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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cohort of 175 patients who underwent successful percutaneous transluminal coronary angioplasty (PTCA) were subjected to a treadmill exercise test to determine the prognostic significance of silent and symptomatic myocardial ischemia during the follow-up (average 11.7 months). The cardiac events during the follow-up were defined as cardiac death, nonfatal myocardial infarction, class III angina, and need for repeat angioplasty or coronary artery bypass surgery. During exercise, 39 patients (22%) had abnormal exercise-induced ST depression without chest pain (Group I). A group of 22 patients (13%) had both exercise-induced chest pain and ST-segment depression (Group II), and 114 patients (65%) had normal exercise test and no chest pain (Group III). The groups were similar in sex distribution, history of previous myocardial infarction, distribution of vessel disease, and presence of left ventricular dysfunction. Group III included more patients with complete revascularization. Follow-up data revealed that cardiac event rates in Groups I and II were significantly higher than in Group III (41%, 41%, vs. 16%) (p less than 0.01). The event rates in Groups I and II with multivessel angioplasty also were significantly higher than in Group III (58%, 61%, vs. 21%) (p less than 0.01). Exercise-induced silent myocardial ischemia is frequently seen early after successful PTCA and is more prevalent in patients undergoing multivessel angioplasty and incomplete revascularization. Both silent and symptomatic ischemia early after PTCA are predictors of an unfavorable prognosis.
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PMID:Silent myocardial ischemia after percutaneous transluminal coronary angioplasty and its prognostic significance. 174 65

Pharmacologic stress testing is an accepted alternative in those patients unable to perform exercise stress testing. The most prevalent form of pharmacologic stress testing remains thallium imaging during vasodilator stress with either dipyridamole or adenosine infusions. More recently, dobutamine stress echocardiography has emerged as a promising new technique for the evaluation of patients with known or suspected coronary disease. The rationale for the use of dobutamine infusion as a stress agent lies in its ability to simulate physical exercise through its beta-receptor agonist activity. This causes a supply-demand mismatch which in turn, creates regional myocardial dysfunction which can be detected by two-dimensional echocardiography. A major advantage in the use of echocardiography over other adjunctive imaging techniques is its ability to detect all forms of anatomic heart disease which may be associated with chest pain or may mimic ischemic chest pain. Our current dobutamine protocol involves stepwise infusion of dobutamine beginning at 5 micrograms/kg/min and increasing to 10, 20, and a peak of 30 micrograms/kg/min in three minute stages. Images are recorded in standard parasternal long axis and short axis, four chamber and two chamber views, digitized and displayed for comparison in a quad screen format. A 16 segment model is used for scoring wall motion abnormalities. Ischemia is considered present when a wall motion abnormality develops in an area with normal or only hypokinetic resting wall motion. The overall accuracy is between 85 and 90% for the detection of patients with coronary disease. In over 600 studies at our institution, no major side effects or complications have occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dobutamine stress echocardiography: diagnostic utility. 175 63

Patients admitted for suspected acute myocardial infarction within 6 hours (mean 3 hours 42 minutes) after onset of symptoms were randomised to double-blind treatment with low-dose oral aspirin or placebo. Early exercise ischemic responses, exercise capacity and resting left ventricular ejection fraction (radionuclide ventriculography) were estimated in 77 survivors 2-4 weeks later. Exercise performance and ejection fraction in patients with confirmed acute myocardial infarction were equal in the two groups. During exercise, patients treated with aspirin had significantly more silent ischemia (ST depression without chest pain) compared to placebo (28% versus 6%; P = 0.015). The occurrence of positive exercise tests (chest pain or ST-segment depression), however, was similar in the two groups. The results indicate that the administration of aspirin early after acute myocardial infarction increases the occurrence of silent ischemia but has no effect on left ventricular function.
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PMID:Increased occurrence of exercise-induced silent ischemia after treatment with aspirin in patients admitted for suspected acute myocardial infarction. 176 36

