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

Treatment of a patient with myocardial infarction might include opiates and sedatives to reduce pain and anxiety, heparin, antiarrhythmic drugs, diuretics which aim at improvement of myocardial function and drugs which might reduce the ischemic area at risk and thus mortality such as beta-blockers, vasodilators and possibly calcium antagonists. Obviously a selection of these and other therapeutic agents should be made for each individual patient. Guidelines for such a selection are presented in this paper. These are based on assessment of the hemodynamic state in a given patient: heart rate, blood pressure and presence or absence of heart failure as determined by non-invasive examination or by hemodynamic monitoring with a pulmonary artery catheter. An attempt should be made to reach an optimal hemodynamic state quickly, preferably within one hour of admission to the coronary care unit: a heart rate between 60 and 80 b.p.m., a systolic blood pressure between 100 and 140 mmHg and absence of signs of heart failure. For this purpose fast-acting intravenous drugs should be employed. Possibly myocardial preservation could also be achieved by prompt recanalization of an occluded coronary artery. At present, however, this is still an experimental procedure which should be further investigated.
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PMID:Practical guidelines for treatment with beta-blockers and nitrates in patients with acute myocardial infarction. 613 71

In patients without heart failure and with exercise-induced angina pectoris, betablockers are still the treatment of choice. The pharmacological differences within the betablockers are of minor importance clinically. Patients with angina at rest, or with a considerably changing effort threshold, are suspect for additional coronary spasms. Here calcium antagonists, and possibly nitrates, should be given first. A combination of these three treatments often proves beneficial. Amiodarone, which in the beginning was only rarely used because of its complex pharmacokinetics, is now generally accepted as an effective and well-tolerated drug for angina. In unstable angina, medical treatment varies according to the differing clinical symptoms. In addition to immobilization and anticoagulation, prolonged pain attacks are treated with intravenous nitrates. If the symptoms persist, combination of antianginal drugs as described above, sometimes in high doses, is necessary in order to postpone selective coronary angiography and bypass operation by one to two weeks. Otherwise these procedures must be performed after intraaortic balloon pumping has been instituted.
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PMID:[Drug therapy of angina pectoris]. 614 37

Benign liver tumors are relatively uncommon and, even when large enough to be symptomatic, they usually remain undiagnosed prior to exploratory laparotomy. Hemangiomas constitute the majority of benign hepatic neoplasms and are 9 times as frequent in females as in males. Most are asymptomatic but abdominal swelling, a mass, or symptoms due to compression of adjacent organs may occur and abdominal hemorrhage is reported in 4.5% of patients. Hepatic hemangioma may produce a large arteriovenous communication serious enough to cause heart failure. Recently an increased frequency of liver tumors, mostly adenomas, has been noted in women taking oral contraceptives (OCs); the cause has been attributed to estrogens. The exact incidence is unknown but believed to be low. It is most common in women in their late 20s who have been on OCs for 7 years or more. The tumor occasionally completely regresses on withdrawal of the OCs. The tumor may be discovered incidentally at laparotomy or may manifest inself by pain, a palpable mass, or catastrophic hemoperitoneum. Hepatic adenoma is usually a solitary lesion and infrequently degenerates into malignancy. Differential diagnosis includes chronic gall bladder disease and peptic ulcer. Focal nodular hyperplasia (FNH) is apparently much less frequently related to OC use and is less likely to bleed seriously than adenoma. Hepatic chemistry is usually normal in adenoma and FNH, but slight increases in serum bilirubin, serum alkaline phosphatase, and serum transaminase may occur. Primary liver cancer (hepatocellular carcinoma or hepatoma) is mostly a disease of males and in the US and Western Europe seldom develops before age 40. Fibrolamellar carcinoma, which characteristically develops in adolescents and young adults, occurs with equal sex incidence. Doubt has been expressed about its relationship to OCs. In the US about 75% of primary hepatocellular carcinomas are associated with cirrhosis, and about 5% of cirrhosis cases develop primary liver cancer. Clinical manifestations of hepatoma have been divided into 5 groups: frank cancer (62.7%), acute abdominal cancer (8%), febrile cancer (8%), occult cancer (16%), and metastatic cancer (5%). Detection of large amounts of alpha fetoprotein has proven useful in diagnosis of hepatocellular carcinoma, but values may be negative in OC users. It has been estimated that 1/3 to 1/2 of all malignant tumors eventually metastasize to the liver.
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PMID:Hepatic neoplasia: selected clinical aspects. 619 95

