Serum Levels Of Cardiac Biomarkers Research Articles

Nutrition Modulation of Cardiotoxicity in Breast Cancer: A Scoping Review.

Advancements in breast cancer therapeutics, such as anthracyclines, are improving cancer survival rates but can have side effects that limit their use. Cardiotoxicity, defined as damage to the heart caused by cancer therapeutics, is characterised by a significant reduction in left ventricular ejection fraction (LVEF) and symptoms of cardiac dysfunction. Multiple oral supplements exist with antioxidant and anti-inflammatory properties that have the potential to lower cardiotoxicity risk and ameliorate the complications associated with left ventricular dysfunction. In this review, we evaluate the current status of using nutritional interventions to modulate cardiotoxicity. We used specific keywords to search for articles that met our predetermined inclusion and exclusion criteria to review the evidence and provide insights for future research. Seven studies were identified as eligible for this review: six focused on oral supplementation strategies in breast cancer patients undergoing chemotherapy, and one focused on nutritional counselling and adherence to the Mediterranean diet in breast cancer survivors' post-treatment. There was a significantly attenuated reduction in LVEF in five studies that monitored cardiometabolic health, and there were significant improvements in blood serum levels of cardiac biomarkers across all studies. Current evidence suggests that appropriate nutritional interventions, alongside chemotherapy, can modulate the risk of cardiotoxic side effects. This highlights the potential of oral antioxidant supplementation and Mediterranean diet counselling to decrease tertiary cancer therapy costs associated with cardiovascular complications.

Protective role of vitamin D3 in a rat model of hyperthyroid-induced cardiomyopathy.

Several studies have reported the cardioprotective effect of vitamin D. Thus, this study aimed to investigate the possible cardioprotective effect of vitamin D3 in hyperthyroid-induced cardiomyopathy rat model. Rats were divided into 3 groups: control group; hyperthyroid group, rats were administrated l-thyroxine sodium daily for 4 weeks; and hyperthyroid+vitamin D3 treated group, rats were treated with l-thyroxine sodium for 4 weeks daily, and received the vitamin D3 for the same duration. After 4 weeks, electrocardiogram (ECG) was recorded. Then, blood samples were collected for biochemical analysis. After that, the final body weight was measured, and the rats were sacrificed. Finally, the hearts were excised, weighed and were prepared for histological examination by hematoxylin and eosin, and immunohistochemistry assessment of caspase-3 and proliferating cell nuclear antigen (PCNA). Hyperthyroid rats showed significant ECG changes, increased serum levels of cardiac biomarkers, fibroblast growth factor-23 (FGF23), malondialdehyde, antioxidant enzymes, tumor necrosis factor-alpha (TNF-α) and relative heart weight compared with the control rats. Vitamin D3 coadministration with l-thyroxine resulted in significant improvement in thyroid profile, ECG parameters, significant decrease of cardiac biomarkers, FGF23, malondialdehyde, TNF-α and relative heart weight, and significant decrease of the antioxidant enzymes compared with the hyperthyroid rats. The histological study was consistent with the biochemical results. Hyperthyroid rats showed upregulation of caspase-3 and PCNA in the myocardium compared with control group. Vitamin D3 treated rats showed downregulation of caspase-3 and PCNA. Vitamin D3 provides cardioprotective effects in hyperthyroid rats.

Oxygenation index and NT-proBNP as predictors of pulmonary hypertension and ventilation/perfusion mismatch in acute pulmonary embolism.

The magnitude of pulmonary artery pressure (PAP) and the extent of ventilation/perfusion (V/Q) mismatch are essential for assessing the prognosis of acute pulmonary embolism (APE). We aimed to develop a model for predicting the status of the pulmonary circulation and arterial gas exchange functions using serum levels of cardiac biomarkers and arterial oxygenation index (OI) values. This single-center, retrospective observational cohort study included 224 patients with APE. Multivariate linear regression and Poisson regression were used to test the statistical association between cardiac biomarkers, OI, PAP, and V/Q mismatch. Diagnostic efficiency was calculated from a receiver operating characteristic (ROC) curve. Serum levels of troponin I (TNI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and arterial OI magnitude significantly correlated with PAP and V/Q mismatches (P < 0.05). Multivariate linear regression showed that NT-proBNP serum levels (β = 0.002, P < 0.001) and OI values (β = -0.022, P = 0.001) significantly influenced PAP. Arterial OI (β = -0.039, P < 0.001) had a significant influence on the percentage of pulmonary vascular obstruction (PVO) as determined by perfusion scanning. Poisson regression showed that OI (odds ratio: 0.995, p < 0.001) was a predictor of the number of lung segments with V/Q mismatches. ROC area under the curve (AUC) values of NT-proBNP and OI predicting pulmonary hypertension were 0.716 and 0.730, respectively, and for V/Q mismatch scanning, the results were 0.601 and 0.634, respectively. Arterial OI and serum levels of cardiac biomarkers may be used as indicators of pulmonary hypertension and V/Q mismatch.

