocardial infarction, stroke and subsequent coronary revascularisation at 5 years., Results: A total of 1719 patients underwent PCI (n=573), CABG (n=572) or MT (n=574) alone. The SS was not considered an independent predictor of 5-year mortality in the PCI (low, intermediate and high SS at 6.5%, 6.8% and 4.3%, respectively, p=0.745), CABG (low, intermediate and high SS at 5.7%, 8.0% and 12.1%, respectively, p=0.194) and MT (low, intermediate and high SS at 6.8%, 6.9% and 6.5%, respectively, p=0.993) cohorts. The SSII (low, intermediate and high SSII at 3.6% vs 7.9% vs 10.5%, respectively, p<0.001) was associated with a higher mortality risk in the overall population. Within each treatment strategy, SSII was associated with a significant 5-year mortality rate, especially in CABG patients with higher SSII (low, intermediate and high SSII at 1.8%, 9.7% and 10.0%, respectively, p=0.004) and in MT patients with high SSII (low, intermediate and high SSII at 5.0%, 4.7% and 10.8%, respectively, p=0.031). SSII demonstrated a better predictive accuracy for mortality compared with SS and rSS (c-index=0.62)., Conclusions: Coronary atherosclerotic burden alone was not associated with significantly increased risk of all-cause mortality. The SSII better discriminates the risk of death., Trial Registration Number: ISRCTN66068876., Competing Interests: Competing interests: MEF has received research grants from Amgen, Novo Nordisk and Novartis. LCG has received the Frederick Banting and Charles Best Canada Graduate Scholarship (Doctoral Research Award) from the Canadian Institutes of Health Research., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: The diagnosis of peri-procedural myocardial infarction is complex, especially after the emergence of high-sensitivity markers of myocardial necrosis., Methods: In this study, patients with normal baseline cardiac biomarkers and formal indication for elective on-pump coronary bypass surgery were evaluated. Electrocardiograms, cardiac biomarkers, and cardiac magnetic resonance imaging with late gadolinium enhancement were performed before and after procedures. Myocardial infarction was defined as more than ten times the upper reference limit of the 99th percentile for troponin I and for creatine kinase isoform (CK-MB) and by the findings of new late gadolinium enhancement on cardiac magnetic resonance. We assessed the release of cardiac biomarkers in patients with no evidence of myocardial infarction on cardiac magnetic resonance., Results: Of 75 patients referred for on-pump coronary bypass surgery, 54 (100%) did not have evidence of myocardial infarction on cardiac magnetic resonance. However, all had a peak troponin I above the 99th percentile; 52 (96%) had an elevation 10 times higher than the 99th percentile. Regarding CK-MB, 54 (100%) patients had a peak CK-MB above the 99th percentile limit, and only 13 (24%) had an elevation greater than 10 times the 99th percentile. The median value of troponin I peak was 3.15 (1.2 to 3.9) ng/mL, which represented 78.7 times the 99th percentile., Conclusion: In this study, different from CK-MB findings, troponin was significantly increased in the absence of myocardial infarction on cardiac magnetic resonance. Thus, CK-MB was more accurate than troponin I for excluding procedure-related myocardial infarction. These data suggest a higher troponin cutoff for the diagnosis of coronary bypass surgery related myocardial infarction., Clinical Trial Registration: http://www.isrctn.com/ISRCTN09454308 . Registered 08 May 2012.

