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)

Left ventricular function was assessed sequentially with biplane cineventriculography in 18 patients with acute myocardial infarction, in whom nonsurgical reperfusion was achieved within 8.2 +/- 6.9 hours (mean +/- standard deviation) after the onset of chest pain with intracoronary infusion of streptokinase (2,000 units/min for 66 +/- 16 minutes). Ejection fraction increased from 51.4 +/- 9.8 percent before reperfusion to 55.9 +/- 9.0 percent immediately after completion of streptokinase infusion (n = 13, p less than 0.01); the length of the akinetic myocardial segment decreased from 10.2 +/- 6.1 to 7.1 +/- 4.9 cm (p less than 0.025). Left ventricular function data before reperfusion and in the chronic stage of infarction (before surgery) were compared with data obtained in two medically treated groups that were matched retrospectively: control group I, nine patients with permanent obstruction of the infarcted vessel; control group II, nine patients with spontaneous recanalization of the initially obstructed vessel. In the acute stage of infarction, ejection fraction and akinetic segment length were comparable in the three groups. In the chronic stage ejection fraction was higher in the study group (57.4 +/- 12.7 percent) than in control group I (43.4 +/- 7.6 percent, probability [p] less than 0.05); the akinetic segment was shorter in the study group (4.5 +/- 6 versus 9.4 +/- 5.5 cm, p less than 0.025). Preservation of R waves was more extensive in the study group. Intraoperative inspection in 10 study group patients and transmural biopsy performed in 3 of these patients revealed the bulk of reperfused myocardium to be viable. It is concluded that jeopardized myocardium was preserved by nonsurgical reperfusion during the acute stage of coronary occlusion.
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PMID:Effects of nonsurgical coronary reperfusion on the left ventricle in human subjects compared with conventional treatment. Study of 18 patients with acute myocardial infarction treated with intracoronary infusion of streptokinase. 705 96

Acute coronary occlusion may cause severe autonomic reactions that can modify the clinical presentation of acute ischemic events. To evaluate whether adaptation in these autonomic reactions exists during repeated short coronary occlusions, heart rate (HR) and its variability in the time and frequency domains were analyzed in 70 patients with significant (50% to 95%) coronary artery stenosis immediately before and during 2 identical balloon occlusions of the vessel (mean 110 seconds). Reactions were compared with the range of nonspecific changes formed by analyzing a control group (n = 13) with no ischemia during balloon inflation in a totally occluded coronary artery. Thus, neither occlusion caused significant changes in HR or HR variability in 29 patients (41%). Vagal activation, as seen by an abnormal increase in HR variability or bradycardia, or both, was observed in 24 patients (34%). HR reactions in this group (p < 0.05) were significantly attenuated during the second occlusion. An opposite reaction (i.e., abnormal decrease in HR variability or tachycardia, or both) was observed in 17 patients (24%). A nonsignificant tendency for attenuation of the reactions was also seen in this group. Severity of chest pain, frequency of ST-segment shifts, or narrowing of pulse pressure were comparable during the 2 occlusions. Thus, a preceding short vessel occlusion-reperfusion cycle seems to attenuate autonomic HR reactions, especially vagal reactions, during subsequent coronary occlusion. Alleviation of extreme autonomic reactions may modify the clinical outcome of coronary occlusion in a beneficial way.
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PMID:Heart rate variability during repeated arterial occlusion in coronary angioplasty. 773 93

Prolonged intravascular infusion of urokinase has proven beneficial in reestablishing patency of chronically occluded peripheral arteries and saphenous vein grafts. This study was performed to assess the efficacy and safety of prolonged urokinase infusion as a prelude to angioplasty in chronically occluded native coronary arteries, that had failed standard angioplasty techniques. Twenty-five patients with objective evidence for ischemia in the distribution of a chronic coronary occlusion were referred for percutaneous intervention. Patients were assessed for any potential exclusions from lytic therapy. Urokinase infusion through both a SOS wire and a stable guiding catheter was continued at 100,000-240,000 units/hr for 8-25 hr; patients then underwent attempted balloon angioplasty. Mean duration of urokinase infusion was 20.6 +/- 7.7 hr (total dose 163,000 +/- 52,447 units/hr). Fibrinogen levels dropped slightly with this (300 +/- 129 to 203 +/- 81 mg/dl, P = 0.02). Angiography posturokinase showed improvement in 7 (28%) with regard to coronary flow (> or = 1 TIMI-grade). Angioplasty was successful in 13 (52%), with final angiographic result revealing thrombus in 5 (20%), or dissection 8 (32%). The infusions were well-tolerated with a low incidence of chest pain, 2 (8%) or ischemic ECG response, 2 (8%); myocardial infarction, 2 (8%); or significant bleeding 2 (8%). All patients survived the procedure, with a length-of-hospital stay = 5.1 +/- 4 days. Use of prolonged preangioplasty intracoronary urokinase infusion can be done safely with success in roughly one-half of patients with chronic total native coronary occlusions who have failed prior attempts at percutaneous intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged urokinase infusion for chronic total native coronary occlusions: clinical, angiographic, and treatment observations. 778 87