Heart failure with preserved ejection fraction: the role of microvascular dysfunction

Aim. To evaluate the relationship between coronary microvascular dysfunction (CMD), biomarkers of cardiac fibrosis and cardiac remodeling (soluble ST2 (sST2), fibroblast growth factor-23 (FGF-23), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), and NT-proBNP), parameters of diastolic dysfunction (DD), and the presence of heart failure with preserved ejection fraction (HFpEF) in symptomatic patients.Materials and methods. Study participants were 59 patients with non-obstructive coronary artery disease (CAD) and preserved left ventricular ejection fraction (LVEF) of 62 (56; 67) %. Non-obstructive CAD was verified by coronary computed tomography angiography. Stress-and rest-myocardial blood flow (MBF) and coronary flow reserve (CFR) parameters were evaluated by CZT SPECT. Serum levels of cardiac biomarkers were measured by the enzyme immunoassay. Two-dimensional transthoracic echocardiography was used to assess DD parameters.Results. Decreased CFR was defined as CFR ≤ 2. Therefore, CMD was defined as the presence of decreased CFR in the absence of flow-limiting CAD. Distribution of patients was performed by CFR values: group 1 included patients with preserved CFR (&gt;2, n = 35), and group 2 encompassed patients with decreased CFR (≤2, n = 24). In 87.5% of cases, patients with CMD were diagnosed with HFpEF, whereas in patients with preserved CFR, heart failure was diagnosed only in 51.4% of cases (p &lt; 0.0001). CFR values were correlated with the left atrial volume (r = –0.527; p = 0.001), E / A ratio (r = –0.321, p = 0.012), and E / e’ (r = –0.307; p = 0.021). Following the ROC analysis, the levels of sST2 ≥ 31.304 ng / ml (AUС = 0.730; р = 0.004) and NT-proBNP ≥ 0.034 pg / ml (AUС = 0.815; р = 0.034) were identified as cut-off values for the presence of CMD in patients with non-obstructive CAD.Conclusion. The obtained data suggest that CMD may play an essential role in HFpEF. The values of CFR were correlated with DD parameters, and decreased CFR was associated with overexpression of biomarkers of cardiac fibrosis and cardiac remodeling. Serum levels of sST2 and NT-proBNP were identified as cut-off values for the presence of CMD in patients with non-obstructive CAD.

Evaluation of Clinical Efficiency of Cardioprotective Therapy in Patients with Acute Myocardial Infarction

