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Myocardial Injury (myocardial + injury)
Selected AbstractsSerum Cardiac Troponin I Concentration in Dogs with EhrlichiosisJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008P.P.V.P. Diniz Background: Ehrlichiosis is a multisystemic disease with the potential to cause cardiomyocyte injury in naturally infected dogs. Hypothesis: Myocardial injury occurs in dogs infected with Ehrlichia canis. Animals: One-hundred and ninety-four dogs from Brazil with clinical and laboratory abnormalities indicative of ehrlichiosis. Sixteen healthy dogs served as controls. Methods: Electrocardiogram, echocardiogram, noninvasive blood pressure measurement, and serum cardiac troponin I (cTnI) concentrations were evaluated. Serologic assays and PCR determined the exposure and infection status for E. canis, Anaplasma spp., Babesia canis vogeli, Bartonella spp., Borrelia burgdorferi, Dirofilaria immitis, Ehrlichia chaffeensis, Ehrlichia ewingii, Leishmania chagasi, and spotted-fever group Rickettsia. Dogs were assigned to groups according to PCR status: E. canis infected, infected with other vector-borne organisms, sick dogs lacking PCR evidence for infection, and healthy controls. Results: E. canis -infected dogs had higher serum cTnI concentrations than controls (median: 0.04 ng/dL; range 0.04,9.12 ng/dL; control median: 0.04 ng/dL; range: 0.04,0.10 ng/dL; P= .012), and acute E. canis infection was associated with myocardial injury (odds ratio [OR]: 2.67, confidence interval [CI] 95%: 1.12,6.40, P= .027). Severity of anemia was correlated with increased risk of cardiomyocyte damage (r= 0.84, P < .001). Dogs with clinical signs of systemic inflammatory response syndrome (SIRS) were at higher risk for myocardial injury than were other sick dogs (OR: 2.55, CI 95%: 1.31,4.95, P= .005). Conclusions and Clinical Importance: Acute infection with E. canis is a risk factor for myocardial injury in naturally infected Brazilian dogs. Severity of anemia and SIRS might contribute to the pathophysiology of myocardial damage. [source] Anti-inflammatory actions of aprotinin provide dose-dependent cardioprotection from reperfusion injuryBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2008J M Carter Background and purpose: Myocardial injury following ischaemia and reperfusion has been attributed to activation and transmigration of polymorphonuclear leukocytes (PMNs) with release of mediators including oxygen-derived radicals and proteases causing damage. Experimental approach: We studied the serine protease inhibitor aprotinin in an in vivo rabbit model of 1 h of myocardial ischaemia followed by 3 h of reperfusion (MI+R). Aprotinin (10 000 Ukg,1) or its vehicle were injected 5 min prior to the start of reperfusion. Key results: Myocardial injury was significantly reduced with aprotinin treatment as indicated by a reduced necrotic area (11±2.7% necrosis as percentage of area at risk after aprotinin; 24±3.1% after vehicle; P<0.05) and plasma creatine kinase activity (12.2±1.5 and 17.3±2.3 IU g,1 protein in aprotinin and vehicle groups, respectively, P<0.05). PMN infiltration (assessed by myeloperoxidase activity) was significantly decreased in aprotinin-treated animals compared to vehicle (P<0.01). Histological analysis also revealed a substantial increase in PMN infiltration following MI+R and this was significantly reduced by aprotinin therapy (44±15 vs 102±2 PMN mm2 in aprotinin vs vehicle-treated animals, P<0.05). In parallel in vitro experiments, aprotinin inhibited neutrophil-endothelium interaction by reducing PMN adhesion on isolated, activated aortic endothelium. Finally, immunohistochemical analysis illustrated aprotinin significantly reduced myocardial apoptosis following MI+R. Conclusions and implications: Inhibition of serine proteases by aprotinin inhibits an inflammatory cascade initiated by MI+R. The cardioprotective effect appears to be at least partly due to reduced PMN adhesion and infiltration with subsequently reduced myocardial necrosis and apoptosis. British Journal of Pharmacology (2008) 155, 93,102; doi:10.1038/bjp.2008.223; published online 9 June 2008 [source] High serum cardiac troponin T concentrations in preterm infants with respiratory distress syndrome,ACTA PAEDIATRICA, Issue 9 2000D Trevisanuto In preterm infants with respiratory distress syndrome (RDS), cardiac function is negatively influenced by the severity of the lung disease. On day 2 of life, cardiac troponin T (cTnT), biochemical marker of myocardial injury, was measured in 46 preterm infants (gestational age ,32 wk), 26 with RDS and 20 without: median (range) 0.38 (0.02,1.57) ,gL vs 0.13 (0.02,0.85) ,gL, respectively. Conclusion: High cTnT concentrations in preterm infants with RDS suggest the presence of myocardial damage in this group of high-risk patients. [source] Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 during cardiac remodelling in ratsACTA PHYSIOLOGICA, Issue 1 2010E. Mustonen Abstract Aim:, Accumulating evidence supports the concept that proinflammatory cytokines play an essential role in the failing heart. We examined the concomitant tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/Fn14 expression in myocytes in vitro as well as in vivo in cardiac remodelling. Methods:, We assessed TWEAK and its receptor Fn14 expression in response to angiotensin (Ang) II, myocardial infarction (MI) as well as to local adenovirus-mediated p38 gene transfer in vivo. The effect of various hypertrophic factors and mechanical stretch was studied in neonatal rat ventricular myocyte cell culture. Results:, Ang II increased Fn14 levels from 6 h to 2 weeks, the greatest increase in mRNA levels being observed at 6 h (6.3-fold, P < 0.001) and protein levels at 12 h (4.9-fold, P < 0.01). TWEAK mRNA and protein levels remained almost unchanged during Ang II infusion. Likewise, a rapid and sustained elevation of Fn14 mRNA and protein levels in the left ventricle was observed after experimental MI. Moreover, local p38 gene transfer increased Fn14 mRNA and protein but not TWEAK levels. Fn14 immunoreactive cells were mainly proliferating non-myocytes in the