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Biomedical subjects

J Mair

Publications and source records attributed to J Mair.

At least 37 records · Page 2Linked to original sources
PubMed1999

Consequences of acute normovolaemic haemodilution on haemostasis during major orthopaedic surgery.

Acute preoperative normovolaemic haemodilution (NHD) is an accepted tool for reducing allogeneic blood transfusion requirements during surgery. At present, little is known of its impact on haemostasis. We have investigated the consequences of NHD on haemostasis by comparing conventional global tests (prothrombin time (PT), activated partial thromboplastin time (aPTT) with more specific measures of coagulation (prothrombin fragment 1 + 2 (F 1 + 2), thrombin-antithrombin III complex (TAT) and fibrinolysis (D-dimer (DD), plasmin-alpha 2-antiplasmin complex (PAP)). Blood samples were collected from two groups (NHD and controls) undergoing elective spinal surgery or pelvic osteotomy until day 3 after operation. The conventional global tests remained within normal limits: there were no significant differences between groups. Although surgery induced significant increases in the more specific measures of coagulation and fibrinolysis, there were no differences between NHD and control patients. Major orthopaedic surgery strongly activates coagulation and fibrinolysis. As the degree of these alterations was similar in haemodiluted and control patients, we suggest that acute preoperative normovolaemic haemodilution itself does not appear to be associated with greater perioperative disturbances in haemostasis.

Adult↗
PubMed1999

Use of biochemical markers in acute coronary syndromes. IFCC Scientific Division, Committee on Standardization of Markers of Cardiac Damage. International Federation of Clinical Chemistry.

This paper presents evidence and suggestions from the IFCC Committee on "Standardization of Markers of Cardiac Damage" (C-SMCD) on the use of biochemical markers for the triage diagnosis of acute coronary syndromes. There is general agreement that both 'early' and 'definitive' biochemical markers of myocardial damage are necessary and that these assays must be available with a turnaround time of 1 h or less. Currently, myoglobin is the marker that most effectively fits the role as an 'early' marker, whereas 'definitive' markers are cardiac troponins. Since the sensitivity of the initial electrocardiogram is only 50% for detecting myocardial infarction, the use of biochemical markers may significantly contribute to the early diagnosis and become relevant when the electrocardiogram is not diagnostic. In addition, new sensitive biochemical markers, particularly the cardiac troponins, are presently the best to detect the presence of minor myocardial cell damage. With regard to this, two decision limits are probably needed for the optimal use of troponins: a low abnormal value suggesting the presence of myocardial damage and a higher value suggesting the diagnosis of myocardial infarction according to traditionally used criteria. Properly designed studies should be performed to establish limits for each commercially available troponin assay. Finally, it is recognized that there is no need for the use of any biochemical marker when the clinical diagnosis is unequivocal, other than for diagnosing reinfarction, estimating the infarct size, and monitoring thrombolytic therapy.

Acute Disease↗
PubMed1999

Proposals from IFCC Committee on Standardization of Markers of Cardiac Damage (C-SMCD): recommendations on use of biochemical markers of cardiac damage in acute coronary syndromes.

This paper presents evidence and suggestions from the IFCC C-SMCD on the use of biochemical markers for the triage diagnosis of acute coronary syndromes. There is general agreement that both 'early' and 'definitive' biochemical markers are necessary and that these assays must be available with a turnaround time of 1 h or less. Currently, myoglobin is the marker that most effectively fits the role as an 'early' marker, whereas 'definitive' markers are cardiac troponins. Since the sensitivity of the initial electrocardiogram is only 50% for detecting myocardial infarction, the use of biochemical markers may significantly contribute to the early diagnosis. New sensitive biochemical markers, particularly the cardiac troponins, are presently the best criterion to detect the presence of small myocardial cell damage. Two decision limits are probably needed for the optimum use of troponins: a low abnormal value suggesting the presence of myocardial damage and a higher value suggesting the diagnosis of myocardial infarction. Additional studies should be performed to establish limits for each commercially available assay. Finally, it is recognized that there is no need for the use of any biochemical marker when the clinical diagnosis is unequivocal, other than for diagnosing reinfarction, estimating the infarct size, and monitoring thrombolytic therapy.

