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)

Between 1988 and 1995, 341 children with acute myeloid leukaemia (AML) were treated on the Medical Research Council Acute Myeloid Leukaemia Trial (MRC AML10). The 5-year overall survival was 57%, much improved on previous trials. However, there were 47 deaths (13. 8%), 11 of which were associated with bone marrow transplantation (BMT). The treatment-related mortality was significant at 13.8%, but decreased in the latter half of the trial from 17.8% in 1998-91 to 9. 6% in 1992-95 (P = 0.03%). The main causes of death were infection (65.9%), haemorrhage (19.1%) and cardiac failure (19.1%). Fungal infection was a significant problem, causing 23% of all infective deaths. Haemorrhage occurred early in treatment, in children with initial white cell counts >100 x 109/l (P = 0.001), and was more common in those with M4 and M5 morphology. Cardiac failure only occurred from the third course of chemotherapy onwards, with 78% (7/9) in conjunction with sepsis as a terminal event. Some deaths could be prevented by identifying those most at risk, and with prompt recognition and aggressive management of complications of treatment. Future options include the prophylactic use of antifungal agents, and the use of cardioprotectants or alternatives to conventional anthracyclines to decrease cardiac toxicity.
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PMID:Treatment-related deaths during induction and first remission of acute myeloid leukaemia in children treated on the Tenth Medical Research Council acute myeloid leukaemia trial (MRC AML10). The MCR Childhood Leukaemia Working Party. 1046 Jun 4

Beta-blockers have been considered for decades as effective agents in preventing coronary events in hypertensive patients. Actually, the scrutiny of the available data arises some doubts over the real value of this pharmacological class. In primary prevention, the clinical benefits of beta-blockers are poorly documented: the studies conducted against placebo (MRC, IPPPSH...) did not show any significant differences regarding the rate of coronary events (except within non smokers); moreover, the beneficial effect of propranolol in preventing sudden deaths and silent myocardial infarctions has been reported byjust one retrospective analysis. Likewise in HAPPHY study, the comparison with diuretics did not emphasize a clear superiority of one of both classes; the better effect of metoprolol regarding overall mortality and fatal coronary events was shown in the pecular subset MAPHY, only. Furthermore, in elderly people, HEP, MRC OA and STOP studies did not find any significant effect of beta-blockers in preventing coronary events, as compared with placebo. However, SHEP study, which involved patients older than 60 years with isolated systolic hypertension receiving first a diuretic, then a beta-blocker(atenolol) in 1/4 of the cases, demonstrated a significant reduction versus placebo both in strokes and in coronary events. Finally, in UKPDS, CAPP, LIFE and CONVINCE studies, atenolol turned out to have a similar efficacy as captopril, losartan and verapamil, in preventing ischemic heart disease. Among the numerous published meta-analyses, that of Psaty pointed out the absence of a primary cardioprotective effect by beta-blockers; more recently, that of Carlberg, emphasized atenolol given alone as the first-line drug to fail in significantly reducing coronary events and strokes. In secondary prevention, some more convincing data may be found in the literature, regarding post myocardial infarction patients (meta-analyses of Staessen, 1982, Yusuf, 1985 and Soriano, 1997), as well as those with stable angina (BIP study in diabetics) or silent ischemia (ASIST study: significant reduction in number and duration of ischemic events by atenolol). Moreover, INVEST study recently showed atenolol and verapamil to have an equivalent efficacy in the hypertensive patients with stable coronary artery disease. Last, hypertension should be reminded as resulting in many cases of heart failure, a pathology where beta-blockers have clearly demonstrated their beneficial effects.
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PMID:[Do beta-blockers prevent coronary events in hypertensive patients?]. 1623 74

