Myocardial Damage (myocardial + damage)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


The ARMYDA trials (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) at Campus Bio-Medico University: rationale, results and future horizons

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 2007
Germano Di Sciascio
Abstract Myocardial protection by atorvastation pretreatment was found in several trials applied to percutaneous coronary intervention by the ARMYDA study group. This article reviews those studies and explores future avenues. [source]


Continuous Coronary Sinus Perfusion Reverses Ongoing Myocardial Damage in Acute Ischemia

ARTIFICIAL ORGANS, Issue 10 2009
Francesco Onorati
Abstract Acute cardiogenic shock or cardiac arrest (CS/CA) before cardiopulmonary bypass (CPB) installation are life-threatening events in acute coronary syndromes. We evaluated whether continuous retrograde warm-blood perfusion (CRWBP) before aortic cross-clamping (ACC), with immediate CPB installation may improve hospital results in these dreadful events. Hospital outcome of 18 coronary artery bypass grafting (CABG) (Group A) with CS/CA before CPB, with immediate CPB installation and CRWBP, has been compared with 24 CABG (Group B) with CS/CA undergoing only immediate CPB installation. No differences have been detected in the mean time to establish CPB (P = 0.655). Electrocardiography normalized in a significantly higher number of CRWBP (P = 0.0001). Group B showed longer CPB (116.2 ± 21.2 min vs. 157.8 ± 32.4; P = 0.0001) and postoperative intra-aortic balloon pumping time course (36.2 ± 5.9 h vs. 77.8 ± 13.2; P = 0.0001). CRWBP reduced postoperative acute myocardial infarction (P = 0.004) and damage (P = 0.033), death (P = 0.026), and need for high inotropic support (0% vs. 37.5%; P = 0.003). Troponin I was significantly lower in Group A (P = 0.013 from coronary sinus; P , 0.0001 at 12, 24, and 48 h postoperatively; P = 0.008 at 72 h), never reaching values suggestive of acute myocardial infarction. Group A had also lower lactate release from aortic declamping to 48 h postoperatively (P , 0.0001). CRWBP improved postoperative left ventricular ejection fraction (EF) (P = 0.017) and wall motion score index (P = 0.041), whereas Group B showed a significant worsening of EF (P = 0.0001) and wall motion score index (P = 0.002). Patients in Group A had shorter intubation time (P = 0.0001), intensive therapy unit (ITU) stay (P = 0.001), and hospital stay (P = 0.0001). CRWBP reverses myocardial damage in patients with CS/CA during acute coronary syndromes, adding a straightforward benefit to hospital survival. [source]


Predictors of cardiac events in high-risk patients undergoing emergency surgery

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
A. OSCARSSON
Background: The aim of this study was to determine the incidence of myocardial damage and left ventricular myocardial dysfunction and their influence on outcome in high-risk patients undergoing non-elective surgery. Methods: In this prospective observational study, 211 patients with American Society of Anesthesiologists classification III or IV undergoing emergent or urgent surgery were included. Troponin I (TnI) was measured pre-operatively, 12 and 48 h post-operatively. Pre-operative N-terminal fragment of B-type natriuretic peptide (NT-proBNP), as a marker for left ventricular systolic dysfunction, was analyzed. The diagnostic thresholds were set to TnI >0.06 ,g/l and NT-proBNP >1800 pg/ml, respectively. Post-operative major adverse cardiac events (MACE), 30-day and 3-months mortality were recorded. Results: Elevated TnI levels were detected in 33% of the patients post-operatively. A TnI elevation increased the risk of MACE (35% vs. 3% in patients with normal TnI levels, P<0.001) and 30-day mortality (23% vs. 7%, P=0.003). Increased concentrations of NT-proBNP were seen in 59% of the patients. Elevated NT-proBNP was an independent predictor of myocardial damage post-operatively, odds ratio, 6.2 [95% confidence interval (CI) 2.1,18.0] and resulted in an increased risk of MACE (21% vs. 2.5% in patients with NT-proBNP ,1800 pg/ml, P<0.001). Conclusion: Myocardial damage is common in a high-risk population undergoing unscheduled surgery. These results suggest a close correlation between myocardial damage in the post-operative period and increased concentration of NT-proBNP before surgery. The combinations of TnI and NT-proBNP are reliable markers for monitoring patients at risk in the peri-operative period as well as useful tools in our risk assessment pre-operatively in emergency surgery. [source]


Serum Cardiac Troponin I Concentration in Dogs with Precapillary and Postcapillary Pulmonary Hypertension

