التفاصيل البيبلوغرافية
| العنوان: |
Plasma Cardiac Troponin-I Concentration in Normal Horses and in Horses with Cardiac Abnormalities. |
| المؤلفون: |
Foreman, Jonathan H., Tennent-Brown, Brett S., Oyama, Mark A., Sisson, D. David |
| المصدر: |
Animals (2076-2615); Jan2025, Vol. 15 Issue 1, p92, 10p |
| مصطلحات موضوعية: |
VENTRICULAR arrhythmia, MYOCARDIAL injury, VENTRICULAR tachycardia, CHEMILUMINESCENCE assay, ATRIAL fibrillation, ARRHYTHMIA |
| مستخلص: |
Simple Summary: Cardiac troponin-I (cTnI) in plasma is used daily as a biomarker indicative of the severity of myocardial damage in humans suffering cardiac ischemia due to coronary artery disease, commonly referred to as "heart attacks". Because troponin is so similar in humans and domestic animal species, human immunoassays are often used to measure cTnI concentrations in domestic animals. All assays should, however, have normal reference ranges specific to the type of assay and the species of concern. We used a human chemiluminescence assay to measure cTnI concentrations in normal ponies, to establish an assay-specific reference range, and in adult horses with clinical cardiac disease confirmed by electrocardiography and ultrasonography. Horses with atrial fibrillation sometimes had mild increases in cTnI, with concentrations outside the reference range. Horses with ventricular arrhythmias had a 10-fold higher median cTnI than horses with atrial fibrillation, confirming the utility of cTnI plasma measurements in horses with suspected ventricular premature contractions or ventricular tachycardia. Ventricular arrhythmias carry a poorer prognosis for survival than atrial fibrillation in horses. Cardiac troponin-I (cTnI) is a highly sensitive and specific marker of myocardial injury detectable in plasma by immunoassay techniques. Inclusion criteria over a 3-year period required a diagnosis of cardiac disease accompanied by electrocardiographic (ECG) and cardiac ultrasound examinations (n = 23) in adult horses (≥2 years of age). A second group of normal adult ponies (n = 12) was studied as a reference group. Heparinized jugular venous blood samples were collected and centrifuged within 30 min, and the plasma was separated and frozen at −70 °C for subsequent batched cTnI analysis. The lower limit of detection was 0.01 ng/mL, and the upper limit was 100 ng/mL of plasma. Normal equine plasma cTnI concentrations ranged from 0.01 to 0.03 ng/mL (n = 12). Horses with non-arrhythmogenic murmurs (n = 4) included tricuspid (0.05 ng/mL cTnI), mitral (0.07), and aortic insufficiencies (0.01, 0.02). Horses with benign atrial fibrillation (n = 8) had a cTnI range of <0.01–0.09 ng/mL, with four horses having cTnI concentrations falling slightly outside the reference range (0.04, 0.05, 0.06, and 0.09). Horses with ventricular arrhythmias (ventricular premature contractions or ventricular tachycardia) and documentable myocardial toxicities or immunological reactions (n = 5) had cTnI concentrations of 0.05, 0.21, 0.31, 15.18, and >100 ng/mL. Horses with ventricular arrhythmias but no documentation of myocardial toxicity (n = 3) had cTnI concentrations of 0.34, 0.46, and 80.42 ng/mL. When grouped by arrhythmia type and compared using the Mann–Whitney Rank Sum Test, the median ventricular arrhythmia cTnI (0.40 ng/mL) was significantly higher than the median atrial fibrillation cTnI (0.04 ng/mL, p < 0.001). It was concluded that horses with myocardial toxicities and ventricular arrhythmias often had severe elevations in plasma cTnI. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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