Cardiac markers in the early diagnosis and management of patients with acute coronary syndrome

Chest pain is a non-specific complaint and is the most frequent reason for patients seeking urgent medical attention. A small group of these patients will have acute coronary syndromes [ACS]. The current diagnostic and triage systems based on clinical history and electrocardiograms are insufficient. They may result in some of these patients being misdiagnosed and being admitted to the wrong units or receiving inappropriate care, treatment and investigations. In some patients, the diagnosis is delayed resulting in the late administration [or no administration] of essential early treatment. A few patients with ACS may be inadvertently discharged from the emergency department leading to serious health and legal implications. These systems also result in the unnecessary admission of a substantial number of patients without ACS. The triage and management of patients with chest pain can be considerably improved by implementation of serial cardiac markers testing that can identify ACS in the very early stages of presentation. This review article will discuss the currently available markers of myocardial damage such as creatine kinase [CK], creatine kinase muscle and brain [CK-MB] [mass and activity], CK-MB isoforms, heart-type fatty acid-binding protein, myoglobin, cardiac troponin T, and cardiac troponin I

Serum level of heart-type fatty acid-binding protein in patients with chronic renal failure

Heart-type fatty acid binding-protein [H-FABP] has been reported to be a potential novel biochemical marker for the early diagnosis of acute myocardial infarction [AMI]. The effect of kidney diseases on the renal handling of H-FABP has not yet been fully evaluated. The aim of this study was to compare the effect of renal failure on the level of H-FABP and cardiac troponin [cTnT] concentrations. The study population was a small group of 16 patients with renal failure [6 females, 10 males aged 30-70 years] on routine regular haemodialysis or peritoneal dialysis. Results: The mean +/- SD of serum urea and creatinine concentration in this group of patients was 19 +/- 9.6 mmol/L and 531.3 +/- 231.2 mmol/L respectively. H-FABP was increased in all 16 patients [81 +/- 53.3 micro g/L]. The cTnT was increased

impact of chronic liver diseases on the level of heart-type fatty acid-binding protein [H-FABP] concentrations

Heart-type fatty acid binding-protein [H-FABP] has been reported to be a potential novel biochemical marker for the early diagnosis of acute myocardial infarction [AMI]. The presence of H-FABP in the liver has not been reported. The aim of this study was to compare the effect of chronic liver diseases on the level of H-FABP concentrations. The effects of chronic liver diseases including infective hepatitis and cirrhosis on the concentration of H-FABP was studied in a small group of patients [n=10, mean age +/- SD = 58.33 +/- 7.19 years]. The serum concentrations of the following markers were measured: H-FABP, alanine aminotransferase [ALT] and bilirubin and compared with a reference control group [20 healthy blood donors, mean age +/- SD = 63.8 +/- 8.01]. The serum concentrations of these markers in the control group as compared to patients with chronic liver disease were as follows [mean +/- SD]: H-FABP = 6.86 +/- 2.21 micro g/L versus 6.44 +/- 3.06 micro g/L [p = NS]; ALT = 29.8 +/- 14.7 U/L versus ALT = 198.67 +/- 122.89 U/L [p < 0.0005] and bilirubin = 9.6 +/- 4.0 micro mol/L versus bilirubin = 100.89 +/- 87.85 micro mol/L [p < 0.0001]. These data illustrate clearly that there is no significant interference with the normal concentration of H-FABP in the presence of liver diseases, despite the significant elevation of liver enzymes and proteins. These data may support a useful role of H-FABP for the diagnosis of myocardial injury in patients with liver diseases