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Biomedical subjects

J Mair

Publications and source records attributed to J Mair.

At least 55 records · Page 3Linked to original sources
PubMed1997

Markers of activated coagulation for early diagnosis of acute myocardial infarction.

Intracoronary thrombosis plays a key role in the pathogenesis of acute myocardial infarction (AMI), and the formation of an occlusive thrombus usually precedes the development of myocardial damage. Therefore we evaluated and compared the early sensitivities of thrombin-antithrombin III complex (TAT), D-dimer, myoglobin, creatine kinase (CK) MB mass concentration, and cardiac troponin T (cTnT) on admission to a coronary care unit (CCU) before heparin or thrombolytic therapy was started. We investigated 31 consecutive patients admitted to CCU for evolving AMI within 6 hours from the onset of infarct-related symptoms; the median delay from chest pain onset to CCU admission was 135 minutes. Of all biochemical markers tested TAT had the highest early sensitivity on admission to the CCU, and TAT was significantly more sensitive than cTnT, CKMB mass, myoglobin, and D-dimer. However, TAT increases give no information about the location of clot formation in the body, and the diagnosis of AMI must be subsequently verified by an increase in more cardiac specific proteins, such as troponins or CKMB.

Acute Disease↗
PubMed1997

Cardiac troponin I to diagnose percutaneous transluminal coronary angioplasty-related myocardial injury.

The purposes of the present study were to evaluate cardiac troponin 1 (cTnl) in the diagnosis of percutaneous transluminal coronary angioplasty (PTCA)-related myocardial injury in comparison with cardiac troponin T (cTnT) and creatine kinase (CK) MB mass concentration, and to investigate the frequency of myocardial injury, as indicated by myocardial protein release, after clinically symptomless side-branch occlusion (SBO) which may occur in the proximity of the attempted stenosis. The final study population comprised 80 patients undergoing elective, single vessel PTCA. Blood samples were drawn before, 6, 24 and 48 h after PTCA. cTnI, cTnT and CKMB mass baseline values were within the reference intervals in all patients (cTnI < 0.1 microgram/l, cTnT < 0.2 microgram/l, CKMB < 5 micrograms/l). Two patients presented with primary failure of PTCA, and visually successful PTCA was performed in all remaining patients. Seven patients (four with SBO) subsequently developed acute myocardial infarction (AMI). Symptomless SBO occurred in 16 patients. In controls (n = 55) there were no significant increases in cTnI, cTnT, or CKMB concentrations compared with baseline values, and all markers stayed within their reference intervals. In half the patients with symptomless SBO (n = 8) all markers were slightly to moderately increased, in two additional patients only CKMB was elevated (cTnI: 0.1-1.0 microgram/l; cTnT: 0.25-0.81 microgram/l and CKMB: 7.9-25.6 micrograms/l). In the majority of patients with primary failure or AMI we found pronounced increases in all tested markers (cTnI: 0.2-12.0 micrograms/l; cTnT: 0.44-12.10 micrograms/l; CKMB: 19.2-423.0 micrograms/l). The results of this study indicate that cTnI is comparably useful to cTnT or CKMB mass for diagnosing myocardial injury in PTCA patients. From our results a preference for one of the tested parameters cannot be clearly derived. Post-procedural cTnI, cTnT, and CKMB mass values are not higher than baseline values in uncomplicated cases, whereas AMI after PTCA leads to pronounced marker increases. SBO, even when symptomless, leads frequently (in about half the patients) to slight marker increases.

Adult↗
PubMed1997

Augmented release of brain natriuretic peptide during reperfusion of the human heart after cardioplegic cardiac arrest.

The aim of the study was to investigate the release of natriuretic peptides during myocardial ischaemia and reperfusion associated with cardioplegic cardiac arrest. Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in paired arterial, central venous and coronary sinus blood samples in 19 patients undergoing elective coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 min after aortic declamping. Peak myocardial BNP release after aortic declamping was significantly higher than baseline values before aortic crossclamping. Both peak and cumulative BNP release during reperfusion correlated significantly with the severity of ischaemia, as assessed by myocardial lactate production. In 3 patients with perioperative myocardial ischaemia, cumulative and peak myocardial BNP release after aortic unclamping was markedly higher than in the remaining 16 uneventful patients. Myocardial ANP release during reperfusion was not significantly different from baseline values before aortic crossclamping. In conclusion, our data demonstrate a significantly enhanced myocardial BNP release early during reperfusion of the human heart after global ischaemia associated with cardioplegic cardiac arrest.

