Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and echocardiographic features of right atrial thrombi were examined in 9 patients, 5 men and 4 women aged 16 to 86 years. The 2D echocardiographic diagnosis was confirmed at autopsy (4 cases) or by the association of severe recurrent pulmonary embolism (5 cases). Three patients had associated ischaemic heart disease and on patient had dilated cardiomyopathy. The clinical presentation was: acute cor pulmonale (5 cases including 2 patients which biventricular myocardial infarction), chronic post-embolic cor pulmonale (1 case), tricuspid valve obstruction (1 case), general ill health with pyrexia (1 case) and heparin-induced thrombocytopenia (1 case). Predisposing factors included: absence of anticoagulent therapy (7 cases), previous supraventricular arrhythmias (2 cases) and right ventricular failure (6 cases, including 2 of right ventricular infarction). In 2 patients the thrombi were relatively immobile and had a wide base of implantation on the interatrial septum; in 1 patient, multiple thrombi were observed lining the right heart cavities from the inferior vena cava to the pulmonary infundibulum. In the other 6 patients, the thrombi were very mobile with a visible pedicule of implantation (2 cases) or totally free (4 cases). The variable polylobulated appearances, completely irregular whirling motion and intermittent prolapse into the tricuspid valve were characteristic features of the latter 4 cases. They disappeared spontaneously (2 cases) or after fibrinolytic therapy (2 cases) in under 36 hours. Three patients were operated with one postoperative death. The global hospital mortality was 22%. The present occasional detection of right atrial thrombosis will certainly become more common if patients with pulmonary embolism, right ventricular infarction or deep venous thrombosis are systematically examined by 2D echocardiography in the acute phase of their illness.
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PMID:[Clinical, echocardiographic and evolutive aspects of right atrial thrombosis]. 308 12

This report reviews the present status of cardiovascular surgery in West Africa and highlights some of the constraints of development in this field.Rheumatic heart disease is still endemic in the tropics, where it constitutes about 20 percent of all cases of cardiovascular disease (CVD) in Nigeria. Endomyocardial fibrosis is a disease of unknown etiology accounting for 10 to 20 percent of cases. Purulent pericarditis is a common complication of pyomyositis and osteomyelitis found in 5 percent of patients. Chronic constrictive pericarditis is a sequela of infective pericarditis found in 5 percent of all cases of CVD. Calcification is found in 30 percent of cases and pericardiectomy can be performed successfully without cardiopulmonary bypass. Infective endocarditis is equally rare, occurring in 2.5 percent of cases; it is a common source of septic emboli to coronary artery and a very difficult disease to treat in the West African environment.Ischemic heart disease is relatively uncommon, accounting for less than 0.5 percent of patients. The rarity of the disease in black Africans has been attributed to dietary habits and environment rather than to racial and psychosocial factors. Congenital heart disease accounts for 5 percent of all cases of CVD in this review. Ventricular septal defect and patent ductus arteriosus are the most common acyanotic defects, while tetralogy of Fallot and transposition of the great arteries are the most common cyanotic defects.Vascular diseases are uncommon in this series, with traumatic injuries accounting for most of the cases. Abdominal aortic aneurysms, peripheral occlusive vascular disease, and atherosclerotic aortic aneurysms are quite rare. This review further confirms the rarity of deep venous thrombosis and pulmonary embolism in Africans.
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PMID:The status of cardiovascular surgery in West Africa. 331 74

In a prospective multicenter study, 244 men with highly or moderately differentiated prostatic cancer in stage I, II or III (VACURG) were consecutively randomized to three groups of treatment: Group A (77 patients) received polyestradiol phosphate (Estradurin, Leo) 80 mg i.m. every fourth week + ethinyl estradiol (Etivex, Leo) 150 micrograms daily, group B (72 patients) estramustine phosphate (Estracyt, Leo) 280 mg twice daily, and group C (76 patients) no therapy. Only men without current or previous other malignancy and without cardiovascular disease were admitted to the study. After 4 1/2 years 125 of the 244 patients had left the study, 9 because of cancer progression (stage IV, VACURG). The most serious complications were cardiovascular, including ischemic heart disease, cardiac decompensation, cerebral ischemia and venous thromboembolism, which occurred in 24 patients from group A and 9 from group B as compared to only one patient in group C. The subgroup superficial or deep venous thrombosis comprised 11 group A and 2 group B patients. Estrogens (E + e) offered as palliative treatment to patients with non-generalized prostatic carcinoma is burdened with a high incidence of serious cardiovascular complications.
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PMID:Cardiovascular complications of estrogen therapy for nondisseminated prostatic carcinoma. A preliminary report from a randomized multicenter study. 352 68