Autonomic mechanisms may have an important role in the clinical presentation of acute coronary occlusion. This research was designed to evaluate the effect of preocclusion stenosis severity on the immediate autonomic heart rate (HR) responses to a subsequent acute occlusion of the coronary artery. HR and its variability in the time and frequency domains were analyzed in patients with mild to moderate (< or = 85%) (group 1, n = 19) and severe (> 85%) (group 2, n = 18) left anterior descending coronary artery stenosis immediately before and during balloon occlusion (mean 108 seconds). The ranges of nonspecific responses were determined by analyzing HR reactions in a control group (n = 13) with no ischemia during balloon inflation of a totally occluded coronary artery. An abnormal increase in HR variability and/or bradycardia as a sign of vagal activation occurred in 6 patients (32%) in group 1 and in 3 patients (17%) in group 2. A significant decrease in HR variability or tachycardia, or both, was observed in 5 patients (26%) in group 1, but in none of the patients in group 2. Compared with the control group, the balloon occlusion of mild to moderate stenosis caused abnormal HR reactions more often than did occlusion of tight stenosis (58% vs 17%, p < 0.05). Balloon occlusions in group 1 caused chest pain (p < 0.01), ST-segment changes (p < 0.001), and narrowing of pulse pressure (p < 0.05) more often than did occlusions of severe stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of preocclusion stenosis severity on heart rate reactions to coronary occlusion. 797 15

A 41-year-old man was admitted because of chest pain at rest. The exercise test and coronary angiography were performed after all antianginal medication was discontinued for 24 hours. During the graded treadmill exercise stress test using the Bruce protocol, the patient had anginal pain with the electrocardiogram (ECG) showing ST segment elevation in leads V1 and V2. A baseline coronary angiogram disclosed 50% stenosis of the first septal branch of the left coronary artery. After a bolus of 0.1 mg ergonovine was administered into the coronary artery, the patient complained of typical anginal pain. Complete occlusion of the first septal branch was demonstrated, associated with significant ST segment elevation in leads V1-V3, right bundle branch block, and electrical axis deviation to the left on the ECG. The coronary occlusion reversed soon after nitroglycerin administration into the coronary artery. We diagnosed a rare case of angina pectoris caused by spasm of the minor branch of coronary artery, and that serial ECG changes might demonstrate ventricular septal ischemia including the cardiac conduction system. ST segment elevation in leads V1-V3 indicated ischemia of the ventricular septum, and right bundle branch block, axis deviation to the left, and increased amplitude of the precordial R wave might be induced by ischemia of the right bundle branch, left anterior bundle branch and septal branch in the cardiac conduction system supplied by the septal branches of the left anterior descending coronary artery.
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PMID:[Rest angina induced by coronary artery spasm at the first septal artery: a case report]. 816 49

Acute myocardial infarction results from the cessation of myocardial blood flow caused by thrombotic occlusion of a coronary artery. Rapid restoration of blood flow to the ischemic myocardium minimizes cardiac damage and improves early and long-term morbidity and mortality. Chest pain is the first symptom of myocardial infarction, but in some patients with silent ischemia, the disease can be diagnosed only in retrospect. In symptomatic patients, myocardial infarction should be accurately and promptly diagnosed so that reperfusion therapy can begin immediately. Electrocardiography is the simplest diagnostic modality. Although regional ST-segment elevation is specific, it is not sensitive. In contrast, new computerized algorithms for electrocardiographic analysis and serial monitoring increase sensitivity without decreasing specificity. In the emergency room, echocardiography is used to diagnose patients with no prior history of coronary artery disease whose electrocardiograms proved nondiagnostic. Time-consuming perfusion nuclear studies are inferior to echocardiography but may nevertheless enable physicians to diagnose myocardial infarction in the emergency room. Although the presence of excess creatine kinase is a sign of myocardial necrosis, its increase is delayed for a few hours after coronary occlusion. Doctors can diagnose myocardial infarction as early as two hours after coronary occlusion with the help of simpler automatic assays of MB-creatine kinase mass that use monoclonal antibodies. Other investigational markers of myocardial necrosis include myoglobin and troponin. Elevation of a circulating protein marker also signifies established necrosis, but physicians hope to achieve reperfusion through therapy before irreversible damage occurs.
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PMID:The earliest diagnosis of acute myocardial infarction. 819 86

