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Query: UMLS:C0018801 (heart failure)
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Of 511 cases of brucellosis studied between December 1983 and February 1986, four (0.8%) had sternoclavicular (STCL) arthritis. Two were male and two female, and only one was younger than 50 years old. All four cases had significantly high specific IgG antibody titres (1 of 1280), measured by the indirect immunofluorescent (IIF) test, and two had Brucella melitensis isolated from their blood. In two cases, STCL arthritis was the presenting problem, and it was associated in one with ankle arthritis, hepatitis, renal impairment, orogenital ulcers and a haematological picture of myelodysplasia; in the other it was a relapsing STCL arthritis. In the remaining two cases, STCL arthritis was part of an extensive osteoarticular disease, which was associated in one with cachexia, liver cirrhosis, heart failure and prostatitis with urine retention, and in the other with severe thrombocytopenia. Excellent results were obtained from six to eight weeks' therapy with streptomycin, rifampicin and cotrimoxazole or tetracycline.
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PMID:Brucellar sternoclavicular arthritis, the forgotten complication. 325 Mar 41

Low-dose cyclosporine (CsA) plus prednisone for induction and maintenance immunosuppression were used in 106 consecutive cadaveric renal transplants. Previous reports of lower initial CsA have described its use in combination with other forms of immunosuppression. An oral CsA dose of 3 mg/kg was given 2-4 hr before operation, and maintenance CsA was started 12 hr post-operatively at 1 or 1.5 mg/kg i.v. every 12 hr for non-functioning and functioning kidneys, respectively. Oral CsA was given at 3 times the i.v. dose and started 2-3 days postoperatively. The CsA dose was adjusted to maintain plasma trough levels, as measured by radio-immunoassay, of 150-200 ng/ml for the first two weeks, 125-175 ng/ml 2-4 weeks posttransplant, and 100-150 ng/ml for the second month after transplant. Between two and six months, the CsA dose was gradually reduced by 33%. Maintenance prednisone was rapidly reduced 5 mg/month to a maintenance dose of 10 mg/day. Graft survivals for low and high-risk patients at one year were 91% and 81%, respectively. Patient survivals for low-and high-risk patients at one year were 97% and 90%, respectively. Patient death was caused by: aspiration (1), suicide (1), cardiac failure (1), Mediterranean fever with colon perforation (1), and traumatic renal artery disruption (1). Except for death, grafts were lost to primary nonfunction (2), accelerated rejection at +/- 12 hr (3), medical noncompliance (1), renal artery thrombosis (1), and vascular rejection (1). Of 106 patients, 26 (25% were treated for rejection with 3.5 g of i.v. methylprednisolone over 10 days; 25/26 (96%) rejections were reversed with methylprednisolone alone. OKT-3 failed to reverse the remaining vascular rejection. All 9 conversions from CsA to azathioprine for toxicity were successful. Our definition of toxicity was rising serum creatinine, normal CsA level, and no response to 7-10 days of i.v. methylprednisolone and no change in biopsy. We were not able to distinguish CsA toxicity and rejection in most biopsies. Average serum creatinines at 1, 6, and 12 months were 1.6 mg/dl, 1.55 mg/dl and 1.65 mg/dl, respectively. We conclude that low-dose CsA plus prednisone can be successfully used for all cadaveric renal transplants without other forms of immunosuppression. Steroid-resistant rejection is extremely rare if adequate time is given for i.v. methylprednisolone treatment. Almost all "steroid-resistant rejections" were found to be CsA toxicity, and they were reversed after conversion to azathioprine.
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PMID:Low-dose cyclosporine for cadaveric renal transplantation. 327 22

The influence of myocardial infarction size, as indicated by the maximum elevation of creatine kinase (CK) and its iso-enzyme CK-MB, on the exercise training response and resting left ventricular function was studied in 15 male patients who underwent exercise training for 8 weeks. Patients were found to divide themselves into two subgroups; those with maximum CK less than or equal to 200 IU/l (n = 7) and greater than or equal to 400 IU/l (n = 8). All were evaluated by treadmill exercise testing (Bruce Protocol), M-mode echocardiography and radionuclide ventriculography before training, immediately after, 3 and 6 months after training. Both of the subgroups showed statistically significant improvements in exercise duration, heart rates for doing equal workloads, energy expenditure and functional aerobic impairment immediately after training which were maintained 3 and 6 months later, with no inter-group differences. Resting left ventricular function, both by radionuclide and echocardiography, did not demonstrate significant changes throughout the study period, again with no inter-group differences. It is suggested that myocardial infarction size in the absence of heart failure does not appear to have a significant influence on the exercise training response and resting left ventricular function in those patients who recovered sufficiently to participate in exercise training.
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PMID:Myocardial infarction size; effect on the training response. 373 67