Aim. To evaluate the efficiency of cardioprotective therapy using intravenous metoprolol in combination with a high dose of atorvastatin in the prevention of myocardial remodeling (MR) and heart failure (HF) in patients with acute ST-segment elevation myocardial infarction (STEMI).Material AND methods. A prospective study included 100 STEMI patients who underwent primary percutaneous intervention (PCI). Depending on the regimens of drug cardioprotection, three groups of patients were formed: the first (2014–2015) — 34 patients who received 80 mg atorvastatin as a part of the basic therapy on the first day of STEMI, then 20–40 mg/day for 30 days. The second group (2017–2018) — 34 patients who received atorvastatin 80 mg/day for a month from the onset of STEMI. The third group (2018–2019) — 32 patients who received intravenous metoprolol tartrate (5–15 mg) and atorvastatin 80 mg/day before PCI for a month from the onset of STEMI. On days 1 and 2 of STEMI and one month later, patients were assessed for serum levels of cardiac biomarkers; on the 1st, 7th days and one month later, echocardiographic studies (EchoCG) were performed. At the end of the observation, clinical and imaging outcomes (MR and HF) were assessed, which were compared with the dynamics of biomarkers between the groups of patients.Results. The combined use of atorvastatin 80 mg/day for a month from the onset of STEMI and a single intravenous injection of metoprolol tartrate (5–15 mg) in the acute phase of STEMI before PCI showed the most significant effects in the prevention of the development of structural and functional myocardial disorders and clinically severe heart failure, and also caused the minimal serum activity of cardiomarkers in the third group of patients in comparison with the first and second groups of patients without this drug combination. Also, correlations between biomarkers and echocardiography indicators were established in the third group of patients who received cardioprotective therapy.Conclusion. The combined use of high-dose atorvastatin for a month with a single intravenous injection of metoprolol tartrate in acute STEMI before PCI prevents the formation of MR and clinically significant HF in the post-infarction period. Comprehensive dynamic assessment of cardiac biomarkers and echocardiography parameters within a month after post-STEMI is a highly informative tools for monitoring the efficiency of cardioprotective therapy.

Evaluation of the Role of Pentraxin 3, B-type Natriuretic Peptide and Troponin I in Acute Carbon Monoxide Cardiotoxicity

Background: Acute carbon monoxide induced cardiotoxicity is one of the main causes of mortality. It is considered as a poor prognostic factor in patients with carbon monoxide intoxication.Although early diagnosis of cardiac injury is often difficult and might be misdiagnosed.This study aimed to assess the role of Pentraxin 3 and B-type natriuretic peptide in comparison with cardiac Troponin I as early predictors of cardiotoxicity in patients presented with acute CO poisoning. Methods: Thirty patients with acute CO poisoning were recruited from PoisonControl Center, Ain Shams University Hospitals. Serum levels of Cardiac biomarkers (Pentraxin3, BNP and Troponin I) were measured on admission and after 10 hours after exposure. Conclusion: Our results revealed that, B-type natriuretic peptide and Troponin I were more reliable cardiac biomarkers in early prediction of cardiotoxicity in acute CO poisoning patients.While Pentraxin3 had low sensitivity and specificity to predict the cardiotoxicity in acute CO poisoning in comparing with BNP and Troponin I

Lactoferrin Ameliorates Azithromycin-induced Cardiac Injury: Insight into Oxidative Stress/TLR4 /NF-κB Pathway

Introduction: Azithromycin, a widely used antibacterial agent, is also considered the cornerstone of the management protocols for COVID-19 infection, particularly in Egypt, due to its antiviral impact and preventive effects against secondary bacterial infections. However, even at pharmacological doses, azithromycin develops rapid cardiac toxicity. Objectives: Our study here aims at investigating the cardioprotective potentials of lactoferrin, a natural compound used primarily for boosting intestinal iron absorption, to counteract azithromycin-induced cardiac toxicity in experimental rats when administered concurrently. Methods: Male Sprague Dawley rats received either lactoferrin (200 mg/kg/day, orally) or saline for 10 days. Induction of cardiac toxicity was initiated on the 6th day via oral administration of azithromycin (20mg/kg/day, orally) for 5 successive days, concurrently with either lactoferrin or vehicle. Cardiac injuries were confirmed via Electrocardiogram (ECG) recording, assessment of cardiac function biomarkers, assessment of cardiac expression of nuclear factor erythroid 2–related factor 2 (Nrf2), interleukin-1β (IL-1β) and IL-10, measurement of cardiac oxidant/antioxidant balance, immunohistochemical staining against toll-like receptor-4 (TLR4), and nuclear factor-κB (NF-κB), and histopathological examination of HE-stained cardiac specimens. Results: Administration of azithromycin denoted a significant cardiac tissue injury as demonstrated by upregulated serum levels of cardiac biomarkers, namely total creatine Kinase (CK), Creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and Alkaline phosphatase (ALP). Furthermore, it upregulated cardiac content of malondialdehyde (MDA) and nitric oxide (NO) and cardiac inflammatory markers, such as TLR4, NF-κB, and IL-1β. Similarly, azithromycin-downregulated reduced glutathione (GSH) cardiac content and the anti-inflammatory protective indicators, IL-10 and Nrf2. Additionally, azithromycin-induced cardiotoxicity was evinced by ECG pattern and histopathologic deterioration. Oral Lactoferrin showed cardioprotective potentials and counteracted the azithromycin-induced cardiac toxicity, downregulating cardiac biomarkers. Moreover, it restored cardiac oxidant/antioxidant balance, decreased cardiac TLR4, NF-κB, and IL-1β expression, and increased IL-10 and Nrf2 expression. Lactoferrin Cardioprotective potentials were also evinced by enhanced ECG pattern and histopathological examination. Conclusion: Finally, we support the use of lactoferrin with azithromycin intake that induced cardiac toxicity.

