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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension increases cardiovascular morbidity and mortality two- to fourfold. The chief hazards are now atherosclerosis and coronary disease. Risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensive patients with a high total/high-density lipoprotein (HDL)-cholesterol ratio, impaired glucose tolerance, high fibrinogen, electrocardiographic (ECG) abnormalities, and who are cigarette smokers. Evidence of organ involvement such as left ventricular function are hallmarks of impending cardiovascular sequelae. Electrocardiogram-left ventricular hypertrophy (ECG-LVH) behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, infarction, cardiac failure, and stroke. Consideration of cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, set goals, and determine the efficacy of treatment. Awaiting evidence of organ involvement is dangerous since the first such evidence is often a sudden death, stroke, or myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure.
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PMID:Risk factors in hypertension. 246 76

beta-Blockers reduce hypertension effectively and safely. However, their overall efficacy is a balance between their influence on blood pressure and their influence on other important risk factors. Thus, whereas a drug may ameliorate the primary blood pressure marker of the syndrome, this effect may be negated by enhancement of aggressive cofactors. The evolution of the beta-blockers exemplifies how this potentially dangerous conflict may be counteracted. The latest "third-generation" agents, such as celiprolol, not only achieve their primary objective of lowering blood pressure, but also have the potential to simultaneously reverse some of the deleterious cofactors. For example, celiprolol reduces the threat of atheroma by lowering serum cholesterol, and enhances the efficacy of myocardial oxygen utilization in heart failure by reducing plasma triglyceride metabolism. Its ability to reduce fibrinogen and its lack of effect on glucose metabolism are additional positive factors. Celiprolol also provides the combined pharmacodynamic advantages of vasodilatation and inotropic support of the heart, and it attenuates the myocardial oxygen-wasting effects of sympathoadrenal stimulation. These attributes all make a positive contribution to cardiovascular risk reversal in the hypertensive patient.
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PMID:Celiprolol and risk factor reversal in hypertension. 248 88

To evaluate the effects of the fibrinolytic system on the development of coronary heart disease (CHD), the level of released plasminogen activator was measured by venous occlusion in 60 CHD cases, and 20 healthy subjects. The level of plasma basic plasminogen activator activity, plasminogen, fibrinogen and serum fibrin degradation products (FDP) were determined also. In comparison with control subjects, a lower level of released plasminogen activator was found in all CHD patients, being especially marked in those with unstable angina pectoris and acute myocardial infarction. The levels of plasma plasminogen, fibrinogen and FDP were also significantly changed in these patients. In acute myocardial infarction patients, the level of released plasminogen activator was lower in cases complicated with heart failure than in those without.
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PMID:Fibrinolytic activity in coronary heart disease. 251 77

Hypertension increases cardiovascular morbidity and mortality two to four-fold. The chief hazards are now atherosclerosis and coronary disease. The risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of the blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensives with a high total/high density lipoprotein (HDL) cholesterol ratio, impaired glucose tolerance, high fibrinogen, those with ECG abnormalities and cigarette smokers. Evidence of organ involvement such as left ventricular hypertrophy, proteinuria or impaired left ventricular function are hallmarks of impending cardiovascular sequelae. The presence of ECG-LVH behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, myocardial infarction, cardiac failure and stroke. Consideration of all cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, and set goals and determine the efficacy of treatment. Waiting until there is evidence of organ involvement is dangerous since the first such evidence is often sudden death, a stroke or a myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure. This can be achieved by hygienic (dietary) measures or pharmacological therapy in those who do not respond to diet alteration, weight control and exercise.
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PMID:An integrated view of hypertension. 260 26

The incidence of venous thrombosis (VT) detected by 125I-labelled fibrinogen was followed in 408 patients with acute myocardial infarction (AMI). Patients were randomized into three groups: a group receiving small doses of heparin (2 X 5000 u. subcutaneously/24 h), and an exercise group (dorsal and plantar flexion of the foot for one minute each hour). VT was present in 13.6% of the control group, in 9% of the group with mini-heparin (an insignificant difference), and in 5.1% of the group with moderate exercise (p less than 0.05). VT was statistically significantly more frequent in patients with acute MI who had heart failure, thrombosis in their medical history, had varices and were non-smokers. The results indicate that even moderate exercise of the lower limbs decreases significantly the incidence of VT in patients with AMI.
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PMID:Deep vein thrombosis and its prevention in patients with acute myocardial infarction. 322 17