Background: The lack of a correlation between myocardial necrosis biomarkers and electrocardiographic abnormalities after revascularization procedures has resulted in a change in the myocardial infarction (MI) definition., Methods: Patients with stable multivessel disease who underwent percutaneous or surgical revascularization were included. Electrocardiograms and concentrations of high-sensitive cardiac troponin I (cTnI) and creatine kinase (CK)-MB were assessed before and after procedures. Cardiac magnetic resonance and late gadolinium enhancement were performed before and after procedures. MI was defined as more than five times the 99th percentile upper reference limit for cTnI and 10 times for CK-MB in percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), respectively, and new late gadolinium enhancement for cardiac magnetic resonance., Results: Of the 202 patients studied, 69 (34.1%) underwent on-pump CABG, 67 (33.2%) off-pump CABG, and 66 (32.7%) PCI. The receiver operating characteristic curve showed the accuracy of cTnI for on-pump CABG, off-pump CABG, and PCI patients was 21.7%, 28.3%, and 52.4% and for CK-MB was 72.5%, 81.2%, and 90.5%, respectively. The specificity of cTnI was 3.6%, 9.4%, and 42.1% and of CK-MB was 73.2%, 86.8%, and 96.4%, respectively. Sensitivity of cTnI was 100%, 100%, and 100% and of CK-MB was 69.2%, 64.3%, and 44.4%, respectively. The best cutoff of cTnI for on-pump CABG, off-pump CABG, and PCI was 6.5 ng/mL, 4.5 ng/mL, and 4.5 ng/mL (162.5, 112.5, and 112.5 times the 99th percentile upper reference limit) and of CK-MB was 37.5 ng/mL, 22.5 ng/mL, and 11.5 ng/mL (8.5, 5.1, and 2.6 times the 99th percentile upper reference limit), respectively., Conclusions: Compared with cardiac magnetic resonance, CK-MB was more accurate than cTnI for diagnosing MI. These data suggest a higher troponin cutoff for the diagnosis of procedure-related MI., (Copyright © 2016 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Objective: Enhanced sodium intake increases volume overload, oxidative stress and production of proinflammatory cytokines. In animal models, increased sodium intake favours ventricular dysfunction after myocardial infarction (MI). The aim of this study was to investigate, in human subjects presenting with ST-segment elevation MI (STEMI), the impact of sodium intake prior the coronary event., Methods: Consecutive patients (n=372) admitted within the first 24 h of STEMI were classified by a food intake questionnaire as having a chronic daily intake of sodium higher (HS) or lower (LS) than 1.2 g in the last 90 days before MI. Plasma levels of 8-isoprostane, interleucin-2 (IL-2), tumour necrosis factor type α (TNF-α), C-reactive protein (CRP) and brain natriuretic peptide (BNP) were measured at admission and at the fifth day. Magnetic resonance imaging was performed immediately after discharge. Total mortality and recurrence of acute coronary events were investigated over 4 years of follow-up., Results: The decrease of 8-isoprostane was more prominent and the increase of IL-2, TNF-α and CRP less intense during the first 5 days in LS than in HS patients (p<0.05). Sodium intake correlated with change in plasma BNP between admission and fifth day (r=0.46; p<0.0001). End-diastolic volumes of left atrium and left ventricle were greater in HS than in LS patients (p<0.05). In the first 30 days after MI and up to 4 years afterwards, total mortality was higher in HS than in LS patients (p<0.05)., Conclusion: Excessive sodium intake increases oxidative stress, inflammatory response, myocardial stretching and dilatation, and short and long-term mortality after STEMI., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Objective: Clinical trials of statins during myocardial infarction (MI) have differed in their therapeutic regimes and generated conflicting results. This study evaluated the role of the timing and potency of statin therapy on its potential mechanisms of benefit during MI., Methods and Results: ST-elevation MI patients (n=125) were allocated into 5 groups: no statin; 20, 40, or 80 mg/day simvastatin starting at admission; or 80 mg/day simvastatin 48 hours after admission. After 7 days, all patients switched their treatment to 20 mg/day simvastatin for an additional 3 weeks and then underwent flow-mediated dilation in the brachial artery. As of the second day, C-reactive protein (CRP) differed between non-statin users (12.0±4.1 mg/L) and patients treated with 20 (8.5±4.0 mg/L), 40 (3.8±2.5 mg/L), and 80 mg/day (1.4±1.5 mg/L), and the daily differences remained significant until the seventh day (P<0.0001). The higher the statin dose, the lower the elevation of interleukin-2 and tumor necrosis factor-α, the greater the reduction of 8-isoprostane and low-density lipoprotein(-), and the greater the increase in nitrate/nitrite levels during the first 5 days (P<0.001). Later initiation of statin was less effective than its early introduction in relation to attenuation of CRP, interleukin-2, tumor necrosis factor-α, 8-isoprostane, and low-density lipoprotein(-), as well as in increase in nitrate/nitrite levels (P<0.0001). At the 30th day, there was no longer a difference in lipid profile or CRP between groups; the flow-mediated dilation, however, was proportional to the initial statin dose and was higher for those who started the treatment early (P=0.001)., Conclusions: This study demonstrates that the timing and potency of statin treatment during MI are key elements for their main mechanisms of benefit. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00906451.