Clinical Feasibility of Biofunctionalized Magnetic Nanoparticles for Detecting Multiple Cardiac Biomarkers in Emergency Chest Pain Patients.

The rapid diagnosis of acute myocardial infarction (AMI) is a clinical and operational priority in emergency departments. Serial serum levels of cardiac biomarkers play a crucial role in the evaluation of patients presenting with acute chest pain, so that an accurate and rapidly responsive assay of cardiac biomarkers is vital for emergency departments. Immunomagnetic reduction (IMR) has been developed for rapid and on-site assays with a small sample volume. IMR kits for three biomarkers [myoglobin, creatine kinase-MB (CK-MB), and troponin-I] have been developed by MagQu Co., Ltd., Taiwan (US patent: US20190072563A1). In this study, we examined correlations between IMR signals and biomarker concentrations. The measurement threshold of the IMR kits, dynamic ranges, interference tests in vitro, and reagent stability were tested. Clinical cases were included with serial IMR measurements to determine the time course and peak of IMR-measured cardiac biomarkers after AMI. The correlations between IMR signals and biomarker concentrations fitted well to logistic functions. The measurement thresholds of the IMR kits (1.03 × 10-8 ng/mL for myoglobin, 1.46 × 10-6 ng/mL for CK-MB, and 0.08 ng/mL for troponin-I) were much lower than the levels detected in the patients with AMI. There was no significant interference in vitro. The peak times of IMR-detected myoglobin, CK-MB, and troponin-I after AMI were 8.2 hours, 24.4 hours, and 24.7 hours, respectively. IMR is an accurate and sensitive on-site rapid assay for multiple cardiac biomarkers in vitro, and may play a role in the early diagnosis of AMI. Clinical trials are needed.

Biochemical and toxicological effect of diazepam in stress-induced cardiac dysfunctions

Diazepam is a medicine of the family benzodiazepine, used to treat various CNS disorders. To date, no study is available for biochemical analysis of diazepam in cardiac dysfunction. This study aimed to determine the effect of diazepam in stress-induced cardiac dysfunctions in rats. Male Wistar Albino rats were divided into four groups with six animals in each group for 90 days of the experimental protocol. Group1 served as a Normal Control (NC), Groups 2, as a Disease Control (DC), Group 3 as a Diazepam Control (DIC), and Group 4 as a Disease + Diazepam Treatment (DDT). Disease Control and Disease + Diazepam Treatment animals exposed to regular stress by forced swimming exercise method for 3 months. Diazepam Control and Disease + Diazepam Treatment received 5 mg/kg/p.o the daily dose of diazepam. At the end of the protocol, animals were sacrificed, heart preserved, blood collected, and utilized for biochemical estimations. Heart weight was increased in DC as compared to NC. Serum levels of cardiac biomarkers, creatine phosphokinase (CPK), creatine kinase-MB (CPK-MB), lactate dehydrogenase (LDH), High sensitivity C-reactive protein (hs-CRP) and troponin I (TnI) were significantly increased in DC as compared to NC. Heart tissue examined for histological changes. The altered serum levels of CPK, CPK-MB, LDH, hs-CRP, and TnI were significantly restored by the treatment of diazepam. Serum levels of Sodium, Potassium, Calcium, and Magnesium was increased in DC animals as compared to NC. The altered ionic level was also restored by the treatment of diazepam. Level of various cardiac markers and ions in the plasma were also slightly elevated in DIC. Histopathological studies are also in agreement with serological examinations and bonafide cardioprotective influences of diazepam in cardiac dysfunction. Conclusively research findings endorse the cardioprotective effect of diazepam in stress-induced cardiac dysfunction in rats.

