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

Sudden fissuring of an atherosclerotic plaque has been suggested as the primary trigger of transient spontaneous ischemia in both the coronary and cerebral circulation. Measurements of urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2, as well as results of Aspirin trials, have suggested that episodic platelet activation at the site of this acute vascular lesion is mediated, at least partly, by enhanced thromboxane (TX) A2 biosynthesis. Thus, episodic increases in metabolite excretion have been detected in unstable angina. Aspirin (75-325 mg/day) prevents about one third of all fatal and nonfatal thrombotic events in this setting. That a similar "dynamic" thrombotic process occurs during the early phase of acute myocardial infarction is suggested by thromboxane metabolite measurements and by the results of the ISIS-2 trial showing a similar impact of short-term Aspirin therapy to that seen in unstable angina. Percutaneous transluminal coronary angioplasty is associated with transiently enhanced TXA2 biosynthesis and Aspirin-suppressable periprocedural thrombotic complications. On the other hand, both non-insulin-dependent diabetes mellitus and type IIa hypercholesterolemia are associated with a relatively reproducible and persisting abnormality of TXA2-dependent platelet function. This association is likely to reflect a systemic rather than localized stimulus to platelet activation and a continuous rather than episodic alteration. Low-dose (50 mg/day) Aspirin can largely suppress thromboxane metabolite excretion in both diseases. Thus, low-dose Aspirin and/or selective prostaglandin H2/TXA2-receptor antagonists may be important tools to test the hypothesis that TXA2-dependent platelet activation represents an important transducer of the enhanced thrombotic risk associated with these metabolic abnormalities.
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PMID:Thromboxane biosynthesis in cardiovascular diseases. 226 Jan 37

The influence of myocardial ischemia on defibrillation success was studied using two different lead orientations in halothane-anesthetized pigs. Ischemia was induced by ligating the left anterior descending artery in its distal third. Controls had loosely tied ligatures placed around the artery at the same site. Ventricular fibrillation was induced by electrical stimulation 30 minutes after coronary artery ligation. Defibrillation used a single truncated pulse of approximately 6 ms duration passed to either: a transvenous electrode catheter (Medtronic, 6880) with the cathode in the apex of the right ventricle and the anode in the superior vena cava-atrial junction region, or the cathode in the apex of the right ventricle and a mesh plaque on the epicardium of the basal lateral left ventricle as anode. Ten seconds after the onset of ventricular fibrillation, defibrillation was attempted with increasing incremental energies until defibrillation was achieved. Fibrillation episodes were repeated at 15-minute intervals until the minimum first shock was successful in defibrillating the animal (i.e., defibrillation threshold). The number of animals successfully defibrillated with a minimum energy above or below 30 J was not different between normal and ischemic animals for either electrode configuration (i.e., 3 out of 20 vs 1 out of 13 for the catheter and 5 out of 6 vs 6 out of 7 for the epicardial plaque, respectively). Also, the cumulative percent success as a function of defibrillation energy was similar in both the normal and ischemic groups. There was a significant reduction in the minimum energy necessary for defibrillation when passing current between the right ventricular apex and the left ventricular epicardial plaque. The present results indicate that, despite differences in lead orientations, acute ischemia in the anesthetized pig does not appear to influence defibrillation success.
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PMID:Internal cardiac defibrillation threshold: effects of acute ischemia. 242 74

In man a close interrelationship exists between hyperadrenergic states, myocardial ischemia, necrosis, infarction and sudden cardiac death. Persistent high catecholamine levels may also be associated with increased vascular endothelial turnover and permeability to calcium and lipoproteins, increased blood velocity, abnormal blood flow patterns and atheroma formation. There are thus good reasons to predict a cardiovascular protective effect of beta-blockers. Animal data indicate that in spite of apparently adverse plasma lipoprotein changes beta-blockers retard atheromatous plaque formation under conditions of high cholesterol diet with or without stress. A slow heart rate, as well as a reduction in calcium influx and inhibition of both esterification of arterial wall cholesterol (by ACAT) and endothelial permeability to lipoproteins, may be central to this process. Beta-blockers benefit a spectrum of conditions related to the atheromatous process and myocardial necrosis. These are silent ischemia; stable (including mixed), unstable and preinfarction angina; periinfarction events (including myocardial rupture and dissection of the ascending aorta); and myocardial necrosis associated with stress conditions such as head injuries and subarachnoid hemorrhage. In one study coronary deaths in hypertensive men, particularly in smokers, were significantly reduced by metoprolol (a beta 1-selective blocker) compared to a diuretic. In contrast in the MRC study of mild hypertension only nonsmoking men with mild to moderate hypertension who received a nonselective beta-blocker appeared to experience fewer myocardial infarctions. Recent clinical data showed that moderate-severe hypertensives who were optimally controlled by atenolol-based treatment over a 10-year period were less likely to die from myocardial infarction than those suboptimally controlled, irrespective of a rise in serum triglyceride levels. Thus the net effect of acute beta-blockade in hyperadrenergic states, including myocardial infarction, is to limit cardiovascular damage. Chronic beta-blockade inhibits atheroma formation (in animals) and beneficially modifies the incidence of stroke and myocardial infarction, which in man are the long-term consequences of hypertension.
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PMID:The beta-receptor, atheroma and cardiovascular damage. 257 Apr 26

