Glycogen Phosphorylase BB: A more Sensitive and Specific Marker than Other Cardiac Markers for Early Diagnosis of Acute Myocardial Infarction

Cardiac markers are used to evaluate functions of heart. However, there are no satisfactory cardiac biomarkers for the diagnosis of acute myocardial infarction (AMI) within 4 h of onset of chest pain. Among novel cardiac markers, glycogen phosphorylase BB (GPBB) is of particular interest as it is increased in the early hours after AMI. The present study was conducted with the objective to find out the sensitivity and specificity of GPBB over other cardiac markers i.e. myoglobin and CKMB in patients of AMI within 4 h after the onset of chest pain. The study includes 100 AMI patients and 100 normal healthy individuals as controls. In all the cases and controls, serum GPBB and myoglobin concentrations were measured by ELISA where as CK-MB was measured by diagnostic kit supplied by ERBA. The sensitivity and specificity of glycogen phosphorylase BB (GPBB) were greater than CK-MB and myoglobin in patients of AMI within 4 h after the onset of chest pain. Hence, glycogen phosphorylase BB (GPBB) can be used as additional biomarker for the early diagnosis of AMI.     

Cardiac troponins and physical exercise. It's time to make a point

The timely diagnosis of acute coronary syndrome (ACS), in particular myocardial infarction (MI), is still one of the most challenging issues in medicine. The introduction into routine laboratory practice of assays for measuring the cardiospecific troponins has dramatically revolutionized the diagnostic approach and the recent development of methods with improved analytical sensibility (i.e., highly sensitivity [HS] assays), has further contributed to improve the negative predictive value of troponin testing but, contextually, has substantially lowered the clinical specificity of these markers. In particular, clinical studies have demonstrated the existence of an exercise-related increase of HS-troponins, with measurable values detectable in up to 94% of athletes undergoing endurance sports. This measurable amount oftroponin in blood would mirror an increased membrane permeability and early troponin release rather than reflecting a clinically threatening myocardial injury. As such, the measurable amount of cardiac troponins as assessed with the novel HS assays requires major clinical focus (i.e., serial measurement of cardiac biomarkers, detailed clinical history-taking, integration with ECG and imaging findings) to prevent misdiagnosis of ACS and/or MI in otherwise healthy persons.     

Evaluation of clinical utility of serum enzymes and troponin—T in the early stages of acute myocardial infarction

Laboratory infarction diagnostics are based on the detection of elevated serum activities of total Creatine Kinase (CK), Creatine Kinase isoensyme MB, (CKMB), Lactate dehydrogenase (LDH), isoenzyme forms of LDH and transaminases. Determination of these cardiac marker enzymes permits a highly sensitive diagnosis of transmural myocardial infarction. In such patients the diagnosis of acute myocardial infarction can be confirmed by the clinical, symptoms, and changes in the ECG in addition to the enzyme assays. The 50 AMI patients selected in the present study were those admitted to the ICCU of Shri Krishna Hospital, Karamsad. The blood samples were taken at the time of admission (ie. within four hours of the start of chest pain). The samples were analyzed for CK, CKMB, SGOT, (Serum glutamate oxaloactate transaminase) αHBDH α-hydroxybutyrate dehydrogenase and troponin T. The serum CKMB activity in AMI showed an increase only 5–6 hours after the commencement of chest pain. The elevation in SGOT and αHBDH was still delayed. At the same time we could observe that the cardiac Troponin T (cTnT) was elevated at the time of admission of the patient itself. This increase of cTnT in AMI patients was 20 times higher than the normal blood donors. The controls included 25 normal blood donors and 25 patients with polytraumatic injuries with no chest contusion. The study shows that cTnT estimation could serve in the early diagnosis of AMI. The increase of cardiac troponin T in AMI patients was 20 times higher than the normal blood donors in AMI patients at the time of admission. Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial cell injury than CKMB activity and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina as well. When the blood of normal blood donors or that of patients with polytraumatic injury was analysed the troponin T values were well within the normal range in both the above categories showing that cardiac troponin T is highly specific for heart tissue. Although CKMB and cardiac troponin T are released soon after the myocardial injury, the release of cardiac troponin T is much earlier than CKMB thereby invalidating the important role of cardiac troponin T in diagnosing AMI. Cardiac troponin T has been shown to be highly sensitive for cardiac injury and not elevated in any other trauma, heavy exercise or skeletal muscle injury. Cardiac troponin T is ordinarily undetectable in healthy individuals, and so its measurement can serve as a powerful tool in the diagnosis of AMI.     