Mapping the link between cardiac biomarkers and chronic periodontitis: A clinico-biochemical study.

Background:Various risk factors are coupled with atherosclerotic complications, such as myocardial infarction and stroke. Periodontitis is considered one of them.Aims and Objectives:The objective of the study is to compare and correlate the occurrences of periodontitis with serum levels of cardiac-biomarkers in patients with coronary heart-disorders.Materials and Methods:Of 70 individuals diagnosed with coronary artery diseases, 32 patients with chronic periodontitis constituted the test group, 31 without chronic periodontitis constituted the control group. Cardiac-biomarkers analyzed were Troponin T, Troponin I, Myoglobin; low density lipoprotein (LDL), high-density lipoprotein, very LDL (VLDL), total cholesterol (TC), and highly sensitive C-reactive protein (Hs-CRP). Periodontal characteristics were drawn from the plaque index (PI) and gingival index, probing depth (PD), clinical attachment loss, and periodontal inflammatory surface area (PISA).Statistical Analysis:In order to separate any association between cardiac biomarkers and clinical parameters of periodontitis, detailed statistical analysis through independent t-test and Pearson test of correlation was done.Results:Statistically significant differences were seen not only in PI, PD, and PISA between both the groups (P < 0.05), but also between various cardiac parameters of test and control groups (P < 0.001). Positive relations were seen in the test group, between cardiac biomarkers such as TC, VLDL, Hs-CRP, and Troponin T with periodontal parameters such as PD and PISA.Conclusion:The study reveals, a strong association between periodontitis and diseases of cardiovascular nature, highlighting the need for awareness and timely medical interventions to prevent periodontitis from scaling up and interfering with the risk of cardiovascular problems.

Noninvasive diagnosis of hereditary transthyretin-related cardiac amyloidosis

Rationale:Cardiac transthyretin amyloidosis is a progressive and fatal cardiomyopathy for which several promising therapies are in development. The diagnosis is frequently delayed or missed because of the limited specificity of clinical manifestations, routine electrocardiogram, echocardiography and the traditional requirement for endomyocardial biopsy confirmation.Patient concerns:A 68-year-old female had suffered from lumbago for 5 years with progressive weakness, numbness in both lower limb.Diagnosis:The patient's clinical signs were not specific, but cardiac amyloidosis was suspected based on relative left ventricular apical sparing of longitudinal strain on echocardiography and continuous elevated serum levels of cardiac biomarkers (ultrasensitive cardiac troponin I and NT-proBNP). She was finally diagnosed hereditary transthyretin-related cardiac amylodosis by specific findings of cardiovascular magnetic resonance imaging (CMR), 99m-technetium pyrophosphate (99mTc-PYP) scintigraphy and genetic testing.Interventions:The patient received medications including diuretics, beta-blockers and angiotensin-converting enzyme inhibitors at the time of hospitalization. Ultimately, however, she refused further treatments and requested discharge from our hospital.Outcomes:A series of noninvasive technique enables the diagnosis of hereditary transthyretin-related cardiac amyloidosis.Lessons:While endomyocardial biopsy is not able to performed, this case demonstrates that a combination of noninvasive techniques, especially CMR, nuclear imaging, and genetic testing, may help us to make a correct diagnosis of hereditary transthyretin-related cardiac amyloidosis.

Traitement de l’amylose AL

AL amyloidosis is caused by the conversion of monoclonal immunoglobulin light chains into amyloid fibrillar aggregates that deposit in tissue and lead to organ dysfunction. Diagnosis is histological and relies primarily on non-invasive biopsies, showing Congo red-positive amorphous deposits containing immunoglobulin light chains, most commonly of lambda isotype. The clinical presentation is extremely polymorphous, due to the large number of organs that can be affected by the disease. The kidneys and the heart are most frequently involved organs, in about two thirds of patients each, responsible for nephrotic syndrome and restrictive cardiomyopathy. Treatment is based on chemotherapy aimed at eliminating the medullary clone producing the pathogenic monoclonal light chains. It is guided by risk assessment, based on the serum levels of cardiac biomarkers. Its effectiveness must be regularly assessed by the serum free light chain assay. Current reference regimens combine an alkylating agent, with high doses of dexamethasone and most often a proteasome inhibitor. They are effective in the majority of patients. The overall prognosis depends on the importance of the initial severity of organ involvement, particularly the heart, and is strongly influenced by the haematological response. The treatment must be rapidly modified in non-responders, especially in those with severe cardiac disease, with the introduction of immunomodulatory drugs and antibodies targeting plasma cells. However, effective therapies for patients with the more severe amyloid cardiopathy are an unmet need. Strategies directly accelerating the removal of amyloid deposits, despite disappointing preliminary results, could further improve the prognosis of this disease.