inflammation area while TWEAK immunoreactivity localized to cardiomyocytes and endothelial cells of the coronary arteries. Hypertrophic agonists and lipopolysaccharide increased Fn14 but not TWEAK gene expression in neonatal rat myocytes, while mechanical stretch upregulated Fn14 and downregulated TWEAK gene expression. Conclusions:, In conclusion, the cardiac TWEAK/Fn14 pathway is modified in response to myocardial injury, inflammation and pressure overload. Furthermore, our findings underscore the importance of Fn14 as a mediator of TWEAK/Fn14 signalling in the heart and a potential target for therapeutic interventions. [source] Erratum: MR imaging in assessing cardiovascular interventions and myocardial injuryCONTRAST MEDIA & MOLECULAR IMAGING, Issue 2 2007Alexis Jacquier Contrast Media and Molecular Imaging, MR imaging in assessing cardiovascular interventions and myocardial injury, Alexis Jacquier, Charles B. Higgins and Maythem Saeed, published in CMMI 2:1, DOI: 10.1002/cmmi122, pp1,15. Contract/Grant Sponsor information relating to Dr. A. Jacquier was absent from the published article. It should be noted that Dr. A. Jacquier was supported by the Société Française de Radiologie, Paris, as a research fellow. [source] MR imaging in assessing cardiovascular interventions and myocardial injuryCONTRAST MEDIA & MOLECULAR IMAGING, Issue 1 2007Alexis Jacquier Abstract Performing an MR-guided endovascular intervention requires (1) real-time tracking and guidance of catheters/guide wires to the target, (2) high-resolution images of the target and its surroundings in order to define the extent of the target, (3) performing a therapeutic procedure (delivery of stent or injection of gene or cells) and (4) evaluating the outcome of the therapeutic procedure. The combination of X-ray and MR imaging (XMR) in a single suite was designed for new interventional procedures. MR contrast media can be used to delineate myocardial infarcts and microvascular obstruction, thereby defining the target for local delivery of therapeutic agents under MR-guidance. Iron particles, or gadolinium- or dysprosium-chelates are mixed with the soluble injectates or stem cells in order to track intramyocardial delivery and distribution. Preliminary results show that genes encoded for vascular endothelial and fibroblast growth factor and cells are effective in promoting angiogenesis, arteriogenesis, perfusion and LV function. Angiogenic growth factors, genes and cells administered under MR-guided minimally invasive catheter-based procedures will open up new avenues in treating end-stage ischemic heart disease. The optimum dose of the therapeutic agents, delivery devices and real-time imaging techniques to guide the delivery are currently the subject of ongoing research. The aim of this review is to (1) provide an updated review of experiences using MR imaging to guide transcatheter therapy, (2) address the potential of cardiovascular magnetic resonance (MR) imaging and MR contrast media in assessing myocardial injury at a molecular level and labeling cells and (3) illustrate the applicability of the non-invasive MR imaging in the field of angiogenic therapies through recent clinical and experimental publications. Copyright © 2007 John Wiley & Sons, Ltd. [source] Elective coronary angioplasty with 60 s balloon inflation does not cause peroxidative injuryEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2002K. Cedro Abstract Background The aim of this study was to evaluate the ongoing controversial issue of whether ischemia/reperfusion during elective coronary angioplasty evokes myocardial peroxidative injury. Design We measured indicators of free radical damage to lipids (free malondialdehyde) and proteins (sulphydryl groups) in coronary sinus blood in 19 patients with stable angina who were undergoing elective angioplasty for isolated stenosis of the proximal left anterior descending coronary artery. Ischemia induced by 60 s balloon inflations was confirmed by lactate washout into coronary sinus after deflation, with immediate and 1 min samples. Peroxidative injury was assessed from washout of (a) malondialdehyde measured directly by high performance liquid chromatography and (b) reduced sulphydryl groups, inverse marker of protein oxidative stress. Results Mean lactate concentration immediately after each deflation increased by 120,150% of the initial value, confirming ischemia and showing that blood originated largely from the ischemic region. Lack of myocardial production of malondialdehyde was confirmed by (a) no arteriovenous differences in individual basal concentrations (aortic, range 0·33,12·03 nmol mL,1, mean 7·82; coronary sinus blood, range 0·52,15·82 nmol mL,1, mean 8·18), and (b) after deflations, mean concentrations were not significantly different from preocclusion value. There was no decrease in concentration of sulphydryl groups throughout angioplasty. Conclusion Elective coronary angioplasty with 60 s balloon inflations is a safe procedure that does not induce peroxidative myocardial injury as assessed by methods used in the present study. [source] Higher arteriovenous fistulae blood flows are associated with a lower level of dialysis-induced cardiac injuryHEMODIALYSIS INTERNATIONAL, Issue 4 2009Shvan KORSHEED Abstract Native arteriovenous fistulae (AVF) remain the vascular access of choice for hemodialysis (HD). Despite being associated with superior long-term outcomes (cf. catheter use), little is known about the systemic hemodynamic consequences of AVFs. Repetitive myocardial injury (myocardial stunning) is an under-recognized common consequence of HD. The aim of this study was to examine the impact of AVF flow (Qa) on dialysis-induced cardiac injury. We studied 50 chronic HD patients. All patients underwent echocardiography (and subsequent quantitative offline analysis) at baseline, during and post dialysis, to assess left ventricular function and the development of regional wall motion abnormalities. Qa was measured using ionic dialysance. Patients were divided into Qa tertiles (<500, mean 291±101 mL/min, 500,1000, mean 739±130 mL/min and >1000, mean 1265±221 mL/min). There were