Effects of Cardiac Contusion in Isolated Perfused Rat Hearts (original) (raw)

Studies on Cardiac Troponin I in patients with Cardiogenic Shock

Journal of Dhaka National Medical College & Hospital, 2013

Despite recent advances in the care of patients with acute coronary disease and the benefits associated with the early use of reperfusion strategies, cardiogenic shock as a complication of acute myocardial infarction continues to be associated with a dismal prognosis. There is a strong relationship between serum cardiac troponin I with cardiogenic shock as a complication of acute myocardial infarction. A case control study was designed to see the association of serum cardiac troponin I with cardiogenic shock. The study was done from July 2008 to June 2009. Sixty subjects were selected as study population which were taken from department of Cardiology, Mymensingh Medical College hospital, Mymensingh. Among them 30 were diagnosed case of cardiogenic shock and 30 were age and sex matched control. It revealed that the mean cardiac troponin- I levels in case group were 15.998±28.31 ng/ml and control group were 0.065 ± 0.08 ng/ml respectively. The study suggest that serum cardiac troponin...

Release kinetics of serum cardiac troponin i in ischemic myocardial injury

Clinical Biochemistry, 1996

Objectives: The study was undertaken to evaluate the release kinetics of cardiac troponin I (c'rn-I) in ischemic myocardial injury. Design and Methods: The reference range for cTn-I was established by determination of cTn-I in sera and plasma obtained from 622 healthy volunteers (Group 1). cTn-I was compared to: (a) Creatine kinase (CK) MB mass and myoglobin in 12 patients with severe skeletal muscle damage (Group 2); (b) CK-MB activity in 48 patients with myocardial infarction (MI) receiving intravenous thrombolysis (Group 3) (in this group, an additional 43 patients with MI were analyzed separately to characterize cTn-I patterns in thrombolyzed and nonthrombolyzed populations); and in 44 patients with unstable angina (Group 4). Results: In Groups 1 and 2, no positive results (>t0.1 pg/L) were obtained. In Group 3, the time-courses of cTn-I were mostly monophasic in form. A pathologic increase occurred earlier in cTn-I than in CK-MB activity (p = 0.0002); the period with increased cTn-I was longer (,o= 0.001), the overall sensitivity of cTn-I (93.9%) was higher than that of CK-MB activity (,c, = 0.00001). cTn-I was more sensitive at admission (,o = 0.0004). In additional patients, the cTn-I peak occurred and cTn-I disappeared significantly later in nonthrombolyzed than in the thrombolyzed group. In Group 4, positive tests results were detected in 45% of patients for cTn-I, 16% for CK-MB activity, and 32% for CK-MB mass. Conclusions: The cTn-I assay appears to be ideally suited for the detection of ischemic myocardial injury in complex clinical situations because of its high specificity; cTn-I indicates myocardial tissue damage in patients with unstable angina and is superior to CK-MB activity and mass in this respect.

Myocardial Injury and the Release of Troponins I and T in the Blood of Patients

Clinical Chemistry, 2020

Background Cardiac troponin I (cTnI) and cTnT are the established biomarkers of cardiomyocyte damage and the recommended biomarkers for the diagnosis of acute myocardial infarction (MI). High-sensitivity immunochemical diagnostic systems are able to measure the cTn concentrations in the blood of a majority of healthy people. At the same time, the concentration of cTn may be increased not only after MI but also because of other pathologies that might affect myocardium. This effect reduces the clinical specificity of cTn for MI and may complicate the diagnosis. Content This review summarizes the existing information regarding the causes and mechanisms that lead to the increase of cTn concentration in blood and the forms of cTn that are present in circulation after MI or other types of myocardial injury. Summary Different etiologies of disease associated with increases of cTn above the 99th percentile and various mechanisms of troponin release from myocardium could result in the appear...

Effects of myocardial ischemia on the release of cardiac troponin I in isolated rat hearts

The Journal of Thoracic and Cardiovascular Surgery, 1996

Background: The twofold aim of this experimental study was (1) to verify the correlation between the duration of ischemia and concentration of cardiac troponin I and (2) to compare the release of cardiac troponin I with histologic findings. Methods: Experiments were done on 18 rat hearts, which were perfused according to the Langendorff method, immediately after excision in group I (control group) and after immersion for 3 hours (group II) and 6 hours (group III) in St. Thomas' Hospital solution at 4 ° C. During reperfusion, the release of cardiac troponin I, creatine kinase isoenzyme MB, and lactate dehydrogenase, the recovery of left ventricular pressure, and heart rates were compared among the three groups. After the experiment, three samples of myocardium (left ventricle, right ventricle, and septum) were taken for histologic examination. Results: Cardiac troponin I

