Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have identified the presence of coronary baroreceptors in animal models. We set up a study to explore the presence of coronary baroreceptors in humans, which was performed with isolated, graded aortic root perfusion in patients during cardiopulmonary bypass. With ethical approval 12 patients with normal coronary arteries, aged 58-75 (mean 69) years undergoing mitral valve surgery were recruited to the study with informed consent. Those with aortic valve incompetence, coronary, or peripheral artery disease and diabetes mellitus were excluded. They were randomized to have their coronary perfusion pressure set low at 50 mmHg for 90 seconds and then adjusted high to 80 mmHg for 90 seconds (group L-H) or the reverse sequence (group H-L). Average arterial pressure and approximately constant systemic flow over 30-second periods were used to calculate vascular resistance (SVR). The first six experiments followed initiation of cardiopulmonary bypass and aortic clamping but before the delivery of cold blood cardioplegia; the blood temperature for these experiments was kept at 32 degrees C. The remaining six were conducted prior to removal of the aortic cross clamp at 37 degrees C. Coronary sinus blood samples were analyzed to exclude myocardial ischemia. Coronary sinus blood samples showed insignificant variation in oxygen saturation, lactate, and troponin T. Three patients were excluded because of unstable blood pressure. In the (L-H) group SVR reduced in 4 of 4 remaining patients (mean -9.4%, range -3.9 to -19.6%). In the (H-L) group SVR increased in three patients (mean +2.0%, range 1.1 to 3.7%) but decreased in two (-8.9% and -15.8%). These preliminary results, although not statistically different, suggest the presence of coronary baroreceptors in humans. The reflex vascular responses are similar to those previously reported in animal models.
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PMID:The coronary baroreflex in humans. 1635 Mar 86

High-risk acute coronary syndrome is characterized by vulnerable-plaque with subocclusive thrombus and down-stream microemboli spreading minor myocardial damage, resulting in non-ST-elevation myocardial infarction. Advances in the understanding of the pathogenesis and consequences of acute coronary syndrome have stimulated development of novel biomarkers, and expanded their role in the different spectrum of the underlying pathophysiology, namely multi-biomarker strategy; consisted of biomarkers for 1) myocardial necrosis(membrane damage to myofibril necrosis), 2) plaque destabilization, 3) myocardial stress(ischemic stress per se and end-diastolic atrial or ventricular wall stress), 4) myocardial ischemia, and 5) inflammatory process. In this article, we review clinical importance of novel biomarkers referring our previous clinical investigation and other reports, especially troponin T for detection of minor myocardial damage associated with vulnerable plaque with thrombus/embolus, heart-type fatty acid -binding protein for earlier detection of myocardial damage and it's role for the rule-out triage, N-terminal pro-BNP for earlier risk stratification in cardiac emergency, and soluble CD40 ligand for earlier identification of plaque destabilization with platelet activation in non-ST-elevation acute coronary syndrome.
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PMID:[Multi-biomarker approach to acute coronary syndrome]. 1661 86

The effects of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker with alpha-/beta-adrenoceptor blocking activities, on myocardial infarct size, apoptosis and necrosis in the rat after myocardial ischemia/reperfusion (45 min/120 min) were investigated. Ten minutes prior to left coronary artery occlusion, rats were treated with vehicle or labedipinedilol-A (0.25 or 0.5 mg/kg, i.v.). In the vehicle group, myocardial ischemia-reperfusion induced creatine kinase (CK) release and caused cardiomyocyte apoptosis, as evidenced by DNA ladder formation and terminal dUTP deoxynucleotidyltransferase nick end-labeling (TUNEL) staining. Treatment with labedipinedilol-A (0.25 or 0.5 mg/kg) reduced infarct size significantly compared to vehicle group (18.75+/-0.65% and 8.27+/-0.29% vs. 41.72+/-0.73%, P<0.01). Labedipinedilol-A also reduced the CK, CK-MB, lactate dehydrogenase (LDH) and troponin T levels in blood. In addition, labedipinedilol-A (0.5 mg/kg) significantly decreased TUNEL positive cells from 19.21+/-0.52% to 9.73+/-0.81% (P<0.01), which is consistent with absence of DNA ladders in the labedipinedilol-A group. Moreover, labedipinedilol-A pretreatment also decreased calcium content in ischemic-reperfused myocardial tissue. In conclusion, these results demonstrate that labedipindielol-A, through reduction of calcium overload and apoptosis, exerts anti-infarct effect during myocardial ischemia-reperfusion and would be useful clinically in the prevention of acute myocardial infarction.
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PMID:Protective effect of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker, on myocardial apoptosis in ischemia-reperfusion injury. 1664 91