Heart-Type Fatty Acid-Binding Protein,in Early Detection of Acute Myocardial Infarction: Comparison with CK-MB,Troponin I and Myoglobin

The study aimed to investigate whether heart-type fatty acid binding protein (H-FABP) measurement provides additional diagnostic value to that of conventional cardiac markers in acute myocardial infarction (AMI) within first 6 h after the onset of symptoms. The study included 120 subjects: 60 AMI cases and 60 age and sex matched controls. The cases and controls were further divided into 2 subgroups depending on the time since onset of chest pain as (1) subjects within 3 h and (2) between 3 and 6 h of onset of chest pain. In all the cases and controls, serum H-FABP concentration was measured by Immunoturbidimetric method, serum Troponin I and myoglobin concentrations by Chemiluminescence immunoassay and serum CK-MB concentration by Immuno-inhibition method. The sensitivity, specificity, positive and negative predictive values of H-FABP were significantly greater than CK-MB and myoglobin but were lesser than Troponin I in patients with suspected AMI in both within 3 h and 3–6 h groups. Receiver operating characteristic curves demonstrated greatest diagnostic ability for Troponin I (AUC = 0.99, p < 0.001) followed by H-FABP (AUC = 0.906, p < 0.001) within 3 h and 3–6 h after the onset of chest pain. In conclusion, the diagnostic value of H-FABP is greater than CK-MB and myoglobin but slightly lesser than troponin I for the early diagnosis of AMI within first 6 h of chest pain. H-FABP can be used as an additional diagnostic tool for the early diagnosis of AMI along with troponin I.     

Pregnancy Associated Plasma Protein-A (PAPP-A) Levels in Acute Coronary Syndrome: A Case Control Study in a Tertiary Care Centre

In recent years, an important objective of cardiovascular research has been to find new markers that would improve the risk stratification and diagnosis of patients presenting with symptoms of acute coronary syndrome (ACS). Established biomarkers for diagnosis of ACS includes troponins and creatine kinase MB (CK-MB). Pregnancy associated plasma protein A (PAPP-A) is an emerging marker which has been described as a marker of plaque instability. PAPP-A is a large metalloproteinase involved in insulin-like growth factor signaling and has been shown to be involved in pathological processes like atherosclerosis. Many studies have been published regarding release of PAPP-A in circulation during ACS. The objective of this study was to evaluate the role of PAPP-A as an early marker of ACS by comparing levels of PAPP-A in patients with acute myocardial infarction (AMI) and unstable angina (UA) with asymptomatic controls. The association of PAPP-A with markers of myocardial necrosis and the association of PAPP-A levels to the presence of risk factors for coronary artery disease was also studied. We measured PAPP-A levels in patients with AMI (30), UA (23) and asymptomatic controls (45). PAPP-A was estimated using PAPP-A US (ultra sensitive) ELISA manufactured by DRG (Germany). PAPP-A levels were significantly elevated in patients with AMI and in patients with UA (mean levels 64.26 ± 1.05 and 36.23 ± 1.05 ng/ml respectively; p < 0.001). Mean PAPP-A levels in controls were 10.68 ± 1.04 ng/ml. In UA cases PAPP-A levels were elevated when the troponin I and CK-MB levels were within the normal range. No correlation was observed between PAPP-A with markers of myocardial necrosis. PAPP-A can serve as a useful biomarker in the diagnosis of ACS, especially UA, where cardiac troponin levels and CK-MB levels are not elevated and ECG changes are inconclusive.     

