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)

A 65 year old woman with history of ischaemic heart disease underwent standard adenosine stress test for myocardial perfusion imaging. She sustained inferior myocardial infarction during the final stages of the stress test. She was admitted to the coronary care unit and received thrombolytic treatment. The patient made an uneventful recovery. Adenosine is widely used for myocardial stress imaging tests and has a good safety profile. So far there has been only one other reported myocardial infarction during adenosine stress test, which was under special circumstances because three days before the test the patient had undergone percutaneous transluminal coronary angioplasty when a severe circumferential dissection was noted. The present patient's case highlights the need to be aware of rare but potentially serious complications of adenosine, even though it generally has an excellent safety record for use in myocardial stress testing.
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PMID:Myocardial infarction during adenosine stress test. 1179 65

Adenosine is an endogenous nucleoside that has been shown to be beneficial for the myocardium in different settings by a large number of experimental studies. In this article, we 1) outline adenosine's metabolic pathways, 2) address cardioprotective properties of adenosine, and 3) discuss possible implications of the two recently published clinical studies disclosing a positive effect of adenosine monophosphate deaminase 1 (AMPD1) gene mutation on cardiovascular survival in heart failure and ischemic heart disease. (Fig. 2, Ref. 84.)
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PMID:Adenosine and cardioprotection: what can we learn from nature's genetic polymorphism? 1244 64

The intrinsic cardiac nervous system is the final common integrator of regional cardiac function. The ischemic myocardium modifies this nervous system. We sought to determine the role that intrinsic cardiac neuronal P(1) purinergic receptors play in transducing myocardial ischemia and the subsequent reperfusion. The activity generated by ventricular neurons was recorded concomitant with cardiac hemodynamic variables in 44 anesthetized pigs. Regional ventricular ischemia was induced by briefly occluding (30 s) the ventral interventricular coronary artery distal to the arterial blood supply of identified ventricular neurons. Adenosine (100 microM) was administered to these neurons via their local arterial blood supply during or immediately after transient coronary artery occlusion. Occlusion was also performed following local administration of adenosine A(1) [8-cyclopentyl-1,3-dipropylxanthine (DPCPX)] or A(2) [3,7-dimethyl-1-propargylxanthine (DMPX)] receptor blocking agents. The activity generated by ventricular neurons was modified by transient coronary artery occlusion and the subsequent reperfusion (||Delta|| 112 +/- 14 and 168 +/- 34 impulses/min, respectively; P < 0.01 vs. preischemic states). Locally administered adenosine attenuated neuronal responses to reperfusion (-75%; P < 0.01 compared with normal reperfusion) but not ischemia. The neuronal stabilizing effects that adenosine elicited during reperfusion persisted in the presence of DMPX but not DPCPX. It is concluded that activation of neuronal adenosine A(1) receptors stabilizes the intrinsic cardiac nervous system during reperfusion.
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PMID:Adenosine A1 receptor activation reduces myocardial reperfusion effects on intrinsic cardiac nervous system. 1267 52

Adenosine (Ado), a naturally occurring autacoid, exerts cardioprotective effects against myocardial ischemia and reperfusion injury, through activation of its receptors type 1 (A1) and 2A (A2A). Since ageing involves a complex change in these effects, we evaluated A1 and A2A gene expression in left (LV) and right ventricle (RV) from 2-, 5-, 12-, and 21-month-old Sprague-Dawley rats. LV end-diastolic (EDD) and end-systolic (ESD) internal dimensions (mm) and LV fractional shortening (FS, %) were measured by M-mode echocardiography. Senescence was associated with a reduction in FS (42+/-1, 38+/-2, 39+/-2 and 35+/-2, in 2-, 5-, 12- and 21-month-old rats; p<0.02) and increases in EDD (7.5+/-0.2, 8.1+/-0.2, 8.5+/-0.2 and 8.8+/-0.2; p<0.001) and ESD (4.2+/-0.1, 4.4+/-0.2, 4.7+/-0.2 and 5.1+/-0.2; p=0.002). Ado A1 mRNA levels were highest in 12 and 21-month-old animals in both ventricles (LV: p<0.001; RV: p=0.001). By contrast, Ado A2A gene expression was lower in the aged LV (p<0.001), but higher in the aged RV (p<0.001). These modifications of Ado receptor gene expression and especially the increase in A1 receptor mRNA may partially explain the stronger antiadrenergic effects of Ado in the senescent heart.
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PMID:Adenosine A1 and A2A receptor cross-talk during ageing in the rat myocardium. 1291 7

