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Myocarditis
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
George Lazaros, Emilia Lazarou, Dimitris Tousoulis
The first scenario includes patients presenting with acute coronary syndrome-like symptoms, such as chest pain. Importantly, coronary artery disease or any possible cardiac or extracardiac condition accounting for these symptoms should be excluded (see also the subsection in this chapter on imaging features in the Diagnosis section). Patients may present with or without troponin elevation. In contrast to coronary syndromes, troponin has sustained release and prolonged plateau in myocarditis.2 C-reactive protein may rise in any subtype of acute myocarditis; however, normal values do not rule out myocardial inflammation.23
Cardiac biomarkers in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are more sensitive and specific markers than CK-MB in detecting myocardial necrosis and have become the preferred biomarkers for the diagnosis of AMI. Troponin is a complex of three proteins that is integral to muscle contraction in skeletal and cardiac muscle, regulating the calcium-mediated interaction between actin and myosin. Its three subunits are TnC, TnI and TnT. Troponin C binds to calcium ions in order to produce movement; troponin T binds to tropomyosin, interlocking it to form a troponin-tropomyosin complex; troponin I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place. Troponin C has an identical amino-acid sequence in both skeletal and cardiac tissues and, thus, it has no potential as a cardiac specific marker. However, troponin T and troponin I have different isoforms in cardiac and skeletal muscle, encoded by separated genes, and consequently, have different amino-acid sequences. The respective cardiac isoforms of TnT (cTnT) and TnI (cTnI) allow production of antibodies that exclusively recognize these myocardial-specific proteins. Higher diagnostic sensitivity and specificity require specimen collection at patient presentation, 6–9 hours later and at 12–24 hours if clinical suspicion is high and earlier results are negative. Indeed, troponin is not considered as an early biomarker of myocardial necrosis: cardiac troponins need 4–10 hours after symptoms onset to appear in serum, and peak at 12–48 hours, remaining then abnormal for several days to two weeks [10–12].
Clinical Reasoning and Diagnostic Errors
Published in Paul Cerrato, John Halamka, Reinventing Clinical Decision Support, 2020
Suppose Mr. Jones, 59 years old, with a history of hypertension, stroke, and elevated lipid levels arrives in the ED complaining of sudden-onset intense sub-sternal chest pain that radiates to his left leg but does not affect his left arm or jaw.22 An experienced clinician would likely begin to think intuitively about this patient’s diagnosis. Mr. Jones’ symptoms suggest coronary ischemia, that is, a loss of blood to the heart tissue. Naturally, the attending physician will want to do a detailed physical examination to look for more clues to help refine the list of differential diagnoses, as well as appropriate lab tests. One finding that stands out in Mr. Jones’ lab readings is an elevated troponin I level. Troponin is a muscle protein that can escape from heart tissue that has been damaged by an MI.
High Dose Methylprednisolone versus Low Dose in Correction of Congenital Acyanotic Heart Disease
Published in Egyptian Journal of Anaesthesia, 2022
Maha Sadek El Derh, Noha Mohamed Abdelaziz, Samar M. Abdel Twab
In this study, 93 patients suffering from congenital acyanotic heart disease, planned for surgical correction, were divided into 3 groups according to the dose of MP received just after induction. They either received a high dose of 30 mg/kg or a low dose of 10 m/kg, and the third group did not receive steroids at all. In our institution, IL 6 is the only available inflammatory marker to be measured. Only 75 patients completed the study; there were significant differences as regard the postoperative ejection fraction measured 6 hours after surgery. The two groups that received MP had a higher EF in comparison to the control group, with no significance between the high-dose group and the low-dose group. Random blood sugar showed highest elevation in the high-dose group at ICU admission and after 24 hours. No differences between groups as regard the rate of wound infection was observed. As regard IL6 measured at ICU and after 24 hours, values were lowest in the high-dose group and higher in the low-dose group, with significant differences between all three groups. Cardiac troponin showed a significant variation only after 24 hours, expressed by the lowest level in the high-dose group, followed by the low-dose group, and the highest troponin level in the control group. These differences were significant only between the high-dose group and the two other groups, and no significance between the low-dose group and the control group was observed.
Azacitidine-induced myopericarditis in acute myeloid leukemia
Published in Baylor University Medical Center Proceedings, 2022
Mahmoud Ismayl, Asmini KC, Abhishek Thandra, Nattapong Sricharoen, Amy Arouni
Hypomethylating agents (AZA and decitabine) have been implicated as cardiotoxic in several case reports.6–9 However, trials evaluating AZA and decitabine for the treatment of myelodysplastic syndrome reported no myopericarditis.10–12 In a case series by Newman et al, three patients had new-onset pericarditis with repeated administration of AZA, which may suggest that cardiotoxicity could be secondary to a hypersensitivity or immune reaction to hypomethylating agents.6 This view was supported by the quick resolution of symptoms with corticosteroids in the three patients in their series.6 In another case by Bibault et al, acute myocarditis secondary to AZA was reported in a 50-year-old patient who presented with intense chest pain.7 The patient had ST elevations on ECG and an elevated troponin level up to 13.1 ng/mL with normal echocardiography and coronary angiography. After 1 week, the troponin level normalized and the chest pain resolved. With a final diagnosis of viral myocarditis, the patient was rechallenged with AZA. A similar scenario occurred on day 4, and cardiac magnetic resonance imaging demonstrated signs of myocarditis.7
Dietary Patterns and Their Association with CVD Risk Factors among Bangladeshi Adults: A Cross-Sectional Study
Published in Journal of the American College of Nutrition, 2021
Farhana Aktar Shammi, Suvasish Das Shuvo, Md Shahariea Karim Josy
Biochemical information such as; blood pressure, troponin-I level, and lipid profile (TC, LDL cholesterol, HDL cholesterol, TG) level was collected from their biochemical report for further analysis. Lipid profiles are categorized into high, borderline high, and normal (27). A digital BP machine (Brand: Omron-JPN500; Origin: Japan) was used to measure the blood pressure level. According to the blood pressure category of the American heart association, subjects were identified as hypertensive. Troponin-I is a cardiac and skeletal muscle protein suitable in the laboratory diagnosis of heart attack and related problems. The higher the amount of Troponin-I in the blood, the more damage there is to the heart. Different laboratories have different cutoff points for “normal” and “probable myocardial infarction”. The normal value of Troponin-I defined by the laboratory of Jashore Sadar Hospital is “Up to 1.3” ng/ml. Total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride ranges were determined according to the recommendations of Adult Treatment Panel (ATP III) of National Cholesterol education programs.