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==Overview== | ==Overview== | ||
[[ | [[Myocardial injury]] is defined as elevated [[troponin]] concentrations without [[sign]] and [[symptom]] indicating overt [[myocardial ischemia]] and is the most common cause of increased [[troponin]] level. Traditionally, elevated [[troponin]] level was eqaul to [[myocardial infarction]]. Diagnosis of [[myocardial injury]] is a challange for clinicians. By improving the laboratory method for detecting high sensitive [[troponin]] and clinical approach to diagnosis of myocardial [[ischemia]], [[patients]] with [[myocardial injury]] due to underlying [[diseases]] were excluded and treated. Evaluation and treatment of [[percipitant]] factors of [[myocardial injury]] including [[sepsis]], [[anemia]], [[chronic kidney disease]], [[cardiomyopathy]] are practically indicated. However, [[patients]] with evidence of [[myocardial injury]] and [[myocardial ischemia]] both have poor short and [[long term outcome]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Latest revision as of 19:06, 10 March 2022
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2]
Synonyms and keywords: Acute myocardial injury, Chronic myocardial injury, Myocardial ischemia, troponin concentration, systemic illness
Overview
Myocardial injury is defined as elevated troponin concentrations without sign and symptom indicating overt myocardial ischemia and is the most common cause of increased troponin level. Traditionally, elevated troponin level was eqaul to myocardial infarction. Diagnosis of myocardial injury is a challange for clinicians. By improving the laboratory method for detecting high sensitive troponin and clinical approach to diagnosis of myocardial ischemia, patients with myocardial injury due to underlying diseases were excluded and treated. Evaluation and treatment of percipitant factors of myocardial injury including sepsis, anemia, chronic kidney disease, cardiomyopathy are practically indicated. However, patients with evidence of myocardial injury and myocardial ischemia both have poor short and long term outcome.
Historical Perspective
- Troponin was first discovered by setsuro ebashi, a Japanese physiologist, in 1963 as a component of muscle contraction. [1]
- In 2000, use of troponin was established as the biomarker of choice in diagnosis of myocardial infarction by European Society of Cardiology (ESC) and American College of Cardiology (ACC).[2]
Classification
- Myocardial injury may be classified into acute and chronic based upon the pattern of troponin concentration.[3]
- Acute myocardial injury is considered when there is a rise and/or fall of cardiac troponin concentrations exceeding the biological and/or analytical variation.[4]
- Chronic myocardial injury may occur when cardiac troponin is greater than 99th-percentile URL without a rise and/or fall over a period of serial measurements ( more than 8 hours) in the conditions such as structural heart disease (hypertensive heart disease, ischemic cardiomyopathy, dilated cardiomyopathy) or secondary to non-cardiac causes such as chronic renal failure.
- Table below shown the classification of myocardial injury and also different types of myocardial infarction:
| Classification | Definition |
|---|---|
| Acute myocardial injury | Dynamic rise and/or fall of troponin concentration
associated with cardiovascular or noncardiovascular causes |
| Chronic myocardial injury | Stable elevated troponin concentration related to cardiovascular or noncardiovascular causes |
| Myocardial infarction type 1 | Myocardial infarction due to plaque rupture, ulceration, or dissection |
| Myocardial infarction type 2 | Myocardial infarction attributable to oxygen supply-demand
mismatch |
| Myocardial infarction type 3 | Sudden cardiac death associated with myocardial infarction |
| Myocardial infarction type 4 | Myocardial infarction associated with percutaneous intervention or stent thrombosis |
| Myocardial infarction type 5 | Myocardial infarction related to cardiac surgery |
Pathophysiology
- The pathogenesis of myocardial injury depends on increased cardiac troponin released by myocardial strain, inflammation, apoptosis, and cell injury, or decreased clearance of cardiac troponin.