no significant differences between the groups in terms of age, sex, diabetes, or resting ejection fraction. Patients with Qa>1000 mL/min had a lower prevalence of left ventricular hypertrophy (55% vs. 76%, P=0.01). Dialysis-induced myocardial stunning (seen in 65% of the patients studied) was significantly and sequentially reduced in those patients with higher Qas. This was seen in a lower number of segments and ventricular regions developing regional wall motion abnormalities, as well as a significantly reduced mean and cumulative percentage reduction in fractional shortening of those ventricular segments affected (,187±37%, ,161±26%, and ,101±25%, respectively, P=0.04). Relatively higher AVF flows appear to be associated with a lower level of observed HD-induced cardiac injury. [source] Anti-ischemic effects of inotropic agents in experimental right ventricular infarctionACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2009M. HEIN Background: Right ventricular (RV) function is an important determinant of survival after myocardial infarction. The efficacy of reperfusion therapy might be increased by the cardioprotective action of inotropic agents, which are used for symptomatic therapy in situations with compromised hemodynamics. Therefore, we used a porcine model of RV ischemia and reperfusion (IR) injury to study the influence of milrinone, levosimendan and dobutamine on the extent and degree of myocardial injury. Methods: IR injury was induced by temporary ligation of the distal right coronary artery for 90 min, followed by 120 min of reperfusion. Treatment was initiated 30 min after coronary artery occlusion. A bolus of milrinone (n=12; 50 ,g/kg) and levosimendan (n=10; 24 ,g/kg) was applied in different groups, followed by continuous infusion of the drugs at 0.5 and 0.2 ,g/kg/min, respectively. The effects on myocardial injury and inflammation were compared with a control (n=12) and a dobutamine group (n=10), where treatment was started with an infusion of 5 ,g/kg/min. Results: Milrinone and levosimendan reduced the resulting infarct size with respect to the area at risk (41.7±10.2%, 45.7±8.1%) when compared with the control group (58.3±6.1%). In contrast, dobutamine had no effect (55.8±7.7%). All drugs reduced the number of neutrophils infiltrating into the different myocardial regions and the circulating levels of interleukin-6. Increased levels of tumor necrosis factor , during reperfusion were only abated by milrinone and levosimendan. Conclusions: Cardioprotective properties of milrinone and levosimendan were demonstrated for the first time in a clinically relevant model of RV infarction. [source] Perioperative myocardial infarction in noncardiac surgery: the diagnostic and prognostic role of cardiac troponinsJOURNAL OF INTERNAL MEDICINE, Issue 1 2002S. LUCREZIOTTI Abstract.,Lucreziotti S, Foroni C, Fiorentini C (Università degli Studi di Milano, Ospedale S. Pado, Milano, Italy). Perioperative myocardial infarction in noncardiac surgery: the diagnostic and prognostic role of cardiac troponins (Review). J Intern Med 2002; 252: 11,20. Despite the number of technologies used, the diagnosis of perioperative myocardial infarction is still a challenge. Studies conducted in surgical series have demonstrated that cardiac troponins (cTns) have both a superior diagnostic sensitivity and specificity, compared with other traditional techniques, and an independent power to predict short- and long-term prognosis. Nevertheless, some points need to be clarified. They include the usefulness of cTns in patients with end-stage renal failure; the standardization of the cTns cut-off for the diagnosis of myocardial injury; the timing of postoperative blood samplings; the cost-effectiveness of a screening in asymptomatic patients; and the possible therapeutic strategies. [source] Bacopa monniera protects rat heart against ischaemia,reperfusion injury: role of key apoptotic regulatory proteins and enzymesJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2010Ipseeta Ray Mohanty Abstract Objectives, Rat isolated hearts were perfused in a Langendorff model to study the cardioprotective effects of Bacopa monniera, a medicinal herb used in the Indian system of medicine, on cardiomyocyte apoptosis and antioxidant status following ischaemia,reperfusion (I-R) injury. Methods, Forty-eight rats were randomly divided into four groups (12 in each group): sham group (no ischaemia,reperfusion injury), B. monniera control group (orally fed B. monniera at a dose of 75 mg/kg, for three weeks); ischaemia,reperfusion control group(subjected to ischaemia,reperfusion-induced myocardial injury) and B. monniera -treated group (same protocol as ischaemia,reperfusion control group except that rats also fed B. monniera). Key findings, Post-ischaemic reperfusion injury resulted in significant cardiac necrosis, apoptosis, depression of heart rate, decline in antioxidant status and elevation in lipid peroxidation. Oral administration of B. monniera per se for three weeks to healthy rats caused augmentation of myocardial antioxidants, superoxide dismutase, catalase and glutathione, along with induction of heat shock protein 72 (HSP72). Ischaemia,reperfusion-induced biochemical and histopathological perturbations were significantly prevented by B. monniera (75 mg/kg) pre-treatment. Interestingly, B. monniera also restored the antioxidant network of the myocardium and reduced myocardial apoptosis, caspase 3 and Bax protein expression. Conclusions, Histopathological studies and myocardial creatine phosphokinase content further confirmed the cardioprotective effects of B. monniera (75 mg/kg) in the experimental model of ischaemia,reperfusion injury. The study provides scientific basis for the putative therapeutic effect of B. monniera in ischaemic heart disease. [source] Protective effects of melatonin against myocardial injury induced by isoproterenol in ratsJOURNAL OF PINEAL RESEARCH, Issue 2 2003Mahmut Acikel Abstract: This study was performed to determine whether melatonin could have a protective effect against myocardial injury (MI) induced by isoproterenol (ISO) in rats. Twenty-four rats were