The significance of troponin T and CK-MB release in coronary artery bypass surgery

Measurement of cardiac markers is an index of care standard in the assessment and diagnosis of cardiovascualr disease. Two of the major cardiac markers are Creatine Kinase isoenzyme CK-MB and Troponin T, which are extensively used in the diagnosis of heart disease. The release of Troponin T and creatine kinase isoenzyme (CK-MB) was investigated in 50 coronary artery bypass surgery patients. Measurement of plasma samples was carried out at five different time points, namely before surgery, 1,6,12,24 hours after surgery. The results indicated that CK-MB level were increased by a factor more than four times compared with the upper limit of baseline (befor surgery). Troponin T concentration showed more than six fold over the upper limit of baseline (before surgert) at 1,6,12,24 hours after surgery. In order to assess the significance of the length of the surgical procedure on the release of Troponin T and CK-MB, the surgery patient were divided into two groups according to the length of the surgical procedure: group I was selected on the basis that the surgical procedure they underwent lasted above 90 minutes and group II with a surgical procedure below 90 minutes. Both Troponin T and CK-MB showed a significant increase in-group I compared to group II. To investigate the likelihood that this effect is party due to myocardial infarction during surgery, the patients were divided into two groups: Group A with some sings of myocardial infarction on Q wave of ECG and group B without any change. The results showed approximately a two-fold increase of these markers in-group A compared to group B. Since these markers reach into blood following damage to myocardial their increase in patients with time course surgery of more than 90 minutes and those with a probability of MI during operation, indicating that these patient fall into a high risk group of repeat (MI) after surgery.     

Serum markers for early diagnosis of non-‘Q’ wave and ‘Q’ wave myocardial infarction

The present study conducted on twenty-five uncomplicated cases of acute myocardial infarction diagnosed by clinical and electrocardiographic findings indicated significantly increased level of cardiac Troponin-T and increased activities of the enzymes total creatine kinase, creatine kinase-MB, aspartate transaminase and lactate dehydrogenase as compared to the twenty-five healthy control subjects. The level of cardiac Troponin-T and the activities of the enzymes total creatine kinase, creatine kinase-MB, aspartate transaminase and lactate dehydrogenase was found to be higher in “Q” wave myocardial infarction patients as compared to the non-“Q” wave and the controls. Since cardiac Troponin-T has been shown to increase in unstable angina and renal failure without cardiac disease and creatine kinase-MB activity has been found to be normal in patients with unstable angina and increase very slightly in patients with renal failure, it was concluded that a combination of cardiac Troponin-T and creatine kinase-MB activity was sufficient for the early diagnosis of acute myocardial infarction.     

A serial follow up study of cardiac marker enzymes during the week after acute myocardial infarction

Laboratory infarction diagnostics are based on the detection of elevated serum activities of creatine kinase (CK) Creatine kinase Isoenzyme MB (CKMB) and Transaminases. Determination of these cardiac marker enzymes permits the diagnosis of transmural myocardial infarction. However in such patients the diagnosis of acute myocardial infarction can be confirmed by the clinical symptoms and changes in the ECG, in addition to the enzyme assays. The 50 AMI patients selected in the present study were those admitted to the ICCU of Shri Krishna Hospital, Karamsad. The blood samples were taken at Zero hours (i.e. at the time of admission of the patient). Within 6 hrs of the starting of chest pain, 1.5 million units of streptokinase were mixed with 100 to 150ml of normal saline and administered by infusion over a period of one hour. The blood samples were further collected at intervals of 6 hrs, 14hrs, 32hrs, 48hrs, 5^th day and 7^th day. The blood samples were analyzed for CK, CKMB, SGOT, α HBDH and Cardiac specific Troponin T. By 6hrs the CK and CKMB values had started rising, the rise continuing at 14hrs with peak values at 32hrs. The CK showed a slight decrease by 48 hrs. The cardiac Troponin T showed wide time window from 4 hrs to 7^th day for detecting myocardial damage. The maximum cardiac Troponin T values were during the first 24hrs. Cardiac Troponin T in serum appears to be a more sensitive and early indicator of myocardial cell injury in comparison to CKMB.     

A comparative study of tumor markers of adenocarcinoma prostate

The present study deals with the evaluation and comparison of the tumor markers for prostatic carcinoma—The Total Acid Phosphatase (ACP Total) and its Prostatic Fraction (ACP PF) estimated by the enzyme kinetic method, an immunoreactive Prostatic Acid Phosphatase (PAP) and Prostate Specific Antigen (PSA) estimated by enzyme immunoassay. The comparison of all four markers revealed that there was no perfect positive correlation between any of these four markers. PSA had shown a better correlation with ACP Total and its prostatic fraction ACP PF. No correlation was observed between PSA and PAP. Of the four markers PAP exhibited a very low sensitivity, positive and negative predictive values. PSA had shown an absolute specificity, sensitivity, positive and negative predictive values for adenocarcinoma prostate. PSA levels in all phases of disease showed a 100% correlation with disease status. Being a marker with very high tissue specificity and sensitivity, it is revolutionizing the diagnosis of prostatic carcinoma. Hence, it could be used effectively for screening of elderly people over 50 years of age who are at high risk for developing prostatic carcinoma for early diagnosis of this disease.     