- It is thought that increased troponin level in patients with advanced kidney disease is caused by either decreased clearance of cardiac troponin, underlying coronary artery disease and the presence of a left ventricular hypertrophy.[5]
- The presence of chronic myocardial injury and cardiac troponin in valvular heart disease such as aortic stenosis may be associated with cardiac mass, replacement fibrosis, and prognosis.[6]
Causes
- Common causes associated with myocardial injury include:
- Cardiovascular causes of chronic myocardial injury:[7]
- Chronic heart failure[8]
- Stable coronary artery disease[11]
- Persistent arrhythmias (atrial fibrillation)[14]
- Noncardiovascular causes of chronic myocardial injury:
- Chronic renal disease[15]
- Cardiovascular causes of acute myocardial injury:
- Myocardial infarction [7]
- Pulmonary embolism
- Myocarditis
- Myopericarditis
- Aortic dissection
- Cardiac surgery or procedures (cardioversion or ablation)
- Hypertension
- Arrhythmias
- Acute heart failure
- Acute valvular heart disease (aortic regurgitation or mitral regurgitation)
- Takotsubo cardiomyopathy
- Cardiac contusions ( chest compressions)
- Noncardiovascular causes of acute myocardial injury:
- Acute renal failure
- Sepsis
- Anemia [19]
- Drug-induced causes (chemotherapy)
- Stroke
- Extreme exertion
Differentiating myocardial injury from other Diseases
- Myocardial injury must be differentiated from myocardial ischemia based on the troponin concentration changes, ECG changes and clinical approach.
Epidemiology and Demographics
- The prevalence of myocardial injury is approximately 12,400 per 100,000 individuals presented in emergency department.[23]
- Between 2010 to 2011, the incidence of myocardial injury was approximately 29,000 per 100,000 individuals with a mortality rate of 39%.[24]
- The incidence of myocardial injury increases with age.
- There is no racial predilection to myocardial injury.
- women are more commonly affected by myocardial injury than men.
Risk Factors
Common risk factors in the development of myocardial injury include:
Screening
- According to the Canadian Cardiovascular Society,cardiac troponin screening for myocardial injury in noncardiac surgery (stayed at least 1 night in hospital ) is indicated for patients with history of:[25]
- Age >45 years old with known cardiovascular disease such as coronary artery disease, cerebral vascular disease, peripheral arterial disease, congestive heart failure,
- Age between 18-64 years old with significant cardiovascular disease scheduled for urgent or semi-urgent surgery (hip fracture)
- Age at least 65 years old
- A Revised Cardiac Risk Score Index (RCRI>1)
Natural History, Complications, and Prognosis
- 60% of cases of abnormal troponin concentrations , and 1 in 8 patients presenting to the hospital will have evidence of myocardial injury.
- Evidence of myocardial injury in chronic heart failure disease was associated with increased all-cause mortality, cardiovascular death, cardiovascular hospitalization.[8]
- Increases in cTnI concentrations in patients undergoing high-dose chemotherapy for aggressive malignant conditions have been correlated with future decreases in left ventricular ejection fraction.
- In patients with chronic kidney disease and end stage renal disease, amyloidosis, pulmonary embolism, increased level of troponin was associated with increased all-cause mortality.[26][27]
- Among patients admitted in emergency department, evidence of acute myocardial injury was associated with higher rate of all cause mortality and heart failure compared with chronic myocardial injury.[28]
- Prognosis is generally poor especially in non-cardiac causes of myocardial injury which have higher in-hospital mortality rate ( compared with cardiac causes of chronic myocardial injury).[29]
- The 5-year mortality rate of patients with myocardial injury is approximately 70%.[30]
Diagnosis
Diagnostic Study of Choice
- There are no established criteria for the diagnosis of myocardial injury. However, in patients with increased level of cardiac troponin, after evaluation about myocardial ischemia, diagnosis and treating the underlying disorders is considered.[3]
History and Symptoms
- The initial workup includes an evaluation about myocardial ischemia.[3]
- If myocardial infarction is ruled out, further assessment involves a detailed history, physical examination, laboratory testing, a 12-lead electrocardiogram, and an echocardiogram.
- Medical history should be taken about:
- Recent procedures (cardiac and non-cardiac)
- Use of cardiotoxic medications ( chemotherapy and substance abuse)
- Activity ( intense exercise regimens)
- Life stressors (takotsubo cardiomyopathy)
- Recent travel
- Comorbidities (specifically cardiovascular, pulmonary, renal )
- The most practical approach is identifying and treating the underlying causes of myocardial injury.
