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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Regional hemodynamics was studied in 120 patients with atherosclerosis obliterans of the iliac and femoral arteries by ultrasonic Dopplerometry. Regional malleolar systolic pressure, malleolar-upper arm index, and regional systolic perfusion pressure deficit (RSPPD) were determined by an elaborated method. The authors analyse the values of regional hemodynamics according to the severity of the trophic disorders and type of the occlusive lesion of the iliac and femoral arteries. It was established that, being an integral characteristic, RSPPD allows the degree of limb ischemia to be characterized quantitatively most informatively with consideration for the condition of the central hemodynamics.
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PMID:[Ultrasonic evaluation of regional hemodynamics in arteriosclerosis obliterans of the iliac and femoral arteries]. 220 74

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

External iliac fibromuscular dysplasia is a rare and usually asymptomatic disorder. We report eight symptomatic patients seen over a 15-year period and review pathophysiologic mechanisms accounting for the three following distinct lower extremity ischemic sequelae: (1) Emboli--episodic focal digital ischemia (blue toe) was seen in three patients. Resection and primary anastomosis of focal iliac ulcerative fibromuscular dysplasia (one patient) or resection and replacement (two patients) removed the embolic source and relieved the symptoms. (2) Chronic ischemia--gradual onset of full leg claudication in four patients was treated by operative graduated intraluminal dilation in three patients and prosthetic bypass in one. Arteriography subsequently showed a remodeled lumen in the three patients who underwent dilation. (3) Dissection--acute onset leg ischemia resulted from presumed dissection of the external iliac segment. After 4 months of conservative management of antiplatelet agents and exercise, symptoms resolved completely, and arteriogram showed spontaneous restoration of a normal lumen in the dissected segment. The clinical presentation of fibromuscular dysplasia may mimic other arterial processes such as atherosclerosis. Diagnosis is made only by arteriography with specific magnification views of the external iliac arteries and careful surveillance of the renal arteries. Appropriate treatment should be tailored to the clinical presenting symptom. For microembolic disease, resection and replacement are required. For chronic ischemia, intraluminal dilation is generally sufficient and durable and has proved to be a simpler and acceptable alternative to replacement or bypass. In acute dissection, surgical intervention may be deferred if the limb is viable to allow spontaneous healing and remodeling. Persistent symptoms may be the only indication for intervention in this ischemic manifestation of external iliac fibromuscular dysplasia.
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PMID:Clinical spectrum of symptomatic external iliac fibromuscular dysplasia. 221 43

Acetylcholine-induced constriction of human coronary arteries in vivo is commonly attributed to endothelial dysfunction. To examine the effects of 2 other important determinants of vascular responses--namely, agonist concentration and the segment of circulation under study--the diameters of proximal, middle and distal segments of the left anterior descending artery (LAD) and coronary sinus oxygen saturation were measured in 10 patients with angiographically normal coronary arteries (group 1) and in 7 patients with coronary atherosclerosis (group 2) after intracoronary acetylcholine was infused at concentrations from 10(-7)M to between 10(-4)M and 10(-2)M. In group 1, acetylcholine caused minor (less than or equal to 6%) but progressive dilatation of the LAD up to 10(-4)M, but constriction, particularly of the distal segments and tertiary branches, occurred at higher concentrations. Over the same concentration range, coronary sinus oxygen saturation rose progressively from a basal level of 36 +/- 3% to a maximum of 72 +/- 3% in the absence of changes in heart rate and blood pressure, suggesting marked progressive dilatation of resistance vessels. Concentrations greater than or equal to 10(-3)M caused intense constriction of distal epicardial vessels and, in some cases, anginal pain and objective signs of ischemia. Conversely, in group 2, acetylcholine (infused only up to 10(-4)M for ethical reasons) failed to cause significant changes in LAD diameter. These data suggest that the local acetylcholine concentration and coronary vascular segment under study may determine the observed response to at least an equivalent extent as does the presence or absence of coronary atherosclerosis, raising the question of whether a constrictor response to intracoronary acetylcholine reliably indicates the presence of coronary atherosclerosis.
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PMID:Response of angiographically normal and atherosclerotic left anterior descending coronary arteries to acetylcholine. 222 Jun 34

Eight patients with severe pedal ischemia in the presence of palpable foot pulses are described. All had atherosclerosis, and seven patients also had diabetes. There were two anatomic patterns of disease, including supramalleolar obstruction with reconstitution of pulsatile flow in three patients and segmental occlusion of the pedal vessels in five. All patients underwent arterial reconstructive surgery. Patency was sustained in six patients, with limb salvage in five and below-knee amputation in one patient for persistent necrosis and infection of an open amputation. Of the two eventual bypass failures, a transmetatarsal amputation continued to heal in one patient, and the other required amputation below the knee. Palpable pedal pulses and satisfactory ankle/brachial indexes did not rule out the presence of surgically correctable distal arterial occlusive disease. Therefore arteriography is indicated in any patient with persistent forefoot ischemia that fails to respond to conservative measures. The safety and patency of the distal reconstructive procedures performed in this series suggest that salvage of weight-bearing tissue and rapid healing, as well as limb salvage, are legitimate indications for revascularization.
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PMID:Indications for distal arterial reconstruction in the presence of palpable pedal pulses. 151 Jul 52