divided into three treatment groups: (1) control (n = 8): saline solution. (2) ISO (n = 8): ISO only. (3) melatonin + ISO (n = 8). Melatonin (10 mg/kg/day, i.p.) was administered 30 min before the initiation of ISO (150 mg/kg/day, s.c.). Drugs and saline were given at 14:00 hr for two consecutive days. At the end of the second day, blood samples were taken from the abdominal aorta shortly after the rats were anesthetized for the purpose of measuring cardiac troponins T (cTnT) and I (cTnI); hearts were removed, preserved and examined microscopically. Additionally, based on the histological changes in myocardial tissue, the rats were divided into three groups: no change, mild changes and moderate and/or marked changes. The mean cTnT and cTnI values were significantly increased in ISO group compared with control group [(1.29 ± 0.22 ng/mL versus 0.46 ± 0.07 ng/mL, P < 0.0001) and (0.56 ± 0.11 ng/mL versus 0.21 ± 0.01 ng/mL, P < 0.001)], respectively, and were significantly reduced in the ISO + melatonin group (0.65 ± 0.06 ng/mL for cTnT and 0.25 ± 0.01 ng/mL for cTnI) compared with the ISO only group (P < 0.01), respectively. cTnT and cTnI values were significantly increased in rats with moderate and/or marked cardiac changes compared with hearts where there were mild changes and no change (P < 0.05). ISO + melatonin group showed less histological changes than the ISO group (P < 0.01). In conclusion, this study revealed a protective effect of melatonin against ISO-induced MI in rats, and its potential clinical application in the treatment of MI. [source] Myocardial perforation by a stick foreign body in a dogJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2008Augusta Pelosi DVM, DACVS Abstract Objective: To report a case of myocardial perforation by a stick foreign body in a dog. Case Summary: A 3-year-old castrated male Labrador Retriever was examined because of a puncture wound seen after an unsupervised run in the woods. The wound was suspected to penetrate into the thoracic cavity on the basis of physical exam and radiographs. Uniform ventricular premature complexes (VPCs) and junctional beats were noted on electrocardiogram (ECG). Thoracotomy was performed and a 6-cm wooden stick was seen protruding from the right ventricle through the pericardium toward the sternum. The stick was removed while purse string sutures were tied around the resultant myocardial defect. Follow-up echocardiography revealed intact intracardiac structures. VPCs were treated with lidocaine and resolved completely within 24 hours of presentation. New or Unique Information Provided: Thoracic trauma can result in myocardial injury; penetration into the myocardium represents a life-threatening situation for the emergency clinician. Cardiac injury should be included in the differential diagnoses of penetrating thoracic foreign bodies. [source] BIOCHEMICAL MARKERS OF CARDIAC INJURY IN NORMAL AND SURVIVING VERSUS NON-SURVIVING SEPTICEMIC NEONATAL FOALSJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue S1 2004SF Peek Although myocardial injury can be a significant component of multiple organ dysfunction (MODS) in association with septicemia in critically ill human patients, it is as yet an undefined clinical entity in equine septicemia. With septicemia as the leading cause of death in neonatal foals, a better understanding of the pathophysiology, diagnosis and treatment of MODS will be important in further improving survival rates. We designed a prospective study to establish normal ranges for cardiac troponin I (cTnI), T (cTnT) and CKMB mass in healthy 24,48 hour old foals, as well as septicemic neonatal foals seen over a 2-year period in a teaching hospital. We also performed a comparison of these biomarkers in surviving and non-surviving septicemic foals. Sepsis was judged on the basis of the presence of any of the 3 following criteria: blood culture positive at admission, admission sepsis score ,11, or 3 or more sites of infection during hospitalization in foals ,14 days of age. cTnI was measured by the ACCESS® (Beckman Coulter), cTnT was measured using the Elecsys 2010® Immunoassay (Roche), and CKMB mass measurements were performed using the Elecsys 2010®. Each parameter was described using range and 95th and 50th percentile. Comparisons were made for each parameter between normal and septic foals as well as surviving and non-surviving septic foals using the non-parametric Wilcoxon's rank sum test. Significance was set at p<0.05. There were 52 control foals and 38 septic foals of which 22 survived. Significant differences were documented for CKMB between septicemic and normal foals, but not for cTnT or cTnI. However, CKMB and cTnT were significantly lower in surviving versus non-surviving septicemic foals. The 50th and 95th percentiles alongside the ranges for the normal foal population were 0.14, 0.49, (0.01,0.51) ,g/L for cTnI, 0.009, 0.03, (0.009,0.04) ,g/L for cTnT and 2.3, 7.4, (0.4,9.3) ,g/L for CKMB. Our findings suggest that myocardial injury is a component of MODS during septicemia in foals, and that quantitatively significant increases in CKMB and cTnT are seen in non-surviving septicemic foals versus survivors. [source] Serum Cardiac Troponin I Concentration in Dogs with EhrlichiosisJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008P.P.V.P. Diniz Background: Ehrlichiosis is a multisystemic disease with the potential to cause cardiomyocyte injury in naturally infected dogs. Hypothesis: Myocardial injury occurs in dogs infected with Ehrlichia canis. Animals: One-hundred and ninety-four dogs from Brazil with clinical and laboratory abnormalities indicative of ehrlichiosis. Sixteen healthy dogs served as controls. Methods: Electrocardiogram, echocardiogram, noninvasive blood pressure measurement, and serum cardiac troponin I (cTnI) concentrations were evaluated. Serologic assays and PCR determined the exposure and infection status for E. canis, Anaplasma spp., Babesia canis vogeli, Bartonella spp., Borrelia burgdorferi, Dirofilaria immitis, Ehrlichia chaffeensis, Ehrlichia ewingii, Leishmania chagasi, and spotted-fever group Rickettsia. Dogs were assigned to groups according