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)

In a multicentre open therapeutic study 64 physicians provided 650 questionnaires of patients who had been treated with the new cardiac glycoside 14-Hydroxy-3beta-[(4-O-methyl-alpha-L-rhamnopyranosyl)oxy]-14beta-bufa-4,20,22-trienolide (meproscillarin, Clift) for more than 3 months; 647 questionnaires had been filled in completely and could be evaluated. The major part of all patients suffering from heart failure of the severity degrees I--III required 2 tablets of 0.25 mg, a smaller part 3 tablets to achieve complete recompensation and/or maintenance of compensation, which was possible in 79% of all cases. The rate of side effects corresponded to that of other cardiac glycosides.
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PMID:[Long-term study with the novel cardiac glycoside meproscillarin (author's transl)]. 34 6

14-Hydroxy-3beta-[4-O-methyl-alpha-L-rhamnopyranosyl)oxy]-14beta-bufa-4,20,22-trienolide (meproscillarin) is a new semisynthetic glycoside for the therapy of cardiac insufficiency. The preparation from proscillaridin and the chemical and physical properties are described.
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PMID:[Meproscillarin, a new semisynthetic cardiac glycoside/chemistry and physical properties (author's transl)]. 58 May 77

In ten patients in heart failure for which they were on long-term administration of digitoxin, the influence of aluminium-magnesium hydroxide gel (Maaloxan) on steady-state digitoxin plasma concentration and renal glycoside excretion was studied. Compared with control values before antacid medication (13.6 +/- 4.4 ng/ml), the administration of 20 ml aluminium-magnesium hydroxide gel three or four times daily for several weeks caused no significant change in digitoxin plasma levels (15.1 +/- 4.9 ng/ml). Daily renal glycoside excretion, as a further measure of bioavailability of digitoxin, was also unchanged by the antacid. Therapeutic plasma concentrations of digitoxin are not influenced by antacids which contain aluminium-magnesium hydroxide, at least not if the antacid is taken 1-2 hours after the digitoxin dose.
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PMID:[Digitoxin blood picture and renal elimination in long-term therapy with aluminum-magnesium hydroxide gel]. 669 64

The authors evaluated the serological response of metronidazole, or 8823 RP-(Hydroxy-2' ethy1)-1-methyl-2 nitro-5 imidazole) in 1307 patients, with Chagas' disease in the acute or chronic stage with age ranging between 6 months to 73 years. 273 patients were in the acute phase: 153 children and 120 adults. Patients in the chronic stage were classified with serological, clinical and cardiological criteria: 1.-POSITIVE SEROLOGY without cardiological signs or symptomatology (EKG, VECTO, ECHO M mode and 2-D, Chest Rx, physiological and pharmacological tests, radiocardiological-HMIBI, MUGA); 2.- POSITIVE SEROLOGY with cardiological signs and symptoms (all cardiological tests were abnormals); 3.- POSITIVE SEROLOGY with cardiomyopathy and cardiac failure. Metronidazole, P.O. or I.V. was utilizing dosages ranging from 15 to 25 mg/Kilo body weight per five days in acute phase and 250 to 500 mg. P.O. in the chronic stage of the disease for 180 days. The drug was well tolerated by all patients in both phases of the disease. Adequate anabolic effect was identified in both stages of the illness. Serological reactions were negative in all patients (100%) without cardiomyopathy. In patients with cardiomyopathy and cardiac failure, the complement fixation test title were similar before and after treatment.
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PMID:[The clinical experience in Panama with metronidazole in treating Chagas' disease in the acute and chronic phases]. 832 50

