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Maternal perception of reduced fetal movement (RFM) is associated with increased risk of stillbirth and fetal growth restriction (FGR). RFM is thought to represent fetal compensation to conserve energy due to insufficient oxygen and nutrient transfer resulting from placental insufficiency. To identify predictors of poor perinatal outcome after maternal perception of reduced fetal movements (RFM). Prospective cohort study. 305 women presenting with RFM after 28 weeks of gestation were recruited. Demographic factors and clinical history were recorded and ultrasound performed to assess fetal biometry, liquor volume and umbilical artery Doppler. A maternal serum sample was obtained for measurement of placentally-derived or modified proteins including: alpha fetoprotein (AFP), human chorionic gonadotrophin (hCG), human placental lactogen (hPL), ischaemia-modified albumin (IMA), pregnancy associated plasma protein A (PAPP-A) and progesterone. Factors related to poor perinatal outcome were determined by logistic regression. 22.1% of pregnancies ended in a poor perinatal outcome after RFM. The most common complication was small-for-gestational age infants. Pregnancy outcome after maternal perception of RFM was related to amount of fetal activity while being monitored, abnormal fetal heart rate trace, diastolic blood pressure, estimated fetal weight, liquor volume, serum hCG and hPL. Following multiple logistic regression abnormal fetal heart rate trace (Odds ratio 7.08, 95% Confidence Interval 1.31-38.18), (OR) diastolic blood pressure (OR 1.04 (95% CI 1.01-1.09), estimated fetal weight centile (OR 0.95, 95% CI 0.94-0.97) and log maternal serum hPL (OR 0.13, 95% CI 0.02-0.99) were independently related to pregnancy outcome. hPL was related to placental mass. Poor perinatal outcome after maternal perception of RFM is closely related to factors which are connected to placental dysfunction. Novel tests of placental function and associated fetal response may provide improved means to detect fetuses at greatest risk of poor perinatal outcome after RFM.

The field of diagnostic cardiac biomarkers has grown exponentially since the development of an assay for aspartate transaminase activity to diagnose myocardial infarction in 1954. The clinician now has a vast array of clinical tools, which include biomarkers of inflammation, ischaemia and necrosis as well as sensitive imaging technology and coronary anatomy intervention at their disposal when evaluating acute coronary syndromes. Previously the World Health Organisation (1979) defined a myocardial infarction (MI) in the presence of two of the following triad: History of chest pain, electrocardiographic (ECG) changes and a rise in cardiac enzymes to twice the upper limit of normal. At this time, creatine kinase and its MB isoenzyme were the preferred biochemical markers. The clinical requirements of early diagnosis, risk stratification and effective treatment have stimulated the development of numerous new and cardiac specific biomarkers (e.g. cardiac troponins). Cardiac troponins are now integral to the diagnosis of MI and have led to the reclassification of MI into either ST elevated MI (STEMI) or non-ST elevated MI (NSTEMI). Subsequent to the release of each new cardiac specific assay there typically follows an array of studies supporting or refuting its efficacy. Many cardiac biomarkers originally proposed with high sensitivity and specificity for ACS are now of questionable clinical value or require the addition of significant caveats once they have been fully evaluated. Indeed, acute exercise often stimulates perturbations in cardiac biomarkers; such as elevations in creatine kinase, cardiac troponins or reductions in Ischemia Modified Albumin (IMA®). Such an influence of exercise upon commercially available cardiac biomarkers may hamper or distort the viability of such assays in the clinical arena. The purpose of this review is to examine the influence of exercise upon a number of established and novel cardiac biomarkers, including markers of necrosis, inflammation, cardiac function and ischemia. We will also address the clinical relevance of such exercise-induced perturbations.

Numerous markers upstream of necrosis have been investigated, including inflammatory cytokines, cell adhesion molecules, acute phase reactants, biomarkers of plaque destabilization and rupture, as well as ischemia [2]. Models of human cardiac ischemia, including elective angioplasty, demonstrate an early rise, peak and fall in IMA following coronary occlusion, with values returning to baseline within 24 h. The combination of IMA, cTn and ECG changes on admission to the emergency department has a 95% sensitivity for diagnosis of myocardial infarction.

