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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal dysfunction is an important predictor of mortality in patients with acute coronary syndrome. Until recently, the Cockcroft-Gault (C-G) equation has been most commonly used to estimate renal function, although the Modification of Diet in Renal Disease (MDRD) equation is now recommended. Which equation better predicts mortality is unclear. Consecutive patients without ST elevation on the initial electrocardiogram admitted for exclusion of myocardial ischemia were included. Admission creatinine was used to estimate renal function, and 30-day and 1-year mortality were compared after classifying patients as having no (estimated glomerular filtration rate [eGFR] > or =60 ml/min/m(2)), moderate (eGFR 30 to 59 ml/min/ m(2)), or severe (eGFR <30 ml/min/m(2)) renal dysfunction using the 2 equations. Of the 4,343 patients (49% women, 64% African-American) included, 16% had troponin I elevations consistent with myocardial infarction, and 1-year mortality was 10%. Agreement between the 2 equations was high (r = 0.87 p <0.001, concordance 86%). Mortality was similar in the 2 renal function classifications, with no significant differences based on race or troponin I status at 30 days or 1 year. However, the area of the receiver operator characteristic curve was significantly larger for predicting 1-year mortality with the C-G equation (0.75 [0.72 to 0.77] vs 0.71 [0.68 to 0.73]; p <0.01); both were superior to creatinine alone (0.68 [0.66 to 0.71]; p <0.01 for both C-G and MDRD). Results for 30-day mortality were similar. In conclusion, the C-G equation appears to be superior to the MDRD equation for predicting short- and long-term mortality in patients admitted for exclusion of ischemia, although differences are minor.
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PMID:Comparison of the modification of diet in renal disease and the Cockcroft-Gault equations for predicting mortality in patients admitted for exclusion of myocardial ischemia. 1860 10

Troponin elevation is usually synonymous with acute coronary syndrome (ACS). Although sensitive for ACS, the elevation of serum troponin, in the absence of clinical evidence of ischemia, should prompt a search for other etiologies of myocardial necrosis. In fact, elevated values of troponin are correlated with myocardial necrosis even though it does not discriminate the mechanism involved. We report a series of seven patients (age range 18-67 years), who presented with complaints of chest discomfort and were found to have regular supraventricular tachycardia (5 patients) and one patient each with atrial fibrillation and ventricular tachycardia. All these patients had elevated troponin I and underwent coronary angiography that revealed normal epicardial coronary arteries. This is first case series in which all patients underwent coronary angiography and none of the patients was hemodynamically unstable at the time of presentation. Patients with elevated troponin due to conditions other than ACS can receive inappropriate and delayed definitive diagnosis and treatment.
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PMID:Troponin elevation in patients with various tachycardias and normal epicardial coronaries. 1867 21

The effects of mexicor (ethylmethylhydroxypyridine succinate) at doses of 50 and 100 mg/kg on myocardial infarct size, serum levels of myocardial markers, and severity of ischemia- and reperfusion-induced arrhythmias were studied in the rat model of myocardial ischemia-reperfusion injury. It was shown that pre-ischemic intravenous infusion of mexicor at a dose of 50 mg/kg resulted in significant reduction of myocardial infarct size and troponin I level. When the dose of mexicor was increased up to 100 mg/kg the infarct-limiting effect was reversed. Both doses of mexicor tested in this study failed to protect the heart from ischemic tachyarrhythmias but decreased the occurrence of persistent reperfusion-induced ventricular fibrillation.
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PMID:[The effects of modulation of cardiac metabolism and antioxidant state on myocardial ischemia-reperfusion injury]. 1906 30

