Investigating the Effect of a Single Infusion of Reconstituted High-Density Lipoprotein in Patients with Symptomatic Carotid Plaques.

BACKGROUND: Elevation of plasma high-density lipoprotein (HDL) cholesterol concentration reduces cardiovascular mortality and morbidity. HDLs have been shown to possess acute anti-inflammatory, antioxidant, and antithrombotic properties. We hypothesize that HDL therapy can acutely alter local and systemic manifestations of plaque instability. METHODS: Forty patients with early symptomatic carotid disease were randomized to either receive reconstituted HDL (rHDL) 40 mg/kg (n = 20) or placebo (n = 20). Carotid endarterectomies were performed 24 hr later. Plaques were obtained intraoperatively and used for measurement of thrombomodulatory genes expression. Plasma samples were collected before the infusion, 24 and 48 hr later to measure changes in systemic markers of plaque instability. RESULTS: No significant differences were noted in thrombomodulatory genes expression between the 2 groups. Systemic levels of tissue factor, matrix metalloproteinase 9 (MMP-9), and monocyte chemotactic factor-1 (MCP-1) were significantly reduced in the rHDL group. However, the effects on MMP-9 and MCP-1 were abolished in the immediate postoperative period. Although rHDL did not affect plasma interleukin-6 levels 24 hr following the infusion, it prevented the significant postoperative elevation seen in the placebo group. CONCLUSIONS: A single infusion of rHDL can acutely alter plasma biomarkers associated with plaque instability and cardiovascular morbidity.

Analytical evaluation of the automated galectin-3 assay on the Abbott ARCHITECT immunoassay instruments.

BACKGROUND: Galectin-3 is secreted from macrophages and binds and activates fibroblasts forming collagen. Tissue fibrosis is central to the progression of chronic heart failure (CHF). We performed a European multicentered evaluation of the analytical performance of the two-step routine and Short Turn-Around-Time (STAT) galectin-3 immunoassay on the ARCHITECT i1000SR, i2000SR, and i4000SR (Abbott Laboratories). METHODS: We evaluated the assay precision and dilution linearity for both routine and STAT assays and compared serum and plasma, and fresh vs. frozen samples. The reference interval and biological variability were also assessed. Measurable samples were compared between ARCHITECT instruments and between the routine and STAT assays and also to a galectin-3 ELISA (BG Medicine). RESULTS: The total assay coefficient of variation (CV%) was 2.3%-6.2% and 1.7%-7.4% for the routine and STAT assays, respectively. Both assays demonstrated linearity up to 120 ng/mL. Galectin-3 concentrations were higher in plasma samples than in serum samples and correlated well between fresh and frozen samples (R=0.997), between the routine and STAT assays, between the ARCHITECT i1000 and i2000 instruments and with the galectin-3 ELISA. The reference interval on 627 apparently healthy individuals (53% male) yielded upper 95th and 97.5th percentiles of 25.2 and 28.4 ng/mL, respectively. Values were significantly lower in subjects younger than 50 years. CONCLUSIONS: The galectin-3 routine and STAT assays on the Abbott ARCHITECT instruments demonstrated good analytical performance. Further clinical studies are required to demonstrate the diagnostic and prognostic potential of this novel marker in patients with CHF.

Age-dependent values of N-terminal pro-B-type natriuretic peptide are superior to a single cut-point for ruling out suspected systolic dysfunction in primary care.

