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

Although vasodilation, direct cardiac actions, or both represent the main properties of calcium channel blockers, there are further pharmacologic effects that may be therapeutically relevant. For example, hemorrheological effects, which have been demonstrated for a variety of calcium antagonists, have received relatively little attention to date. Hemorrheology describes the mechanics of blood and its components. It is of particular interest in the context of cardiovascular disease, as it has been shown that under certain conditions (reduced pump function, impaired vasomotor reserve), parameters of blood fluidity may be crucial for tissue perfusion. Whole-blood viscosity is the dominating factor in large arteries. For geometrical reasons, plasma viscosity and the rheological properties of blood cells may become of paramount importance at the microcirculatory level. In ischemic states, erythrocytes may be depleted of ATP, which they need for maintenance of normal shape and for transformation. This results in rigidification of the red blood cell and hindrance of its passage in the microcirculatory bed. Hence, blood flow deteriorates with the consequence of further unfavorable changes of the "milieu interieur," leading to the induction of a vicious cycle. Although effects on several hemorrheological parameters, for example, whole-blood viscosity, plasma viscosity, and red cell aggregation, can be demonstrated for various calcium channel blockers, the main rheological effects of these compounds are believed to consist in the improvement of erythrocyte deformability. When the ATP-dependent calcium pump is impaired in ischemia, calcium channel blockers may inhibit the slow inward transmembrane calcium flux and prevent the accumulation of intracellular calcium.
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PMID:The effects of calcium channel blockers on blood fluidity. 170 14

Cardiac arrhythmias may present in a variety of ways in the primary care setting. They may or may not be accompanied by related symptoms. Rhythm disturbances span the continuum of posing no risk to the patient to being life-threatening. The importance of a thorough history and physical examination to detect the presence of cardiovascular disease or related factors cannot be overemphasized. An ECG is essential for the accurate identification of cardiac arrhythmias. Evaluation and management of cardiac rhythm disturbances often requires collaboration with medical practitioners and possible specialist referral. The primary care nurse practitioner must be able to recognize the important red flags in clinical practice such as cardiac syncope, ischemia, or failure. Finally, an understanding of the diagnostic and therapeutic measures used for arrhythmia evaluation and management will facilitate appropriate patient education, counseling, and follow-up.
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PMID:A primary care approach to cardiac arrhythmias. 184 Sep 34

Exposure of the vessel wall to hypoxemia is a central feature of ischemic cardiovascular disease. This led us to examine the perturbation of endothelial cell properties under hypoxia. An atmosphere of pO2 of 12 mmHg is not lethal to the endothelial cells for up to five days, but barrier function was impaired. Increased passage of macromolecule tracers were observed in time- and dose-dependent manner and electron microscopy demonstrated small gaps (0.5-1.0 micron) between cells. Expression of the anticoagulant cofactor thrombomodulin was also perturbed: thrombomodulin activity and antigen decreased in parallel. Northern blots showed almost complete suppression of thrombomodulin in hypoxic culture. Furthermore, synthesis of other proteins, such as fibronectin, was slightly enhanced under hypoxia. In addition to the suppression of these anticoagulant cofactor, hypoxic endothelial cell displayed a noval procoagulant activity distinct from tissue factor. Further study revealed that hypoxic endothelial cultures directly activated Factor X, as assessed by functional assays and SDS-PAGE. In addition to this no activation of Factor IX or prothrombin was observed. The hypoxia-induced Factor X activator was membrane-associated, required calcium to form Factor Xa, was inhibited by HgCl2 but not by PMSF, and had Km approximately 25 micrograms/ml. Co-incubation of hypoxic cultures with cycloheximide prevented the expression of this activity, suggesting that protein synthesis is required for its expression. These functional perturbations of endothelial cells were reversible following reoxygenation. These data indicate that hypoxia imposes a selective perturbation on endothelial cell function, suggesting the possible contribution of hypoxemia to vascular dysfunction in ischemia.
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PMID:Modulation of endothelial function by hypoxia: perturbation of barrier and anticoagulant function, and induction of a novel factor X activator. 196 56