to PCR status: E. canis infected, infected with other vector-borne organisms, sick dogs lacking PCR evidence for infection, and healthy controls. Results: E. canis -infected dogs had higher serum cTnI concentrations than controls (median: 0.04 ng/dL; range 0.04,9.12 ng/dL; control median: 0.04 ng/dL; range: 0.04,0.10 ng/dL; P= .012), and acute E. canis infection was associated with myocardial injury (odds ratio [OR]: 2.67, confidence interval [CI] 95%: 1.12,6.40, P= .027). Severity of anemia was correlated with increased risk of cardiomyocyte damage (r= 0.84, P < .001). Dogs with clinical signs of systemic inflammatory response syndrome (SIRS) were at higher risk for myocardial injury than were other sick dogs (OR: 2.55, CI 95%: 1.31,4.95, P= .005). Conclusions and Clinical Importance: Acute infection with E. canis is a risk factor for myocardial injury in naturally infected Brazilian dogs. Severity of anemia and SIRS might contribute to the pathophysiology of myocardial damage. [source] Cardiac Troponin I in Pastured and Race-Training Thoroughbred HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2003Wade Phillips Cardiac troponin I (cTnI), a myocardial polypeptide, is a highly sensitive and specific biomarker of myocardial injury in people and dogs. The structure of cTnI is highly conserved across species, and equine myocardium has high reactivity with human immunoassays. The purpose of this study was to describe cTnI concentrations in normal pastured and race-training Thoroughbred horses. Ten horses on pasture and 10 horses in race training were studied. Horses were considered normal on the basis of physical examination, training performance, electrocardiography (ECG), and echocardiography. Serum cTnI concentrations were determined with a colorimetric immunoassay. The assay has an analytical sensitivity of 0.04 ng/mL. Serum cTnI concentrations in race-training horses were not significantly different from those of pastured horses. When groups were combined, mean cTnI concentration (±SD) was 0.047 ± 0.085 ng/mL, and the median was 0 (range, 0-0.35 ng/mL). The 90th percentile for both groups combined was 0.11 ng/mL. This study establishes a preliminary reference range for serum cTnI in normal Thoroughbred horses. Key words: Cardiac disease; Cardiac markers; Creatine kinase; Myocarditis. [source] EPR oximetry in the beating heart: Myocardial oxygen consumption rate as an index of postischemic recoveryMAGNETIC RESONANCE IN MEDICINE, Issue 4 2004Govindasamy Ilangovan Abstract Oxygen plays a critical role in the pathophysiology of myocardial injury during both ischemia and subsequent reperfusion (I/R). Thus, oxygen concentration is an important variable to measure during I/R. In the present work, electron paramagnetic resonance (EPR)-based oximetry was used to measure the oxygen concentration during a series of I/R episodes and oxygenation levels were correlated with the contractile and hemodynamic functions of the heart. A custom-developed electronically tunable surface coil resonator working at 1.1 GHz was used to determine tissue pO2 in the beating heart. Microcrystalline particulate of lithium phthalocyanine was used as an EPR oximetry probe. Isolated and perfused rat hearts were subjected to 1 or 3 hr durations of preischemic perfusion, followed by 15-min I/R cycles. In hearts perfused for 3 hr prior to 15-min I/R cycles, the myocardial pO2 decreased gradually on subsequent reperfusions of three successive I/R cycles. However, in hearts perfused for 1 hr there was almost 100% recovery of myocardial pO2 in all three I/R cycles. The extent of oxygenation recovered in each reperfusion cycle correlated with the recovery of hemodynamic and contractile function. The results also showed that the oxygen consumption rate of the heart at the end of each I/R episode decreased in direct proportion to the functional recovery. In summary, it was observed that the amount of myocardial oxygen consumption during I/R could provide a reliable index of functional impairment in the heart. Magn Reson Med 51:835,842, 2004. © 2004 Wiley-Liss, Inc. [source] Mapping ischemic risk region and necrosis in the isolated heart using EPR imagingMAGNETIC RESONANCE IN MEDICINE, Issue 6 2003Murugesan Velayutham Abstract Reperfusion of ischemic tissue is a common event in the treatment of heart attack and stroke. To study disease pathogenesis, methods are required to measure tissue perfusion and area at risk, as well as localized regions of injury. While histology can provide this information, its destructive nature precludes assessment of time course. Thus, there is a critical need for a noninvasive technique to obtain this information. To map myocardial redox state as a possible index of cellular ischemia and viability, electron paramagnetic resonance (EPR) imaging experiments were performed on isolated rat hearts before and after the onset of regional ischemia using nitroxide spin labels. With coronary artery occlusion, the EPR images clearly showed the risk region as a void of lower intensity that reversed upon reperfusion. The extent of risk region in the heart was similar in EPR imaging and histological measurements. The unique information obtained regarding the time course of changes in redox metabolism of the risk region and normal myocardium can provide important insights regarding the mechanisms of myocardial injury during and following ischemia. Magn Reson Med 49:1181,1187, 2003. © 2003 Wiley-Liss, Inc. [source] Review: Neutrophil gelatinase-associated lipocalin: A troponin-like biomarker for human acute kidney injuryNEPHROLOGY, Issue 4 2010PRASAD DEVARAJAN ABSTRACT Acute kidney injury (AKI) is a common and serious condition, the diagnosis of which currently depends on functional markers such as serum creatinine measurements. Unfortunately, creatinine is a delayed and unreliable indicator of AKI. The lack of early biomarkers of structural kidney injury (akin to troponin in acute myocardial injury) has hampered our ability to translate promising experimental therapies to human AKI. Fortunately, understanding the early stress response of the kidney to acute injuries has revealed a