Common symptoms associated with underlying causes of myocardial injury include:
- Pleuritic chest pain may suggest pulmonary embolism, pneumonia, or myocarditis.
- Chest discomfort radiating to the back may suggest aortic dissection.
- Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema may suggest heart failure disease
- Syncope, angina, dyspnea may suggest valvular heart disease
- Palpitations, syncope may be seen in patients with cardiac arrhythmias
- Fevers, chills may suggest infection
Physical Examination
- There are no specific physical examination findings associated with myocardial injury. However, cardiovascular evaluation and systemic organs assessment is warranted as follows:
- Check of vital signs
- Cardiovascular system: heart rate and rhythm, murmurs, presence of congestion
- Pulmonary system: wheezing, rhonchi, crackles
- Detecting origin of infection
Laboratory Findings
Laboratory investigation consistent with the diagnosis of myocardial injury include: [3]
- Serial cardiac troponin measurement
- Renal function testing (chronic kidney disease)
- Natriuretic peptide (heart failure)
- Complete blood cell count (anemia or infection)
- D-dimer (pulmonary embolism, aortic dissection)
- C-reactive protein (infectious and inflammatory markers)
- Serial cardiac troponin samples should be obtained for differentiating between acute or chronic myocardial injury.
- In patients suspected MI, given a third sample of troponin without the pattern of rising and falling (in 26% of patients) and also ECG changes may be helpful to differentiate from myocardial injury.[31]
Electrocardiogram
There are no specific ECG findings associated with myocardial injury. Findings on an ECG suggestive of myocardial injury may include:[3]
- Evidence of ischemia, infarction
- Arrhythmias
- Acute right ventricular strain
- Conduction disease
- Structural disease ( left ventricular hypertrophy).
X-ray
There are no x-ray findings associated with myocardial injury.
Echocardiography or Ultrasound
Echocardiography may be helpful in the diagnosis of underlying causes of myocardial injury.
- Findings on an echocardiography associated with myocardial injury include:
CT scan
There are no CT scan findings associated with myocardial injury. However, a CT scan may be helpful in suspicion of pulmonary thromboembolism or aortic dissection.
MRI
Cardiac MRI may be helpful when there is clinically suspicion of myocarditis or infiltrative cardiomyopathy as the underlying causes of myocardial injury.
Other Imaging Findings
There are no other imaging findings associated with myocardial injury.
Other Diagnostic Studies
There are no other diagnostic studies associated with myocardial injury.
Treatment
Medical Therapy
- There is no established consensus regarding the routine management of myocardial injury. However, treating the underlying precipitant factors such as heart failure, chronic kidney disease is recommended.
- WOSCOPS study showed that pravastatin reduced hs-cTnI in patients without previous MI by the means of 13% leading to reduced future risk of MI .However, the role of pravastatin in acute phase of nonischemic myocardial injury is uncertain.[32]
- Use of dabigatran in patients with myocardial injury after noncardiac surgery was associated with reduced risk of major vascular event rate. However, this trial was terminated early and medication discontinuation rates were high. [33]
- The efficacy of Sodium-glucose cotransporter 2 inhibitors such as canagliflozin in patients with diabetes mellitus type 2 and myocardial injury was a delay of the rise in troponin over 2 years as well as diuresis, reduce blood pressure, and improve left ventricular remodeling.[34]
Surgery
Surgical intervention is not recommended for the management of myocardial injury.
Primary Prevention
There are no established measures for the primary prevention of myocardial injury.
Secondary Prevention
There are no established measures for the secondary prevention of myocardial injury.
References
- ↑ Perry SV (April 2008). "Background to the discovery of troponin and Setsuro Ebashi's contribution to our knowledge of the mechanism of relaxation in striated muscle". Biochem Biophys Res Commun. 369 (1): 43–8. doi:10.1016/j.bbrc.2007.11.185. PMID 18365325.
