Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Compared to non-smokers, chronic smokers are at increased risk of developing atherosclerotic vascular disease, myocardial infarction, unstable angina and sudden death. The acute systemic hemodynamic response to smoking includes an increase in the heart rate, arterial pressure, cardiac output and myocardial contractility. These acute effects are primarily mediated by activation of the sympathetic nervous system. In patients with heart disease, smoking may cause a deterioration in cardiac performance. In the coronary circulation, smoking induces coronary vasoconstriction which can be prevented by alpha-adrenergic blockade, nitrates and calcium channel blockers. Non-selective beta-adrenergic blockade potentiates both the systemic and coronary vasoconstrictor effect of smoking. Other adverse effects of smoking on the cardiovascular system include a reduction in high-density lipoprotein (HDL) cholesterol, an increase in platelet reactivity and an increase in fibrinogen concentrations. These effects on systemic and coronary hemodynamics, lipid metabolism and hemostasis may contribute to the long-term adverse consequences of smoking.
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PMID:Smoking and cardiovascular function. 228 53

Forty six patients aged 18-39 years with transient ischaemic attacks (TIA) were studied; two thirds were women. Twenty five patients had attacks accompanied by headache, and seven gave a history of common migraine. Only four of 27 angiograms were abnormal; no operable carotid lesion was demonstrated. Over a mean follow up period of 10 years stroke or myocardial infarction (AMI) occurred in all four patients who presented major cerebrovascular risk factors, but in only two of the remaining 42 patients. Thus irrespective of age thromboembolic TIA is a harbinger of stroke or AMI. However, most TIAs under the age of 40 years are caused by a non-embolic benign vascular disorder. The clinical characteristics, long-term prognosis, and possible pathogenesis, for such attacks are often indistinguishable from those of classical migraine. In the absence of cardiovascular risk factors, arteriography does not provide much diagnostic and prognostic information.
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PMID:Transient ischaemic attacks in young patients: a thromboembolic or migrainous manifestation? A 10 year follow up study of 46 patients. 229 92

Selective coronary angiography to determine the prevalence of coronary artery disease (CAD) has been performed in patients with abdominal aortic aneurysm (AAA). Thirty patients in this series consisted of 26 men and 4 women with an age range of 48-87 years (mean +/- SD: 67.5 +/- 8.2 years). As the atherosclerotic risk factors, cigarette smoking was present in 19 patients (63.3%), hypertension was in 18 (60%), hypercholesteremia was in 10 (33.3%), and diabetes mellitus was in 2 (6.7%). Cerebral vascular disease was present in 11 patients (36.7%). Regarding CAD, angina pectoris or old myocardial infarction was found in 9 patients (30%), and abnormal electrocardiography (ECG) was in 16 patients (53.3%). Coronary angiography prior to operation of AAA was performed to 22 patients (73.3%), and 15 patients (68.2%) among them had significant coronary artery stenosis, and 9 patients underwent myocardial revascularization (4 CABG, 5 PTCA). CAD was frequently complicated both in patients without symptoms or ECG abnormalities and in less than 65-year patients. In order to prevent fatal myocardial infarction, we recommend routine coronary angiography to patients with AAA. And if necessary, myocardial revascularization must be indicated prior to aneurysmectomy.
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PMID:[Coronary artery disease in patients with abdominal aortic aneurysm]. 237 12

Coronary artery disease and myocardial infarction are frequently associated with major conduction abnormalities, but the correlation between the vascular disease and the specific conduction system is not obvious. Anyhow, in cases of acute occlusive vascular disease, the correlation might be more obvious. 31 cases of acute coronary arterial occlusion with myocardial infarction were studied correlating with ECG changes as well as pathologic lesions present in the conduction system. Results showed that histologic changes of the conductive system were usually related with the condition of blood supply and the site and size of the infarction. Additionally, the area of the damaged conductive tissue should be large enough to produce ECG changes. Otherwise the functional changes might be compensated or recovered. Myofibrillar degeneration was obtained in the conduction tissue in the majority of the cases reported, and its clinical significance remains to be clarified.
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PMID:[Pathologic features of conduction system in myocardial infarction]. 238 7