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010
C. Guglielmini
Background: Pulmonary hypertension (PH) is a disease condition leading to right-sided cardiac hypertrophy and, eventually, right-sided heart failure. Cardiac troponin I (cTnI) is a circulating biomarker of cardiac damage. Hypothesis: Myocardial damage can occur in dogs with precapillary and postcapillary PH. Animals: One hundred and thirty-three dogs were examined: 26 healthy controls, 42 dogs with mitral valve disease (MVD) without PH, 48 dogs with pulmonary hypertension associated with mitral valve disease (PH-MVD), and 17 dogs with precapillary PH. Methods: Prospective, observational study. Serum cTnI concentration was measured with a commercially available immunoassay and results were compared between groups. Results: Median cTnI was 0.10 ng/mL (range 0.10,0.17 ng/mL) in healthy dogs. Compared with the healthy population, median serum cTnI concentration was increased in dogs with precapillary PH (0.25 ng/mL; range 0.10,1.9 ng/mL; P < .001) and in dogs with PH-MVD (0.21 ng/mL; range 0.10,2.10 ng/mL; P < .001). Median serum cTnI concentration of dogs with MVD (0.12 ng/mL; range 0.10,1.00 ng/mL) was not significantly different compared with control group and dogs with PH-MVD. In dogs with MVD and PH-MVD, only the subgroup with decompensated PH-MVD had significantly higher cTnI concentration compared with dogs with compensated MVD and PH-MVD. Serum cTnI concentration showed significant modest positive correlations with the calculated pulmonary artery systolic pressure in dogs with PH and some echocardiographic indices in dogs with MVD and PH-MVD. Conclusions and Clinical Importance: Serum cTnI is high in dogs with either precapillary and postcapillary PH. Myocardial damage in dogs with postcapillary PH is likely the consequence of increased severity of MVD. [source]


Pharmacodynamic interaction of captopril with garlic in isoproterenol-induced myocardial damage in rat

PHYTOTHERAPY RESEARCH, Issue 5 2010
Syed Mohammed Basheeruddin Asdaq
Abstract It is known that various preparations of garlic and angiotensin-converting enzyme (ACE) inhibitor such as captopril (CAP) have beneficial effects on the left ventricular function and cardiovascular events after myocardial infarction (MI) when used individually. There is no reported interaction between garlic homogenate (GH) and CAP during and after acute MI. Thus the purpose of the current study was to evaluate the possible pharmacodynamic interaction of GH with CAP on isoproterenol (ISO)-induced myocardial damage in rat. Female Wistar albino rats were treated with GH at three different doses of 125; 250 and 500,mg/kg orally for 30 days and CAP (30,mg/kg, p.o.) was incorporated in the interactive groups during the last seven days of GH treatment. Myocardial damage was induced by administration of ISO (150,mg/kg, s.c.) for two consecutive days. Biochemical parameters were studied in serum and heart tissue homogenate of all animals. The GH 250,mg/kg was found to dislodge the effect of ISO on superoxide dismutase and catalase and retained the activities of LDH and CK-MB. Incorporation of CAP during GH treatment provided further protection to myocardium from injury. However, higher dose of GH alone or with CAP failed to prevent damaging effect of ISO. Histopathological determinations confirmed biochemical findings. Thus it is concluded that the combination needs to be used carefully when garlic is consumed at high doses. Copyright © 2009 John Wiley & Sons, Ltd. [source]


High serum cardiac troponin T concentrations in preterm infants with respiratory distress syndrome,

ACTA PAEDIATRICA, Issue 9 2000
D 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]


Ischaemic preconditioning is related to decreasing levels of extracellular adenosine that may be metabolically useful in the at-risk myocardium: an experimental study in the pig

ACTA PHYSIOLOGICA, Issue 1 2010
A. Waldenström
Abstract Aim:, ,Pre-treatment' with short repetitive periods of ischaemia (ischaemic preconditioning) has proved to be a powerful mechanism for modification of the extent of myocardial damage following acute coronary artery occlusion. The exact mechanism of protection induced by ischaemic preconditioning is not known. We herewith put forward a contributing component for protection with preconditioning involving a shift in the adenylate kinase (AK) equilibrium reaction in favour of adenosine triphosphate (ATP) formation. Methods:, A coronary artery was occluded in anaesthetized thoracotomized pigs to induce ischaemic preconditioning as well as a longer period of ischaemia. Microdialysis probes were inserted in ischaemic and control myocardium and were infused with 14C- adenosine with two different specific activities. 14C-lactate was identified and measured in the effluent. Results:,14C-adenosine was taken up by non-preconditioned and preconditioned myocardium during ischaemia. Significantly increased levels of 14C-lactate were recovered in preconditioned myocardium. 14C-adenosine with high specific activity resulted in a specific activity of lactate that was 2.7 times higher than that of lactate after administration of 14C-adenosine with low specific activity. Mass spectrography verified the identity of 14C-lactate. Conclusions:, Preconditioning up-regulates a new metabolic pathway (starting with 5,-nucleotidase and ending up with lactate) resulting in ATP formation in the micromolar range on top of another effect terminating in a useful shift in the AK equilibrium reaction in favour of ATP generation in the millimolar range. Although the up-regulation of the purine nucleoside phosphorylase pathway is clearly demonstrated, its biological relevance remains to be proved. [source]


Intracardiac Echocardiography in Patients with Pacing and Defibrillating Leads: A Feasibility Study