Adult↗
PubMed1997

Cardiac troponin I and troponin T: are enzymes still relevant as cardiac markers?

Creatine kinase (CK) MB and lactate dehydrogenase (LDH) isoenzyme 1 are not heart-specific. By contrast, the regulatory proteins troponin I and troponin T are expressed in three different isoforms, one for slow-twitch skeletal muscle fibers, one for fast-twitch skeletal muscle fibers, and one for cardiac muscle (cTnI, cTnT). cTnI and cTnT are usually not detectable in patients without myocardial damage, which is a prerequisite for high diagnostic performance. After acute myocardial infarction (AMI) cTnI, cTnT, and CKMB mass have a comparable early sensitivity. cTnI and cTnT usually peak in parallel except for patients without reperfusion in whom cTnI peaks about 1 day and cTnT approximately 3-4 days after onset of AMI. Both stay increased for at least 4-5 days. cTnT tends to stay increased longer than cTnI. Because the sensitivities of cTnI and cTnT for myocardial injury are comparable, their specificities are the main topic of current debate. Recent reports on mismatches of cTnI and cTnT in patients with renal failure and myopathy without other evidence for myocardial injury suggest that cTnT could be reexpressed similar to CKMB and LDH-1 in chronically damaged human skeletal muscle. In contrast to cTnT, CKMB, and LDH-1, cTnI is not expressed in skeletal muscle during fetal development. So far, an increase in cTnI has been reported only after myocardial damage. Because of currently higher costs, troponin measurement should be restricted at present to clinical settings that really require their high specificity. Based on its distinct functional association with the metabolism of acute ischemic myocardium and according to initial clinical results, glycogen phosphorylase isoenzyme BB is a promising enzyme for the early detection of ischemic myocardial damage.

Biomarkers↗
PubMed1997

Muscular adaptation and strength during the early phase of eccentric training: influence of the training frequency.

We investigated the effects of different training frequencies on maximum isometric voluntary contraction (MVC) force and plasma concentrations of muscle proteins during the early phase of eccentric training. MVC and plasma concentrations of creatine kinase (CK) and slow-twitch skeletal (cardiac beta-type) myosin heavy chain (MHC) fragments were measured before and 4 and 7 d after performing the first and last training task. Training tasks, which comprised 70 high-force eccentric contractions involving the thigh muscles (single leg), were performed under supervision in three groups (A, B, C) at the beginning and at the end of the study period (7 wk). In addition, groups A (N = 10) and B (N = 10) trained during the study period starting 1 wk after the first training task. Group A performed one training task once a week for 5 wk and group B (N = 10) twice a week for 2 wk and three times a week during the subsequent 3 wk. In all three groups the first training task resulted in delayed CK and MHC peaks and decrements in MVC, which were comparable (P > 0.05). Only training regimen B resulted in a significant increase in the MVC. Compared with the first training task training regimens, A and B significantly (P < 0.01) reduced the increase in serum muscle protein and muscle function impairment. The responses to the last training task did not differ significantly between groups A and B. In group C the responses after the second training task did not differ significantly from those observed after the first task. Our results suggest that, compared with group A, additional eccentric exercise in group B is the essential basis for the increase in muscle strength during the early phase of eccentric training without further benefits for muscular adaptation. In group C we found no muscular adaptation.

Adaptation, Physiological↗
PubMed1997

Skeletal troponin I as a marker of exercise-induced muscle damage.

