It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease.

https://www.cmaj.ca/content/cmaj/173/10/1191.full.pdf

Troponin: the biomarker of choice for the detection of cardiac injury

Background— Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction Methods and Results— We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers Echocardiography included conventional measures as well as tissue Doppler–derived strain and strain rate imaging Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) All subjects completed the race Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decrea

Myocardial Injury and Ventricular Dysfunction Related to Training Levels Among Nonelite Participants in the Boston Marathon

Current guidelines for the diagnosis of non-ST-segment elevation myocardial infarction are largely based on an elevated troponin level. While this rapid and sensitive blood test is certainly valuable in the appropriate setting, its widespread use in a variety of clinical scenarios may lead to the detection of troponin elevation in the absence of thrombotic acute coronary syndromes. Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure, can be associated with an increase in troponin level. These elevations may arise from various causes other than thrombotic coronary artery occlusion. Given the lack of any supportive data at present, patients with nonthrombotic troponin elevation should not be treated with antithrombotic and antiplatelet agents. Rather, the underlying cause of the troponin elevation should be targeted. However, troponin elevation in the absence of thrombotic acute coronary syndromes still retains prognostic value. Thus, cardiac troponin elevations are common in numerous disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome. While troponin is a sensitive biomarker to "rule out" non-ST-segment elevation myocardial infarction, it is less useful to "rule in" this event because it may lack specificity for acute coronary syndromes.

Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded.

Exercise-Induced Cardiac Troponin Elevation: Evidence, Mechanisms, and Implications

A routine of regular exercise is highly effective for prevention and treatment of many common chronic diseases and improves cardiovascular (CV) health and longevity. However, long-term excessive endurance exercise may induce pathologic structural remodeling of the heart and large arteries. Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias. Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening. However, this concept is still hypothetical and there is some inconsistency in the reported findings. Furthermore, lifelong vigorous exercisers generally have low mortality rates and excellent functional capacity. Notwithstanding, the hypothesis that long-term excessive endurance exercise may induce adverse CV remodeling warrants further investigation to identify at-risk individuals and formulate physical fitness regimens for conferring optimal CV health and longevity.

/pdf/potential-adverse-cardiovascular-effects-from-excessive-4mr7fjmgxp.pdf

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

This study provides biochemical evidence that ultraendurance exercise may cause subclinical myocardial damage, even in well-trained cyclists. The cellular nature of this damage and its clinical relevance remain unknown at present.

Plasma levels of cardiac troponin I after prolonged strenuous endurance exercise.

For a further depiction of exercise-induced cardiac dysfunction, N-terminal pro-brain natriuretic peptide (NT-pro-BNP) and cardiac troponin T (cTnT) were measured in recreational cyclists (n = 29) during the Otztal Radmarathon 2004. In all subjects, NT-pro-BNP significantly increased from 28 ± 21 to 278 ± 152 ng/L immediately after the race (p

Effect of competitive marathon cycling on plasma N-terminal pro-brain natriuretic peptide and cardiac troponin T in healthy recreational cyclists.

As long as the clinical meaning of exercise-induced release of cardiac troponins is uncertain, it should be considered as biochemical evidence for subclinical myocardial damage With regard to the extraordinary cardiopulmonary strains of ultraendurance races, we recommend athletes who regularly participate in such events to undergo thorough cardiovascular medical examinations to ascertain any subtle evidence of myocardial dysfunction

Effect of the “Race Across The Alps” in elite cyclists on plasma cardiac troponins I and T

The physiological effects of ultraendurance exercise are poorly investigated. The present case report describes the exercise intensity of ultraendurance cycling and its physiological impacts on various organ functions in an amateur cyclist performing the Otztal Radmarathon twice en bloque in a circuit of 2 identical laps (distance 460 km; cumulative altitude difference 11,000 m). In a pre-race laboratory test the athlete's performance capacity was measured as the maximal aerobic power (VO2max= 70 ml.kg(-1).min(-1)), a maximal power output (5.7 W.kg(-1)) and lactate threshold of 89%. The overall intensity during the ride was moderate (HRmean = 131 b.min(-1); %HRmax = 0.71) and significantly declined during the course of the race. Extensive biochemical laboratory testing performed pre- and post-race excluded major exercise-induced organ disturbances. For further confirmation and better understanding of the physiological effects of ultra-cycle events future studies of larger athlete populations are required.

Rudolf Pfister

Papers

Plasma levels of cardiac troponin I after prolonged strenuous endurance exercise.

Effect of competitive marathon cycling on plasma N-terminal pro-brain natriuretic peptide and cardiac troponin T in healthy recreational cyclists.

Effect of the “Race Across The Alps” in elite cyclists on plasma cardiac troponins I and T

Physiological effects of an ultra-cycle ride in an amateur athlete - a case report.