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

Heart failure is a frequent human disease, partly related to anomalous activation of the defense systems, following a cardiovascular aggression. Increases in the prevalence of heart failure have been observed in the so-called occidental culture countries, probably due to the increased prevalence of cardiovascular risk factors, ageing population, and heart failure patients' survival. During the last two decades, intensive investigation in the human and non-human set have contributed to better knowledge of the patophysiology, the prevention and the therapeutic approach of heart failure. The Authors reviewed on some aspects of the neurohumoral activation in heart failure, with therapeutic implications.
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PMID:[Heart failure: neurohumoral approach to treatment]. 1130 12

Patients with insulin resistance or type 2 diabetes have a particularly high risk for heart failure and a poor prognosis once they develop heart failure. The choice of drugs for the management of heart failure in these patients should be directed at changing the natural history of the disease. The various drugs available for the treatment of heart failure, including ACE inhibitors and beta-adrenergic blockers, are known to be beneficial and should be given as first-line agents. Aggressive risk-factor modification and tight blood pressure and glycemic control are crucial. Much work is needed to establish the safety and efficacy of various oral antidiabetic agents, especially the TZDs, for which the theoretic benefits are substantial and overall morbidity and mortality impact remain ill-defined.
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PMID:Cardiomyopathy and heart failure in diabetes. 1172 99

Children with chronic cyanotic heart disease often develop systemic-to-pulmonary artery collateral vessels that can be deleterious at the time of a Fontan procedure because of excessive pulmonary blood flow with resultant ventricular volume overload. We therefore occlude all significant collateral arteries during preoperative cardiac catheterization. From June 1993 to September 2001, 137 children ranging from 1.5 to 18.3 years old (median, 2.4 years), underwent a fenestrated lateral tunnel Fontan procedure. Of these, 130 (95%) had a previous bidirectional Glenn anastomosis, including 43 (31%) with a Norwood procedure. Preoperatively, 52 children (38%) required occlusion of collateral vessels. Two of five perioperative deaths (operative survival, 96%) resulted from excessive pulmonary blood flow; one from unrecognized collateral arteries and one from uncontrollable collateral arteries. Postoperatively, 29 children (22%) required coil occlusion of collateral vessels for elevated pulmonary artery pressures, heart failure, or prolonged chest tube drainage. At follow-up of 1.5 months to 8.3 years (mean, 4.1 years), there have been four late deaths (two from pneumonia, two secondary to heart failure); nine patients underwent cardiac transplantation for refractory heart failure. Ten of 11 patients with ventricular failure required occlusion of significant collateral vessels postoperatively. Hemodynamically significant collateral arteries are common in Fontan candidates. Aggressive control can result in good early and medium-term survival. After the Fontan operation, the presence of significant collateral vessels may be a marker for eventual cardiac failure; 11 of the 29 patients who required postoperative coil placement went on to transplantation or died of heart failure.
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PMID:Management of aortopulmonary collateral arteries in Fontan patients: occlusion improves clinical outcome. 1199 64

From May 1998 to April 2000, we performed partial left ventriculectomy (PLV) in 3 pediatric patients with dilated cardiomyopathy (DCM). At the time of the surgery, their age ranged from eight months to three years. The first patient eventually had to receive a heart transplant, but all patients treated with PLV are alive to this day. Patient #1 was diagnosed with DCM at the age of five months, PLV was done on a semi-urgent basis at the age of eight months, when medium dose IV catecholamine therapy and mechanical ventilation were required. Fraction shortening (FS) as shown by echocardiography increased postoperatively from 8% to 15% along with marked clinical improvement. Her heart failure deteriorated three months after the surgery, and received a heart transplant in the United States when she was one year and two months old. Patient #2 developed severe heart failure two months after correction of a ventricular septal defect. Aggressive medical therapy failed to improve his condition, therefore PLV was done on an elective basis at the age of three years and five months. [The patient was initially hospitalized and underwent low dose catecholamine.] Postoperative course was well. The ventriculography one year after surgery showed an improvement of the left ventricular FS from 12% to 27% after PLV. He was still doing well at his most recent check up. Patient #3 was diagnosed with DCM as a neonate. PLV was done on an elective basis at the age of two years and five months. Her postoperative course was generally well. FS on echocardiography increased postoperatively from 10% to 25% along with marked clinical improvement. The timing of performing PLV is the most essential factor for postoperative course in our experiences. We consider that the best timing is when aggressive catecholamine infusion or mechanical ventilation is required. The mid-term outcome of PLV of pediatric patients is considered to be acceptable. We believe that PLV should be considered as a viable option for severe DCM patients.
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PMID:Mid-term outcome after partial left ventriculectomy in pediatric patients. 1239 1