The antitumor activity of 5-fluorouracil (5-FU), combined either with bleomycin or adriamycin plus radiation, was studied in a controlled randomized clinical trial. Sixty-one previously untreated inoperable esophageal cancer patients entered the study and 56 have been evaluated: 58 male and 3 female patients with a mean age of 57 years (range 37-74). Concerning localization of the tumors in the esophagus, 2 were in the upper third, 36 in the middle third and 18 in the lower third. The length of the filling defects in the esophagogram (X-ray) was in 9 patients less than 5 cm, in 31 5-8 cm, and in 16 patients greater than 8 cm. Squamous cell carcinoma was found in 51 patients, adenocarcinoma in 3, and anaplastic (squamous cell) carcinoma in 2 patients. Modality A consisted of a combination of 5-FU (10 mg/kg i.v. 2 X weekly, 4 weeks) and bleomycin (10 mg/m2 i.v., 2 X 4 weeks) which was given concurrently with radiation (3600-4000 rad - 1000 rad weekly). In modality B the combination of 5-FU (same dose) and adriamycin (30 mg/m2 i.v. day 1, 2, 23 and 24) was applied with the same schedule and dosage of radiation. Seventy-five percent of the patients (21/28) have responded to treatment (CR + PR) in modality A, with 11 complete and 10 partial responses. In arm B, response was recorded in 64% of patients (18/28), with 2 complete and 16 partial responses. The difference in complete responses (39% vs 8%) was statistically significant (P less than 0.05). The median remission duration in complete responders was 12 months in modality A (range 6-18 months), and 6.8 months in modality B (range 3-10 months). All the responses occurred in patients with squamous cell carcinoma, except one partial response in a case of adenocarcinoma. As far as the age is concerned (less than 55 vs greater than 55 years), no significant difference in response rate was found (67% vs 71%). More favorable results were observed in the group of patients with less than 10% weight loss (79% vs 63%). Toxicity was moderate (myelosuppression, cardiotoxicity), but one treatment-related death (pulmonary fibrosis, cardiac failure) was recorded in arm A, as well as one death (rupture of aorta) in group B. Approximately 60% of patients in both modalities suffered from severe mucositis and retrosternal pain. The results of the study showed that the combination of 5-FU with adriamycin and particularly with bleomycin, given concurrently with lower radiation dosage, is an effective palliative treatment for inoperable esophageal cancer.
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PMID:The value of two combined chemoradiotherapy approaches in the treatment of inoperable esophageal cancer. 620 Sep 79

The incidence rate of chest wall invasion in bronchogenic carcinoma is difficult to estimate, but is possibly as high as 5%. These cancers can be locally extensive without systemic dissemination. From 1973 to 1982, 9 patients in our hospital underwent en bloc pulmonary and partial chest wall resection for bronchogenic carcinoma with local invasion of the thoracic wall. All the patients were male, their ages ranging from 49 to 67 years. Pain was the most prominent symptom. Bronchoscopy examination revealed no tumors in 7 of the 9 patients, in one a tumor was seen in the apex of the right lower lobe and in another in the apex of the right upper lobe. Seven lobectomies and 2 pneumonectomies were performed. The macroscopic size of the tumour ranged from 3 to 17 cm, the number of partially resected ribs ranged from 1 to 4. In 8 cases squamous cell carcinoma was found, in one adenocarcinoma. After operation 7 patients were classified as T3N0M0 and 2 as T3N1M0. One T3N0M0 patient died shortly after operation due to a lung embolism. Two out of the 6 patients with T3N0M0 neoplasm survived more than 5 years, none of the patients with T3N1M0 neoplasm survived more than 3 months. Late deaths were due to recurrent carcinoma in the chest wall (2 cases), cerebral metastasis (1 case), cardiac failure (1 case) and unknown causes (2 cases). In cases where the lymph nodes are not involved, the survival rate is not unfavorably influenced by chest wall invasion. In the literature the mean operative mortality rate is 12%, the median survival time approximately one year and the mean 5-year survival rate 18%; resection is also of great importance in relieving pain.
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PMID:Chest wall resection for bronchogenic carcinoma. 620 97