Acute Disease↗
PubMed1999

Proposals from the IFCC Committee on Standardization of Markers of Cardiac Damage (C-SMCD): strategies and concepts on standardization of cardiac marker assays.

The search for sensitive and specific biochemical markers of cardiac damage has resulted in development of methods for the measurement of cardiac markers such as myoglobin, CK-MB mass and the cardiac troponins (cardiac troponin I and cardiac troponin T). There have been new clinical applications of already known markers based on improved, reformulated methods which often depend on advanced technologies. These developments are connected with analytical and interpretative challenges for the laboratory manager and for the clinician. In this situation, it is essential that international professional societies develop comprehensive and carefully elaborated guidelines for the quality management and use of these measurements and their results. Several professional associations have formed committees working on different issues regarding the measurement of biochemical markers of cardiac damage. Recognizing the huge interest in this field and substantial diagnostic relevance of these markers, the IFCC has established the Committee on "Standardization of Markers of Cardiac Damage" (C-SMCD) in 1997 inviting the already operating American and European groups to designate some of their members into the new committee. The task of the IFCC C-SMCD is to coordinate the different activities of the national groups, with preparation of international documents and recommendations under the auspices of IFCC and to initiate various standardization activities. The establishment of consensus/reference methods as well as development of primary and secondary matrix reference materials for markers of cardiac damage are extremely important in order to achieve comparability of test results, thus leading to an effective patient care.

Biomarkers↗
PubMed1999

Natriuretic peptides in assessment of left-ventricular dysfunction.

The heart secrets two different natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which have potent vasorelaxant, diuretic, and natriuretic actions. They are main tools in the body's defense against volume overload and hypertension. The natriuretic peptides (NP) are synthetized as prohormones. The C-terminal endocrinological active peptides and their N-terminal prohormone fragments are found in plasma. The NP system is maximally activated in ventricular dysfunction. However, NP:s are also increased in patients with renal failure or pulmonary hypertension, and increases may be found in arterial hypertension or liver cirrhosis. Among all NP and prohormone fragments currently BNP is the most promising candidate analyte for routine diagnosis. BNP is also superior to other neurohormones for diagnosis of left-ventricular dysfunction (LVD) or estimating prognosis in LVD or during the subacute phase of myocardial infarction. For primary care physicians BNP measurement is useful to decide which patient with suspected heart failure warrants further investigation, particularly when assessment of left ventricular function is not readily available. BNP has an excellent negative predictive value particularly in high risk patients. For the cardiologists the NP:s are helpful for monitoring therapy and disease course in LVD patients and for estimating prognosis in LVD and myocardial infarction patients. There is now sufficient evidence to encourage physicians to gain experience with NP as a supplement in the diagnosis of patients suspected of having heart failure. An increase in BNP is serious enough to warrant follow-up examinations.

Atrial Natriuretic Factor↗
PubMed1999

Skeletal muscle injury induced by eccentric muscle action: muscle proteins as markers of muscle fiber injury.

Muscular overuse after high force eccentric muscle action is associated with structural damage of the contractile apparatus that can be observed as Z-line steaming and myofibrillar disruption. Mechanical stress is the major contributing factor for inducing muscle injury, which initiates a cascade of processes resulting in skeletal muscle damage. Disturbances in Ca2+ homeostasis with elevated intracellular [Ca2+] activates the nonlysomal cysteine protease, calpain. Calpain is assumed to play an important role in triggering the response of skeletal muscle protein breakdown, of inflammatory changes, and of regeneration processes in response to eccentric muscle action. The inflammatory response is attributed to changes in hormone and cytokine levels in blood and skeletal muscle. To assess the amount of skeletal muscle damage, plasma CK activity and plasma myoglobin levels have been widely used as markers for muscle injury. As the cytosolic proteins do not necessarily reflect the amount of structural damage, structurally bound proteins such as myosin heavy chains and troponin have been investigated. This paper briefly reviews the cascade of events causing muscle cell injury after unaccustomed eccentric muscle action and the potential of muscle proteins as markers of skeletal muscle damage.