AIMS: The study evaluated the use of age-related decision limits for N-terminal pro-B-type natriuretic peptide (NT-proBNP), for ruling out suspected systolic dysfunction in symptomatic patients in primary care, compared with the present standards. METHODS AND RESULTS: Data were obtained from 5508 patients from 10 studies in the UK, New Zealand, Europe, and USA. All have had NT-proBNP analysis and echocardiography. The median age was 62 years (range 18-100 years) with a prevalence of reduced left ventricular systolic function (left ventricular ejection fraction < or =40%) of 18%. In a receiver operating characteristic curve analysis, overall area under the curve (AUC) was 0.89. When looking at different age groups, AUC was highest (0.95) for <50 years, intermediate (0.90) for 50-75 years, and lowest (0.82) for >75 years. Using optimized decision limits, sensitivity, specificity, and negative predictive values (NPVs) were: <50 years (50 ng/L): 99.2, 57.2, and 99.7%; 50-75 years (75 ng/L): 95.9, 51.0, and 96.8%; and >75 years (250 ng/L): 87.9, 53.7, and 92.4%, respectively. Using only a single decision value (125 ng/L for all ages) gave sensitivities of 89.1, 91.9, and 94.3%; specificities of 84.0, 69.1, and 29.3% and NPVs of 97.7, 97.6, and 93.4%. A decision value of 400 ng/L for all ages gave much lower sensitivities. CONCLUSION: In a large population of patients in primary care, the use of age-stratified NT-proBNP decision limits considerably improves performance over current standards, with an excellent NPV for exclusion of reduced left ventricular systolic function.

Clinical utility of cardiac troponin measurement in COVID-19 infection.

The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.

Defective endovascular trophoblast invasion in the first trimester is associated with increased maternal serum ischemia-modified albumin.

BACKGROUND: Ischemia-modified albumin (IMA), a protein elevated in cardiac ischemia, is also increased to supra-physiological levels in early normal pregnancy. This finding supports the hypothesis that normal trophoblast development is stimulated by a hypoxic intrauterine environment. The aim of this study was to examine whether first trimester IMA levels are further elevated with defective trophoblast development. METHODS: Prospective study of healthy women with singleton pregnancies undergoing nuchal translucency assessment at 11-14 weeks. First trimester maternal serum IMA concentrations in those subsequently developing pre-term pre-eclampsia (n = 19) were compared to randomly chosen controls with normal pregnancy outcome (n = 69). RESULTS: Median first trimester serum IMA concentrations were significantly higher in women who subsequently developed pre-eclampsia (median 126.5 kU/L, interquartile range (IQR) 114.33-134.36 kU/L) when compared to those with normal pregnancy outcome (median 115.01 kU/L, IQR 102.29-124.81 kU/L, P = 0.02). CONCLUSIONS: Maternal serum IMA levels are elevated in the first trimester in women with pre-eclampsia, a clinical manifestation of defective endovascular trophoblast development. This suggests that abnormally high intrauterine hypoxia and subsequent reperfusion oxidative damage may be associated with defective trophoblast development. First trimester serum IMA may be a potential biomarker for abnormal placental development.

Multiple molecular forms of circulating cardiac troponin: analytical and clinical significance.

Cardiac troponin T (cTnT) and I (cTnI) are highly specific and sensitive biomarkers of myocardial cell damage and are now accepted as the 'gold standard' diagnostic test for acute coronary syndrome and supersede the classical muscle enzyme biomarkers. While the understanding of the development and structure of the troponins has advanced, detailed biochemistry of the troponin molecules is complex and poorly understood. Many post-translational molecular forms of troponin are known to exist. The diversity of these circulating forms may have a clinical impact and the notion of a disease-specific troponin protein signature has been suggested. However, the effects of these multiple forms on commercial assay performance and their impact clinically are currently unknown and should be the focus of future research and assay design.

Cardiac troponin I measurement using the ACS:180 to predict four-year cardiac event rate.

BACKGROUND: This study aimed at evaluating the ability of cardiac troponin I (cTnI) measurement on the ACS:180 for prognostic risk stratification. Sequential admissions to the coronary care unit of a busy district general hospital were studied. All patients were followed up for a maximum of 4.3 years and cardiac events, either cardiac death, readmission with acute myocardial infarction or admission with acute unstable angina were documented. METHODS: Blood samples were taken on admission and at 4 and 12 h. A serum aliquot was taken and stored frozen at -70 degrees C. The frozen aliquots were subsequently analysed for cTnI by chemiluminescent immunoassay using an ACS:180. Patients were categorized into those with or without ST segment elevation on the presenting electrocardiogram. The optimized decision threshold for mortality and event prediction was then determined by log-rank analysis and by construction of Kaplan-Meier survival plots. RESULTS: A total of 289 patients (196 men) median age 65.3 years, range 27.4-87.9 years were studied. Out of this, 139 had ST elevation myocardial infarction (STEMI) and 150 had suspected non-STEMI (NSTEMI). Full data were available from 278 patients. Admission cTnI did not predict any of the endpoints in the STEMI group. In patients admitted with suspected NSTEMI, admission and peak cTnI predicted increased risk of death or readmission with acute myocardial infarction. In addition, peak cTnI predicted increased risk of death. CONCLUSION: A cTnI exceeding 0.16 microg/L on admission or during hospital stay predicted an increased cardiac event rate at four years in patients admitted with suspected NSTEMI.