Patients on maintenance peritoneal dialysis (PD) are frequently complicated with volume overload. In this study, we sought to evaluate troponin T testing alone or in combination with echocardiographic measures in predicting cardiovascular congestion in PD patients. This was a prospective study of 222 chronic PD patients with echocardiography and measurement of serum troponin T carried out at baseline. Patients were followed for 3 years or until death. The end point was first episode of cardiovascular congestion. Troponin T emerged as an independent predictor of cardiovascular congestion (hazard ratio, 2.98, 95% confidence intervals (CI), 1.19-7.42) in a multivariable Cox regression model, including also left ventricular mass index (LVMi) and ejection fraction (EF). Patients with troponin T>median (0.06 microg/l) and EF<or=50% and patients with troponin T>median but EF>50% had a 3.10-fold (95% CI, 1.71-5.63) and 1.88-fold (95% CI, 1.05-3.38) adjusted risk of cardiovascular congestion, respectively, than those with troponin T<or=median and EF>50%. Patients with troponin T>median and LVMi>or=median (96.23 g/m2.7) had a 2.68-fold (95% CI, 1.39-5.19) adjusted risk of cardiovascular congestion than those with troponin T<or=median and LVMi <median. In conclusion, troponin T predicts cardiovascular congestion in chronic PD patients without acute myocardial ischemia and provides incremental prognostic value for cardiovascular congestion when used in combination with LVM and EF. This easily available parameter adds significant value to echocardiography in identifying PD patients at risk of cardiovascular congestion.
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PMID:Troponin T, left ventricular mass, and function are excellent predictors of cardiovascular congestion in peritoneal dialysis. 1687 Dec 51

The role of iron in the pathogenesis of cardio-vascular disorders is still controversial. We studied the effects of iron perturbations on myocardial injury upon temporary ischemia/reperfusion. C57BL/6J male mice were injected with iron dextran for 2 weeks while controls received saline. Mice were then subjected to 30 min of myocardial ischemia and subsequent reperfusion for 6-24 h. Tissue damage was quantified histologically and by troponin T determination. The expressions of tumor necrosis factor-alpha (TNF-alpha), superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) were investigated in non-ischemic and ischemic regions of both groups. After myocardial ischemia and reperfusion, troponin T levels, as a marker of myocardial damage, were significantly reduced in iron-treated mice as compared to control mice (P < 0.05). Under the same conditions the infarction area and damage score were significantly lower in iron-treated animals. In parallel, TNF-alpha and SOD expressions were increased in infarcted regions of iron-treated mice as compared to controls, whereas myocardial iNOS expression was significantly lower in iron-treated mice. Although, iron challenge increased radical formation and TNF-alpha expression in vivo, this did not result in myocardial damage which may be linked to the parallel induction of SOD. Importantly, iron treatment inhibited iNOS expression. Since, an increased nitric oxide (NO) formation has been linked to cardiac damage after acute myocardial infarction, iron may exert short time cardio-protective effects after induction of ischemia/reperfusion via decreasing iNOS formation.
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PMID:Short term protective effects of iron in a murine model of ischemia/reperfusion. 1692 72