Comorbidities, are common in COPD, have been associated with poor outcomes and are thought to relate to systemic inflammation. To investigate comorbidities in relation to systemic inflammation and outcomes we recorded comorbidities in a well characterized cohort (ECLIPSE study) for 2164 clinically stable COPD subjects, 337 smokers and 245 non-smokers with normal lung function. COPD patients had a higher prevalence of osteoporosis, anxiety/panic attacks, heart trouble, heart attack, and heart failure, than smokers or nonsmokers. Heart failure (Hazard Ratio [HR] 1.9, 95% Confidence Interval [CI] 1.3-2.9), ischemic heart disease (HR 1.5, 95% CI 1.1-2.0), heart disease (HR 1.5, 95% CI 1.2-2.0), and diabetes (HR 1.7, 95% CI 1.2-2.4) had increased odds of mortality when coexistent with COPD. Multiple comorbidities had accumulative effect on mortality. COPD and cardiovascular disease was associated with poorer quality of life, higher MRC dyspnea scores, reduced 6MWD, higher BODE index scores. Osteoporosis, hypertension and diabetes were associated with higher MRC dyspnea scores and reduced 6MWD. Higher blood concentrations of fibrinogen, IL-6 and IL-8 levels occurred in those with heart disease. Comorbidity is associated with poor clinical outcomes in COPD. The comorbidities of heart disease, hypertension and diabetes are associated with increased systemic inflammation.
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PMID:Comorbidity, systemic inflammation and outcomes in the ECLIPSE cohort. 2379 63

Heart failure is a public health problem and a great economic burden for patients and healthcare systems. Suppression of the renin-angiotensin system (RAS) by angiotensin-converting enzyme (ACE)-inhibitors remains the mainstay of treatment for heart failure. However, the abundance of ACE inhibitors makes it difficult for doctors to choose.We performed this network meta-analysis of ACEIs in patients with heart failure in order to address this area of uncertainty.We searched PubMed, Embase, CENTRAL, and Medline.Any randomized controlled trial evaluating the efficacy and safety of captopril, enalapril, lisinopril, ramipril, or trandolapril or combined interventions of 2 or more of these drugs.Two reviewers extracted the data and made the quality assessment. At first, we used Stata software (version 12.0, StataCorp, College Station, TX) to make traditional pairwise meta-analyses for studies that directly compared different interventions. Then, network meta-analysis was performed using WinBUGS (version 1.4.3, MRC Biostatistics Unit, Cambridge, UK).A total of 29 studies were included. Lisinopril was associated with a higher rate of all-cause mortality compared with placebo (odds ratio 65.9, 95% credible interval 1.91 to 239.6) or ramipril (14.65, 1.23 to 49.5). Enalapril significantly reduced systolic blood pressure when compared with placebo (standardized mean differences -0.6, 95% credible interval -1.03 to -0.18). Both captopril (odds ratio 76.2, 95% credible interval 1.56 to 149.3) and enalapril (274.4, 2.4 to 512.9) were associated with a higher incidence of cough compared to placebo.Some important outcomes such as rehospitalization and cardiac death were not included. The sample size and the number of studies were limited, especially for ramipril.Our results suggest that enalapril might be the best option when considering factors such as increased ejection fraction, stroke volume, and decreased mean arterial pressure. However, enalapril was associated with the highest incidence of cough, gastrointestinal discomfort, and greater deterioration in renal function. Trandolapril ranked first in reducing systolic and diastolic blood pressure. Ramipril was associated with the lowest incidence of all-cause mortality. Lisinopril was the least effective in lowering systolic and diastolic blood pressure and was associated with the highest incidence of all-cause mortality.
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PMID:Comparison of the Efficacy and Safety of Different ACE Inhibitors in Patients With Chronic Heart Failure: A PRISMA-Compliant Network Meta-Analysis. 2687 74

