2.50
Hdl Handle:
http://hdl.handle.net/10755/157888
Type:
Presentation
Title:
Cardiac and Non-Cardiac Causes of Troponin I Elevations
Abstract:
Cardiac and Non-Cardiac Causes of Troponin I Elevations
Conference Sponsor:Western Institute of Nursing
Conference Year:2006
Author:Wung, Shu-Fen, PhD, RN, ACNP, FAHA, FAAN
P.I. Institution Name:The University of Arizona
Title:Associate Professor
Contact Address:School of Nursing, 1305 N Martin Avenue, Tucson, AZ, 85721-0203, USA
Contact Telephone:520-626-4305
Co-Authors:Diana Wong and Heather Hiscox, MPH
Cardiac troponin is the most sensitive and specific biochemical marker of myocardial damage and is routinely measured in patients presenting with acute coronary syndrome (ACS), including non-ST-elevation myocardial infarction (NSTEMI), ST-elevation-MI (STEMI), and unstable angina (UA). However, myocardial damage can occur from a variety of mechanisms other than acute ischemia. Knowledge about the potential elevations of troponin in these conditions may help discriminate acute MI from other causes. Methods: A total of 1,220 subjects with suspected myocardial infarction enrolled in a prospective study were evaluated. Among those, 210 (17%) had an elevated troponin I level. Discharge summaries were reviewed for cardiac and noncardiac diagnoses. The mean troponin I level was calculated. Results: Cardiac causes of troponin I elevation include NSTEMI (n=95, 45%), STEMI (n=72, 34%), UA (n=15, 7%), arrhythmia (n=5, 2%), hypertension/cardiomyopathy (n=3, 2%), and bypass surgery (n=1, 1%). Noncardiac causes of elevated troponin I include renal failure/insufficiency (n=5, 2%), hypoxia (n=4, 2%), pulmonary embolism (n=1, 1%), and sepsis (n=1, 1%). Six subjects (3%) had false-positive troponin I elevations and no specific cause for these elevations can be identified. Twenty-eight subjects (13%) experienced troponin I elevations but were not diagnosed with ACS. Three of the five subjects with arrhythmia had troponin I elevation after cardioversion. The mean troponin I levels was highest in subjects with STEMI, NSTEMI, hypoxia, UA, followed by renal failure/insufficiency (Table 1). Conclusion: Although ACS is the most common cause of troponin I elevation, one in eight subjects has elevated troponin I that is caused by other cardiac or noncardiac causes than ACS. Understanding these differential causes of troponin elevations may help clinicians to discriminate acute cardiac events from other diagnoses. Header: Table 1: Troponin I values (ng/ml) by discharge diagnosis; Final Diagnosis / n / Frequency / Mean ñ SD / Range / Median; STEMI / 72 / 0.34/ 101 ñ 223.46 / 1.7-1,768 / 38.5; NSTEMI / 95/ 0.45/ 15.76 ñ 27.74 / 0.2-220/ 7.6 ; Hypoxia/Pulmonary / 4 0 / .02 4./ 25 ñ 3.29/ 1.4-9 / 3.3; UA / 15/ 0.07 / 3.76 ñ 3.97 /.05-12.9/ 2.1; Renal failure/insufficiency/ 5 0.02/ 3.72 ñ 5.32 /.06-12.9 / 2.2; HTN/cardiomyopathy / 3 / 0.02/ 2.53 + 4.13/ 0.08-7.3/ 0.22; Arrhythmia / 5 / 0.02/ 0.89 + 1.17/ 0.05-2.5/ 0.07;
Heart failure / 2/ 0.01/ 0.15 + 0.07/ 0.14-0.15 / 0.15. [SD = standard deviation, HTN = hypertension]
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Western Institute of Nursing

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleCardiac and Non-Cardiac Causes of Troponin I Elevationsen_GB