- ↑ Antman, Elliott; Bassand, Jean-Pierre; Klein, Werner; Ohman, Magnus; Lopez Sendon, Jose Luis; Rydén, Lars; Simoons, Maarten; Tendera, Michal (2000). "Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction". Journal of the American College of Cardiology. 36 (3): 959–969. doi:10.1016/S0735-1097(00)00804-4. ISSN 0735-1097.
- ↑ 3.0 3.1 3.2 3.3 3.4 McCarthy, Cian P.; Raber, Inbar; Chapman, Andrew R.; Sandoval, Yader; Apple, Fred S.; Mills, Nicholas L.; Januzzi, James L. (2019). "Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays". JAMA Cardiology. 4 (10): 1034. doi:10.1001/jamacardio.2019.2724. ISSN 2380-6583.
- ↑ Twerenbold, R.; Jaffe, A.; Reichlin, T.; Reiter, M.; Mueller, C. (2012). "High-sensitive troponin T measurements: what do we gain and what are the challenges?". European Heart Journal. 33 (5): 579–586. doi:10.1093/eurheartj/ehr492. ISSN 0195-668X.
- ↑ Januzzi, James; Gaggin, Hanna; Wolf, Myles; Christenson, Robert H; Hise, Michael; Duh, Show-Hong; Kelley, Walter; Seliger, Stephen L; deFilippi, Christopher (2012). "Interpreting Cardiac Troponin Results from High-Sensitivity Assays in Chronic Kidney Disease without Acute Coronary Syndrome". Clinical Chemistry. 58 (9): 1342–1351. doi:10.1373/clinchem.2012.185322. ISSN 0009-9147.
- ↑ Chin, C. W. L.; Shah, A. S. V.; McAllister, D. A.; Joanna Cowell, S.; Alam, S.; Langrish, J. P.; Strachan, F. E.; Hunter, A. L.; Maria Choy, A.; Lang, C. C.; Walker, S.; Boon, N. A.; Newby, D. E.; Mills, N. L.; Dweck, M. R. (2014). "High-sensitivity troponin I concentrations are a marker of an advanced hypertrophic response and adverse outcomes in patients with aortic stenosis". European Heart Journal. 35 (34): 2312–2321. doi:10.1093/eurheartj/ehu189. ISSN 0195-668X.
- ↑ 7.0 7.1 Sandoval, Yader; Smith, Stephen W.; Sexter, Anne; Thordsen, Sarah E.; Bruen, Charles A.; Carlson, Michelle D.; Dodd, Kenneth W.; Driver, Brian E.; Hu, Yan; Jacoby, Katherine; Johnson, Benjamin K.; Love, Sara A.; Moore, Johanna C.; Schulz, Karen; Scott, Nathaniel L.; Apple, Fred S. (2017). "Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical Transition to High-Sensitivity Cardiac Troponin I". The American Journal of Medicine. 130 (12): 1431–1439.e4. doi:10.1016/j.amjmed.2017.05.049. ISSN 0002-9343.
- ↑ 8.0 8.1 Aimo, Alberto; Januzzi, James L.; Vergaro, Giuseppe; Ripoli, Andrea; Latini, Roberto; Masson, Serge; Magnoli, Michela; Anand, Inder S.; Cohn, Jay N.; Tavazzi, Luigi; Tognoni, Gianni; Gravning, Jørgen; Ueland, Thor; Nymo, Ståle H.; Brunner-La Rocca, Hans-Peter; Genis, Antoni Bayes; Lupón, Josep; de Boer, Rudolf A.; Yoshihisa, Akiomi; Takeishi, Yasuchika; Egstrup, Michael; Gustafsson, Ida; Gaggin, Hanna K.; Eggers, Kai M.; Huber, Kurt; Tentzeris, Ioannis; Tang, Wai H.W.; Grodin, Justin; Passino, Claudio; Emdin, Michele (2018). "Prognostic Value of High-Sensitivity Troponin T in Chronic Heart Failure". Circulation. 137 (3): 286–297. doi:10.1161/CIRCULATIONAHA.117.031560. ISSN 0009-7322.