Objective: The study we assessed how often patients who are manifesting a myocardial infarction (MI) would not be considered candidates for intensive lipid-lowering therapy based on the current guidelines., Methods: In 355 consecutive patients manifesting ST elevation MI (STEMI), admission plasma C-reactive protein (CRP) was measured and Framingham risk score (FRS), PROCAM risk score, Reynolds risk score, ASSIGN risk score, QRISK, and SCORE algorithms were applied. Cardiac computed tomography and carotid ultrasound were performed to assess the coronary artery calcium score (CAC), carotid intima-media thickness (cIMT) and the presence of carotid plaques., Results: Less than 50% of STEMI patients would be identified as having high risk before the event by any of these algorithms. With the exception of FRS (9%), all other algorithms would assign low risk to about half of the enrolled patients. Plasma CRP was <1.0mg/L in 70% and >2mg/L in 14% of the patients. The average cIMT was 0.8±0.2mm and only in 24% of patients was ≥1.0mm. Carotid plaques were found in 74% of patients. CAC ≥100 was found in 66% of patients. Adding CAC ≥100 plus the presence of carotid plaque, a high-risk condition would be identified in 100% of the patients using any of the above mentioned algorithms., Conclusion: More than half of patients manifesting STEMI would not be considered as candidates for intensive preventive therapy by the current clinical algorithms. The addition of anatomical parameters such as CAC and the presence of carotid plaques can substantially reduce the CVD risk underestimation., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Background: Myocardial contrast echocardiography has been used for determination of infarct size (IS) in experimental models. However, with intermittent harmonic imaging, IS seems to be underestimated immediately after reperfusion due to areas with preserved, yet dysfunctional, microvasculature. The use of exogenous vasodilators showed to be useful to unmask these infarcted areas with depressed coronary flow reserve. This study was undertaken to assess the value of adenosine for IS determination in an open-chest canine model of coronary occlusion and reperfusion, using real-time myocardial contrast echocardiography (RTMCE)., Methods: Nine dogs underwent 180 minutes of coronary occlusion followed by reperfusion. PESDA (Perfluorocarbon-Exposed Sonicated Dextrose Albumin) was used as contrast agent. IS was determined by RTMCE before and during adenosine infusion at a rate of 140 mcg.Kg(-1).min(-1). Post-mortem necrotic area was determined by triphenyl-tetrazolium chloride (TTC) staining., Results: IS determined by RTMCE was 1.98 +/- 1.30 cm2 and increased to 2.58 +/- 1.53 cm2 during adenosine infusion (p = 0.004), with good correlation between measurements (r = 0.91; p < 0.01). The necrotic area determined by TTC was 2.29 +/- 1.36 cm2 and showed no significant difference with IS determined by RTMCE before or during hyperemia. A slight better correlation between RTMCE and TTC measurements was observed during adenosine (r = 0.99; p < 0.001) then before it (r = 0.92; p = 0.0013)., Conclusion: RTMCE can accurately determine IS in immediate period after acute myocardial infarction. Adenosine infusion results in a slight better detection of actual size of myocardial damage.