We have previously demonstrated that brief episodes of tachycardia prior to a prolonged occlusion of a coronary artery, followed by reperfusion, substantially reduce the infarct size. Adenosine receptors and mitochondrial ATP-dependent K(+) channels mediate this effect. Since preconditioning can be induced or reverted by maneuvers that increase or decrease [Ca(2+)](i), respectively, and tachycardia increases [Ca(2+)](i), we studied the participation of sarcoplasmic reticulum and Ca(2+) in the preconditioning effect of tachycardia. We measured the effect of ischemia and tachycardia on Ca(2+) uptake and release by sarcoplasmic reticulum vesicles isolated from left ventricular canine myocardium. Myocardial ischemia increased Ca(2+)-release rate constants and decreased both the initial rates of Ca(2+) uptake and [(3)H]-ryanodine binding by sarcoplasmic reticulum. In addition, ischemia induced a decrease in the pentameric form of phospholamban and in the content of ryanodine-receptor Ca(2+)-release channel protein. All these effects were reverted in hearts preconditioned with tachycardia. Furthermore, tachycardia by itself increased [(3)H]-ryanodine binding, Ca(2+)-release rate constants and the protein levels of ryanodine-receptor Ca(2+)-release channels and the ATP-dependent Ca(2+) pump. These results suggest that tachycardia preserves the integrity of the sarcoplasmic reticulum preventing the excess of release and the decrease of uptake of Ca(2+) produced by ischemia, thereby avoiding cytosolic Ca(2+) overload. This sarcoplasmic reticulum protection could partly explain the preconditioning effect of tachycardia.
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PMID:Effect of tachycardia on myocardial sarcoplasmic reticulum and Ca2+ dynamics: a mechanism for preconditioning? 1465 69

Adenosine and verapamil have successfully been used in the treatment of clinical no-reflow after direct angioplasty for acute myocardial infarction. However, their effects on anatomic perfusion defects in experimental myocardial ischemia/reperfusion are unknown. Thus the area of no-reflow (ANR), visualized after in-vivo staining of perfused tissue by thioflavin S (% of the risk area, RA, blue dye), and regional myocardial blood flow (radioactive microspheres) were determined in anesthetized open-chest rabbits after 30 minutes of occlusion and 120 minutes of reperfusion. Adenosine, administered intravenously during the entire reperfusion period, reduced vascular resistance in the RA at 120 minutes of reperfusion by 39% compared with controls (P < 0.053). However, in every animal, sizable perfusion defects developed and the ANR with adenosine treatment (29 +/- 3%) was not significantly different from saline controls (35 +/- 6%). Intravenous verapamil, given during the entire reperfusion period, reduced vascular resistance in the RA by 54% at 120 minutes of reperfusion (P < 0.03). But perfusion defects, visible in every animal, were similar in size between verapamil (38 +/- 5%) and saline (35 +/- 6%) groups. Therefore, neither treatment prevented or attenuated perfusion defects after ischemia/reperfusion despite reducing vascular resistance in the RA; hence vasospasm is not a major contributor to microvascular perfusion defects in this model.
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PMID:Effects of adenosine and verapamil on anatomic no-reflow in a rabbit model of coronary artery occlusion and reperfusion. 1508 70

