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)

With use of semiselective xenon-133 injections and gamma camera recording, myocardial scintigrams were obtained in a series of 20 patients with angina pectoris, abnormal exercise electrocardiograms and normal coronary arteries. Ten patients (Group I) exhibited localized perfusion defects and the other 10 (Group II) a hjemogenous uptake of the tracer. Group I was characterized by more past myocardial infarctions and, most significantly, by male preponderance (P less than 0.001). Computer analysis of regional xenon-133 washout curves revealed that every patient in Group I had a reduced flow rate in the area of the perfusion defect (P less than 0.001). A comparison of this group with 26 patients with similarly abnormal scintigrams but coronary arterial obstruction revealed that myocardial perfusion was 16 to 18 percent greater in the group with normal coronary arteries. In three patients of this group, myocardial perfusion rates were not augmented by atrial pacing in contrast to the response in patients with coronary arterial obstruction. The data demonstrated localized perfusion abnormalities in half of the patients with angina pectoris and normal coronary arteries and constitute evidence that a metabolic disorder is not the sole mechanism for ischemia in this syndrome.
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PMID:Regional myocardial perfusion abnormalities on xenon-133 imaging in patients with angina pectoris and normal coronary arteries. 84 56

Transmural myocardial infarction occurred in a 48-year-old woman with syndrome X -- atypical angina pectoris and angiographically normal coronary arteries. Before the infarction her electrocardiogram had been normal at rest but showed ischemia after exercise. Angiography 3 months after infarction revealed a normal coronary tree but hypokinesia of the posterior left ventricular wall.
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PMID:Syndrome X: case report. 84 23

Angina with "normal coronary arteries" might best be thought of as "angina with coronary dysfunction". It seems likely that this syndrome is due to inadequate regional myocardial perfusion with manifestations similar to those seen when ischemia results from occlusive coronary artery disease. The prognosis of the disorder is favorable, but occasional catastrophic events occur. It appears likely that maldistribution of perfusion results from dynamic changes affecting proximal, and perhaps distal coronary vessels, potentially mediated by vasoactive substances released from platelets precipitating or exacerbating coronary arterial spasm. Clarification of the pathogenesis of the syndrome should permit implementation of more effective therapy and prevention of the rare malignant sequelae of this disorder.
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PMID:Angina with "normal coronary arteries". A misnomer. 84 83

The relation between myocardial release of prostaglandin and myocardial ischemia was studied in 12 selected patients with multivessel coronary artery disease. These 12 were chosen for analysis because they experienced angina pectoris, ischemic electrocardiographic changes and decreased myocardial lactate uptake during atrial pacing. Simultaneous aortic and coronary sinus blood samples were obtained at rest, during angina and after recovery and were assayed for prostaglandins F, E and A with radioimmunoassay. Cardiac release of prostaglandin F was observed during angina in 11 of 12 patients. Aortic prostaglandin levels remained constant throught each study. During angina, the mean aortovenous difference (+/- standard error) was -0.30 +/- 0.04 ng/ml (P less than 0.001) for prostaglandin F and -0.10 +/- 0.03 ng/ml (Pless than 0.001) for prostaglandin E. There was no significant release of prostaglandin A. Blood samples were also drawn at subanginal heart rates in two patients. Prostaglandin F was released only during angina. In three control patients with a chest pain syndrome and normal coronary arteries, comparable atrial pacing produced no release of prostaglandin F, E or A. These results, together with the known vascular and metabolic actions of prostaglandins, suggest that these pharmacologically active compounds may also play a physiologic role in the cardiac response to ischemia in man.
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PMID:Cardiac prostaglandin release during myocardial ischemia induced by atrial pacing in patients with coronary artery disease. 84 31

Twenty-one long-term survivors of out of hospital sudden cardiac death due to ventricular fibrillation underwent radionuclide angiography and myocardial imaging with thallium-201. In 13 patients images were obtained at rest and after maximal treadmill exercise; 11 of these 13 (85 percent) had an image defect in one or both studies. Eleven of the 21 patients (52 percent) had a defect in the image obtained at rest. The magnitude of myocardial image defects was typically great; some patients had an image abnormality without other clinical evidence (angina, S-T depression) of ischemia. The mean ejection fraction, assessed in 16 patients with radionuclide angiography, was 0.41 +/- 0.15 (standard deviation); in 5 of the 16 ejection fraction was normal (more than 0.50) and in 3 it was severely abnormal (less than 0.25). Thus, noninvasive radionuclide studies defined a broad spectrum of ischemic and ventriculographic abnormalities in survivors of sudden cardiac death. Further application of these noninvasive studies may identify those at high risk.
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PMID:Myocardial imaging and radionuclide angiography in survivors of sudden cardiac death due to to ventricular fibrillation: preliminary report. 87 Nov 11