Sudden cardiac death (SCD) due to acute myocardial infarction (AMI) is mostly the result of ventricular fibrillation (VP) which is an electrical accident appearing on the basis of electrical instability of the myocardium. In addition to the chronic electrical instability predisposing to ventricular arrhythmias the trigger effect of a precipitating factor also seems necessary which may disrupt the normal sequence of cardiac contractions. In view of this hypothesis the following strategy of therapeutic interventions aimed at preventing SCD from AMI seems to be logical: Prophylactic measures to prevent pathological processes underlying chronic electrical instability of the heart i.e. elimination of identified risk factors of ischemic heart disease. Protection from SCD due to AMI: by using drugs which could, prevent further electrical destabilization as shifts in myocardial and plasma ionic balance, in pH, in pCO2, accumulation of potentially arrhythmogenic metabolites: Inhibit the trigger effect of sudden changes: in hemodynamics, in the autonomic nervous outflow and balance. The general supportive measures include therapeutic interventions which are not directly connected with appearance of lethal arrhythmias but may indirectly contribute to their development as pain, arterial Hb desaturation, deep vein thrombosis. Some of the measures listed above are capable of limiting the size of the developing infarct, a major determinant of the future conditions of life and prognosis of the patient. In the prehospital phase of AMI when two thirds of all coronary deaths occur general supportive measures and drug treatment of life threatening arrhythmias should be applied simultaneously. Sedatives and anxiolytics, furthermore analgetics are widely used. They are however often associated with bradycardia and sometimes with hypotension. This latter is dominant in patients with inferior infarction, showing a parasympathetic hyperactivity, when atropine treatment is needed. Sympathetic hyperactivity responds to analgesia and sedation but beta blockers may be required to reduce increased MVO2. These agents belong to the group of anti-ischemic drugs. The beneficial anti-ischemic action of beta-blockers is mostly due to their negative chronotropic and inotropic effect. A direct metabolic action was shown by use as well as the presence of a positive steal phenomenon in the experimental angina model in dogs. Anti-ischemic action of coronary vasodilators. The most reliable drug for preventing or abolishing anginal attack is still the classic nitroglycerin. On the other hand persantine a potent coronary dilator failed to protect against anginal attack in man.
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PMID:[Pharmacological possibilities for the prevention of complications following myocardial infarction]. 382 Nov 31

The scientific basis for the statement that cigarette smoking increases the risk of serious cardiovascular side effects from oral contraceptive (OC) use is reviewed. The published literature and the new statistical analyses of the data are examined. Attention is directed to 3 broad categories of relevant vascular disease--deep vein thrombosis and pulmonary embolism, stroke--both occlusive and hemorrhagic, and ischemic heart disease. Within each category, the epidemiologic relationship of cigarette smoking alone, of OC use, and of a combination of the 2 is addressed. This review of smoking and OC use as risk factors for major classes of cardiovascular disease reveals little convincing evidence for an interaction of the smoking and OC use. Essentially all of the data have been interpreted to indicate that OC use is a risk factor for cardiovascular disorders derive from retrospective case-control studies, which continue to be a subject of controversy. The role of smoking as a risk factor appears to be little questioned in the case of myocardial infarction, and the evidence suggests that it may also be a factor in hemorrhagic stroke. There is little evidence to implicate smoking in the pathogenesis of thrombotic stroke in young women, and several publications suggest that it has a protective effect for deep vein thrombosis. In sum, evidence for an interaction of smoking and OC use has been reported but is deemed to be weak. A major existing difficulty is the methodological problems that are inherent in epidemiologic investigations, both retrospective and prospective. While conservatism could thus withhold needed and effective contraception, the recommendation is for the OC user to forego smoking.
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PMID:Smoking, oral contraceptives, and thromboembolic disease. 612 53