Biomarkers of Myocardial Injury and Inflammation after Permanent Pacemaker Implantation: The Lead Fixation Type Effect.

Permanent pacemaker implantation is accompanied by minor myocardial damage, indicated by elevated serum levels of cardiac biomarkers. Aim of this prospective study was to comparably investigate the lead fixation type effect on the extent of myocardial injury and inflammation following pacemaker implantation, and to assess the possible clinical implications. Cardiac troponin I (cTnI) and C-reactive protein (CRP) were measured at baseline, 6 and 24h after implantation in 101 patients, categorized into the active and passive lead fixation group. Patients were followed up for clinical adverse events or abnormal pacing parameters at 24h, 7 and 30 days post-procedure. cTnI increased at 6h post-procedure (p<0.05) in 23.8% of patients, and returned to baseline after 24h. The passive group demonstrated significantly higher cTnI at 6h compared to the active group (p=0.006). CRP increased significantly at 6h, and maintained an upward trend after 24h (p<0.01) in both groups. The active group demonstrated significantly higher CRP at 6h compared to the passive group. We did not identify an association of positive biomarkers with adverse events. cTnI and CRP can increase early after permanent pacemaker implantation, indicating mechanical myocardial injury and inflammation. The extent of these biomarkers elevation depends on the lead fixation type, and is not related to worse short-term prognosis.

Role of dexmedetomidine in myocardial protection during beating coronary artery bypass grafting.

Background: On-pump CABG is associated with a high risk of myocardial injuries and other complications that result into myocardial ischemia and arrhythmias. OPCAB surgery may reduce, although not entirely eliminate, these myocardial injuries. This prospective study was designed to determine whether the intraoperative use of Dexmedetomidine could reduce the incidence of myocardial injuries after off pump CABG. Methods: A total of 100 patients who underwent off-pump coronary artery bypass surgery were included and randomly divided into Dexmedetomidine treated and Control groups (groups B and A, respectively) 50 patients in each groups. Following the first vascular anastomosis grafting, the patients in group B received a loading dose of 0.5 μg/kg/10min of Dexmedetomidine via central venous catheter followed by a continuous infusion of 0.5 μg/kg/hr of Dexmedetomidine. The infusion was discontinued at the end of surgery. In group A, 0.9% physiological saline was infused using identical methods to group B. Results: The primary outcomes measured included serum levels of cardiac biomarkers like CPK-MB & Trop I. Secondary outcomes included hemodynamic stability, ischemia or arrhythmia events & post-operative ICU stay. Dexmedetomidine use significantly reduced postoperative CPK-MB (26.38 ± 7.11 v/s 30.48 ± 9.84, P=0.019) & Trop I (0.678 ± 0.742 v/s 1.011 ± 0.67, P=0.021) at 24 & 48 hours respectively. Intraoperative dexmedetomidine therapy also reduced the risk of overall complications. Conclusion: Intra operative administration of low-dose dexmedetomidine reduces myocardial damage during off-pump coronary artery bypass grafting surgery as indicated by significantly decreased level of cardiac biochemical markers, CK-MB and cTnI post-operatively.