The utility of skeletal troponin I (sTnI) as a plasma marker of skeletal muscle damage after exercise was compared against creatine kinase (CK), myoglobin (Mb), and myosin heavy chain (MHC) fragments. These markers were serially measured in normal physical education teacher trainees after four different exercise regimens: 20 min of level or downhill (16% decline) running (intensity: 70% maximal O2 uptake), high-force eccentric contractions (70 repetitions), or high-force isokinetic concentric contractions of the quadriceps group (40 repetitions). Eccentrically biased exercise (downhill running and eccentric contractions) promoted greater increases in all parameters. The highest plasma concentration were found after downhill running (median peaks: 309 U/l CK concentration (-CK-)), 466 microgram/l Mb concentration (-Mb-), 1,021 microU/l MHC concentration (-MHC-), and 27.3 microgram/l sTnI concentration ([sTnI]). Level running produced a moderate response (median peaks: 178 U/l -CK-, 98 microgram/l -Mb-, 501 microU/l -MHC-, and 6.6 microgram/l [sTnI]), whereas the concentric contraction protocol did not elicit significant changes in any of the markers assayed. sTnI increased and peaked in parallel to CK and stayed elevated (>2.2 microgram/l) for at least 1-2 days after exercise. In contrast to MHC, sTnI is an initial, specific marker of exercise-induced muscle injury, which may be partly explained by their different intracellular compartmentation with essentially no (MHC <0.1%) or a small soluble pool (sTnI: median 3.4%).

Adult↗
PubMed1997

Progress in myocardial damage detection: new biochemical markers for clinicians.

New clinical requirements for triaging chest pain patients challenge the abilities of the current cardiac markers. Serial measurements of myoglobin, creatine kinase (CK) isoenzyme MB (CKMB) mass, or CK isoforms in emergency rooms help to rapidly rule out acute myocardial infarction (AMI). However, within the first 3 to 4 h from chest pain onset, their sensitivities are too low to contribute significantly to AMI diagnosis during this period. CKMB and lactate dehydrogenase (LDH) isoenzyme 1 are not heart-specific, which hampers reliable diagnosis in patients with concomitant skeletal muscle damage. By contrast, the regulatory proteins troponin I and troponin T are expressed in three different isoforms: one for slow-twitch skeletal muscle fibers, one for fast-twitch skeletal muscle fibers, and one for cardiac muscle (cTnI, cTnT); cardiac-specific cTnI and cTnT assays are already available for routine use. cTnT and cTnI are the most promising markers for risk stratification in patients with unstable angina pectoris. Recent reports on increased cTnT in patients with renal failure or myopathy without evidence of myocardial injury and undetectable cTnI suggest that cTnT could be reexpressed similar to CKMB and LDH-1 in chronically damaged human skeletal muscle. Therefore, cTnI is probably the most heart-specific marker. Among the recently proposed new markers for early AMI diagnosis: glycogen phosphorylase isoenzyme BB (GPBB), fatty acid binding protein, phosphoglyceric acid mutase isoenzyme MB, enolase isoenzyme alpha beta, S100a0, and annexin V, GPBB is the most promising because it increases as early as 1 to 4 h from chest pain onset and its early release appears to be essentially dependent on ischemic myocardial injury.

Animals↗
PubMed1996

Cardiac troponin I in the diagnosis of myocardial injury and infarction.

We used a cardiospecific enzymoimmunometric assay to measure cardiac troponin I (cTnI) in samples serially drawn from 78 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (Braunwald class III), 22 multi-traumatized patients, and in 30 athletes after eccentric exercise, as well as in 101 non-traumatic chest pain patients on admission to the emergency department. cTnI assay crossreactivity with crude human skeletal muscle homogenates was < 0.1%. cTnI could not be detected in athletes or multi-traumatized patients except for 2 trauma patients with myocardial damage. Increased cTnI concentrations were found in 6 of 7 patients with unstable angina at rest and in all AMI patients. After AMI, cTnI increased about 3.5 h (median) after the onset of chest pain, reached peak values parallel to CKMB, and stayed increased for at least 4 days. Cardiac troponin T (cTnT) increased and mostly peaked parallel to cTnI. cTnT sensitivity on the 7th day after AMI was significantly higher than that of cTnI. In contrast to cTnI, cTnT mostly showed a second, usually smaller, peak about day 4 after AMI. During the first 4 h after the onset of chest pain and before thrombolytic therapy the sensitivities of myoglobin (0.43) and CKMB mass (0.56) were significantly higher than those of both troponins (cTnI, 0.29; cTnT, 0.25). Areas under receiver operator characteristic curves indicated only moderate diagnostic accuracies of bio-chemical markers for early AMI diagnosis in non-traumatic chest pain patients that cTnI is a highly sensitive and specific marker for myocardial damage which is suitable for early and late diagnosis.