The AKI in intensive care has been widely treated by international and national guidelines. The treatment of AKI in patients not requiring admission in Intensive Care Unit, but often hospitalized in Nephrology Unit, it is showed of less relevance. For over 5 years we have used for the treatment of AKI of patients admitted in Nephrology Unit an intermittent slow technique, implemented in approximately 600 patients with AKI for a total of about 3000 treatments. In this study we report the clinical results obtained in 100 consecutive patients referred to our Nephrology Unit from 1st January 2014. We excluded the patients with AKI and lactic acidosis by metformin, which were treated with CVVHDF. The Dialysis Protocol provides a slow low efficiency intermittent treatment called SLE-HDF (Sustained Low Efficiency Hemo-Dia-Filtration), with 10-hour duration, 1.5 L/h dialysate for a patient up to 75 kg, 2 L/h up to 85 kg, 2.5 L/h over 85 kg. Half of the dialysate was used in convention in post and half in diffusion. Endpoints were the recovery of renal function and the survival of the patient. On each patient was calculated on at least one seat, the Kt/V urea (UKt/V). Were studied 100 patients, 45 females and 55 males, with mean age 79.4 + 11 years. The weight was 74 kg + 18 kg at the start of treatment. The 65% of patients had diuresis < to 500 ml/24 hours. The causes of AKI were: 41% heart failure, 31 % AKI on MRC, 7% rhabdomyolysis, 6% Hepato-renal Syndrome, 4% sepsis, 11 % other causes. Major comorbidities were heart disease (63%), diabetes (50%), COPD (38%), age over 85 years, cancers 23, liver disease 16, hypotension requiring amine 15, sepsis 10. In total in the 100 patients, 512 treatments were performed, average 5.12 + 3.7. The mean UKt/V was 0.4 + 0.05 per session. The deaths were 43. Patients discharged were 57. Of these, 43 had a recovery of renal function. Fourteen patients have not recovered renal function and were admitted for chronic dialysis treatment. In conclusion, our protocol of SLE-HDF, which uses volumes of dialysate sharply lower than used in literature, has been shown to be effective in correcting the biochemical profile of the patient with AKI. The clinical results are considered satisfactory, having obtained the improvement in 57% of patients, considering that the 43 deaths, 10 were suffering from Hepato-cirrhosis and 13 from malignant neoplasm. Further studies are needed to confirm our findings.
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PMID:[The treatment of AKI in nephrology hospitalization: the SLE-HDF 15 litres in 10 hours]. 2870 Jan 86

Angiotensin-converting enzyme (ACE-I) inhibitors and ARBs have shown real efficacy in reducing blood pressure, proteinuria, in slowing the progression of chronic kidney disease (MRC) and in clinical improvement. in patients with heart failure, diabetes mellitus and ischemic heart disease. However, their use is limited by some side effects such as the increase in serum potassium (K), which can be particularly severe in patients with renal insufficiency. In the 23,000 patients followed by the PIRP project of the Emilia-Romagna Region, hyperkalaemia at the first visit (K> 5.5 mEq / L) was present in about 7% of all patients. The prevalence of K values> 5.5 mEq / L increased in relation to the CKD stage, reaching 11% in patients in stage 4 and 5. Among patients with values of K> 5.5 at baseline, 44.8% were in therapy with ACE-I / ARB inhibitors, 3.8% with anti-mineralcortoid and a further 3.9% concurrently taking SRAA-blocking agents and K-sparing diuretics. Counter-measures to avoid the onset of hyperkalemia during treatment with drugs that block the RAAS range from the low-K diet, to diuretics and finally to drugs that promote fecal elimination of K. Among these, polystyrene sulfonates, which have more than 50 years of life, exchange K with sodium or calcium. These drugs, however, in chronic use, can lead to sodium or calcium overload and cause dangerous intestinal necrosis. Recently two new highly promising drugs have been introduced on the market for the treatment of hyperkalemia, the patiromer and sodium zirconium cyclosilicate. The patiromer, which is a potassium-calcium exchanger, acts at the level of the colon where there is a higher concentration of K and where the drug is most ionized. Sodium zirconium cyclosilicate (ZS-9) is a resin with micropores of well-defined dimensions, placed in the crystalline structure of the zirconium silicate. The trapped K is exchanged with other protons and sodium. However, even these drugs will have to demonstrate their long-term efficacy and safety to be considered true partners of RAAS blockers in some categories of patients.
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PMID:[Hyperkalemia as a limiting factor in the use of drugs that block the Renin Angiotensin Aldosterone System (RAAS)]. 2978 83