Animals↗
PubMed1998

Insertion/deletion polymorphism in the angiotensin-converting enzyme gene is associated with atrial natriuretic peptide activity after exercise.

An insertion/deletion polymorphism in the gene coding for the angiotensin-converting enzyme (ACE) is strongly associated with ACE activity. This polymorphism may be a marker for an increased risk for cardiovascular events. Our study examined a possible relationship between the D/I polymorphism and myocardial release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Ninety-six individuals with normal or impaired left ventricular function were included in the study. ANP and BNP plasma levels were measured at rest and after exposure to physical stress. At rest no association of ACE genotypes with ANP and BNP was found. After exercise homozygotes with the genotype DD had significantly higher ANP plasma levels than homozygotes with the genotype II. In contrast to ANP, BNP levels were not significantly different between genotype groups after exercise. Differences in site of production and mode of release between ANP and BNP might explain this difference. We hypothesize that our result might represent a variability gene effect of the ACE gene locus on endocrine processes in the heart during exposure to physical stress.

Adult↗
PubMed1998

Glycogen phosphorylase isoenzyme BB to diagnose ischaemic myocardial damage.

Glycogen phosphorylase isoenzyme BB (GPBB) is a key enzyme of glycogenolysis. Its degree of association with the sarcoplasmatic reticulum glycogenolysis complex depends essentially on the metabolic state of the myocardium. With the onset of tissue hypoxia, when glycogen is broken down, GPBB is converted from a structurally bound into a cytoplasmatic form. Considerable amounts of GPBB are only found in human heart and brain. In the first clinical studies GPBB was the most sensitive marker for the diagnosis of acute myocardial infarction within 4 h of chest pain onset. GPBB also increases early in patients with unstable angina and reversible ST-T alterations in the resting electrocardiogram at hospital admission, which could be useful for risk stratification. GPBB is sensitive for the detection of perioperative ischaemic myocardial damage and infarction in patients undergoing coronary artery bypass grafting. The diagnostic specificity of GPBB in non-traumatic chest pain patients was comparable to creatine kinase MB. These results indicate that GPBB is a sensitive marker for ischaemic myocardial damage.

Angina Pectoris↗
PubMed1998

Myocardial damage after minimally invasive coronary artery bypass grafting on the beating heart.

BACKGROUND: In conventional coronary artery bypass grafting, the rate of perioperative myocardial infarction is reported in the 2% to 6% range; however, significantly higher rates are observed if sensitive myocardial marker proteins are used to detect perioperative myocardial damage. For minimally invasive direct coronary artery bypass grafting, few data are available concerning myocardial marker protein release. METHODS: Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 +/- 8.5 years) received minimally invasive direct coronary artery bypass grafting procedures via minithoracotomy on the beating heart. Electrocardiography and transesophageal and transthoracic echocardiography as well as determination of creatine kinase-MB mass concentration and cardiac troponin I level were used for ischemic monitoring. RESULTS: One patient had a perioperative myocardial infarction according to standard criteria and died despite mechanical circulatory support. Determination of cardiac troponin I level showed small but definitive ischemic damage in 4 of 9 patients (44%) who presented transient ischemic signs intraoperatively or postoperatively. In 2 of these 4 patients pathologic findings could be detected on angiographic restudies. CONCLUSIONS: Subclinical myocardial injury is a common event in minimally invasive coronary artery bypass grafting on the beating heart. Cardiac troponin I could serve as an adequate diagnostic tool for diagnosis of perioperative myocardial infarction in minimally invasive direct coronary artery bypass grafting.

Aged↗
PubMed1998

Effect of age and multiple mating on the mating behavior of Culicoides nubeculosus (Diptera: Ceratopogonidae).