number of potential biomarkers. The discovery, translation and validation of neutrophil gelatinase-associated lipocalin (NGAL), possibly the most promising novel AKI biomarker, is reviewed. NGAL is emerging as an excellent stand-alone troponin-like structural biomarker in the plasma and urine for the early diagnosis of AKI, and for the prediction of clinical outcomes such as dialysis requirement and mortality in several common clinical scenarios. The approach of using NGAL as a trigger to initiate and monitor therapies for AKI, and as a safety biomarker when using potentially nephrotoxic agents, is also promising. In addition, it is hoped that the use of sensitive and specific biomarkers such as NGAL as endpoints in clinical trials will result in a reduction in required sample sizes, and hence the cost incurred. Furthermore, predictive biomarkers like NGAL may play a critical role in expediting the drug development process. However, given the complexity of AKI, additional biomarkers (perhaps a panel of plasma and urinary biomarkers) may eventually need to be developed and validated for optimal progress to occur. [source] The Ischemia-Modified Albumin in Relation to Pacemaker and Defibrillator ImplantationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2008EFTIHIA SBAROUNI M.D. Background: Ischemia-modified albumin (IMA) is considered a marker of myocardial ischemia whereas cardiac enzymes are released when cardiac necrosis occurs. It has previously been shown that permanent pacemaker-defibrillator insertion is associated with myocardial injury expressed as cardiac enzyme rise. Objective: We assessed whether pacemaker-defibrillator implantation also induces changes in IMA plasma levels and whether, therefore, myocardial ischemia precedes necrosis. Methods: We studied 64 consecutive patients undergoing pacemaker or defibrillator implantation; 43 were men and 21 women and their age was 70 ± 11 years (range 23,84 years). Blood samples were collected at baseline, six hours and 48 hours following the procedure. IMA measured by the albumin cobalt binding test (ACB, Integra 800 analyzer), as well as creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB) and cardiac troponin I (Tn-I) were evaluated. Results: Data analysis showed that compared to baseline measurements, IMA increased at six hours (P = 0.015) and at 48 hours (P = 0.003)[97.6 ± 10.2 vs 101.4 ± 10.7 vs 102.1 ± 9.2 U/mL at baseline, six hours and 48 hours, respectively]; similarly, CK increased at six hours (P = 0.0001) and remained high at 48 hours (P = 0.0001) [74.9 ± 49.9 vs 136.1±186.7 vs 115.2 ± 63.9 mIU/mL], while CK-MB increased at six hours (P = 0.0001), but returned to baseline values at 48 hours (P = 0.05) [0.90 ± 0.89 vs 1.27 ± 134 vs 0.71 ± 0.63 ng/mL] and Tn-I increased at six hours (P = 0.0001) and returned to baseline levels at 48 hours (P = 0.32) [0.057 ± 0.23 vs 0.16 ± 0.36 vs 0.03 ± 0.045 ng/mL]. Conclusion: Permanent pacemaker-defibrillator insertion is associated with myocardial ischemia and necrosis. [source] Effect of Transvenous Cardiac Resynchronization Therapy Device Implantation on Cardiac Troponin I ReleasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2007TIMUCIN ALTIN M.D. Background: Pacemaker and implantable cardioverter defibrillator (ICD) implantation increases cardiac troponin I (cTnI) levels which indicates myocardial injury. During implantation of a cardiac resynchronization therapy (CRT) device, balloon inflation for coronary sinus (CS) venogram, cannulation of CS side branch, and electrode advancement may interfere with CS drainage and, hence, may decrease the washout of toxic metabolites from the heart. Thus, CRT implantation may further increase cTnI levels. In this study, we investigated the effects of CRT implantation on cTnI release. Methods: We included 10 patients (mean age = 57 ± 15 years) in whom a successful transvenous CRT system was implanted (CRT group). Twenty patients (mean age = 65 ± 10 years) who underwent a transvenous pacemaker or ICD implantation were included as the control group. Blood samples for cTnI were drawn at baseline and at six, 12, 18, and 24 hours thereafter. Results: Baseline median cTnI levels were similar in CRT and control groups (0.03 ng/mL vs 0.02 ng/mL, respectively; P = 0.1). Postoperative cTnI levels during 24 hours were significantly higher in the CRT group (P < 0.05) by two-way repeated measures of analyis of variance. Post hoc analysis revealed that cTnI levels were higher at the 6th, 12th, 18th, and 24th hours compared to baseline levels (P < 0.001, P < 0.001, P < 0.01, and P < 0.01, respectively). There was a significant difference in the area under the curves (AUCs) of cTnI measurements (1.79 hr·ng/mL in the CRT group and 0.78 hr·ng/mL in the control group, P < 0.05). Conclusion: Postoperative cTnI levels were higher after CRT implantation than simple pacemaker/ICD implantation. This may be due to CS manipulation during CRT implantation. [source] Bone marrow stem cells regenerate infarcted myocardiumPEDIATRIC TRANSPLANTATION, Issue 2003Donald Orlic Abstract: Heart disease is the leading cause of death in the United States for both men and women. Nearly 50% of all cardiovascular deaths result from coronary artery disease. Occlusion of the left coronary artery leads to ischemia, infarction, necrosis of the affected myocardial tissue followed by scar formation and loss of function. Although myocytes in the surviving myocardium undergo hypertrophy and cell division occurs in the border area of the dead tissue, myocardial infarcts do not regenerate and eventually result in the death of the individual. Numerous attempts have been made to repair damaged myocardium in animal models and in humans. Bone marrow stem cells (BMSC) retain the ability throughout adult life to self-renew and differentiate into cells of all blood lineages. These adult BMSC have recently been shown to have the capacity to differentiate into multiple specific cell types in tissues other than bone marrow. Our research is focused on the capacity of BMSC to form new cardiac myocytes and coronary vessels following an induced myocardial infarct in adult mice. In