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)

This study was performed to assess the value of washout rate analysis of quantitative exercise thallium-201 emission computed tomography in vasospastic angina patients without significant coronary stenosis. Quantitative analysis of both thallium-201 perfusion and washout rate before and after drug treatment was performed in 48 patients with vasospastic angina and no significant coronary artery stenosis. All of the patients attained more than 90% of their age-predicted heart rate during each exercise test. Before drug treatment, 26 patients exhibited exercise-induced ischemia (perfusion defects on stress polar map), 17 did not exhibit exercise-induced ischemia (normal stress and washout rate polar maps), and the remaining 5 patients showed no perfusion defects, but did show extensive abnormal washout rates. On coronary angiography, multivessel coronary spasm was documented in 12 of the 26 patients with exercise-induced ischemia, in 7 of the 17 patients without exercise-induced ischemia and in 4 patients with an extensive abnormal washout rate and a normal stress polar map. In the 17 patients without exercise-induced ischemia, the mean washout rate was significantly decreased (p < 0.05) in association with a significant decrease in the double product (p < 0.05) after drug treatment. Of the 26 patients with exercise-induced ischemia, 18 (group 1) showed an increase in the mean washout rate with improved perfusion defect after drug treatment. The remaining 8 patients (group 2) showed a decrease in the mean washout rate with improved perfusion defect after drug treatment, which increased significantly on repeat exercise test performed after additional increased doses of antianginal drugs were administered (p < 0.01). The number of patients with multivessel coronary spasm was significantly high in group 2 (p < 0.01). Thirteen patients showed an extensive abnormal washout rate before drug treatment, including 8 patients with exercise-induced ischemia and 5 patients with no perfusion defects, who showed an increased mean washout rate after drug treatment (p < 0.05). These findings indicate that washout rate analysis aids in the diagnosis in vasospastic angina patients with exercise-induced ischemia. Some patients with exercise-induced ischemia can not be detected by thallium-201 perfusion analysis alone, especially those with multivessel coronary spasm and when this procedure is performed after drug treatment. In addition, a high frequency of abnormal washout rate in vasospastic angina may result not only from exercise-induced ischemia due to main epicardial coronary artery spasm, but also from microspasm, or impairment of microcirculation or myocyte.
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PMID:Assessment of quantitative exercise thallium-201 emission computed tomography in patients with vasospastic angina--value of washout rate analysis. 806 9

Despite the increasing evidence that alterations in coronary vascular tone can and do occur in patients with anginal syndromes, only in a minority of such patients with Prinzmetal's angina is there decisive evidence that the coronary vasodilation induced by calcium channel antagonists (CCAs) plays a specific therapeutic role. CCAs may also give therapeutic benefit in a number of conditions in which coronary vasoconstriction may contribute to ischemia, such as hyperventilation, cold-induced angina, or silent ischemia not caused by an increase in heart rate. Thus, the decision of whether or not to use CCAs in angina syndromes will often have to be made on grounds other than what appears to be a minor role of vasospasm in the overall spectrum of angina. There are preliminary indications that the long-term prognosis may be different among different categories of CCAs.
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PMID:Calcium channel antagonists in the management of anginal syndromes: changing concepts in relation to the role of coronary vasospasm. 855 88