Beta-thromboglobulin (beta TG) plasma levels were measured by radioimmunoassay in 14 patients with acute myocardial infarction (MI), in 13 with myocardial ischemia and recurrent episodes of angina and in 14 subjects with a past history of MI. Increased beta TG plasma values were observed in patients with acute MI and with myocardial ischemia whereas subjects with a past history of MI showed results not significantly different from normal subjects. Daily measurements in acute MI showed in five cases a second peak of beta TG values which suggests the occurrence of a deep vein thrombosis. The increased platelet consumption in MI was not related with the extent of the necrosis. We suggest, therefore, that platelet activation is associated with myocardial ischemia rather than necrosis.
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PMID:Beta-thromboglobulin in patients with acute and chronic coronary artery disease. 618 23

The risk of thromboembolism in oral contraceptive (OC) users is evaluated based on findings of major cohort studies conducted in England, the US, and Denmark. Since approximately 25% of Danish Women aged 15-45 use OCs, such an assessment is timely and critical. A study by the Royal College of General Practitioners (RCGP) found a slightly higher risk of venous thrombosis and pulmonary embolism, especially postoperatively (deep venous thrombosis). Major risk was found only with the use of high estrogen-content pills. No connection between OC use and subarachnoidal bleeding could be established according to the latest studies. In a US study examining 182 cases of apoplexy cerebri of thrombotic origin in comparison with 98 controls, the risk was 9.5 times higher on OC users. However, 74% of the patients with cerebral thrombosis were smokers vs. 43% of controls. The high gestagen component of pills was implicated in the increased risk. In a case control study, the risk of myocardial infarct was found 4 times higher in OC users and 20 times higher in smokers who used OCs. Another study of the RCGP supported these findings: myocardial infarct was .3/1000 women per year in pill users vs. .15 in nonusers, and the risk of death from ischemic heart disease was 6.4 times higher among users. These risk factors were also borne out by Danish data: the number of women aged 35-39 and 40-45 dying of ischemic heart disease between 1951-1981 rose slightly, but there was no significant increase after 1967, when low-dose OCs were introduced; in recent years there has been a decline. To establish a firm link between the use of the estrogen and gestagen components of OCs and thromboembolic disease, further investigations must be conducted in view of recently introduced low-dose pills.
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PMID:[The pill and thrombosis]. 651 90

The authors review the importance of echocardiography and duplex examination of the blood vessels of the lower extremities for early diagnosis of thromboembolic attacks. Echocardiographic examination rules out other causes of the patient's complaints such as myocardial infarction, heart defects, ischaemic heart disease and others. The main role of echocardiography is, however, detection of symptoms of an acute rise of the blood pressure in the right heart or symptoms of its failure. The most valuable symptom is dilatation of the right branch of the pulmonary artery and dilatation of the right ventricle found in as many as 75% patients. It is also useful to assess by the Doppler method the dextrolateral systolic pressure from tricuspidal regurgitation. For pulmonary embolism a regurgitation rate of 2.8-3.8 m/s is typical. The correlation coefficient is, however, lower than when the dimensions of the right and left ventricle are used. Evidence of deep venous thrombosis does not reveal pulmonary embolism but has the same therapeutic consequences. Duplex sonography has a 95-100% sensitivity and specificity in acute thrombosis. In recurrent thrombosis it is necessary to use a combination of the two methods. Concurrent echocardiography and duplex sonography of the blood vessels of the lower extremities makes it possible to start prompt treatment in 70-80% of the patients. In the remainder for diagnosis of thromboembolic attacks other methods must be used.
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PMID:[Ultrasound in the diagnosis of thromboembolism]. 814 Jul 53

Plasminogen activator inhibitor-1 plays a major role in the fibrinolytic system as the main physiological inhibitor of both tissue-type and urinary-type plasminogen activators. The inhibitor is present in plasma in small amounts and derives mainly from endothelial cells. Positive correlations have been reported between plasma levels and different parameters, such as serum triglycerides, insulin plasma levels and body mass index. Moreover, high plasma inhibitor concentrations have been observed in different disease states, but it must be stressed that plasminogen activator inhibitor-1 behaves as an acute-phase reactant and measurement of plasma levels is not significant in the acute phase of the disease. A possible predictive value of inhibitor levels for thrombotic events such as deep vein thrombosis and ischemic heart disease has been studied. On the basis of available studies, the predictive value is not clear for venous thrombosis, whereas plasminogen activator inhibitor-1 levels can predict some coronary events, at least in subgroups of young patients with a first myocardial infarction. It remains to be established if treatments able to reduce plasma inhibitor levels lead to a decrease in the risk of thromboembolic events.
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PMID:Predictive value for thrombotic disease of plasminogen activator inhibitor-1 plasma levels. 851 17

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
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PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59


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