Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year old female had a fever about 39 degrees C of unknown origin for 2 days. Soon she developed pain in the bilateral lower extremities followed by gait disturbance and vesicorectal disorder. Prednisolone was administered with an improvement. However, she developed paresthesia in the upper extremities 1 month later, and then gradually paraplegia another 5 month later. Nystagmus, painful tonic spasm, facial spasm, and visual disorder also appeared. These symptoms repeatedly exacerbated and remitted with administration of prednisolone. We examined this patient at age 53, CBC, blood chemistry, urinalysis, ECG and chest X-ray were normal. Serum IgG and IgA level were decreased. CSF protein content and IgG level were remarkably increased. EEG showed diffuse theta activities. MRI studies revealed high intensity signals in the putamen, deep frontal and periventricular white matter region. Pulse therapy of methylprednisolone was performed effectively for several times. She died of respiratory and heart failure 6 years after the onset. Autopsy revealed bilateral continuous cystic lesions along the lateral ventricles extending from the frontal tips of anterior horns to the occipital tips of posterior, and further, to the temporal tips of lateral horns; the caudate-callosal angeles (Wetterwinkel) were more severely and widely affected bilaterally. There were also old and fresh demyelinated lesions scattered in the cerebral white matter, brainstem, cerebellum, and spinal cord. Although this case is considered to have typical MS from clinical and pathological findings, there have been only a few reports of MS with such continuous cystic lesions in the cerebral hemispheres as seen in this case.
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PMID:[An autopsy case of multiple sclerosis with bilateral continuous cystic lesions along lateral ventricles and caudate-callosal angles (Wetterwinkel)]. 179 16

Heart transplantation (HTx) has now become an accepted treatment modality for end-stage heart disease. The limited supply of suitable donor organs imposes constraints upon the decision of who should be selected for transplantation. Usually patients are candidates for HTx, who remain NYHA functional class III or IV despite maximal medical therapy. Further criteria are low left ventricular ejection fraction (less than 20%) with heart rhythm disturbances class IIIA-V (LOWN), which are associated with poor prognosis. Additionally, the suffering of the patient and also the course of heart failure are essential for judging the urgency of HTx. Contraindications are absolute in patients with untreated infections, fixed pulmonary vascular resistance (PVR) above 8 WOOD-degrees, severe irreversible kidney and liver disease, active ventricular or duodenal ulcers and acute, psychiatric illness. HTx is relatively contraindicated in patients with diabetes mellitus, age over 60 years, PVR above 6 WOOD-degrees and an unstable psychosocial situation. To prevent rejection of the transplant heart, live-long immunosuppressive therapy is needed. Most immunosuppressive regimes consist of Cyclosporine A and Azathioprine (double drug therapy) or in combination (tripple drug therapy) with Prednisolone. For monitoring of this therapy, control of hole blood cyclosporine A level and white blood count is needed. Rejection episodes can be suspected if there is a greater than 20 mmHg decrease of systolic blood pressure, elevated body temperature, malaise, tachycardia or heart rhythm disturbance. The diagnosis of cardiac rejection can be established by endomyocardial biopsy. Measurement of the voltage of either the surface or intramyocardial ECG, echocardiography with special consideration to early left ventricular filling time as well as immunological methods are additionally used tools. Graft sclerosis as the main risk factor of the late transplant period remains an unsolved problem.
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PMID:[Therapy of terminal heart failure using heart transplantation]. 192 Dec 33

Two patients suffering from dilated Cardiomyopathy (CMP) had to undergo orthotopic heart transplantation (HTX). In both cases, the postoperative period was without any complications. The immunosuppression consisted of Cyclosporin-A and Azathioprine including a one week prophylactic treatment with Antithymocyte Globuline (ATG). Four months postoperatively, they developed clinical signs of heart failure. The endomyocardial biopsies showed rejection at stage I according to Billingham's grading plus a fine interstitial fibrosis. Therefore, the Cyclosporin treatment was suspended and replaced by conventional immunosuppression consisting of Prednisolone and Azathioprine. Acute heart failure was managed by catecholamines in combination with aggressive diuretic therapy. After three weeks, both patients recovered. 12 weeks later, one died because of an acute rejection episode. The other is in good condition, with conventional immunosuppression at the present time. A vascular process caused by Cyclosporin-A as the pathogenic mechanism is considered. The absence of rejection signs in the biopsies as well as the remarkable improvement of heart failure after withdrawal of Cyclosporin-A support this possibility.
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PMID:Cyclosporin-A induced heart failure after orthotopic heart transplantation. 244 Jan 40