We identified 420 medically treated and 231 surgically treated patients (coronary graft plus myocardial surgery in 30%) who had severe left ventricular dysfunction manifest by an ejection fraction below 0.36 and markedly abnormal wall motion. Compared with medically treated patients, those treated surgically had more severe angina (56.7% vs 29.0% class III or IV; p less than .001), less heart failure as predominant symptom (11.1% vs 18.8%; p less than .003), more severe coronary disease (66.7% vs 50.2% three-vessel disease; p less than .001), a greater concentration of left main coronary artery lesions greater than 70% (12.6% vs 3.8%: p less than .001), and a greater estimated extent of jeopardized myocardium (p less than .001). Multivariate regression analysis of survival, which adjusts for the above covariates, showed that surgical treatment prolonged survival (p less than .05), although it ranked below severity of heart failure symptoms, age, ejection fraction, and left main stenosis greater than 70% in determining prognosis. Surgical benefit was most apparent for patients with ejection fractions below 0.26 who had a 43% 5 year survival with medical treatment vs 63% with surgery. Surgically treated patients experienced substantial symptomatic benefit compared with medically treated patients if their presenting symptoms were predominantly angina; however, there was no relief of symptoms caused primarily by heart failure. We conclude that patients with predominantly ischemic pain symptoms, despite poor left ventricular function, benefit from surgery; however, operative mortality in this high-risk subset must equal or better the 6.9% obtained in this study.
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PMID:Results of coronary artery surgery in patients with poor left ventricular function (CASS). 635 78

Intracoronary streptokinase infusion is an exciting new technique, it is feasible and relatively safe, and it can restore antegrade coronary flow in 80% of the patients with an evolving myocardial infarction. Current data indicate that successful reperfusion apparently is associated with improved left ventricular function. The ultimate benefit, a significant decrease in mortality, has not yet been established. Furthermore many questions have not been answered: what is the optimal dosage of streptokinase? How should it be administered: systemic, intracoronary or super selective? Which thrombolytic agent should we use? How can we prevent reocclusion? What is the role of PTCA or acute surgery? A major shortcoming of this technique is the impact on equipment and personnel together with the rather low percentage (25%) of patients with evolving myocardial infarction, in whom this technique is applicable. Of course, although not within the scope of this article, this i.c. streptokinase treatment will have to be compared with other interventions which may reduce morbidity and mortality in patients with acute myocardial infarction. Thus, antegrade flow with i.c. streptokinase can be restored in patients with an evolving myocardial infarction. The main question is: should you do so? Until now, management of patients with an acute myocardial infarction has been conservative and is directed to treatment of pain, arrhythmias and heart failure. At the moment this approach can be considered respectable. For those who propose active management and believe in i.c. streptokinase treatment, until now, insufficient scientific data are available to back this up. For those who have doubts, but like to be active, the best is to put their patients in a well-conducted randomized trial. This will eventually resolve the question: you can, but should you? However, even if i.c. streptokinase is proven to be beneficial to the patient, this technique will not receive widespread application because of its great impact on limited health resources.
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PMID:Intracoronary streptokinase in acute evolving myocardial infarction: you can, but should you? 637 4

