Which labs are consistent with the mi diagnosis

It should be done within 10 minutes of being admitted to hospital. An ECG measures the electrical activity of your heart. Every time your heart beats, it produces tiny electrical impulses. An ECG machine records these signals onto paper, allowing your doctor to see how well your heart is functioning. An ECG is painless and takes about 5 minutes to do. During the test, flat metal discs electrodes are attached to your arms, legs and chest.

Wires from the electrodes are connected to the ECG machine, which records the electrical impulses. This corresponds to the area of damage inflicted on the heart. A heart attack is a form of acute coronary syndrome ACS , where there is a significant blockage in the coronary arteries. An STEMI is the most serious type of heart attack where there is a long interruption to the blood supply.

This is caused by a total blockage of the coronary artery, which can cause extensive damage to a large area of the heart. The availability of sensitive and in particular highly specific biomarkers of myocardial damage, such as the cardiac troponins cTn has led to a conceptual change in the definition and diagnosis of myocardial infarction in the second half of the s [1—3]. As a result the combination of symptoms and an increase above the reference limit in these specific biomarkers, preferably cardiac troponin were considered as diagnostic for MI [4, 5].

In the acute setting diagnosis relies on biomarkers, if the electrocardiogram is not conclusive. This is clearly the case for all patients with non-cardiac chest pain in whom the diagnosis of MI and ACS has to be ruled out, but also for many patients with unstable angina or non-ST-elevation myocardial infarction. Therefore, guidelines for the appropriate diagnosis and treatment in these cases have been issued and are regularly updated by the American and European professional associations [6, 7].

One limitation of the assays for cTn was their limited analytical sensitivity [8]. Thus, the first generations of these assays were not able to reliably quantify the low concentration of cTn in plasma from healthy persons. This situation has significantly improved with the advent of more sensitive cTn assays in recent years. Large clinical studies have shown that these assays can improve the diagnostic work-up of patients with acute chest pain and suspected MI [9—11].

This has already induced changes in the guidelines for diagnosis of MI [6]. At present we have not reached the end of this development. The current status of the available assays has been reviewed recently [13]. The advent of high sensitive hs cTn assays raise several questions regarding the definition of myocardial infarction, rule-in and rule-out of myocardial infarction, as well as when and how to treat patients with increased cTn concentrations according to the hs-cTn assays.

A major point is the increased analytical and diagnostic sensitivity of the assays and its impact on the diagnosis and definition of MI. These issues have been amply reviewed and discussed in the literature, recently [6, 14—16]. They are therefore not the topic of this short review. Another interesting question relates to the role of other biomarkers in the diagnosis of myocardial infarction or the acute coronary syndrome.

Many biomarkers of myocardial damage have been proposed and used in the past, because it was apparent that the conventional cTn assays did not perform ideally. Are these markers obsolete now or can they still improve diagnosis based on hs-cTn? This question has been asked in the past for several of the traditional MI-markers, e. In addition, to markers of ischemia and necrosis, several novel non-specific biomarkers have been identified in recent years that might add diagnostic information in the setting of suspected acute coronary syndrome or myocardial infarction.

The use of alternative markers has been reviewed in detail previously [17]. However, most of the studies evaluated in this review neither compared the alternative markers with cTn nor assessed the potential added value. Furthermore, hs-cTn assays were not evaluated at all limiting the relevance of these older studies. As indicated above, all these known and novel alternative biomarkers can be divided into two groups.

Group 1 are biomarkers related to myocardial damage or necrosis. The second group constitutes biomarkers related to the response of the body to acute stress or injury. These markers are non-specific for myocardial damage, but may be highly sensitive in combination with a specific marker of myocardial damage. In Table 1 the relevant biomarkers are summarized. While the markers indicating myocardial damage all have been investigated for their potential to substitute for cTn, the non-specific stress markers have mostly been used in combination with cTn trying to improve early diagnosis of myocardial infarction.

It should be noted that many biomarkers have been tested for their prognostic potential in the past, e. While these markers may be included in the therapeutic decision-making in the future, they are not specific for MI and therefore of limited value in making the diagnosis of MI.

Therefore, these markers are also not in the focus of this short review. Myoglobin is a low molecular 17 kDa cytosolic protein of striated muscle. It is able to bind oxygen and serves as an oxygen reservoir for the muscle cell in cases of increased demand.

