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)

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.
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PMID:Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death. 207 44

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

To examine whether acute myocardial ischemia activates the coagulation system and platelet activation in the coronary circulation, we measured plasma levels of fibrinopeptide A and beta-thromboglobulin in the coronary sinus and the aortic root simultaneously in 15 patients with coronary spastic angina before and after the left coronary spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Fifteen patients with chest pain but normal coronary arteries and no coronary spasm served as controls. The coronary sinus-arterial difference of fibrinopeptide A increased markedly (p less than 0.001) from 0.1 +/- 0.2 to 4.3 +/- 0.7 ng/ml after the anginal attacks in the coronary spastic angina group. However, fibrinopeptide A levels remained unchanged after the attacks in the stable exertional angina group and after intracoronary injection of acetylcholine in the control group. Plasma beta-thromboglobulin levels remained unchanged after the attacks in both patient groups and after acetylcholine in the control group. Our data indicate that coronary spasm induces thrombin generation and may lead to thrombus formation in the coronary artery involved, but pacing-induced ischemia does not activate the coagulation system.
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PMID:Fibrinopeptide A is released into the coronary circulation after coronary spasm. 214 92

The possible options for the management of acute pain are quite numerous and continue to expand as our understanding of the mechanisms of pain becomes increasing sophisticated. Many of the options discussed have been available for years, and their present underutilization may be a reflection of the lack of emphasis on the importance of management of acute pain. An illustration of this would be our present ritual of prescribing narcotics postoperatively, a longstanding, but unfortunately inadequate practice. Because of poor selection and scheduling of doses, postoperative analgesia is typically a less than satisfactory experience for many patients convalescing in a hospital following surgery. The clinician should of course be guided by the clinical situation itself in order to determine what modality or combination of modalities may be appropriate for pain management. Certain techniques, such as continuous local anesthetic infusions, may warrant an escalated level of monitoring and ancillary care. Other techniques, such as the infiltration of a wound with local anesthetic or the addition of a nonsteroidal anti-inflammatory agent to a regimen of mild oral narcotics are so simple that excluding them from patient care is almost callous and inconsiderate. Attention to the mechanisms of pain that may be present in a given situation, whether it be muscle spasm, ischemia, inflammation, edema, or nerve injury, may guide the clinician toward a more rational approach in managing that pain.
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PMID:Non-narcotic modalities for the management of acute pain. 218 13

Rupture of an atherosclerotic plaque associated with partial or complete thrombotic vessel occlusion is fundamental to the development of ischemic coronary syndromes. Plaques that produce only mild-to-moderate angiographic luminal stenosis are frequently those that undergo abrupt disruption, leading to unstable angina or acute myocardial infarction. Plaques with increased lipid content appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages appear to play an important role in atherogenesis, perhaps by participating in the uptake and metabolism of lipoproteins, secretion of growth factors, and production of enzymes and toxic metabolites that may facilitate plaque rupture. In addition, the particular composition or configuration of a plaque and the hemodynamic forces to which it is exposed may determine its susceptibility to disruption. Exposure of collagen, lipids, and smooth muscle cells after plaque rupture leads to the activation of platelets and the coagulation cascade system. The resulting thrombus may lead to marked reduction in myocardial perfusion and the development of an unstable coronary syndrome, or it may become organized and incorporated into the diseased vessel, thus contributing to the progression of atherosclerosis. In unstable angina, plaque disruption leads to thrombosis, which is usually labile and results in only a transient reduction in myocardial perfusion. Release of vasoactive substances, arterial spasm, or increases in myocardial oxygen demand may contribute to ischemia. In acute myocardial infarction, plaque disruption results in a more persistent thrombotic vessel occlusion; the extent of necrosis depends on the size of the artery, the duration of occlusion, the presence of collateral flow, and the integrity of the fibrinolytic system. Thrombi that undergo lysis expose a highly thrombogenic surface to the circulating blood, which has the capacity of activating platelets and the coagulation cascade system and may lead to thrombotic reocclusion. Measurements aimed at reversing the process of atherosclerosis via cholesterol reduction and enhanced high density lipoprotein activity are encouraging. Active research is being focused on the development of new antithrombotic tools, such as inhibitors of thrombin, thromboxane, and serotonin receptor antagonists, and monoclonal antibodies aimed at blocking platelet membrane receptors or adhesive proteins. These compounds may prove useful when immediate and potent inhibition of the hemostatic system is desired. Intensive research is still needed in the areas of pathogenesis and therapeutic intervention in atherosclerosis.
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PMID:Atherosclerotic plaque rupture and thrombosis. Evolving concepts. 220 64

Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along its endothelial surface that occur in response to vessel injury; (2) the delayed onset of a neurological deficit following subarachnoid hemorrhage, thought to be due to ischemia or infarction of a portion of the brain; or (3) the combination of these two features (symptomatic vasospasm). The arterial contraction of intracranial arterial spasm typically develops a few days after the rupture of an intracranial aneurysm and lasts 2 to 3 weeks. Such arterial spasm can also occur in other conditions such as head trauma. If it is severe enough it can lead to cerebral infarction. The pathogenesis of this condition is still unclear. Many ingenious attempts have been made to prevent or treat cerebral vasospasm, but most have failed. The best current approach is to ensure adequate blood volume, and to elevate the patient's blood pressure (especially if the aneurysm has been secured by an early operation). The continuing investigation of drugs such as calcium channel blocking agents to improve the cerebral circulation has begun to provide additional help.
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PMID:Cerebral vasospasm. 222 95