ECHOCARDIOGRAPHY, Issue 6 2008
Maria Grazia Bongiorni M.D.
Background: Lead extraction, an important and necessary component of treatment for many common device and lead-related complications, is a procedure that can provoke much anxiety in even the most experienced operators given the potentially serious complications. The principal impediment to lead extraction is the body's response to an intravascular foreign body with matrix intravascular neoformation, which causes the lead to adhere to the endocardium or vascular structure, increasing the risk of vascular or myocardial damage with lead removal. Fluoroscopic visualization, the commonly visualization used tool, has several limits in terms of anatomical structures visualization. The aim of this study was to assess the safety and feasibility of intracardiac echocardiography (ICE) in patients undergoing pacing and defibrillating leads before and during a transvenous device removal, and its potential role in detecting intracardiac leads and areas of fibrous adherence. Methods: ICE interrogation was performed in 25 consecutive patients with pacing and defibrillating implantable cardioverter defibrillators (ICD) leads before and during device removal. Results: A programmed ICE analysis was completed in 23 out of 25 patients with excellent resolution, providing a "qualitative-quantitative" information on anatomical structures, cardiac leads, and related areas of fibrous adherence. No ICE-related complications occurred. Conclusions: ICE evaluation is safe and feasible in patients with pacing and defibrillating leads before and during transvenous lead removal, offering an excellent visualization of cardiac leads and related areas of adherence. ICE can assist pacing and ICD lead removal and could improve procedure efficacy and safety. [source]


SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2009
G. Y. Oudit
Abstract Background, Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1,7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction. Materials and methods, We studied mice infected with the human strain of the SARS-CoV and encephalomyocarditis virus and examined ACE2 mRNA and protein expression. Autopsy heart samples from patients who succumbed to the SARS crisis in Toronto (Canada) were used to investigate the impact of SARS on myocardial structure, inflammation and ACE2 protein expression. Results, Pulmonary infection with the human SARS-CoV in mice led to an ACE2-dependent myocardial infection with a marked decrease in ACE2 expression confirming a critical role of ACE2 in mediating SARS-CoV infection in the heart. The SARS-CoV viral RNA was detected in 35% (7/20) of autopsied human heart samples obtained from patients who succumbed to the SARS crisis during the Toronto SARS outbreak. Macrophage-specific staining showed a marked increase in macrophage infiltration with evidence of myocardial damage in patients who had SARS-CoV in their hearts. The presence of SARS-CoV in the heart was also associated with marked reductions in ACE2 protein expression. Conclusions, Our data show that SARS-CoV can mediate myocardial inflammation and damage associated with down-regulation of myocardial ACE2 system, which may be responsible for the myocardial dysfunction and adverse cardiac outcomes in patients with SARS. [source]


Myocardial lipofuscin-laden lysosomes contain the apoptosis marker caspase-cleaved cytokeratin-18

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2008
A. Soleiman
ABSTRACT Background Acute coronary syndrome is related to increased circulatory concentration of soluble apoptosis specific caspase-cleaved cytokeratin-18 (ccCK-18). Potential cardiac sources of this intermediate filament derivative have not been investigated to date. Materials and methods Paraffin embedded tissue of normal myocardium, and chronically damaged samples of ischaemic, congestive and hypertrophic cardiomyopathy were analysed by histology and by CK-8, CK-18, ccCK-18 immunohistochemistry (each group, n = 15). Antibody specificity of the ccCK-18 antibody M30 was checked by immunoblotting on lysed myocardium and enriched myocardial lysosomes. Results ccCK-18 and CK-18 but not CK-8 were present in all forms of cardiomyopathy, most prominently in ischaemic cardiomyopathy while only traces were detectable immunohistochemically in normal myocardium. Weak CK-18 and strong ccCK-18 staining co-localized to lysosomes with cardiac age pigment lipofuscin. Weak staining of CK-18 was detected in the cytoplasm of coronary endothelia. Conclusion Our study reveals that cardiac lipofuscin-laden lysosomes contain ccCK-18, a marker of apoptosis and its precursor CK-18. This ccCK-18 pool might contribute to increased systemic levels of ccCK-18 in acute coronary syndrome thus monitoring myocardial damage. [source]


Structural myocardial changes after coronary artery surgery

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2000
F. Eberhardt
Background Postoperative contractile dysfunction or ,myocardial stunning' has been described after coronary artery bypass grafting (CABG). In the present study we sought to determine if and to what extent clinical, structural and histochemical evidence of myocardial changes associated with stunning could be found in patients after CABG and cold crystalloid cardioplegia. Materials and methods Left ventricular (LV) biopsies were obtained from CABG patients (n = 10) prior to and at the end of cardiopulmonary bypass (CPB). These biopsies were immunostained for the inducible heat-shock protein 70 (HSP-70i), intercellular adhesion molecule-1 (ICAM-1) and actin. ATP was measured by bioluminescence. Results Biopsies pre-CPB showed no evidence of myocardial damage as HSP-70i was absent and a regular actin cross-striation pattern and only constitutive ICAM-1-expression were present. After CPB we found significantly increased HSP-70i and ICAM-1 levels as well as a deranged actin cross-striation pattern with a widening of actin bands. ATP levels declined from 10 mmol L,1 pre-CPB to 4.9 mmol L,1 after CPB. Correspondingly, coronary sinus effluent showed a significant lactate production. Although, cardiac function determined by transoesophageal echocardiography did not deteriorate, significant inotropic support was necessary to maintain cardiac output. Conclusions Our results present clinical and structural evidence of ,myocardial stunning' after CABG and cold crystalloid cardioplegia. Increased HSP-70i and ICAM-1 expression, as well as a deranged actin cross-striation pattern, might be structural markers to determine ,myocardial stunning' in clinical settings. [source]


Effects of melatonin and caffeic acid phenethyl ester on testicular injury induced by myocardial ischemia/reperfusion in rats