- ↑ . doi:10.3969/j.issn.1671-5411.2014.02.011. Missing or empty
|title=(help) - ↑ Kubo, Toru; Kitaoka, Hiroaki; Yamanaka, Shigeo; Hirota, Takayoshi; Baba, Yuichi; Hayashi, Kayo; Iiyama, Tatsuo; Kumagai, Naoko; Tanioka, Katsutoshi; Yamasaki, Naohito; Matsumura, Yoshihisa; Furuno, Takashi; Sugiura, Tetsuro; Doi, Yoshinori L. (2013). "Significance of High-Sensitivity Cardiac Troponin T in Hypertrophic Cardiomyopathy". Journal of the American College of Cardiology. 62 (14): 1252–1259. doi:10.1016/j.jacc.2013.03.055. ISSN 0735-1097.
- ↑ Januzzi, James L.; Suchindran, Sunil; Coles, Adrian; Ferencik, Maros; Patel, Manesh R.; Hoffmann, Udo; Ginsburg, Geoffrey S.; Douglas, Pamela S. (2019). "High-Sensitivity Troponin I and Coronary Computed Tomography in Symptomatic Outpatients With Suspected CAD". JACC: Cardiovascular Imaging. 12 (6): 1047–1055. doi:10.1016/j.jcmg.2018.01.021. ISSN 1936-878X.
- ↑ Aeschbacher, Stefanie; Schoen, Tobias; Bossard, Matthias; van der Lely, Stephanie; Glättli, Kathrin; Todd, John; Estis, Joel; Risch, Martin; Mueller, Christian; Risch, Lorenz; Conen, David (2015). "Relationship Between High-Sensitivity Cardiac Troponin I and Blood Pressure Among Young and Healthy Adults". American Journal of Hypertension. 28 (6): 789–796. doi:10.1093/ajh/hpu226. ISSN 0895-7061.
- ↑ Røsjø, Helge; Andreassen, Johanna; Edvardsen, Thor; Omland, Torbjørn (2011). "Prognostic Usefulness of Circulating High-Sensitivity Troponin T in Aortic Stenosis and Relation to Echocardiographic Indexes of Cardiac Function and Anatomy". The American Journal of Cardiology. 108 (1): 88–91. doi:10.1016/j.amjcard.2011.02.346. ISSN 0002-9149.
- ↑ van den Bos, E. J.; Constantinescu, A. A.; van Domburg, R. T.; Akin, S.; Jordaens, L. J.; Kofflard, M. J. M. (2011). "Minor elevations in troponin I are associated with mortality and adverse cardiac events in patients with atrial fibrillation". European Heart Journal. 32 (5): 611–617. doi:10.1093/eurheartj/ehq491. ISSN 0195-668X.
- ↑ Apple, Fred S.; Murakami, MaryAnn M.; Pearce, Lesly A.; Herzog, Charles A. (2002). "Predictive Value of Cardiac Troponin I and T for Subsequent Death in End-Stage Renal Disease". Circulation. 106 (23): 2941–2945. doi:10.1161/01.CIR.0000041254.30637.34. ISSN 0009-7322.
- ↑ Heresi, G.A.; Tang, W.H.W.; Aytekin, M.; Hammel, J.; Hazen, S.L.; Dweik, R.A. (2012). "Sensitive cardiac troponin I predicts poor outcomes in pulmonary arterial hypertension". European Respiratory Journal. 39 (4): 939–944. doi:10.1183/09031936.00067011. ISSN 0903-1936.
- ↑ Riley, Elise D.; Hsue, Priscilla Y.; Vittinghoff, Eric; Wu, Alan H.B.; Coffin, Phillip O.; Moore, Peter K.; Lynch, Kara L. (2017). "Higher prevalence of detectable troponin I among cocaine-users without known cardiovascular disease". Drug and Alcohol Dependence. 172: 88–93. doi:10.1016/j.drugalcdep.2016.11.039. ISSN 0376-8716.