Today's definition of coronary artery disease (CAD) comprises two forms: obstructive and non-obstructive CAD. The 31-72% chance of a life-threatening event-like a myocardial infarction-with non-obstructive CAD is well documented in numerous studies. The objective in modern strategies of diagnosis and therapy should therefore be expedient identification of patients at high risk for coronary events, who will benefit from a customized therapy. Before initiating diagnostic procedures of CAD, a well defined strategy should be pursued. There are two possible primary objectives: ASSESSMENT OF THE INDIVIDUAL RISK FOR A CORONARY EVENT: Assessment of the individual "absolute" risk for a coronary event is not possible using single traditional risk factors. The individual risk can be estimated by integrating several of the traditional risk factors into a scoring system. These so-called risk scores (e.g. Framingham score and Procam score), however, have been associated with shortcomings: insufficient discrimination of high-risk from low-risk individuals. The calcium score has therefore become increasingly established; this Agatston score is independent of the traditional risk factors, so there is no correlation between Agatston and Procam scores. Today, the calcium score is considered the superior test for identifying individuals at high risk for a coronary event and its use is recommended by the European Society of Cardiology (ESC) guidelines for prevention of cardiovascular diseases. PROOF OR EXCLUSION OF A HEMODYNAMICALLY SIGNIFICANT CORONARY STENOSIS: Another concept is the definitive proof or exclusion of a hemodynamically "significant" coronary narrowing. The probability of an obstructive CAD is traditionally assessed by the type of chest pain, age, gender and stress-ECG. In patients with a low probability of an obstructive CAD, cardiac catheterization is not indicated, whereas in patients with a high probability of a hemodynamically significant coronary stenosis, an invasive strategy should be performed. Since non-invasive coronary angiography (CTA) with cardiac-CT has been shown to provide a high negative predictive value, CTA (with good imaging quality) is suitable for ruling out a significant obstructive CAD in the group at intermediate risk for an obstructive CAD. Another approach could be a functional test to initially prove a relevant, inducible myocardial ischemia: In a large cohort it was shown that patients will only prognostically benefit from revascularization procedures if the ischemic myocardial area is greater than 10%. Therefore, the assessment of the extent of myocardial ischemia is the domain of modern stress imaging tests. Stress-echocardiography and myocardial scintigraphy have almost the same sensitivity (74-80%, 84-90%, respectively) and specificity (84-89%, 77-86%, respectively), which are considerably higher than for stress-ECG. Cardiac MR is most suitable for the assessment of myocardial perfusion, because it traces the first pass dynamics of gadolinium at rest and during stress in reproducible slices at an acceptable spatial and a high temporal resolution without ionizing radiation. Whether the non-invasive coronary angiography with cardiac-CT and the Adenosin-perfusion imaging with cardiac-MR will completely replace diagnostic cardiac catheterization and stress-echocardiography as well as myocardial scintigraphy remains to be evaluated in further studies.
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PMID:[Impact of both cardiac-CT and cardiac-MR on the assessment of coronary risk]. 1641 70

Adenosine is well known to be a cardioprotective substance in ischemic heart disease. However, the modulation of adenosine receptors and the production and degradation of endogenous adenosine in chronic heart failure (CHF) are not fully understood. We analyzed the gene expression patterns of adenosine-related genes in human failing and nonfailing myocardium using DNA microarray analysis and quantitative real time-polymerase chain reaction (RT-PCR). DNA microarray analysis revealed that the gene expression of adenosine A2a, A2b, and A3 receptors (A2aR, A2bR, and A3R) as well as that of adenosine deaminase (ADA) decreased in failing myocardium. The down-regulation of these genes was verified by quantitative RT-PCR. We also measured the activities of these adenosine metabolism-related enzymes in failing myocardium and cardiac adenosine levels in patients with CHF. In CHF patients, we observed the decreased enzyme activity of ADA and the elevation of cardiac adenosine levels in CHF patients. To enhance the signaling of adenosine receptors, we increased plasma adenosine levels using dipyridamole, which decreased the severity of CHF. The gene expression of A2aR, A2bR, A3R, and ADA was decreased in the failing hearts, and this decrease may impair adenosine-related signal transduction. The activities of adenosine-related enzymes were altered, thus increasing the myocardial adenosine levels; this increase may compensate for the impairment of adenosine-related signal transduction in patients with CHF. The impairment of adenosine-related signal transmission contributes to the pathophysiology of CHF.
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PMID:Impact of adenosine receptor signaling and metabolism on pathophysiology in patients with chronic heart failure. 1803 66