The goal of the study was to determine whether postconditioning protects against different ischemia durations in the rabbit. Rabbits were assigned to a 20-, 25-, 45- or 60-min coronary occlusion followed by 24-h of reperfusion. Rabbits received no further intervention (control) or were postconditioned with four cycles of 30-s occlusion and 30-s reperfusion after myocardial infarction. Plasma levels of troponin I were quantified throughout reperfusion. In control conditions, infarct sizes (% area at risk using triphenyltetrazolium chloride) after 20, 25, 45 and 60 min of coronary occlusions were 23+/-3, 51+/-4, 70+/-3 and 81+/-3 %, respectively. With 20 and 25 min occlusion, postconditioning reduced infarct size by 43+/-10 and 73+/-21 %, respectively. On the other hand, with 45 or 60 min occlusion, postconditioning had no significant effects on infarct size (61+/-3 and 80+/-2 % of area at risk). Preconditioning protocol was performed with 25- and 60-min coronary occlusion. As expected, preconditioning significantly reduced infarct size. In conclusion, in the rabbit, the cardioprotection afforded by postconditioning is limited to less than 45 min coronary occlusion.
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PMID:Is postconditioning effective in prevention against long-lasting myocardial ischemia in the rabbit? 1909 26

Mesenchymal stem cells (MSCs) have the capacity to differentiate into osteoblasts, chondrocytes, adipocytes, myocytes, and cardiomyocytes. Several established methods are presently available for in vitro isolation of MSCs from bone marrow. However, the duration necessary to culture them can be a major handicap to cell-based therapies needed for such urgent cardiovascular conditions as acute myocardial infarction and acute hindlimb ischemia. The best timing of cardiomyocyte differentiation induction after MCS isolation and expansion is still an unresolved issue. Our goal was to investigate the possibility of obtaining functional cardiomyocytes from rat MSC within a shorter time period. We examined MSCs' colony-forming capacity, CD90 and CD34 immunoreactivity during the 14 days of culturing. Cardiomyocyte differentiation was induced by 5-azacytidine. Immunohistochemic staining, together with intracellular Ca2+ measurement experiments, revealed that MSCs do not differentiate into any specific cell lineage but show the characteristics of MSCs on both the 9th and 14th days of the culture. To check the potential for differentiation into cardiomyocytes, experiments with caffeine application and depolarization with KCl were performed. The cells possessed some of the specific biochemical features of contracting cells, with slightly higher capacities on the 14th day. Cells from 9th and 14th days of the culture that were treated with 5-azacytidine had a higher expression of cardiac-specific markers such as troponin I, alpha-sarcomeric actin, and MEF2D compared with the control groups. This study illustrates that it is possible to get functional cardiomyocytes from in vitro MSC culture in a shorter time period than previously achieved. This reduction in time may provide emergency cases with access to cell-based therapies that may have previously been unavailable.
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PMID:Timing of induction of cardiomyocyte differentiation for in vitro cultured mesenchymal stem cells: a perspective for emergencies. 1923 78

Exercise-induced ST-segment elevation in lead aVR accompanied by ST-segment elevation in lead V1 might be a specific finding of left main coronary artery (LMCA) stenosis. Lead aVR and lead v1 ST segment elevation has been reported, during an attack of chest pain, in patients with LMCA disease with ST segment depression in leads V3, V4 and V5 (with maximal depression in V4). ST-segment elevation in lead aVR in patients with angina at rest can be related to transmural ischemia of the basal part of the interventricular septum, frequently due to LMCA or multivessel coronary disease too. 3-vessel coronary artery disease (CAD) and LMCA disease show a frequent combination of leads with abnormal ST segments during chest pain with ST-segment depression in leads I II V4-V6, and ST-segment elevation in lead aVR. When ST-segment status in lead aVR combines with troponin T, ST-segment elevation in lead aVR and positive troponin T on admission are useful predictors of LMCA or 3-vessel CAD. We present a case of acute myocardial infarction with significant left main coronary artery stenosis, significant 3-vessel coronary artery disease and elevated troponin I at admission in an 83-year-old Italian woman. Also this case focuses attention on the importance of the recognition of the patterns suspected for LMCA and/or 3-vessel coronary disease.
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PMID:Acute myocardial infarction with significant left main coronary artery stenosis, significant 3-vessel coronary artery disease and elevated troponin-I at admission. 1935 9