This communication will discuss the spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases, and will focus on ischemic heart disease. The hypothesis is regarded as a separate model or paradigm, and is based on the principle that spasm of resistance vessels directly induces symptoms in these conditions. Resistance vessels help maintain vascular homeostasis through autoregulatory mechanisms, and spasm of resistance vessels is considered to represent 'inappropriate' activation of these mechanisms by disease states, which are equated with risk factors. For ischemic heart disease, the most important risk factor is stenotic coronary artery disease, and the concept asserts that severe ischemia secondary to coronary artery disease causes sufficient tissue injury to incite injury-spasm of resistance vessels. While it is universally accepted that occlusions of epicardial arteries by stenotic coronary artery disease, spasm, and thromboses directly induce clinical symptoms, the hypothesis suggests that these occlusions have other roles. The concept accepts all current treatments of ischemic heart disease, but as this disorder is viewed differently, a significantly different direction of research is proposed for improving its treatment and prevention.
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PMID:The spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases. 225 73

Myocardial reperfusion injury will be discussed in context to the spasm of resistance vessel concept of ischemic heart disease. This hypothesis attributes symptoms in this disorder directly to primary spasm of resistance vessels, and is based in part on a study of no-reflow which provided evidence that no-reflow is due to ischemia-induced injury-spasm of resistance vessels. Studies of no-reflow and reperfusion injury are rather similar, and the concept asserts that ischemia-induced injury-spasm causing no-reflow is involved in reperfusion injury. It is recognized that oxygen free radicals cause both myocardial and vascular injury during reperfusion injury, and the concept suggests that vascular injury contributes significantly to reperfusion injury by inducing the sequence of injury-spasm, no-reflow, fresh ischemia, and fresh ischemic reperfusion injury. In keeping with this, the possible involvement of spasm and no-reflow in reperfusion injury occasionally is mentioned. However, it seems to be generally accepted that reperfusion injury is due essentially solely to direct myocardial injury by free radicals, and possible reasons will be explored for a relative disinterest in spasm and no-reflow in reperfusion injury.
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PMID:Myocardial reperfusion injury: an assessment by the spasm of resistance vessel concept of ischemic heart disease. 225 93

Shenshao Tongguan Pian (SSTGP) is composed chiefly of saponins from the stem and leaf of Ginseng and Radix Paeoniae Alba, etc. The authors applied this remedy for the treatment of angina pectoris of CHD. From 1982-1988, the authors carried out a randomized double blind trial on altogether 565 cases of CHD divided into an experimental group to be treated with SSTGP and a control group treated with another TCM proprietory medicine, Dan Qi Pian, that had been used for many years clinically. The total effective rate of treating angina pectoris was 94.71% and ECG improvement rate 63.38% in experimental group whereas 66.99% and 23.38% respectively in the control group, the difference being very significant (P less than 0.01). Experiments with animals proved that SSTGP had more potent actions on CV system, such as dilatation of coronary arteries, promotion of coronary perfusion flow, lowering oxygen consumption of heart muscle, resisting the coronary spasm, anoxia and ischemia of heart muscle elicited by pituitrin, and prolongation of survival time of mice under anoxic state. In addition, laboratory examination also revealed SSTGP could promote the left ventricular output, lower the blood viscosity and inhibit the aggregation of blood platelets. Both acute and chronic toxicity tests showed SSTGP has no toxicity nor side effects. Therefore SSTGP is a new, safe and effective TCM proprietory remedy for CHD and angina pectoris.
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PMID:[Clinical and experimental study of shenshao tongguan pian in treating angina pectoris of coronary heart disease]. 226 17

The timing of surgery for the ruptured aneurysm (SAH) remains controversial. After the period of delayed surgery, the early surgery is now more and more frequently advocated. This paper, study our experience in aneurysm surgery in two different periods, considering only patients admitted in grades I to IV, excluding grade V patients (deep coma, decerebration). During the former period (1972-1984) 328 patients were admitted and considered for delayed surgery, usually during the second week following SAH. 94.5% of patients were operated upon. 5.5% patients died before surgery, from ischemia (3%) or from rebleeding (2.5%). 38.5% were admitted between (D.O-D3) after SAH, D.O being the day of SAH. Only 5.7% were operated upon between D.O-D3. The higher peak of surgery was during the second week (41.8%) and during the third week (39.2%). During the later period (1985-1988) 106 patients were admitted, 50% of them between D.O and D3 after SAH. Every patient was operated upon. The patients admitted between D.O and D3 were operated upon as follows: between D.O and D3 = 32.1%, between D4 and D6 = 22.6%, between D7 and D15 = 34%, after D16 = 11.3%. The analysis of these sub-groups demonstrates that the distribution was related to the age and clinical status. Patients being awake and under 50 years of age were considered for early surgery. Patients being obnubilated or stuporous, and over 50 years of age were planned for delayed surgery. Angiographic spasm and extension of blood in CT Scan were taken in consideration to a lesser degree.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The same question for the past 20 years: when should a ruptured intracranial aneurysm be surgically treated? (Experience with 434 cases)]. 228 2


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