The clinical effects of intravenous streptokinase in patients with acute myocardial infarction were compared with those of intracoronary streptokinase in a randomized, prospective study. Comparisons were also made with a historical control group. Fifty patients were entered into the study at 2.4 +/- 1.2 hr after onset of pain, and 27 were assigned to intravenous and 23 to intracoronary therapy. The doses of streptokinase averaged 212,000 U ic and 845,000 U iv (0.75 X 10(6) U/5 hr, n = 14 or 10(6) U/1 hr, n = 13). Results of studies of the two intravenous dosage schedules were similar and so were combined. Streptokinase was administered at 2.8 +/- 1.0 hr after onset of pain in the intravenous and at 4.3 +/- 1.4 hr in the intracoronary drug group (p less than .001). Convalescent (day 10) radionuclide ejection fractions were 54 +/- 14% for the intravenous and 50 +/- 16% for the intracoronary drug group. Change in ejection fraction from day 1 to 10 tended to be greater after intravenous drug: 5.1% (p less than .08) vs 1.2% (NS). Semiquantitative regional wall motion indexes in the infarct zone showed significant and similar modest improvement from admission to day 10 in both groups (p less than .02). Accelerated enzyme-release kinetics were noted after both therapies. Times of peak enzyme levels for patients on intravenous and intracoronary drug were, respectively, 12.5 +/- 5.0 and 11.5 +/- 4.3 hr for creatine kinase MB isoenzyme and 31.7 +/- 11.8 and 28.1 +/- 12.7 hr for lactic dehydrogenase (LDH). Peak LDH-1 level was lower in patients receiving intravenous drug than in the historical control group (p less than .05). Electrocardiographically summed ST segments diminished rapidly after therapy in both groups; Q wave development was similar and overall R wave loss was equivalent and less extensive compared with in historical control subjects. Infarct pain requiring morphine was diminished similarly in both treatment groups. Incidence of early arrhythmias and heart failure also did not differ. Posttherapy ischemic events and early surgery tended to be more common in the intracoronary group and bleeding was more common in the intravenous group. Intravenous drug did not decrease early hospital mortality (intravenous drug = 5, historical control = 4, intracoronary drug = 1); the differences in this parameter among groups were not significant. At convalescent angiographic evaluation, anterograde perfusion was present in 73% of those receiving intravenous and 76% of those receiving intracoronary drug.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A randomized trial of intravenous and intracoronary streptokinase in patients with acute myocardial infarction. 638 54

The main feature of venous thrombosis on endocardial pacing electrodes are described with reference to 7 cases: the incidence is relatively low (0.4 to 4 p. 100) and the diagnosis obvious in the typical axillary-subclavian form associated with pain, oedema and collateral circulation. Diagnosis is mainly clinical and rehoplethysmography, rather than venography with its potential complications, is the complementary investigation of choice. Internal jugular, innominate vein, vena cava and intracardiac thrombosis may also occur. The vena cava syndromes are observed mainly in patients with multiple electrodes. Atrial or ventricular endocavitary thrombosis may give rise to hemodynamic signs of cardiac failure or to thromboembolism which may be fatal. Operational technique is an important factor in the etiology of early thrombosis especially when the approach vein is ligatured. In the late period, the loss of venous mobility due to the presence of a foreign body makes the vessel susceptible to compression in the cervico-brachial region. The mainstay of treatment is anticoagulation with intravenous or subcutaneous heparin with mobilisation and elevation of the affected arm. Fibrinolysis may be indicated in superior vena cava syndromes (case no 1), the results being better when therapy is instituted early on. Long term anticoagulation is not indicated (case no 7) and may even be dangerous in elderly patients with multiple electrodes.
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PMID:[Thrombophlebitis on intravenous cardiac stimulator electrodes]. 641 55

The hour of day of primary ventricular tachycardia (VT) in the acute phase of myocardial infarction was studied in 63 consecutive patients without cardiac failure or antiarrhythmic therapy, admitted to hospital less than 6 hours after the onset of chest pain. There were 19 women and 44 men, with an average age of 63 years. The site of infarction was anterior in 23 cases, posterior in 34 cases and circumferential in 6 cases. The cardiac rhythm was analysed from the 6th hour following the onset of chest pain for 4 days, using a HP 98220 A computerised analyser CPK levels were measured daily. Ventricular tachycardia occurred in 73% of cases with no significant difference between daytime (18 patients) and night time (28 patients). The patients developing VT did not differ from the remainder with respect to age, sex, or site of ECG changes, but peak CPK levels were significantly higher than in patients without VT. The risk of VT decreased slowly as the interval from the onset of chest pain increased and fell practically to zero after the 40th hour. Diurnal and nocturnal VT were independent of age, sex or site of infarct. However, nocturnal VT correlated independently of the time of onset of chest pain to high values of CPK. There was no difference with respect to age, sex, location of infarct or incidence of ventricular tachycardia between infarcts with pain starting during the day, and infarcts with pain starting at night. However, when the pain started during the day, the peak CPK was significantly higher and there were significantly more attacks of nocturnal ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Time of occurrence of primary ventricular tachycardia in the acute phase of myocardial infarction]. 643 67


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