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

The authors present the Minnesota Heart Failure Criteria (MHFC), derived using latent class analysis from widely available items in the Framingham Criteria. The authors used 1995 and 2000 data on hospitalized Minnesota Heart Survey subjects discharged after myocardial infarction or heart failure (N = 7,379). Selected Framingham Criteria variables (dyspnea, pulmonary rales, cardiomegaly, interstitial or pulmonary edema on chest radiograph, S(3) heart sound, tachycardia) plus left ventricular ejection fraction were used. The discriminatory power of the MHFC was evaluated using age- and sex-adjusted 2-year mortality. A five-class latent class analysis model was collapsed into cases and noncases. Mortality estimates discriminated noncases (18%) from cases (43%) (p < 0.001). The MHFC performed better than previous truncated criteria (Framingham Criteria: 26% noncases, 43% cases; Duke Criteria: 29%, 40%; Killip Score: 31%, 44%; Boston Score: 28%, 45%). In a subset of patients admitted for heart failure (n = 5,128), the MHFC identified all but 2% (116/4,746) of cases found with a nearly full version of the Framingham Criteria. In terms of prognostic value, the MHFC are as precise as or more precise than several previous sets of truncated criteria. They closely approximate a nearly full version of the Framingham Criteria but require many fewer variables and can facilitate epidemiologic case-finding for heart failure.
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PMID:Prognostic value of a novel classification scheme for heart failure: the Minnesota Heart Failure Criteria. 1670 56

Activation of the renin-angiotensin system (RAS), with ensuing aldosterone excess, detrimentally affects outcome in patients with hypertension and heart failure (HF). RAS blockade with angiotensin (Ang) 1-converting enzyme inhibitors (ACEIs) or Ang II type 1 receptor blockers (ARBs) is beneficial in such conditions. However, aldosterone secretion can persist despite these treatments. Hence, mechanisms besides Ang II acquire the role of aldosterone secretagogue. The RALES and EPHESUS studies have shown that this aldosterone "escape" or "breakthrough" is an important factor, because it is a determinant of outcome in HF patients. Endothelin (ET)-1, which stimulates aldosterone secretion via both A (ETA) and B (ETB) receptor subtypes, and which is increased in HF, is a candidate for the "aldosterone breakthrough." Moreover, the novel ET peptide ET-1(1-31) is involved in adrenocortical growth. Therefore, findings suggesting a role for the ET-1 system as an aldosterone secretagogue, along with the potential usefulness of endothelin antagonists for the prevention of "aldosterone breakthrough," are discussed.
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PMID:Aldosterone breakthrough during RAS blockade: a role for endothelins and their antagonists? 1714 26

OBJECTIVES.: We sought to study the incidence and clinical correlates of elevated filling pressures in ST-elevation myocardial infarction (STEMI) patients, without physical signs of heart failure and treated with primary coronary angioplasty. BACKGROUND.: Haemodynamic data, as measured with a Swan-Ganz catheter, are not routinely obtained in STEMI patients. At admission, low blood pressure, increased heart rate, sweating, increased respiration rate, rales, oedema, and a third heart sound are indicative of heart failure. METHODS.: All consecutive STEMI patients were monitored by a Swan-Ganz catheter and central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), pulmonary artery pressure (PAS) and cardiac index (CI) were measured. To investigate the clinical correlates of the haemodynamic status patients were classified according to previously defined haemodynamic criteria. RESULTS.: We studied 90 patients, aged 60.5+/-13.1 year, 76% were male. Mortality at 30 days was 2/90 (2.2%). Patients with impaired haemodynamics presented later and had larger myocardial infarct sizes. CVP, PCWP and PAS were above normal in 36 (40%) patients. CONCLUSION.: A large proportion of STEMI patients without physical signs of heart failure have elevation of right- as well as left-sided cardiac filling pressures. (Neth Heart J 2007;15:95-9.).
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PMID:Haemodynamic patterns in ST-elevation myocardial infarction: incidence and correlates of elevated filling pressures. 1761 67

Mineralocorticoid signaling pathway plays a pivotal role in cardiovascular physiopathology. Evidences from clinical and experimental studies have linked mineralocorticoid hormones with cardiovascular morbiditiy and mortality. Thus, antagonist of the mineralocorticoid receptor (AMR) has reappeared. In addition, a novel mineralocorticoid receptor antagonist has been developped, named eplerenone, which lack the side effect of former ARMs as gynecomastia. Based on two studies named RALES et EPHESUS, guidelines of the european and american societies of cardiology recommend the use of ARMs as a treatment for cardiac failure NYHA III and IV, and post-infarct cardiac failure (ejection fraction < 40%).
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PMID:[Aldosterone receptor antagonists]. 1764 55

