[Magnesium and congestive heart failure--a clinical study of magnesium levels in patients with congestive heart failure].
Explore the source record for details and available documents.
Adolescent↗
SEARCH · PubMed Health
Results for “CONGESTIVE HEART FAILURE”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Molecular genetics of congestive heart failure.
The manifestation of congestive heart failure occurs secondary to a great variety of cardiac or systemic disorders that share a temporal or permanent loss of cardiac function. In order to enhance our knowledge about the genetics of heart failure it is mandatory to analyse the aetiologic factors of these underlying disorders separately. Monogenic forms of congestive heart failure have initially been described by observant physicians in consecutive generations of affected families. Molecular genetic analyses of these families subsequently allowed us to localise and identify some of the genes that cause hypertrophic, dilative, or restrictive cardiomyopathies, congenital heart disease, as well as a number of inborn errors of metabolism. However, the great majority of patients develops heart failure as a final consequence of multifactorial conditions such as hypertension, cardiac hypertrophy, or coronary artery disease. Each of these conditions may be the product of a complex equation that includes environmental and genetic factors. Indeed, some of these factors may be harmful, others protective and for most it takes decades before a phenotype will be clinically detectable. Given this complex scenario it was not unexpected that early studies on candidate genes came up with partially controversial information. This review aims to summarize and to comment on the principal findings of this work.
Animals↗
Management of elderly patients with congestive heart failure--design of the Trial of Intensified versus standard Medical therapy in Elderly patients with Congestive Heart Failure (TIME-CHF).
BACKGROUND: Little is known about the management of elderly patients with congestive heart failure (CHF) although they represent the majority of the CHF population. Therefore, the TIME-CHF study was set up (1) to evaluate the medical management of very old patients (> or = 75 years) with CHF compared with younger patients (60-74 years), (2) to compare an intensified with a standard treatment approach, and (3) to differentiate between systolic and diastolic dysfunction (ejection fraction < or = 45% vs > 45%). METHODS: In a prospective single-blinded multicenter trial, 824 symptomatic patients, CHF hospitalization within the last year and elevated NT-BNP, are randomized to an intensified versus a standard medical therapy. Treatment strategies follow the published guidelines with the aim to reduce symptoms to NYHA class < or = II (standard) or, additionally, NT-BNP levels below twice the upper limit of normal (intensified). The primary end points are 18-month hospitalization-free survival and quality of life. RESULTS: By the end of 2004, 297 patients have been included, 147 randomized to intensified and 150 to standard therapy. Mean age in the older age group was 82 +/- 4 years (n = 174) and 69 +/- 4 years in the younger group (n = 123), respectively. Ejection fraction was > 45% in 26% and 10%, respectively. Significant comorbidities were present in 93% of patients. CONCLUSION: TIME-CHF will be the first prospective randomized trial to comprehensively study the management of elderly patients with CHF. It will provide unique information comparing two treatment strategies in two age groups irrespective of ejection fraction regarding prognosis, quality of life, as well as resource utilization and costs.
Aged↗
The incidence and prevalence of congestive heart failure in Rochester, Minnesota.
Although congestive heart failure is a fairly common clinical syndrome and the societal costs associated with its care are high, relatively little is known about the incidence or prevalence of the condition in the community. Using the resources of the Rochester Epidemiology Project, we identified all 46 persons 0 through 74 years of age who had a new diagnosis of congestive heart failure during 1981 and all 113 persons with a prevalent diagnosis on Jan. 1, 1982, in the city of Rochester, Minnesota. After confirming the diagnosis in the medical record by using criteria similar to those in the Framingham study, we found the annual incidence of congestive heart failure to be 110 per 100,000 after adjusting for age. Incidence rates were higher among male than among female study subjects (157 versus 71 per 100,000). In both male and female subjects, the incidence generally increased with advancing age, reaching 1,618 per 100,000 and 981 per 100,000, respectively. Prevalence rates on Jan. 1, 1982, demonstrated similar patterns. Overall, the prevalence of congestive heart failure was higher among male than among female subjects (327 versus 214 per 100,000) and increased exponentially with advancing age, reaching almost 3% in both sexes. Survival after a diagnosis of congestive heart failure was extremely poor, with only 80% alive at 3 months and 66% at 1 year. These data underscore the effect of congestive heart failure in the community and provide estimates of the number of persons who might benefit from early intervention.