Cardiac biomarkers in chronic renal disease.

Cardiac biomarkers have a complex interrelationship with disease pathophysiology in patients with renal dysfunction. The underlying clinical condition results in a direct effect on the normal release and clearance of cardiac troponins and natriuretic peptides. Although initial reports suggested that this might prove a major limitation in the routine clinical use of these markers, a combination of improved assay performance and a better understanding of the underlying biochemistry of these markers in health and disease has clarified the situation. Renal dysfunction does not provide a significant practical limitation to the use of cardiac biomarkers for diagnosis in acute presentation of cardiovascular disease. The direct relationship between cardiac biomarkers and renal dysfunction reflects the high incidence of cardiovascular disease and cardiac death in patients with renal dysfunction and end-stage renal disease. Elevations of the cardiac troponins are prognostic in patients with renal dysfunction and represent global diffuse myocardial injury. Elevations of natriuretic peptides also occur due to abnormalities of ventricular function. In addition, background levels will be affected by fluid and electrolyte abnormalities due to renal dysfunction. This will directly affect vascular volume and fluid distribution altering atrial and ventricular wall tension and hence rates of natriuretic peptide release and production. The challenge is for the renal physician to translate the potential for cardiovascular disease monitoring conferred by these biomarkers into improved patient management.

Mitral annular calcification predicts mortality and coronary artery disease in end stage renal disease.

BACKGROUND: We sought to determine whether mitral annular calcification (MAC) predicts mortality and cardiac disease in a group of renal transplant candidates. METHODS: Hundred and forty patients were prospectively studied. All had echocardiography and coronary angiography. Significant coronary artery disease (CAD) was defined as luminal stenosis >70% by visual estimation in at least one coronary artery. RESULTS: There were 21 deaths over a follow-up period of 2.2+/-0.7 years. MAC occurred in 56 patients (40%) and was associated with higher mortality (p=0.04). Patients with MAC were older (p=or<0.001), had larger left ventricular (LV) end systolic (p=0.005) and LV end diastolic (p=0.04) diameter, larger left atrial diameter (p=0.001), lower LV fractional shortening (p=0.003), larger LV mass index (p=0.04) and higher mitral E/Ea ratio (p=0.03) compared to those without. Plasma calcium (p=0.002), phosphate (p=0.004), cardiac troponin T (p=0.03), N-terminal Pro-B-type natriuretic peptide (p=0.004) concentrations were higher in those with MAC but gender, total cholesterol, haemoglobin and creatinine were similar in the two groups. The proportion diabetic (p=0.03), on dialysis (p=0.05), with significant CAD (p=or<0.001), taking calcium containing phosphate binders (p=0.02) and Vitamin D3 (p=0.04) was significantly higher in those with MAC. Significant CAD (OR 12, 95% CI 3.25, p=0.001) was the only independent associate of MAC. CONCLUSIONS: MAC is associated with increased mortality and significant CAD in ESRD. These patients have increased LV cavity size, poorer LV systolic function, higher LV filling pressures compared to patients without MAC.

The role of existing and novel cardiac biomarkers for cardioprotection.

Cardioprotection is an all-encompassing term for physico-biochemical or therapeutic interventions which slow or ameliorate the progression of cardiomyocyte necrosis. There are a number of established and novel biomarkers to assess coronary artery disease at initiation, ischemia, necrosis and myocardial dysfunction. Established biomarkers such as creatine kinase-MB, cardiac troponins and natriuretic peptides have been utilized for the assessment of cardioprotection, especially during surgery. Novel markers are currently being investigated for detection and risk assessment in patients with acute coronary syndromes. Ischemia-modified albumin is used for the early detection of cardiac ischemia and could be a potential biomarker for assessing the early cardioprotective effects of damage-limiting interventional measures.