- ↑ Segre, Carlos Alexandre Wainrober; Hueb, Whady; Garcia, Rosa Maria Rahmi; Rezende, Paulo Cury; Favarato, Desiderio; Strunz, Celia Maria Cassaro; Sprandel, Marília da Costa Oliveira; Roggério, Alessandra; Carvalho, Ana Luiza de Oliveira; Maranhão, Raul Cavalcante; Ramires, José Antonio Franchini; Filho, Roberto Kalil (2015). "Troponin in diabetic patients with and without chronic coronary artery disease". BMC Cardiovascular Disorders. 15 (1). doi:10.1186/s12872-015-0051-z. ISSN 1471-2261.
- ↑ Bellotto, Fabio; Fagiuoli, Stefano; Pavei, Andrea; Gregory, Shawn A.; Cati, Arianna; Silverj, Elisabetta; Plebani, Mario; Zaninotto, Martina; Mancuso, Tommaso; Iliceto, Sabino (2005). "Anemia and ischemia: Myocardial injury in patients with gastrointestinal bleeding". The American Journal of Medicine. 118 (5): 548–551. doi:10.1016/j.amjmed.2005.01.026. ISSN 0002-9343.
- ↑ Puelacher, Christian; Lurati Buse, Giovanna; Seeberger, Daniela; Sazgary, Lorraine; Marbot, Stella; Lampart, Andreas; Espinola, Jaqueline; Kindler, Christoph; Hammerer, Angelika; Seeberger, Esther; Strebel, Ivo; Wildi, Karin; Twerenbold, Raphael; du Fay de Lavallaz, Jeanne; Steiner, Luzius; Gurke, Lorenz; Breidthardt, Tobias; Rentsch, Katharina; Buser, Andreas; Gualandro, Danielle M.; Osswald, Stefan; Mueller, Christian; Seeberger, Manfred; Christ-Crain, Mirjam; Cuculi, Florim; Badertscher, Patrick; Nestelberger, Thomas; Wussler, Desiree; Flores, Dayana; Boeddinghaus, Jasper; Sabti, Zaid; Giménez, Maria Rubini; Kozhuharov, Nikola; Shrestha, Samyut; Kloos, Wanda; Lohrmann, Jens; Reichlin, Tobias; Freese, Michael; Meissner, Kathrin; Kaiser, Christoph; Buser, Andreas (2018). "Perioperative Myocardial Injury After Noncardiac Surgery". Circulation. 137 (12): 1221–1232. doi:10.1161/CIRCULATIONAHA.117.030114. ISSN 0009-7322.
- ↑ Lim, Wendy (2006). "Elevated Cardiac Troponin Measurements in Critically Ill Patients". Archives of Internal Medicine. 166 (22): 2446. doi:10.1001/archinte.166.22.2446. ISSN 0003-9926.
- ↑ Punukollu, Gopikrishna; Gowda, Ramesh M; Khan, Ijaz A; Mehta, Nirav J; Navarro, Victor; Vasavada, Balendu C; Sacchi, Terrence J (2004). "Elevated serum cardiac troponin I in rhabdomyolysis". International Journal of Cardiology. 96 (1): 35–40. doi:10.1016/j.ijcard.2003.04.053. ISSN 0167-5273.
- ↑ Lee, Kuan Ken; Noaman, Ala; Vaswani, Amar; Gibbins, Matthew; Griffiths, Megan; Chapman, Andrew R.; Strachan, Fiona; Anand, Atul; McAllister, David A.; Newby, David E.; Gray, Alasdair J.; Mills, Nicholas L.; Shah, Anoop S.V. (2019). "Prevalence, Determinants, and Clinical Associations of High-Sensitivity Cardiac Troponin in Patients Attending Emergency Departments". The American Journal of Medicine. 132 (1): 110.e8–110.e21. doi:10.1016/j.amjmed.2018.10.002. ISSN 0002-9343.
- ↑ Sarkisian, Laura; Saaby, Lotte; Poulsen, Tina S.; Gerke, Oke; Jangaard, Nikolaj; Hosbond, Susanne; Diederichsen, Axel C.P.; Thygesen, Kristian; Mickley, Hans (2016). "Clinical Characteristics and Outcomes of Patients with Myocardial Infarction, Myocardial Injury, and Nonelevated Troponins". The American Journal of Medicine. 129 (4): 446.e5–446.e21. doi:10.1016/j.amjmed.2015.11.006. ISSN 0002-9343.