Ischemia modified albumin: A novel marker for acute coronary syndrome

Early identification of patients with acute myocardial infarction is of prime importance due to the associated very high mortality. Only 22% of the patients presenting at emergency cardiology care with chest pain have coronary disease. A number of biochemical tests like CKMB and Troponin-T/I have been introduced for early detection of the coronary syndrome (ACS). Ischemia modified albumin (IMA) has been recently introduced as a marker of myocardial ischemia. We estimated serum IMA in four sequential samples from 25 patients admitted to ICCU. Twenty five healthy volunteers formed the control group from which the normal range was derived. IMA was significantly raised in ischemia patients than in controls as well as compared to the patients who did not have cardiac ischemia. IMA demonstrated good discrimination between the ischemic and the non-ischemic patients with an Odds Ratio of 16.9 (6.29–46.87) than CKMB which showed an Odds Ratio of 2.07 (1.18–6.08). Sensitivity and specificity of IMA for the detection of ACS was 78.0% and 82.7% compared to 58.0% and 60.0%, respectively for the CK-MB assay. The area under the ROC curve of IMA for ischemic v/s non-ischemic patients was 0.834. IMA appears to be developing into a new and very potent marker, of cardiac ischemia.     

Modeling of dielectrophoretic transport of myoglobin molecules in microchannels

Myoglobin is one of the premature identifying cardiac markers, whose concentration increases from 90 pg∕ml or less to over 250 ng∕ml in the blood serum of human beings after minor heart attack. Separation, detection, and quantification of myoglobin play a vital role in revealing the cardiac arrest in advance, which is the challenging part of ongoing research. In the present work, one of the electrokinetic approaches, i.e., dielectrophoresis (DEP), is chosen to separate the myoglobin. A mathematical model is developed for simulating dielectrophoretic behavior of a myoglobin molecule in a microchannel to provide a theoretical basis for the above application. This model is based on the introduction of a dielectrophoretic force and a dielectric myoglobin model. A dielectric myoglobin model is developed by approximating the shape of the myoglobin molecule as sphere, oblate, and prolate spheroids. A generalized theoretical expression for the dielectrophoretic force acting on respective shapes of the molecule is derived. The microchannel considered for analysis has an array of parallel rectangular electrodes at the bottom surface. The potential and electric field distributions are calculated using Green’s theorem method and finite element method. These results also compared to the Fourier series method, closed form solutions by Morgan et al. [J. Phys. D: Appl. Phys. 34, 1553 (2001)] and Chang et al. [J. Phys. D: Appl. Phys. 36, 3073 (2003)]. It is observed that both Green’s theorem based analytical solution and finite element based numerical solution for proposed model are closely matched for electric field and square electric field gradients. The crossover frequency is obtained as 40 MHz for given properties of myoglobin and for all approximated shapes of myoglobin molecule. The effect of conductivity of medium and myoglobin on the crossover frequency is also demonstrated. Further, the effect of hydration layer on the crossover frequency of myoglobin molecules is also presented. Both positive and negative DEP effects on myoglobin molecules are obtained by switching the frequency of applied electric field. The effect of different shapes of myoglobin on DEP force is studied and no significant effect on DEP force is observed. Finally, repulsion of myoglobin molecules from the electrode plane at 1 KHz frequency and 10 V applied voltage is observed. These results provide the ability of applying DEP force for manipulating nanosized biomolecules such as myoglobin.     

Cardiac indexes, cardiac damage biomarkers and energy expenditure in professional cyclists during the Giro d'Italia 3-weeks stage race

Introduction

The study of cardiac response to strenuous and continuous exercise is crucial to understanding the physiology of endurance. N-terminal proB-type natriuretic peptide (NT-proBNP) is a potential marker for monitoring myocardial wall stress, and troponins (TnT and TnI) are widely used in the diagnosis of cardiac ischemia and infarction. Strenuous exercise may generate transitory ischemia, myocardial stress, and diastolic left ventricular dysfunction, inducing the increased production of both these biomarkers. We measured changes in NT-proBNP and TnT in elite cyclists during a 3-week stage race, a model of strenuous exercise.