Early observations that the regular use of aspirin (acetylsalicylic acid, ASA), a nonsteroidal anti-inflammatory agent, seemed to protect against myocardial infarction and reduce platelet aggregation made this substance the most frequently used drug in large clinical trials. The objectives of these studies were to reduce thromboembolic complications in arterial cardiovascular diseases (prevention of myocardial infarction in unstable angina, secondary prevention of acute myocardial infarction, and increased patency of aortocoronary bypass grafts) and to reduce platelet deposition on artificial surfaces (artificial heart valves and hemodialysis shunts). Despite the recent synthesis of more selective inhibitors of arachidonic acid metabolism in blood platelets, and a multitude of questions concerning optimal dose, schedule, and mode of action that still remain open, ASA continues to be the most frequently used drug in arterial vascular disorders. Because of the frequent and potentially serious side effects of aspirin, mainly on the gastrointestinal tract, less toxic ways of inhibiting eicosanoid metabolism in blood platelets are attracting more and more interest. Among these, the alimentary substitution of omega-3 fatty acids for a competitive inhibition of the omega-6-arachidonic acid metabolism seems the most promising. Results with fish-oil diet raise the question of whether substitution of polyunsaturated lipid acids influence only platelet metabolism, or whether the action of "anti-platelet" drugs or diet in cardiovascular disorders is mediated primarily by leukocytes or monocytes. This new dietary principle, which possibly corrects only a poor alimentary habit of civilization, could open simple and adequate ways for even a primary prophylaxis of vascular disease by diet alone or, at least for therapeutic aims, in combination with drugs.
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PMID:Drugs or diet: do they protect against degenerative cardiovascular disease? 246 42

Plasminogen activator inhibitor-1 (PAI-1) is an important physiological inhibitor of fibrinolysis. It circulates in blood both in free active form and in inactive form complexed with tissue type plasminogen activator (t-PA). Control mechanisms for its synthesis and release from hepatocytes and endothelial cells are important in the pathogenesis of thrombosis. Possible risk factors for myocardial infarction include high insulin and PAI-1 levels, which correlate with one another in healthy subjects, and fibrinogen, which together with PAI-1, is an acute-phase reactant. We therefore studied the interrelationships between PAI-1, plasma insulin, and acute-phase proteins in 67 patients with angina pectoris. Plasma insulin correlated strongly (r = 0.59, p less than 0.001) with PAI activity, free PAI-1 antigen (r = 0.60, p less than 0.001), and total PAI-1 antigen (r = 0.58, p less than 0.001). The acute-phase proteins, fibrinogen and C-reactive protein, correlated significantly with t-PA antigen, total PAI-1 antigen, and PAI-1/t-PA complexes but not with PAI activity or free PAI-1. The results suggest that insulin stimulates synthesis and release of free PAI-1 (probably via hepatocytes as previously shown with cell culture) and that endothelial cell synthesis and release of t-PA, together with PAI-1, reflects a nonspecific acute-phase response to chronic vascular disease. Hyperinsulinemia found in patients with angina pectoris could play a role in the development of myocardial infarction via the induction of high plasma PAI-1 activity.
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PMID:Plasma plasminogen activator inhibitor-1 in angina pectoris. Influence of plasma insulin and acute-phase response. 247 Mar 43

High blood pressure (BP) is associated with increased risk of vascular disease, including myocardial infarction and stroke. Since drugs that lower BP will reduce the risk of those complications of hypertension that are due to high pressure (strokes due to small-vessel disease, including lacunar infarction and intracerebral hemorrhage due to rupture of microaneurysms, heart failure, and renal failure), it has been assumed that such drugs would also reduce the risk of myocardial infarction due to atherosclerosis. However, in addition to hypertension, many other factors are involved in the atherosclerotic process including blood lipids such as cholesterol, blood platelets, and arterial flow disturbances such as turbulence and vortex formation. Some drugs that lower BP have unwanted effects on blood lipids and arterial flow patterns, which are thought to offset the benefit of BP reduction, whereas other drugs have beneficial effects on such factors. Ames has calculated that the adverse effects of antihypertensive drugs on lipids are enough to completely offset the benefit of treating mild hypertension. We have shown that antihypertensive drugs have different effects on blood velocity, and that these effects are associated with differences in the effects of drugs on arterial flow disturbances at the site of carotid stenosis in man, such that propranolol reduced, and hydralazine increased, the occurrence of abnormal high-velocity flow patterns associated with turbulence and vortex formation. In cholesterol-fed hypertensive rabbits (one-kidney Goldblatt), propranolol was more effective than hydralazine in preventing the occurrence of aortic atherosclerosis, even though hydralazine lowered blood pressure more effectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and atherosclerosis: effects of antihypertensive drugs on arterial flow patterns. 248 Nov 60