Adolescent↗
Clinical correlates of elevated plasma natriuretic peptides and Big endothelin-1 in a population of ambulatory patients with heart failure. A substudy of the Italian Network on Congestive Heart Failure (IN-CHF) registry. IN-CHF Investigators.
BACKGROUND: Activation of neuroendocrine factors plays a major role in the pathophysiology and progression of heart failure. The aim of the present study was 1) to assess the clinical correlates of elevated plasma natriuretic peptides [atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)] and Big endothelin-1 in a population of 180 ambulatory patients from the Italian registry of heart failure (Italian Network on Congestive Heart Failure, IN-CHF) in 22 clinical centers, 2) to assess the within-patient variability of plasma BNP concentration, and 3) to evaluate the analytical agreement for BNP determination between a core laboratory and local sites. METHODS: ANP and BNP were measured with specific immunoradiometric methods, Big endothelin-1 with an enzyme immunoassay. RESULTS: Elevated BNP was associated with severe mitral valve regurgitation (odds ratio 8.546, 95% confidence interval 1.879-38.510, p = 0.0052); high circulating concentrations of ANP and BNP were found in older patients, and in patients with higher NYHA functional class or reduced left ventricular ejection fraction. Elevated plasma concentration of Big endothelin-1 was a strong and independent predictor of atrial fibrillation (odds ratio 4.001, 95% confidence interval 1.531-10.454, p = 0.0047). Plasma concentration of BNP was reasonably stable at 3-month interval in patients with mild-to-moderate heart failure (mean between-visit difference -1.5+/-45 pg/ml, n = 96). There was a satisfactory analytical agreement between the central laboratory and sites, over a broad range of concentrations (2-1133 pg/ml, n = 283) with a slope for the best line fitted by linear regression of 1.09 (r2 = 0.96). CONCLUSIONS: BNP assay may become an appropriate tool for routine clinical practice in patients with congestive heart failure.
Aged↗
The neurohumoral axis in congestive heart failure.
The incidence of congestive heart failure is increasing in the United States. This common syndrome is characterized not only by impaired ventricular function but also by an increase in some endogenous vasoconstrictor substances, including norepinephrine, angiotensin II, and arginine vasopressin. Although activation of the systems that release these substances is presumed to be compensatory (to maintain perfusion pressure during inadequate flow), the sympathetic nervous system, renin-angiotensin-aldosterone system, and arginine vasopressin may contribute to the pathogenesis of the syndrome. The excessive vasoconstriction present in heart failure likely produces a further burden on the failing myocardium. New strategies in therapy are being developed to counteract the activation of vasoconstrictor forces in congestive heart failure. Data indicate that selective blockade of the renin-angiotensin system is useful. Preliminary data suggest that inhibition of the sympathetic nervous system may be helpful, and inhibition of vasopressin in animals with heart failure is being studied. New and more selective therapy for heart failure may come from these studies.
Animals↗
Congestive heart failure: meet the challenge.
Congestive heart failure is an increasingly common, complex disease process with far reaching consequences for patients and caregivers. Thorough knowledge of the pathophysiology, assessment, and management of congestive heart failure affords nurses the opportunity to improve patient functional status and quality of life.
Heart Failure↗
Rationale for the Atrial Fibrillation and Congestive Heart Failure (AF-CHF) trial.