In this review we report our recent findings of histopathological features of plaque instability and the association with Mycoplasma pneumoniae (MP) and Chlamydia pneumoniae (CP) infection, studying thrombosed coronary artery segments (CAS) of patients who died due to acute myocardial infarction. Vulnerable plaques are known to be associated with fat atheromas and inflammation of the plaque. Here we demonstrated that vulnerability is also related with focal positive vessel remodeling that maintains relatively well preserved lumen even in the presence of large atheromatous plaques. This phenomena may explain why the cinecoronariography may not detect large and dangerous vulnerable plaques. Greater amount of these bacteria in vulnerable plaques is associated with adventitial inflammation and positive vessel remodeling: the mean numbers of lymphocytes were significantly higher in adventitia than in the plaque, good direct correlation was obtained between numbers of CD20 B cells and numbers of CP infected cells in adventitia, and between % area of MP-DNA in the plaque and cross sectional area of the vessel, suggesting a cause-effect relationship. Mycoplasma is a bacterium that needs cholesterol for proliferation and may increase virulence of other infectious agents. In conclusion, co-infection by Mycoplasma pneumoniae and Chlamydia pneumoniae may represent an important co-factor for plaque instability, leading to coronary plaque thrombosis and acute myocardial infarction, since larger amount of these bacteria strongly correlated with histological signs of more vulnerability of the plaque. The search of CMV and Helicobacter pilori in these tissues resulted negative.

Background: The diagnosis of peri-procedural myocardial infarction is complex, especially after the emergence of high-sensitivity markers of myocardial necrosis.Methods: In this study, patients with normal baseline cardiac biomarkers and formal indication for elective on-pump coronary bypass surgery were evaluated. Electrocardiograms, cardiac biomarkers, and cardiac magnetic resonance imaging with late gadolinium enhancement were performed before and after procedures. Myocardial infarction was defined as more than ten times the upper reference limit of the 99th percentile for troponin I and for creatine kinase isoform (CK-MB) and by the findings of new late gadolinium enhancement on cardiac magnetic resonance. We assessed the release of cardiac biomarkers in patients with no evidence of myocardial infarction on cardiac magnetic resonance.Results: Of 75 patients referred for on-pump coronary bypass surgery, 54 (100%) did not have evidence of myocardial infarction on cardiac magnetic resonance. However, all had a peak troponin I above the 99th percentile; 52 (96%) had an elevation 10 times higher than the 99th percentile. Regarding CK-MB, 54 (100%) patients had a peak CK-MB above the 99th percentile limit, and only 13 (24%) had an elevation greater than 10 times the 99th percentile. The median value of troponin I peak was 3.15 (1.2 to 3.9) ng/mL, which represented 78.7 times the 99th percentile.Conclusion: In this study, different from CK-MB findings, troponin was significantly increased in the absence of myocardial infarction on cardiac magnetic resonance. Thus, CK-MB was more accurate than troponin I for excluding procedure-related myocardial infarction. These data suggest a higher troponin cutoff for the diagnosis of coronary bypass surgery related myocardial infarction.Clinical Trial Registration: http://www.isrctn.com/ISRCTN09454308 . Registered 08 May 2012. [ABSTRACT FROM AUTHOR]