Comparative Study of Potential Diagnostic Biomarkers in Myocardial Infarction with Survival and Myocardial Infarction without Survival

ABSTRACT Introduction Because of the varied presentation and associated high mortality, the identification of patients with acute myocardial infarction (MI) is very critical for patient management and has a bearing on the prognosis. The goal of present study was to correlate the diagnostic value of cardiac biomarkers in MI with survival and MI without survival. Materials and methods Diagnostic case—control study was conducted on 110 MI patients presenting to the Emergency Department within 12 hours of acute chest pain, and 120 healthy age- and sex-matched volunteers formed the control group. Serum ischemia-modified albumin (IMA), troponin I (TnI), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate transaminase (AST) were measured. Statistical software SYSTAT version 12 was used to analyze the data. The results were expressed in mean ± standard deviation. Comparisons of study groups and study groups with control groups were done by applying Z test. Correlation was tested by Student's t-test at 5% (p = 0.05) and 1% (p = 0.01) level of significance. Results Mean levels of serum IMA, TnI, CK-MB, LDH, and AST levels were significantly higher (p &lt; 0.01) in patients with MI as compared with healthy controls. Serum levels of cardiac biomarkers were significantly elevated (p &lt; 0.01) in MI patients without survival as compared with MI with survival. Conclusion The serum levels of biomarkers were increased in MI without survival as compared with MI with survival. These study data prove that these changes might be helpful to obtain a comprehensive view of the infarct size and severity of vascular stenotic lesions. How to cite this article Patil SM, Bankar M, Padalkar R, Phatak A. Comparative Study of Potential Diagnostic Biomarkers in Myocardial Infarction with Survival and Myocardial Infarction without Survival. Indian J Med Biochem 2017;21(2):106-111.

Effects of N-Acetylcysteine on the Cardiac Remodeling Biomarkers and Major Adverse Events Following Acute Myocardial Infarction: A Randomized Clinical Trial

The aims of this study were to evaluate the effects of N-acetylcysteine (NAC) on cardiac remodeling and major adverse events following acute myocardial infarction (AMI). In a prospective, double-blind, randomized clinical trial, the effect of NAC on the serum levels of cardiac biomarkers was compared with that of placebo in 98 patients with AMI. Also, the patients were followed up for a 1-year period for major adverse cardiac events (MACE), including the occurrence of recurrent myocardial infarction, death, and need for target vessel revascularization. In patients who received NAC, the serum levels of matrix metalloproteinase (MMP)-9 and MMP-2 after 72 h were significantly lower than those in the placebo group (p = 0.014 and p = 0.045, respectively). The length of hospitalization in patients who received NAC was significantly shorter than that in the placebo group (p = 0.024). With respect to MACE, there was a significant difference between those who received NAC (14 %) and those patients on placebo (25 %) (p = 0.024). Re-infarction took place in 4 % of patients in the NAC group as compared with 16.7 % in patients who received placebo (p = 0.007). NAC can be beneficial in preventing early remodeling by reducing the level of MMP-2 and MMP-9. Moreover, NAC decreased the length of hospital stays in patients after AMI. By decreasing MACE, NAC could possibly be introduced as a 'magic bullet' in the pharmacotherapy of patients with AMI. Further studies are needed to elucidate NAC's role in this population.

Association of glomerular filtration rate with high-sensitivity cardiac troponin T in a community-based population study in Beijing

ObjectiveThe reduced level of glomerular filtration rate (GFR) is an independent risk factor for cardiovascular disease (CVD) mortality and persistently elevated cardiac biomarkers are frequently observed in patients with end-stage...

Cardiovascular Effects of Cocaine

The use of cocaine has evolved from chewing the leaves of the Erythroxylon coca bush thousands of years ago, to purification of cocaine hydrochloride over 100 years ago and its use in tonics and elixirs (at one time in popular cola drinks), to insufflating and injecting the fine, white, water-soluble, powder form, to a smokable freebase form called “crack,” which became popular in the 1980s.1 In 2007, 2.1 million Americans had recent cocaine use; 1.6 million met criteria for cocaine dependence or abuse.1 Cocaine accounted for 31% of all visits to the emergency department related to drug misuse or abuse.1 From 1971 to 1987, the incidence of deaths caused by cocaine overdose increased 20-fold in Dade County, Florida.2 In a consecutive series of 233 emergency visits by cocaine-using patients, 56% presented with cardiovascular complaints, including 40% with chest pain.3 A minority of these patients have acute myocardial infarction (MI) (≈6%),4,–,7 and overall mortality is low (<1%).3,–,5,8,–,10 However, cocaine is associated with a number of cardiovascular diseases, including MI, heart failure, cardiomyopathies, arrhythmias, aortic dissection, and endocarditis. Identifying patients with acute disease is challenging. This review describes the relationship between cocaine and various cardiovascular diseases, as well as appropriate diagnostic evaluation and therapies. ### Molecular Cocaine stimulates the sympathetic nervous system by inhibiting catecholamine reuptake at sympathetic nerve terminals,11,12 stimulating central sympathetic outflow,11 and increasing the sensitivity of adrenergic nerve endings to norepinephrine (Figure 1).12 Cocaine also acts like a class I antiarrhythmic agent (local anesthetic) by blocking sodium and potassium channels, which depresses cardiovascular parameters.13 Of these 2 primary, opposing actions, enhanced sympathetic activity predominates at low cocaine doses, whereas the local anesthetic actions …