Background Elevated serum cardiac troponin T (cTnT) and I (cTnI) can occur in patients with chronic kidney disease. Differences in cTn concentrations between cTnT and cTnI have been reported but the mechanism of such discrepancy has not been investigated. This study investigates the clearance of cTn with the aid of an in vitro model of haemodialysis (HD). Methods Serum was obtained before and after a single session of dialysis from 53 patients receiving HD and assayed for cTnT and cTnI. An in vitro model of the dialysis process was used to investigate the mechanism of clearance of cTn during HD. Results Serum cTnI was significantly lower (p=0.043) following a session of HD whereas cTnT concentrations were similar to those obtained before HD. Using an in vitro model of dialysis, it was demonstrated that cTnI is not dialysed from the vascular compartment but adheres to the dialyser membrane. Conclusions The adherence of cTnI to the dialyser membrane is responsible for the observed decrease in serum cTnI following a session of dialysis. The adherence of cTnT or T-I-C complex to the dialyser membrane could not be demonstrated and supports the observation that pre-HD and post-HD serum concentrations of cTnT are similar.

All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article.

Cardiac troponins (cTn) are considered to be the ‘gold standard’ biomarkers for the diagnosis of acute coronary syndrome (ACS) a pathological spectrum which includes cardiac ischemia, angina, myocardial infarction and ultimately cardiac failure. The growing evidence base for the diagnostic and prognostic use of cTn in ACS has resulted in a universal redefinition of acute myocardial infarction (AMI). A diagnosis of AMI includes the detection of an elevated cTn (or CK-MB) with at least one measurement within 24 hours of the cardiac episode being >upper 99th percentile of a reference population, in conjunction with evidence of myocardial ischemia. A number of high sensitivity immunoassays with claims of superior imprecision and a definable 99th percentile have been produced. Clinically, these have two important impacts. First, there is a drive to change the values into whole numbers by the application of a unit change which carries the scope for confusion. Secondly, the near-normal Gaussian distribution of sensitive cTn in healthy subjects will increase the frequency of cTn positivity in the non-ACS population. The problem is to decipher if such minor elevations in cTn are of clinical concern. What is certain is that AMI remains a clinical not a biochemical diagnosis and the interpretation of cTn concentrations should be made according to the clinical context. Srčani troponini (cTn) smatraju se »zlatnim standardom« među biomarkerima za dijagnostikovanje akutnog koronarnog sindroma (ACS), patološkog spektra koji obuhvata srčanu ishemiju, anginu, infarkt miokarda i konačno prestanak rada srca. Sve veći broj dokaza koji idu u prilog dijagnostičkoj i prognostičkoj upotrebi cTn u ACS doveo je do opšteg ponovnog definisanja akutnog infarkta miokarda (AMI). Dijagnoza AMI uključuje detekciju povišenog cTn (ili CK-MB) - najmanje jednom u 24 časa od srčane epizode izmeren je nivo > gornjeg 99. procenta referentne populacije - uz dokaze o ishemiji miokarda. Izrađeno je nekoliko veoma osetljivih imunoeseja s navodno superiornom nepreciznošću i 99. procentilnom vrednošću koji se može definisati. U kliničkom smislum, oni imaju dvojaku važnost. Prvo, postoji težnja da se vrednosti promene u cele brojeve, menjanjem jedinice koja unosi zabunu. Drugo, gotovo normalna Gaussova raspodela osetljivog cTn kod zdravih subjekata povećaće učestalost pozitivnog cTn u populaciji bez ACS. Problem je kako utvrditi da li su ti blago povišeni nivoi cTn od kliničkog značaja. Ono što je sigurno jeste da AMI ostaje klinička a ne biohemijska dijagnoza i da se tumačenje koncentracije cTn mora izvoditi u skladu s kliničkim kontekstom.

The primary study aim was to determine whether ischemia-modified albumin (IMA) predicts adverse outcome in patients attending the emergency department (ED) with acute chest pain. Ischemia-modified albumin is a sensitive marker of myocardial ischemia. However, little is known about its ability to predict outcome in patients presenting to the ED with acute chest pain. We prospectively studied 207 patients who presented to the ED with acute chest pain suggestive of acute coronary syndrome within 3 h of the onset of symptoms. Blood samples for IMA assessment were obtained on admission. We evaluated a 30-day combined end point (cardiac death, myocardial infarction, recurrent angina) and 1-year all-cause mortality. A total of 31 (15%) patients experienced the 30-day composite end point and 16 patients (7.7%) died during the 1-year follow-up. Short-term combined end point (9.6% vs 20.4%, P = 0.03) and 1-year mortality rate (11.7% vs 3.8%, log rank 3.978, P = 0.046) were significantly higher in patients with IMA levels >93.3 U/ml compared to patients with lower IMA. On multivariate analysis, IMA remained an independent predictor of both 30-day combined end point (odds ratio 1.04, 95% confidence interval [CI] 1.01–1.07, P = 0.01) and 1-year mortality (hazard ratio 1.038, 95% CI 1.006–1.070, P = 0.018). Ischemia-modified albumin is an independent predictor of short-and long-term adverse outcomes in patients presenting to the ED with typical acute chest pain.