Hydroxyl radicals (OH) are involved in the development of reperfusion injury and myocardial failure. In the acute phase of the OH-mediated diastolic dysfunction, increased intracellular Ca(2+) levels and alterations of myofilaments may play a role, but the relative contribution of these systems to myocardial dysfunction is unknown. Intact contracting cardiac trabeculae from rabbits were exposed to OH, resulting in an increase in diastolic force (F(dia)) by 540%. Skinned fiber experiments revealed that OH-exposed preparations were sensitized for Ca(2+) (EC(50): 3.27+/-0.24 x 10(-6) versus 2.69+/-0.15 x 10(-6) mol/L; P<0.05), whereas maximal force development was unaltered. Western blots showed a proteolytic degradation of troponin T (TnT) with intact troponin I (TnI). Blocking of calpain I by MDL-28.170 inhibited both TnT-proteolysis and Ca(2+) sensitization, but failed to prevent the acute diastolic dysfunction in the intact preparation. The OH-induced diastolic dysfunction was similar in preparations with intact (540+/-93%) and pharmacologically blocked sarcoplasmic reticulum (539+/-77%), and was also similar in presence of the L-type Ca(2+)-channel antagonist verapamil. In sharp contrast, inhibition of the reverse-mode sodium-calcium exchange by KB-R7943 preserved diastolic function completely. Additional experiments were performed in rat myocardium; the rise in diastolic force was comparable to rabbit myocardium, but Ca(2+) sensitivity was unchanged and maximal force development was reduced. This was associated with a degradation of TnI, but not TnT. Electron microscopic analysis revealed that OH did not cause irreversible membrane damage. We conclude that OH-induced acute diastolic dysfunction is caused by Ca(2+) influx via reverse mode of the sodium-calcium exchanger. Degradation of troponins appears to be species-dependent but does not contribute to the acute diastolic dysfunction.
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PMID:Hydroxyl radical-induced acute diastolic dysfunction is due to calcium overload via reverse-mode Na(+)-Ca(2+) exchange. 1201 65

Immunization against components of the renin-angiotensin system offers a potential alternative to daily medication in some patients with hypertension or heart failure. Our primary objective was to determine whether a sustained antibody titre to Ang I (angiotensin I) can be achieved in hypertensive patients. The secondary objective was to determine whether the antibodies block the renin system. Patients (n=27) with essential hypertension responsive to an ACEi (angiotensin-converting enzyme inhibitor) or ARB (angiotensin blocker) were randomly assigned to receive three or four injections of the Ang I vaccine PMD3117 or aluminium hydroxide (Alhydrogel trade mark ) over a 6 week period. Antibody titre was measured prior to each injection and every 30 days until disappearance. Indices of renin blockade were changes in renin and aldosterone (blood and urine) and a within-patient comparison of the pre- and post-vaccination rise in 24 h ambulatory blood pressure after 2 weeks of withdrawal of ACEi or ARB. The anti-(Ang I) antibody titre rose from the second injection in both regimes and peaked on day 64. Median half-life was 85 (95% CI, 44 and 153) days (where CI is confidence interval). Vaccination did not influence blood pressure, but significantly blunted the fall in plasma renin following withdrawal of ACEi or ARB. At 42 days after the first injection, aldosterone excretion was decreased by PMD3117 to 6 (95% CI, 1 and 31)% of values in patients receiving Alhydrogel trade mark (P=0.012). In patients with essential hypertension, PMD3117 generated a prolonged antibody response to Ang I. Biochemical measurements show evidence of blockade of the renin system, but higher titres will be required to achieve a decrease in blood pressure.
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PMID:Randomized double-blind placebo-controlled study of an angiotensin immunotherapeutic vaccine (PMD3117) in hypertensive subjects. 1510 32

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, reduce morbidity and mortality in patients with coronary artery disease (CAD). Because CAD is the major cause of heart failure (HF) in developed countries, prevention of CAD may result in reduced HF. Evidence from randomized trials on lipid reduction (Cholesterol and Recurrent Events and the Scandinavian Simvastatin Survival Study) has shown statins to decrease progression to HF. Recently, many beneficial effects of statins have been demonstrated beyond cholesterol lowering. These agents improve endothelial function, exhibit anti-inflammatory properties, and prevent cardiac hypertrophy. Experimental studies have shown attenuation of left ventricular remodeling after myocardial infarction, possibly through reduced oxidative stress. However, no clinical evidence exists to support an effect on ventricular remodeling. Small, short-lasting clinical studies have also suggested that statin therapy might be associated with improved survival in ischemic and nonischemic HF.
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PMID:Do statins prevent heart failure in patients after myocardial infarction? 1603 39