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005
Mukaddes E
Abstract Experimental studies indicate that ischemia/reperfusion (I/R) causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative injury on testicular damage following myocardial I/R injury and the effects of antioxidant agents, melatonin and caffeic acid phenethyl ester (CAPE), on testicular injury were investigated. As far as we know, this is the first report demonstrating that myocardial I/R induces damage to the testes. Thirty-two male Wistar rats were randomly divided into four groups: sham operation (SO), I/R + vehicle, I/R + melatonin, and I/R + caffeic acid phenethyl ester. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Serum nitric oxide (NO) and malondialdehyde (MDA) levels and morphological changes were examined. I/R was accompanied by a significant increase in serum MDA and NO levels, whereas, melatonin and CAPE administration significantly reduced these values. Melatonin was more efficient in reducing MDA levels than CAPE (P < 0.05). I/R induced myocardial damage, manifested as the histopathological evidence of intracellular vacuolization, interstitial edema, neutrophil infiltration and coagulative necrosis. I/R + vehicle group showed many histological alterations such as focal tubular atrophy, and degeneration and disorganization of the seminiferous epithelium in testes. The number of atrophic tubules and degenerating cells was significantly higher in I/R + vehicle group than that of SO group. Melatonin and CAPE significantly reduced the number of degenerating cells; additionally, melatonin reduced the number of atrophic tubules (P < 0.05). Our results indicate that myocardial I/R induces severe testicular damage and antioxidant agents, especially melatonin, have protective effects on testicular injury after myocardial I/R. Our data emphasize that oxygen-based reactants may play a central role in remote organ injury. [source]


Perioperative myocardial damage and cardiac outcome in patients-at-risk undergoing non-cardiac surgery

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2010
A. O. Tibblin
No abstract is available for this article. [source]


Opposite effects of uracil and adenine nucleotides on the survival of murine cardiomyocytes

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2008
Alessia Mazzola
Abstract We previously showed that the human heart expresses all known P2X and P2Y receptors activated by extra-cellular adenine or uracil nucleotides. Despite evidence that, both in humans and rodents, plasma levels of ATP and UTP markedly increase during myocardial infarction, the differential effects mediated by the various adenine- and uracil-preferring myocardial P2 receptors are still largely unknown. Here, we studied the effects of adenine and uracil nucleotides on murine HL-1 cardiomyocytes. RT-PCR analysis showed that HL-1 cardiomyocytes express all known P2X receptors (except for P2X2), as well as the P2Y2,4,6,14 subtypes. Exposure of cardiomyocytes to adenine nucleotides (ATP, ADP or BzATP) induced apoptosis and necrosis, as determined by flow-cytometry. Cell death was exacerbated by tumour necrosis factor (TNF)-,, a cytokine implicated in chronic heart failure progression. Conversely, uracil nucleotides (UTP, UDP and UDPglucose) had no effect ,per se', but fully counteracted the deleterious effects induced by adenine nucleotides and TNF-,, even if added to cardiomyocytes after beginning exposure to these cell death-inducing agents. Thus, exposure of cardiomyocytes to elevated concentrations of ATP or ADP in the presence of TNF-, contributes to cell death, an effect which is counteracted by uracil-preferring P2 receptors. Cardiomyocytes do not need to be ,primed' by uracil nucleotides to become insensitive to adenine nucleotides-induced death, suggesting the existence of a possible ,therapeutic' window for uracil nucleotides-mediated protection. Thus, release of UTP during cardiac ischaemia and in chronic heart failure may protect against myocardial damage, setting the basis for developing novel cardioprotective agents that specifically target uracil-preferring P2Y receptors. [source]


Predictors of cardiac events in high-risk patients undergoing emergency surgery

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
A. OSCARSSON
Background: The aim of this study was to determine the incidence of myocardial damage and left ventricular myocardial dysfunction and their influence on outcome in high-risk patients undergoing non-elective surgery. Methods: In this prospective observational study, 211 patients with American Society of Anesthesiologists classification III or IV undergoing emergent or urgent surgery were included. Troponin I (TnI) was measured pre-operatively, 12 and 48 h post-operatively. Pre-operative N-terminal fragment of B-type natriuretic peptide (NT-proBNP), as a marker for left ventricular systolic dysfunction, was analyzed. The diagnostic thresholds were set to TnI >0.06 ,g/l and NT-proBNP >1800 pg/ml, respectively. Post-operative major adverse cardiac events (MACE), 30-day and 3-months mortality were recorded. Results: Elevated TnI levels were detected in 33% of the patients post-operatively. A TnI elevation increased the risk of MACE (35% vs. 3% in patients with normal TnI levels, P<0.001) and 30-day mortality (23% vs. 7%, P=0.003). Increased concentrations of NT-proBNP were seen in 59% of the patients. Elevated NT-proBNP was an independent predictor of myocardial damage post-operatively, odds ratio, 6.2 [95% confidence interval (CI) 2.1,18.0] and resulted in an increased risk of MACE (21% vs. 2.5% in patients with NT-proBNP ,1800 pg/ml, P<0.001). Conclusion: Myocardial damage is common in a high-risk population undergoing unscheduled surgery. These results suggest a close correlation between myocardial damage in the post-operative period and increased concentration of NT-proBNP before surgery. The combinations of TnI and NT-proBNP are reliable markers for monitoring patients at risk in the peri-operative period as well as useful tools in our risk assessment pre-operatively in emergency surgery. [source]