Congestive heart failure and atrial fibrillation (AF) are two important and growing problems in medicine and cardiology. Both conditions often coexist and complicate each other's management. Two therapeutic strategies are available for patients with AF and congestive heart failure: the first aims at restoring and maintaining sinus rhythm, whereas the second focuses exclusively on optimizing ventricular rate. Prior studies of AF and congestive heart failure were not randomized and most were retrospective. Although some studies suggested that AF had no effect on survival, in most recent large congestive heart failure trials, AF was reported to be an independent risk factor for mortality or major morbidity. The primary objective of the Atrial Fibrillation in Congestive Heart Failure (AF-CHF) trial is to compare the two widely used treatment strategies with respect to cardiovascular mortality. AF-CHF is a prospective, multicenter trial that will randomize 1450 CHF patients with left ventricular ejection fraction (LVEF) < or =35% and a documented recent episode of atrial fibrillation to either a rhythm control or a rate control strategy. From recent trial data, we anticipate an 18.75% 2-year cardiovascular mortality in the rate control arm and a 25% event reduction in the rhythm control group. As of December 2003, 960 patients have been randomized. Enrollment is expected to be completed in September 2004 with a minimum follow-up of 2 years.
Atrial Fibrillation↗
Acute effects of digitalis and enalapril on the neurohormonal profile of chagasic patients with severe congestive heart failure.
Chagasic patients with congestive heart failure are usually treated with digitalis and converting enzyme inhibitors. According to the neurogenic and dysautonomic theories, chagasic patients would not benefit from these drugs. To clarify this controversial issue, we have studied patients with congestive heart failure and suspected Chagas' heart disease. All patients received intravenous methyl-digoxin for 24 h and oral enalapril for 96 h. Blood samples for plasma norepinephrine, aldosterone and renin were taken at baseline, after acute digitalization and following enalapril. Based on the serology for Chagas' disease, the patients were divided into non-chagasic and chagasic patients. In the chagasic group three patients were in functional class III and 3 were in functional class IV. In the non-chagasic group five patients were in functional class III and 2 were in functional class IV. Both groups had a marked and quantitatively similar degree of neurohormonal activation. All patients improved at least one functional class and lost more than 5 kg of body weight with treatment. The chagasic patients had a statistically significant reduction in plasma norepinephrine (2262 +/- 1407 to 865 +/- 390, P < 0.008, pg/ml, M +/- S.D.), plasma aldosterone (330 +/- 168 to 155 +/- 75, P < 0.01, pg/ml, M +/- S.D.) and plasma renin activity (14 +/- 13 to 2 +/- 1.6 ng/ml per h, M +/- S.D., P < 0.05), with digitalis. Following enalapril, norepinephrine and aldosterone there was a further but non-significant reduction, when compared to postdigitalis values. These results indicated that chagasic patients do benefit from digitalis and enalapril. Furthermore, the prominent and significant reduction in all three neurohormones suggest that the parasympathetic and sympathetic systems of these chagasic and non-chagasic patients, are responding to the neuromodulatory effects of digitalis and enalapril.
Aldosterone↗
Reversible renal failure after combined treatment with enalapril and frusemide in a patient with congestive heart failure.
A patient with congestive heart failure and moderate renal insufficiency developed severe reversible non-oliguric renal failure while on frusemide and enalapril. Renal failure developed when enalapril was given in the presence of pronounced sodium depletion. When positive sodium balance was restored the plasma creatinine concentration began to fall while angiotensin converting enzyme inhibition remained effective and blood pressure was stable. These observations suggest that the degree of sodium depletion plays an important role in the tendency for angiotensin converting enzyme inhibitors to induce renal failure in patients with congestive heart failure and moderate renal insufficiency. Restoration of a positive sodium balance promotes the recovery of renal function after the combined administration of angiotensin converting enzyme inhibitors and diuretics.
Acute Kidney Injury↗
Baroreflex regulation of regional blood flow in congestive heart failure.