Background: Diabetic patients may be more susceptible to myocardial injury after coronary interventions. Thus, the aim of this study was to assess the release of cardiac biomarkers, CK-MB and troponin, and the findings of new late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) in patients with type 2 diabetes mellitus after elective revascularization procedures for multivessel coronary artery disease (CAD). Methods: Patients with multivessel CAD and preserved systolic ventricular function underwent either elective percutaneous coronary intervention (PCI), off-pump or on-pump bypass surgery (CABG). Troponin and CK-MB were systematically collected at baseline, 6, 12, 24, 36, 48 and 72 h after the procedures. CMR with LGE was performed before and after the interventions. Patients were stratified according to diabetes status at study entry. Biomarkers and CMR results were compared between diabetic and nondiabetics patients. Analyses of correlation were also performed among glycemic and glycated hemoglobin (A1c) levels and troponin and CK-MB peak levels. Patients were also stratified into tertiles of fasting glycemia and A1c levels and were compared in terms of periprocedural myocardial infarction (PMI) on CMR. Results: Ninety (44.5%) of the 202 patients had diabetes mellitus at study entry. After interventions, median peak troponin was 2.18 (0.47, 5.14) and 2.24 (0.69, 5.42) ng/mL (P = 0.81), and median peak CK-MB was 14.1 (6.8, 31.7) and 14.0 (4.2, 29.8) ng/mL (P = 0.43), in diabetic and nondiabetic patients, respectively. The release of troponin and CK-MB over time was statistically similar in both groups and in the three treatments, besides PCI. New LGE on CMR indicated that new myocardial fibrosis was present in 18.9 and 17.3% (P = 0.91), and myocardial edema in 15.5 and 22.9% (P = 0.39) in diabetic and nondiabetic patients, respectively. The incidence of PMI in the glycemia tertiles was 17.9% versus 19.3% versus 18.7% (P = 0.98), and in the A1c tertiles was 19.1% versus 13.3% versus 22.2% (P = 0.88). Conclusions: In this study, diabetes mellitus did not add risk of myocardial injury after revascularization interventions in patients with multivessel coronary artery disease. [ABSTRACT FROM AUTHOR]

Several lines of clinical evidence show that AMI frequently occurs at sites with mild to moderate degree of coronary stenosis. The degree of luminal stenosis depends on plaque deposition and degree of vessel remodeling, features poorly assessed by coronary angiography. This postmortem study tested the hypothesis that the size of coronary atheroma and the type of remodeling distinguish culprit lesion responsible for fatal AMI from equi-stenotic nonculprit lesion in the same coronary tree. The main coronary branches from 36 consecutive patients with fatal AMI were studied. The culprit lesion (Group 1) and an equi-stenotic nonculprit segment (Group 2) obtained in measurements of another coronary branch from the same patient were compared. Morphometry and plaque composition was assessed in both groups. Compared to Group 2, Group 1 had larger areas of: plaque \(9.6 vs. 4.7 mm^2\), vessel \(12.7 vs. 7.4 mm^2\) and lumen \(1.7 vs. 1.2 mm^2\); (P<.01). Positive remodeling was more frequent in Group 1 than Group 2: 21/30 (70%) vs. 8/26 (31%). Plaque area correlated positively with lipid core and macrophages and negatively with fibrosis and smooth muscle cells. Atherosclerotic plaques that cause fatal thrombosis are more frequently positively remodeled and tend to be larger than nonculprit plaques with the same degree of cross-sectional stenosis. We tested whether arterial remodeling and plaque size vary between segments containing a fatal thrombosed plaque versus an equi-stenotic nonculprit plaque. Culprit vessel segments had higher cross-sectional areas of intimal plaque and of vessel wall than equi-stenotic nonculprit plaques. The cross-sectional area of the vessel correlated positively with both the lipid core area and \(CD68^+\) macrophage content, and negatively with fibrosis area and smooth muscle cell content. These results add elements explaining limitations of angiography in identifying plaques and provide new insights into the role of remodeling in plaque instability., Other Research Unit

An abstract of the paper "Characterization of Peri-Infarct Zone by CMR Is a Robust Predictor of Major Adverse Events and Is Strongly Associated With Systemic Inflammatory Response Post-Myocardial Infarction," by Andrei Sposito and colleagues is presented.