Materials and methods:

The study population was 9 professional cyclists participating in the 2011 Giro d’Italia. Pre-analytical and analytical phases scrupulously followed official recommendations. Anthropometric data, net energy expenditure and cardiac indexes (rate, diastolic and systolic blood pressure) were recorded. Blood samples were drawn pre-race (day −1) and at days 12 and 22; NT-proBNP and highly sensitive-troponin (Hs-TnT) concentrations were assayed and corrected for plasma volume changes.

Results:

Body-mass index decreased and energy expenditure increased by 52% during the race. NT-proBNP concentrations increased [day −1: 23.52 ng/L (9.67–34.33); day 12: 63.46 ng/L (22.15–93.31); P = 0.039; day 22: 89.26 ng/L (34.66–129.78) vs. day −1; P < 0.001] and correlated with heart rate (r = −0.51; P = 0.006), systolic pressure (r = 0.39; P = 0.046) and energy expenditure (r = 0.70; P < 0.001). TnT concentrations did not vary, but a widened TnT amplitude distribution was observed.

Conclusions:

Increases in NT-proBNP correlated with higher energy expenditure over a 3-week cycling stage race, possibly indicating myocardial stress.     

Troponin T and Heart Type Fatty Acid Binding Protein (h-Fabp) as Biomarkers in Patients Presenting with Chest Pain

Acute coronary syndrome (ACS) is a term for a range of clinical signs and symptoms suggestive of myocardial ischemia. It results in functional and structural changes and ultimately releasing protein from injured cardiomyocytes. These cardiac markers play a major role in diagnosis and prognosis of ACS. This study aims to assess the efficacy of heart type fatty acid binding protein (h-FABP) as a marker for ACS along with the routinely used hs-TropT. In our observational study, plasma h-FABP (cut-off 6.32 ng/ml) and routinely done hs-Trop T (cutoff 0.1 and 0.014 ng/ml) were estimated by immunometric laboratory assays in 88 patients with acute chest pain. Based on the clinical and laboratory test findings the patients were grouped into ACS (n = 41) and non-ACS (n = 47). The diagnostic sensitivity, specificity, NPV, PPV and ROC curve at 95 % CI were determined. Sensitivity of hs-TropT (0.1 ng/ml), hs-TropT (0.014 ng/ml) and h-FABP were 53, 86 and 78 % respectively and specificity for the same were 98, 73 and 70 % respectively. Sensitivity, specificity and NPV calculated for a cut-off combination of hs-TropT 0.014 ng/ml and h-FABP was 100, 51 and 100 % respectively. These results were substantiated by ROC analysis. Measurement of plasma h-FABP and hs-TropT together on admission appears to be more precise predictor of ACS rather than either hs-Trop T or h-FABP.     

Biochemical markers for alcohol consumption

A variety of laboratory tests are available to assist in the diagnosis of alcohol consumption and related disorders. The levels of intake at which laboratory results become abnormal vary from person to person. Laboratory tests are particularly useful in settings where cooperativeness is suspected or when a history is not available. Several biochemical and hematological tests, such as γ-glutamyltransferase (GGT) activity, aspartate aminotransferase (AST) activity, high-density lipoprotein cholesterol (HDL-C) content of serum, and erythrocyte mean corpuscular volume (MCV) are established markers of alcohol intake. Their validity as markers is based largely on correlations with recent intake at a single time point and on decreases in elevated values when heavy drinkers abstain from alcohol. These readily available laboratory tests provide important prognostic information and should be integral part of the assessment of persons with hazardous alcohol consumption. There are several other markers with considerable potential for more accurate reflection of recent alcohol intake. These include carbohydrate deficient transferrin, β-hexosaminidase, acetaldehyde adducts and the urinary ratio of serotonin metabolites, 5-hydroxytryptophol and 5-hydroxyindoleacetic acid. These markers provide hope for more sensitive and specific aids to diagnosis and improved monitoring for intake.     

