Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many patients presenting to the emergency department with suspected acute myocardial infarction have an initial electrocardiogram (ECG) non-diagnostic for acute injury or ischemia. Continuous ST segment monitoring devices have been used by physicians in the past to diagnose ischemia in the ambulatory outpatient population and to identify coronary occlusion in postthrombolytic and postsurgical patients. We report three patients with suspected acute myocardial infarction who underwent real-time continuous 12-lead ST segment monitoring with frequent serial ECGs on a microprocessor-controlled device during their initial emergency department evaluation. Continuous 12-lead ECG monitoring revealed significant changes on the ECG in all three cases presented, with a resultant change in emergency department therapy. Interestingly, all of these patients had significant ECG changes in the absence of recurrence of chest pain. We believe real-time continuous 12-lead ST segment monitoring with frequent serial ECGs can identify patients with an initially nondiagnostic or atypical ECG who may benefit from early interventional therapy.
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PMID:Continuous 12-lead electrocardiograph monitoring in the emergency department. 844 74

Changes in leukotriene C4 levels during different degrees of myocardial ischemia in humans were examined by comparing radioimmunoassay measures of leukotriene C4 plasma levels obtained during transient and prolonged myocardial ischemia. Leukotriene C4 levels in systemic arterial and coronary sinus blood were determined in patients with chronic stable angina before and after myocardial ischemia induced either by exercise (supine bicycle ergometer exercise stress testing; n = 14; age, 52 +/- 8 years) or by coronary occlusion during angioplasty (n = 14; age 53 +/- 7 years). Temporal changes of leukotriene C4 were also followed in arterial and pulmonary artery blood within 24 h after the onset of chest pain (acute phase), and 1 day, 1 week, and 1 month later in 22 patients with acute myocardial infarction (AMI) (12 patients with thrombolytic therapy, age 61 +/- 10 years; 10 patients without thrombolytic therapy, age 60 +/- 11 years). Clinical characteristics, including coronary risk factors and the severity of coronary artery disease, were not significantly different among the groups. Exercise-induced myocardial ischemia and coronary occlusion did not induce any significant leukotriene C4 changes in the chronic stable angina patients, whereas AMI patients had significantly higher plasma leukotriene C4 levels in both arterial and pulmonary artery blood in the acute phase compared with those of chronic stable angina patients (arterial blood, 471 +/- 164 pg/ml and 477 +/- 235 pg/ml vs. 275 +/- 254 pg/ml or 240 +/- 66 pg/ml, p < 0.05; pulmonary artery blood in AMI, 543 +/- 162 pg/ml vs. 234 +/- 125 pg/ml or 225 +/- 64 pg/ml, coronary sinus blood in chronic stable angina, p < 0.05). These results suggest that leukotriene C4 is involved more in prolonged myocardial ischemia than in transient myocardial ischemia, and that leukocyte function might play a significant role in the pathogenesis of patients with AMI.
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PMID:Change of plasma leukotriene C4 during myocardial ischemia in humans. 867 56

Myocardial infarction is the result of acute thrombotic occlusion of a coronary artery secondary to rupture of an atherosclerotic plaque. Intracoronary ultrasonic examinations (ICUS) were performed in patients with acute myocardial infarction in order to describe intraluminal ultrasonic findings at the site of an acute coronary occlusion. Coronary angiography and ICUS studies were performed consecutively within 6 h after the onset of chest pain in 50 patients with acute myocardial infarction (AMI) prior to percutaneous coronary angioplasty (PTCA). Following angiographic documentation of a proximal occlusion, a 3.5 mechanical ultrasound catheter (30 MHz) was advanced successfully through the lesion in 42 of 50 patients (84%). In 37 of the 42 patients (88.1%), ICUS differentiated between pulsatile, low echogenic, intraluminal material suggesting thrombus, and mural more highly echogenic atherosclerotic plaque. A negative imprint of the ICUS catheter was documented within the low echogenic material in 25 of 42 (60%) patients with AMI. Low echogenic intraluminal material was found in 31 of 42 (73.4%) segments proximal to the highly echogenic plaque and in 28 of 42 (66.7%) segments distal to it, indicating pre- and post-stenotic thrombus in AMI. The plaque appeared eccentric in 32 of 42 patients (76.2%) with AMI. Cross-sectional area stenosis due to highly echogenic plaque averaged 48 +/- 14%. Calcification of plaque was evident in 35 of 42 patients (83.3%) and the surface of the plaque was rough in 30 of 42 (42.4%). Fissures were found in 10 (23.8%) and a dissection was detected in four (9.5%) cases.
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PMID:Intravascular ultrasound imaging in patients with acute myocardial infarction. 874 38