dc.identifier.urihttp://hdl.handle.net/10755/157888-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Cardiac and Non-Cardiac Causes of Troponin I Elevations</td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Western Institute of Nursing</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2006</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Wung, Shu-Fen, PhD, RN, ACNP, FAHA, FAAN</td></tr><tr class="item-institute"><td class="label">P.I. Institution Name:</td><td class="value">The University of Arizona</td></tr><tr class="item-author-title"><td class="label">Title:</td><td class="value">Associate Professor</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">School of Nursing, 1305 N Martin Avenue, Tucson, AZ, 85721-0203, USA</td></tr><tr class="item-phone"><td class="label">Contact Telephone:</td><td class="value">520-626-4305</td></tr><tr class="item-email"><td class="label">Email:</td><td class="value">shufen@nursing.arizona.edu</td></tr><tr class="item-co-authors"><td class="label">Co-Authors:</td><td class="value">Diana Wong and Heather Hiscox, MPH</td></tr><tr><td colspan="2" class="item-abstract">Cardiac troponin is the most sensitive and specific biochemical marker of myocardial damage and is routinely measured in patients presenting with acute coronary syndrome (ACS), including non-ST-elevation myocardial infarction (NSTEMI), ST-elevation-MI (STEMI), and unstable angina (UA). However, myocardial damage can occur from a variety of mechanisms other than acute ischemia. Knowledge about the potential elevations of troponin in these conditions may help discriminate acute MI from other causes. Methods: A total of 1,220 subjects with suspected myocardial infarction enrolled in a prospective study were evaluated. Among those, 210 (17%) had an elevated troponin I level. Discharge summaries were reviewed for cardiac and noncardiac diagnoses. The mean troponin I level was calculated. Results: Cardiac causes of troponin I elevation include NSTEMI (n=95, 45%), STEMI (n=72, 34%), UA (n=15, 7%), arrhythmia (n=5, 2%), hypertension/cardiomyopathy (n=3, 2%), and bypass surgery (n=1, 1%). Noncardiac causes of elevated troponin I include renal failure/insufficiency (n=5, 2%), hypoxia (n=4, 2%), pulmonary embolism (n=1, 1%), and sepsis (n=1, 1%). Six subjects (3%) had false-positive troponin I elevations and no specific cause for these elevations can be identified. Twenty-eight subjects (13%) experienced troponin I elevations but were not diagnosed with ACS. Three of the five subjects with arrhythmia had troponin I elevation after cardioversion. The mean troponin I levels was highest in subjects with STEMI, NSTEMI, hypoxia, UA, followed by renal failure/insufficiency (Table 1). Conclusion: Although ACS is the most common cause of troponin I elevation, one in eight subjects has elevated troponin I that is caused by other cardiac or noncardiac causes than ACS. Understanding these differential causes of troponin elevations may help clinicians to discriminate acute cardiac events from other diagnoses. Header: Table 1: Troponin I values (ng/ml) by discharge diagnosis; Final Diagnosis / n / Frequency / Mean &ntilde; SD / Range / Median; STEMI / 72 / 0.34/ 101 &ntilde; 223.46 / 1.7-1,768 / 38.5; NSTEMI / 95/ 0.45/ 15.76 &ntilde; 27.74 / 0.2-220/ 7.6 ; Hypoxia/Pulmonary / 4 0 / .02 4./ 25 &ntilde; 3.29/ 1.4-9 / 3.3; UA / 15/ 0.07 / 3.76 &ntilde; 3.97 /.05-12.9/ 2.1; Renal failure/insufficiency/ 5 0.02/ 3.72 &ntilde; 5.32 /.06-12.9 / 2.2; HTN/cardiomyopathy / 3 / 0.02/ 2.53 + 4.13/ 0.08-7.3/ 0.22; Arrhythmia / 5 / 0.02/ 0.89 + 1.17/ 0.05-2.5/ 0.07;<br/>Heart failure / 2/ 0.01/ 0.15 + 0.07/ 0.14-0.15 / 0.15. [SD = standard deviation, HTN = hypertension]</td></tr></table>en_GB
dc.date.available2011-10-26T20:18:06Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T20:18:06Z-
dc.description.sponsorshipWestern Institute of Nursingen_GB
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