The authors report the principal clinical models in which inhibitors of platelet aggregation were used to prevent the clinical complications of atherosclerosis. The models at risk which were considered include unstable angina, TIAs, myocardial infarction and atherosclerotic vascular disease of the lower limbs. Overall, the studies suggest the value of this therapy for the prevention of cardiovascular accidents. TIAs, unstable angina and myocardial infarction are the models which provide the best evidence for this; however, the effectiveness of this therapy in peripheral vascular disease, while showing positive results, needs to confirmed by further clinical studies. Lastly, therapy with inhibitors of platelet aggregation has been shown to be useful in the prevention of aortocoronary bypass occlusion; however, its efficacy has been shown only when therapy is initiated early.
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PMID:Clinical use of antiplatelet therapy. 251 Nov 6

Aspirin inhibits thromboxane and prostaglandin formation in platelets and in vascular cells. It prevents platelet aggregation by irreversible acetylation of cyclooxygenase, a key enzyme in arachidonic acid metabolism. On the basis of its antiplatelet effect, aspirin has been assessed during the past two decades in patients with a history of myocardial infarction, stroke, transient ischemic attack or unstable angina. A meta-analysis of randomized controlled trials of long-term aspirin treatment for the secondary prevention of vascular disease indicated that aspirin (300-1500 mg daily) significantly reduced fatal and non-fatal vascular events. More recently aspirin (160 mg daily) produced a significant reduction in hospital vascular mortality and in non-fatal events in patients with suspected acute myocardial infarction. The combination of aspirin and streptokinase was significantly better than either drug alone. On the other hand, two primary prevention trials of aspirin in healthy doctors did not show any modification of vascular mortality despite an overall reduction of non-fatal myocardial infarction. Resolution of some problems related to the mechanism of action of aspirin and to selection of trial populations will possibly increase the benefit/risk ratio of aspirin treatment for the prevention of vascular disease.
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PMID:Aspirin, platelets and prevention of vascular disease. 251 99

Laser angioplasty with the pulsed dye laser and integral ball-tipped optical fibres was used for primary treatment of occlusive femoropopliteal vascular disease in 26 limbs of 24 patients, all of whom warranted operative intervention. 19 had "critical ischaemia", 8 had pedal ulceration, and 4 had distal gangrene. The delivery device consisted of the laser fibre loaded retrogradely into a standard 6 mm balloon angioplasty catheter, and was introduced through a common femoral artery cutdown in an attempt to recanalise femoropopliteal occlusions of a mean length of 21 cm (range 3-49). Angiographic recanalisation was achieved with a mean energy of 250 J (range 38-727 J) in 23 of the 26 limbs; in each case the channel created by the laser fibre was augmented by balloon angioplasty. Technical failure occurred in 3 patients, due to wall dissection, persistent side-branch entry, and incomplete lesion penetration, respectively. Acute occlusion within 48 h occurred in 2 diabetic patients with very poor run-off and distal gangrene, and early failure occurred in another patient due to inadequate balloon dilatation. 1 patient with segmental tibial disease below a technically successful recanalisation did not show clinical improvement. Several patients had coexisting coronary artery disease, 3 of whom died of myocardial infarction--all with patent femoropopliteal vessels. In the 21 survivors, 14 vessels remained patent at a median of 7 months' follow-up.
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PMID:Peripheral laser angioplasty with pulsed dye laser and ball-tipped optical fibres. 257 65


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