In a 94-year-old male with a history of atrial fibrillation, aortic stenosis, heart failure, apical thrombus, arterial hypertension, aneurysm of the abdominal aorta, and a urinary bladder carcinoma, cardiologic investigations revealed pulmonary rales, enlarged heart, absolute arrhythmia, and positive troponin-, myocardial thickening, enlarged cardiac cavities, hypocontractility, aortic stenosis, slight aortic insufficiency, severe mitral insufficiency, and surprisingly left ventricular hypertrabeculation. Upon neurological investigations, a polyneuropathy was suspected but a myopathy not completely excluded. The presented case shows that LVHT occurs also in nonagenarians and is associated with neuromuscular disease and positive troponin-T, in the absence of ischemic heart disease or severe renal failure. The cause of troponin-T-positivity remains multi-factorial.
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PMID:Noncompaction and neuromuscular disease with positive troponin-T in a nonagenerian. 1792 84

Acute decompensated heart failure (ADHF) has emerged as a major healthcare problem. It causes approximately 3% of all hospitalizations in the United States, with the direct medical cost of these hospitalizations estimated at $18.8 billion per year. Early recognition, risk stratification, and evidence-based treatment are crucial in reducing the morbidity, mortality, and costs associated with this disorder. Classic signs and symptoms of ADHF, such as rales, dyspnea, and peripheral edema, may be absent at hospital presentation and, even when present, are not specific to this disorder. As a result, serum B-type natriuretic peptide level is now used to rapidly and accurately detect ADHF. Multivariate analyses have identified renal dysfunction, hypotension, advanced age, hyponatremia, and comorbidities as significant and independent mortality risk factors. Based on these factors, mortality risk can be stratified from very low to very high using published algorithms that have been validated in independent populations. Evidence-based guidelines for the treatment of ADHF are available from both the European Society of Cardiology and the Heart Failure Society of America. In general, an intravenous loop diuretic, either alone or in combination with a vasodilator, is recommended as initial therapy in patients with volume overload, depending on the patient's clinical status. Use of inotropic agents should be limited to the small subset of patients with low-output syndrome and significant hypotension. In any event, frequent monitoring of clinical response is essential, with subsequent therapy determined by this response. Finally, focused patient education during hospitalization may help reduce readmissions for ADHF.
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PMID:Hospitalized patients with acute decompensated heart failure: recognition, risk stratification, and treatment review. 1908 91

The cardiovascular and cardiorenal disease continuum comprises the transition from cardiovascular risk factors to endothelial dysfunction and atherosclerosis, to clinical complications such as myocardial infarction (MI) and stroke, to the development of persistent target-organ damage and, ultimately, to chronic congestive heart failure (CHF), end-stage renal disease or premature death. The renin-angiotensin-aldosterone system (RAAS) is involved in all steps along this pathway, and RAAS blockade with ACE inhibitors or angiotensin AT(1)-receptor antagonists (angiotensin receptor blockers; ARBs) has turned out to be beneficial for patient outcomes throughout the disease continuum. Both ACE inhibitors and ARBs can prevent or reverse endothelial dysfunction and atherosclerosis, thereby reducing the risk of cardiovascular events. These drugs have further been shown to reduce end-organ damage in the heart, kidneys and brain. Aldosterone antagonists such as spironolactone and eplerenone are increasingly recognized as a third class of RAAS inhibitor with potent risk-reducing properties, especially but not solely with respect to the inhibition of cardiac remodelling and the possible prevention of heart failure. In secondary prevention, head-to-head comparisons of ACE inhibitors and ARBs, such as the recent ONTARGET study, provided evidence that, in addition to better tolerability, ARBs are non-inferior to ACE inhibitors in the prevention of clinical endpoints such as MI and stroke in cardiovascular high-risk patients. However, the combination of both ramipril and telmisartan at the maximally tolerated dosage achieved no further benefits and was associated with more adverse events such as symptomatic hypotension and renal dysfunction. In acute MI complicated by heart failure, the VALIANT trial has shown similar effects of ACE inhibition with captopril and ARB treatment with valsartan, but dual RAAS blockade did not further reduce events. In CHF, meta-analyses of RESOLVD, ValHeFT and CHARM-ADDED have shown that combined RAAS inhibition with an ACE inhibitor and ARB significantly reduced the morbidity endpoint in certain patient subgroups compared with standard therapy. However, in clinical practice, dual RAAS blockade is rarely employed, as seen, for instance, in the CORONA trial. The RALES and EPHESUS trials, investigating the effects of aldosterone blockade on cardiovascular outcomes in CHF patients, revealed that the addition of an aldosterone antagonist to standard heart failure therapy conferred powerful relative risk reductions for both morbidity and mortality. Future studies will elucidate whether this also holds true for patients who are asymptomatic or who have heart failure with preserved ejection fraction. In selected patients with renal disease, several studies have suggested that combined RAAS blockade brings about additional renoprotective antiproteinuric effects independent of blood pressure reduction, and large trials with robust endpoints are underway. In summary, combined therapy with several RAAS inhibitors is not recommended for all patients along the cardiorenovascular continuum. Patients with CHF with incomplete neuroendocrine blockade, as indicated, for example, by repetitive cardiac decompensation or refractory symptoms, might benefit from dual therapy as long as safety issues are well controlled. Finally, novel pharmacological agents such as the direct renin inhibitor aliskiren may provide additional therapeutic tools, but their role has yet to be established.
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PMID:Optimal antagonism of the Renin-Angiotensin-aldosterone system: do we need dual or triple therapy? 2056 30