In patients with congestive heart failure (CHF), the distribution of the cardiac output is altered. Cardiopulmonary and arterial baroreceptors normally can regulate regional blood flow, but their contribution in heart failure is not known. To examine the role of baroreceptors in the regulation of regional blood flow in CHF, the effect of lower body negative pressure (LBNP) on forearm, renal, and splanchnic blood flow was evaluated in 12 patients with heart failure. Incremental LBNP at -10 and -40 mmHg decreased central venous pressure but had not effect on systolic blood pressure or pulse pressure. Renal blood flow decreased from 505 +/- 63 to 468 +/- 66 ml/min during LBNP -10 mmHg (P less than 0.05) and to 376 +/- 74 ml/min during LBNP -40 mmHg (P less than 0.01). Splanchnic blood flow decreased from 564 +/- 76 to 480 +/- 62 ml/min during LBNP -10 mmHg (P less than 0.01) and to 303 +/- 45 ml/min during LBNP -40 mmHg (P less than 0.01). Forearm blood flow did not decrease during LBNP -10 mmHg or -40 mmHg. To determine whether the absence of limb vasoconstriction during LBNP was confined to abnormalities in the baroreflex arc or was secondary to impaired end-organ responsiveness, six patients with heart failure and six normal subjects received an intrabrachial artery infusion of phenylephrine. Phenylephrine increased forearm vascular resistance comparably in each group. These data demonstrate that baroreceptors can regulate splanchnic and renal but not limb vascular resistance in patients with congestive heart failure and may contribute to the redistribution of blood flow that occurs in this disorder.
Aged↗
Hemorrhagic ascites due to congestive heart failure.
Ascites due to congestive heart failure (CHF) is characteristically serous in gross appearance. Although hemorrhage into ascites commonly indicates a malignant or inflammatory cause, cirrhosis of the liver is a well known cause of bloody ascites. We report a case of hemorrhagic ascites due to biventricular congestive heart failure in which workup for other causes was negative and hemorrhage cleared after 4 months. In as much as the mechanism of ascites is similar in both cirrhosis and CHF, we propose that a similar mechanism could cause bleeding into ascites in CHF.
Aged↗
Hemodynamic responses to indoramin at rest and during exercise in congestive heart failure.
Twenty patients with congestive heart failure underwent hemodynamic studies before and over 10 hours after the administration of 25, 50, and 75 mg of indoramin, an alpha 1-adrenergic antagonist. Hemodynamic studies were repeated during exercise after the administration of the optimal dose of indoramin. The drug reduced resting and exercise pulmonary capillary wedge pressure, right atrial pressure, systemic blood pressure and vascular resistance, and pulmonary artery pressure and vascular resistance. Resting and exercise stroke volume and cardiac output rose in response to the fall in vascular resistances. Heart rate was not altered at rest or during exercise. The first dose of the alpha 1 blocker indoramin elicits a significant reduction in ventricular preload and afterload and augmentation of ventricular performance in patients with congestive heart failure.
Aged↗
New approaches to managing congestive heart failure.
The appreciation that congestive heart failure is not merely a disorder of myocardium has led to a substantial alteration in the treatment of this disease. The use of angiotensin-converting enzyme inhibitors is increasing as their well-demonstrated mortality and symptomatic benefits become better publicized and known. Although diuretics and digoxin continue to remain standard additions to angiotensin-converting enzyme inhibitors for the therapy of congestive heart failure, investigations of these and other agents continue. For example, acceptance of beta-blockade as a potentially beneficial therapeutic intervention increased in the past year with the publication of the Cardiac Insufficiency Bisoprolol Study (CIBIS), the largest controlled trial to date. Similarly, survival studies of vasodilators and positive inotropic agents such as vesnarinone are ongoing. Even the effects of exercise in severely ill patients (who were previously advised to be sedentary) are being studied. With the understanding that heart failure is a systemic disease and that controlled trials are needed because many of our assumptions prove to be incorrect, we can expect continued improvement in the management of heart failure.
Heart Failure↗
Effects of red rest and prazosin in congestive heart failure.
