Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 248 patients with giant cell arteritis, 34 had evidence that the disease affected the aorta or its major branches. Symptoms suggestive of large artery involvement were intermittent claudication of an extremity, paresthesias, and Raynaud's phenomenon. Physical findings included absent or decreased large artery pulses and bruits over large arteries. Four patients presented with decreased upper extremity pulses as the initial manifestation of their arteritis. Nine other patients under treatment for temporal arteritis or polymyalgia rheumatica first developed evidence of large artery involvement as corticosteroid therapy was tapered or discontinued. Angiography, performed in 10 patients, was helpful in indicating arteritis rather than atherosclerosis as the cause of large artery disease. Three patients died with aortic rupture, and, at autopsy, widespread giant cell arteritis was found. However, when corticosteroids were given in adequate doses, the response was favorable in most patients; intermittent claudication decreased and the pulses improved.
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PMID:Large artery involvement in giant cell (temporal) arteritis. 120 May 25

A 38 year old woman with systemic lupus erythematosus (SLE) was admitted because of epigastralgia and fever. The diagnosis of SLE was made 22 years ago based on Raynaud's phenomenon, butterfly rash, hair loss, photosensitivity and positive antinuclear antibody. She had episodes of consciousness disturbance, transient visual disturbance of the left eye, and a necrosis of the left big toe. She underwent artificial arthroplasty of bilateral femoral heads 11 years ago, when multiple aseptic necroses of thirteen bones were found, and when anti-cardiolipin (CL) antibody was found to be positive. An echogram of abdomen suggested an obstruction of superior mesenteric artery (SMA) when she was admitted. Selective angiography revealed a complete obstruction of SMA and splenic artery, and incomplete obstruction of celiac artery. Conservative treatment with urokinase infusion and prednisolone 50 mg/day was not effective, and small intestine and right colon were resected on the 23rd hospital day. The pathological examination showed thrombosis of SMA. There was no evidence of arteritis or atherosclerosis. Anti-CL antibody and lupus anticoagulant were positive on admission, but the level of both anti-DNA antibody and complement was normal. Therefore, it was suggested that the thrombosis was related with anti-phospholipid antibody. The characteristic clinical feature were multiple aseptic bone necroses and thromboses of several arteries. We discussed the relationship of thrombosis and the etiology of multiple bone necrosis in this case with anti-phospholipid antibody.
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PMID:[A systemic lupus erythematosus patient with multiple aseptic bone necroses, thrombosis of superior mesenteric artery and anti-phospholipid antibody]. 144 87

The antiphospholipid syndrome was diagnosed in 19 of 1078 patients treated between 1987 and 1991. All patients with antiphospholipid syndrome had either anticardiolipin antibody (16/19) or lupus anticoagulant (10/19); three patients had thrombocytopenia, eight patients had a prolonged partial thromboplastin time, and 10 patients had an elevated erythrocyte sedimentation rate. The most common site of involvement was the cerebral circulation (nine patients), manifested by transient ischemic attacks or stroke. Eight patients had upper extremity disease, characterized by symptoms of Raynaud's phenomenon, with angiographic lesions involving the brachial, radial, ulnar, and/or digital arteries. Lower extremity disease occurred in seven patients, with clinical presentations similar to those of atherosclerosis and varying angiographic patterns. In comparison with the population having atherosclerosis, patients with arterial manifestations of antiphospholipid syndrome were more likely to be women (13 of 19 versus 411 of 1078, p less than 0.02), were significantly younger (46.2 years versus 63.6 years, p less than 0.0001), did not smoke (1 of 19 patients versus 700 of 1078, p less than 0.0001), had a higher percentage of upper extremity involvement (8 of 18 versus 13 of 1078, p less than 0.0001), and had a higher incidence of early graft failure (9 of 12 grafts versus 13 of 371 grafts, p less than 0.0001). The syndrome is associated with the repetitive failure of vascular reconstructions and occlusion of native vessels. Antiphospholipid syndrome should therefore be suspected in young, female, nonsmokers with vascular disease, especially those with involvement of the upper extremity, cerebrovascular disease with normal findings on extracranial carotid angiography, and premature graft failure.
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PMID:Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis. 172 74