Results of early studies support the concept that steroid treatment may reduce mortality from acute myocardial infarction. This double-blind, randomized, 1118-patient study was performed to determine if methylprednisolone sodium succinate (MPSS, Solu-Medrol Sterile Powder, The Upjohn Company) reduced 28-day mortality following myocardial infarction complicated by cardiac failure. Treatment with 30 mg/kg intravenous MPSS (maximum dose, 3 g) resulted in 28-day mortality rates of 11.7% with MPSS and 9.9% with placebo when treatment was initiated within six hours of the onset of chest pain (Group 1). Mortality rates at 28 days were 10.4% with MPSS and 14.7% with placebo when the treatment was initiated 6-12 hours after onset of chest pain (Group 2). In the late-treatment group, six-month mortality rates were 13.7% with MPSS and 20.3% with placebo (p = 0.08). Analysis of data by life table methods showed similar survival rates between MPSS- and placebo-treated patients in Group 1. In Group 2, survival rates were increased in MPSS-treated patients in the intervals from 48 hours through seven days (p = 0.04) and from three months through six months (p = 0.03). A Cox regression analysis showed that the relative risk of death for Group 1 patients was similar, regardless of treatment; Group 2 patients on MPSS had a significantly decreased relative risk of death (p less than 0.01). MPSS treatment was not associated with increased incidence of myocardial rupture, cardiac aneurysm, early malignant ventricular arrhythmias, or other adverse cardiac events.
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PMID:Methylprednisolone as an intervention following myocardial infarction. The Solu-Medrol Sterile Powder AMI Studies Group. 287 3

In studies of patients with cardiac failure following an acute myocardial infarction, 1114 patients were followed for 7-day mortality. In the 45% of patients receiving diuretics on day 1, the death rate was twice that of patients not receiving diuretics. In patients treated 6 to 12 hours following the onset of chest pain, mortality was 2.8 times that of patients treated within 6 hours of the onset of chest pain. Randomization to methylprednisolone sodium succinate (MPSS, Solu-Medrol Sterile Powder, The Upjohn Company) did not improve the low mortality rates of those patients who did not need diuretics nor who were treated early. However, patients who were treated late and who needed diuretics and who were randomized to MPSS had a death rate half that of those who received placebo.
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PMID:Positive synergism between diuretics and methylprednisolone following acute myocardial infarction. 352 10

We report the case of a 92-year-old man with a 13-year history of occupational asbestos exposure who presented with a complaint of dyspnea. In September 2001, bilateral pleural effusions were revealed on chest radiography, and continued to progress despite treatment for heart failure. Chest CT revealed calcification of the pleura but no abnormal findings in the lung fields. Both pleural effusions were exudative and lymphocytes were the predominant cells contained in them. Antituberculous chemotherapy had no effect on the exudates. In March 2002, thoracoscopy was performed under local anesthesia (medical thoracoscopy). Plaque was recognized on the parietal pleura; however, the serosal surfaces of the parietal and visceral pleura were smooth, and no evidence of malignancy, especially malignant mesothelioma, was noted. The patient's condition was diagnosed as benign asbestos pleural effusions. Prednisolone was administered, and these effusions gradually decreased. Cases of benign asbestos pleural effusion occurring simultaneously with massive bilateral effusions are rare. Thoracoscopy aided in the differential diagnosis of this case.
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PMID:[A case of benign asbestos pleural effusion suspected on thoracoscopic examination under local anesthesia]. 1283 42

A 15-year-old Japanese man was referred for evaluation of heart failure. Conventional heart failure therapy had little effect, and severe left ventricular dysfunction as well as elevated erythrocyte sedimentation rate persisted. Magnetic resonance angiography showed aortic dilatation with wall thickening characteristic of Takayasu's arteritis. An endomyocardial biopsy specimen revealed infiltration of natural killer cells and gamma delta T lymphocytes, which play major roles in vascular injury of Takayasu's arteritis. Prednisolone administration provided great benefits to cardiac function. These findings suggest that autoimmune cytotoxic mechanisms similar to those in arterial tissue may contribute to cardiac impairment in Takayasu's arteritis.
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PMID:Takayasu myocarditis mediated by cytotoxic T lymphocytes. 1580 18