A polymorphism of glycoprotein IIb/IIIa has been associated with myocardial infarction and restenosis after percutaneous coronary intervention. The influence on outcome and the interaction of the PlA1 genotype with classic risk factors for coronary artery disease (CAD) were characterized in patients with chronic CAD followed prospectively for 3 years. PlA1 genotypes were assessed in 592 patients enrolled in the Medical, Angioplasty, or Surgery Study II, a randomized trial comparing treatments for patients with CAD and preserved left ventricular function. The incidence of the composite end point of cardiac death, myocardial infarction, and refractory angina requiring revascularization were determined in each genotype group. Risk was assessed with the Cox proportional-hazards model. The clinical characteristics and treatment of each genotype were similar. Although the composite end point tended to be more common in patients with the PlA2 allele, only smokers with the PlA2 allele had a significantly increased incidence of the composite end point (p = 0.01). Moreover, a 2.2-fold increased risk was apparent in smokers with the PlA2 allele (p = 0.03). Thus, taken together, these data provide support for the interaction effect between smoking and the PlA1 gene variant. Smokers with the PlA2 polymorphism of platelet glycoprotein IIIa are at greater risk for subsequent cardiac events in stable coronary disease. [Copyright &y& Elsevier]

Background: To date, patients displaying stable angina with or without a previous acute coronary event have been grouped together and are offered nowadays, similar clinical approach. However, from clinical experience, increasing doubt exists whether they behave clinically in the same way. In the current study, we investigated whether differences might exist in the clinical, angiographic and biological parameters between these two distinct clinical presentations. Methods: The cardiovascular risk factor profile, clinical evolution, angiographic data, white blood cell (WBC) count and plasma concentrations of lipids and fibrinogen were compared between two groups of patients with longstanding stable angina. The first group consisted of 160 subjects who had undergone myocardial infarction (MI) as the first manifestation of coronary artery disease (CAD) and had no further coronary event. The second group was composed of 226 subjects who had effort-induced angina but never experienced an acute coronary event. The mean period between the first CAD manifestation and entry into the study was 7±6 years for MI group and 7±4 years for patients with uneventful angina. Results: MI patients displayed 8% higher WBC count (P=0.038), 20% higher fibrinogen (P=0.001), 12% lower HDL cholesterol (P=0.02), 8% lower apoA1 (P=0.005) and 46% higher lipoprotein (a) (P=0.005) than patients who presented an uneventful clinical course. Upon multivariate logistic regression analysis, fibrinogen (OR=1.14; 95% CI=1.08–1.28; P=0.033), lipoprotein (a) (OR=1.19; 95% CI=1.05–1.34; P=0.0036) and HDL cholesterol levels (OR=0.97; 95% CI=0.94–0.99; P=0.0095) remained independently associated with the pre-existence of MI. Patients with prior MI evolved more frequently towards clinically refractory angina (P=0.04). In addition, fibrinogen levels were independently associated with evolution to clinically refractory angina (OR=1.03; 95% CI=1.005–1.550; P=0.0448). Conclusions: Stable CAD patients with a prior MI differ from those who display an uneventful effort-induced angina in their biological profile and their evolution towards clinically refractory angina. [Copyright &y& Elsevier]

Introduction: Release of creatine kinase (CK-MB) and high-sensitivity cardiac troponin (hs-cTn) is common after revascularization procedures and represents myocardial injury. However, correlation between release of cardiac biomarkers and prognostic impact in a long-term follow-up is controversial. Hypothesis: To evaluate prognostic utility of elevation ofcardiac biomarkers in a long-term follow-up. Methods: Stable multivessel coronary disease patients who underwent percutaneous or surgical revascularization were included. Cardiac biomarkers were collected before and after procedures. Primary outcome was a composite of death, myocardial infarction, additional revascularizationor hospitalization for cardiac cause. Results: In a median follow-up of 4 years, 202 patients were followed, of whom 136 (67.3%) underwent coronary artery bypass grafting (CABG) and 66 (32.7%) underwent percutaneous coronary intervention (PCI). Fifty-nine (29.2%) and 47 (23.2%) patients had a peak of CK-MB (> 26.35 ng/ml) and a peak of hs-cTn (> 5.67 ng/ml). During follow-up, primary outcome was documented in 16 patients (7.9%). In CABG patients, CK-MB elevation above 26.35 ng/ml was associated toincreased risk of primary outcome (p log-rank 0.04; HR 5.49, 95% CI: 1.1-27.44; p = 0.03). In percutaneous group, release of troponin above 5.67 ng / ml was also associated to higher risk of primary outcome (p log-rank 0.04, HR 5.6, 95% CI: 1.07-29.2; p = 0.04). Conclusion: In this sample, release of cardiac biomarkers after myocardial revascularization procedures was a predictor of cardiovascular events. [ABSTRACT FROM AUTHOR]