Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Moderate use of alcohol has shown protective effects in coronary artery disease, while excessive use has been associated with cardiomyopathy and hypertension. Since alcohol is a vasodilator, we postulated that it might have protective effects when administered acutely in the setting of ischemia/reperfusion. Therefore, we studied the acute effects of alcohol on myocardial infarction in a rabbit model. Anesthetized, open chest rabbits were subjected to a 30 minute coronary artery occlusion followed by 4 hours of reperfusion. Rabbits were randomized to a control group (n = 20), receiving an infusion of 10 ml normal saline, intravenously, over 10 minutes via a Harvard pump, or an alcohol group (n = 20), receiving a diluted solution of 100% ethanol (1 ml/kg diluted in normal saline to 10 ml total solution) infused in a similar fashion. This infusion regimen resulted in an average blood alcohol level of 110 mg/dl (range 77-129) tested in five rabbits within the study. Ten minutes after in fusion, a marginal branch of the circumflex artery was occluded. Regional myocardial blood flow during coronary occlusion and reperfusion was measured using radioactive microspheres. Myocardial ischemic area at risk (AR) was assessed by blue dye injection and myocardial necrosis (AN) by triphenyltetrazolium chloride (TTC) staining. The mean regional coronary blood flow in ischemic tissue was 0.04 +/- 0.01 ml/min/g in the control group versus 0.03 +/- 0.01 ml/min/g in the experimental group (p = NS) and averaged 1.74 ml/min/g (control) to 1.98 ml/min/g (alcohol) in the nonischemic tissue. All rabbits received comparable ischemic insult: Collateral blood flow and AR were similar in both groups. An overall analysis showed no significant reduction in infarct size (expressed as the percent of necrotic tissue within the area at risk) in the alcohol group (23 +/- 3%) compared with the control group (27 +/- 4%). In conclusion, alcohol did not reduce infarct size in the rabb it model.
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PMID:Acute Ethanol Does Not Protect Against Ischemic/Reperfusion Injury in Rabbit Myocardium. 1061 80

Coronary artery disease is highly prevalent in patients with end-stage renal disease, and accounts for much of their observed morbidity and mortality. Despite this, diagnosing myocardial disease in this population remains problematic, because many patients present with abnormal baseline electrocardiograms, frequently compounded by silent or atypical symptoms. Conventionally used enzymatic markers of cardiac injury have not resolved this dilemma because of their poor specificity in end-stage renal disease. In particular, nonspecific elevations in creatinine kinase-muscle brain enzyme, a widely accepted marker of cardiac injury, have been consistently observed in the absence of other demonstrable evidence for cardiac injury. Recently, the cardiac troponins (troponin I and troponin T) have emerged as more sensitive markers for cardiac ischemia, facilitating rapid bedside diagnosis and early risk stratification. Unfortunately, cardiac troponin T shows poor specificity in end-stage renal disease, possibly because of variable expression in extracardiac tissues. On the other hand, troponin I consistently maintains a high sensitivity and specificity, and is the most sensitive marker for ischemic heart disease in this patient population.
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PMID:Current markers of myocardial ischemia and their validity in end-stage renal disease. 1063 Aug 19

Injury to the cardiovascular system causes an elevated expression of endothelin-1 (ET-1) and activation of several important signaling pathways including the mitogen-activated kinase (MAPK) cascade. The activation of these pathways has been implicated in the pathogenesis of cardiovascular disease caused by hypoxia, infections, and ischemia /reperfusion injury, cardiomyopathy and restenosis after balloon angioplasty. Important downstream targets of the MAPK and ET-1 pathways are the cell cycle regulatory molecules (cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors). Regulation of these molecules contributes to remodeling throughout the cardiovascular system. In addition, cell cycle molecules are important in the regulation of angiogenesis. These new data have led to the development of potential therapeutic modalities targeting these regulatory molecules in order to ameliorate various cardiovascular disease states.
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PMID:Cell cycle molecules and diseases of the cardiovascular system. 1076 98