Prognostic value of combination of heart-type fatty acid-binding protein and ischemia-modified albumin in patients with acute coronary syndromes and normal troponin T values

JOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 1 2009
Cui Liyan
Abstract Recent studies have suggested that heart-type fatty acid-binding protein (H-FABP) may detect ongoing myocardial damage involved in the progression of acute coronary syndromes (ACS). This study was prospectively designed to examine whether the combination of H-FABP, a marker for ongoing myocardial damage, and ischemia-modified albumin (IMA), a marker for myocardial ischemia, would effectively diagnose patients with ACS. H-FABP values above 1.5,µg/l can be correctly measured via an ELISA and 6,µg/l is the currently used cut-off value (1,3). We measured serum H-FABP and IMA of 108 patients on admission within 12,hr after onset of chestpain and normal troponin T. serum samplesfrom ACS group (n=82) had decreased capacity of ACB [64 (61,67),U/ml] compared with non-ACS ischemic chest pain group (n=26) samples [75 (71,78),U/ml] (P<0.05). The combination of IMA and H-FABP usually had better sensitivity [96.3% (92.2,100%)] (P<0.05) and accuracy [92.6 (87.7,97.5%)] (P<0.05) than when individually used. Thus, the combination of H-FABP and IMA measurements after initiation of chest pain may be highly effective for risk stratification in patients with ACS and normal cardiac troponin T. J. Clin. Lab. Anal. 23:14,18, 2009. © 2009 Wiley-Liss, Inc. [source]


Effect of elevated concentration of alkaline phosphatase on cardiac troponin I assays

JOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 4 2001
Amitava Dasgupta
Abstract Troponin I is the regulatory subunit of troponin complex associated with the actin thin filament within muscle cells. Cardiac troponin I (cTnI) is a good marker for diagnosis of myocardial damage. Several immunoassays are available for determination of cTnI in serum. The Stratus cTnI fluorometric enzyme immunoassay (Dade International) uses alkaline phosphatase (ALP) substrate. The microparticle enzyme immunoassay (MEIA) for cTnI (Abbott Laboratories) also uses ALP conjugate. On the other hand, the chemiluminescent assay (CLIA) for cTnI (Bayer Diagnostics) does not use ALP. ALP activity may frequently be elevated in serum of patients being evaluated for suspected myocardial infarction. Therefore, we studied the potential interference of ALP in cTnI assays. Serum pools were prepared from patients, and various concentrations of ALP solution were added to different aliquots. The cTnI concentrations were measured by the Stratus, MEIA, and CLIA assays. We observed no interference of ALP in the MEIA and CLIA assay for cTnI. On the other hand, we observed significant positive interference of ALP when cTnI concentrations were measured using the Stratus. J. Clin. Lab. Anal. 15:175,177, 2001. © 2001 Wiley-Liss, Inc. [source]


The Intracoronary Electrocardiogram in Percutaneous Coronary Intervention

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2009
ANDY SC YONG M.B.B.S.
The technique of obtaining an epicardial electrocardiogram trace by connecting the guidewire during coronary angioplasty to an electrocardiogram lead has been used since 1985. The intracoronary electrocardiogram appears to be more sensitive than the surface electrocardiogram in detecting transient ischemia, particularly in the territory of the left anterior descending and left circumflex coronary arteries. Importantly, recent studies have shown the intracoronary electrocardiogram to be particularly useful in demonstrating pre- and postconditioning during interventional procedures, predicting periprocedural myocardial damage, and in the determination of regional viability in the catheterization laboratory. Barriers to the use of the intracoronary electrocardiogram in the clinical setting include the lack of standardized methods for acquiring and analyzing the intracoronary electrocardiogram, and the lack of commercially available continuous intracoronary monitoring systems to permit analysis while performing coronary interventions. Facilitating these relatively simple technical developments may permit optimal integration of the intracoronary electrocardiogram into the catheterization laboratory. [source]


Cardiovascular magnetic resonance reveals similar damage to the heart of patients with becker and limb-girdle muscular dystrophy but no cardiac symptoms

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2009
Ali Yilmaz MD
Abstract Cardiac involvement in patients with a sarcoglycanopathy (limb-girdle muscular dystrophy) has been described previously; however, this is the first cardiovascular magnetic resonance (CMR) study in such a patient demonstrating an interesting pattern of myocardial damage using late gadolinium enhancement (LGE) imaging. Moreover, the wall motion abnormality and the subepicardial pattern of LGE in this patient with a sarcoglycanopathy is in agreement with the findings in another patient with Becker muscular dystrophy. The predominance of LGE in the subepicardial layers of the left ventricular inferolateral wall suggests that such a myocardial damage pattern represents a nonspecific cardiac phenotype in response to exaggerated mechanical stress in this region, at least in patients with a sarcoglycanopathy or dystrophinopathy. J. Magn. Reson. Imaging 2009;30:876,877. © 2009 Wiley-Liss, Inc. [source]


Protective effect of Nardostachys jatamansi on oxidative injury and cellular abnormalities during doxorubicin-induced cardiac damage in rats