The mechanisms of severe vascular injury during surgery of the hip joint are depicted with reference to the authors' own patient series and a review of the literature. Massive arterial hemorrhage is most commonly caused by the tip of a Hohmann retractor. Special care must be given to placement of the proximal retractor directly against the pelvis behind the anterior lip of the acetabulum, and this must be checked with the finger tip. Other mechanisms of injury are: massive venous bleeding can result if a coil of pelvic vein is rolled up with a Kirschner wire; arterial thrombosis can be caused by the polymerization heat of bone cement; or intimal dissection can be caused by pressure of a retractor or loosening of an intimal plaque, resulting in ischemia of the corresponding limb; arterio-arterial embolism can originate from appositional thrombus formation on a chronically weakened arterial wall; false aneurysms may be due to instrumental arterial injury; and arteriovenous fistulae can be caused by a piercing instrument. Laceration of the external iliac or common femoral artery is best treated by interposition of a saphenous vein graft. Angiological examination before and immediately after hip surgery is advocated.
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PMID:[Vascular complications in surgery of the hip joint]. 260 75

Recent work has now clearly established that coronary arterial thrombosis is the direct cause of acute myocardial infarction. This thrombotic event occurs when a pre-existing atherosclerotic plaque ruptures or fissures, thereby exposing underlying thrombogenic material to the circulation. Platelets are thus activated and the clotting cascade is initiated. It is as yet unclear why a previously stable atherosclerotic plaque should fissure or rupture. However, suggested mechanisms include release of vasoactive substances from activated platelets, coronary arterial vasomotion, mechanical stress fatigue of the atherosclerotic plaque, and rupture of vasa vasorum within the atherosclerotic plaque. The resultant cessation of myocardial blood flow produces specific biochemical and physiological alterations secondary to myocardial ischemia. Intracellular acidosis, loss of high-energy phosphates, reduced sensitivity of contractile proteins to calcium, and accumulation of inorganic phosphate and lipid, all occur within the ischemic myocyte. Diastolic compliance is markedly reduced by ischemia followed by cessation of systolic contractile activity. Most of these alterations are reversible if ischemia is relieved promptly. Prolonged ischemia leads to delayed biochemical and physiological recovery and/or cell necrosis.
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PMID:The pathophysiology of acute myocardial infarction. 266 57

The principal common pathway for myocardial ischemia is an oxygen supply-demand imbalance; more recently, greater emphasis has been placed on limitations of myocardial blood supply, as well as excessive myocardial oxygen demand. Myocardial ischemia is a metabolic event resulting from inadequate oxygen delivery to local tissues. The physiologic effects of ischemia are observed through abnormalities in left ventricular function, electrocardiographic changes, and often, by angina pectoris. Prognostic and therapeutic outcomes are significantly related to the pathophysiology of the underlying coronary lesion. Because myocardial ischemia often occurs without symptoms, clinical distinctions based on angina stability may more appropriately be represented by stable or unstable ischemic syndromes that incorporate silent ischemia. Stable ischemic syndromes occur secondary to coronary plaques, whereas unstable syndromes are the result of active lesions caused by plaque rupture with local thrombus and vasoreactivity that produce intermittent critical decreases in coronary supply. The prognosis of patients with stable ischemia is related to the extent of myocardium at jeopardy and overall left ventricular function. In contrast, unstable syndromes are associated with a worse short-term prognosis, which may be predictable by the presence of silent ischemia or left ventricular dysfunction or both. Therapeutic decisions based on an improved pathophysiologic understanding of ischemic mechanisms as well as the physiologic impact of therapy on cardiac function can enhance efficacy while avoiding adverse effects. Calcium channel blockers appear to afford certain advantages in the treatment of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing concepts in the pathophysiology of myocardial ischemia. 267 86