- ↑ Puelacher, Christian; Bollen Pinto, Bernardo; Mills, Nicholas L.; Duceppe, Emmanuelle; Popova, Ekaterine; Duma, Andreas; Nagele, Peter; Omland, Torbjørn; Hammerer-Lercher, Angelika; Lurati Buse, Giovanna (2021). "Expert consensus on peri-operative myocardial injury screening in noncardiac surgery". European Journal of Anaesthesiology. 38 (6): 600–608. doi:10.1097/EJA.0000000000001486. ISSN 0265-0215.
- ↑ Apple, Fred S; Ler, Ranka; Young, Amy; Brunelli, Steven M; Gilbertson, David; Wu, Alan H B; Hu, Yan; Cao, Jing; Love, Sara A; Herzog, Charles A; Sandoval, Yader (2016). "Prognostic Value of Serial Changes in High-Sensitivity Cardiac Troponin I and T over 3 Months Using Reference Change Values in Hemodialysis Patients". Clinical Chemistry. 62 (4): 631–638. doi:10.1373/clinchem.2015.251835. ISSN 0009-9147.
- ↑ La Vecchia, L (2004). "Increased cardiac troponin I on admission predicts in-hospital mortality in acute pulmonary embolism". Heart. 90 (6): 633–637. doi:10.1136/hrt.2003.019745. ISSN 0007-0769.
- ↑ Kadesjo, Erik; Roos, Andreas; Siddiqui, Anwar J.; Desta, Liyew; Lundback, Magnus; Holzmann, Martin (2019). "ACUTE VERSUS CHRONIC MYOCARDIAL INJURY AND OUTCOMES". Journal of the American College of Cardiology. 73 (9): 105. doi:10.1016/S0735-1097(19)30713-2. ISSN 0735-1097.
- ↑ Ilva, Tuomo J.; Eskola, Markku J.; Nikus, Kjell C.; Voipio-Pulkki, Liisa-Maria; Lund, Juha; Pulkki, Kari; Mustonen, Harri; Niemelä, Kari O.; Karhunen, Pekka J.; Porela, Pekka (2010). "The Etiology and Prognostic Significance of Cardiac Troponin I Elevation in Unselected Emergency Department Patients". The Journal of Emergency Medicine. 38 (1): 1–5. doi:10.1016/j.jemermed.2007.09.060. ISSN 0736-4679.
- ↑ Chapman, Andrew R.; Shah, Anoop S.V.; Lee, Kuan Ken; Anand, Atul; Francis, Oliver; Adamson, Philip; McAllister, David A.; Strachan, Fiona E.; Newby, David E.; Mills, Nicholas L. (2018). "Long-Term Outcomes in Patients With Type 2 Myocardial Infarction and Myocardial Injury". Circulation. 137 (12): 1236–1245. doi:10.1161/CIRCULATIONAHA.117.031806. ISSN 0009-7322.
- ↑ Bjurman, Christian; Larsson, Mårten; Johanson, Per; Petzold, Max; Lindahl, Bertil; Fu, Michael L.X.; Hammarsten, Ola (2013). "Small Changes in Troponin T Levels Are Common in Patients With Non–ST-Segment Elevation Myocardial Infarction and Are Linked to Higher Mortality". Journal of the American College of Cardiology. 62 (14): 1231–1238. doi:10.1016/j.jacc.2013.06.050. ISSN 0735-1097.
- ↑ Ford, Ian; Shah, Anoop S.V.; Zhang, Ruiqi; McAllister, David A.; Strachan, Fiona E.; Caslake, Muriel; Newby, David E.; Packard, Chris J.; Mills, Nicholas L. (2016). "High-Sensitivity Cardiac Troponin, Statin Therapy, and Risk of Coronary Heart Disease". Journal of the American College of Cardiology. 68 (25): 2719–2728. doi:10.1016/j.jacc.2016.10.020. ISSN 0735-1097.
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