The purpose of this study is to determine whether left ventricular dysfunction following coronary artery spasm by 123I-BMIPP myocardial imaging. To reveal the clinical efficacy of 123I-BMIPP SPECT, 20 patients with vasospastic angina were studied using resting, 3-hour delayed image with 123I-BMIPP and exercise, 3-hour delayed image with 201Tl SPECT. 123I-BMIPP uptake was decreased compared to 201Tl (discordant) in 12 patients (60%) and in 49/100 myocardial segments (49%). The extent and severity score in resting image with 123I-BMIPP were significantly larger than that in delayed image with 201Tl (p < 0.01). In 123I-BMIPP SPECT, the severity score in the latest ischemia were significantly larger than that in others. The incidence of a complete agreement of decreased 123I-BMIPP uptake and coronary artery spasm was significantly higher (75%) than that in 201Tl (28%, p < 0.01). Furthermore, compared to 201Tl uptake, decreased 123I-BMIPP uptake much more corresponded to reduced wall motion in 9 of patients with mismatching. The severity of regional wall motion abnormality was significantly correlated with severity score of 123I-BMIPP. Late redistribution in delayed image with 123I-BMIPP was seen in 6 patients. The regional washout rate and the severity of regional wall motion abnormality in 6 patients was significantly lower than that in others (p < 0.05). Thus, metabolic abnormality assessed by 123I-BMIPP is well associated with left ventricular asynergy and spastic region in patients with vasospastic angina. In conclusion, 123I-BMIPP SPECT may sensitively delineate the impaired myocardium following coronary artery spasm, and it is very useful in diagnosing and estimating the severity of vasospastic angina.
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PMID:[Evaluation of myocardial damage using 123I-BMIPP imaging in patients with vasospastic angina]. 874 4

To characterize the vasospastic angina patients with exercise-induced ischemia, we measured hemostasis (platelet factor 4; PF4, fibrinopeptide A; FPA) and fibrinolytic parameters (tissue plasminogen activator antigen; t-PA, free plasminogen activator inhibitor-1 antigen; free PAI-1) in 15 normal subjects and 33 vasospastic angina patients without significant coronary artery stenosis (less than 50% stenosis). All of the vasospastic angina patients began to feel chest pain within 3 months before diagnostic coronary angiography. Blood samples were obtained from all of the study patients at 8:30-9:30 am before exercise 201Tl emission computed tomography. Vasospastic angina patients were divided into 2 groups; 15 patients with exercise-induced ischemia (group 1) and 18 patients without exercise-induced ischemia (group 2). On coronary angiography, the severity of coronary artery stenosis at the site of spasm in group 1 (34 +/- 5%) was greater than that in group 2 (18 +/- 3%). Plasma FPA and PF 4 levels in group 1 were also significantly higher than those in normal subjects and group 2. Plasma t-PA and free PAI-1 levels in group 1 were significantly higher than those in normal subjects and group 2. Plasma levels of free PAI-1 group 2 were also significantly higher than those in normal subjects. The present study demonstrated that all of the patients with vasospastic angina had impaired fibrinolysis, and these patients with exercise-induced ischemia showed enhanced platelet activation, an enhanced coagulation system, and advanced atherosclerotic lesions. These results suggest that vasospastic angina with exercise-induced ischemia puts patients at increased risk for thrombus formation.
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PMID:Characteristics of vasospastic angina with exercised-induced ischemia--analysis of parameters of hemostasis and fibrinolysis. 880 21

The authors discuss the transient ischemic Q waves in various situations. Five cases are presented. Two patients had exercise-induced Q waves, one patient had right bundle branche block-dependent Q waves, one patient had transient Q waves after thrombolytic therapy and one patient had transient Q waves caused by Prinzmetal angina. Profound ischemia may not result in necrosis but may cause myocardial stunning. Myocardial stunning may be accompanied by deranged electrophysiologic activity with transient loss of electromotive forces.
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PMID:[Transient Q-waves in coronary disease]. 910 23