A solid-phase sandwich fluorescence immunoassay using nanocrystals of a fluorogenic precursor, fluorescein diacetate (FDA), conjugated with monoclonal antibodies for the detection of C-reactive protein (CRP), is described. FDA nanocrystals were coated with distearoylglycerophosphoethanolamine (DSPE), modified with amino(poly(ethylene glycol))(PEG(2000)-Amine) as an interface for coupling biomolecules. CRP was chosen as a model analyte because of its widely accepted role as a marker for acute inflammation and prospective heart failure. A low limit of detection (1.10 microg l(-1)) and high precision (CV = 2.72-9.48%) were achieved. Following the immunoreaction, the monoclonal anti-CRP conjugated nanocrystals were released by hydrolysis and dissolution instigated by the addition of a large volume of organic solvent-sodium hydroxide mixture. Using human serum samples from 66 patients with high heart attack risk and 19 healthy blood donors, this CRP fluorescence immunoassay showed a good correlation to the commercially available, turbidimetric immunoassay for CRP. This result was corroborated by the Bland-Altman plot that showed a mean difference between the two methods of only 0.36+/-1.46 mg l(-1). The study demonstrates that the organic fluorogenic FDA nanocrystals can be applied for the detection of CRP, which is a clinically interesting plasma protein with a low limit of detection.
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PMID:Fluorogenic nanocrystals for highly sensitive detection of C-reactive protein. 1679

Hydroxyl radicals (*OH) are involved in the pathogenesis of ischemia-reperfusion injury and are observed in clinical situations, including acute heart failure, stroke, and myocardial infarction. Acute transient exposure to *OH causes an intracellular Ca(2+) overload and leads to impaired contractility. We investigated whether upregulation of sarcoplasmic reticulum Ca(2+)-ATPase function (SERCA) can attenuate *OH-induced dysfunction. Small, contracting right ventricular papillary muscles from wild-type (WT) SERCA1a-overexpressing (transgenic, TG) and SERCA2a heterogeneous knockout (HET) mice were directly exposed to *OH. This brief 2-min exposure led to a transient elevation of diastolic force (F(dia)) and depression of developed force (F(dev)). In WT mice, F(dia) increased to 485 +/- 49% and F(dev) decreased to 11 +/- 3%. In sharp contrast, in TG mice F(dia) increased only to 241 +/- 17%, whereas F(dev) decreased only to 51 +/- 5% (P < 0.05 vs. WT). In HET mice, F(dia) rose more than WT (to 597 +/- 20%, P < 0.05), whereas F(dev) was reduced in a similar amount. After approximately 45 min after *OH exposure, a new steady state was reached: F(dev) returned to 37 +/- 6% and 32 +/- 6%, whereas F(dia) came back to 238 +/- 28% and 292 +/- 17% in WT and HET mice, respectively. In contrast, the sustained dysfunction was significantly less in TG mice: F(dia) and F(dev) returned to 144 +/- 20% and 67 +/- 6%, respectively. Before exposure to *OH, there is decrease in phospholamban (PLB) phosphorylation at Ser16 (pPLBSer16) and PLB phosphorylation at Thr17 (pPLBThr17) in TG mice and an increase in pPLBSer16 and pPLBThr17 in HET mice versus WT. After exposure to *OH there is decrease in pPLBSer16 in WT, TG, and HET mice but no significant change in the level of pPLBThr17 in any group. The results indicate that SERCA overexpression can reduce the *OH-induced contractile dysfunction in murine myocardium, whereas a reduced SR Ca(2+)-ATPase activity aggravates this injury. Loss of pPLB levels at Ser16 likely amplifies the differences observed in injury response.
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PMID:SERCA overexpression reduces hydroxyl radical injury in murine myocardium. 1679 16

Over the past 2 decades our understanding of the pathologic mechanisms that lead to heart failure (HF) has evolved from simplistic hemodynamic models to more complex models that have implicated neurohormonal activation and adverse cardiac remodeling as important mechanisms of disease progression. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have become a standard part of the armamentarium in the prevention and treatment of coronary artery disease. Apart from their lipid-lowering capabilities, statins seem to have non-lipid-lowering effects that impact neurohormonal activation and cardiac remodeling. This review will examine the potential benefits of statins in HF patients with ischemic and nonischemic cardiomyopathy as well as potential concerns regarding the use of statins in these patients.
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PMID:Experimental and clinical basis for the use of statins in patients with ischemic and nonischemic cardiomyopathy. 1822 51


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