Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed a closed chest animal model that allows noninvasive monitoring of cardiac high energy phosphate metabolism before, during, and for at least 3 weeks after a myocardial infarction. Ten beagles underwent 2 h of coronary occlusion followed by 3 weeks of reperfusion. Myocardial high energy phosphates from 12-ml voxels were noninvasively tracked using 31P two-dimensional chemical shift imaging. Gadolinium enhanced 1H MRI identified the zone at risk, and radioactive microspheres assessed regional blood flow and partition coefficients. Occlusion of the left anterior descending coronary artery produced infarcts that were 13.7+/-8.8% (mean+/-SD) of the left ventricular volume. Rapid changes in the phosphocreatine and inorganic phosphate levels were observed during occlusion, whereas adenosine triphosphate levels decreased more slowly. All metabolites recovered to base-line levels 2 weeks after occluder release. Multiple inorganic phosphate peaks in the infarct voxel spectra indicated that more than one metabolically compromised tissue zone developed during occlusion and reperfusion. Microsphere data indicating three distinct blood flow zones during ischemia and reperfusion (<0.3, 0.3-0.75, and >0.75 ml/min/g) supported the grouping of pH values into three distinct metabolic distributions.
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PMID:Myocardial infarction in a canine model monitored by two-dimensional 31P chemical shift spectroscopic imaging. 932 25

The article presents a case of subacute coronary artery thrombosis investigated by classic methods, coronary angiography, and MRI. T1- and T2-weighted images showed high signal intensity within the lumen of the right coronary artery corresponding to the methemoglobin content of the thrombus. Dynamic sequence images with intravenous gadolinium contrast agent displayed lack of right coronary artery enhancement, confirming coronary occlusion. The coronarography revealed the same finding. MRI appears to be a promising method of coronary thrombosis assessment.
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PMID:Subacute coronary artery thrombosis: MRI findings. 938 90

The objectives of this study were to define the relationship between the first order constant of Gd-DTPA transfer (K1) and the myocardial blood flow (MBF) at rest and to compare it with an equivalent relationship obtained for positron emission tomography (PET). In a canine model of permanent coronary occlusion (n = 4), myocardial and blood time concentration curves obtained by 13N-ammonia PET and Gd-DTPA-enhanced MRI were fitted by a one-compartment model to determine K1. A linear relationship was observed between MRI-derived K1 and MBF measured by microspheres (K1 = 0.88 x flow -0.015, R = 0.95), which compares favorably with the equivalent relationship derived from PET (K1 = 0.74 x flow +0.16, R = 0.88). The results of this preliminary study suggest that, at rest and distal to a permanently occluded coronary artery, myocardial perfusion quantification by MRI is possible and can challenge PET.
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PMID:Quantification of myocardial perfusion by MRI after coronary occlusion. 970 11

Previous studies in a model of ischemia/reperfusion using a constant infusion of Gd-DTPA have shown that distribution volume (lambda) is increased in infarcted myocardial tissue. This study examined this technique in the setting of permanent coronary artery occlusion. Ten beagles underwent permanent occlusion of a coronary artery for 2 days (N = 3), 1 week (N = 4), or 3 weeks (N = 3). Imaging was performed at 2 days and, depending on the length of occlusion, 1 week, 2 weeks, and 3 weeks to follow changes in lambda in vivo. At sacrifice, (201)Tl was injected and the extent of the hyperenhanced region was compared to pathology. lambda was increased in infarcted tissue by 2 days post occlusion and this increase persisted for 3 weeks. At sacrifice, lambda correlated strongly with (201)Tl uptake (r = -0.86 to -0.95, P < 0.05; i.e., lambda increased in infarcted tissue) and the size of the hyperenhanced region was comparable to pathological infarct size (slope 1.006, r = 0.96, P < 0.0001). Thus, beyond 2 days after coronary occlusion, MRI, during a constant infusion of Gd-DTPA, can assess myocardial viability regardless of the success of reperfusion. Magn Reson Med 44:309-316, 2000.
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PMID:Contrast-enhanced MRI for the assessment of myocardial viability after permanent coronary artery occlusion. 1091 31