Twelve patients with congestive heart failure were monitored with invasive and noninvasive techniques to evaluate the effect of vasodilator treatment. During the 18 hours of strict bed rest before administration of prazosin, the hemodynamics improved substantially while only small and transient heModynamic changes were observed after introduction of prazosin. At 6 weeks' control the effect of vasodilator treatment with prazosin, 3 mg x 4, was lost. The beneficial results often credited to vasodilators in studies on congestive heart failure might in part be due to the concomitant bed rest introduced during the monitoring of the patients.
Adult↗
Metabolic and cardiovascular benefits deriving from beta-adrenergic blockade in chronic congestive heart failure.
Ten patients with congestive heart failure were given metoprolol (50 mg/day) or placebo during a double-blind, crossover, randomized study. After a run-in period of 4 weeks, metoprolol and placebo were administered over a period of 3 months, which was separated by a washout period of 4 weeks. At the end of the run-in, metoprolol, and placebo periods, all patients underwent metabolic (oral glucose tolerance and hyperinsulinemic glucose clamp tests) and noninvasive cardiologic (New York Heart Association classification, bimodal echocardiographic left ventricular end-diastolic determination, maximal oxygen consumption, left ventricular radionuclide ejection fraction) tests. Our results show that beta-adrenergic blockade significantly enhances insulin-mediated suppression of hepatic glucose output (p less than 0.005) and increase in glucose uptake (p less than 0.01) with a concurrent improvement in New York Heart Association functional class (p less than 0.05) and the multistage exercise treadmill test score (p less than 0.05). After administration of metoprolol all changes in glucose turnover parameters were found to correlate with the decrease in basal plasma free fatty acid levels. In conclusion, our findings confirm the beneficial cardiologic effects of beta-adrenergic blockade in congestive heart failure and demonstrate that metoprolol is also useful for reversing the metabolic damage caused by exaggerated plasma norepinephrine levels.
Aged↗
Medical management of congestive heart failure.
The syndrome of congestive heart failure can result from a variety of cardiac disorders of which left ventricular dysfunction is the most common. The clinical presentation is determined by the interaction between cardiac dysfunction and a series of compensatory mechanisms that are activated throughout the body. Therapy for this disorder is best approached through an understanding of this complex relationship and an appreciation for the influence of preload, afterload, and contractility on cardiac performance. Recent important advances in therapy include the use of combined diuretic therapy, a better understanding of the value of the digitalis glycosides, and evidence that angiotensin-converting enzyme (ACE) inhibitors can relieve symptoms and prolong life. More intensive therapy earlier in the course of congestive heart failure appears to have some clinical benefit. The use of ACE inhibitors during this phase may delay progression of the underlying left ventricular dysfunction. Future therapy will be influenced by the results of ongoing trials that are testing both new agents and expanded indications for drugs that are currently available.
Cardiac Output↗
Effects of exercise training in patients with congestive heart failure: a critical review.
Congestive heart failure is a potentially debilitating disorder that affects a significant number of patients. The age-adjusted death rate has doubled over the past decade. Patients live an average of 4 to 5 years, and nearly all suffer from fatigue and breathlessness, which limits exercise capacity and produces a poor quality of life. Patients have usually been advised to avoid exercise because of concerns that they would experience a further decline in cardiac function. However, it has been demonstrated that exercise capacity is not related to the degree of left ventricular systolic dysfunction. This has led to the suggestion that peripheral changes in skeletal muscle and blood supply may play a major role in determining the exercise capacity of patients with congestive heart failure. Studies have demonstrated abnormalities of skeletal muscle blood flow, metabolism and structure, all of which are consistent with the impaired performance observed in these patients. Although the effects of exercise training have been examined in only a relatively few number of patients, the results have been promising. Exercise training has been found to improve exercise capacity and reduce symptoms. However, to our knowledge no data exist as to the impact of exercise training on left ventricular function, hospital stay or mortality in this population. Even though the early results are promising, they require confirmation of feasibility, clinical benefit and safety in larger, long-term randomized trials. It should be determined whether training has a long-term beneficial impact on measures more closely related to daily activities and quality of life. Ultimately, it would be important to determine whether training has an impact on mortality and morbidity.
Clinical Trials as Topic↗