Aggressive treatment of hypertension is effective in reducing both microvascular and macrovascular complications in type 2 diabetes, and target BP less than 130/85 or 130/80 mmHg are now recommended. Inhibition of renin angiotensin aldosterone system (RAAS) plays an essential role in the treatment of hypertension and diabetes-related complications. Studies focusing on renal end-points suggest that angiotensin-converting enzyme inhibitors (ACE-I) are more effective than other traditional agents in reducing the onset of clinical proteinuria in both type 1 and type 2 diabetic patients with incipient nephropathy, mainly in normotensive ones (secondary prevention). However, several small trials in type 2 diabetic patients with overt nephropathy (tertiary prevention) failed to demonstrate a specific renoprotective role for ACE-I, at variance with type 1 diabetes. Three recent large trials address the question of whether angiotensin II receptor blockers (ARB) prevent the development of clinical proteinuria or delay the progression of nephropathy in type 2 diabetes. The IRMA study showed that irbesartan is more effective than conventional therapy in preventing the development of clinical proteinuria and in favoring the regression to normoalbuminuria for comparable BP control in patients with incipient nephropathy. The IDNT and RENAAL trials showed that ARB are more effective than traditional antihypertensive therapies in reducing progression toward end-stage renal failure (ESRF) in type 2 diabetic patients with overt nephropathy independently of changes in BP. Moreover, a reduction in hospitalizations for heart failure was demonstrated for ARB-treated patients compared with placebo. Furthermore, the LIFE study showed that losartan is more effective than conventional therapy in reducing cardiovascular morbidity and mortality in a cohort of diabetic patients with hypertension and left ventricular hypertrophy. In conclusion, ARB seem to be effective in both preventing renal damage and reducing progression toward ESRF in type 2 diabetic patients. Thus, the guidelines for the prevention and treatment of diabetic nephropathy are now changed. In type 1 diabetes ACE-I are the first-choice drug; in type 2 diabetes, ARB are considered first-choice drugs in secondary prevention as well as ACE-I and have been now elected the unique first-choice drug in tertiary prevention of ESRF. Finally, ARB should be considered as the first-choice drug in cardiovascular prevention too, as well as ACE-I.
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PMID:Renal and cardiovascular protection in type 2 diabetes mellitus: angiotensin II receptor blockers. 1246 18

Autonomic functions, such as increased sympathetic and parasympathetic activity and the brain's suprachiasmatic nucleus, higher nervous centres, depression, hostility and aggression appear to be important determinants of heart rate variability (HRV), which is, itself, an important risk factor of myocardial infarction, arrhythmias, sudden death, heart failure and atherosclerosis. The circadian rhythm of these complications with an increased occurrence in the second quarter of the day may be due to autonomic dysfunction as well as to the presence of excitatory brain and heart tissues. While increased sympathetic activity is associated with increased levels of cortisol, catecholamines, serotonin, renin, aldosterone, angiotensin and free radicals; increased parasympathetic activity may be associated with greater levels of acetylecholine, dopamine, nitric oxide, endorphins, coenzyme Q10, antioxidants and other protective factors. Recent studies indicate that hyperglycemia, diabetes, hyperlipidemia, ambient pollution, insulin resistance and mental stress can increase the risk of low HRV. These risk factors, which are known to favour cardiovascular disease, seem to act by decreasing HRV. There is evidence that regular fasting may modulate HRV and other risk factors of heart attack. While exercise is known to decrease HRV, exercise training may not have any adverse effect on HRV. In a recent study among 202 patients with acute myocardial infarction (AMI), the incidence of onset of chest pain was highest in the second quarter of the day (41.0%), mainly between 4.0-8.0 AM, followed by the fourth quarter, usually after large meals (28.2%). Emotion was the second most common trigger (43.5%). Cold weather was a predisposing factor in 29.2% and hot temperature (> 40 degrees celsius) was common in 24.7% of the patients. Dietary n-3 fatty acids and coenzyme Q10 have been found to prevent the increased circadian occurrence of cardiac events in our randomized controlled trials, possibly by increasing HRV. We have also found that n-3 fatty acids plus CoQ can decrease TNF-alpha and IL-6 in AMI which are pro-inflammatory agents. There is evidence that dietary n-3 fatty acids canenhance hippocampal acetylecholine levels, which may be protective. Similarly, the stimulation of the vagus nerve may inhibit TNF synthesis in the liver and acetylecholine, the principal vagal neurotransmitter, significantly attenuates the release of pro-inflammatory cytokines TNF-alpha, interleukin 1,6 and 18, but not the anti-inflammatory cytokine IL-10 in experiments. Therefore, any agent which can enhance brain acetylecholine levels, may be used as a therapeutic agent in protecting the suprachiasmatic nucleus, higher nervous centres, vagal activity and sympathetic nerve activity which are known to regulate the body clock and HRV and the risk of SCD and heart attack.
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PMID:Brain-heart connection and the risk of heart attack. 1265 78