Thirteen patients, seven with acute myocardial infarction and six survivors of sudden death after sport, underwent coronary angiography within a mean of 104 min after the onset of symptoms. The admission electrocardiogram showed transmural myocardial ischemia in all patients. The ischemia-related vessel was occluded in all cases of sudden death and in three cases of acute myocardial infarction. Reperfusion was achieved in eight vessels: after intracoronary streptokinase in three, after intracoronary nitroglycerin in three, and mechanically in two. Coronary spasm was demonstrated in three vessels, and coronary thrombi, in four. The coronary lesion was described as either concentric in two or eccentric with irregular borders in eight. There was a high incidence of eccentric lesions consistent with ruptured plaques. The acute coronary angiographic findings of acute myocardial infarction and sudden death after sport are similar. Physical exercise can provoke myocardial infarction and sudden death probably by inducing plaque rupture that can evoke coronary spasm, thrombosis, or both.
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PMID:Myocardial infarction and sudden death after sport: acute coronary angiographic findings. 276 51

Atheromatous plaques of the vertebral artery ostium are usually smooth and cause hemodynamic ischemia in the vertebro-basilar territory only when stenosis is severe. A case of crescendo vertebro-basilar attacks is reported and related to an ulcerated plaque of the vertebral artery ostium. The patient underwent surgical endarterectomy after failure of an antiplatelet treatment. He has remained asymptomatic for six months. Diagnosis of vertebral artery ulceration is difficult by ultrasonics or digitalized arteriography because of the small diameter of the vessel and its posterior origin. The frequency of ulcerated plaques of the subclavio-vertebral intersection is probably underestimated in the literature Labauge et al. (1987) emphasized recently the risk of cerebellar infarction during the natural history of vertebral artery occlusion. Crescendo vertebro-basilar transient ischemic attacks can be caused by a plaque rupture of of the vertebral ostium which leads secondarily to vertebral artery occlusion. Therapeutic options for atheromatous lesions of the posterior circulation are not clearly defined by controlled studies. In the reported case and in series reported in the literature, surgery would appear to be an efficient procedure with low mortality and morbidity.
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PMID:[Emboligenic ulcerated plaque of the foramen of the vertebral artery]. 279 11

"Blue toe syndrome" refers to digital ischemia of the foot in the presence of palpable or Doppler audible pedal pulses. This clinical syndrome is caused by microembolization to small vessels from a proximal source. The use of percutaneous transluminal atherectomy is described in the treatment of embologenic superficial femoral artery lesions in seven patients. All seven had prompt healing of the ischemic toes, and none required surgical revascularization or amputation. One patient developed a recurrent stenosis at the atherectomy site and had a second episode of digital ischemia, which was treated by means of atherectomy with a larger device. Histologic study of atherectomy specimens suggests that emboli arise from adherent fibrinoplatelet aggregates or thrombus and less often from cholesterol-rich atheromatous plaque. Although either percutaneous transluminal angioplasty or atherectomy can be used to treat the underlying stenosis, percutaneous atherectomy offers the advantage of nonsurgical removal of embologenic material and provides material for histologic study. Percutaneous atherectomy is an effective method of treating embologenic superficial femoral stenoses in patients with ipsilateral blue toe syndrome.
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PMID:Blue toe syndrome: treatment with percutaneous atherectomy. 281 88

Contrast-enhanced computed tomography of the neck permits low-risk evaluation of morphologic complications of carotid plaque, including (and foremost) calcification. To investigate the patterns and clinical significance of calcified deposits in the cervical carotid arteries using computed tomography we studied 40 patients with unilateral symptoms of hemispheric ischemia. Calcium deposits observed in the external, internal, and common carotid arteries were oriented in space and individually scored. We found calcified deposits in 39 patients. Stepwise multiple regression of the data provided evidence strongly suggesting a correlation between advancing age and calcium scores. Calcium was more heavily concentrated in the posterior half of arteries (p less than 0.01), in particular of the internal and common carotid arteries, and always in relation to an atheromatous plaque, suggesting a causative link to hemodynamic forces within the arteries. There was no difference in calcification scores between symptomatic and asymptomatic sides, indicating that calcium deposits do not contribute to the development of symptoms.
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PMID:Computed tomographic study of cervical carotid calcification. 281 80


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