Coronary angioplasty provides an ideal model for studying ischemic preconditioning in humans. Four coronary occlusions, each lasting 5.2 +/- 1.3 min, separated by 3 min of reperfusion, were performed during angioplasty of isolated stenosis of the left anterior descending artery of 18 patients with stable angina and normal left ventricular function. The ischaemia was evaluated and compared during the first and fourth coronary occlusion with the aid of clinical, electrocardiographic, echocardiographic and metabolic parameters. We analysed: 1) interval to chest pain and its intensity; 2) degree of ST change on the intracoronary electrocardiogram; 3) regional wall motion abnormalities on 2D echocardiography; 4) coefficient of myocardial lactate extraction. The results showed that during the fourth occlusion: chest pain occurred later (93 +/- 57 vs 60 +/- 49 s; p < 0.05) and ST elevation was less (0.69 +/- 0.5 vs 1.03 +/- 0.8; p < 0.05). During the fourth occlusion, there was a delay in appearance and a decrease in the regional wall motion abnormalities: anterior wall hypokinesia occurred later: 26 +/- 15 vs 19 +/- 19 s (p = 0.08). Akinesia observed in 10 patients out of 13 (77%) during the first occlusion, was only observed in 8 patients (62%) and dyskinesia, observed in 5 patients out of 13 (38%) during the first occlusion was not observed thereafter in any patient. The production lactate was less important during the fourth occlusion than during the first one: -3 +/- 17% vs -12 +/- 19% (p < 0.05). This study confirms that, in man, preconditioning allows myocardial adaptation to successive episodes of acute ischaemia.
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PMID:[Myocardial adaptation to ischemia. A study during repeated prolonged coronary occlusions in angioplasty]. 876 98

A 56-year-old male cigarette smoker, without other risk factors for arterial disease and no history of heart disease or thrombotic events, was admitted as an emergency case because of chest pain shortly after a fall. He had a right coronary artery occlusion, which was managed with angioplasty and stenting. A large thrombotic occlusion in the distal aorta probably occurred simultaneously with the coronary occlusion, became symptomatically manifest and was diagnosed when the chest pain subsided after stenting. This thrombus was successfully treated with the new platelet inhibitor abciximab.
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PMID:[Large arterial thrombosis. Rapid recanalization with a new thrombocyte inhibitor]. 941 Oct 93

It has recently been suggested that inflammation may play an important role in the pathogenesis of acute ischemic syndromes. It may therefore be important to relate their clinical features with plasma indexes of inflammation. We have studied leukocyte, platelet and fibrinogen blood levels in 57 consecutive patients with acute myocardial infarction admitted to our Intensive Care Unit within 90 min after the onset of chest pain and treated with primary coronary angioplasty. Patients were divided into two groups on the basis of blood leukocyte levels: Group A, 24 patients, 17 males, mean age 54.2 +/- 13.7 years, with high blood leukocytes and Group B, 33 patients, 28 males, mean age 60.9 +/- 10.3 years, with normal blood leukocytes. Group A patients also had higher serum fibrinogen (p = 0.05) and blood platelet levels (p < 0.05). The stenosis observed after guidewire advancement was significant (> 75%) in 33% of the patients with leukocytosis vs 94% of the others (p < 0.01). No difference between the two groups was observed in the success rate of coronary angioplasty and prevalence of stent placement (100 vs 97%, and 43 vs 42% of the patients of Group A and B, respectively). In contrast, a tendency to rethrombosis requiring Rheopro administration was observed in 62% Group A patients vs 21% Group B patients (p < 0.01). In conclusion, the finding of leukocytosis in the acute phase of myocardial infarction suggests that coronary occlusion is mainly caused by a coronary thrombus occurring at the site of a non significant stenosis. In contrast, when blood leukocytes are normal, the underlying coronary stenosis is more often critical and the thrombotic process is less important. The high blood leukocytes, platelet and fibrinogen levels of Group A patients are consistent with a significant role of inflammation in the pathogenesis of the thrombotic process while hemodynamic and local mechanical factors are probably more important in patients with normal blood leukocytes.
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PMID:[Etiopathogenesis of acute myocardial infarction: role of early leukocytosis]. 985 7

In this article we have outlined the current rationale and role of invasive management in ACS. For the majority of patients with ACS, who are either at high risk or unstable, invasive management is a critical element in breaking the sequence of recurrent ischemia leading to early cardiac events (Fig. 11). Secular trends in the care of cardiovascular patients predict even more sophisticated, invasive methods of treating coronary occlusion in the future. A futurist's view on this subject may envision the following type of scenario. A patient with prior CAD experiences persistent chest pain and notifies the emergency medical system. The paramedics arrive, and perform a rapid fingerstick cardiac biomarker panel and ECG. The results are interpreted by an emergency physician via a telecommunication system, and the patient is determined to be at high risk. He or she is triaged to a center capable of angioplasty and bypass surgery. On the way to the hospital, the patient is treated with aspirin, IV heparin, and an IV glycoprotein IIb/IIIa inhibitor. The patient undergoes triage angiography within 1 hour of hospital arrival, culprit lesion(s) are identified, and a revascularization plan is made--setting a critical pathway that is definitive. This vision is not far off on the horizon. We anticipate additional clinical trial results will help form the decision points in this optimal treatment scenario, which for a large proportion of patients will involve invasive management.
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PMID:Early use of coronary angiography and intervention. 1038 33

