The ED applicability of the troponins is severely limited, however, because values remain normal in most patients with acute cardiac events as long as 6 hours following symptom onset. Myoglobin appeared promising as a marker of early cardiac ischemia but appears to be only marginally more sensitive than CK-MB assays early after symptom onset and less sensitive than CK-MB at 8 hours or more after chest pain starts.
Rapid serial myoglobin assessment, however, appears highly useful as an early marker of AMI. The marker has a very narrow diagnostic window. The clinician is left with several tests that are highly effective in correctly identifying patients with AMI or at high risk for AMI , but none that can dependably exclude patients with acute coronary syndromes soon after chest pain onset. Although it is recognized that normal values obtained within 6 hours of symptom onset do not exclude an acute coronary syndrome, patients at low clinical risk and having normal cardiac marker tests could be provisionally admitted to low-acuity hospital settings or ED observation.
Also, there was no difference in the hospital placement of patients in critical care and non- critical care beds. The availability of early markers was associated with more hospital admissions as compared to the control group, as the number of patients discharged from the ED was decreased in the stat versus control groups Conclusions: The availability of 0- and 1-h myoglobin and CK-MB results after ED evaluation had no effect on the use of thrombolytic therapy for patients presenting with AMI, and it slightly increased the number of patients admitted to the hospital who had no evidence of acute myocardial necrosis.
Abstract Objectives: The purpose of this study was to assess whether the immediate availability of serum markers would increase the appropriate use of thrombolytic therapy. Also, a trend detected in serial measurements provides better information than single measurements. Therefore, MI is unlikely if CK is not increased in patients with chest pain and a failure of elevated CK levels to fall indicates that there is an extension of the infarct.
It is shown that in high-risk patients, even minor elevations have important prognostic implications. The relative index is a very useful index to helps differentiate between CK from the myocardium, skeletal muscle, or from neural damage. It is calculated as:. Rather than the enzyme activity of CK and CK-MB, the CK mass estimated is found to be of better diagnostic value, but the costs being considerable is not easily available. Because there is a lag period for the elevation of CK-MB levels after onset of chest pain, other potential markers such as myoglobin and troponins were pursued.
Troponins are the contractile proteins in muscle cells, which present very early in the bloodstream, 3 to 9 hours post infarct. Cardiac-specific isoforms have been identified, and among the three troponins in the contractile component of the myocardium, troponin-I and troponin-T are widely used.
Cardiac troponin cTn I, increases in 4 to 6 hours, peaks at 12 hours, and returns to basal levels in 3 to 10 days, whereas troponin-T stays elevated for 12 to 48 hours and falls to normal in 10 days. The introduction of a high-sensitivity troponin hs-Trop assay has been very useful in patients with non—ST-elevation myocardial infarction NSTEMI , which allows diagnosis by a single blood test, thus permitting early treatment than otherwise might be advised.
The hsTn assays are also of value in prognostication in patients with acute heart failure AHF if seen in detectable values, as seen in a study by Xue et al. Thus tropinins play a significant role in assessment of cardiac dysfunction. The small heme protein that assists in oxygen transport in all muscle tissues, is released within 1 hour and rises more rapidly than cTn or CK-MB, peaks in nearly 8 to 10 hours, and returns to normal within 24 hours. Thus, it is a sensitive early indicator of cardiac damage, and though nonspecific to the myocardium, it has found use as an excellent negative predictor of myocardial injury.
When the circulating serum albumin comes into contact with the ischemic heart tissue, a novel marker of ischemia is produced by the structural modification of albumin at the N-terminal end, which is used for the estimation. IMA rises within 6 hours of an infarct and remains elevated for 12 hours. The drawback with IMA is that it is induced by conditions such as extracellular hypoxia, acidosis, etc. It is a very stable low-molecular-weight 14—15 kDa protein present in the myocardial cytoplasm.
These are involved in the transport of fatty acids from the cell membrane to the mitochondria for oxidation. Due to their small size, they are easily diffused through the interstitial space and appear in 1 to 3 hours after onset, peak levels are achieved in 6 hours, and return to normal in 24 hours. Use of H-FABP may improve diagnostic ability, but the presence of easily available specific markers such as troponins has made it of an additive value only.
Natriuretic peptides are a group of structurally similar but genetically distinct molecules that are involved in the sodium and water excretion, thus lowering of blood pressure. Different biomarkers and their concentrations with relation to time after an AMI.
Furthermore, it modulates diuresis, natriuresis, vasodilation, inhibition of renin and aldosterone, and helps reduce the blood pressure. An acute phase protein synthesized by the liver, C-reactive protein CRP is mostly stimulated by the cytokine, interleukin IL CRP levels are thought to differ by sex and ethnicity and increase in acute illness.
An intermediary amino acid, homocysteine is an independent risk factor for the development of atherosclerosis. Hyperhomocysteinemia causes intimal thickening, disruption of the elastic lamina, smooth muscle hypertrophy, and platelet aggregation, and hence is directly implicated in vascular injury.
It is therefore useful marker for risk assessment, and regular assays are available for the same. It is another inflammatory marker, a signaling protein that reflects both inflammation and platelet interaction with the plaque and is found increased in ACS. Also, assays are cumbersome and not adaptable for diagnosis. Several biomarkers that are used currently and in the past decade are listed as follows. Also called platelet-activating factor, is synthesized by lymphocytes and monocytes and produces highly atherogenic lipid fragments that cause endothelial adhesion.
It is mostly used as a research tool and in risk stratification. It is a degranulation product of the white blood cells WBCs and is elevated in the blood vessels where a plaque is present and found to be increased in coronary artery disease and ACS. Commercial assays are available for myeloperoxidase, but types of specimen collected have shown variation.
This protein is a metalloproteinase and a member of the insulin-like growth factor family of proteins. Elevated levels are indicative of an ongoing neovascularization process in the coronary arteries and an incipient plaque rupture. However, there is no established correlation with available markers; rather, it is an indicator of adverse CV events and not used routinely.
It is released from phospholipids on cleavage and is suggested to indicate necrosis and ischemia. Again, it has been considered to be of value in prognostication. It is member of IL-1 family and is believed to play a role in the cardiac remodeling and signal inflammation by its interaction with IL
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