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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet function and thromboxane A2 release were measured in 71 patients admitted to a coronary care unit with a provisional diagnosis of acute myocardial infarction (AMI). All measurements were carried out within twenty-four hours of admission. Of these, 35 patients had the diagnosis of AMI confirmed. The remainder (n = 36), who did not have AMI (NMI), were divided into two groups: those (n = 18) with an unequivocal history of previous vascular disease and those without vascular disease (n = 18). Platelet aggregation and thromboxane A2 (TXA2) release were significantly increased in the AMI group when compared with those in the NMI without vascular disease group or a healthy control group with similar age and sex distribution. Aggregation and TXA2 release in the NMI patients with vascular disease were greater than those in controls and did not differ significantly from those in the AMI group. Patients in the AMI or NMI with vascular disease groups who were taking beta-blockers or calcium channel antagonists at the time of admission showed significantly less platelet aggregation than those who were not taking these drugs. Heparin, added in vitro at therapeutic concentrations, induced significantly more aggregation in patients in the AMI and NMI with vascular disease groups than in the NMI without vascular disease group. We conclude that: platelets obtained from patients with AMI are hyperaggregable and release more TXA2; platelets from patients with significant vascular disease are hyperaggregable, even in the absence of AMI, although they are not as hyperaggregable as those from AMI; treatment with nifedipine and beta-blockers protects these patients from platelet hyperaggregability; heparin induces significant aggregation of platelets from patients with AMI and NMI with vascular disease. These observations are of importance in considering the pathogenesis and treatment of AMI and ischemic heart disease.
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PMID:Platelet function in patients admitted with a diagnosis of myocardial infarction. 288 May 35

The coronary-subclavian steal syndrome involves the siphoning of blood from the myocardium through an internal mammary artery graft because of a proximal subclavian artery stenosis or occlusion, and results in myocardial ischemia. With the increased use of the internal mammary artery for myocardial revascularization, the potential exists for recurrence of angina pectoris in patients who have or in whom develops high-grade stenosis or occlusion of the subclavian artery, because of the coronary-subclavian steal syndrome. The coronary-subclavian steal syndrome can be prevented by the identification of patients with or at risk to develop subclavian artery occlusive disease. All patients undergoing cardiac catheterization prior to coronary artery bypass grafting in which use of the internal mammary artery is anticipated should be evaluated for the presence of upper extremity and cerebrovascular ischemia, the presence of cervical or supraclavicular bruits, and an upper extremity blood pressure differential of 20 mm Hg or greater. Patients with these findings or with evidence of diffuse atherosclerotic vascular disease should have brachiocephalic arteriography at the time of coronary arteriography to identify significant subclavian artery occlusive disease. When this is demonstrated, use of the internal mammary artery as a free graft instead of an in situ graft or use of saphenous vein grafts is indicated. Patients in whom recurrent angina develops following coronary artery bypass grafting that included an internal mammary artery graft should have coronary arteriography to evaluate the presence of coronary-subclavian steal syndrome, and brachiocephalic arteriography. Carotid-subclavian bypass grafting, probably best done with a prosthetic conduit, is the procedure of choice for management of the coronary-subclavian steal syndrome.
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PMID:The coronary-subclavian steal syndrome: report of a case and recommendations for prevention and management. 289 38

Thirteen patients presented with brief, repetitive, stereotyped transient ischemic attacks, large artery atherostenoses or occlusions with impaired collateral flow to a cortical perfusion borderzone, and orthostatic hypotension (OH). OH was caused by diabetes mellitus, aging, and treatments for ischemic heart disease and hypertension. Medical management of OH often eliminated the need for stroke prevention measures such as surgery or anticoagulation. Focal cerebral hypoperfusion from the combination of occlusive vascular disease and OH may be an underreported, treatable cause of TIA and stroke.
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PMID:Orthostatic hypotension as a risk factor for symptomatic occlusive cerebrovascular disease. 290 10