Prednisolone (PSL) therapy is the gold standard treatment in patients with cardiac sarcoidosis (CS). However, clinicians often have difficulty in deciding whether to discontinue PSL therapy in long-term management. Sixty-one consecutive patients with CS were divided into 2 groups based on the discontinuation of PSL during the median follow-up period of 9.9 years. PSL was discontinued in 12 patients because of improvement of clinical findings. There were no significant differences between the 2 groups in age, gender, left ventricular ejection fraction (LVEF), findings of imaging techniques, incidence of fatal arrhythmias and heart failure, and dose of PSL. After discontinuation of PSL, 5 patients had cardiac death, and discontinuation of PSL was significantly associated with higher cardiac mortality compared with continuation (p = 0.035). Although patients with discontinuation had improvement of LVEF after PSL treatment, LVEF decreased after discontinuation of PSL. Furthermore, discontinuation of PSL was associated with greater percent decrease in LVEF compared with continuation (p = 0.037) during the follow-up period. In conclusion, in the long-term management of patients with CS, discontinuation of PSL was associated with poor clinical outcomes and decreased LVEF, suggesting the importance of PSL maintenance therapy.
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PMID:Effect of Discontinuation of Prednisolone Therapy on Risk of Cardiac Mortality Associated With Worsening Left Ventricular Dysfunction in Cardiac Sarcoidosis. 2680 58

A 42-year-old woman presented with fever, dyspnea, lower-leg edema, significant pulmonary congestion, pleural effusion, and severely reduced left ventricular contractions. She was resistant to treatment for heart failure, including catecholamines, furosemide, phosphodiesterase III inhibitors, and human atrial natriuretic peptide, and antibiotics failed to reduce her inflammation. She had renal dysfunction and hypocomplementemia and was positive for anti-nuclear and anti-ds-DNA antibodies. The patient was diagnosed with myocarditis and pleurisy associated with systemic lupus erythematosus (SLE). Prednisolone administration improved her general condition, reducing inflammation and improving left ventricular function. On day 1, an electrocardiography (ECG) revealed a T-wave inversion similar to a T-U complex configuration in leads II, aVF, and V3-6. By day 8, however, ECG showed prolonged corrected QT (QTc) and T-wave alternans (alternating beat-to-beat T-wave patterns) in lead V3-6. Careful ECG monitoring should be used to identify potentially fatal ventricular arrhythmias during the recovery phase of SLE-related myocarditis. <Learning objective: This was a case of significant T-wave alternans (TWA) during recovery from systemic lupus erythematosus (SLE)-related myocarditis. Fatal ventricular arrhythmia appears to be a risk during recovery from myocardial damage caused by SLE. Up to now, there have been no published case reports of TWA during this period. Patients with myocarditis should be carefully monitored for arrhythmia, even after ventricular function and inflammation have improved with prednisolone therapy.>.
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PMID:T-wave alternans in a case with systemic lupus erythematosus-related myocarditis. 3027 27

Myocardial calcification, a rare disease that leads to chronic or acute heart failure and with a poor prognosis, occurs in patients with abnormal calcium-phosphorus metabolism. The association between myocardial calcification and tumor lysis syndrome has not been reported to date. A 50-year-old man with hyperthermia and general malaise presented to our hospital and was clinically diagnosed with B-lymphoblastic leukemia (B-ALL) and febrile neutropenia accompanied by septic shock. Prednisolone was administered for tumor reduction. Two to three hours later, electrocardiography demonstrated ST elevation in V4-6, and blood tests showed elevated levels of cardiac enzymes. Transthoracic echocardiogram revealed diffuse severe hypokinesis with decreased left ventricular ejection fraction. Additionally, blood tests showed that serum phosphorus level increased to 8.0 mg/dl, which was likely due to tumor lysis syndrome. Circulatory and respiratory failure due to left heart failure progressed, and he died 3 days after administration of prednisolone. Pathological autopsy revealed diffuse proliferation of atypical B-lymphoblasts in the bone marrow, which led to the pathological diagnosis of B-ALL, accompanied by necrosis. On the cut surface of the heart, the left ventricle was dilated, and patchy yellowish-brown areas were present in the epicardial-side of the myocardium and spread through the circumferential wall of the left ventricle and interventricular septum. Microscopically, myocardial fibers were granularly basophilic in that area and were revealed as calcium deposits by Von Kossa staining. He was diagnosed with myocardial calcification. The drastic increase in the serum phosphorus level caused by tumor lysis syndrome seemed to be associated with myocardial calcification.
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PMID:Myocardial calcification in a patient with B-lymphoblastic leukemia accompanied by tumor lysis syndrome. 3149 34


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