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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary artery obstruction during cardiac catheterization is a rare but serious complication that has been reported to occur in 0.15 to 0.5% of cases. The most common causes of intraprocedural coronary occlusion include thromboembolism, air embolism, and coronary dissection. This report describes the angiographic findings of a patient who developed chest pain with electrocardiographic evidence of myocardial ischemia due to obstruction of the right coronary artery by an aortic valve tumor.
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PMID:Aortic valve tumor: an unusual cause of coronary obstruction during cardiac catheterization. 234 8

Recognition that myocardial infarction is caused by coronary thrombosis has stimulated a search for a safe, rapidly acting, and effective thrombolytic regimen. Tissue plasminogen activator (t-PA) can provide relatively clot-selective thrombolysis, but one quarter of patients fail to achieve reperfusion, lysis speed is not optimal, and higher doses have been associated with an increased incidence of hemorrhagic stroke. We report the results of a multicenter study of pro-urokinase, a second naturally occurring plasminogen activator that has structural similarities to t-PA but has a different mechanism of action. Pro-urokinase was administered 3.9 +/- 1.1 hours after the onset of chest pain to 40 patients with acute myocardial infarction with angiographically confirmed complete coronary occlusion (TIMI grade 0). After a 90-minute intravenous infusion of pro-urokinase (4.7-9 million units, 36-69 mg) 51% (20 of 39) of the patients demonstrated reperfusion (TIMI grade 2 or 3) occurring 64.8 +/- 22.3 minutes after initiation of therapy. Fibrinogen levels fell only 10 +/- 17% from baseline, confirming the fibrin specificity of pro-urokinase. As with t-PA, however, this specificity was only relative. alpha 2-Antiplasmin decreased to 39% and plasminogen decreased to 64% of initial values. Fibrinogen degradation products increased 63% and the fibrin-specific D-dimer increased 8.7-fold. Thus, pro-urokinase produces relatively clot-selective coronary thrombolysis similar to that produced by t-PA, but the use of either pro-urokinase or t-PA alone in higher doses would be likely to produce more nonspecific effects.
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PMID:Clot-selective coronary thrombolysis with pro-urokinase. 249 4

Technetium-99m isonitrile is a new myocardial perfusion imaging agent that accumulates according to the distribution of myocardial blood flow. However, unlike thallium-201, it does not redistribute over time. This imaging agent was used with serial quantitative planar imaging to assess the initial risk area of infarction, its change over time and the relation to infarct-related artery patency in 30 patients with a first acute myocardial infarction. Twenty-three of 30 patients were treated with recombinant tissue-type plasminogen activator (rt-PA) within 4 h after the onset of chest pain. Seven patients were treated in the conventional manner without thrombolytic therapy. Technetium-99m isonitrile was injected before or at the initiation of thrombolytic therapy, and imaging was performed several hours later. These initial images demonstrated the area at risk. Repeat imaging was performed 18 to 48 h later and at 6 to 14 days after the onset of myocardial infarction to visualize the ultimate extent of infarction. The initial area at risk varied greatly (range defect integral 2 to 61) both in patients treated with rt-PA and in those who received conventional treatment. For the total group, the initial imaging defect decreased in size in 20 patients and was unchanged or larger in 10 patients. Patients with a patent infarct-related artery had a significantly greater decrease in defect size than did patients with persistent coronary occlusion (-51 +/- 38% versus -1 +/- 26%, p = 0.0001). All patients with a decrease in defect size greater than 30% had a patent infarct-related artery. In 12 patients who also had predischarge quantitative exercise thallium-201 imaging, good agreement existed between the extent and severity of myocardial perfusion defect on the last technetium-99m isonitrile study before discharge and that noted on delayed thallium-201 imaging. It is concluded that serial planar technetium-99m isonitrile myocardial imaging in patients with acute myocardial infarction undergoing thrombolytic therapy offers a new quantitative noninvasive approach for assessment of the initial risk zone as well as the success of reperfusion.
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PMID:Serial quantitative planar technetium-99m isonitrile imaging in acute myocardial infarction: efficacy for noninvasive assessment of thrombolytic therapy. 250 12