A common complication of percutaneous coronary intervention (PCI), no-reflow is predominantly encountered during interventions in degenerated saphenous vein grafts and is associated with a marked increase in short-term mortality risk. Etiologically, no-reflow is complex and multifactorial. Microembolic debris from dilated target sites, sustained diffuse microvascular spasm, and pathophysiologic alterations from initial ischemic insults and subsequent reperfusion injuries result in persistence of myocardial ischemia despite angiographic evidence of restored vessel patency. Treatments to prevent or reverse no-reflow include antiplatelet medications to interfere with platelet aggregation. However, insufficient evidence exists demonstrating benefits with their prophylactic use in humans. Distal protection devices target microemboli, but soluble vasoactive factors may elude capture, contributing to downstream vasospasm. Intracoronary administration of vasodilators during PCI address a root cause of no-reflow. Adenosine, nitroprusside, verapamil, nicardipine and others have been evaluated clinically, showing improvements across a range of surrogate TIMI flow grade and frame count and real endpoints (wall motion indices and elevated CPK). Nicardipine may be particularly well-suited for prevention or reversal of no-reflow, demonstrating pharmacologic protection equal or superior to mechanical distal protection devices. The consistent and often dramatic mitigation of no-reflow by adjunctive use of vasodilators supports the role of microvascular spasm as a major, modifiable cause of the syndrome and a critical therapeutic target. A further large-scale, prospective, randomized, controlled clinical study is warranted to confirm prior findings, determine the optimal dosing regimen, and whether treatment or prevention of no-reflow confers clinically relevant outcome benefits.
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PMID:Pharmaceutical interventions for the management of no-reflow. 1859 1

This study investigated plasma brain natriuretic peptide (BNP) levels in normotensive and hypertensive patients with suspected coronary artery disease during radionuclide pharmacological stress testing. Twenty-seven normotensive patients (15 males, aged 63.0+/-4.5 years and 12 females, aged 63.0+/-4.1 years) and 38 essential hypertensive patients (25 males, aged 63.3+/-3.3 years and 13 females, aged 64.6+/-2.6 years) with chest pain and exercise stress testing inconclusive for coronary artery disease underwent myocardial perfusion single-photon emission computed tomography (SPECT) using adenosine infusion. SPECT identified patients without (16 normotensive and 22 hypertensive) and patients with (11 normotensive and 16 hypertensive) transient perfusion defects. Basal BNP levels in normotensive patients without transient myocardial ischemia (3.1+/-1.2 fmol/ml) were significantly (P<0.01) lower than those observed in normotensive patients with transient ischemia (8.2+/-1.2 fmol/ml), whereas BNP levels in hypertensive patients without transient ischemia (8.2+/-1.0 fmol/ml) did not significantly differ from those in hypertensive patients with transient ischemia (8.1+/-2.0 fmol/ml). No significant difference was found in BNP levels between males or females either in normotensive or hypertensive patients without or with ischemia. Adenosine infusion did not significantly change BNP levels in any subject group without or with myocardial perfusion defects. Our findings show that increases in BNP allow early detection of myocardial ischemia in normotensive patients, but not in hypertensive patients with suspected coronary artery disease. Adenosine-induced myocardial ischemia does not affect BNP production already activated by coronary artery disease in normotensive patients and by hemodynamic changes in hypertensive patients.
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PMID:Plasma brain natriuretic peptide at rest and after adenosine-induced myocardial ischemia in normotensive and essential hypertensive patients with suspected coronary artery disease. 1895 35


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