Loss of membrane permeability caused by ischemia leads to cellular sodium accumulation and myocardial edema. This phenomenon has important implications to left ventricular structure and function in the first hours after myocardial infarction. We hypothesized that during this period of time, after prolonged coronary occlusion and complete reflow, the rate of myocardial sodium accumulation is governed by microvascular integrity. We used 3-dimensional (23)Na MRI to monitor myocardial sodium content changes over time in an in vivo closed-chest canine model (n=13) of myocardial infarction and reperfusion. Infarcts with microvascular obstruction (MO) defined by both radioactive microspheres and contrast-enhanced (1)H MRI showed a slower rate of sodium accumulation as well as lower blood flow at 20 minutes and 6 hours after reperfusion. Conversely, the absence of MO was associated with faster rates of sodium accumulation and greater blood flow restoration. In addition, infarct size by (23)Na MRI correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced (1)H MRI at 9 hours after reperfusion. We conclude that in reperfused myocardial infarction, sodium accumulation is dependent on microvascular integrity and is slower in regions of MO compared with those with patent microvasculature. Finally, (23)Na MRI can be a useful tool for monitoring in vivo myocardial sodium content in acute myocardial infarction.
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PMID:Microvascular integrity and the time course of myocardial sodium accumulation after acute infarction. 1102 99

Nicorandil is an adenosine triphosphate-sensitive potassium channel opener with a nitrate-like effect. It is approved for clinical use in Europe and Japan as an antianginal drug. The purpose of this investigation was to assess the acute effects of nicorandil therapy on microvascular injury using the blood pool MR contrast medium, NC100150 injection (Clariscan). Microvascular injury was produced in 24 rats using 45 min of coronary occlusion / 3 hr reperfusion. Nicorandil was infused at 15 min of occlusion and during reperfusion. Control animals received a saline solution. MR imaging was used to characterize microvascular permeability, quantify the extent of microvascular injury, LV volume, and wall thickness. Hyperenhancement at 30 min after administration of 0.05 mmol/kg Clariscan mapped the extent of ischemia-induced loss of microvascular integrity. The accumulation of Clariscan in the injured region was significantly suppressed in nicorandil compared to control rats. Nicorandil reduced the extent of microvascular injury from 44 +/- 2% to 18 +/- 2% (P < 0.01) and true infarction size from 29 +/- 2% to 12 +/- 1%. The extent of the hyperenhanced region correlated with the true size of area at risk at autopsy. On spin-echo MRI during end-diastole, nicorandil reduced LV end-diastolic volume and preserved wall thickness in remote myocardium; both parameters are markers of LV dilatation caused by acute infarction (remodeling). In conclusion, blood pool contrast-enhanced MRI has the potential to depict and quantify the extent of microvascular permeability and injury. Nicorandil suppressed microvascular permeability, reduced infarction size, and improved LV function in early postinfarction reperfusion.
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PMID:Blood pool contrast-enhanced MRI detects suppression of microvascular permeability in early postinfarction reperfusion after nicorandil therapy. 1197 68

Following myocardial infarction (MI), contractile dysfunction develops not only in the infarct zone but also in noninfarcted regions of the left ventricle remote from the infarct zone. Inflammatory activation secondary to MI stimulates inducible nitric oxide synthase (iNOS) induction with excess production of nitric oxide. We hypothesized that the anti-inflammatory effects of selective A(2A)-adenosine receptor (A(2A)AR) stimulation would suppress inflammation and preserve cardiac function in the remote zone early after MI. A total of 53 mice underwent 60 min of coronary occlusion followed by 24 h of reperfusion. The A(2A)AR agonist (ATL146e, 2.4 microg/kg) was administered intraperitoneally 1, 3, and 6 h postreperfusion. Because of the 1-h delay in treatment after MI, ATL146e had no effect on infarct size, as demonstrated by contrast-enhanced cardiac MRI (n = 18) performed 24 h post-MI. ATL146e did however preserve global cardiac function at that time by limiting contractile dysfunction in remote regions [left ventricle wall thickening: 51 +/- 4% in treated (n = 9) vs. 29 +/- 3% in nontreated groups (n = 9), P < 0.01]. RT-PCR, immunohistochemistry, and Western blot analysis indicated that iNOS mRNA and protein expression were significantly reduced by ATL146e treatment in both infarcted and noninfarcted zones. Similarly, elevations in plasma nitrate-nitrite after MI were substantially blunted by ATL146e (P < 0.01). Finally, treatment with ATL146e reduced NF-kappaB activation in the myocardium by over 50%, not only in the infarct zone but also in noninfarcted regions (P < 0.05). In conclusion, A(2A)AR stimulation after MI suppresses inflammatory activation and preserves cardiac function, suggesting the potential utility of A(2A)AR agonists against acute heart failure in the immediate post-MI period.
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PMID:Stimulation of A2A-adenosine receptors after myocardial infarction suppresses inflammatory activation and attenuates contractile dysfunction in the remote left ventricle. 1628 33

