Cardiac Necrosis Markers Research Articles

Aplicabilidad de la nueva definición de infarto de miocardio y opinión de los cardiólogos españoles

The Working Group on Ischemic Heart Disease and Coronary Care Units of the Spanish Society of Cardiology evaluated the applicability of a new definition of infarction in Spanish hospitals, its current use, and the opinion of Spanish cardiologists. A telephone survey was made (from late 2001 to early 2002) in Spanish hospitals to evaluate the availability of troponin or creatine kinase MB mass determinations. A questionnaire was sent to all members of the Spanish Society of Cardiology to query about the availability of determinations of cardiac necrosis markers at their respective hospitals, use of the new definition, and whether they agreed with the new definition. An important proportion of Spanish hospitals cannot determine myocardial necrosis markers (troponin or creatine kinase MB mass), mainly due to low-volume activity (fewer than 200 beds). The new definition of myocardial infarction was used by Spanish cardiologists always (24%), frequently (31%), sometimes (17%), seldom (14%), and never (11%). Agreement with the definition was complete in 21%, almost complete in 33%, half and half in 26%, rare in 10%, and absent in 7% of Spanish cardiologists. A large percentage of Spanish hospitals cannot use the new definition of myocardial infarction because they cannot determine specific cardiac necrosis markers. Spanish cardiologists are not generally using the new definition and many do not agree with it.

Drugs modifying nitric oxide metabolism affect plasma cholesterol levels, coagulation parameters, blood pressure values and the appearance of plasma myocardial necrosis markers in rabbits: opposite effects of L-NAME and nitroglycerine.

Various experiments have shown that decreased nitric oxide values alter plasma lipid levels or coagulation parameters or blood pressure values or cause myocardial necrosis phenomena, but it is not clear whether these alterations are reciprocally connected, or whether nitric oxide changes are involved in the appearance of some coronary disease risk factors (lipid, coagulation, blood pressure alterations) and myocardial necrosis. We modified nitric oxide levels in rabbits using L-NAME (a NO synthase blocker) or nitroglycerine (a NO donor), and simultaneously evaluated variations in total and HDL cholesterol levels, some coagulation parameters, mean blood pressure values and myocardial necrosis patterns. L-NAME lowered plasma nitric oxide values, increased plasma total cholesterol and decreased HDL cholesterol levels, enhanced the amount of plasma fibrinogen, shortened prothrombin times, elevated the mean blood pressure values and caused the appearance of cardiac necrosis markers (c-troponin I, creatine kinase) in plasma and coagulative necrosis lesions in the myocardium. The administration of nitroglycerine to rabbits treated with L-NAME increased plasma nitric oxide levels and reversed the biochemical lesions caused by L-NAME. Our data show that the studied alterations in cholesterol values, coagulation parameters, increased mean blood pressure values and myocardial necrosis markers are strictly related to modified plasma nitric oxide levels, and that the regulation of nitric oxide metabolism affects the presence or absence of some coronary disease risk factors (lipid, coagulation and blood pressure alterations) and plasma indicators of myocardial necrosis.

Cardiac necrosis markers associated with low nitric oxide levels in the plasma of rabbits after treatment with vasopressin: protective effects of nitroglycerin administration

It has been reported that the administration of vasopressin induces myocardial ischaemia in rats, which causes electrocardiographic ST segment alterations according to many authors. But rat electrocardiogram (ECG) lacks ST segment. Consequently it appears important to study the effects of vasopressin in rabbits, which show ST segment present in the ECG. Since cardiac necrosis markers are released in the plasma of humans with myocardial infarction, as well as in a variety of experimental models of myocardial necrosis, it is possible that the same may occur in rabbits with myocardial ischaemia induced by vasopressin. The main aim of this study was to investigate whether the administration of vasopressin causes the appearance of specific myocardial necrosis markers, such as cardiac troponin I, myoglobin or creatine kinase MB (CK MB) in rabbits in the presence or absence of modified ECG profile, and to also verify whether these markers are associated with the alterations in some coagulation parameters, that are known to be induced by vasopressin. As the effects of vasopressin are counteracted by nitric oxide (NO), another aim was to verify whether vasopressin also affects plasma NO levels and whether the administration of a NO donor can reverse these effects. Vasopressin was administered to rabbits and caused ischaemic alterations such as electrocardiographic changes, and significantly increased the levels of plasma cardiac necrosis markers (c-troponin I, myoglobin and CK MB). It also elevated diastolic blood pressure (BP), lowered heart rate (HR), increased procoagulation activity, and lowered plasma NO levels. The appearance of heart necrosis, demonstrated by plasma cardiac necrosis markers in the animals receiving vasopressin, was attributed to a drug-induced increase in vasoconstriction and coagulation activity. The intense vasoconstriction and thrombosis may lead to endothelium necrosis and a consequent drop in NO production. The administration of the NO donor nitroglycerin (NG) in the vasopressin treated animals restored NO values, and was capable of preventing the appearance of the plasma cardiac necrosis markers and altered coagulation values. The protective activity of NG was attributed to NO release, which lowers BP values and counteracts coagulation activity in vasopressin-treated animals. The described procedure may also be proposed for the study of early ischaemic myocardial lesions and the screening of NO donors preventing myocardial damage.