We encountered a patient with hypertrophic cardiomyopathy complicated with exercise-induced myocardial ischemia. Exercise-stress 99mTc-tetrofosmin imaging demonstrated reversible ischemia in the lateral wall, whereas resting fatty acid imaging with a new beta-methyl branched fatty acid analogue, I-123-15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid (123I-9-MPA), showed impaired uptake and accelerated washout kinetics in the inferoapical and posteroseptal walls but not in the ischemia-related region. These findings suggest that the metabolic derangement is closely related to cardiomyopathy per se rather than exercise-induced myocardial ischemia in this patient with hypertrophic cardiomyopathy and a spastic coronary lesion so that myocardial perfusion and 123I-9-MPA imagings may contribute to clarifying the etiological background of impaired myocardial fatty acid metabolism.
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PMID:Impaired myocardial accumulation of 15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid in a patient with hypertrophic cardiomyopathy and exercise-induced ischemia due to vasospasm. 1077 May 82

The effect of beta-blocker (propranolol) on the metabolism and contraction of doxorubicin-induced cardiomyopathy during pacing or ischemia was examined by the phosphorus 31-nuclear magnetic resonance (31 P-NMR) in Langendorff hearts of chronically treated rabbits after cumulative doses of 16 mg doxorubicin/kg. After 8 weeks of doxorubicin treatment, beta-blocker (propranolol) was given orally over a period of 2 weeks for a cumulative dose of 1.4 mg/kg. Isolated hearts were paced at higher heart rates, or hearts were perfused on low flow. Adenosine triphosphate (ATP), creatine phosphate (PCr), inorganic phosphate (Pi), pH, left ventricular systolic developed pressure (LVDev P), and coronary flow were measured. The hearts were divided into three experimental groups: Group I consisted of controls, Group II consisted of doxorubicin treatment, and Group III consisted of doxorubicin treatment with propranolol. Group II showed a significant decrease of ATP during pacing (48 +/- 2%) and during low flow (61 +/- 6%) compared with Group I (86 +/- 9% at pacing, 94 +/- 6% on low flow). But Group III showed a significantly marked improvement of ATP during pacing (95 +/- 10%) and during low flow (83 +/- 3%) compared with Group II. Furthermore, Group II showed a significant decrease of LVDev P during pacing (69 +/- 6 mm Hg) and during low flow (63 +/- 3 mm Hg) compared with Group I (101 +/- 5 mm Hg at pacing, 95 +/- 9 mm Hg on low flow). But Group III showed a significantly marked improvement of LVDev P during pacing (93 +/- 5 mm Hg) and during low flow (83 +/- 14 mm Hg) compared with Group II. In conclusion, propranolol had a significant beneficial effect on metabolism and contraction during high-energy demand and during low oxygen supply of doxorubicin cardiomyopathy.
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PMID:Effect of beta-blocker on metabolism and contraction of doxorubicin-induced cardiotoxicity in the isolated perfused rabbit heart. 1082 57

Nuclear medicine techniques have been applied to cardiomyopathy as well as in ischemic heart diseases. Various types of radiopharmaceutical including 201Tl and 99mTc-labeled perfusion tracers, 123I-labeled fatty acid(BMIPP), sympathetic function (MIBG) and tracers for myocardial injuries have been used. Perfusion imaging identifies stress-induced ischemia associated with myocardial damage. Recent application of gated SPECT enables simultaneous assessment of ventricular function. 123I-BMIPP and MIBG can detect metabolic abnormality, which has diagnostic and prognostic value for hypertrophic cardiomyopathy. The MIBG uptake index, heart-to-mediastinum ratio, is known to show good prognostic value for estimating dilated cardiomyopathy. Nuclear medicine plays unique roles for evaluating functional and metabolic derangement in cardiomyopathy.
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PMID:[Nuclear medicine imaging for cardiomyopathy]. 1088 87