Ischemic colitis, or more properly colonic ischemia, became a clear clinical entity in the past 25 years. Yet, early diagnosis of this disease with its various presentations remains a difficult task. A 10-year review at our hospital identified 38 patients with colonic ischemia for comparison with the authors' previous experience and with data from the literature. Several important factors emerge: (1) Twice as many cases occurred after operations (34% in this series vs. 16% in the past), probably because fewer and fewer spontaneous cases were hospitalized. (2) Sixteen patients required operative intervention for colonic ischemia with a mortality of 62 per cent, while those treated nonoperatively had a mortality of 14 per cent. Seven of eight postoperative patients who required a second operative procedure for their colonic ischemia died. A high clinical suspicion is necessary in the postoperative patient, as colonic ischemia appears to be more severe among these patients. Moreover, the high incidence of associated cardiovascular disease indicates that early diagnosis, as well as monitoring of the "at-risk" patient, is needed for improvement in survival to occur. New monitoring methods, such as tonometry, may help accomplish this goal.
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PMID:Ischemic colitis. An ever-changing spectrum? 199 67

Left ventricular hypertrophy caused by cardiovascular disease is a marker as well as a contributing factor for cardiovascular morbidity and mortality. Ventricular tachycardia, complex ventricular arrhythmias, and silent ischemia are more prevalent in patients with left ventricular hypertrophy than in those without. Echocardiography is more sensitive and more specific than electrocardiography in diagnosing the entity. Treatment of the underlying disorder may cause regression of left ventricular hypertrophy which, Framingham Heart Study data suggests, may reduce the incidence of cardiovascular events.
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PMID:Left ventricular hypertrophy. Significance in cardiac morbidity and mortality. 213 88

Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Hyperinsulinemia also occurs in patients with angiographically proved atherosclerosis without ischemia and thus appears to be related to arterial disease and not to be a nonspecific response to tissue injury. Fasting insulin levels and insulin responses to intravenous stimuli, including glucose, tolbutamide, and arginine, are normal, suggesting a gastrointestinal factor may be involved in the increased insulin response to oral glucose. In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower high-density lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels. Total and low-density lipoprotein (LDL) cholesterol is less closely related to hyperinsulinemia. Upper-body adiposity is associated (in separate studies) with coronary heart disease, diabetes, hyperinsulinemia, and hypertriglyceridemia. Insulin and blood pressure are closely related in both normotensive and hypertensive people. Although obesity and diabetes are often found in hypertensive people, hyperinsulinemia also occurs in nonobese nondiabetic hypertensive people. Thus, hyperinsulinemia is closely associated with a cluster of cardiovascular risk factors, i.e., hypertriglyceridemia, low HDL levels, hypertension, hyperglycemia, and upper-body obesity. There is a possibility that insulin has a role in the sex differences in ischemic heart disease incidence and their absence in diabetes, but additional work is required for its clarification. Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions. Insulin stimulates lipid synthesis in arterial tissue; the effect of insulin is influenced by hemodynamic factors and may be localized to certain parts of the artery. In physiological concentrations, insulin stimulates proliferation and migration of cultured arterial smooth muscle cells but has no effort on endothelial cells cultured from large vessels. Insulin also stimulates cholesterol synthesis and LDL binding in both arterial smooth muscle cells and monocyte macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insulin and atheroma. 20-yr perspective. 199 42

The diagnosis of silent myocardial ischemia in the aged remains controversial. In this study to evaluate the basic state of silent ischemia in the aged, a total of 972 consecutive autopsy cases (mean 79.0 yrs of age) were analyzed in terms of coronary atherosclerotic diseases. The following results were obtained: (1) Severe coronary occlusive lesions simultaneously detected in the three major coronary arterial branches were found in 85 cases (8.7%), of which 10 (12%) had neither history of angina nor myocardial infarction (MI), which may correspond to one representation of silent ischemia. (2) There were 218 cases of MI (22.4%), of which 106 (49%) were never documented to have MI during life. The latter may correspond to unrecognized MI. It was considered to be caused by 1) small or middle-sized MI in 66 cases and 2) lateral or nontransmural MI in 29 out of 40 large MI cases (more than 4.9 cm in diameter). (3) 30 cases (54%) out of 56 fresh and large MI with a correct diagnosis revealed no chest pain. This is an incidence of painless MI in the aged. This painless group showed a significant difference in the incidence of a correct diagnosis of MI (51% vs 89%), combined arrhythmia (47% vs 79%) and the association of CVD (47% vs 11%) compared with chest pain group.
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PMID:Silent myocardial ischemia in the aged: a retrospective study from the evaluation of necropsy hearts. 262 71