Usefulness of ferroxidase activity of ceruloplasmin in the diagnosis of Wilson’s disease

Serum ceruloplasmin is one of the most commonly used screening tests for Wilson’s disease. However immunological assays for ceruloplasmin are not recommended for diagnosis and management of Wilson’s disease through calculation of free copper index. Enzymatic methods using non-physiological substrates have toxicity and stability problems, making them difficult to automate. Ferroxidase assays may be a satisfactory alternative for measuring serum ceruloplasmin. The o-dianisidine hydrochloride manual method for estimation of serum ceruloplasmin enzyme activity was compared with an automated method using the ferroxidase activity of ceruloplasmin in measurement in a double blind study in 91 consecutive patients screened for Wilson’s disease. The o-dianisidine and ferroxidase methods both successfully identified 7 patients with Wilson’s disease. Values for these 7 patients in the o-dianisidine and ferroxidase methods were median 5.0 (range 0–16.0 U/L) and median 45.0 (range 4–166 U/L) respectively. There were 7 other positive values (<62 U/L) with the o-diansidine method and 2 (<200 U/L) with the ferroxidase method, where WD was not confirmed. ROC curves for both methods showed area under the curve of 0.998 for o-dianisidine and 0.997 for ferroxidase. Using literature cut off values of 62 U/L and 200 U/L respectively both methods had 100% sensitivity and specificity was 91.7% (o-dianisidine) and 97.6% (ferroxidase). For the o-dianisidine assay, specificity was improved to 98.8% using a cut off of 22.5 U/L. In the 84 persons (46 adults and 38 children) in whom the diagnosis of Wilson’s disease was not established, the mean value for ceruloplasmin activity by the o-dianisidine and ferroxidase methods was 124.7 ± 48.7 U/L and 571.4 ± 168.1 U/L respectively. There were no significant differences between sex or age of patients (p > 0.29). In a subsequent evaluation with 372 specimens, the Pearson correlation coefficient between the assays was 0.908, p < 0.01, slope 4.06, intercept 265.8, with the manual assay as the x-axis. The ferroxidase assay is a suitable replacement for the o-dianisidine assay in detecting patients with Wilson’s disease.     

Comparative study of serum myoglobin and creatine kinase MB isoenzyme in the detection of acute myocardial infarction

Serum creatine kinase MB isoenzyme (CKMB) and myoglobin have been studied in 35 cases with myocardial infarction. Increased values for both serum CKMB and myoglobin have been found in all the patients in the second sample collected 4 hr. after admission while in 22 patients in the first sample collected immediately after admission. Thus, the present study shows a good correlation between serum CKMB and myoglobin and therefore, suggests the possibility of using the serum myoglobin estimation in early detection of myocardial infarction either alone or in combination with the serum CKMB.     

β-Adrenoreceptor Agonist Isoproterenol Alters Oxidative Status,Inflammatory Signaling,Injury Markers and Apoptotic Cell Death in Myocardium of Rats

Sustained high levels of circulating catecholamines are reported to induce cardiotoxicity. Isoproterenol (ISP), a synthetic catecholamine has been widely employed to induce myocardial injury, though the role of inflammation and apoptosis is not well established. This study was designed to investigate the underlying mechanism of oxidative damage, inflammatory signaling, cell death in ISP induced myocardial infarction in rats. Wistar albino rats were divided in two groups: group I (sham control) and group II (ischemic control). ISP (85 mg/kg, s.c.) was administered at an interval of 24 h to group II for two consecutive days. On day third, after 48 h of the first injection of ISP, blood was collected from retro orbital plexus of rat eyes to estimate the biochemical parameters. Glutathione (GSH) and superoxide dismutase (SOD) were measured for antioxidant status. Similarly, malondialdehyde (MDA) was measured as an index of lipid peroxidation. Cardiac markers (SGOT, CK-MB, TropI and LDH) and pro-inflammatory cytokines (IL-6, CRP and TNF-α) were also estimated in ISP-induced rats. At the end of experiments animals were sacrificed for histopathological studies. GSH and SOD showed significant decrease after ISP challenge as compared to sham (control) group (p < 0.01) while MDA level, increased significantly (p < 0.01). ISP, also increased the level of cardiac markers and markers of inflammation significantly (p < 0.01), which was further verified by histopathological studies of the heart tissues. The study confirmed that ISP causes detrimental changes in the myocardium by altering cardiac and inflammatory markers, which leads to severe necrosis. The deleterious effects produced by ISP substantiate its suitability as a novel animal model for evaluation of cardioprotective agents/drugs.     