The structure of the NH2-terminal region of troponin T (TnT) is hypervariable among the muscle type-specific isoforms and is also regulated by alternative RNA splicing. This region does not contain binding sites for other thin filament proteins, but alteration of its structure affects the Ca2+ regulation of muscle contraction. Here we report a truncated cardiac TnT produced during myocardial ischemia reperfusion. Amino acid sequencing and protein fragment reconstruction determined that it is generated by a posttranslational modification selectively removing the NH2-terminal variable region and preserving the conserved core structure of TnT. Triton X-100 extraction of cardiac muscle fibers promoted production of the NH2-terminal truncated cardiac TnT (cTnT-ND), indicating a myofibril-associated proteolytic activity. Mu-calpain is a myofibril-associated protease and is known to degrade TnT. Supporting a role of mu-calpain in producing cTnT-ND in myocardial ischemia reperfusion, calpain inhibitors decreased the level of cTnT-ND in Triton-extracted myofibrils. Mu-calpain treatment of the cardiac myofibril and troponin complex specifically reproduced cTnT-ND. In contrast, mu-calpain treatment of isolated cardiac TnT resulted in nonspecific degradation, suggesting that this structural modification is relevant to physiological structures of the myofilament. Triton X-100 treatment of transgenic mouse cardiac myofibrils overexpressing fast skeletal muscle TnT produced similar NH2-terminal truncations of the endogenous and exogenous TnT, despite different amino acid sequences at the cleavage site. With the functional consequences of removing the NH2-terminal variable region of TnT, the mu-calpain-mediated proteolytic modification of TnT may act as an acute mechanism to adjust muscle contractility under stress conditions.
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PMID:Selective deletion of the NH2-terminal variable region of cardiac troponin T in ischemia reperfusion by myofibril-associated mu-calpain cleavage. 1698 28

Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic mediators, release of cytokines, leukocyte accumulation, and subsequent severe tissue injury. In this regard, activation of transcription factors (i.e., NFkappaB) and de novo protein synthesis or inflammatory protein degradation seems to play an important role. In the present study, we analyzed the cardiac protein expression following myocardial ischemia (60 min) and reperfusion (180 min) in a rabbit model utilizing two-dimensional electrophoresis and nanoHPLC/ESI-MS/MS for biochemical protein identification. To achieve cardioprotective effects, we used a novel highly selective small molecule C1s inhibitor administered 5 min prior to reperfusion. The reduction of myocardial injury was observed as diminished plasma creatine kinase activity in C1s-INH-248-treated animals (65.2+/-3 vs. 38.5+/-3 U/g protein after 3 h of reperfusion, P<0.05). With proteome analysis we were able to detect 509+/-21 protein spots on the gels of the 3 groups. A pattern of 480 spots with identical positions was found on every gel of myocardial tissue of sham animals, vehicle and C1s-INH-248-treated animals. We analyzed 11 spots, which were identified by mass spectrometry: Superoxide dismutase, alpha-crystallin-chain-B, mitochondrial stress protein, Mn SOD, ATP synthase A chain heart isoform, creatine kinase, and troponin T. All of these proteins were significantly decreased in the vehicle group when we compared to sham-treated animals. Treatment with C1s-INH-248 preserved levels of these proteins. Thus, blocking the classical complement pathway with a highly specific and potent synthetic inhibitor of the activated C1 complex archives cardio-protection by altering and preserving different anti-inflammatory and cytoprotective cascades.
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PMID:Proteome analysis of myocardial tissue following ischemia and reperfusion--effects of complement inhibition. 1704 55

A 62-year-old man with non-topic severe persistent asthma and chronic obstructive disease suffered severe asthma exacerbation. Epinephrine was repeatedly injected subcutaneously (0.3mg x 8 times in four hours) in addition to intravenous methylprednisolone for his severe asthma. Despite these treatments, his symptoms steadily deteriorated and thus he was transferred to our hospital. He did not have chest pain or a sensation of compression, while ECG on admission demonstrated ST elevation, loss of R-wave progression, negative T waves and QT interval prolongation, suggesting ischemic heart disease. Nonetheless creatine kinase and its MB isozyme were within normal range and myosin light chain I and troponin T were only mildly elevated. Echocardiography demonstrated apical dyskinesia and hypersystole in the basal region of the heart. Finally this case was diagnosed as Takotsubo cardiomyopathy, probably due to catecholamine-mediated myocardial stunning by overuse of epinephrine for acute severe asthma exacerbation. Abnormal findings of ECG and echocardiography became normal without any specific treatments for the heart.
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PMID:[Case of bronchial asthma complicated with Takotsubo cardiomyopathy after frequent epinephrine medication]. 1708 35

