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)

A 62-year-old world record marathon runner was found to have silent ischemia manifested by a very abnormal stress test, whereas at autopsy nine months later, there was virtually no coronary atherosclerosis nor other disease of the coronary microvasculature. However, there was focal fibrosis of the papillary muscles consistent with remote ischemia secondary to possible CV. It is postulated that endurance-related high catecholamine levels might have been responsible.
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PMID:A world record marathon runner with silent ischemia without coronary atherosclerosis. 201 5

We studied the lipidic metabolism and the atherogenic risk factors non related to lipidic metabolism in two groups of patients: group 1 with only coronary disease and group 2 with coronary disease and atherosclerosis in the cerebral and/or peripheric artery territories. Patients of group 2 showed a cholesterol, cLDL, and B-apoprotein titers significantly higher than group 1. Systolic and diastolic blood pressure were higher in group two. Also the incidence of diabetes mellitus in group 2 was higher than in group 1. In a stepwise discriminating analysis the diastolic arterial pressure and cholesterol titers were the parameters with a greatest predictive potential for the presence of localized or generalized ischemic disease. B-apoprotein was the lipidic parameter with the greatest predictive potential. All together these data suggest that in coronary patients, a discrete increase in plasma cholesterol can imply a risk of suffering ischemia in some other arterial territories. Diastolic blood pressure, cholesterol and diabetes mellitus are the factors with the highest predictive potential for the generalization of arteriosclerosis.
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PMID:[Factors associated with generalized forms of arteriosclerosis in patients with coronary disease]. 209 Nov 13

The very first presentation of ischemic heart disease--acute infarction, sudden death, or unstable angina--most often occurs abruptly. The first approximation that it occurs as a random event only when a certain "threshold severity" of coronary atherosclerosis has gradually developed, although widely accepted, should perhaps be reconsidered and expanded on the basis of the following considerations. Acute coronary occlusion leading to myocardial infarction often occurs at the site of mild or noncritical coronary stenoses. Conversely, in patients with chronic angina severe coronary stenoses can remain unchanged for years with no detectable progression. When a coronary artery occludes, the size of infarction can vary greatly, and when ischemia and infarction occur, malignant arrhythmias occur in some patients but not in others. Thus, in a second approximation, ischemic heart disease should be considered as the result of the variable combination of three major components: a) A very variable chronic atherosclerotic background, which can result from a variety of pathologic processes; b) A number of acute ischemic stimuli, which can unpredictably impair myocardial blood flow as a result of coronary thrombosis and/or vasoconstriction; c) A variable response of the heart to a sudden reduction of coronary blood flow in terms of collateral perfusion and malignant arrhythmias. Therefore, at one extreme end of the spectrum in any individual, ischemic syndromes may present predominantly as a result of an extremely large chronic background component. At the other extreme, powerful acute ischemic stimuli can unexpectedly impair blood supply by coronary thrombosis, constriction, or their combination, in the presence of a mild chronic atherosclerotic background.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of myocardial ischemia. 209 77

In patients with coronary artery disease, angina pectoris provides an unreliable underestimation of disease activity and risk. Unheralded myocardial infarction and sudden death are common clinical presentations. Furthermore, objective testing, in hospital and more recently during the patient's normal daily activities, has demonstrated frequent and asymptomatic episodes of ischemia, as indicated by transient ST-segment depression. Since the underlying pathophysiologic disturbances of myocardial perfusion appear to be similar in painful and painless episodes, it seems appropriate to consider them together as the "total ischemic burden" on the myocardium. Research into this functional expression of coronary disease has indicated that active ischemia is associated with an increased risk of morbid events in all clinical subgroups of patients, including those with stable angina, unstable angina, peripheral vascular disease and following myocardial infarction. If this is confirmed in prospective trials, the assessment of total ischemic burden is likely to become part of the clinical investigation of patients with coronary disease. Clinical trials testing the efficacy of interventions will need to examine the effect on ischemic activity during normal daily life, in addition to symptoms and exercise tolerance. Evidence is still required to demonstrate whether therapy aimed at reducing the total ischemic burden will prolong life. The total ischemic burden provides a marker to follow the dynamic changes of the atherosclerotic lesion. Future research may have to concentrate on treatment aimed at altering the natural history of obstructive coronary atherosclerosis in order to affect the long-term outlook for patients with coronary artery disease.
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PMID:Total ischemic burden in patients with coronary artery disease. 209 78

The approach to a proximal LAD stenosis in an asymptomatic patient depends on a number of factors. Most important among these are the presence and extent of ischemia, anatomic considerations, and the functional status of the myocardium subserved by the vessel. In patients with functionally and hemodynamically insignificant disease with no ischemia, it is appropriate simply to follow the patient and to modify the risk factors for atherosclerosis if they exist. All three of the currently available modalities are appropriate in individual patients, including medical management, percutaneous balloon angioplasty, and surgical revascularization. In ambiguous cases, the available studies suggest no benefit from aggressive strategies; therefore, a conservative approach that minimizes side effects and complications of treatment is best.
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PMID:Should the asymptomatic patient with a significant proximal LAD stenosis undergo PTCA? 211 33