Low nitric oxide values associated with low levels of zinc and high levels of cardiac necrosis markers detected in the plasma of rabbits treated with L-NAME.

Nitric oxide plays a key role as a vasodilating agent and its deficiency is associated with ischemic heart diseases. The aim of this study was to induce biochemical alterations associated with ischemic heart lesions by blocking nitric oxide synthase. L-NAME, a nitric oxide synthase inhibitor, was administered to rabbits and its effects on blood pressure, plasma levels of nitric oxide, zinc and cardiac necrosis markers, heart histology, and electrocardiographic profile were examined. L-NAME administration reduced the nitric oxide levels and consequently increased the diastolic blood pressure. It also caused small areas of myocardial coagulative necrosis, whose dispersed nature made it undetectable by electrocardiograph, and decreased the plasma levels of zinc, which is involved in the enzymatic activities that remove the peroxides damaging the myocardium. This model is proposed for the development of drugs affecting nitric oxide levels with the aim of controlling coronary ischemia.

Evaluation of Stratus CS stat fluorimetric analyser for measurement of cardiac markers Troponin I (cTnI), creatine kinase MB (CK-MB), and myoglobin.

Myoglobin, CK-MB, and Troponin I (cTnI) are cardiac muscle necrosis markers that are useful for detecting acute myocardial infarction (AMI). The Stratus CS (Dade Behring, Inc.) is a discrete fluorimetric immunoassay analyser designed for the determination of the three cardiac markers from a single sample of whole blood or plasma. Overall analytical performances of the Stratus CS provided by Dade Behring were evaluated according to the French Society of Clinical Biology guidelines. Within-run imprecision (n = 20) for the three parameters at three levels gave values under 5%, whereas CVs for between-run imprecision (n = 20) were under 6%. The sensitivities were 0.03 microg/L for cTnI and 0.4 microg/L for CK-MB. Linearities extended from 0-50 microg/L for cTnI, 0-140 microg/L for CK-MB, and 1-900 microg/L for myoglobin. The results, particularly those obtained on whole-blood samples, correlated well with those obtained on Stratus II. We did not find any interference with haemolysis, icterus, or lipemia. The system was very easy to use, and fulfills the requirements for the analysis of the three cardiac markers in patients with acute chest pain in emergency situations.

Fibronectin accumulation within cardiac myocytes in rats with elevated plasma angiotensin II

Elevation in plasma angiotensin II (AngII) is associated with cardiac myocyte necrosis. Myocyte necrosis followed by wound healing and fibrosis represents a structural remodeling of the myocardium thought to contribute to abnormal myocardial function. Fibronectin (FN) is generally considered an early component of the healing process that precedes collagen accumulation. To better understand the time course of this remodeling process involving both cardiac myocytes and extracellular matrix, (i.e., FN and collagen), we used two animal models: (1) endogenous activation of the renin-angiotensin system by surgical induction of renovascular hypertension and (2) exogenous AngII administration (150 ng/min/kg). Animals were killed at different time points within the first two weeks. Both “cellular” (cFN) and “plasma” (pFN) FN immunolabeling were compared with collagen distribution (picrosirius red stain), together with histopathologic (hematoxylin-eosin stain) and ultrastructural examination of cardiac myocytes. In each experimental group, the pattern and time course of FN immunolabeling was coincident with histopathologic evidence of myocyte injury and/or remodeling. We found different patterns of FN labeling of cardiac myocytes: (a) homogenous intracellular distribution in necrotic myocytes, most obvious on days 1 and 2; (b) patchy intracellular distribution in nonnecrotic myocytes starting on day 4; and (c) marking internalized capillaries. Both FNs were codistributed throughout the myocardium of each ventricle; however, cFN was less pronounced and not seen in mature scars. Ultrastructural examination revealed different kinds of intramyocytic inclusions, characterized by vacuoles containing fibrillar/flocculent material, remnants of unknown origin, or internalized capillaries. We conclude that FNs are markers of cardiac myocyte necrosis and early interstitial remodeling and that renovascular hypertension and AngII administration exhibit the same time course and pattern of FN and collagen expression.