Patients presenting with Raynaud's phenomenon pose differential diagnostic problems. The question is whether the discolorations are a symptom of the benign primary type or a symptom of an underlying disease, mostly a connective tissue disease or an atherosclerotic occlusive disease, both having major prognostic implications. To evaluate whether Raynaud patients can be classified properly in the above-mentioned categories on clinical grounds we evaluated 225 patients using a checklist dealing with signs and symptoms supposed to be specific for primary Raynaud's phenomenon or the two major types of the secondary form. Complaints that started before the age of 20, reactive hyperaemia at the end of an attack and discolorations of the earlobes and the nose have a high predictive value for primary Raynaud's phenomenon. Trophic skin disturbances are rare in the latter but are rather specific for connective tissue diseases. In the case of arterial obstructive disease, the feet are always involved and risk factors associated with atherosclerosis are often present, whereas this type is specifically encountered in men in whom the complaints started over the age of 50 [corrected], and in whom signs of atherosclerotic vessel wall disease were seen elsewhere. In conclusion, in most patients who present with a Raynaud's phenomenon a complete history and physical examination are sufficient for a correct diagnosis. Supplementation with determination of anti-nuclear antibodies, measurements of the capillary perfusion and of the finger skin systolic pressure completes the diagnostic classification.
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PMID:The diagnostic value of clinical signs and symptoms in patients with Raynaud's phenomenon. A cross-sectional study. 207 8

The present article deals with the pathophysiological role of serotonin in cardiovascular disease and in other disorders that are accompanied by cardiovascular pathophysiological events. The distribution of serotonin over various organs and tissues and the presence of several types of 5-HT receptors would suggest a rather important physiological role of serotonin. However, a modest serotonergic role could only be shown for the microcirculation and for the regional circulation of the brain and the intestinal wall. An important pathological role of serotonin in the carcinoid syndrome, in migraine, and in peripheral vascular disease is beyond debate, although many details remain to be established. The possibility that serotonergic mechanisms contribute to Raynaud's phenomenon and other vasospastic disorders is the subject of present discussions, although firm evidence for this view is not widely available. An involvement of peripheral serotonin in the genesis and maintenance of essential hypertension seems very unlikely, although vascular damage due to hypertension is probably enhanced by serotonin released from aggregating platelets. This ancillary process is, in particular, to be anticipated in older patients, with vascular walls predamaged by atherosclerosis. For this reason, pharmacological blockade of 5-HT2 receptors may be of potential therapeutic benefit in this category of patient. Finally, the involvement of central serotonergic mechanisms in hypertensive disease cannot be ruled out.
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PMID:Pathophysiological relevance of serotonin. 244 63

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

The etiological study of a series of 30 cases of digital arteritis, shows that there may be various causes at the origin of a digital arteritis. In elderly patients, atherosclerosis appears as the most frequent cause. At a middle age, digital arteritis frequently occurs in a context of vasomotor pathology: in this case, sclerodermis is a frequent cause to examine systematically but some cases are secondary to a Raynaud's phenomenon, apparently idiopathic. Other etiologies: traumatic, hematologic, iatrogenic... may be pointed out; but in some cases, digital arteritis occurs alone without any apparent reason.
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PMID:[Etiologic diversity of digital arteritis]. 357 29