The purpose of this study was to evaluate the ability of novel semiselective matrix metalloproteinase inhibitors (MMPI) to protect myocardial structure-function in the setting of ischemia-reperfusion injury. For this purpose, an isolated rat model of myocardial stunning and infarction was used. Isolated hearts were subjected to 20-30 minutes of global no-flow ischemia and 30-minute reperfusion. Myocardial performance was assessed as the product of the heart rate and left ventricular developed pressure (rate-pressure product, RPP). Coronary flow rates, ventricular weights, indicators of muscle (troponin I), and fibrillar collagen damage (collagen opalation) were measured. Four MMPI were tested: 2 non-hydroxamate, semiselective inhibitors (PY-2 and 1,2-HOPO-2) and 2 broad-spectrum inhibitors (PD166793 and CGS27023A). The non-hydroxamate, semiselective inhibitors were shown to be nontoxic in cocultures of cardiac cells. Results indicate that semiselective inhibitors (in particular 1,2-HOPO-2) yield improved cardiac performance (approximately 23% higher RPP vs. controls) and coronary flow rates (approximately 22%), reducing muscle (approximately 25%) and fibrillar collagen damage (approximately 60%). Evidence suggests the involvement of matrix metalloproteinase-2 in these actions. Interestingly, broad-spectrum inhibitors only show modest improvement (approximately 8% higher RPP vs. controls) without affecting the other measured parameters. In conclusion, semiselective MMPI can act as cardioprotectors in isolated perfused rat hearts. Protection is observed in all structural components of the myocardium translating into improved contractile function. Based on these findings, non-hydroxamate, semiselective MMPI warrant further studies as to their ability to protect ischemic myocardium in the in vivo setting.
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PMID:Effects of novel semiselective matrix metalloproteinase inhibitors on ex vivo cardiac structure-function. 1936 78

The present study investigates whether 3-(R)-[3-(2-methoxyphenylthio-2-(S)-methylpropyl]amino-3,4-dihydro-2H-1,5-benzoxathiepine bromhydrate (F 15845), a new, persistent sodium current blocker, can reduce the ischemic Na(+) accumulation and exert short- and long-term cardioprotection after myocardial infarction. First, F 15845 concentration-dependently reduced veratrine-induced diastolic contracture (IC(50) = 0.14 microM) in isolated atria. Second, F 15845 from 1 microM preserved viability in 54.2 +/- 12.5% of isolated cardiomyocytes exposed to lysophosphatidylcholine. Third, the effect of F 15845 on intracellular Na(+) of isolated hearts from control and diabetic db/db mice was monitored using (23)Na-nuclear magnetic resonance spectroscopy. F 15845 (0.3 microM) significantly counteracted [Na(+)](i) increase during no-flow ischemia in control mouse hearts. In diabetic db/db mouse hearts, the reduction in [Na(+)](i) was delayed relative to control. However, it was more marked and maintained upon reperfusion. The cardioprotective properties after myocardial infarction associated with short- (24-h) and long-term (14-day) reperfusion were measured in anesthetized rats. After 24-h reperfusion, F 15845 (5 mg/kg) significantly reduced infarct size (32.4 +/- 1.7% with vehicle and 24.2 +/- 3.4% with F 15845; P < 0.05) and decrease of troponin I levels (524 +/- 93 microg/l with vehicle versus 271 +/- 63 microg/l with F 15845; P < 0.05). It is important that F 15845 limits the long-term expansion of infarct size (35.2 +/- 2.6%, n = 19 versus 46.7 +/- 1.6%, n = 27 in the vehicle group; P < 0.001). Overall, F 15845 attenuates [Na(+)](i) and prevents (or reverses) contractile and biochemical dysfunction in ischemic and remodeling heart. F 15845 constitutes a new generation of cardioprotective agent.
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PMID:3-(R)-[3-(2-methoxyphenylthio-2-(S)-methylpropyl]amino-3,4-dihydro-2H-1,5-benzoxathiepine bromhydrate (F 15845) prevents ischemia-induced heart remodeling by reduction of the intracellular Na+ overload. 1951 69