Intracoronary infusion of oxygenated Fluosol during percutaneous transluminal coronary angioplasty has been shown to reduce chest pain and preserve contractile function. In spite of this evidence for reduced severity of myocardial ischemia, ST elevation is frequently observed on the electrocardiogram. To determine if Fluosol produces ST segment elevation by a mechanism other than myocardial ischemia, closed-chest dogs underwent three interventions: (1) an infusion of oxygenated Fluosol into the unoccluded left anterior descending (LAD) coronary artery; (2) an identical infusion of unoxygenated Ringer's lactate; and (3) a transient occlusion of the LAD coronary artery. Open-artery infusions were chosen to minimize ischemia by permitting antegrade coronary blood flow. ST segments were monitored continuously and contrast left ventriculography was performed to assess regional systolic function. Coronary occlusion for 1 minute resulted in significant ST segment elevation from baseline (0.8 +/- 0.2 to 3.2 +/- 0.6 mm, p less than 0.05) and marked depression in regional ejection fraction (45 +/- 7% to -3 +/- 4%, p less than 0.05). Infusion of Fluosol produced a similar degree of ST segment elevation (0.9 +/- 0.3 to 2.8 +/- 0.4 mm, p less than 0.05), but no change in regional ejection fraction. Ringer's lactate infusion also resulted in ST segment elevation associated with preservation of regional contractility. Because regional systolic function (a sensitive indicator of regional ischemia) was preserved and an open-artery infusion was used, it is concluded that intracoronary infusion of Fluosol causes ST segment elevation by a mechanism other than myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation of ST segment elevation and regional wall motion with open-artery, intracoronary Fluosol. 252 47

Currently there is no accepted method for measurement of myocardial infarct size in humans. Analysis of both global and regional left ventricular function provides an indirect indication of extent of myocardial necrosis. Acute coronary occlusion results in cessation of function and in some cases dilatation of the involved myocardial segment. Often there is reciprocal hyperfunction of the non-ischemic segments resulting in little impairment of global ventricular function. Average global left ventricular function does not change from hospital admission through hospital discharge in patients with acute myocardial infarction, treated conventionally. With successful coronary reperfusion, however, both regional and global ventricular function have been reported to improve over several weeks after the initial ischemic insult. Improvement in ventricular function is most likely to occur in patients with collaterals or some preservation of antegrade flow to the involved myocardial segment who successfully undergo reperfusion. Return of function occurs in 82% of patients successfully treated within two hours after onset of chest pain. Approximately 50% of patients successfully treated two to 18 hours after onset of chest pain have demonstrated significant improvement in function. Patients admitted with normal ventricular function are less likely to demonstrate improved global ventricular function than those admitted with ejection fractions less than 45%. Acute PTCA with or without thrombolysis may result in a greater return in function than thrombolysis alone. Delayed revascularization more than 48 hours after successful reperfusion does not appear to affect ventricular function a late follow-up but may improve probability of survival. Patients discharged with ejection fractions greater than 45% clearly have an improved prognosis compared to those with depressed ejection fractions post-myocardial infarction.
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PMID:Changes in ventricular function associated with coronary reperfusion in acute myocardial infarction. 293 4

Increases in electrocardiographic R-wave amplitude in humans have been described with positive and negative dynamic exercise test findings, episodes of variant angina and myocardial ischemia and infarction. The role of factors other than acute reversible ischemia in the genesis of these R-wave size alterations is unclear. To evaluate the contribution of acute ischemia to changes in R-wave size in the absence of other confounding variables, electrocardiograms were recorded before and during coronary angioplasty balloon inflation. The frontal leads and V1, V2, V5 and V6 were recorded during the last 10 seconds of coronary occlusion in 20 patients and intracoronary epicardial electrograms were recorded continuously during balloon inflation in 10 patients. Inflations were 8 +/- 2 atm for 52 +/- 36 seconds. Chest pain occurred in 26 of 30 patients with balloon inflation and ST elevation occurred in 22. No significant increases in R amplitude were noted in any lead or in the sum of the R waves in all leads, including intracoronary electrograms. In contrast, R amplitude tended to decrease. The initial decrease in both surface and epicardial R amplitude was similar to the first of the biphasic changes observed in animal models. An increase in R-wave amplitude is not by itself always a marker for myocardial ischemia, but depends on severity and duration of the process.
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PMID:R wave of the surface and intracoronary electrogram during acute coronary artery occlusion. 294 13

A 61-year-old man with unstable angina underwent emergency angioplasty of a proximal left anterior descending coronary stenosis. This was successful but a major first septal branch involved in the stenosis was occluded following the procedure. Recovery was uncomplicated, however, without chest pain or other evidence of myocardial infarction. Predischarge treadmill stress testing was negative for ischaemia but two hours afterwards abrupt coronary occlusion required a second emergency angioplasty procedure. Recanalization of the left anterior descending artery was achieved and the first septal branch was shown to be fully patent. Spasm probably accounted for the side branch occlusion which complicated the first procedure but the mechanism of the abrupt coronary occlusion following stress-testing is unclear.
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PMID:Reversible occlusion of a side branch and the left anterior descending coronary artery following angioplasty. 295 5