Eight hundred Jordanians with liver enlargement were studied: 369 (46%) were males and 431 (54%) females. Ages ranged between 13 and 85 years, with a mean of 47.4%: 766 cases demonstrated a single pathological process while 34 cases showed two or more processes. The most significant findings were: congestion secondary to cardiac failure in 323 cases (38.5%); inflammatory and parasitic processes in 192 cases (22.9%), including acute hepatitis (81 cases), hydatid cyst (63 cases), chronic hepatitis (27 cases), liver abscess (19 cases), brucellosis (one case) and malaria (one case); malignancy in 164 cases (19.6%); liver cirrhosis in 80 cases (9.5%); fatty metamorphosis in 47 cases (5.6%); metabolic and genetic disease in 11 cases (1.3%); miscellaneous conditions in nine cases (1.1%); and 15 apparently normal individuals (1.8%). Cardiac failure was the most frequent cause of hepatomegaly in this sample of Jordanians. Inflammatory processes were the second major cause, followed by malignancy and cirrhosis of the liver.
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PMID:Patterns of hepatomegaly in Jordanians: a prospective study of 800 cases. 407 96

Chronic therapy with propranolol has been shown to reduce the incidence of sudden death in patients with hypertrophic cardiomyopathy (HCM). However, the long-term effect of beta blockade on exercise capacity has not been studied adequately. Therefore, 32 patients with HCM (21 men), mean age of 47 years (range = 14 to 80 years), were evaluated for dyspnea and chest pain and underwent stress testing (ST) prior to therapy. At entry, ST was contraindicated in four patients, because of heart failure (three patients) and sustained supraventricular tachycardia (one patient). The remaining patients completed 4.9 +/- 3.2 min (mean +/- S.D.) of the Bruce protocol with a functional aerobic capacity (FAC) of 51 +/- 28%. All were placed on propranolol, unless a beta blocker with other characteristics was indicated. Dosage was adjusted to achieve a standing heart rate of 60 beats/min unless adverse effects occurred. At last follow-up, 25 patients were receiving 501 +/- 147 mg propranolol/day while the remainder received nadolol or metoprolol. On the most recent ST, patients exercised 6.6 +/- 3.1 min (38% increase), while mean FAC increased by 24% (both P less than 0.05). The FAC improved by more than 15% in 21, by less than 15% in five, was unchanged in five and was worse in only one, a noncompliant patient. The 21 patients with an FAC increment much greater than 15% exercised longer at entry than the remaining 11 (6.6 +/- 3.3 vs 3.9 +/- 2.8 minutes, P less than 0.05). The mean peak ST blood pressure-heart rate product of the group decreased from 26 550 to 17 898 (P less than 0.05), while the symptom scores of dyspnea and chest pain declined from 2.2 +/- 0.8 to 0.8 +/- 0.7 and from 1.4 +/- 1.0 to 0.3 +/- 0.8, respectively (both P less than 0.001). We conclude that beta blockade produces sustained improvement in exercise capacity. Improvement was greatest in those with the least initial impairment, and appears to be related to a reduction in blood pressure-heart rate product.
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PMID:Long-term medical management of hypertrophic cardiomyopathy: usefulness of propranolol. 668 31

A 20 year-old white man was admitted with fever and weight loss since 60 days previous to his admission and cardiac failure (functional class IV). The heart was enlarged in the echocardiographic examination without valvular involvement. Liver biopsy showed granulomatous hepatitis with a necrosis focus. The patient was treated with a combination of venous dilators and digital. Serum agglutination test for Brucella showed a titer of 1/250, and complement fixation 1/40. Seven days later, agglutination titer was 1/4000. He was treated with rifampin and trimethoprimsulfametoxazol. He got better; fever disappeared, and the signs of cardiac failure improved. Brucellosic myocarditis is an uncommon complication of brucellosis in the absence of endocarditis. In our knowledge, this case would be the first reported in Argentina and the third in adult patients out of the five cases reported worldwide.
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PMID:[Febrile syndrome: myocarditis and brucellosis]. 756 52

A feasibility and reproducibility study of cardiac output measurement by CO2 rebreathing was performed in normal subjects and in patients with compensated cardiac failure. The measurements were performed at rest and at the second stage of the Bruce protocol in normal subjects (N = 12) with a good reproducibility (r = 0.81) after an interval of two days. In patients with stable cardiac failure (N = 17), the cardiac outputs were 9.4 +/- 3.9 l/min and 9.3 +/- 3.1 l/min by measuring the arterial pCO2 and end-expiratory CO2 compared with the theoretical value of 9.9 +/- 2 l/min. The non-invasive measurement of cardiac output by the CO2 rebreathing method was well tolerated by patients and is reliable and reproducible.
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PMID:[Measurement of cardiac output by CO2 rebreathing technique. A study of reproducibility in the normal subject; application to cardiac insufficiency]. 821 69