Myocardial injury due to ischemia-reperfusion (I-R) damage remains a major clinical challenge. Its pathogenesis is complex including endothelial dysfunction and heightened oxidative stress although the key driving mechanism remains uncertain. In this study we tested the hypothesis that the I-R process induces a state of insufficient L-arginine availability for NO biosynthesis, and that this is pivotal in the development of myocardial I-R damage. In neonatal rat ventricular cardiomyocytes (NVCM), hypoxia-reoxygenation significantly decreased L-arginine uptake and NO production (42 +/- 2% and 71 +/- 4%, respectively, both P < 0.01), maximal after 2 h reoxygenation. In parallel, mitochondrial membrane potential significantly decreased and ROS production increased (both P < 0.01). NVCMs infected with adenovirus expressing the L-arginine transporter, CAT1, and NVCMs supplemented with L-arginine both exhibited significant (all P < 0.05) improvements in NO generation and mitochondrial membrane potentials, with a concomitant significant fall in ROS production and lactate dehydrogenase release during hypoxia-reoxygenation. In contrast, L-arginine deprived NVCM had significantly worsened responses to hypoxia-reoxygenation. In isolated perfused mouse hearts, L-arginine infusion during reperfusion significantly improved left ventricular function after I-R. These improved contractile responses were not dependent on coronary flow but were associated with a significant decrease in nitrotyrosine formation and increases in phosphorylation of both Akt and troponin I. Collectively, these data strongly implicate reduced L-arginine availability as a key factor in the pathogenesis of I-R injury. Increasing L-arginine availability via increased CAT1 expression or by supplementation improves myocardial responses to I-R. Restoration of L-arginine availability may therefore be a valuable strategy to ameliorate I-R injury.
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PMID:Reduced L-arginine transport contributes to the pathogenesis of myocardial ischemia-reperfusion injury. 1954 85

Our objectives were to evaluate the prognostic value of several biomarkers in patients with acute coronary syndrome (ACS) through an evaluation of the 30-day clinical outcomes. Multiple biomarkers have emerged as potentially useful in risk stratification of ACS. Specifically, markers of vascular inflammation and oxidative stress might be helpful in the determination of clinical outcomes. We evaluated patients presenting with chest pain. ACS was defined by symptoms of cardiac ischemia plus electrocardiographic changes or positive troponin I. Levels of serum troponin I, high sensitivity C-reactive protein, serum choline, and free F(2)-isoprostane were obtained. Patients were followed up for 30 days (n = 108) with determination of nonfatal myocardial infarction, congestive heart failure, need for revascularization, and death. Of the 108 patients, 26 had a cardiac event. Free F(2)-isoprostane and choline levels (but not high-sensitivity C-reactive protein levels) predicted 30-day cardiac events. To determine the value of choline and F(2)-isoprostane levels in predicting 30-day cardiac events, receiver operating curves were generated. The optimal cutoff point of these markers was a serum F(2)-isoprostane level of 124.5 pg/ml (r = 0.82) and a serum choline level of 30.5 mumol/L (r = 0.76). F(2)-isoprostane and choline had a positive predictive value of 57% and 44% and a negative predictive value of 90% and 89%, respectively. In conclusion, serum choline and free F(2)-isoprostane are predictors of cardiac events in ACS. A model that includes an array of biomarkers, including troponin, choline, and free F(2)-isoprostane, might be useful in predicting patients at greater risk of future events in ACS.
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PMID:Usefulness of elevations in serum choline and free F2)-isoprostane to predict 30-day cardiovascular outcomes in patients with acute coronary syndrome. 1969 37


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