The mating behavior of the biting midge Culicoides nubeculosus (Meigen) may be divided into a number of stages, including resistance behavior of the female before copulation. A previous study indicated that resistance behavior is a method through which the female assesses the fitness of the male, allowing some degree of mate choice. Our study used behavioral and electrophysiological techniques to investigate whether insect age and the reproductive status of the females influenced mating behavior. Virgin females became increasingly receptive to mating attempts as they aged, with reduced resistive behavior and a reduction in the time required for genital union. With increasing male age, the duration of copulation increased, possibly related to the time required for the transfer of sperm. Previously mated females were very resistant to further attempts to mate by males. Secondary matings were achieved only through the persistent efforts of males, although when successful, there were no differences in the duration of the mating process from matings with virgin females. Virgin female C. nubeculosus release a volatile sex pheromone which is detected by the males' antennae. Electrophysiological recordings from male antennae indicated that mated females have a continued but reduced output of this pheromone, which may allow males to distinguish virgin from mated females. The findings of the study are discussed in relation to possible methods of mate choice in this species.

Age Factors↗
PubMed1998

No release of cardiac troponin I during major orthopedic surgery after acute normovolemic hemodilution.

BACKGROUND: Normovolemic hemodilution is a well-accepted method for intraoperative blood salvage. However, some controversy exists concerning the possible risk of myocardial fiber injury as consequence of the reduced oxygen content. Laboratory diagnosis of perioperative myocardial fiber injury is difficult, since biochemical markers are elevated postoperatively due to the surgical trauma. Cardiac troponin I (cTnI) is a new, highly sensitive and specific marker for the detection of myocardial injury. The aim of our study was to investigate whether normovolemic hemodilution in patients with major orthopedic surgery (13 hemodiluted patients, 15 control) induces a release of cTnI. METHODS: cTnI as a highly specific and sensitive cardiac parameter, as well as total creatine kinase (CK), creatine kinase isoenzyme MB mass (CKMB mass) and myoglobin were measured after induction of anesthesia, after normovolemic hemodilution, prior to retransfusion of blood components, 3 h after surgery, and on the first and third postoperative days. RESULTS: Prior to retransfusion of blood components the hematocrit was decreased to 25.4 +/- 1.2% (mean +/- SEM; range: 18%-34%) in the control group and to 20.2 +/- 0.8% (mean +/- SEM; range: 17%-24%) in the hemodilution group. Total CK, CKMB mass as well as myoglobin concentration increased significantly in both groups, reaching their maxima within the first day of surgery. In contrast, cTnI was below the detection limit of assay (< 0.5 micrograms/L) at any time. CONCLUSIONS: We suggest that pre- and intraoperative hemodilution to a hematocrit of approximately 20% by maintaining normovolemia does not induce myocardial fiber injury in patients without preexisting cardiac diseases.

Adult↗
PubMed1998

Early assessment of exercise induced skeletal muscle injury using plasma fatty acid binding protein.

OBJECTIVE: To test whether fatty acid binding protein (FABP) is a useful plasma marker for the early detection of exercise induced skeletal muscle injury in healthy subjects. METHODS: Plasma concentrations of FABP and myoglobin (Mb) were measured in six healthy physical education teacher trainees after 20 minutes of downhill running (16% incline; mean lactate 4 mmol/l; 70% (VO2MAX). Creatine kinase (CK) was measured for comparison. RESULTS: Significant increases were found in plasma FABP (mean peak level 50 micrograms/l), Mb (823 micrograms/l), and CK (491 U/l). Mb and FABP concentrations were already significantly elevated (p < 0.05) at 30 minutes, but CK not until two hours after exercise. Whereas Mb and FABP decreased to normal levels within 24 hours, CK activity remained elevated until 48 hours. The Mb to FABP ratio in plasma after exercise induced muscle injury was 15.0 (1.3) (mean (SEM)) (range 7.4-31.1), which is within the range of ratios calculated for skeletal muscle tissue contents of Mb and FABP, but different from the reported plasma ratio after myocardial injury (4-6). CONCLUSIONS: After eccentric exercise induced muscle injury, plasma FABP and Mb increase and decrease more rapidly than CK, indicating that both FABP and Mb are more useful than CK for the early detection of such injuries and the monitoring of injury during repeated exercise bouts. In addition, the Mb to FABP ratio in the plasma identifies the type of muscle injured.

Adult↗
PubMed1998

Rebound increase of plasminogen activator inhibitor type I after cessation of thrombolytic treatment for acute myocardial infarction is independent of type of plasminogen activator used.