Several emerging cardiac markers constitute strong predictors among patients with coronary artery disease. In particular, brain natriuretic peptide (BNP), troponin T (TnT), and C-reactive protein (CRP) are related to increased risk of recurrent ischemic events and death. However, little is known about the utility of these biomarkers in combination. This study examined risk assessment in patients with coronary artery disease and preserved systolic function. We studied 208 consecutive patients (138 men, 70 women) with stable angina, unstable angina, and non-Q-wave myocardial infarction whose plasma BNP, TnT, and CRP levels were measured at hospital admission. All recruited patients underwent echocardiographic examination, and selective coronary angiography was performed. After adjusting for clinical presentation, age, gender, and common risk factors, BNP was demonstrated as a strong predictor of heart failure (6 months, odds ratio [OR] 2.03, 95% confidence interval [CI] 1.24 to 2.9, p <0.01; 12 months, OR 2.65, 95% CI 1.69 to 3.5, p <0.001) and mortality at 3, 6, and 12 months (p <0.001). BNP was also significantly related to extent of coronary artery disease and left anterior descending artery involvement (p <0.01). Patients with a BNP level >80 pg/ml in all 3 groups had a significantly poorer prognosis with increased incidence of heart failure and death. CRP was related to recurrent ischemic events (infarct or recurrent angina, OR 1.4, 95% CI 1.14 to 2.08, p <0.01) and was associated with major cardiac revascularization at 12 months (OR 1.51, 95% CI 1.29 to 1.73, p <0.001). TnT demonstrated a mild correlation with recurrent infarct or angina at 12 months (OR 1.1, 95% CI 0.96 to 1.22, p <0.05) but appeared related to multivessel coronary artery disease (OR 1.47, 95% CI 1.05 to 1.99, p <0.01). In conclusion, BNP appears to be associated with a long-term increased risk of mortality and heart failure in patients with apparently mild risk. BNP is also associated with a larger extent and greater severity of myocardial ischemia. Early BNP measurement could provide incremental information to TnT and CRP, and it may be the strongest independent predictor of cardiac outcome in subjects without left ventricular dysfunction or enlargement.
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PMID:Brain natriuretic peptide and other risk markers for outcome assessment in patients with non-ST-elevation coronary syndromes and preserved systolic function. 1713 22

Gastric perforation in association with incarceration of a hiatus hernia rarely features on a list of differential diagnoses of acute chest pain. A patient presented to the emergency department with acute chest pain characteristic of myocardial ischaemia. Several risk factors for ischaemic heart disease (IHD) were present. Investigations revealed normal cardiac enzymes and normal electrocardiography both initially and at 90 mins. A chest radiograph demonstrated the presence of a hiatus hernia. The patient was diagnosed with, and treated for, unstable angina. A troponin T test at 12 h post-admission was normal. The patient's clinical condition continued to deteriorate. The source of her pain was found to be gastric perforations in association with an incarcerated hiatus hernia. Her postoperative course was complicated by pulmonary and intra-abdominal sepsis necessitating admission to the intensive care unit where she remained for 23 days. This case highlights the challenge that non-cardiac chest pain presents to the acute care physician. Patients who present with risk factors for and symptoms consistent with a diagnosis of IHD may have non-cardiogenic pathology which can be life-threatening.
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PMID:Gastric perforation secondary to incarcerated hiatus hernia: an important differential in the diagnosis of central crushing chest pain. 1765 2


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