Effects of interaction of vitamin A and <Emphasis Type="Italic">Rauwolfia vomitoria</Emphasis> root bark extract on marker enzymes of cardiac diseases

Serum creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and aspartate aminotransferase (AST) are key players in the diagnostic study of cardiac complications. These enzymes are specific diagnostic markers of myocardial infarction and hypertension is a disease condition characterized with a wide range of complications, including myocardial infarction. In this study, we determined the effects of interaction of vitamin A and Rauwolfia vomitoria (RV) root bark extract on marker enzymes of cardiac diseases. CK and CK-MB activities had significant decrease in the group of animals with concomitant administration of vitamin A (40 IU/kg body wt.) and 150 mg/kg body wt. of RV root bark extract. At the interaction of vitamin A with 300 mg/kg body wt. RV root bark extract, CK-MB only showed significant (p ≥ 0.05) decrease while CK decreased insignificantly. Also at the interaction of vitamin A with 300 mg/kg body wt. RV root bark extract, AST increased significantly but decreased significantly at the interaction of vitamin A (40 IU/kg body wt.) and 150 mg/kg body wt. of RV root bark extract. Our findings showed that vitamin A dose did not lower the activities of cardiac marker enzymes. However, concomitant administration of RV root bark extract at 150 mg/kg body wt. with vitamin A shows significant reduction in the activities of CK, CK-MB and AST. These findings suggest that interaction of vitamin A with RV root bark extract would be a meaningful ethno-pharmaceutical approach in the management of myocardial infarction and treatment of hypertension.     

Hospital based preliminary study on osteoporosis in postmenopausal women

The awareness of osteoporosis has grown world wide in recent years. This silently progressing metabolic bone disease is widely prevalent in India, and osteoporotic fractures are a common cause of morbidity and mortality in adult Indian men and women. Rapid bone loss occurs in postmenopausal women due to hormonal factors which lead to increased risk of fractures. Biochemical markers of bone metabolism are used to assess skeletal turnover. A cross-sectional study of 150 pre- and post menopausal women was carried out at S.D.M College of Medical Sciences and Hospital, Dharwad, during the period of May 2005 to September 2005. The study group consisted of 75 Premenopausal women in the age group of 25–45 years and 75 Postmenopausal women in the age group of 46–65 years. Bone formation markers (Total Calcium, lonised calcium, Phosphorus, Alkaline phosphatase), and bone resorption markers (Urinary Hydroxyproline) were analysed in pre and post menopausal women. Bone formation markers, Total and lonised calcium were significantly decreased (p<0.001) and Alkaline phosphatase was significantly increased (p<0.001) in postmenopausal women compared to premenopausal women. Bone resorption markers, Urinary hydroxyproline excretion was significantly increased (p<0.001) in postmenopausal women. The results from this study suggest that simple, easy, common biochemical markers can still be used to assess the bone turnover in postmenopausal women and hence their risk of developing osteoporosis and fractures.     

Biochemical advances in detection of the acute coronary syndromes: Implications for therapeutic decisions

In this paper, I have attempted to place the evolving insights of the pathophysiology of coronary atherosclerosis in the context of the conventional perspective of clinical medicine. We strive to prevent death and to relieve suffering. Our clinical tools are critical but limited. Troponin, a biomarker of unprecedented organ specificity, in the context of the appropriate setting of new chest pain (or its equivalent syndrome), is an extraordinary aid to clinical diagnosis. Highly effective therapy is evolving which reduces loss of myocardium, undoubtedly reducing not only acute death but progression to congestive heart failure. Even if the newer therapies of the GpIIb/IIIa platelet antagonists and antithrombins are not yet widely employed, or may not be available to some physicians, the convincing demonstration of myocardial injury by troponin presents objective evidence to both the patient and the attending physician that serious compliance with a program of risk reduction must be urgently considered. Hoeg has described the mosaic of risk factors beyond the conventional and often ignored basic ones (JAMA, 1997, 277, 1387–1390). He provides thoughtful hope and encouragement for both patient and physician to do more in prevention of the subsequent predictable progression. We should look on a troponin positive vague unstable angina event as similar to a tremor which preceeds a subsequent earthquake. Although the mass of myocardium lost in such an episode may be small, it is a warning of the major acute myocardial infarction which can be predicted to follow at a later time if the course of the individual patient is not altered. Troponin is the objective evidence.