Extramedullary hematopoiesis (EMH) after fetal development is uncommon and is most often seen in patients who have hematologic disorders. EMH unassociated with hematologic disease is rare. After the recent observation of EMH in a myocardial infarct, we sought to determine the frequency and clinicopathologic setting of EMH in myocardial tissues submitted for pathologic examination. Hematoxylin and eosin (H&E)-stained sections from 805 consecutive myocardial samples (207 surgical specimens, 598 autopsy specimens) were examined retrospectively. The presence of immature erythroid or myeloid cell clusters in intramyocardial capillaries or stroma was considered sufficient for the diagnosis of EMH. Immunoperoxidase studies confirming the nature of the hematopoietic cell infiltrate were performed in selected cases. Foci of EMH (often multiple) were identified in 15 of 207 surgical hearts (7.2%) and in 22 of 598 autopsy hearts (3.7%). Patient ages (exclusive of premature infants) ranged from 2 weeks to 73 years (median, 13 years). Twenty-four of 37 (65%) EMH-positive cases were associated with infarcts in various stages of repair (accounting for 11 of 68 [16.2%] of all infarcts in surgical specimens and 13 of 86 [15.1%] of infarcts in autopsy specimens). Acute infarcts less than 72 hours old, excluding those with acute extension, were not associated with EMH. Viral myocarditis and myocardial hypertrophy with fibrosis accounted for primary diagnoses in the nonischemic, EMH-positive surgical cases, whereas seven of nine nonischemic, EMH-positive autopsy cases involved premature or term infants with no obvious myocardial disease. Another autopsy patient had sarcoidosis with myelophthisic involvement of her bone marrow and represented one of only two cases overall in which a hematopoietic disorder was coexistent or suspected. Myocardial EMH is relatively common after myocardial infarct but is rarely encountered in normal or nonischemic myocardium. Its presence in healing but not early acute stages of infarct suggests that EMH results from inflammation- or repair-associated trophic factors, not from ischemia itself.
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PMID:Myocardial extramedullary hematopoiesis: a clinicopathologic study. 1091 38

Cardiomyopathy (CM) comprises a heterogeneous group of diseases, including ischemic (ICM) and dilative (DCM) forms. The pathogenesis of primary DCM is not clearly understood. Recent studies in mice show that vascular endothelial growth factor (VEGF) is involved in ICM. Whether VEGF plays a role in human CM is unknown. We examined the mRNA and protein expression of VEGF and its receptors in hearts of patients with end-stage DCM and ICM and in healthy individuals using real-time polymerase chain reaction and Western blotting. Number of capillaries, area of myocytes, and collagen were calculated in cardiac biopsies using transmission electron microscopy. In DCM, except for VEGF-C, mRNA transcript levels of VEGF-A(165), VEGF-A(189), and VEGF-B and the protein level of VEGF-A and VEGF-R(1) were downregulated compared with controls (P:<0.05). However, in ICM, mRNA transcript levels of VEGF isoforms and protein levels of VEGF-C were upregulated. The vascular density was decreased in DCM but increased in ICM compared with controls (P:<0. 05). Muscular hypertrophy was not different for ICM and DCM, although DCM had more collagen (P:<0.05). Blunted VEGF-A and VEGF-R(1) protein expression and downregulated mRNA of the predominant isoform of VEGF-A, VEGF-A(165), to our knowledge shown here for the first time, provide evidence that the VEGF-A defect in DCM is located upstream. Whether downregulation of certain VEGF isoforms in DCM is a cause or consequence of this disorder remains unclear, although upregulated VEGF levels in ICM are most likely the result of ischemia.
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PMID:Selective downregulation of VEGF-A(165), VEGF-R(1), and decreased capillary density in patients with dilative but not ischemic cardiomyopathy. 1102 98