Angiotensin converting enzyme (ACE) inhibitors are of proven value in patients with severe chronic heart failure (CHF). Studies of the effects of ACE inhibitors on exercise capacity and quality of life in mild CHF have produced conflicting results. We have studied the effects of quinapril, a new ACE inhibitor with a relatively short plasma half-life, in mild CHF. Once daily (o.d.) dosing was compared with twice daily (b.i.d.) dosing in a three-way cross-over, double-blind, placebo-controlled trial. Thirty-two patients (two female), mean age 59 (range 32-76) years were enrolled in three cardiology centres in the U.K. in 29 patients, and non-ischaemic in three. The mean (range) radionuclide ejection fraction was 20.4% (8%-47%). Following full familiarization with the protocol, the treadmill exercise time (modified Bruce protocol) was determined for each patient during a placebo run-in phase, and at the end of each of three 8-week double-blind treatment phases with quinapril o.d., quinapril b.i.d. (maximal total daily dose 20 mg) and placebo. Three patients were withdrawn due to adverse events while receiving quinapril (unstable angina, exacerbation of CHF and arrhythmia); there were no deaths and no patient was withdrawn due to hypotension. Mean exercise time (the primary end-point) was 65 s and 53 s longer in patients receiving quinapril o.d. and b.i.d. respectively compared to placebo (both P < 0.01, ANOVA). There was no significant period effect during the trial and no significant difference between the two quinapril dosing regimens. Quinapril had no significant effect on secondary end-points including ejection fraction, functional class and quality of life.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A multicentre, double-blind, placebo-controlled trial of quinapril in mild, chronic heart failure. 845 62

The slope of the linear relationship between ventilation (V(E)) and carbon dioxide production (VC0(2)) has been thought to indicate that VC0(2) is one of the major stimuli to V(E). A group of 15 normal subjects undertook different incremental treadmill exercise protocols to explore the relationship between V(E) and VCO(2). An incremental protocol using 1 instead of 3-min stages of exercise resulted in an increase in the V E to VCO(2) ratio [26.84 (SEM 1.23) vs 31.08 (SEM 1.36) (P <0.008) for the first stage, 25.24 (SEM 0.86) vs 27.83 (SEM 0.91) (P <0.005) for the second stage and 23.90 (SEM 0.86) vs 26.34 (SEM 0.81) (P = 0.001) for the third stage]. Voluntary hyperventilation to double the control level of V(E) during exercise resulted in an increase in the V(E) to VCO(2) slope [from 21.3 (SEM 0.71) for the control run to 35.1 (SEM 1.2) for the hyperventilation run (P <0.001)]. Prolonged hyperventilation (5 min) during exercise at stage 2 of the Bruce protocol resulted in a continued elevation of VCO(2) and the V(E)/VCO(2) slope. A steady state of V(E) and metabolic gas exchange can only be said to have been present after at least 3 min of exercise. Voluntary hyperventilation increased the slope of the relationship between V(E) and VCO(2). End-tidal carbon dioxide fell, but remained within the normal range. These results would suggest that a non-carbon dioxide factor may have been responsible for the increase we found in V(E) during exercise, and that factors other than increased dead space ventilation can cause an increased ventilation to VCO(2) slope, such as that seen in some pathophysiological conditions, such as chronic heart failure.
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PMID:Factors which alter the relationship between ventilation and carbon dioxide production during exercise in normal subjects. 886 83

Sudden cardiac death is a common cause of mortality in patients with congestive heart failure. Asymptomatic ventricular arrhythmia has been attributed as the cause for increased overall mortality in such patients. We conducted a prospective randomised single-blind placebo-controlled trial with low-dose amiodarone to assess its efficacy in reducing mortality in severe congestive heart failure and its effect on exercise tolerance, left ventricular systolic function and ventricular ectopic activity. Patients were randomised to receive amiodarone (n = 36) 400 mg/day orally for one month followed by a maintenance dose of 200 mg/day, or to a standard treatment (n = 40) according to intention-to-treat principle. There were 10 cardiac deaths in the amiodarone-treated group and 16 in the control group. Significant improvement was noted in exercise time in the treadmill test (modified Bruce Protocol) among patients in the amiodarone-treated group while no such statistical difference was detectable in the placebo group. Side-effects in the amiodarone group included asymptomatic rise in hepatic enzymes (three-fold) in 6 percent and proarrhythmia in 3 percent of patients. Nausea was reported in one patient and rash in one. Though low-dose amiodarone proved to be an effective antiarrhythmic agent, it failed to live up to the expectation of improving sudden cardiac death in patients with severe chronic heart failure and asymptomatic ventricular ectopy.
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PMID:Low-dose amiodarone in severe chronic heart failure. 890 21


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