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)

Over the last 5 to 8 years, numerous clinical studies have been conducted evaluating the effects of coronary ischemia on disparity of ventricular repolarization (VR) as assessed by determination of QT dispersion from the surface electrocardiogram. From findings in patients with acute myocardial infarction, stable coronary disease, and vasospastic angina there is convincing evidence that acute coronary ischemia augments inhomogeneity in VR. In some studies, this was associated with the occurrence of ventricular arrhythmias. In general, therefore, these clinical observations confirm previous experimental work. One should keep in mind, however, various problems inherent to the current technology used to determine QT dispersion from the surface electrocardiogram. Whereas some of these technological limitations can be overcome in carefully designed and conducted clinical studies, these methodological shortcomings have so far precluded the routine use of QT dispersion in taking care of patients with acute coronary syndromes. It remains to be seen whether further refinements in technology will enable clinicians to incorporate assessment of disparity of VR in daily practice in an attempt to further improve care of patients with acute coronary syndromes.
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PMID:Effect of coronary ischemia on QT dispersion. 1076 13

The objective of the present study was to investigate the differences between coronary hyperresponsiveness without ischemia and vasospastic angina in an ergonovine provocation test using multivariate analysis. We have sometimes experienced a more than 50% narrowing response of vascular diameter without ischemia in a coronary response to ergonovine. We studied 107 patients with less than 50% stenosis in a coronary arteriogram. Their vascular responses to ergonovine were measured and the patients were divided into three groups, as follows: Group 1 had 50% or less vascular narrowing response without ischemia; Group 2 had a vascular hyperresponsiveness of more than 50% narrowing response without ischemia; and Group 3 experienced a hyperresponsiveness with ischemia. The degree of coronary response was found to be related to smoking, inpaired glucose tolerance (IGT) and the Gensini score by multiple regression analysis. A multiple logistic analysis revealed that the Gensini score and smoking were significant predictive factors for Group 3 (odds ratio: 1.20 and 8.97). The only factor different between Group 2 and Group 1 was gender. The coronary hyperresponsiveness to ergonovine without ischemia differs from vasospastic angina in the degree of coronary atherosclerosis and smoking habits. The patients with hyperresponsiveness had similar characteristics to those with atypical chest pain rather than vasospastic angina, except for a gender difference.
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PMID:Differences between coronary hyperresponsiveness to ergonovine and vasospastic angina. 1098 46

We briefly described recently developed methods for testing cardiac electrophysiological phenomena such as 24-hour Ambulatory ECG, high resolution ECG, body surface mapping ECG, heart rate variability, QT and QT dispersion, and T wave alternans. Of these methods ambulatory ECG monitoring is important and useful for detecting malignant arrhythmias and ischemia attacks, especially in cases of vasospastic angina. Using this method, it is possible to quantitatively analyze arrhythmia and elucidate the pathophysiology of vasospastic angina. The monitoring system is useful not only for diagnosis, but also for assessing treatment efficacy. Heart rate variability is currently used for analyzing the autonomic nervous system; however, the exact meaning of each index still remains to be confirmed. The concept of QT dispersion was recently introduced as an index for detecting dispersion of ventricular repolarization and QT dispersion is still controversial. T wave alternans monitoring has been recently introduced as a new method of assessing the microvolt level of T wave alternans, which has been hypothesized to correlate with the occurrence of arrhythmic events in myocardial infarction. The possible roles of these methods and their applications for clinical practice are discussed.
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PMID:[Electrophysiological tests in clinical laboratory]. 1145 37