Between May 1991 and February 1992, 31 consecutive patients were included in a prospective study, the aims of which were to determine the criteria of early coronary revascularisation after intravenous thrombolysis in the acute phase of myocardial infarction. The rise in serum myoglobin, the ST segment elevation, accelerated idioventricular rhythm and the evolution of chest pain were analysed. All patients underwent coronary angiography. Twenty-six were revascularized and 5 remained with coronary occlusion. Two types of serum myoglobin curves were demonstrated. Those with a sudden , decrease and a well defined peak in the first 4 hours were specific for revascularisation and easily identified (Group A: 16 patients). The graphs with a progressively rising slope to a peak after the 4th hour were observed in patients with coronary occlusion, but also in 10 patients with recanalized arteries (Group B). No significant difference was demonstrated with regards to the clinical and coronary angiographic parameters between patients in Group A and Group B. On the other hand, the time between the onset of chest pain and peak myoglobin was shorter in Group A (298 +/- 81 min) than in recanalised patients in Group B (380 +/- 54 min) (p < 0.05). The difference in the profile of the serum myoglobin could therefore reflect restoration of arterial flow in myocardial cells which had not suffered the same period of ischemia. ST segment elevation may increase, decrease of remain stable at 120 minutes in patients revascularised and those remaining occluded. In 9 patients, the ST elevation increased compared with the initial electrocardiogram .(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Early clinical, electrocardiographic and biological criteria of reperfusion after intravenous fibrinolysis during the acute phase of myocardial infarction]. 827 57

A case report of the sudden death of a 64-year-old man, three months after successful percutaneous transluminal coronary angioplasty (PTCA). He was admitted because of non-Q-wave acute myocardial infarction. Coronary angiography showed 90% stenosis in the anterior descending artery (No. 6). PTCA was successful, but the proximal portion of anterior descending artery was dissected because the balloon slipped from the dilated site during inflation. Acute coronary occlusion was not observed. However, he died suddenly shortly after he complained of severe chest pain three months after PTCA. Histologically, the site of the dissecting artery showed that the intima and media of the arterial wall was disrupted and the lumen was severely stenotic with cellular proliferation. This dissection of the coronary artery is also important because rapid and severe stenosis was induced by the artery's being badly injured.
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PMID:[A case of sudden death three months after successful PTCA]. 833 31

Silent myocardial ischemia is a marker in patients with coronary artery disease identifying those at high risk for subsequent cardiac events. During provoked myocardial ischemia some patients with angina pectoris do not develop chest pain. Are there clinical, angiographic or electrocardiographic differences between patients with chest pain as compared with patients without chest pain during provoked myocardial ischemia? Coronary angioplasty is a well-established method for the treatment of coronary stenosis, but it is also an interesting model for the study of myocardial ischemia as a result of coronary occlusion. We monitored 114 patients with angina pectoris during coronary angioplasty with dynamic, computerized vectorcardiography. During inflation of the balloon 33 of 114 patients had silent ischemia. Patients with silent myocardial ischemia had similar reasons for terminating the preangioplasty exercise test and where on similar anti-ischemic drug regimes. Silent myocardial ischemia was significantly associated with a history of diabetes, presence of collaterals, a history of less severe previous angina and less ST segment changes during angioplasty as compared with patients with painful ischemia. It is suggested that during coronary angioplasty silent ischemia may be caused by a less severe degree of ischemia, possibly as a result of the protective effect of collaterals.
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PMID:Silent myocardial ischemia during coronary angioplasty. 837 30

A 53-year-old-man afflicted with combined valvular heart disease and atrial fibrillation was admitted to our department complaining of chest pain. ST elevation on ECG (II, III, aVF) and elevated CPK value were recognized. He was diagnosed as having acute myocardial infarction, and percutaneous transluminal coronary recanalization was performed immediately. The coronary angiogram showed occlusions at the proximal left branch (#12). But these lesions could not be recanalized by 960000 IU urokinase administration. The cineangiogram after one month revealed perfect recanalization of these occlusions. Mitral stenosis with neovascularity to the left atrium and aortic regurgitation were recognized. We supposed this infarction caused by coronary embolism originated from left atrial thrombi. Acute myocardial infarction associated with mitral stenosis has been reported in fifteen cases previously in Japan, but only three cases revealed coronary occlusion in the acute phase with normal coronary artery in the chronic stage. However, there has been no report, except for this case, demonstrating occlusion in two coronary arteries at the same time. So, our case is the first report of the involvement of two coronary artery occlusions.
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PMID:[A case of coronary artery embolism associated with combined valvular heart disease]. 843 64


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