Two clinical trials will be reviewed, RALES(1) and ILLUMINATE.(2) In RALES, low-dose spironolactone in addition to standard of care, produced a 30% improvement in survival in progressive heart failure, commonly assumed to reflect deleterious effects of aldosterone, with spironolactone competing with aldosterone for cardiac mineralocorticoid receptors. Recent evidence, however, points to cortisol rather than aldosterone as the hormone activating cardiac mineralocorticoid receptors, under conditions of tissue damage, and spironolactone as acting by mechanisms other than receptor blockade. ILLUMINATE compared the effects of torcetrapib, a cholesterol ester transport protein inhibitor, in combination with atorvastatin vs. atorvastatin alone, and was terminated after excess mortality was found in the torcetrapib arm. Subjects receiving torcetrapib showed effects consistent with increased aldosterone secretion, subsequently confirmed on patient samples and in vitro. In animal experiments, the pressor effect of torcetrapib was abolished by adrenalectomy but not by administration of trilostane, an inhibitor of aldosterone secretion. Although aldosterone (and probably cortisol) excess is involved in the off-target effects of torcetrapib, they may also involve secretion of endogenous oubain from the adrenal glomerulosa. This possibility may explain the enigma of aldosterone being homeostatic in chronic sodium deficiency, but deleterious in the presence of inappropriate sodium levels.
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PMID:Aldosterone, hypertension and heart failure: insights from clinical trials. 2063 15

Aldosterone is present and active all along the cardiovascular continuum. Excessive tissue production occurs in cardiovascular diseases including myocardial infarction (MI) and heart failure, resulting in a multitude of adverse effects in the cardiovascular system necessitating pharmacologic blockade of this neurohormone. Both human and animal studies have consistently proven the beneficial effects of antialdosteronics in the improvement of: 1) endothelial function, 2) modulation of inflammatory mechanisms between blood and the vascular wall and 3) reduction of tissue proliferation and cardiovascular remodeling leading to different severities of cardiovascular damage. These basic mechanisms of anti-aldosterone therapy strongly support the promising data observed in major clinical trials with aldosterone blockers in cardiovascular diseases, specially in heart failure patients. Whereas aldosterone receptor blockers were initially viewed as potassium-sparing diuretics there has been a clear change of concept in the past 10 years, mainly following the positive results of RALES with spironolactone in chronic heart failure, followed by EPHESUS using eplerenone in patients with systolic dysfunction post MI. The significant positive results in both studies were a clear support for the inclusion of this pharmacologic intervention as first line treatment in most international guidelines for the management of heart failure. More recent and ongoing studies are exploring the usefulness of this type of intervention in preventing vascular and myocardial hypertrophy and remodeling in refractory hypertensive and some hyperfibrotic syndromes. There are also provocative studies investigating in the possibility of inhibiting atherosclerosis. More recently, some studies are suggesting the benefit of aldosterone blockade in sleep apnea. In addition, two large multicentric trials, TOPCAT and EMPHASIS are analyzing the potential use of antialdosteronics in patients with cardiac insufficiency and preserved systolic function and the possibility of extending their indication in systolic heart failure to Phase II respectively. New compounds, blocking the synthesis of aldosterone instead of blocking its receptor are being developed, and initial Phase 2 studies are positive. All of the above results are very interesting, show an optimistic future and are consolidating and enlarging the spectrum of aldosterone blockade in cardiovascular disorders every day.
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PMID:Aldosterone inhibition and cardiovascular protection: more important than it once appeared. 2067 26

The clinical efficacy of aldosterone inhibition in heart failure was proved in two important clinical trials, RALES and EPHESUS, which demonstrated a reduction in mortality with aldosterone receptor blocker therapy in patients with severe and post-MI heart failure.The echocardiographic study AREA IN-CHF evaluated, for the first time, the effectiveness of aldosterone receptor blocker therapy in patients with mild to moderate heart failure (NYHA class II). The AREA IN-CHF rationale and results can be considered the pathophysiological background of the survival study EMPHASIS-HF conducted in a similar population of patients. On May 27, 2010 it was announced the earlier discontinuation of the recruitment to the EMPHASIS-HF that had an estimated end date around October 2011. Discontinuation is related to the excess of benefit in reducing risk of cardiovascular death or hospitalization for heart failure, obtained by antialdosteronic therapy.
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PMID:[Antialdosteronic therapy in mild chronic heart failure: from AREA IN-CHF to EMPHASIS-HF]. 2113 77


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