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 2 2006
Rajakannu Subashini
Nardostachys jatamansi is a medicinally important herb of Indian origin. It has been used for centuries in the Ayurvedic and Unani systems of medicine for the treatment of various ailments. We have evaluated the effect of N. jatamansi (rhizomes) on the biochemical changes, tissue peroxidative damage and abnormal antioxidant levels in doxorubicin (adriamycin)-induced cardiac damage. Preliminary studies on the effect of the graded dose of extract showed that 500 mg kg,1 orally for seven days was found to be optimum and hence all further study was carried out with this particular dose. Rats administered doxorubicin (15 mg kg,1, i.p.) showed myocardial damage that was manifested by the elevation of serum marker enzymes (lactate dehydrogenase, creatine phosphokinase, aspartate aminotransaminase and alanine aminotransaminase). The animals showed significant changes in the antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase) and lipid peroxidation levels. Pretreatment with N. jatamansi extract significantly prevented these alterations and restored the enzyme activity and lipid peroxides to near normal levels. Restoration of cellular normality accredits the N. jatamansi with a cytoprotective role in doxorubicin-induced cardiac damage. [source]


Thrombin generation during reperfusion after coronary artery bypass surgery associates with postoperative myocardial damage

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 7 2006
P. RAIVIO
Summary.,Background: Cardiopulmonary bypass and coronary artery bypass grafting (CABG) result in significant thrombin generation and activation of fibrinolysis. Thrombin contributes to myocardial ischemia,reperfusion injury in animal studies, but the role of thrombin in myocardial damage after CABG is unknown. Objectives: We measured thrombin generation and fibrin turnover during reperfusion after CABG to evaluate their associations with postoperative hemodynamic changes and myocardial damage. Methods: One hundred patients undergoing primary, elective, on-pump CABG were prospectively enrolled. Plasma prothrombin fragment F1+2 and D-dimer were measured preoperatively and at seven time points thereafter. Mass of the Mb fraction of creatine kinase (Ck-Mbm) and troponin T (TnT) were measured on the first postoperative day. Results: Reperfusion induced an escalation of thrombin generation and fibrin turnover despite full heparinization. F1+2 during early reperfusion associated with postoperative pulmonary vascular resistance index. F1+2 at 6 h after protamine administration correlated with Ck-Mbm (r = 0.40, P < 0.001) and TnT (r = 0.44, P < 0.001) at 18 h postoperatively. Patients with evidence of myocardial damage (highest quintiles of plasma Ck-Mbm and TnT) had significantly higher F1+2 during reperfusion than others (P < 0.002). Logistic regression models identified F1+2 during reperfusion to independently associate with postoperative myocardial damage (odds ratios 2.5,4.4, 95% confidence intervals 1.04,15.7). Conclusions: Reperfusion caused a burst in thrombin generation and fibrin turnover despite generous heparinization. Thrombin generation during reperfusion after CABG associated with pulmonary vascular resistance and postoperative myocardial damage. [source]


Serum Cardiac Troponin I Concentration in Dogs with Ehrlichiosis

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008
P.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]


Prospective Clinical Evaluation of Serum Cardiac Troponin T in Dogs Admitted to a Veterinary Teaching Hospital

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2002
Teresa C. DeFrancesco
The purpose of this study was to measure serum cardiac troponin T (cTnT) with a commercially available human enzyme-linked immunoassay (ELISA) test in various groups of dogs, including those undergoing doxorubicin chemotherapy. Serum samples were obtained from 6 groups of dogs: (1) normal adult dogs (n = 15); (2) dogs with asymptomatic dilated cardiomyopathy (n = 5); (3) dogs with congestive heart failure (n = 10); (4) dogs with untreated neoplasia (n = 20); (5) dogs with skeletal muscle trauma (n = 10); and (6) dogs with neoplasia receiving doxorubicin chemotherapy (n = 4). One serum sample was obtained from each of the normal dogs, those with asymptomatic cardiomyopathy, those with congestive heart failure, and those with untreated neoplasia. Serum samples were obtained serially from the dogs that were undergoing doxorubicin chemotherapy; samples were collected before doxorubicin (30 mg/m2) administration and then 1,5,7, and 14 days after administration throughout 6 cycles for a cumulative total dose of 180 mg/m2. All normal dogs, dogs with untreated neoplasia, and dogs with asymptomatic dilated cardiomyopathy had cTnT concentrations below the lower limits of detection for the assay used (<0.05 ng/mL). Detectable concentrations of cTnT were found in 3 dogs with congestive heart failure and in 2 dogs with skeletal muscle trauma. Detectable concentrations also were found in both dogs that had received 180 mg/m2 of doxorubicin. We conclude that dogs with congestive heart failure and those with skeletal muscle trauma and dogs with neoplasia receiving high-dose doxorubicin chemotherapy may have increased serum cTnT concentration, which may be suggestive of myocardial damage. [source]


Cardiac Troponin I in Feline Hypertrophic Cardiomyopathy

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2002
William E. Hemdon
Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05,10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2= .354; P= .009) but not with the diastolic thickness of the interventricular septum (P= .8467) or the left atrium: aorta ratio (P= .0652). Furthermore, cats with congestive heart failure at the time of cTnl analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P= .0095 and P= .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM. [source]


