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

Recent concepts about post-infarction left ventricular remodeling, which is the basis for heart failure in these patients, as well as its prevention by ACE inhibitors are briefly summarized. Those data were the rationale for the SAVE trial. The most important initial aspects of this trial (general objective, pre-specified endpoints, inclusion and exclusion criteria, etc.) are then described as well as the basal characteristics of the respective cohort. The most important results of the SAVE trial, now in press, are subsequently presented. Several clinical guidelines, derived from these results, are then suggested. Finally, some new questions, both clinical and pathophysiological, and originated by the results from the SAVE results, are commented.
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PMID:[The SAVE trial: rational basis, results, and reflections]. 147 63

The case of a 46-year-old patient who underwent orthotopic heart transplantation for treatment of end-stage heart failure as a result of ischemic heart disease is reported. Four months after transplantation a grade II rejection episode was complicated by ventricular fibrillation. Lidocaine and procainamide intravenously did not effectively prevent recurrence. An increase of antirejection therapy in combination with flecainide acetate effectively prevented further episodes of ventricular fibrillation. This case demonstrates that recurrent ventricular fibrillation can be a complication of acute rejection.
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PMID:Ventricular fibrillation during acute rejection after heart transplantation. 149 46

In a retrospective study we analyse two populations of aged patients in congestive heart failure, one treated with ACE inhibitors other not and the other with conventional therapy. Both populations received the same medication (diuretics and digitalis) and are equivalent in age, sex distribution, NYHA functional class and echocardiographic left ventricular parameters. Comparing the mortality of the two populations at the first, second and third year of follow-up, a statistically significant reduction in mortality was found on the ACE inhibitors treated population, at the first year. However, this reduction did not reach statistical significance at second and third years. The results are similar to trials in which the effects of ACE inhibitors are studied on general populations in heart failure.
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PMID:[Effect of converting enzyme inhibitors in cardiac insufficiency mortality in the elderly]. 150 88

The effects of flosequinan and enalapril on exercise capacity (bicycle exercise duration), quality-of-life symptomatology (visual analogue scales) and New York Heart Association (NYHA) grading, were compared in 61 patients with chronic heart failure (NYHA, grade III). Bicycle exercise duration improved similarly with flosequinan (+27%) and enalapril (+18%); in patients completing the study, flosequinan produced a significantly greater increase in exercise time at week 12, compared with enalapril (P = 0.02). Improvements in visual analogue scores relating to general health, energy and vitality, ability to perform physical activities and breathing performance, were equivalent for both drugs. Changes in NYHA classification showed that 27 (55%) of 49 patients completing the study had improved by at least one NYHA grade (15 (68%) patients on flosequinan; 12 (44%) on enalapril). The overall safety and tolerability of the two treatments was similar; 18 patients reported adverse effects while on flosequinan, compared with 19 patients on enalapril. Neither treatment was associated with any clinically important changes in haematological or biochemical variables, although some treatment-related effects were observed. This study confirms that flosequinan achieved similar efficacy to enalapril in the symptomatic relief of chronic heart failure. The effect of flosequinan on survival in chronic heart failure has not been tested; pending such studies, our data suggest that it may prove a useful alternative therapy in patients where ACE inhibitors are contraindicated or poorly tolerated.
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PMID:A double-blind, parallel-group comparison of flosequinan and enalapril in the treatment of chronic heart failure. 150 60