Directional coronary atherectomy (DCA) was used in 74 patients with an average age of 56 years. They were categorized into three different groups depending on the indications for atherectomy. Group I included all patients who had atherectomy as their primary intervention (n = 26), because they were assumed to be unsuitable for PTCA. Group II consisted of patients in whom DCA was used after failed balloon dilatation with unsuccessful but uneventful treatment (n = 20). Group III (n = 28) included cases where DCA was performed as a "rescue" or "bail-out" procedure after failed PTCA resulted in critical ischemia (ECG changes, chest pain, hypotension, and shock). The target lesions were located in LM 2, LAD 52, RCA 16, ACVB 4. The mean length of lesion was 8 mm (2-25 mm). The overall success rate was 94%. The mean stenosis was reduced from 90.6 +/- 10% to 17.2 +/- 14.8% in cases with primary success. The presently available follow-up angiography (n = 31) showed six restenoses. Major complications occurred in seven cases (death: 0, myocardial infarction: 2, CABG within 24 h: 5). Histological analysis revealed highly cellular areal as a major characteristics of a coronary lesion and also of restenotic tissue. Tissue of the lamina elastica was present in 44% and of media in 14%. Thrombus was found only rarely. Ultrastructure showed a significant amount of extracellular matrix in the primary coronary lesions and isolated smooth muscle cells without gap-junctions. RER, mitochondria were typical for the synthesizing type of smooth muscle cell. In restenotic tissue a focal high density of smooth muscle cells with increased synthesizing activity and gap-junctions was present. Endothelial cells (and macrophages) were found only rarely. Furthermore, altered smooth muscle cells from restenotic tissue showed a significantly increased migration and proliferation. Our results show that DCA is a safe and effective technique that can extend the use of percutaneous procedures and provide a promising, nonsurgical option in cases of failed PTCA. Histological analysis revealed a proliferative process as a characteristics of restenosis development.
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PMID:[Current status of directional coronary atherectomy in interventional cardiology]. 179 47

Results of our prospective, randomised pilot trial to evaluate the clinical effects and the angiographic correlates of early thrombolysis in patients with unstable angina are reported. Sixty-seven patients had coronary angiography 10 +/- 8 (median 7) hours after an episode of transient chest pain at rest with reversible ischaemic changes on the electrocardiogram. Patients with left main disease (4), or diffuse coronary disease and unidentified ischemia-producing lesions (13) were excluded, as were those without severe (greater than or equal to 70%) stenosis (10). Intracoronary thrombus was identified at angiography in 7 patients (17%) and complex coronary lesions in 5 (12%) of the remaining 40 patients who were randomised to either intracoronary streptokinase 250,000 IU followed by intravenous heparin along with conventional treatment (20 patients), or to conventional treatment alone (20 patients). All patients received Aspirin. No differences between the streptokinase and the conventional treatment groups were observed with respect to demographic and clinical characteristics at admission to the study. During observation in the intensive care unit for 3 +/- 1 days, 8 patients (40%) with streptokinase and 10 (50%) with conventional treatment were free from angina and infarction (p = 0.75; 95% confidence interval for the difference in response rates = -20 to 40%). There were no bleeding complications and no patient died. Patients enrolled in our study had fewer coronary thrombi at angiography than currently reported. Our data did not show that adjunct treatment with streptokinase and heparin is superior to conventional treatment alone in these patients.
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PMID:Intracoronary streptokinase in unstable angina: a prospective randomised study. 180 19

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evidence of congestive heart failure, had their circulating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31-67; pro ANF 31-67) and creatine phosphokinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31-67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p less than 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1-98 and pro ANF 31-67 levels in these patients were within our normal range and significantly lower (p less than 0.001) than seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.
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PMID:Acute and sustained release of the atrial natriuretic factor prohormone N-terminus with acute myocardial infarction. 182 42

Long-term low-flow oxygen therapy can lead to improved exercise capacity and improved hemodynamics in selected patients with pulmonary hypertension. We report a patient who presented with severe exercise limitation and anginal chest pain that appeared to result from pulmonary hypertension and predominantly right ventricular ischemia. Acute oxygen therapy led to relief of pain but no change in exercise capacity or of pulmonary hypertension. After eight months of oxygen therapy, the patient's pulmonary hypertension was unchanged, but right ventricular hypertrophy and marked increases in exercise cardiac output and exercise capacity developed. Thus, oxygen can relieve right ventricular angina and facilitate the development of compensatory hypertrophy.
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PMID:Relief of right ventricular angina and increased exercise capacity with long-term oxygen therapy. 183 Aug 39

