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)

In choosing a pharmacologic agent for stress testing, the clinician must keep a number of things in mind, such as the diagnostic utility of the agent or in what situations a vasodilator or catecholamine will be the better choice. Although all stress agents produce similar diagnostic accuracy for CAD, vasodilators have a higher cardiac uptake than catecholamines, and the addition of exercise improves the heart/background contrast ratios. With regard to physiologic comparisons, exercise or dobutamine will double coronary perfusion compared with baseline flow, but vasodilators produce a threefold or fourfold increase. The clinician should also keep in mind that adenosine will produce the shortest duration of hyperemia, whereas dobutamine and arbutamine produce a longer effect, and dipyridamole has the longest duration. If electrophysiologic considerations are important, exercise and catecholamines accelerate sinoatrial and atrioventricular conduction and are not typically associated with heart block. In contrast, adenosine can cause transient atrioventricular block, but this rarely occurs with dipyridamole. Clinical factors also must be considered. Although clinical utility of pharmacologic stress agents in the first 24 hours after infarction has not been demonstrated, the prognostic utility of vasodilators in the subsequent 2- to 4-day period has been shown. With patients with pulmonary disease (asthma) who do not have wheezing, dipyridamole can be used, but dobutamine or arbutamine should be used in patients with recent respiratory failure or bronchospasm before testing. In patients with left bundle branch block, vasodilators are the preferred stress agents rather than synthetic catecholamines or dynamic exercise. In the first crossover thallium imaging, there was good overall agreement in segmental perfusion comparing adenosine and dipyridamole, but there was a tendency for adenosine to detect more ischemia. The clinical significance (if any) for these findings has yet to be determined.
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PMID:Comparison of pharmacologic stress agents. 898 83

A stress test that can be performed intraoperatively might be valuable for cardiac risk stratification in patients needing urgent noncardiac surgery and for early evaluation of coronary reserve in patients undergoing aortocoronary bypass surgery. Therefore, we evaluated the sensitivity and safety of rapid atrial pacing combined with electrocardiography and transesophageal echocardiography for inducing and detecting provokable demand ischemia in 20 anesthetized patients with multivessel coronary artery disease. Rapid atrial pacing induced ST segment changes or new segmental wall motion abnormalities (SWMA), which were defined as evidence of induced ischemia in 15 of the 20 patients. Unexpectedly, the new SWMA normalized during the first beat after abrupt cessation of pacing in three patients who did not show any ST segment changes. Simultaneously, left ventricular preload was severely decreased during pacing and recovered to baseline immediately when pacing was abruptly discontinued. Rapid atrial pacing was safe in all patients, but the target heart rate could not be achieved because of heart block or arterial hypotension in 4 of the 20 patients. These findings raise the question of whether rapid atrial pacing is the most appropriate approach for inducing provokable demand ischemia in anesthetized patients. However, its potential usefulness for predicting adverse cardiac outcomes has not been evaluated and would require larger studies. In addition, the immediate normalization of new SWMA after abrupt cessation of pacing in some patients calls into question the validity of new SWMA as evidence of myocardial ischemia when left ventricular preload is severely decreased.
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PMID:Rapid atrial pacing for detecting provokable demand ischemia in anesthetized patients. 917 88

We hypothesized that by limiting the Na+ and Ca2+ loading by a blocker/inhibitor of the Na+ channel (lidocaine), Na+ overload (R56865: N-[1-[4-(4-fluorophenoxy)butyl]-4-piperidinyl]-N-methyl-2-benzothiazo lamine), Ca2+ channel (verapamil), Na+ -H+ exchange (ethylisobutyl amiloride) or of Na+ -Ca2+ exchange (No. 7943: 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate), it should be possible to reduce ischemia/reperfusion-induced arrhythmias. To test this hypothesis, we used anaesthetized rats subjected to 5 min of coronary artery occlusion followed by 10 min of reperfusion to study antiarrhythmic effects of above compounds on reperfusion-induced ventricular premature beats, ventricular tachycardia, and reversible and irreversible ventricular fibrillation. Compound or saline was administered as an intravenous bolus injection at 5 min before ischemia. Pretreatment with lidocaine (5 mg/kg), verapamil (0.63 mg/kg), R56865 (0.63 mg/kg) or ethylisobutyl amiloride (1.25 mg/kg) significantly reduced or abolished all types of ventricular arrhythmias. However, pretreatment with verapamil was associated with second or third degree heart block in 3 out of 12 animals. Pretreatment with No. 7943 did not significantly influence the ischemia/reperfusion-induced ventricular arrhythmias. The present results suggest that both intracellular Na+ -and Ca2+ -loading play important roles in reperfusion-induced ventricular arrhythmias and the inhibition of Na+ -Ca2+ exchange to limit Ca2+ loading probably does not play any important role in ischemia/reperfusion-induced arrhythmias in anaesthetized rats.
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PMID:Ischemia/reperfusion-induced arrhythmias in anaesthetized rats: a role of Na+ and Ca2+ influx. 998 7