Both experimental and single-center clinical studies have shown that myocardium at risk, residual collateral flow, and duration of coronary occlusion are important determinants of final infarct size. The purpose of this study was to replicate these results on a multicenter basis to demonstrate that perfusion imaging using different camera and computer systems can provide reliable assessments of myocardium at risk and collateral flow. Sequential tomographic myocardial perfusion imaging with technetium-99 (Tc-99m) sestamibi was performed in 74 patients with first time myocardial infarction, who were enrolled in a multicenter, randomized, double-blind, placebo-controlled pilot study of poloxamer 188 as ancillary therapy to thrombolysis. All patients underwent thrombolysis within 6 hours of the onset of chest pain. Tc-99m sestamibi was injected intravenously at the initiation of thrombolytic therapy, and tomographic imaging was performed 1 to 6 hours later to assess myocardium at risk. Collateral flow was estimated noninvasively from the acute sestamibi images by 3 methods that assess the severity of the perfusion defect. Final infarct size was determined at hospital discharge by a second sestamibi study. Myocardium at risk (r = 0.61, p <0.0001) and radionuclide estimates of collateral flow (r = 0.58 to 0.66, all p <0.0001) were significantly associated with final infarct size. These associations were independent of the treatment center. On a multivariate basis, myocardium at risk (p = 0.003), the radionuclide estimate of collateral flow (p = 0.03), and treatment arm (p = 0.04) were all independent determinants of infarct size. Time to thrombolytic therapy showed only a trend (p = 0.10). The treatment center was not significant (p = 0.42). Myocardium at risk and collateral flow are important determinants of infarct size that are independent of treatment center. Tomographic imaging with Tc-99m sestamibi can provide noninvasive assessments of these parameters in multicenter trials of thrombolytic therapy.
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PMID:Determinants of infarct size after thrombolytic treatment in acute myocardial infarction. 1039 61

In spite of recent advances in secondary prevention, sudden cardiac death has remained a major public health problem as the majority of fatalities occur in subjects without a history of severe heart disease. Abrupt rupture of a vulnerable plaque resulting in thrombotic occlusion of a coronary artery is a common cause of sudden death in this population. Coronary occlusion does not, however, invariably lead to sudden death but may cause acute myocardial infarction or exacerbation of chest pain. Extensive studies in experimental animals and increasing clinical evidence indicate that autonomic nervous activity has a significant role in modifying the clinical outcome. Sympathetic hyperactivity favours the genesis of life-threatening ventricular tachyarrhythmias while vagal activation exerts an antifibrillatory effect. Strong afferent stimuli from the ischaemic myocardium impair arterial baroreflex and may lead to dangerous haemodynamic instability. Studies with a human angioplasty model have shown that there is wide interindividual variation in the type and severity of autonomic reactions during the early phase of abrupt coronary occlusion, a critical period for out-of-hospital cardiac arrest. The site of the occlusion is not a significant determinant of the reactions, whereas the severity of a coronary stenosis, adaptation or ischaemic preconditioning, beta-blockade and gender seem to affect the autonomic reactions and occurrence of complex ventricular arrhythmias. Clinical and angiographic factors are, however, poor predictors of autonomic reactions in an individual patient. Recent studies have documented a hereditary component for autonomic function, and genetic factors may also modify the clinical manifestations of acute coronary occlusion.
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PMID:Autonomic mechanisms and sudden death after abrupt coronary occlusion. 1048 Jul 54

In acute myocardial infarction, the perfusion status frequently fluctuates with rapid occurrences of coronary occlusion followed by myocardial ischemia. In patients with unstable angina, most episodes of ischemia are not accompanied by chest pain. In these patients it is important to be able to monitor the results of medical treatment non-invasively to establish the need for further intervention. It is not feasible to perform coronary angiography in all patients with acute myocardial infarction to evaluate patency of the infarct-related artery. Furthermore, even in a patent artery, no reflow may be present in the myocardial tissue. Angiography is therefore not the perfect golden standard to compare noninvasive ischemia monitoring with. Prognosis seems to be a better standard for comparison. This review indicates that vectorcardiography monitoring may identify myocardial reperfusion at an early stage and gives valuable prognostic information both in patients with unstable angina and acute myocardial infarction with low interobserver variability.
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PMID:Vectorcardiography: a tool for non-invasive detection of reperfusion and reocclusion? 1069 89


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