Regional anesthesia is often preferred over general anesthesia for patients with cardiovascular disease because of presumed decreased risk of perioperative myocardial ischemia. However, few studies have addressed this issue directly. To determine whether the type of anesthesia is independently associated with myocardial ischemia, records of 134 patients undergoing peripheral vascular grafting under general or regional anesthesia were examined. There were no significant differences preoperatively between groups in ASA class, age, sex, or prevalence of angina, diabetes, or hypertension. Twelve patients developed myocardial ischemia or infarction within 7 days of operation; 11 of these 12 patients had received regional anesthesia (p less than 0.015). The association between anesthetic approach and perioperative myocardial ischemia or infarction remained after adjustment for preoperative factors associated with ischemia or with type of anesthesia. General anesthesia does not appear to be associated with increased risk of myocardial ischemia, and stringent recommendations to avoid it in this population may be unfounded. A clinical trial is needed to define more clearly the risks and benefits of different types of anesthesia in high-risk patients.
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PMID:Regional versus general anesthesia in high-risk surgical patients: the need for a clinical trial. 227 Nov 99

In patients with neuropathologic processes leading to disturbed cerebrovascular autoregulation, sudden increases in arterial blood pressure may lead to a sudden elevation in cerebral blood flow and intracranial pressure. Therefore, sudden increases in arterial pressure should be assiduously avoided in the perioperative period. Hypertensive episodes may occur at any time during anesthesia, but are more likely to occur (1) during laryngoscopy and intubation, (2) at the time of skin incision, (3) at extubation, and (4) during awakening. In patients with cardiovascular disease, such hypertensive episodes may also cause deterioration of the cardiovascular situation. Catecholamines are the principal mediators of such intraoperative hypertensive reactions. There are 2 options available to the anesthesiologist: (1) attempt to suppress this response after it has occurred, or (2) prevent its occurrence at the outset. Treatment of hypertension often relies on agents that relax vascular smooth muscle. In patients with compromised intracranial compliance, however, cerebral vasodilation must be avoided because it leads to an increase in cerebral blood volume. This, in turn, may raise intracranial pressure and result either in herniation of brain contents or a decrease in cerebral perfusion pressure leading to brain ischemia. Different pharmacologic means of preventing or suppressing such intraoperative hypertensive reactions are reviewed. Many of the drugs reviewed resulted in adverse effects that could preclude their use in patients with reduced intracranial compliance. Alpha- and beta-adrenergic receptor blockers can safely be administered to such patients.
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PMID:Treatment of intraoperative hypertensive emergencies in patients with intracranial disease. 264 55

Loss of consciousness is rare in the absence of transient or persistent insult to the diencephalon or mesencephalon. We found three patients with severe atherosclerotic stenosis or occlusion of both internal carotid arteries who experienced brief loss of consciousness. Common characteristics were the absence of clinical or electroencephalographic seizure activities, significant cardiovascular disease, or a history suggestive of vasovagal syncope. Angiographically, the patients had widely patent vertebrobasilar circulation and collaterals from vertebrobasilar to carotid circulation. Episodic loss of consciousness disappeared after carotid endarterectomy. We concluded that bilateral hemispheric ischemia caused brief loss of consciousness, but selective focal ischemia in the subcortical structures superimposed on widespread bihemispheric ischemia may have been responsible. Since loss of consciousness is rare in carotid occlusive diseases, systemic and vertebrobasilar causes must be carefully ruled out in each instance.
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PMID:Brief loss of consciousness in bilateral carotid occlusive disease. 275 25


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