Little is known concerning the effect of oxidative stress on the expression of antioxidative enzymes in the decompensated cardiac hypertrophy of spontaneously hypertensive rats (SHR), considered as a model of dilative cardiomyopathy in man. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were characterized in isolated perfused hearts of 18 month old SHR and the age-matched normotensive control Wistar-Kyoto (WKY) rats, before and after 30 min infusion of 25 microM H(2)O(2). After infusion of H(2)O(2), aortic flow decreased in WKY from 26.2 +/- 2.2 to 16.0 +/- 0.8 ml/min (p <.05) but not in SHR (18.2 +/- 1.9 vs. 20.7 +/- 2.2 ml/min). This protection was related to the higher myocardial activities of GPx, MnSOD and CuZnSOD in SHR, compared with those of the WKY group. Although total SOD activity in the SHR fell after H(2)O(2) exposure (to 1.81 +/- 0.13 from 3.56 +/- 0.49 U/mg of protein), catalase activity increased (to 2.46 +/- 0.34 from 1.56 +/- 0.29 k min(-1)mg(-1)protein), compared with the pre-infusion period (p <.05 in each case). In additional studies, hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The results obtained in ischemic/reperfused hearts show the same changes in enzyme activities measured as it was observed in H(2)O(2) perfused hearts, indicating that oxidative stress is independent of the way it was induced. The higher catalase activity derived from elevated mRNA synthesis. The antioxidative system in dilative cardiomyopathic hearts of SHR is induced, probably due to episodes of oxidative stress, during the process of decompensation. This conditioning of the antioxidative potential may help overcome acute stress situations caused by reactive oxygen species in the failing myocardium.
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PMID:Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts. 1103 13

The echocardiographic examination is generally performed in patients with heart failure and it often gives a significant contribution to the differential diagnosis. Firstly, the evaluation of left ventricular pump function by measuring the ejection fraction (EF) can distinguish patients with heart failure into two different groups, with depressed or preserved EF. The most frequent causes of heart failure and depressed EF are coronary artery disease, idiopathic dilated cardiomyopathy (DCM) and hypertensive heart disease. Although the echocardiographic features of coronary artery disease versus idiopathic DCM may be similar, the demonstration of inducible ischemia at dobutamine echocardiographic test suggests the presence of significant coronary artery disease and may be useful in the selection of cases for coronary arteriography. The association of left ventricular hypertrophy, hypokinesis and, sometimes, significant dilation is compatible with hypertensive heart disease or end-stage hypertrophic cardiomyopathy. No useful echocardiographic findings can identify the patients with genetic DCM or affected by myocarditis from other cases with idiopathic DCM. Some advanced cases of right ventricular dysplasia/cardiomyopathy may show a biventricular involvement and mimic DCM; these patients are usually characterized at echo by predominant right ventricular dilation and multiple a-dyskinetic bulges in the absence of pulmonary hypertension. Very difficult to manage are the patients with significant left ventricular dysfunction and severe valvular heart disease (such as aortic stenosis or mitral regurgitation). According to the literature, the left ventricular systolic function is relatively preserved (EF > 40%) in 30-40% of patients with heart failure. In these cases a diastolic dysfunction may be hypothesized. Echo-Doppler evaluation can be helpful in the recognition of signs of increased left ventricular stiffness ("restrictive filling pattern") and of increased filling pressures. In the differential diagnosis one must first consider the most frequent heart disorders that may present with this clinical syndrome, coronary artery disease and hypertensive heart disease. Furthermore, other less common diseases characterized by heart failure due to predominant diastolic dysfunction are the following: hypertrophic and restrictive cardiomyopathies, infiltrative heart diseases, such as amyloidosis, and constrictive pericarditis. Restrictive cardiomyopathy is characterized by heart failure and preserved left ventricular EF in the absence of significant ventricular dilation and hypertrophy; typical, although not pathognomonic, echocardiographic features are atrial enlargement ad restrictive filling pattern. In distinguishing constrictive pericarditis from restrictive cardiomyopathy useful Doppler signs are the wide respiratory variability in flow velocities at mitral and tricuspid levels, due to increased ventricular interdependence caused by the presence of an abnormally rigid pericardium.
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PMID:[Contribution of echocardiography to the diagnosis of patients with chronic heart failure]. 1106 13


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