Adult↗
PubMed1996

Mating behavior of Culicoides nubeculosus (Diptera:Ceratopogonidae).

The mating behavior of the biting midge Culicoides nubeculosus (Meigen) was characterized by a number of distinct stages using laboratory-bred insects (48-h-old males and 24- to 48-h-old females). Contact appeared to be required to initiate mating by the male, and most mating attempts involved some degree of female resistance to mate. It is suggested that the female may assess the fitness of the male by the vigor of his response to her unreceptive behavior.

Animals↗
PubMed1996

Natriuretic peptides and cyclic guanosine 3',5'-monophosphate in asymptomatic and symptomatic left ventricular dysfunction.

BACKGROUND: Screening for patients with asymptomatic left ventricular dysfunction is of considerable importance because they may benefit from early treatment with angiotensin converting enzyme inhibitors. It has been suggested that atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and cyclic guanosine 3',5'-monophosphate (cGMP) might be useful markers for screening. OBJECTIVE: To compare directly the power of the three immunoreactive forms of ANP (CT-ANP, beta-ANP, NT-ANP) and BNP and cGMP to detect asymptomatic left ventricular dysfunction. METHODS AND RESULTS: Radionuclide ventriculography was used to study left ventricular ejection fraction in 37 patients with asymptomatic left ventricular dysfunction, 32 patients with mild to moderate congestive heart failure, and 38 controls. CT-ANP, NT-ANP, beta-ANP, BNP, and cGMP were measured at rest and 3 minutes after exercise. Plasma BNP was the most sensitive marker for patients with asymptomatic left ventricular dysfunction but it reached only a sensitivity of 58% and a specificity of 76% at rest and a sensitivity of 65% and a specificity of 84% after exercise. Combined measurements of all natriuretic peptides and cGMP did not improve the power to detect asymptomatic left ventricular function above that of a single BNP measurement. CONCLUSIONS: Although natriuretic peptides and cGMP measured at rest and three minutes after ergometry may be useful for monitoring left ventricular dysfunction they are unlikely to be suitable for more general routine screening for completely asymptomatic left ventricular dysfunction.

Adult↗
PubMed1995

Serum cardiac troponin T and creatine kinase-MB elevations in murine autoimmune myocarditis.

BACKGROUND: We used a murine model of autoimmune myocarditis to investigate systematically whether serum markers of myocardial cell injury, that is, cardiac troponin T (TnT) and the MB isoenzyme of creatine kinase (CK-MB) are useful for the diagnosis of inflammatory heart disease. METHODS AND RESULTS: Fifty-two A.SW mice were immunized with cardiac myosin to induce myocarditis. The disease was evident on day 12 after the initial immunization in 14 of 22 immunized mice, on day 16 in 7 of 10 mice, on day 19 in 6 of 10 mice, and on day 23 in 5 of 10. The severity of myocarditis increased between days 12 and 16 and remained constant thereafter. TnT was elevated in a considerable number of mice with myocarditis, resulting in a diagnostic sensitivity (number of marker elevations per number of mice with myocarditis) of 0.43 on day 12, 0.71 on day 16, and 0.50 on day 19. CK-MB elevations were not seen on day 12 but resulted in a diagnostic sensitivity of 0.71 on day 16 and of 0.33 on day 19. No elevations of CK-MB or TnT were observed on day 23. All elevations were specific for the disease, as none of the mice lacking myocarditis showed increased markers. CONCLUSIONS: In murine autoimmune myocarditis, TnT is a more sensitive marker for the disease than CK-MB. Elevations clearly indicate myocarditis, but negative test results do not exclude the presence of the disease. These data suggest that the determination of CK-MB and, in particular, of TnT, can be useful for the diagnostic evaluation of patients with suspected myocarditis.

Animals↗