Evaluation of ischaemia-modified albumin as a marker of myocardial ischaemia in end-stage renal disease.

The early diagnosis of myocardial ischaemia is problematic in patients with ESRD (end-stage renal disease). The aim of the present study was to determine whether IMA (ischaemia-modified albumin) increases during dobutamine stress and detects myocardial ischaemia in patients with ESRD. A total of 114 renal transplant candidates were studied prospectively, and all received DSE (dobutamine stress echocardiography). IMA levels were taken at baseline and 1 h after cessation of DSE. A total of 35 patients (31%) had a positive DSE result. Baseline IMA levels were not significantly different in the DSE-positive and -negative groups. The increase in IMA was significantly higher in the DSE-positive group compared with those with no ischaemic response (26.5 +/- 19.1 compared with 8.2 +/- 9.6 kU/l respectively; P = 0.007; where kU is kilo-units). From ROC (receiver operator charactertistic) curve analysis, the optimal IMA increase to predict an ischaemic response was 20 kU/l, with a sensitivity of 81% and a specificity of 72% [area under the curve, 0.80 (95% confidence interval, 0.44-0.94); P = 0.03]. There were 18 deaths, ten of which were cardiac in nature over a follow up period of 2.25 +/- 0.71 years. An increase in IMA > or = 20 kU/l was associated with significantly worse survival (P = 0.02). In conclusion, IMA is a moderately accurate marker of myocardial ischaemia in ESRD. Patients with an increase in IMA > or = 20 kU/l during DSE had significantly worse survival.

Markers of muscle ischemia, necrosis, and inflammation following uterine artery embolization in the treatment of symptomatic uterine fibroids.

OBJECTIVE: The objective of the study was to quantify markers of myometrial ischemia, necrosis, and inflammation in women undergoing uterine artery embolization (UAE). STUDY DESIGN: Women with symptomatic fibroids were randomized to treatment with UAE (n = 14) or abdominal myomectomy (n = 11). Peripheral venous blood samples were taken before and after the procedure, at 24 hours and 6 weeks. Creatine kinase (CK) and ischemia-modified albumin (IMA) were measured as markers of necrosis and ischemia. Inflammation was assessed by measurement of C-reactive protein (CRP). OUTCOME MEASURES: Changes in the markers following UAE and myomectomy were measured. RESULTS: Following UAE, no change was seen in CK or IMA, but CRP was raised only at 6 weeks. At 24 hours after myomectomy, there were significant rises in all 3 markers, with a return to normal by 6 weeks. CONCLUSION: No significant ischemia or necrosis occurs in the myometrium following UAE, whereas the delayed rise in CRP is likely to reflect necrosis in fibroids.

Evidence of cardiomyocyte necrosis in glycogen storage disease type II.

Adult-onset glycogen storage disease type II (GSD-II), unlike the infantile form, is not normally associated with coexisting cardiovascular pathologies. In infantile onset GSD-II, cardiomyopathy is a common feature, and mutations in the genes for cardiac troponin T and I are likely to be involved. This case report describes a 39-year-old man with no classical risk factors for premature cardiac disease who presented with central chest pain and shortness of breath. Serum aspartate transaminase (AST) had been consistently elevated for 15 years. Adult GSD-II had been diagnosed two years previously by muscle biopsy. On presentation, there was an elevated serum creatine kinase and AST. Electrocardiography and echocardiography were both normal, and an acute coronary syndrome was ruled out. Cardiac Troponin T (cTnT) was found to be positive at 0.1 microg/L using a Cardiac Reader, subsequently confirmed on an Elecsys 1010 (both from Roche Diagnostics, Lewes, UK). cTnT may therefore be a useful biomarker in examining subclinical cardiac involvement in GSD-II patients.

Cardiac troponins: from myocardial infarction to chronic disease.

Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to date has been developed: cardiac troponin (cTn) assays. For the past decade, cTn has been regarded as the gold-standard marker for acute myocardial necrosis: the pathological hallmark of acute myocardial infarction (AMI). Whilst cTn is the cornerstone for ruling-out AMI in patients presenting with a suspected acute coronary syndrome (ACS), elevated cTn is frequently observed in those without clinical signs indicative of AMI, often reflecting myocardial injury of 'unknown origin'. cTn is commonly elevated in acute non-ACS conditions, as well as in chronic diseases. It is unclear why these elevations occur; yet they cannot be ignored as cTn levels in chronically unwell patients are directly correlated to prognosis. Paradoxically, improvements in assay sensitivity have meant more differential diagnoses have to be considered due to decreased specificity, since cTn is now more easily detected in these non-ACS conditions. It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasizing the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasizing a need to understand the mechanisms of such release. This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases.

Ischemia-modified albumin predicts mortality in ESRD.

BACKGROUND: The primary study aim is to determine whether ischemia-modified albumin (IMA) levels predict mortality in patients with end-stage renal disease (ESRD). The secondary aim is to determine characteristics of patients with elevated IMA levels. METHODS: A prospective observational study of 114 renal transplantation candidates was performed. All underwent coronary angiography and dobutamine stress echocardiography. The primary end point is total mortality. RESULTS: During a follow-up period of 2.25 +/- 0.71 years, there were 18 deaths; 10 were cardiac related. Diabetes, severe coronary artery disease, positive dobutamine stress echocardiography result, cardiac troponin T (cTnT) level, IMA level, left ventricular (LV) end-systolic diameter, LV ejection fraction, left atrial size, and mitral peak velocity of early filling (E)/early diastolic velocity (Ea) ratio all predicted mortality. The receiver operating characteristic area under the curve for mortality prediction was similar for IMA and cTnT levels. An IMA level of 95 KU/L or greater (n = 46) predicted mortality with a sensitivity of 76% and specificity of 74%. cTnT level of 0.06 ng/mL or greater (> or = 0.06 microg/L; n = 51) predicted mortality with a sensitivity of 75% and specificity of 72%. Thirty-eight patients (33%) had both IMA and cTnT levels elevated. With multivariate analysis, a positive dobutamine stress echocardiography result (P = 0.003), combined elevated IMA and cTnT levels (P = 0.005), and E/Ea ratio (P = 0.009) were independent prognostic factors. IMA and cTnT levels alone were not independent predictors of mortality. Patients with an elevated IMA level had a significantly larger LV size, decreased LV systolic function, and greater E/Ea ratio compared with those without an increased level. CONCLUSION: IMA level predicts mortality in patients with ESRD. Patients with elevated levels have larger LV size, decreased systolic function, and greater estimated LV filling pressures.

Comparison of biomarker strategies for rapid rule out of myocardial infarction in the emergency department using ACC/ESC diagnostic criteria.

OBJECTIVE: Creatine kinase MB isoenzyme (CK-MB) mass and rate of change of CK-MB have been proposed as superior to cardiac troponin measurement for very early exclusion of acute myocardial infarction (AMI). All three markers were examined prospectively in patients presenting to the Emergency Department (ED) for rule out of AMI. METHODS: Consecutive admissions to the ED with undifferentiated chest pain were initially assessed clinically and by electrocardiography. A total of 786 patients (490 male, median age 52.5 years) considered at low risk of AMI had blood drawn on admission. If the first sample was less than 12 h from onset of chest pain, a second sample was then drawn at least 2 h later and at least 6 h from onset of chest pain. CK-MB mass was measured on the first sample and CK-MB mass and cardiac troponin T (cTnT) were measured on the second sample. Measurement of cTnT was using an Elecsys 2010 with the third generation assay (Roche Diagnostics, Lewes, UK). Assay coefficient of variation (CV) was 5.8% and 5.7% at 0.47 and 11.5 microg/L, respectively, with measuring range 0.01-25.0 microg/L; analytical sensitivity of 0.01 microg/L and functional sensitivity of 0.03 microg/L. CK-MB (mass) was measured by electrochemiluminesence using an Elecsys 2010 (Roche Diagnostics). The assay CV was 4.0% at 5.89 microg/L and 4.1% at 60.5 microg/L, with a detection limit of 0.1 microg/L and an upper measuring limit of 500 microg/L. Myocardial infarction was diagnosed if either sample had a CK-MB of more than 5 microg/L, if there was a change in CK-MB (DeltaCK-MB) of more than 1.5 microg/L or if the cTnT was more than 0.05 microg/L. When AMI was excluded, patients proceeded to stress electrocardiography and reattended 72 h from presentation for follow up phlebotomy for cTnT measurement. A final diagnosis of AMI was made according to American College of Cardiology/ European Society of Cardiology criteria using a cut-off of 0.05 microg/L cTnT in any of the samples. Diagnostic efficiency was compared by receiver operator characteristic (ROC) curve analysis with comparison of area under the curve (AUC) for four strategies: admission CK-MB measurement; 6-h post-pain CK-MB measurement; DeltaCK-MB; and 6-h post-pain cTnT measurement. RESULTS: On admission the AUC for CK-MB was 0.830 (95% confidence interval [CI] 0.757-0.904). At 6 h post pain the respective values were: CK-MB 0.939 (95% CI 0.889-0.988); DeltaCK-MB 0.948 (95% CI 0.906-0.990); and cTnT 0.989 (95% CI 0.966-1.0). CONCLUSION: cTnT at 6 h has high diagnostic sensitivity for AMI and is superior to CK-MB mass and DeltaCK-MB even using a low cut-off value.

