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Cardiac biomarkers in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Cardiac markers are used in the diagnosis and risk stratification of patients with chest pain and suspected acute coronary syndrome (ACS). The cardiac troponins, in particular, have become the cardiac markers of choice for patients with ACS. Indeed, cardiac troponin is central to the definition of acute myocardial infarction (MI) in the consensus guidelines from the European Society of Cardiology (ESC) and the American College of Cardiology (ACC): These guidelines recommend that cardiac biomarkers should be measured at presentation in patients with suspected MI, and that the only biomarker that is recommended to be used for the diagnosis of acute MI at this time is cardiac troponin due to its superior sensitivity and accuracy [5–7].
The incidence and potential mechanism of side-branch occlusion after implantation of bioresorbable scaffolds: Insights from ABSORB II
Published in Yoshinobu Onuma, Patrick W.J.C. Serruys, Bioresorbable Scaffolds, 2017
Yuki Ishibashi, Takashi Muramatsu, Yohei Sotomi, Yoshinobu Onuma, Patrick W.J.C. Serruys
Despite advances in interventional technology, the incidence of postprocedural cardiac marker elevation has not substantially decreased since the first serial assessment 20 years ago. As of now, these postprocedural cardiac marker elevations are considered to represent periprocedural myocardial injury (PMI) with worse long-term outcome potential.
Coronary artery disease and regional left ventricular function
Published in Andrew R. Houghton, MAKING SENSE of Echocardiography, 2013
An acute coronary syndrome occurs when an atherosclerotic plaque ruptures, exposing the lipid-rich core to the bloodstream. This leads to the rapid formation of a thrombus which acutely obstructs flow down the coronary artery. If this leads to necrosis of a portion of myocardium, cardiac markers (e.g. troponins) will be released into the circulation, and the detection of these markers is one of the key diagnostic features of a myocardial infarction. Unstable symptoms without a rise in cardiac markers is termed unstable angina.
The efficacy and safety of tadalafil in the management of erectile dysfunction with diabetes and blood circulation issues
Published in The Aging Male, 2023
Jong Seung Lee, Seung-ho Hong, Hwa Yeon Sun, Hyunseung Jin, Byung Yeon Yu, Yong-jin Cho, Jin young Chang, Byung Wook Yoo
After the daily administration of tadalafil 5 mg to patients with diabetes, laboratory testing showed a non-significant decrease in HbA1c from 7.47% to 7.37% and LDL-cholesterol from 91.30% to 90.85%. AST levels significantly decreased from 35.35 U/L to 23.65 U/L. The blood circulation improvement test at the fingertip capillary showed significantly increased results in the apical limb width from 13.10 to 14.65 µm (p = .04829) and flow from 9035.50 to 11946.65 µm3/s (p = .04405). The width increased non-significantly from 35.40 to 37.55 µm, and the speed from 81.50 124.10 µm/s. Troponin, a cardiac marker, showed no significant change before and after administration at 0.01 ng/mL, respectively (p = .3446). No statistically significant changes pre- and post-measurements occurred for PSA (1.50–1.28 ng/mL), testosterone (482.20–473.85 ng/dL), and EKG (Heart rate: 73.20–73.90 bpm, the Pulse rate: 169.70–172.50, QT: 375.45–385.15), further supporting the safety of the daily administration of low-dose tadalafil (Table 3).
Gallic acid and sesame oil exert cardioprotection via mitochondrial protection and antioxidant properties on Ketamine-Induced cardiotoxicity model in rats
Published in Toxin Reviews, 2023
Ahmad Salimi, Mohammad Shabani, Deniz Bayrami, Armin Saray, Nastaran Farshbaf Moghimi
The present study showed a significant increase in the cardiac markers (creatine kinase, lactate dehydrogenase and troponin) following the ketamine administration, which are used to determine myocardial injury. It has been shown in various studies that the increase these mentioned cardiac markers may be due to the disruption of the mitochondrial membrane, ROS formation and oxidative stress in cardiac tissue (Peoples et al.2019, D’Oria et al.2020, Mongirdienė et al.2022). Also, it has been claimed that ketamine can cause oxidative damage by suppressing the production of antioxidants such as total GSH and increasing the lipid peroxidation markers such as MDA in the heart tissue (Cetin et al.2015, Ahiskalioglu et al.2018). In our study, MDA as the end product of lipid peroxidation, was found to be high and GSH levels were decreased in comparison to control group in cardiac tissue. This indicates that ketamine increases oxidative stress in the heart. Lipid peroxidation markers such as MDA, ROS formation and increased oxidative stress have been implicated in the pathogenesis and progression of heart failure by ketamine in previous studies (Cetin et al.2015, Ahiskalioglu et al.2018, Çömez et al.2020). In the literature, ketamine has been shown to significantly increase the amount of MDA in the cardiac tissue even after a single dose (Cetin et al.2015). Also, we confirmed ketamine-induced cardiotoxicity by histopathological examination, which is consistent with other studies in the literature.
Bad players in AL amyloidosis in the current era of treatment
Published in Expert Review of Hematology, 2023
Natalia Kreiniz, Morie A. Gertz
Cardiac involvement is the most important prognostic factor that defines the survival of ALA patients. Thus, in 2004 cardiac markers – cardiac troponin T (cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) – were incorporated into the Mayo clinic staging system for ALA [4]. In 2012, this model was updated, and a third prognostic parameter – the difference between involved and uninvolved free light chains (dFLC) – was added [5]. Each parameter scores 1 point. Stage I is 0 points, stage II is 1 point, stage III is 2 points, and stage IV is 3 points. According to this staging system, the 5-year survival of patients with stage IV ALA is less than 14%. Other groups adopted these cardiac markers in their risk stratification systems. The modified European staging system subdivided Mayo 2004 stage III patients into A and B subgroups, according to the NT-proBNP threshold of 8500 ng/L [6,7]. The Boston model used brain natriuretic peptide (BNP) instead of NT-proBNP and cTnI instead of cTnT. According to this model, the cutoff for BNP was 81 pg/ml, and an additional threshold of 700 pg/ml was used to define patients with the worst prognosis [8] (Table 1).