Fifty patients with 65 popliteal aneurysms underwent reconstructive procedures (mean age 64). Atherosclerosis is almost the exclusive cause of popliteal aneurysms. Most of the cases showed an acute ischemia, while he others were asymptomatic or presented a complication of venous occlusion or neural compression. Numerous cases were found incidentally at amputations (these were not included). The best operational method is ligation of the aneurysm sometimes with partial resection and autologous venous graft bypass. The immediate results were excellent in all cases, loss of limb was observed in only three.
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PMID:[Popliteal aneurysm. Our experience in 65 cases]. 223 54

Current noninvasive diagnostic techniques have limited accuracy for detection of coronary artery disease (CAD) in symptomatic and (particularly) asymptomatic patients with silent disease. Furthermore, no standard noninvasive method provides reliable diagnostic information on the location of the coronary arteries involved, the severity of stenosis, the presence of collaterals and myocardial viability. Based on greater than 1,000 cardiac studies at the University of Texas, cardiac positron emission tomography (PET) with either generator-produced rubidium-82, cyclotron-produced N-13 ammonia, or F-18 deoxyglucose is suitable for 4 routine diagnostic purposes: (1) noninvasive diagnosis of CAD in either symptomatic or asymptomatic subjects with a sensitivity of 95 to 98% and specificity of 95 to 100%. This accuracy is now sufficient to schedule diagnostic catheterization and multivessel angioplasty with surgical backup on the basis of the PET scan. At the University of Texas we carry out PET in asymptomatic and symptomatic patients to direct those with mild disease to cholesterol-lowering reversal therapy and those with severe disease to percutaneous transluminal coronary angioplasty (PTCA); (2) assessment of physiologic severity of coronary artery stenosis as compared to automated quantitative coronary arteriographic analysis. Changes in stenosis severity are followed before and after interventions including PTCA, bypass surgery, vasodilator drugs and cholesterol control regimens for reversal of coronary atherosclerosis; (3) imaging myocardial infarction, ischemia, viability, zone at risk and sizing of these pathophysiologic processes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Positron emission tomography and interventional cardiology. 223 2

When an obstruction of a cerebral vessel is hemodynamically relevant and insufficiently collateralized--and when the mechanisms of compensation are exhausted--it can lead to ischemia. The second and more common way a vascular obstructive lesion can become symptomatic is the shedding of emboli to the periphery. The extra-/intracranial arterial bypass (EIAB), most often constructed as an anastomosis between the superficial temporal artery (STA) and a cortical branch of the middle cerebral artery (MCA), increases cerebral blood flow when all the mechanisms of compensation are exhausted. When not, it augments the cerebral perfusion reserve. If cerebral ischemia is due to embolism, the therapy of choice is elimination of the embolic source. When using the EIAB in hemodynamically caused ischemia, there are two indications: a therapeutic and a prophylactic one. Differentiation between functional and structural damage of neurons is difficult. Because reversible longlasting functional loss is rare, we reject it as a therapeutic indication. The prophylactic EIAB has to overcome the hemodynamic consequences of an intentional or spontaneous obstruction of extra- or intracranial cerebral vessels. Currently, neither the asymmetry of cerebral perfusion nor a decrease of the the cerebral perfusion reserve are established as risk factors for future ischemic cerebral events. If the MCA is to be occluded, a prophylactic EIAB is indicated: When the intention is to occlude the ICA with its extensive collateral system, the necessity for a bypass has to be evaluated. Most often, spontaneous occlusion of cerebral vessels is of atherosclerotic origin. Because no reliable method exists to differentiate between embolic (arterio-arterial) and hemodynamic ischemia; and since the spontaneous course of atherosclerosis is not predictable, the prophylactic indications for EIAB are unresolved. Nevertheless, many uncontrolled studies have shown a good prophylactic effect after the EIAB. The randomized international EC/IC Bypass Study, which is not accepted without reservation, denies any advantage of the EIAB in treating atherosclerotic vessel lesions when compared to medication with aspirin. Our experience leads us to believe that a prophylactic effect of the EIAB, even with atherosclerotic vessel obstruction, cannot be denied point blank. On the other hand, our experience also confirms that the EIAB should not be the standard treatment for atherosclerotic vessel obstruction. Considering the broad differences in the individual architecture of the cerebral vascular system and its varied amounts of acquired vascular lesions and through the spontaneous development of collaterals, the indications for EIAB, which in some circumstances is very effective, must be assessed for each individual patient.
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PMID:[Cerebral bypass surgery]. 229 2

Acute acalculous cholecystitis is a virulent disease of uncertain etiology observed most commonly in critically ill patients. Although the precise mechanism is unknown, the most commonly postulated theories regarding its pathogenesis are bile stasis, sepsis, and ischemia. The role of ischemia in this process, whose etiology is multifactorial, has been difficult to elucidate. Consequently, we report two patients who developed acute acalculous cholecystitis without apparent risk for the disease other than severe visceral atherosclerosis. Both patients had symptomatic mesenteric vascular disease requiring revascularization and developed fulminant acalculous cholecystitis temporally related to exacerbation of their visceral ischemia. These cases suggest that patients with visceral atherosclerosis may be at increased risk for acute acalculous cholecystitis, perhaps due to impaired mucosal resistance when other factors, such as bile statis and sepsis, are also present.
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PMID:Does visceral ischemia play a role in the pathogenesis of acute acalculous cholecystitis? 230 85


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