China
Africa
Explore chapters and articles related to this topic
Acute coronary syndromes
Published in Henry J. Woodford, Essential Geriatrics, 2022
Two cardiac troponin blood tests are used in series to detect significant change. The timing and diagnostic cut-off values depend on the specific assay used. Careful clinical evaluation is needed in conjunction with testing. Troponin tests can also be elevated in pulmonary embolism and aortic dissection, also in association with chest pain.2 Small rises with non-ACS diagnoses are more common in older people.9 NSTEMI is usually diagnosed by the presence of either acute cardiac-type chest pain or relevant ECG changes plus evidence of a myocardial injury (e.g. rise in cardiac troponins). In unstable angina there is no myocyte necrosis, the risk of death is lower and people benefit less from aggressive therapies.
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
Atypical variant takotsubo cardiomyopathy secondary to pheochromocytoma
Published in Baylor University Medical Center Proceedings, 2022
Nikhil Kokkapuni, Michelle Thieu, Sinan Ali Bana, Reba Cherian, Amy Haberman
A 39-year-old woman presented to the emergency department with acute onset chest pain associated with headache and diaphoresis. She reported similar symptoms intermittently for the past 7 years. Prior cardiac and neurology workup were negative, and she had been given the diagnosis of anxiety disorder. She did not use alcohol, tobacco, or illicit drugs. Physical examination was unremarkable. Laboratory findings were significant for an elevated troponin level of 2.67 ng/mL. Electrocardiogram was normal. She was admitted for non–ST elevation myocardial infarction. She underwent cardiac catheterization, which demonstrated no coronary artery disease. Intraoperative ventriculogram revealed a left-ventricular ejection fraction of 45% with global hypokinesis and akinesis of the mid-anterior and mid-inferior walls compatible with atypical/inverted takotsubo cardiomyopathy (Figure 1).