Recently, there has been some controversy concerning calcium antagonists, suggesting the need for further debate on this heterogeneous class of drugs. Three chemical families, dihydropyridines (DHP), phenylalkylamines (verapamil) and benzothiazepines (diltiazem) bind to the type L receptors of the calcium channels with different binding, modulation and tissue selectivity characteristics. DHP are selective for type L receptors and block the extracellular portion of the channel leading to vigorous vasodilatation and little or no cardiodepressive effect. Diltiazem and verapamil also interfere with type T channel receptors. These drugs have a cardiodepressive and a bradycardia effect. Verapamil blocks the intracellular portion of the calcium channel at the site where part of the catecholamine effect occurs, leading to less reflex sympathetic activation than with other calcium antagonists (namely DHP). Deleterious sympathetic stimulation is proportional to the intensity and degree of rapid onset of arterial vasodilatation and is attenuated with slow-release formulations. Calcium antagonists in general have an anti-angina effect but high-dose short-acting DHP can cause excessive vasodilatator leading to subsequent ischemia. In chronic stable angina, slow-release verapamil has been shown to have a preventive clinical effect comparable to that of beta blockers. Slow-release nifedipine is effective and safe but must be associated with betablockers. In unstable angina, only those calcium antagonists with a bradycardia effect appear to have an effect similar to beta blockers. Beta blockers are nevertheless to be preferred in these patients (excepting Prinzmetal angina) until results of convincing clinical studies are available. After the initial phase of myocardial infarction, again only calcium antagonists with a bradycardia effect have been shown to have a beneficial effect, in patients without cardiac failure: diltiazem in infarction without Q-wave and verapamil in all infarctions, in case of residual ischemia to reduce the risk of recurrence.
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PMID:[Calcium antagonists in ischemic heart disease]. 941 Oct 6

Iodinated fatty acid compounds have an important role in early detection of myocardial abnormalities and provide insights into pathological states in the heart. Among them, 15-(p-iodophenyl)-3R,S-methyl pentadecanoic acid (BMIPP) has been most widely used providing excellent images of the left ventricular myocardium due to high myocardial uptake and long retention. The previous chapters have focused on the basic characters and clinical applications of this compound. However, the precise mechanisms of myocardial kinetics should be further investigated under various conditions. Most of the studies showed reduced BMIPP uptake relative to perfusion in a variety of myocardial disorders, whereas an increase in BMIPP uptake relative to perfusion is often reported. The potential mechanisms of such conflicting results are discussed, but basic studies should be performed to clarify such results in detail. There are a number of clinical values of this compound. Since alteration of fatty acid is observed in the repetitive ischemia, BMIPP can be used for detecting severe ischemic episodes. The concept of 'ischemic memory' imaging can be applied for patients with unstable or vasospastic angina at rest and for those with acute myocardial infarction with successful revascularization to identify the risk area. The discordant decrease in BMIPP uptake relative to perfusion is often seen in ischemic but viable myocardium, and therefore, the combined imaging of BMIPP and perfusion can be used for assessment of tissue viability. Furthermore, abnormal BMIPP uptake is most often observed in hypertrophic cardiomyopathy, and thus, this compound can be used for an early detection and differential diagnosis of the cardiomyopathy. Although BMIPP imaging seems to be quite promising in many fields, the number of patient data remain limited. In this respect, a multicenter study with a vast majority of patients is warranted to confirm these important values of BMIPP. In addition, this attractive tracer should be available all over the world to confirm its clinical value in the near future.
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PMID:Future aspects of BMIPP. 1045 6

Reperfusion injury refers to cellular death or dysfunction caused by restoration of blood flow to previously ischemic tissue. This should be differentiated from the normal reparative processes that follow an ischemic insult. Four types of reperfusion injury have been described in the literature: (1) lethal reperfusion injury, (2) nonlethal reperfusion injury (myocardial stunning), (3) reperfusion arrhythmias, and (4) vascular injury (including the "no-reflow" phenomenon). There is continued debate whether reperfusion itself is capable of killing viable myocytes, which otherwise would have survived the ischemic insult. However, there is firm evidence for the existence of myocardial stunning following various ischemic syndromes, including reperfusion therapy for acute myocardial infarction, unstable angina pectoris, vasospastic angina, effort-induced ischemia, coronary artery bypass surgery, and cardiac transplantation. Reperfusion arrhythmia is more common after short ischemic episodes than after long ischemic periods. Thus, while reperfusion arrhythmias in the setting of acute myocardial infarction are relatively rare, reperfusion arrhythmias may be an important cause of sudden death. The "no-reflow" phenomenon has been described following reperfusion in patients with acute myocardial infarction. Three major components have been proposed as mediators of reperfusion injury: (1) oxygen free radicals, (2) the complement system, and (3) neutrophils. Numerous experimental studies have shown short-term benefit by blocking various stages of the postischemic inflammatory response. Oxygen free radicals scavangers, complement inhibition, leukocyte depletion, and the use of antibodies against various adhesion molecules have shown a reduction of infarct size in many ischemic/reperfusion experimental models. However, many of these agents failed to show a benefit in the clinical setting. Moreover, the long-term benefit of such intervention is still unknown.
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PMID:Pathobiology and Clinical Impact of Reperfusion Injury. 1060 22