Two-dimensional contrast perfusion echocardiography was performed in 14 patients who underwent percutaneous transluminal coronary angioplasty to test the efficacy of this new technique for defining the area at risk of dyskinesis during acute coronary occlusion. In nine patients (group A) selective coronary injection of echocontrast medium through the central lumen of the angioplasty catheter was performed immediately before balloon inflation. This produced regional myocardial enhancement that defined the area of dyskinesis after balloon inflation. In five patients (group B) who underwent left coronary angioplasty, echocontrast medium was injected through the introducer catheter positioned in the left main coronary artery during balloon inflation. In each case this produced regional myocardial enhancement remote from the area of dyskinesis. There were no complications related to the intracoronary echocontrast injections, which produced no discernible exacerbation of chest pain or left ventricular contractile dysfunction. These data indicate that selective coronary injection of echocontrast medium defines the perfusion territory of the artery injected and also provides a means of identifying the area at risk of dyskinesis after balloon occlusion of the artery.
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PMID:Contrast perfusion echocardiography: identification of area at risk of dyskinesis during percutaneous transluminal coronary angioplasty. 295

Acute myocardial ischemia is known to cause impairment of both left ventricular systolic and diastolic function. To further investigate these changes as well as their relation to common clinical variables (electrocardiographic [ECG] changes and chest pain), 32 patients were evaluated with Doppler echocardiography during coronary angioplasty. Doppler indexes of left ventricular diastolic function included the ratios of peak early to late and peak early to mean diastolic velocities as well as the ratios of early to late and first third to total velocity integral (one-third filling fraction). All diastolic indexes showed significant impairment by 15 seconds after coronary occlusion (ratio peak early to late filling velocity: 1.11 versus 0.96, p less than 0.01; ratio peak early to mean filling velocity: 1.9 versus 1.7, p less than 0.01; ratio early to late velocity integral: 1.58 versus 1.25, p less than 0.01; one-third filling fraction: 41.2 versus 37.7, p less than 0.01). Left ventricular systolic function was evaluated during coronary occlusion both qualitatively, as assessed by the appearance of a new wall motion abnormality on two-dimensional echocardiography (mean 28.8 seconds), and quantitatively by measurement of systolic percent area change on the two-dimensional short-axis view as well as the Doppler echocardiographic stroke integral index. Systolic indexes did not show significant change until 30 seconds after balloon inflation (percent area change: 42.8 versus 29.2, p less than 0.01; stroke integral index: 11.04 versus 9.36, p less than 0.01). ECGs were performed at 15 second intervals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of left ventricular systolic and diastolic dysfunction during transient myocardial ischemia produced by angioplasty. 295 30

The detection of regional myocardial dysfunction due to acute ischemic event has been limited almost entirely to experimental animal models. In human subjects, it has been limited to the observations during spontaneously-occurring or exercise-induced ischemic events. Recently, percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to study such dysfunction as the result of repeated interruptions of coronary blood flow. Echocardiograms and electrocardiograms were simultaneously recorded immediately before, during, and after 21 episodes of complete interruptions of coronary blood flow by PTCA in 11 patients. No patient had asynergy of the left ventricle either by two-dimensional echocardiography (2DE) or angiography. All patients had isolated single coronary artery stenosis including the left anterior descending artery in nine, left circumflex artery in one and right coronary artery in one. Recordings of M-mode and 2DE were successfully obtained in 10 patients. After balloon inflation, regional asynergy in the distribution of the instrumented coronary artery appeared in all 10 patients. Hypokinesis developed 9 +/- 3 (means +/- SD) sec after balloon inflation and progressed rapidly to akinesis or dyskinesis. At the same time, decreased systolic thickening of the left ventricular wall appeared in some patients in relation to the development of regional asynergy. However, systolic thinning of the left ventricular wall was not noted in all. The regional asynergy preceded ischemic electrocardiographic changes and had no relation to chest pain. Left ventricular wall motion began to normalize 12 +/- 3 sec after balloon deflation. Thereafter, transient hyperkinesis of the left ventricle developed. The first ischemic electrocardiographic change was a negative U wave which appeared 13 +/- 7 sec after coronary occlusion and remained 3 to 4 sec. Tall T waves were recorded at 28 +/- 12 sec and significant ST elevations developed 31 +/- 11 sec, after balloon inflation. These electrocardiographic changes invariably occurred only after the onset of wall motion abnormalities. Normalization of T waves was recognized at 17 +/- 16 sec and ST segment deviation were no longer present at 18 +/- 10 sec, after reperfusion. These electrocardiographic changes also preceded normalization of regional myocardial dysfunction. In conclusion, left ventricular wall motion abnormalities after coronary occlusion invariably precede the electrocardiographic changes, and begin to normalize after reperfusion prior to the electrocardiographic recovery.
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PMID:[Mechanical and electrocardiographic sequence of coronary artery occlusion: an echocardiographic study during coronary angioplasty]. 296 73


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