We examined whether angina pectoris (AP) occurring shortly before the onset of acute myocardial infarction (AMI) can render the right ventricle and the conducting tissue resistant to ischemia in 75 patients with an inferior wall AMI. Each patient had total occlusion in the proximal right coronary artery and underwent successful coronary angioplasty < or =24 hours from the onset. We divided patients into 2 groups based on presence or absence of antecedent AP < or =24 hours before the system onset: group 1 (absent) = 57 patients; group 2 (present) = 18 patients. Collateral circulation was more frequently observed in group 2 than in group 1 (group 1 vs 2, 28% vs 61%, p <0.01). Elevation in ST segment > or =1 mm in lead V4R, hemodynamic right ventricular dysfunction, and frequency of high-degree heart block were more frequent in group 1 than in group 2 (75% vs 44%, 79% vs 39%, 53% vs 11%, p <0.05, respectively). Multivariate analysis demonstrated that antecedent AP is the only factor related to these complications. Thus, episodes of AP occurring shortly before onset may restrain development of ischemic damage of the right ventricle and conducting tissue, and are associated with better clinical and functional outcomes among patients with an inferior wall AMI.
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PMID:Antecedent angina pectoris as a predictor of better functional and clinical outcomes in patients with an inferior wall acute myocardial infarction. 1007 14

Mortality rates for coronary artery disease are greater in elderly patients. Although prodromal angina occurring shortly before an acute myocardial infarction (MI) has protective effects against ischemia, this effect has not been well documented in older patients. This study investigated whether angina 1 week before a first MI provides protection in this group of patients. A total of 290 consecutive elderly (>64 years old, n = 143) and adult patients (<65 years old, n = 147) with a first MI were examined to assess the effect of preceding angina on the short- and long-term prognosis. Elderly patients with a history of prodromal angina were less likely than those without angina to experience in-hospital death, heart failure, or the combined end point of in-hospital death and heart failure (6% vs 20.4%, p = 0.02; 10% vs 23.7%, p = 0.07; 14% vs 32.3%, p = 0.01, respectively). Left ventricular function was more frequently depressed (ejection fraction <40%) in elderly patients without (44.8%) than with (26%, p = 0.04) preinfarction angina, and the incidence of arrhythmias (complete heart block and ventricular fibrillation) was greater in the former group (16.1% vs 4%, p = 0.03). Multivariate analysis confirmed that the presence of preinfarction angina was an independent predictor of in-hospital death and heart failure in older patients (odds ratio 0.28, p = 0.009). The occurrence of angina 1 week before a first MI may confer protection against in-hospital adverse outcomes, and may preserve left ventricular function in older patients.
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PMID:Does angina the week before protect against first myocardial infarction in elderly patients? 1186 66

This study was performed to determine the impact of electrocardiogram (ECG) interpretation on urgent patient care decisions by internal medicine (IM) and emergency medicine (EM) resident physicians. Six clinical scenarios and ECGs were given to 31 IM residents and 31 EM residents at a university medical center. Based on the ECG interpretation, the residents were asked to select the best patient management from a list of choices. IM and EM residents were equally likely to choose the correct management for complete heart block (90% IM v 97% EM, P = NS), and pulseless ventricular tachycardia (VT) (94% IM v 97% EM, P = NS). IM residents were less likely to choose the correct management for acute posterior wall myocardial infarction (MI) (26% IM v 74% EM, P <.0001) and unstable supraventricular tachycardia (SVT) (87% IM v 100% EM, P <.05). Residents in both programs were equally likely to misinterpret left ventricular hypertrophy (LVH) (23% IM and 16% EM, P = NS) and benign early repolarization (BER) (48% IM and 52% EM, P = NS) as acute myocardial ischemia when presented with a clinical history not suggestive of cardiac ischemia. IM and EM residents were equally likely to choose the correct management for complete heart block and pulseless VT. Compared with EM residents, IM residents were less likely to choose the correct management of posterior wall MI and unstable SVT. Both IM and EM residents were prone to misinterpreting LVH and BER as acute myocardial ischemia. Resident education in both specialties should focus on ECG interpretation skills to improve patient management decisions.
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PMID:Variation in patient management based on ECG interpretation by emergency medicine and internal medicine residents. 1199 38

