Review
Mechanism of Troponin Elevations in Patients With Acute Ischemic Stroke

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Ischemic heart disease and cerebrovascular diseases frequently co-exist in the same patient, and similar risk factors are shared. For 60 years, experimental, observational, and clinical trial data have incessantly indicated that neurologically induced myocardial injury exists. Since the introduction of troponin in the diagnosis of acute myocardial infarction, this marker has been measured in a number of other conditions as well. One of these conditions is acute ischemic stroke, causing diagnostic dilemmas for clinicians. Because various electrocardiographic alterations have also been reported in these patients, it has been suggested that elevated troponin levels are somehow neurologically mediated, thus not caused by direct cardiac release. In conclusion, this review examines the available studies that systematically measured troponin in patients with acute ischemic stroke to properly interpret troponin elevations in these patients.

Section snippets

Assays Used to Measure Troponin

Troponin acts as a muscle-regulatory protein and consists of 3 subunits: T, I, and C. Although cardiac troponin C, the calcium-binding subunit, is identical to the troponin C expressed in skeletal muscle, cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are specific to the heart.15 Troponin appears in the bloodstream 5 to 6 hours after AMI. Peak concentrations appear after 18 to 24 hours, and, despite gradual decreases, concentrations can stay elevated for up to 10 to 14 days. Today, the

Prevalence and Causes of Troponin Elevation in Patients With Ischemic Stroke

Existing studies of troponin elevations in patients with acute ischemic stroke are listed in Table 2, Table 3. Although it seems that a large body of evidence is available, the interpretation of these studies remains unclear in clinical practice. One reason why data of cardiac markers in patients with ischemic stroke are difficult to interpret is the hypothesis that the cerebrovascular event may endanger the heart in some kind of direct manner, leading to the elevation of troponin and creatine

Evidence of Myocardial Infarction

In 2000, the European Society of Cardiology and the American College of Cardiology recognized the role of biomarkers and made elevations (increase-and-decrease patterns) in their levels the cornerstone of the diagnosis of AMI.20 With this definition in mind, only few of the stroke studies (Table 2) featured serial measurements of cardiac markers and concomitant electrocardiographic (ECG) recordings.24, 26, 31, 35, 37 In our own previous work, we identified only 7 of 244 patients (3%) with

Prognostic Value of Troponin in Acute Ischemic Stroke

Troponin elevations confer a very well defined increase of cardiovascular mortality and risk for reinfarction in patients with acute coronary syndrome.38 Currently available data in patients with acute coronary syndrome reveal no threshold below which elevations of troponin are without negative implications for prognosis.39 Similarly, the prognostic implication of troponin in patients with ischemic stroke has been scrutinized by several investigators (Table 3).22, 23, 25, 31, 32, 33, 34, 35, 37

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  • Cited by (0)

    1

    Dr. Jensen was supported by a grant from the Danish Heart Foundation, Copenhagen, Denmark.

    2

    Dr Atar has received grants from the National Association of Norway for Public Health (the Norwegian Council for Heart and Vessels), Olso; the Eastern Regional Health Authority of Norway, Hamar; and the Aker University Hospital Research Foundation, Oslo, Norway.

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