this paper we will review the data we have previously published from studies on the regenerative capacity of BMSC in acute ischemic myocardial injury. In one experiment donor BMSC were injected directly into the healthy myocardium adjacent to the injured area of the left ventricle. In the second experiment, mice were treated with cytokines to mobilize their BMSC into the circulation on the theory that the stem cells would traffic to the myocardial infarct. In both experimental protocols, the BMSC gave rise to new cardiac myocytes and coronary blood vessels. This BMSC-derived myocardial regeneration resulted in improved cardiac function and survival. [source] Protective effect of Lycium barbarum on doxorubicin-induced cardiotoxicityPHYTOTHERAPY RESEARCH, Issue 11 2007Yan-Fei Xin Abstract The objective of this work was to explore the hypothesis that Lycium barbarum (LB) may be protective against doxorubicin (DOX)-induced cardiotoxicity through antioxidant-mediated mechanisms. Male SD rats were treated with distilled water or a water extract of LB (25 mg/kg, p.o.) daily and saline or DOX (5 mg/kg, i.v.) weekly for 3 weeks. Mortality, general condition and body weight were observed during the experiment. DOX-induced cardiotoxicity was assessed by electrocardiograph, heart antioxidant activity, serum levels of creatine kinase (CK) and aspartate aminotransferase (AST) and histopathological change. The DOX group showed higher mortality (38%) and worse physical characterization. Moreover, DOX caused myocardial injury manifested by arrhythmias and conduction abnormalities in ECG (increased QT and ST intervals and ST elevation), a decrease of heart antioxidant activity, an increase of serum CK and AST, as well as myocardial lesions. Pretreatment with LB significantly prevented the loss of myofibrils and improved the heart function of the DOX-treated rats as evidenced from lower mortality (13%), normalization of antioxidative activity and serum AST and CK, as well as improving arrhythmias and conduction abnormalities. These results suggested that LB elicited a typical cardioprotective effect on DOX-related oxidative stress. Furthermore, in vitro cytotoxic study showed the antitumor activity of DOX was not compromised by LB. It is possible that LB could be used as a useful adjunct in combination with DOX chemotherapy. Copyright © 2007 John Wiley & Sons, Ltd. [source] Proteomic insights into cardiac cell death and survivalPROTEOMICS - CLINICAL APPLICATIONS, Issue 6 2008W. Robb MacLellan Abstract Cardiovascular disease is the leading cause of death and disability in the developed world. To design novel therapeutic strategies to treat and prevent this disease, better understanding of cardiac cell function is necessary. In addition to (and, indeed, in combination with) genetics, physiology and molecular biology, proteomics plays a critical role in our understanding of cardiovascular systems at multiple scales. The purpose of this review is to examine recent developments in the field of myocardial injury and protection, examining how proteomics has informed investigations into organelles, signaling complexes, and cardiac phenotype. [source] Cardiac Allograft Hypertrophy: A New Target for Therapy, a Surrogate Marker for Survival?AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2009G. Torre-Amione Long-term heart transplant survival may not simply be limited by allograft vasculopathy, but also by diffuse myocardial injury in form of left ventricular hypertrophy. See also article by Raichlin et al in this issue on page 132. [source] Procyanidins Produce Significant Attenuation of Doxorubicin-Induced Cardiotoxicity via Suppression of Oxidative StressBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2009Wei Li The major side effect of doxorubicin is oxidative injury-related cardiotoxicity, which has dramatically hindered its usage. Procyanidins from grape seeds are potent free radical scavengers that have been shown to protect against anthracycline-induced cardiotoxicity. In the present study, we tested whether procyanidins would prevent the doxorubicin-induced cardiotoxicity in rats. Rats were intraperitoneally treated with doxorubicin at a cumulative dose of 15 mg/kg with and without pre-administration of procyanidins. Our data showed that doxorubicin led to cardiac function deterioration, myocardial injury and increased oxidative stress in cardiac tissues. The cardiac function deterioration by doxorubicin included increased QT-interval and ST-interval in electrocardiograph (ECG) and decreased left ventricular developed pressure. Doxorubicin-induced myocardial injury was shown by the increased creatine kinase, alanine aminotransferase and aspartate aminotransferase in serum as well as in myocardial lesions. Pretreatment with procyanidin (150 mg/kg daily) effectively hindered the adverse effects of doxorubicin, such as myocardial injury and impaired heart function. Procyanidin pretreatment attenuated cytoplasmic vacuolization, increased left ventricular developed pressure and improved the ECG. The cardioprotective effect of procyanidin corresponded to the decrease of lipid peroxidation and the increase of cardiac antioxidant potency in doxorubicin-treated rats that were also given procyanidin. An in vitro cytotoxic study showed that procyanidins did not attenuate the antineoplastic activity of doxorubicin to A549 adenocarcinoma cells. All the above lines of evidence suggest that procyanidins protect cardiomyocytes from doxorubicin-induced cardiotoxicity via suppression of oxidative stress. [source] Cardiac troponin I predicts outcome after ruptured abdominal aortic aneurysm repairBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2005A. L. Tambyraja Background: Cardiac troponin I (cTnI) is a highly sensitive and specific marker for myocardial injury that predicts mortality in patients with acute coronary syndromes. This study examined the relationship between perioperative cTnI levels and clinical outcome in patients with ruptured abdominal aortic aneurysm (AAA). Methods: Consecutive patients who underwent operative repair of a ruptured AAA over a 22-month interval and