Baseline serum levels of cardiac biomarkers in patients with stable coronary artery disease

Stable coronary artery disease (CAD) can cause repetitive reversible myocardial ischaemia, and it seems to be possible that reversibly injured myocardium releases small amounts of soluble cytoplasmic proteins. Hence, the aim was to evaluate the effect of stable CAD on baseline serum levels of cardiac biomarkers. We studied 68 consecutive outpatients referred for gated myocardial perfusion imaging. Before a treadmill exercise test, blood samples for measurement of creatine kinase (CK), CK-myocardial band (CK-MB) mass, myoglobin, aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were collected. Normal perfusion patterns were detected in 29 (43%) patients (group 1) and perfusion defects were detected in 39 (57%) patients (group 2). Baseline serum levels of biomarkers except CK were significantly higher in group 2 (p=0.001). Stable CAD increases baseline levels of CK-MB mass, myoglobin, AST and LDH in the serum and this increase is related to the extent and severity of the perfusion defect and to some extent the ejection fraction of the left ventricle.

Powerful Risk Stratification in Patients with AL Using Serum Cardiac Biomarkers.

Introduction: We previously reported that serum cardiac biomarkers are among the most powerful predictors of overall survival. This observation was based on outcomes of more than 300 patients with primary systemic amyloidosis (AL) receiving either low dose chemotherapy or high dose chemotherapy with peripheral blood stem cell transplant (PBSCT). Not all institutions use the N-terminal pro-brain natriuretic peptide (NTproBNP) assay, but rather the B-type natriuretic peptide (BNP) assay. We therefore determined the relative utility of BNP in patients with AL undergoing PBSCT and up-dated our results using our NTproBNP-troponin T staging system. Methods: Between 4/10/96 and 2/24/05, 164 patients with AL undergoing PBSCT had measurements of serum cardiac biomarkers. All BNP measurements were done on fresh serum (Biosite Inc., San Diego). The NTproBNP (Roche Diagnostics, Indianapolis, IN) and troponin T (TnT) (Roche Diagnostics, Indianapolis, IN) measurements were done on either stored serum or on fresh samples as previously reported. Follow-up for patients was through March 2005.Results: Between 5/1/03 and 2/15/05, 72 patients had BNP measurements pre-transplant. The median value was 167 pg/ml (range 5 to 7739). Forty-two of these patients also had an NTproBNP measured. There was good agreement between the two tests in the 42 patients that had both measurements (rho 0.823, p<0.0001). To further test the relationship between the two tests, we evaluated the correlation between BNP and NTproBNP using 204 simultaneous measurements from 106 patients (rho=0.89, p<0.0001). Next, we tested the prognostic utility of BNP. Using a cut-off point of 120 pg/L (the upper limit of normal for women over the age of 70 and the 50th percentile of all measurements in our data set), we found that BNP was prognostic for survival post-transplant. It was independent of TnT values, and patients could be divided into 3 risk categories using these two measurements (low risk if both values were low, high-risk if both were high, and intermediate if either was high). This system was highly predictive of overall survival (Figure A). We next compared the BNP-TnT staging system to our previously reported NTproBNP-TnT staging system in the 42 patients that had all 3 values pre-transplant. The correlation between the two staging systems was excellent (rho=0.91, p<0.0001). Follow-up for the 100 patients who had been reported previously is now 26.9 months. As shown in Figure B, the NTproBNP-TnT system predicts for overall survival post transplant.Conclusions: Serum levels of cardiac biomarkers are invaluable prognostic markers in patients with AL. Preliminary data would suggest that a BNP-TnT system is as useful as the NTproBNP-TnT system. [Display omitted]