Systemic lupus erythematosus (SLE) is a well-known acute and/or chronic multisystem disease of complex autoimmune nature, having predilection for cardiovascular system. While its cardiac manifestations have been adequately studied, there is paucity of information on its vascular manifestations. Accordingly, we studied the incidence of vascular manifestations in 50 consecutive SLE patients seen at our institutions and in private practice during the past 12 years. Systemic hypertension (44%) was the most common vascular manifestation followed by vasculitis (30%), Raynaud's phenomenon (26%), telangiectasis (20%), premature coronary atherosclerosis (6%), digital ulceration (6%), thrombophlebitis (6%), pulmonary hypertension (4%) and portal hypertension (4%). Diffuse systemic vasculitis similar to polyarteritis nodosa was rare (2%). Often more than one lesion was found in the same patient. The clinical diagnosis of these vascular manifestations in the context of the primary disease (SLE) usually does not pose any difficulty except when they antedate it. We also studied the pathology and pathogenesis of some of these vascular lesions in both autopsy and biopsy specimens by both light microscopy and immunofluorescent techniques. Our results as well as those of others who also studied these lesions indicate that immune complex deposition and subsequent complement activation play an important role in the pathogenesis of vasculitis, coronary arteritis and premature coronary atherosclerosis. Corticosteroids and vasodilators remain the drugs of choice for the management of the majority of the symptoms arising from the vascular lesions of SLE.
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PMID:Vascular manifestations of systemic lupus erythematosus. 372 68

We evaluated left ventricular function in 10 scleroderma patients with signs and symptoms suggestive of congestive heart failure. M-mode and two-dimensional echocardiography demonstrated normal to increased systolic function in all patients. The presence of pulmonary venous congestion on the chest radiograph was not useful in assessing left ventricular systolic function. Five of nine patients with normal to increased left ventricular ejection fraction (LVEF) had increased cardiothoracic ratios and increased pulmonary vascular markings. Left ventricular hypertrophy was associated with a worse New York Heart Association functional class, more pulmonary vascular congestion, and greater left atrial size. In the presence of normal systolic function and ventricular hypertrophy, diminished left ventricular diastolic compliance may account for the cardiac dysfunction in these patients. Cold pressor testing induced peripheral Raynaud's phenomenon in nine of nine patients; however, no ST segment changes or chest pain was provoked. In seven of nine patients there was no abnormal fall in LVEF. The mechanism for the fall in ejection fraction seen in two patients may be related to an increase in afterload or myocardial ischemia secondary to coronary atherosclerosis. We found little to suggest that a myocardial Raynaud's phenomenon affects left ventricular perfusion or systolic function. Clinical signs and symptoms of congestive failure as well as chest radiographs are poor indicators of impaired systolic function in scleroderma patients. Based on these findings, it appears that evaluation of left ventricular systolic function should include echocardiographic or angiographic study before such patients are treated for heart failure with inotropic agents.
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PMID:Left ventricular function at rest and during Raynaud's phenomenon in patients with scleroderma. 650 43

The clinical and pathologic findings are reported in seven consecutive patients with progressive and fatal pulmonary hypertension which was not explained by predisposing cardiac or pulmonary diseases. Pulmonary arterial lesions consisted of atherosclerosis of the elastic pulmonary arteries, and medial hypertrophy and concentric laminar fibrosis of the muscular pulmonary arteries in seven patients, plexiform lesions in six patients and necrotizing vasculitis in one patient. Pulmonary emboli were not identified. Five patients had manifestations of autoimmune disease, including laboratory abnormalities (positive antinuclear antibody, positive latex agglutination for rheumatoid factor, hypergammaglobulinemia or antimitochondrial antibody) in four, necrotizing vasculitis in one, Raynaud's phenomenon in two and clinical evidence of multisystem collagen vascular disease in two. Five patients had liver disease which developed prior to or concomitant with the onset of pulmonary hypertension. At autopsy, one patient had prominent periportal fibrosis and four had macronodular (postnecrotic) cirrhosis (active in three and inactive in one). Four of these five patients with liver disease and pulmonary hypertension had evidence of autoimmune phenomena. The findings in the seven patients suggest an association between autoimmune disease, plexogenic pulmonary hypertension and liver disease of the chronic active hepatitis-postnecrotic cirrhosis type.
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PMID:Severe pulmonary hypertension associated with macronodular (postnecrotic) cirrhosis and autoimmune phenomena. 742 41


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