Symptoms, signs, hemodynamic and electrocardiographic responses of 12 patients with acute myocardial infarction were studied before, during and after three activities: activity I, sitting upright; activity II, walking to the adjacent toilet; and activity III, walking on a treadmill set at 1.2 mph (1.9 km/hr) at 0, 3 and 6% successive gradients. The three activities were studied respectively at three, six and ten days (means) after infarction. Weakness was the most commonly occurring symptom. Mean systolic blood pressure fell 9 mm Hg upon assumption of the upright position (activity I) and was sustained for the five minutes of sitting. The systolic blood pressure drop was only 3.5 mm Hg with activity II. During activity III, one patient developed angina. Between rest and the 6% treadmill gradient, systolic blood pressure, heart rate and pressure-rate product rose 29 mm Hg, 26 beats/minute and 64 units, respectively. Electrocardiographic evidence of ischemia was observed in two patients during activity I, in two patients during activity II, and in one patient during activity III, but was insufficient for stopping the activities. Similarly, two patients developed minor arrhythmias, one with activity I and one with activity III. The use of this low-level treadmill test before discharging the patient from the hospital proved to be safe and feasible for obtaining objective data to assess the patients' ability to perform activities requiring equal exertion at home. Successful performance of these three activities before leaving the hospital should provide useful criteria for discharge of a patient with myocardial infarction.
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PMID:Progressive ambulation and treadmill testing of patients with acute myocardial infarction during hospitalization: a feasibility study. 87 Dec 37

To evaluate whether elevated arterial free fatty acids (FFA) increase myocardial oxygen demand and ischemia, 15 fasting patients with coronary artery disease underwent a standardized atrial pacing test before (PTI) and during (PT2) heparin infusion. The patients were monitored for clinical and electrocardiographic (ECG) manifestations of ischemia. Myocardial extraction of lactate, inorganic phosphate, oxygen and FFA was measured before and during each PT. The control arterial FFA was 0.65 +/- 0.03 micromole/ml and rose to 1.83 +/- 0.16 micromole/ml during heparin influsion. Myocardial oxygen extraction at rest and during PT was not affected by the increase in arterial FFA. Seven patients asymptomatic during PT1 did not develop ischaemic manifestations during PT2. In eight patients with angina during both PTs, increased arterial FFA concentration did not modify the severity of anginal pain, the amount of ST-segment depression and the myocardial balance of lactate or inorganic phosphate. Elevation of arterial FFA by heparin neither increased myocardial oxygen extraction at rest or during pacing nor accentuated ischemic manifestations during PT.
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PMID:Effect of increased free fatty acids on myocardial oxygen extraction and angina threshold during atrial pacing. 87 27

The intraaortic balloon was attempted for therapy in 94 patients and successfully placed in 86. The balloon catheter could not be passed through the femoral or iliac artery in 12 patients (13 percent) of the group; in 4 of these the balloon was inserted through an aortic arch graft. The medical indications were cardiogenic shock and preinfarction angina. Ten of the 14 patients in the group with shock survived when treated with an aortic balloon without emergency surgery. Indications for balloon pumping in the surgical group included inability to wean the patient from the pump-oxygenator, postoperative shock and prophylactic placement of the balloon for poor ventricular function. Inability to remove a patient from pump-oxygenator support was the most common surgical indication, and 47 percent of patients were long-term survivors. Only 1 of the 17 patients for whom balloon pumping was used prophylactically died. Complications occurred in 17 percent of the entire group of 86 patients although the rate for medical patients with cardiogenic shock was 50 percent. The most common complication was arterial insufficiency requiring removal of the balloon. Four patients had permanent damage to the legs from ischemia, one patient requiring bilateral amputation. The overall incidence of serious arterial obstruction was 10 percent. Other complications included balloon displacement with arterial obstruction and pericardial tamponade from anticoagulant agents resulting in death.
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PMID:Results and complications of intraaortic balloon pumping in surgical and medical patients. 90 40

Using labelled microspheres, the effect of norepinephrine (NE) infusions (15 microgram and 30 microgram/min) on coronary blood flow and its intramyocardial distribution during ischemia was studied. The results reported here show that in the ischemic myocardium, the ratio of endocardial to epicardial flow was 0.67. This value became 1.0 in dogs receiving NE at a dose of 30 microgram/min. Since an adrenergic discharge is known to accompany angina in man, these data suggest that an imbalance between the endocardial and epicardial blood flow might not be present in this clinical condition.
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PMID:Effect of norepinephrine on intramyocardial distribution of blood flow in normal and ischemic myocardium. 90 50

Prinzmetal's variant angina is commonly referred to as a syndrome apart from the usual spectrum of atherosclerotic disease. 2 well-studied patients with this form of angina gave past histories compatible with classical angina. They were found to have, in addition to severe atheromatous lesions, coronary artery spasm resulting in complete obstruction of the vessel during Prinzmetal attacks. The concomitant electrocardiographic ST segment elevations are probably the reflection of transmural ischemia injury resulting from the transient complete occlusion of the corresponding coronary artery. Electrocardiograms taken during milder resting anginal attacks showed minimal nonspecific changes of the electrocardiogram or T wave inversions which may possibly reflect less severe ischemia, secondary to milder coronary spasm. These observations support the possibility that at least in some cases, Prinzmetal's angina may just be a phase in the life history of patients with atherosclerotic disease, during which recurrent severe coronary spasms may occur.
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PMID:Another look at Prinzmetal's variant angina. 91 86


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