The aim of this study was to examine 24h patterning in the symptoms indicative of third-degree atrio-ventricular (AV) heart block. We found a total of 227 cases (126 men and 101 women) of third-degree AV block that had been diagnosed by the Emergency Medical Department of the St. Anna Hospital in Ferrara, Italy between 1990 and 2001. Determination of the hour of onset of symptomatic third-degree AV block, however, was possible and listed in the records of only 161 or 70.9% of the cases (92 men and 69 women). The onset time of every event was categorized into one of four 6h spans of the 24h: night (00:00-05:59h), morning (06:00-11:59h), afternoon (12:00-17:59h), and evening (18:00-23:59h). The onset of the symptoms of third-degree AV block in the sample of 161 cases was significantly greater in the morning between 06:00 and 11:59h than any other 6h span of the day and night (chi2-test; p < 0.001). The same phenomenon was substantiated in the subgroup of the 92 males (chi2; p < 0.0001), although it could not be detected for the smaller subgroup of 69 women. The 24h pattern, with morning preference, in the onset of symptomatic third-degree AV block is similar to the one in sudden cardiac death and cardiogenic cardiac arrest. The etiology of the 24h pattern in symptomatic AV block is unknown; it may be an expression of intrinsic biological rhythmicity within the heart tissue or its control system, and/or the timing of environmental triggers resulting in coronary ischemia.
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PMID:Morning preference in onset of symptomatic third-degree atrioventricular heart block. 1218 3

It is of interest that the drugs having the most significant impact on total and sudden death mortality are those without direct electrophysiologic actions on myocardial excitable tissue. This observation may provide insight into mechanisms responsible for ventricular tachyarrhythmias causing cardiac arrest. One way to think about ventricular fibrillation is that it is the final common pathway of an electrically unstable heart. After all, the heart can "die" in only three major ways: electromechanical dissociation, asystole and heart block, and ventricular fibrillation, with the latter most common. It is the "upstream" events provoking the electrical instability that these drugs probably act upon (i.e., ischemia, fibrosis). Although we unquestionably need to pursue investigations into the electrophysiology of these ventricular tachyarrhythmias, more studies need to investigate the drugs affecting upstream events, because these agents appear to yield the greatest dividends, at least for the present. This article reviews these drugs and how they may be effective.
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PMID:Use of nonantiarrhythmic drugs for prevention of sudden cardiac death. 1295 May 27

The association between chronic kidney disease and cardiovascular death is accounted for, in part, by higher rates of serious arrhythmias. Research shows an independent relationship between worsened renal function and atrial fibrillation, heart block, ventricular tachycardia, ventricular fibrillation, and asystole. These higher rates also associate with underlying structural heart disease including left ventricular hypertrophy, cardiac fibrosis, valvular disease, and left ventricular systolic and diastolic dysfunction. In addition, chronic intermittent ischemia is implicated in the arrhythmias observed during hemodialysis. The superimposed conditions of acidosis and fluxes in both potassium and magnesium also contribute to higher rates of arrhythmias. Baseline estimated glomerular filtration rate is linked to worsened outcomes and increased defibrillation thresholds in patients receiving implantable cardioverter defibrillators. Preventive strategies include meticulous management of electrolytes, baseline treatment for cardiovascular disease, and when indicated, implantable cardioverter defibrillators. Future research into the mechanisms and prevention of sudden cardiac death in patients with chronic kidney disease is warranted.
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PMID:Chronic kidney disease and sudden death: strategies for prevention. 1473 22

Current consensus guidelines recommend postoperative electrocardiographic surveillance only in patients at relatively high risk of postoperative major cardiac complications, but the usefulness of electrocardiograms after major noncardiac surgery is unknown. We prospectively studied 3,570 patients who underwent major noncardiac procedures and had electrocardiograms performed in the recovery room. Rates of major cardiac complications (acute myocardial infarction, pulmonary edema, ventricular fibrillation or primary cardiac arrest, and complete heart block) were higher in patients who had new postoperative electrocardiographic abnormalities consistent with ischemia (ST-T elevation or depression or T-wave abnormalities compatible with ischemia) compared with those without ischemia (6.7% vs 1.9%, p <0.001). Multivariate analysis, after adjusting for pre- and intraoperative clinical data, indicated that the presence of ischemia on the immediate postoperative electrocardiogram was an independent predictor of major cardiac complications (odds ratio 2.2, 95% confidence interval 1.2 to 3.9, p <0.01). When patients were stratified by a preoperative Revised Cardiac Risk Index, ischemia on the immediate postoperative electrocardiogram identified patients with a higher risk of major cardiac complications in low- and high-risk subsets (odds ratio 4.9, 95% confidence interval 1.6 to 15 in lower risk patients; odds ratio 2.0, 95% confidence interval 1.0 to 3.7 in higher risk patients). We conclude that the immediate postoperative electrocardiogram is a valuable tool to adjust risk stratification, even in patients who have lower risks when undergoing noncardiac surgery.
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PMID:Value of immediate postoperative electrocardiogram to update risk stratification after major noncardiac surgery. 1547 15


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