It has been shown that manganese-enhanced MRI (MEMRI) can safely depict the myocardial area at risk in models of coronary occlusion-reperfusion for at least 2 h after reperfusion. To achieve this, a solution of MnCl(2) is injected during coronary occlusion. In this model, the regional function quantification deficit of the stunning phase cannot be assessed before contrast injection using MR tagging. The relaxation effects of manganese (which remains in normal cardiac myocytes for several hours) may alter the tags by increasing tag fading and hence the quality of strain measurement. Therefore, we evaluated the feasibility of cardiac MR tagging after manganese injection in normal rats. Six normal Sprague-Dawley rats were imaged in vivo using complementary spatial modulation of magnetization (C-SPAMM) at 1.5 T, before and 15 min after intraperitoneal injection of MnCl(2) solution (~17.5 micromol kg(-1)). The contrast-to-noise ratio of the tag pattern increased significantly (P < 0.001) after injection and remained comparable to the control scan in spite of the higher myocardial relaxation rate caused by the presence of manganese. The measurements of circumferential strain obtained from harmonic phase imaging analysis of the tagged images after MnCl(2) injection did not differ significantly from the measurements before injection in the endocardial, mid-wall, and epicardial regions. In particular, the transmural strain gradient was preserved. Thus, our study suggests that MR tagging could be used in combination with MEMRI to study the acute phase of coronary artery disease.
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PMID:Feasibility of complementary spatial modulation of magnetization tagging in the rat heart after manganese injection. 1733 Sep 27

The aim of this study was to measure the myocardial area at risk in rat, using MRI and manganese injection during a coronary occlusion/reperfusion model at 1.5T. A sequential protocol with occlusion and MnCl2 injection immediately followed by MRI was used with the assumption that MnCl2-induced contrast persistence is enough to accurately image the area at risk 90 min after occlusion. A total of 15 adult rats underwent a single 30-min episode of coronary occlusion followed by reperfusion. MnCl2 was injected (25 micromol/kg) at the beginning of the occlusion for 11 rats (group 1) and 6 h after reperfusion for four animals (group 2). A deficit of signal enhancement was observed in all rats. Hypoenhancement area in group 1 was correlated to the area at risk delineated by methylene blue (r=0.96, P<0.0001) whereas in group 2 it was correlated to the infarct area given by triphenyltetrazolium chloride (TTC) solution (r=0.98, P=0.003). The area at risk size was significantly correlated with left ventricle ejection fraction (LVEF), end-systolic volume and anterolateral wall thickening. This work demonstrates that hypoenhanced zone obtained after manganese injection during occlusion represents the area at risk and not only the infarct zone.
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PMID:In vivo myocardial infarct area at risk assessment in the rat using manganese enhanced magnetic resonance imaging (MEMRI) at 1.5T. 1850 88

The activation of adenosine 2A receptors before reperfusion following coronary artery occlusion reduces infarct size and improves ejection fraction (EF). In this study, we examined the effects of delaying treatment with the adenosine 2A receptor agonist ATL146e (ATL) until 1 h postreperfusion. The infarct size and EF were serially assessed by gadolinium-diethylenetriaminepentaacetic acid-enhanced MRI in C57BL/6 mice at 1 and 24 h postreperfusion. The infarct size was also assessed by 2,3,5-triphenyltetrazolium chloride staining at 24 h. Mice were treated with ATL (10 microg/kg ip) either 2 min before reperfusion (early ATL) or 1 h postreperfusion (late ATL) following the 45-min coronary occlusion. The two methods used to assess infarct size at 24 h postreperfusion (MRI and 2,3,5-triphenyltetrazolium chloride) showed an excellent correlation (R=0.96). The risk region, determined at 24 h postreperfusion, was comparable between the control and ATL-treated groups. The infarct size by MRI at 1 versus 24 h postreperfusion was 25+/-1 vs. 26+/-1% of left ventricular mass (means+/-SE) in control mice, 16+/-2 versus 17+/-2% in early-ATL mice, and 24+/-2 versus 25+/-2% in late-ATL mice (intragroup, P=not significant; and intergroup, early ATL vs. control or late ATL, P<0.05). EF was reduced in control mice but was largely preserved between 1 and 24 h in both early-ATL and late-ATL mice (P<0.05). In conclusion, after coronary occlusion in mice, the extent of myocellular death due to ischemia-reperfusion injury is 95% complete within 1 h of reperfusion. The infarct size was significantly reduced by ATL when given just before reperfusion, but not 1 h postreperfusion. Either treatment window helped preserve the EF between 1 and 24 h postreperfusion.
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PMID:Timing of adenosine 2A receptor stimulation relative to reperfusion has differential effects on infarct size and cardiac function as assessed in mice by MRI. 1884 40


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