Plasma concentrations of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), and D-dimer were investigated in 50 patients treated intravenously for acute myocardial infarction with either streptokinase (n = 23), urokinase (n = 17), or recombinant t-PA (rt-PA, n = 10). The fibrinolytic variables were measured by enzyme immunoassay on admission; 1, 2, 4, 6, 8, 12, and 24 h later; and then daily until day 7 after admission. In each subgroup of patients treated with different thrombolytic agents, PAI-1 increased significantly (P < 0.01) approximately 3 h after cessation of thrombolytic therapy. PAI-1 peak concentrations did not differ significantly (P = 0.82) among these three subgroups. t-PA and D-dimer did not differ significantly (P > 0.14) among subgroups except for higher t-PA in the rt-PA group attributable to detection of the therapeutically administered exogenous rt-PA by the t-PA assay. Our findings demonstrate a marked PAI-1 increase after thrombolytic therapy for acute myocardial infarction, which seems to be a common, drug-independent antifibrinolytic rebound phenomenon in response to thrombolytic treatment.

Adult↗
PubMed1998

Effects of prolonged strenuous endurance exercise on plasma myosin heavy chain fragments and other muscular proteins. Cycling vs running.

BACKGROUND: This study evaluates creatine kinase, myosin heavy chain, and cardiac troponin blood levels following three types of exercise: 1) short-distance uphill or downhill running; 2) alpine ultramarathon; and 3) alpine long-distance cycling. METHODS EXPERIMENTAL DESIGN: Comparative field study; follow-up up to 10 days. SETTING: Department of Sports Medicine. All biochemical markers were analysed at the Department of Medical Chemistry and Biochemistry. PATIENTS OR PARTICIPANTS: Subjects included healthy, trained males (N = 53). All subjects were nonsmokers and free from medication prior to and during the study. Each volunteer was an experienced runner or cyclist, who had at least once successfully finished the Swiss Alpine Marathon of Davos or the Otztal-Radmarathon before. INTERVENTIONS: Running or cycling. MEASURES: Plasma concentrations of creatine kinase, myosin heavy chain fragments and cardiac troponins were measured to diagnose skeletal and cardiac muscle damage, respectively. RESULTS: Skeletal muscle protein release is markedly different between uphill and downhill running, with very little evidence for muscle damage in the uphill runners. There is considerable muscle protein leakage in the ultramarathoners (67 km distance; 30 km downhill running). In contrast, only modest amounts of skeletal muscle damage are found after alpine long-distance cycling (230 km distance). CONCLUSIONS: This study proves that there is slow-twitch skeletal muscle fiber damage after prolonged strenuous endurance exercise and short-distance downhill running. Exhaustive endurance exercise involving downhill running and short-distance downhill running lead to more pronounced injury than strenuous endurance exercise involving concentric actions. From our results there is no reason for suggesting that prolonged intense exercise may induce myocardial injury in symptom-less athletes without cardiac deseases.

Adult↗
PubMed1998

Different intracellular compartmentations of cardiac troponins and myosin heavy chains: a causal connection to their different early release after myocardial damage.

We investigated the net myocardial release of creatine kinase isoenzyme MB (CKMB), myoglobin, cardiac troponin T (cTnT), cardiac troponin I (cTnI), and cardiac beta-type myosin heavy chain (beta-MHC) into the coronary circulation after cardioplegic cardiac arrest in humans. Cardiac markers were measured in paired arterial, central venous, and coronary sinus blood in 19 patients undergoing elective coronary artery bypass grafting (CABG) before aortic cross-clamping and 1, 5, 10, and 20 min after aortic declamping. cTnT and cTnI were released into the coronary sinus in parallel to each other and almost simultaneously to myoglobin and CKMB within 20 min of reperfusion. In contrast, no beta-MHC was released in the same patients during the study period. The average soluble cTnT and cTnI pools in right atrial appendages of 11 patients with right atrial and right ventricular pressures within reference values were comparable and were approximately 8% of total myocardial troponin content. The soluble beta-MHC pool was <0.1% in all patients. Our results demonstrate the impact of the different intracellular compartmention of regulatory and contractile proteins on their early release from damaged myocardium.

Adult↗