Reperfusion injury refers to cellular death or dysfunction caused by restoration of blood flow to previously alchemic tissue. This should be differentiated from the normal reparative processes that follow an ischemic insult. Four types of reperfusion injury have been described in the literature: (1) lethal reperfusion injury, (2) nonlethal reperfusion injury, (myocardial stunning), (3) reperfusion arrhythmias, and (4) vascular injury (including the "no-reflow" phenomenon). There is continued debate whether reperfusion itself is capable of killing viable myocytes, which otherwise would have survived the ischemic insult. However, there is firm evidence for the existence of myocardial stunning following various ischemic syndromes, including reperfusion therapy for acute myocardial infarction, unstable angina pectoris, vasospastic angina, effort-induced ischemia, coronary artery bypass surgery, and cardiac transplantation. Reperfusion arrhythmia is more common after short ischemic episodes than after long ischemic periods. Thus, while reperfusion arrhythmias in the setting of acute myocardial infarction are relatively rare, reperfusion arrhythmias may be an important cause of sudden death. The "no-reflow" phenomenon has been described following reperfusion in patients with acute myocardial infarction. Three major components have been proposed as mediators of reperfusion injury: (1) oxygen free radicals, (2) the complement system, and (3) neutrophils. Numerous experimental studies have shown short-term benefit by blocking various stages of the postischemic inflammatory response. Oxygen free radicals scavengers, complement inhibition, leukocyte depletion, and the use of antibodies against various adhesion molecules have shown a reduction of infarct size in many ischemic/reperfusion experimental models. However, many of these agents failed to show a benefit in the clinical setting. Moreover, the long-term benefit of such intervention is still unknown.
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PMID:Pathobiology and Clinical Impact of Reperfusion Injury. 1063 61

Endothelin-1 (ET-1) induces severe pathologic conditions such as coronary spasm followed by vasospastic angina pectoris and acute myocardial infarction. The related pathophysiologic mechanisms have remained obscure. Endothelin-1 receptor (ET(A) and ET(B)) is reported to couple with several types of G protein-involved pathways that participate in phospholipase C activation and atrial myofibrils organization into sarcomeric units. Here we demonstrate that ET-1 induces histologic and pathologic dysfunction in the rabbit myocardium and that such pathologic events are prevented by the Rho-kinase inhibitor fasudil. Although the bolus injection of ET-1 (1.4 nmol/kg) via the auricular vein of the rabbit induced only transient T-wave elevation, irreversible, severe histologic changes were observed in papillary muscles of the ventricle, and multifocal myocardial necrosis with infiltration of neutrophils and macrophages in the left ventricle occurred. Oral administration of fasudil (10 mg/kg) significantly reduced the occurrence of myocardial injury determinants, whereas conventional Ca2+ channel blockers (nifedipine, diltiazem) and a K+ channel opener (nicorandil; 10 mg/kg, p.o. each) showed a lesser or no effect on such determinants. These results suggest that ET-1 induces severe myocardial dysfunction based not only on the occurrence of vasospastic ischemia but also on its direct effects on the myocardium.
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PMID:The protein kinase inhibitor fasudil protects against ischemic myocardial injury induced by endothelin-1 in the rabbit. 1067 51


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