survived for more than 24 h were entered into a prospective observational cohort study. Levels of cTnI were measured immediately before, and at 24 and 48 h after surgery, and related to clinical outcome. Results: Of 62 patients who underwent attempted operative repair of ruptured AAA, 50 (81 per cent) survived for more than 24 h and were included in this study. Twenty-three (46 per cent) of the 50 had a detectable cTnI level at one or more time points during the first 48 h. Of these, 11 patients had clinical or electrocardiographic evidence of an acute cardiac event and 12 did not; five patients in each of these two groups died. Of 27 patients with no increase in cTnI in the first 48 h, only three died (P = 0·031 and P = 0·043 respectively, relative to the groups with detectable cTnI). Conclusion: Approximately half of patients who survived repair of ruptured AAA for more than 24 h sustained a detectable myocardial injury within the first 48 h. A perioperative increase in the level of cTnI, with or without clinically apparent cardiac dysfunction, was associated with postoperative death. Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] The impact of micro troponin leak on long-term outcomes following elective percutaneous coronary intervention,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 6 2009Richard V. Milani MD Abstract Objective: To evaluate the clinical impact of microleaks of troponin, which are below the reference standard defining troponin elevation, on cardiovascular outcomes in stable coronary patients undergoing elective percutaneous coronary intervention (PCI). Background: Troponin elevation, either pre- or post-PCI, has been shown to predict poor cardiovascular outcomes. However, troponin measurements that are above the limit of detection but below the 99th percentile limit defining elevation ("microleak") have uncertain clinical significance. Methods: We assessed subsequent myocardial infarction (MI) and death over a mean follow-up of 4.2 years in 2,272 patients undergoing elective PCI, where baseline troponins were normal and follow-up troponins were obtained 12,24 hr post-PCI. Patients were divided into three groups based on post-PCI troponin levels: Group 1 (n = 1,313) nondetectable; group 2 (n = 587) microleak, and group 3 (n = 372) elevated suggesting myocardial necrosis. Results: The combined endpoint of MI and death was similar in groups 2 and 3 (50.3 vs. 51.9%, respectively, P = NS), which was significantly more than group 1 patients (35.6%, P < 0.01) over the follow-up period. Multivariate analysis of patients in groups 1 and 2 demonstrated that troponin microleak was an independent predictor of MI and death (P = 0.01). Conclusions: Microleak of troponin following elective PCI suggests myocardial injury and predicts an increased risk of subsequent MI and death. Troponins should be routinely assessed following PCI, and preventive therapies are needed to reduce micro and macro troponin elevation in the PCI setting. © 2009 Wiley-Liss, Inc. [source] Myocardial cell injury is common in children with septic shockACTA PAEDIATRICA, Issue 3 2009Rakesh Lodha Abstract Objective: To determine the prevalence of myocardial cell injury in children with septic shock by estimating the levels of biochemical markers of myocardial injury, troponin I (TnI) and creatine kinase MB (CK-MB). Patients: Children aged 3 months to 16 years were admitted to paediatric intensive care unit (PICU) with septic shock. Children with sepsis without shock and children with hypovolaemic shock were enrolled as controls. Measurements and Main Results: Serum TnI and CK-MB levels were measured at admission and serially at 24 h, 48 h and 96 h in children with septic shock, while baseline measurement of the same markers was taken from the controls. In total, 88% (15/18) of children with septic shock had elevated TnI levels compared with 25% (5/20) with sepsis and 6.7% (1/15) with hypovolaemic shock (p < 0.001). Serial TnI levels at admission, 24 h, 48 h and 96 h were higher in the nonsurvivors. There was a positive correlation between the baseline TnI levels and the predicted mortality using the paediatric index of mortality (PIM2) scores at admission (r = 0.51, p = 0.03). Conclusion: A majority of children with septic shock have evidence of myocardial cell injury. The estimation of serum TnI levels may help in better prognostication of children with septic shock. [source] Prophylactic Implantation of Cardioverter Defibrillators in Idiopathic Nonischemic Cardiomyopathy for the Primary Prevention of Death: A Narrative ReviewCLINICAL CARDIOLOGY, Issue 5 2010Cihan Cevik MD, FESC Implantable cardioverter defibrillator (ICD) therapy reduces sudden cardiac death rates and reduces mortality in patients with ischemic heart disease and low ejection fractions. One-third of the deaths in patients with nonischemic cardiomyopathy are sudden. However, the efficacy of ICDs in the primary prevention of death in these patients is less clear. The most common cause of mortality in patients treated with ICDs is heart failure progression. ICD shocks can cause direct myocardial injury, fibrosis, inflammation, and adverse psychological outcomes, and these changes may contribute to the ventricular dysfunction in patients who already have a significantly depressed ejection fraction. We have reviewed the published randomized controlled trials and meta-analysis of prophylactic ICD therapy in the primary prevention of death in patients with nonischemic cardiomyopathy. The individual randomized controlled trials do not report a statistically significant reduction of mortality unless the ICD treatment is added to cardiac resynchronization therapy, but the meta-analysis did show a significant mortality reduction and favored ICD therapy in these patients. Medical management of many study participants was suboptimal, at least based on current guidelines. The patients with non-ischemic cardiomyopathy have good outcomes with medical therapy, and ICD therapy in this relatively low-risk population needs better selection criteria. Copyright © 2010 Wiley Periodicals, Inc. [source] | ||||||||||||||||||||||||||||||||||