A total of 189 patients with uncomplicated myocardial infarction were selected at random for early or late mobilization and discharge from hospital. Patients were admitted to the study after 48 hours in a coronary care unit if they were free of pain and showed no evidence of heart failure or significant dysrhythmia. Randomization was achieved by monthly cross-over of the three medical wards to which the patients were discharged. One group of patients was mobilized immediately and discharged home after a total of nine days in hospital, and the second group was mobilized on the ninth day and discharged on the 16th day. Out-patient assessment was carried out six weeks after admission. No significant differences were observed between the groups in terms of mortality or morbidity, as reflected by the incidence of recurrent chest pain or myocardial infarction, heart failure, dysrhythmia, or venous thromboembolism detected either clinically or by (125)I-labelled fibrinogen scanning.
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PMID:Comparison of mobilization after two and nine days in uncomplicated myocardial infarction. 483 62

This review examines the incidence, natural history, diagnosis, prophylaxis, and management of deep vein thrombosis (DVT) and pulmonary embolism (PE) in neurosurgical patients. Recent studies estimate the incidence of postoperative DVT detected by fibrinogen scanning in neurosurgical patients to be 29% to 43%. Specific factors that enhance the risk of venous thromboembolism include previous DVT, surgery, immobilization, advanced age, obesity, limb weakness, heart failure, and lower extremity trauma. Clinical diagnosis of venous thromboembolism is unreliable but can be augmented by noninvasive screening tests such as iodine-125-fibrinogen scanning, Doppler ultrasonography, and impedance plethysmography. As prophylactic measures, mini-dose heparin and external pneumatic compression of the legs have decreased the incidence of DVT in clinical studies of neurosurgical patients. However, no prophylactic measure has been convincingly shown to prevent PE in neurosurgical patients. Thrombi involving the popliteal, deep femoral, and iliac veins appear most likely to cause significant PE. Anticoagulation therapy constitutes standard management of DVT and PE; however, in neurosurgical patients the potential for precipitating intracranial or intraspinal hemorrhage may necessitate vena caval interruption. This appears to be an effective alternative to anticoagulation.
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PMID:Deep vein thrombosis and pulmonary emboli in neurosurgical patients: a review. 638 85

Of 20 patients who presented to our hospital with the histologically confirmed diagnosis of SLE, nine met the criteria of presence of both a rapidly progressive disease state and contraindications for conventional therapy required for admission to our plasma exchange programme. Five patients improved; two patients progressed to end-stage renal failure; two patients died as a result of complications of advanced SLE. Severe lupus erythematosus (SLE) is usually treated with a combination of steroids and cytotoxic drugs. Even when treated with high dose therapy some patients develop life-threatening complications, such as renal failure, heart failure and respiratory insufficiency. Moreover, both treatment with high dose of corticosteroids and long lasting cytotoxic therapy may produce troublesome side-effects, including severe infections, gastroduodenal ulcers, bone marrow depressions and lymphomas (1, 2). One of the manifestation of SLE is the presence of antibodies against ds-DNA and ss-DNA. These antibodies can either react with DNA bound to te basement membrane and induce an inflammatory reaction (3), or can form circulating immune complexes which deposit in tissues and may impair the function of lymphocytes or macrophages in the RES (4, 5). The presence of anti-DNA-antibodies appears to be secondary to enhanced B-cell activity along with a depression of suppressor T-cells function proteins mediating the inflammatory process, such as fibrinogen, may deposit in membranes already compromised by the disease. Even though the pathogenic mechanisms operating in SLE are not completely understood, it can be expected, from a theoretical point of view, that the extracorporeal removal of any immunopathogens could improve the disease state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma exchange in systemic lupus erythematosus. 664 35

The incidence over 7 days of isotopically-detected calf and popliteal vein thrombosis was determined in a group of 60 diabetic patients admitted to hospital with myocardial infarction, heart failure or stroke, or for abdominal surgery. The result was compared with the incidence in 60 control subjects matched for age, sex and presenting diagnosis. Twenty-one diabetic patients developed positive 125I-fibrinogen scans, compared with 19 control subjects; this difference is not significant. We conclude that diabetes is not associated with an enhanced risk of thrombosis in veins. It is therefore possible that the arterial and capillary abnormalities found in diabetes may arise from mechanisms other than a generalised thrombotic tendency.
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PMID:Venous thrombosis in diabetes mellitus. 666 79

A randomised trial was undertaken in one hundred patients with heart failure and/or chest infection to determine whether low-dose subcutaneous heparin induced the frequency of deep vein thrombosis (DVT) in the legs. Heparin, (5000 units 8 hourly) significantly reduced the frequency of DVT, diagnosed by the 125I-fibrinogen scan technique, from 26 to 4 per cent (p less than 0.01). Heparin was started within 12 hours of admission to hospital and continued until the patient was fully mobile. Heparin did not cause bleeding problems except for a 20 per cent incidence of injection site bruising. We therefore recommend prophylaxis with low-dose subcutaneous heparin in patients with heart failure or chest infection who require more than three days bed rest.
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PMID:Prevention of deep vein thrombosis in medical patients by low-dose heparin. 729 71


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