Cardiac Effects of Electrical Stun Guns: Does Position of Barbs Contact Make a Difference?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2008
DHANUNJAYA LAKKIREDDY M.D.
Background:The use of electrical stun guns has been rising among law enforcement authorities for subduing violent subjects. Multiple reports have raised concerns over their safety. The cardiovascular safety profile of these devices in relationship to the position of delivery on the torso has not been well studied. Methods:We tested 13 adult pigs using a custom device built to deliver neuromuscular incapacitating (NMI) discharge of increasing intensity that matched the waveform of a commercially available stun gun (TASER® X-26, TASER International, Scottsdale, AZ, USA). Discharges with increasing multiples of output capacitances were applied in a step-up and step-down fashion, using two-tethered barbs at five locations: (1) Sternal notch to cardiac apex (position-1), (2) sternal notch to supraumbilical area (position-2), (3) sternal notch to infraumbilical area (position-3), (4) side to side on the chest (position-4), and (5) upper to lower mid-posterior torso (position-5). Endpoints included determination of maximum safe multiple (MaxSM), ventricular fibrillation threshold (VFT), and minimum ventricular fibrillation induction multiple (MinVFIM). Results:Standard TASER discharges repeated three times did not cause ventricular fibrillation (VF) at any of the five locations. When the barbs were applied in the axis of the heart (position-1), MaxSM and MinVFIM were significantly lower than when applied away from the heart, on the dorsum (position-5) (4.31 ± 1.11 vs 40.77 ± 9.54, P< 0.001 and 8.31 ± 2.69 vs 50.77 ± 9.54, P< 0.001, respectively). The values of these endpoints at position-2, position-3, and position-4 were progressively higher and ranged in between those of position-1 and position-5. Presence of ventricular capture at a 2:1 ratio to the delivered TASER impulses correlated with induction of VF. No significant metabolic changes were seen after standard NMI TASER discharge. There was no evidence of myocardial damage based on serum cardiac markers, electrocardiography, echocardiography, and histopathologic findings confirming the absence of significant cardiac effects. Conclusions: Standard TASER discharges did not cause VF at any of the positions. Induction of VF at higher output multiples appear to be sensitive to electrode distance from the heart, giving highest ventricular fibrillation safety margin when the electrodes are placed on the dorsum. Rapid ventricular capture appears to be a likely mechanism of VF induction by higher output TASER discharges. [source]


Pharmacodynamic interaction of captopril with garlic in isoproterenol-induced myocardial damage in rat

PHYTOTHERAPY RESEARCH, Issue 5 2010
Syed Mohammed Basheeruddin Asdaq
Abstract It is known that various preparations of garlic and angiotensin-converting enzyme (ACE) inhibitor such as captopril (CAP) have beneficial effects on the left ventricular function and cardiovascular events after myocardial infarction (MI) when used individually. There is no reported interaction between garlic homogenate (GH) and CAP during and after acute MI. Thus the purpose of the current study was to evaluate the possible pharmacodynamic interaction of GH with CAP on isoproterenol (ISO)-induced myocardial damage in rat. Female Wistar albino rats were treated with GH at three different doses of 125; 250 and 500,mg/kg orally for 30 days and CAP (30,mg/kg, p.o.) was incorporated in the interactive groups during the last seven days of GH treatment. Myocardial damage was induced by administration of ISO (150,mg/kg, s.c.) for two consecutive days. Biochemical parameters were studied in serum and heart tissue homogenate of all animals. The GH 250,mg/kg was found to dislodge the effect of ISO on superoxide dismutase and catalase and retained the activities of LDH and CK-MB. Incorporation of CAP during GH treatment provided further protection to myocardium from injury. However, higher dose of GH alone or with CAP failed to prevent damaging effect of ISO. Histopathological determinations confirmed biochemical findings. Thus it is concluded that the combination needs to be used carefully when garlic is consumed at high doses. Copyright © 2009 John Wiley & Sons, Ltd. [source]


Integrated cardiac and vascular assessment in Takayasu arteritis by cardiovascular magnetic resonance

ARTHRITIS & RHEUMATISM, Issue 11 2009
Niall G. Keenan
Objective This study was undertaken to evaluate the value of cardiovascular magnetic resonance (CMR) in the assessment of patients with Takayasu arteritis (TA). Methods Sixteen patients with TA and 2 populations comprising 110 normal volunteers were prospectively recruited. All patients with TA underwent a CMR protocol including measurement of carotid artery wall volume, assessment of left ventricular (LV) volumes and function, and late gadolinium enhancement for the detection of myocardial scarring. Results Carotid artery wall volume, total vessel volume, and the wall:outer wall ratio were elevated in TA patients compared with controls (wall volume 1,045 mm3 in TA patients versus 640 mm3 in controls, P < 0.001; total vessel volume 2,268 mm3 in TA patients versus 2,037 mm3 in controls, P < 0.05; wall:outer wall ratio 48% in TA patients versus 32% in controls, P < 0.001). The lumen volume was reduced in TA (1,224 mm3 versus 1,398 mm3 in controls, P < 0.05). In TA, LV function was more dynamic, with reduced end-systolic volume (mean ± 95% confidence interval ejection fraction 74 ± 3% versus 67 ± 1% in controls, P < 0.001; LV end-systolic volume 19 ± 4 ml/m2 versus 25 ± 1 ml/m2 in controls, P < 0.001). Myocardial late gadolinium enhancement was present in 4 (27%) of 15 patients, indicating previously unrecognized myocardial damage. Conclusion Our findings indicate that an integrated method of cardiovascular assessment by CMR in TA not only provides good delineation of vessel wall thickening, but has also demonstrated dynamic ventricular function, myocardial scarring, and silent myocardial infarction. CMR has benefits compared with other approaches for the assessment and followup of patients with TA, and has potential to identify patients most at risk of complications, allowing early preventative therapy. [source]