Fifty-six patients with a mean age of 58 years, 14 females and 42 males, all with dominant systolic heart failure (33 in functional class 3 and 4) were randomised to receive either added placebo or added enalapril to their heart failure medication. There were 13 patients in this group who had their trial drug switched after a certain period to allow direct but blind comparison between placebo and enalapril. Cardiac mortality with enalapril was 32 per cent compared to 48 per cent with placebo at intervals after initiating therapy of 20.0 +/- 19.4 versus 14.3 +/- 11.5 months respectively. When compared to a preceding control period, 80 per cent of the enalapril patients improved in contrast to 21 per cent of the placebo. However, when a comparison was made directly between enalapril and placebo, enalapril was better in 31 per cent and placebo was better in 8 per cent of the patients. It is concluded that in certain patients with systolic heart failure from non-valvular and non-hypertensive causes, enalapril is beneficial when added to the conventional treatment. An argument is also presented that to cost-effectively identify the group who will benefit, a short term ACE-I trial after the conventional antifailure therapy can be considered in all patients with systolic heart failure.
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PMID:Double-blind evaluation of enalapril in patients with systolic heart failure. 150 91

Electrolyte abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. Magnesium and potassium deficiencies play an important role in the development of cardiac arrhythmias. Magnesium is essential for the maintenance of intracellular potassium concentration. Although there are conflicting data regarding the prevalence of hypomagnesemia in patients with chronic heart failure (the values range from 7-37%), multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal controls. As magnesium and potassium are mainly intracellular ions, measurements in serum or plasma are of limited value to assess magnesium status. There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for mononuclear cells or erythrocytes or for myocardial and skeletal muscle. Loop diuretics (e.g. furosemide) are supposed to cause a substantial loss of both magnesium and potassium in the plasma and intracellular space. The potassium-sparing diuretics amiloride and triamterene are reported to also exert magnesium-sparing effects. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion. Low magnesium and potassium concentrations increase cardiac glycoside toxicity. In contrast, elevated levels of magnesium decrease the sensitivity of human myocardium to antiarrhythmogenic actions of cardiac glycosides, without affecting maximally developed tension. Moreover, magnesium increases binding affinity of cardiac glycosides to the receptor. The antiarrhythmic action of magnesium is suspected to be mediated by a reduced sensitivity to electrophysiological changes induced by Ca2+, thus indicating Ca2+ antagonistic properties of magnesium. Magnesium deficiency has also been implicated in sudden death, notably in patients with congestive heart failure. Therefore, when treating congestive heart failure, one must consider how to prevent depletion of electrolytes or how to replete potassium and magnesium in deficiency states.
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PMID:Heart failure and electrolyte disturbances. 150 35

A questionnaire on the treatment of congestive heart failure was distributed to physicians in the medical departments of five hospitals in the Oslo area. The 117 (81%) respondents selected first, second and third line therapy in the treatment of mild, moderate and severe heart failure. Diuretics and restrictions on sodium/water dominated as first line therapy for mild heart failure; less than 5% suggested ACE-inhibitors or digitalis. Some differences in priorities were revealed for moderate and severe heart failure. The majority again suggested diuretics and restrictions on sodium/water, but 20% preferred ACE-inhibitors, which were also stated as second or third line therapy by 60% of the physicians. Less than 50% chose digitalis or nitrates as one of the three first therapies.
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PMID:[Treatment of heart failure. A questionnaire among Norwegian hospital physicians]. 141 51

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congestive heart failure in elderly readmitted patients]. 152 7

Nitrate derivatives are venous vasodilators which are effective in reducing the symptoms of pulmonary congestion. The beneficial action on exercise capacity was recently demonstrated in the Veterans II Study in association with Hydralazine and has also been suggested by other trials. The reduction in mortality from cardiac failure was demonstrated in the Veterans I Study in association with Hydralazine compared to conventional digitalo-diuretic therapy but seems less important than that obtained by angiotensin converting enzyme inhibitors. The phenomenon of tolerance seems to be related to the use of high doses in continuous therapy and may be countered by discontinuous use of the drug during the 24 hour period. Tolerance seems to be related to neuro-hormonal factors and perhaps to depletion of SH groups. Simultaneous use of nitrates and ACE inhibitors seems to be an interesting therapeutic concept.
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PMID:[Nitrate derivatives and cardiac insufficiency]. 153 Apr 25

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.
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PMID:Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs. 153 67


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