Cardiac Troponin: a New Biochemical Marker for Peri-operative Myocardial Injury

European Journal of Vascular and Endovascular Surgery, 2001

who have objective evidence of MI. 6 The ECG is difficult to interpret in the post-operative setting and often Peri-operative myocardial infarction (MI) occurs in does not display the classical ST segment elevation of acute myocardial infarction. 7 Lastly, even if there is a 5-10% of patients undergoing major vascular surgery, is fatal in 50% of these cases and in total will account significant rise in creatine kinase leaked from dying myocardial cells (CK-MB) this may be masked by for more than 50% of all post-operative deaths. 1 An even larger proportion of operated patients will suffer large quantities of creatine kinase (CK) released from skeletal muscle as the result of direct surgical trauma cardiac complications, which may be fatal or non-fatal, that are not demonstrably related to peri-operative or ischaemia/reperfusion injury. 8 This makes the CK/ CK-MB ratio difficult to interpret. MI. 2 These complications may have metabolic causes, but are perhaps more likely to be due to myocardial infarction that cannot be detected by the standard diagnostic tests for peri-operative MI. 3,4 This injury Micro-infarction and the acute coronary may be referred to as minor myocardial injury or syndromes micro-infarction.

Effect of Treatment on Ventricular Function and Troponin I Proteolysis in Reperfused Myocardium

Journal of Molecular and Cellular Cardiology, 2002

Effects of ischemia time and treatment interventions upon troponin I (TnI) proteolysis and function of reperfused myocardium were examined in isolated, perfused rabbit hearts. Hearts were randomized to 90 min aerobic perfusion, 15 min low-flow (1 ml/min) ischemia (I) and 60 min reperfusion (R) or 60 min low-flow I and 60 min R. Hearts subject to 60 min I and 60 min R received either no treatment, -arginine treatment, or treatment with oxygen free radical (OFR) scavengers (mercapto-proponylglycine, catalase and superoxide dismutase). Hearts from cholesterol-fed rabbits were also studied after 60 min I and R. Isovolumic LV pressure and heart rate were recorded throughout and Western analysis of ventricular myocardium, using 3 specific antibodies, detected intact TnI (29 kDa) and TnI fragment (25 kDa). Hearts subject to 15 min I had minimal irreversible injury (TTC negative region=0.6±0.4% LV) but hearts subject to 60 min I had more extensive injury (TTC negative=40.7±5.8% LV). Recovery of rate-pressure product after 15 min I and 60 min R (56±9% of baseline) was better than after 60 min I and 60 min R (23±9%, P<0.01). Both arginine and OFR scavengers were associated with better recovery of function after 60 min I, (66±7% and 72±3% of baseline respectively, P<0.01 v no treatment) but cholesterol hearts had poor recovery after 60 min I (37±8%). The 25 kDa TnI (% total TnI immunoreactivity) was 8.7±0.9% in controls, 10.0±1.6% after 15 min I and 60 min R, and 17.4±2.4% after 60 min I and 60 min R (P<0.01 v controls and 15 min I). The proportion of 25 kDa TnI was increased in all hearts after 60 min I and did not change with treatment (-arginine 16.8±1.8%, OFR scavengers 16.0±3.2%, cholesterol 14.0±1.9%). There was no relation between proportion of 25 kDa TnI and recovery of function. Samples from freshly excised rabbit hearts and human right atria also had 25 kDa TnI (relative intensities 8.5±2.3% and 5.1±2.6% respectively). Although TnI fragmentation increases after prolonged ischemia and reperfusion, the functional recovery of stunned myocardium is independent of degree of TnI fragmentation.

The Role of Troponin in Blunt Cardiac Injury After Multiple Trauma in Humans

World journal of surgery, 2016

The incidence of cardiac injury in immediate fatalities after blunt trauma remains underestimated, and reliable diagnostic strategies are still missing. Furthermore, clinical data concerning heart-specific troponin serum levels, injury severity score (ISS), catecholamine treatment and survival of patients on admission to the hospital have rarely been interrelated so far. Therefore, the object of the present study was to identify predictive parameters for mortality in the context of blunt cardiac injury. This retrospective observational study included 173 severely injured patients with an ISS ≥25 admitted to the University Hospital of Ulm, a level 1 trauma center, during 2009-2013 . Furthermore, 83 blunt trauma victims who died before hospital admission were subjected to postmortem examination at the Institute of Legal Medicine, University of Ulm, during 2009-2014. ISS, cardiac injury and associated thoracic injuries were determined in both groups. Furthermore, in the hospitalized pa...

A Review on Role of Cardiac Troponins in Acute Coronary Syndrome

Troponins are structural cardiac muscle proteins that are released during myocyte damage and necrosis. Cardiac troponins are absent in the plasma of a healthy subject, so that small elevations are indicative of myocardial damage. However modern assays are extremely sensitive and can detect low level of myocardial damage. Troponins are highly specific and sensitive marker. The concentration of troponins in the blood increases during an acute myocardial infarction, enabling clinician to quickly initiate appropriate therapy. So they are useful in diagnosing patients with acute coronary syndrome and for predicting the response during drug therapy. This review describes the role of cardiac troponins in acute coronary syndrome.