This report describes the nuclear cardiology procedures available for use as diagnostic techniques in patients with definite or suspected cardiovascular disease. The usefulness of myocardial imaging, radionuclide angiocardiography and other radionuclide cardiovascular imaging techniques is classified within specific disease states. The clinical utility of each technique is graded from I to IV, depending on the clinical importance of the technique (I = most important; IV = not indicated). A grade of V is given for methods now considered to be in their research phase. The usefulness of these methods is discussed in patients with acute ischemic heart disease, chronic ischemic heart disease, valvular heart disease, pulmonary vascular disease and hypertensive heart disease. Selected references are provided.
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PMID:Guidelines for Clinical Use of Cardiac Radionuclide Imaging, December 1986. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Cardiovascular Procedures (Subcommittee on Nuclear Imaging). 294 47

In non-obese, non-diabetic patients suffering acute myocardial infarction, angina pectoris, previous myocardial infarction and peripheral vascular disease, the plasma levels of glucose, insulin, C-peptide and glucagon were determined in basal condition and during an intravenous glucose tolerance test. In the four groups there was a high frequency of glucose intolerance. Basal hyperinsulinism was present in all groups; in groups; in those which maintained normal glucose tolerance there was a high B-cell response to the sugar. Basal hyperglucagonemia was found in the early stage of acute ischemic heart disease, in patients with previous myocardial infarction and in those with peripheral vascular disease. The elevated plasma glucagon levels may play a role in the complex disturbance of carbohydrate metabolism present in patients with atherosclerotic vascular disease.
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PMID:Carbohydrate metabolism and plasma levels of insulin and glucagon in patients with atherosclerotic vascular disease. 304 64

Prostacyclin (PGI2) release by human aortic tissue obtained at surgery was assessed in patients (n = 23) with ischaemic heart disease undergoing coronary artery bypass grafting (group 1) patients (n = 14) undergoing surgery for aortic stenosis (group 2), patients (n = 4) undergoing surgery for aortic regurgitation (group 3), and patients (n = 8) with ischaemic heart disease taking aspirin (group 4). Although there was a highly significant correlation between (a) intimal and medial PGI2 production and (b) medial PGI2 production and aortic diameter, there was no correlation between intimal PGI2 production and aortic diameter. Aspirin intake (75-150 mg daily) was associated with a pronounced inhibition (95%) of aortic PGI2 production. This inhibition of aortic PGI2 secretion by aspirin may account for the variable efficiency of aspirin in altering the natural history of vascular disease.
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PMID:Release of prostacyclin from the human aorta. 307 12

Patients with insulin dependent diabetes mellitus who develop proteinuria may die prematurely, whereas those who do not develop this complication have a comparatively normal life span. The excess mortality in diabetics with proteinuria is from cardiovascular as well as renal disease, but the reason is unclear. Risk factors for vascular disease were therefore assessed in 22 insulin dependent diabetics with proteinuria, but not renal failure, who were matched for sex, age, duration of diabetes, and glycated haemoglobin (HbA1) values with a similar number who had normal urinary albumin excretion rates. Macrovascular disease (ischaemic heart disease and peripheral vascular disease) was present in 10 patients with proteinuria but in only three with normal albumin excretion rates, and proliferative retinopathy was detected in 11 and four patients in the two groups. There was no significant excess of smokers in the group with proteinuria. Blood pressure was, however, higher in the patients with proteinuria--mean systolic pressure 161 (SD 18) mm Hg compared with 135 (19) mm Hg (95% confidence interval of difference between means 15 to 38 mm Hg); mean diastolic pressure 90 (SD 12) mm Hg compared with 79 (15) mm Hg (confidence interval 3 to 19 mm Hg). The concentration of serum high density lipoprotein (HDL) cholesterol isolated by precipitation was lower in the patients with proteinuria (confidence interval 0.02 to 0.41 mmol/l). Their concentration of HDL2 cholesterol isolated by ultracentrifugation was also decreased (confidence interval 0.02 to 0.40 mmol/l), whereas HDL3 cholesterol tended to be increased (confidence interval -0.01 to 0.23 mmol/l). There was also a trend for serum cholesterol concentrations to be higher in the presence of proteinuria (confidence interval -0.39 to 1.20 mmol/l). The aggregation of risk factors for atherosclerosis in insulin dependent diabetes mellitus complicated by proteinuria helps to explain the increased prevalence of ischaemic heart disease and peripheral vascular disease reported in these patients. Early renal disease in insulin dependent diabetes may have an important role in hypertension and altered lipoprotein metabolism.
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PMID:Influence of proteinuria on vascular disease, blood pressure, and lipoproteins in insulin dependent diabetes mellitus. 311 68