More than one third of all Americans have high or high-normal blood pressure and are at risk for stroke, cardiovascular disease, kidney disease, and heart failure. Many of these are not diagnosed or are inadequately treated. The large number of untreated individuals at risk for the complications of hypertension, or who have not achieved goal pressures on therapy, require a concerted effort by health care professionals to screen and treat this condition. Aggressive identification and treatment of even high-normal hypertension can reduce adverse outcomes. The importance of aggressive management is outlined in this article.
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PMID:Aggressive blood pressure management. 1268 May 69

Cardiovascular disease (CVD) is an enormous health care burden in the United States (US) and is responsible for approximately 40% of all US deaths annually. Heart failure (HF) represents the final stage of the continuum of CVD and is increasing in incidence. Between 1970 and 2000, hospital discharges for HF in the US increased 145%. This trend appears to be related to rising life expectancy and the aging of the population. Once HF develops, the long-term prognosis continues to be dismal.Hypertension is a major risk factor for CVD and the most common risk factor for the development of HF. The results of clinical trials such as the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) have helped to clarify the importance of optimizing antihypertensive therapy to reduce CVD risks and development of HF. The trial also confirmed the need for multiple antihypertensive medications to reach recommended blood pressure (BP) goals in most patients. Aggressive lowering of BP is critical to help reduce the risk of CVD and help prevent the development of HF.
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PMID:The burden of cardiovascular disease: following the link from hypertension to myocardial infarction and heart failure. 1451 95

With increasing cardiac dysfunction, a complex neurohormonal response results in increasing circulating levels of an array of plasma hormones. Increments in plasma levels of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) and their amino-terminal congeners are more closely related to cardiac structure and function and to cardiovascular prognosis than changes in other plasma neurohormones. Reports suggest that changes in plasma BNP levels in the course of treatment of acutely decompensated heart failure provide a more powerful prognostic indicator of the likelihood of survival or recurrent decompensation than symptomatic assessment. This observation requires a randomised controlled trial in which changes in peptide levels determine aggression and duration of in-patient therapy in order to establish whether this indicator can improve results from management of acute in-patient heart failure. Plasma BNP or NT-proBNP is a powerful independent predictor of mortality and morbidity in long-term follow-up of heart failure cohorts. In addition, it appears likely to be a good predictor of beneficial response to the addition of beta blockade to anti-heart failure pharmacotherapy. Finally, adjustment of therapy for heart failure according to serial measurements of NT-proBNP promises to improve outcomes in comparison with adjusting therapy according to unassisted clinical acumen.
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PMID:NT-proBNP in heart failure: therapy decisions and monitoring. 1498 87

Pharmacologic therapy of heart failure appears to have reached its zenith. Few new agents are likely to replace conventional therapy. It is time for a paradigm shift in heart failure management. Aggressive surgical strategies to remodel the failing ventricle will shape heart failure therapy in the decade ahead. The articles that follow will describe in detail the advances that have been made in "crossing the boundary" to surgical treatment of advanced heart failure.
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PMID:Management of heart failure: crossing boundary over to the surgical country. 1505 80


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