Myoglobin is rapidly liberated into the extracellular space during muscular damage or necrosis. As myoglobin is present in skeletal muscle, its use in the diagnosis of MI has been limited by the low specificity for myocardial damage. Nevertheless myoglobin has been regarded as the most sensitive biomarker of myocardial damage in the past. In fact, high diagnostic sensitivity is still reported as the major strength of myoglobin in a recent guideline [7].

Even some recent studies adding myoglobin to conventional cTn suggest an improved diagnostic value [18]. With the advent of more sensitive cTn assays this view must be revised and studies using conventional cTn assays as comparison should no longer be performed. It should be noted that this TnI assay does not yet fulfil the criteria of high sensitivity see above [10].

Even 2 h after the onset of chest pain myoglobin did not provide higher diagnostic sensitivity than the hs-cTnI assay. Accordingly, it is not surprising that the addition of myoglobin to hs-cTnI did not improve the diagnostic performance of hs-cTnI alone [19]. These data are in line with several other studies comparing the value of myoglobin with hs-cTn [20, 21].

In summary, the supposed higher sensitivity of myoglobin for the early diagnosis of myocardial infarction does not hold in times of hs-TnI assays.

Therefore, the use of myoglobin in this setting is at least questionable. While the early tests were based on enzyme activity, CK-MB mass is currently measured by various ligand binding assays. There is now ample evidence that CK-MB mass determination is inferior to conventional cTn so that its use has not been advocated any more before the advent of hs-cTn.

Thus, for the diagnosis of acute MI in the setting of an emergency room or chest pain unit, CK-MB cannot be recommended. However, due to the prolonged elevation of cTn after an acute MI, CK-MB may be of value in the setting of suspected reinfarction or after cardiac surgery. Glycogen phosphorylase is an enzyme involved in cellular glycogen metabolism.

It is associated with glycogen in the sarcoplasmatic reticulum as a homodimer of approximately 97 kDa. Glycogen phosphorylase catalyzes the initial step of glycogen degradation, There are three isoforms B, M, and L which are present in brain and heart B , muscle including myocardium M , and liver L. The BB homodimer has been evaluated for its ability to improve the diagnosis of MI.

Myocardial ischemia increases the degradation of glycogen. Exhibition and Sponsorship. Trainee Prizes. Roche Scientific E-Poster Display. Pathology Education Outreach Grants. Past Pathology Update Programs. Future Pathology Updates. About Overview Annual Report. History of the College. What Is Pathology? Promotional Material. Myocardial infarction. Key Information Appropriate Tests Hospital admission should not be deferred, pending investigation.

Tests available include: Cardiac Troponin I or Troponin T - which are both very sensitive and specific and are the recommended laboratory tests for the diagnosis of MI. See Cardiac risk assessment. Reference Thygesen K et al. Eur Heart J ; Thygesen K et al. J Am Coll Cardiol ; Apple FS et al.

Clin Chem ; External Links. Page last updated:. Privacy Legal Sitemap Disclaimer Mail. It's extremely important to participate in this program. People who attend cardiac rehab after a heart attack generally live longer and are less likely to have another heart attack or complications from the heart attack. If cardiac rehab is not recommended during your hospitalization, ask your doctor about it.

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition. Having a heart attack is scary, and you might wonder how it will affect your life and whether you'll have another one. Fear, anger, guilt and depression are all common after a heart attack. Discussing them with your doctor, a family member or a friend might help. Or consider talking to a mental health provider or joining a support group. It's important to mention signs or symptoms of depression to your doctor.

Cardiac rehabilitation programs can be effective in preventing or treating depression after a heart attack. Some people worry about having sex after a heart attack, but most people can safely return to sexual activity after recovery. When you can resume sexual activity will depend on your physical comfort, emotional readiness and previous sexual activity.

Ask your doctor when it's safe to have sex. Some heart medications can affect sexual function. If you're having problems with sexual dysfunction, talk to your doctor. A heart attack usually is diagnosed in an emergency setting. However, if you're concerned about your risk of heart attack, see your doctor to check your risk factors and talk about prevention.

If your risk is high, you might be referred to a heart specialist cardiologist. When you make the appointment, ask if there's anything you need to do in advance, such as restrict your diet. You might need to fast before a cholesterol test, for example.