Twenty-four patients with poor risk factors underwent an extra-anatomic bypass operation for aortoiliac occlusive disease and subclavian steal syndrome. A femoro-femoral bypass was performed on 5 patients, an axillo-femoral bypass on 15, a subclavian-subclavian bypass on 2 and an ascending aorta-femoral bypass on 2. There was only one operative death and there were 2 late deaths (8.3%). The patients were 20 males and 4 females with a mean age of 69.3 years. Among risk factors, high age (70 year old) was present in half of the patients, ischemic heart disease in 9, and cerebral vascular disease in 8. Seventy-five percent of the patients were suffering from two or more dysfunctions. During the limited follow-up period from 8 to 94 months (mean 46.1 months) there was a 96% patency rate. We had good results using externally supported ring graft and by the administration of prostaglandin E1 and ticlopidine during the pre and postoperative period.
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PMID:[Extra-anatomic bypass grafting for vascular occlusive disease in the upper and lower extremities]. 317 84

In a prospective study of 87 patients with TIA or minor stroke (48 men and 39 women, average age 65 years) a history of ischaemic heart disease (IHD) was present in 30 (angina in 25 and myocardial infarction (MI) in 19, 14 having both). The London School of Hygiene Questionnaire did not confirm the diagnosis of IHD in 7 patients, but did detect a further 5 patients with angina and/or MI. The Minnesota coding of the ECG revealed 5 patients with asymptomatic suspect IHD and 15 with probable IHD (a total of 23%). Cardiomegaly (cardiothoracic ratio greater than 0.5) was present in 28 patients, 9 with a history of MI and 8 with a history of angina. These findings indicate that IHD is common in patients with cerebral vascular disease. As both probable IHD on Minnesota coding of the ECG and the presence of cardiomegaly are highly predictive of a poorer outcome, the findings add further weight to the argument that, amongst patients with minor cerebral ischaemia, a sub-group at high risk of death due to IHD can be detected by using simple methods rather than by performing routine coronary angiography on all patients as has been suggested in recent times.
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PMID:Unreported symptomatic and asymptomatic ischaemic heart disease in patients presenting with TIA or minor stroke detected by the London School of Hygiene Cardiovascular Questionnaire and Minnesota coding of a routine ECG. 326 47

Epidemiologic studies clearly link cigarette smoking with vasoocclusive cardiovascular disease. Postmortem studies provide evidence of accelerated atherogenesis in asymptomatic smokers. However, the rapid regression of cardiovascular risk within the first year of quitting smoking is difficult to explain solely in terms of vascular disease. Recent evidence indicates that plasma fibrinogen, which has been prospectively associated with the risk of ischemic heart disease, is elevated in smokers. Similarly, results from studies investigating thromboxane metabolite excretion in urine confirm those involving radiolabeled platelet turnover, suggesting that platelets are activated in the circulation of chronic smokers. Altered hemostatic function, either as a direct result of smoking or caused by smoking-induced vascular damage, may account for the more rapidly reversible component of cardiovascular risk observed in chronic smokers.
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PMID:Cigarette smoking and hemostatic function. 327 16


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