Clinical and physiologic evidence indicates that maximal coronary vasodilation is not achieved in a large number of patients with use of the standard dose of dipyridamole (0.56 mg/kg body weight over 4 min). The feasibility, safety and accuracy of technetium-99m hexakis 2-methoxy-2-isobutyl isonitrile (Sestamibi) scintigraphy associated with intravenous high dose dipyridamole (0.56 mg/kg over 4 min followed 4 min later by an additional 0.28 mg/kg over 2 min) were evaluated in a multicenter study. Planar myocardial perfusion images were obtained at rest and after dipyridamole in 101 patients with effort chest pain and no prior myocardial infarction. High dose dipyridamole (62 patients) was used when typical chest pain or electrocardiographic (ECG) signs of ischemia, or both, did not occur during or after the standard dose (39 patients). With high dose dipyridamole, 34 patients had pain (18 patients) or ECG signs of ischemia (ST depression greater than or equal to 2 mm) (8 patients), or both (8 patients), whereas the other 28 patients had Sestamibi injection in the absence of symptoms or ECG changes. All patients underwent coronary angiography: 81 had significant coronary artery disease (greater than or equal to 50% reduction of lumen diameter) (affecting one vessel in 38, two vessels in 19 and three vessels in 24 patients) and 20 patients had normal coronary arteries. The overall sensitivity, specificity and predictive accuracy of Sestamibi scintigraphy were 81%, 90% and 83%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Accuracy and safety of technetium-99m hexakis 2-methoxy-2-isobutyl isonitrile (Sestamibi) myocardial scintigraphy with high dose dipyridamole test in patients with effort angina pectoris: a multicenter study. Italian Group of Nuclear Cardiology. 183 17

The main cause of death in Kawasaki disease is myocardial infarction due to thrombotic occlusion of a coronary aneurysm. Intracoronary thrombolytic treatment was performed in 15 patients with Kawasaki disease with giant coronary aneurysms. Three patients had acute myocardial infarction, four demonstrated silent myocardial infarction, three suffered chest pain and five did not show ischemia features but had massive thrombus in the coronary aneurysms. Urokinase was infused into the coronary aneurysms as a bolus of 8,000 to 10,000 units/kg via a catheter over 10 minutes. Partial but significant coronary recanalization was achieved after injection of urokinase in a patient with acute myocardial infarction. Complete resolution of massive intracoronary thrombi was observed in 3 of 15 patents, and partial resolution was recognized in 4 cases. In 7 patients, the size of thrombus did not change. Recurrence of the thrombus was observed in 4 patients by serial two-dimensional echocardiography. Urokinase was readministered and two showed significant reduction in the thrombus. All patients have been followed for more than 2 years with longest 8 years (mean: 3.3 yrs), and none have had a recurrence of myocardial infarction or died. These findings suggest that intracoronary urokinase is useful for the treatment and prevention of myocardial infarction in Kawasaki disease.
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PMID:Intracoronary urokinase in Kawasaki disease: treatment and prevention of myocardial infarction. 185 11

Myocardial ischemia must be the first concern of every emergency physician in evaluating chest pain in the adult patient. Any suspicion of myocardial ischemia must be promptly evaluated and admitted. The American College of Emergency Physicians has recently published a standards document on the care of chest pain in the adult patient. The emergency physician must be familiar with this document. Once myocardial ischemia and other life-threatening causes are ruled out, one can consider that cervical disk disease may be the cause of chest pain. The authors present two cases of patients who presented to the Emergency Department with signs and symptoms consistent with cardiac ischemia. Both patients were found to have herniated cervical disks. Subsequent surgical repair completely relieved their symptoms. Evaluation of the literature reveals that this entity was well described from 1950 to the 1960s. Most recent discussions do not mention disk herniation as even an infrequent cause of chest pain. If there is no life-threatening disease present, one should consider cervical disk disease.
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PMID:Herniated cervical disk presenting as ischemic chest pain. 186 3


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