Continuous Coronary Sinus Perfusion Reverses Ongoing Myocardial Damage in Acute Ischemia

ARTIFICIAL ORGANS, Issue 10 2009
Francesco Onorati
Abstract Acute cardiogenic shock or cardiac arrest (CS/CA) before cardiopulmonary bypass (CPB) installation are life-threatening events in acute coronary syndromes. We evaluated whether continuous retrograde warm-blood perfusion (CRWBP) before aortic cross-clamping (ACC), with immediate CPB installation may improve hospital results in these dreadful events. Hospital outcome of 18 coronary artery bypass grafting (CABG) (Group A) with CS/CA before CPB, with immediate CPB installation and CRWBP, has been compared with 24 CABG (Group B) with CS/CA undergoing only immediate CPB installation. No differences have been detected in the mean time to establish CPB (P = 0.655). Electrocardiography normalized in a significantly higher number of CRWBP (P = 0.0001). Group B showed longer CPB (116.2 ± 21.2 min vs. 157.8 ± 32.4; P = 0.0001) and postoperative intra-aortic balloon pumping time course (36.2 ± 5.9 h vs. 77.8 ± 13.2; P = 0.0001). CRWBP reduced postoperative acute myocardial infarction (P = 0.004) and damage (P = 0.033), death (P = 0.026), and need for high inotropic support (0% vs. 37.5%; P = 0.003). Troponin I was significantly lower in Group A (P = 0.013 from coronary sinus; P , 0.0001 at 12, 24, and 48 h postoperatively; P = 0.008 at 72 h), never reaching values suggestive of acute myocardial infarction. Group A had also lower lactate release from aortic declamping to 48 h postoperatively (P , 0.0001). CRWBP improved postoperative left ventricular ejection fraction (EF) (P = 0.017) and wall motion score index (P = 0.041), whereas Group B showed a significant worsening of EF (P = 0.0001) and wall motion score index (P = 0.002). Patients in Group A had shorter intubation time (P = 0.0001), intensive therapy unit (ITU) stay (P = 0.001), and hospital stay (P = 0.0001). CRWBP reverses myocardial damage in patients with CS/CA during acute coronary syndromes, adding a straightforward benefit to hospital survival. [source]


Regulation and Role of the Presynaptic and Myocardial Na+/H+ Exchanger NHE1: Effects on the Sympathetic Nervous System in Heart Failure

CARDIOVASCULAR THERAPEUTICS, Issue 2 2007
Kirsten Leineweber
ABSTRACT In acute myocardial ischemia and in chronic heart failure, sympathetic activation with excessive norepinephrine (NE) release from and reduced NE reuptake into sympathetic nerve endings is a prominent cause of arrhythmias and cardiac dysfunction. The Na+/H+ exchanger NHE1 is the predominant isoform in the heart. It contributes to cellular acid,base balance, and electrolyte, and volume homeostasis, and is activated in response to intracellular acidosis and/or activation of guanine nucleotide binding (G) protein-coupled receptors. NHE1 mediates its signaling via protein kinases A (PKA) or C (PKC). In cardiomyocytes, NHE1 is restricted to specialized membrane domains, where it regulates the activity of pH-sensitive proteins and modulates the driving force of the Na+/Ca2+ exchanger. During acute ischemia/reperfusion and in heart failure the activity/amount of NHE1 is increased, leading to intracellular Ca2+ overload and promoting structural (apoptosis, hypertrophy) and functional (arrhythmias, hypercontraction) myocardial damage. In sympathetic nerve endings, increased NHE1 activity results in the accumulation of axoplasmic Na+ that diminishes the inward and/or favors the outward transport of NE via the neuronal norepinephrine transporter (NET). The increased NE levels within the nerve,muscle junction facilitate the sustained stimulation of myocardial ,- and ,-adrenoceptors (ARs), which in turn aggravate the increases in myocardial NHE1 activity and the associated deleterious effects. Furthermore, the responsiveness of the ,-AR declines overtime, which results in further release of NE, initiating a vicious cycle. Accordingly, NHE1 is a potential candidate for targeted intervention to suppress this feedback loop. [source]


Cardiovascular Protective Effects of Resveratrol

CARDIOVASCULAR THERAPEUTICS, Issue 3 2004
Silvia Bradamante
ABSTRACT Resveratrol (3,4,,5-trihydroxy-trans-stilbene), a phytoalexin found in grape skins, peanuts, and red wine, has been reported to have a wide range of biological and pharmacological properties. It has been speculated that at low doses (such as consumed in the common diet) resveratrol may have cardioprotective activity. In this article we describe recent in vitro and in vivo studies in animal models. The results of these studies suggest that resveratrol modulates vascular cell function, inhibits LDL oxidation, suppresses platelet aggregation and reduces myocardial damage during ischemia-reperfusion. Although the reported biological data indicate that resveratrol is a highly promising cardiovascular protective agent, more studies are needed to establish its bioavailability and in vivo cardioprotective effects, particularly in humans. [source]