The importance of a prothrombotic state as a cause of ischemic stroke in young adults is ill defined. We examined 46 unselected patients under age 50 years with cerebral ischemia for anticardiolipin antibody (aCL) and lupus anticoagulants (LA), over a 3-year-period. Age- and sex-matched patients with other neurologic diseases served as a noncerebral ischemia comparison group to test whether (1) stroke/transient ischemic attacks (TIA) in young people is associated with aCL and/or LA, and (2) their presence is specific to cerebral ischemia. In the stroke/TIA group, 21 patients had aCL or LA and 25 had neither, whereas in the control group, 2 patients had aCL and 24 had neither. Equal numbers of stroke/TIA patients with and without antiphospholipid antibodies (aPL) had other stroke risk factors. Patients with aPL and cerebral ischemia, however, had a more frequent history of multiple events than those without them. These antibodies occur with undue frequency in young patients with stroke/TIA and are not associated with a concurrent diagnosis of systemic lupus in most cases. A coexistent aPL-associated prothrombotic state may be a key determinant of whether patients with atherosclerosis, mitral valve prolapse, or other structural lesions experience recurrent ischemia.
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PMID:Antiphospholipid antibodies and cerebral ischemia in young people. 211 4

After an extensive analysis of the world literature (121 references), beginning from the first reported case by Antopol and Kugel, 1933, the general review of the problem stressed especially the following morphologic characteristics and clinical significance of the anomalous origin of the left circumflex coronary artery (LCxA) from the right coronary artery (RCA): The place of the anomalous origin of LCxA from RCA among all other variations and anomalies of LCxA. The anatomical and topographical characteristics of LCxA originating from RCA in normal heart as well as in congenital heart diseases--CHD (especially complete transposition of great arteries--TGA). The formal genesis of LCxA from RCA according to original new Ogden's theory, taking into account the dual origin of the coronary arteries and the peritruncal angioblastic ring that surrounds the developing aorta and pulmonary artery. The frequencies of the origin of LCxA from RCA in autopsy and coronarography series. The importance of LCxA (by its origin and/or caliber) in determination of the right, left or codominance of the coronary arteries including the peculiarities in cases of isolated aortic stenosis and bicuspid aortic valve. The importance of recognizing LCxA from the RCA during implantation of artificial aortic, mitral and tricuspid heart valves, during mitral valve anuloplasty, closure of ostium primum defect as well as during aorto-coronary venous bypass. The LCxA from RCA, especially its proximal segment, shows more frequent and an earlier, faster and heavier obstructive atherosclerosis, causing different manifestations of coronary heart disease and sudden death. Also, mitral insufficiency can be caused by ischemia of the papillary muscles of the left ventricle. The awareness of the possibility that LCxA may arise from the RCA can prevent many complications during cannulations of the coronary arteries for diagnostic coronarography and myocardial perfusion during heart operations. The authors presented their 30 autopsied cases of LCxA from RCA, analysing morphological and topographic data as well as their clinical significance and association with other CHD. There were 6 isolated cases and 24 cases associated with other CHD (20 with TGA and 4 with other CHD). Our first autopsied case of LCxA from RCA was diagnosed as associated with tetralogy of Fallot in 1964. During the period 1964-1985 we had 1015 cases of CHD (including 132 cases of TGA).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic morphology and clinical significance of the anomalous origin of the left circumflex coronary artery from the right coronary artery. General review and autopsy analysis of 30 cases]. 213 27

Successful recanalization of isolated femoropopliteal occlusions by laser-assisted balloon angioplasty has been widely reported. However, the utility of this approach in other sites remains undetermined. The potential of laser-assisted balloon angioplasty in the treatment of a broad spectrum of lower extremity atherosclerosis was explored. Seventy-seven limbs in 69 patients were treated with laser-assisted balloon angioplasty by means of a percutaneous approach. Technical success was achieved in 62/77 (81%), with 52/77 (68%) open at discharge. At a mean of 8.6 months' follow-up, cumulative patency was 50% at 6 months and 42% at 9 months. In 10 cases initial guide wire placement was not possible; primary laser probe passage was technically successful in six, with two open at latest follow-up. Eleven patients underwent laser therapy without balloon angioplasty of distal sites with technical success in eight; at most recent follow-up five were open at the site of sole laser therapy. Complications were frequent. Bleeding requiring transfusion occurred in six, with three patients requiring emergency surgery; worsened ischemia necessitating urgent arterial bypass grafting developed in five patients. In this series laser angioplasty carried significant complications and a high failure rate. Widespread application of this procedure should await further clinical investigation.
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PMID:Expanded indications for laser-assisted balloon angioplasty in peripheral arterial disease. 224 13

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58

We review below published studies of endothelium-dependent vasodilation in vivo. Endothelium-dependent vasodilation has been demonstrated in conduit arteries in vivo and in the cerebral, coronary, mesenteric, and femoral vascular beds as well as in the microcirculation of the brain and the microcirculation of cremaster muscle. The available evidence, although not complete, strongly suggests that the endothelium-derived relaxing factor generated by acetylcholine in the cerebral microcirculation is a nitrosothiol. The endothelium-derived relaxing factor generated by bradykinin in this vascular bed is an oxygen radical generated in association with enhanced arachidonate metabolism via cyclooxygenase. In the microcirculation of skeletal muscle, on the other hand, the vasodilation from bradykinin is mediated partly by prostacyclin and partly by an endothelium-derived relaxing factor similar to that generated by acetylcholine. Basal secretion of endothelium-derived relaxing factor is controversial in vivo but is usually present in vitro. On the other hand, it appears that endothelium-derived relaxing factor mediates flow-dependent vasodilation in both large vessels and in the microcirculation in vivo. The generation and release of endothelium-derived relaxing factor from endothelium may be abnormal in a variety of conditions including acute and chronic hypertension, atherosclerosis, and ischemia followed by reperfusion. Several mechanisms for these abnormalities have been identified. These include inability to generate endothelium-derived relaxing factor or destruction of endothelium-derived relaxing factor by oxidants after its release in the extracellular space. These abnormalities in endothelium-dependent relaxation may contribute to the vascular abnormalities in these conditions.
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PMID:Endothelium-derived relaxing factors. A perspective from in vivo data. 217 Feb 74


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