Electrical alternans represents a variation in the morphology of electrocardiographic complexes on an every-other-beat basis in an ABABAB... pattern. Apparent electrical alternans associated with pericardial effusion results from rotation of the heart in the pericardial sac, and not true alternation in electrical conduction patterns. In contrast, true electrical alternans results from an alternation in electrical conduction patterns in the heart itself. Repolarization alternans is true electrical alternans associated with the ST segment and T wave of the electrocardiogram (ECG). Here we will focus on T-wave alternans (TWA) and its association with susceptibility to ventricular tachyarrhythmias. Electrical alternans was reported in the literature as early as 1909. Historically, electrical alternans has been regarded as a fairly rare electrocardiographic abnormality. Case reports of electrical alternans have been associated with a variety of disease states, including acute ischemia, Prinzmetal's angina, a variety of electrolyte abnormalities, and the long QT syndrome. Interestingly, patients born with the prolonged QT syndrome have a very high incidence of sudden cardiac death at an early age. Schwartz and Malliani showed that patients with the prolonged QT syndrome who do not demonstrate alternans at rest, may evidence alternans during stress such as emotional excitement. Thus, over the years electrical alternans has been associated anecdotally with conditions associated with an increased risk of ventricular arrhythmias. In 1948, Kalter reviewed the world literature on electrical alternans and found a total of 41 reported cases. In addition, he reviewed clinical ectrocardiograms from 6059 patients and found five new cases (incidence of less than 1 in 1000 patients). Interestingly, he found a very high mortality, 62%, associated with this condition. Despite the clinical associations reported in the literature, the consensus view of electrical alternans until recent years has been that alternans is an electrocardiographic curiosity rarely encountered in clinical practice which, when identified, does not have specific clinical significance.
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PMID:Clinical utility of T-wave alternans. 1154 10

This report describes a case of an unusual association between vasospastic angina, coronary myocardial bridging, and Brugada syndrome. The patient complained of chest pain followed by rhythmic palpitation and syncope. Brugada syndrome ECG markers were documented with transient ST-segment elevation in lateral leads. A coronary angiogram showed a myocardial bridging in the left anterior descending artery and coronary vasospasm was reproduced after intracoronary ergonovine injection in the circumflex coronary artery. Ventricular fibrillation was induced by programmed electrical stimulation. The described association can be important because interaction between ischemia and Brugada syndrome electrophysiological substrate could modulate individual susceptibility to life-threatening ventricular tachyarrhythmias.
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PMID:Brugada syndrome: a case report of an unusual association with vasospastic angina and coronary myocardial bridging. 1199 81

Diagnostic usefulness of 99mTc-MIBI myocardial SPECT at rest was examined in 39 cases of coronary vasospastic angina pectoris who were diagnosed by a positive reaction to ergonovine provocation. SPECT was performed 45 minutes (early image) and 3 hours (delayed image) after the intravenous injection of approximately 600 MBq of MIBI. Decrease in accumulation was ranked by four defect scores (0: normal; 1: slight decrease; 2: moderate decrease; 3: severe decrease) and the total defect score was evaluated semiquantitatively. The washout rate between the normal area and the spasm area was also evaluated quantitatively using bull's eye. As a result, 15 cases (15/39; 38.4%) showed decreased accumulation in the early image and 27 cases (27/39; 69.2%) showed decreased accumulation in the delayed image. All of the cases which showed decreased accumulation in the early image had decreased accumulation in the delayed image as well. In 6 cases (6/34; 17.6%) showed ST wave changes during exercise ECG and 16 cases (16/34: 47%) showed decreased accumulation in the exercise myocardial SPECT. The washout rate of MIBI in the decreased accumulation area was significantly higher than that of the normal area. Of 32 ergonovine induced vasospastic area, 23 areas (72%) exhibited decreased accumulation in the delayed image for the same area. Decreased accumulation in the delayed image in MIBI was due to the enhanced washout, which, in turn, indicated declined retention of MIBI by mitochondrial membrane. In coronary vasospastic angina pectoris, spasm induced ischemia was thought to have an effect on the mitochondria. This study suggested that even with a normal exercise ECG and exercise myocardial SPECT, there's a strong possibility of coronary vasospastic angina pectoris if a decreased accumulation was found in the delayed image in the MIBI myocardial SPECT at rest. Hence, in diagnosing coronary vasospastic angina pectoris, the delayed image in the MIBI myocardial SPECT at rest was believed to be useful.
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PMID:[Rest delayed images on 99mTc-MIBI myocardial SPECT as a noninvasive screen for the diagnosis of vasospastic angina pectoris]. 1205 20