Ischemia modified albumin is a sensitive marker of myocardial ischemia after percutaneous coronary intervention.

BACKGROUND: Ischemia modified albumin (IMA; Ischemia Technologies, Inc) blood levels rise in patients who develop ischemia during percutaneous coronary intervention (PCI). It is not known whether IMA elevations correlate with increases in other markers of oxidative stress, ie, 8-iso prostaglandin F2-A (iP). METHODS AND RESULTS: We compared IMA versus iP plasma levels in 19 patients (mean age 62.8+/-11.9 years) undergoing PCI and 11 patients (mean age 64+/-13.6 years) undergoing diagnostic angiography (controls). In the PCI patients, blood samples for IMA and iP were taken from the guide catheter before PCI and after balloon inflations, and from the femoral sheath 30 minutes after PCI. IMA was measured by the albumin cobalt binding (ACB) test and plasma iP by enzyme immunoassay. During PCI, all 19 patients had chest pain and 18 had transient ischemic ST segment changes. IMA was elevated from baseline in 18 of the 19 patients after PCI. Median IMA levels were higher after PCI (101.4 U/mL, 95%CI 82 to 116) compared with baseline (72.8 U/mL, CI 55 to 93; P<0.0001). Levels remained elevated at 30 minutes (87.9 U/mL, CI 78 to 99; P<0.0001) and returned to baseline at 12 hours (70.3 U/mL, CI 65 to 87; P=0.65). iP levels were raised after PCI in 9 of the 19 patients. However, median iP levels were not significantly different immediately (P=0.6) or 30 minutes after PCI (P=0.1). In the control group, IMA and iP levels remained unchanged before and after angiography (P=0.2 and 0.16, respectively). CONCLUSIONS: IMA is a more consistent marker of ischemia than iP in patients who develop chest pain and ST segment changes during PCI.

Cardiac troponins as biomarkers of drug- and toxin-induced cardiac toxicity and cardioprotection.

Cardiac troponin T and I (cTnT, cTnI) are sensitive biochemical markers of myocardial cell necrosis and have been adopted as the gold standard tests for acute myocardial infarction. Subtle elevations in cTn above the detection limits of the currently available commercial assays confers poor prognosis. These markers are superior to classical enzyme markers of necrosis due to their cardiospecificity. The diagnosis of drug-induced cardiac toxicity using the classical enzymes is problematic due to the high elevations of these markers in skeletal muscle necrosis. cTnT and cTnI are now being adopted as sensitive biomarkers of drug-induced cardiac toxicity.

Comparison of ischemia-modified albumin levels in patients undergoing percutaneous coronary intervention for unstable angina pectoris with versus without coronary collaterals.

This study compared ischemia-modified albumin levels, a marker of ischemia in patients undergoing percutaneous coronary intervention. Ischemia-modified albumin levels were significantly lower in patients with collateral circulation compared with those without collateral circulation.