ATP-sensitive K(+) (K(ATP)) channels comprise the pore-forming subunit (Kir6.1 or Kir6.2) and the regulatory subunit sulfonylurea receptors (SUR1 or SUR2). K(ATP) channels with different combinations of these subunits are present in various tissues and regulate cellular functions. From the analysis of mouse models with targeted deletion of the gene encoding the pore-forming subunit Kir6.1 or Kir6.2, functional roles of K(ATP) channels in various organs have been clarified. Kir6.1(-/-) mice showed sudden death associated with ST elevation and atrioventricular block in ECG, a phenotype resembling Prinzmetal angina in humans. Kir6.2(-/-) mice were more susceptible to generalized seizure during hypoxia than wild-type (WT) mice, suggesting that neuronal K(ATP) channels, probably composed of Kir6.2 and SUR1, play a crucial role for the protection of the brain against lethal damage due to seizure. In Kir6.2(-/-) mice lacking the sarcolemmal K(ATP) channel activity in cardiac cells, ischemic preconditioning failed to reduce the infarct size, suggesting that sarcolemmal K(ATP) channels play an important role in cardioprotection against ischemia/reperfusion injuries in the heart. Mitochondrial K(ATP) channels have been also proposed to play a crucial role in cardioprotection, although the molecular identity of the channel has not been established. Nicorandil and minoxidil, K(+) channel openers activating mitochondrial K(ATP) channels, decreased the mitochondrial membrane potential, thereby preventing the Ca(2+) overload in the mitochondria of guinea-pig ventricular cells. SURs are the receptors for K(+) channel openers and the activating effects on sarcolemmal K(ATP) channels in cardiovascular tissues could be modulated by the interaction of nucleotides. Due to the molecular diversity of the accessory and pore subunits of K(ATP) channels, there would be considerable differences in the tissue selectivity of K(ATP) channel-acting drugs. Studies of Kir6.1 and Kir6.2 knockout mice indicate that K(ATP) channels are involved in the mechanisms of the protection against metabolic stress. Further clarification of physiological as well as pathophysiological roles of K(ATP) channels may lead to a new therapeutic strategy to improve the quality of life.
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PMID:[Molecular and functional diversity of ATP-sensitive K+ channels: the pathophysiological roles and potential drug targets]. 1293 42

ATP-sensitive K+ channels (KATP channels) are present in various tissues, including pancreatic beta-cells, heart, skeletal muscles, vascular smooth muscles, and brain. KATP channels are hetero-octameric proteins composed of inwardly rectifying K+ channel (Kir6.x) and sulfonylurea receptor (SUR) subunits. Different combinations of Kir6.x and SUR subunits comprise KATP channels with distinct electrophysiological and pharmacological properties. Recent studies of genetically engineered mice have provided insight into the physiological and pathophysiological roles of Kir6.x-containing KATP channels. Analysis of Kir6.2 null mice has shown that Kir6.2/SUR1 channels in pancreatic beta-cells and the hypothalamus are essential in glucose-induced insulin secretion and hypoglycemia-induced glucagon secretion, respectively, and that Kir6.2/SUR2 channels are involved in glucose uptake in skeletal muscles. Kir6.2-containing KATP channels in brain also are involved in protection from hypoxia-induced generalized seizure. In cardiovascular tissues, Kir6.1-containing KATP channels are involved in regulation of vascular tonus. In addition, the Kir6.1 null mouse is a model of Prinzmetal angina in humans. Our studies of Kir6.2 null and Kir6.1 null mice reveal that KATP channels are critical metabolic sensors in acute metabolic changes, including hyperglycemia, hypoglycemia, ischemia, and hypoxia.
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PMID:Roles of ATP-sensitive K+ channels as metabolic sensors: studies of Kir6.x null mice. 1556 8

Coronary collateral circulation usually develops as a consequence of recurrent ischemia associated with severe stenosis. In exceptional cases, it can develop with moderate coronary lesions if there is severe recurrent vasospasm. In this situation, the presenting clinical features of vasospastic angina (i.e., effort angina with ST-segment depression) can be identical to those of a severe permanent lesion. We present a patient who exhibited effort angina and ST-segment depression on treadmill testing. Angiography showed severe right coronary artery stenosis and the development of coronary collateral circulation from the other main artery. After repeated intracoronary bolus injection of nitroglycerin, only a moderate stenosis was still apparent and the collateral circulation had disappeared.
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PMID:[Moderate coronary lesion with severe vasospasm and the development of collateral circulation in a patient with effort angina and ST-segment depression]. 1605 35

The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications.
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PMID:Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis. 1754 22


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