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

In the mid 1990s, various organizations published guidelines for the management of chronic heart failure. Subsequent advances in pharmacologic treatment, however, warranted the release of recommendations that accounted for the new developments. Hence the publication in 1999 of the "Consensus recommendations for the management of chronic heart failure." Although there are measures patients can take to help prevent development of heart failure, the recommendations focus primarily on pharmacologic treatment of left ventricular systolic dysfunction. The discussion includes examination of the role of diuretics, ACE inhibitors, beta blockers, cardiac glycosides, as well as alternate agents such as angiotensin II receptor blockers. All of these agents can be used to help achieve a key management goal: decrease disease progression and thereby decrease the risk of hospitalization and death.
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PMID:Chronic heart failure. Examining consensus recommendations for patient management. 1113 54

Clinical and basic science research has repeatedly confirmed the importance of the renin-angiotensin-aldosterone system in the pathophysiology of chronic heart failure. Accordingly, blockade of this system by angiotensin-converting enzyme (ACE) inhibitors has assumed a central role in the treatment of heart failure. Recently, angiotensin II receptor blockers (ARBs) have gained prominence as a possible substitute for ACE inhibitors in therapy for heart failure. However, clinical data compiled on this use of ARBs have shown them to be useful only as alternative therapy in ACE inhibitor-intolerant patients. Continuing large-scale clinical investigations may lead to an expansion of their role in therapy for various cardiovascular diseases.
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PMID:The role of angiotensin receptor blockers in the management of chronic heart failure. 1123 98

The management of heart failure has evolved in parallel with advances in the understanding of the disease process. Inotropes and diuretics are used to combat pump failure and fluid overload. While no convincing data has emerged regarding the long-term safety of inotropes, new exciting data concerning the role of diuretics, especially aldactone, has led to a renewed interest in this class of drug therapy. Angiotensin converting enzyme inhibitors (ACE inhibitors) were noted to not only affect symptomatology but also decrease mortality by interfering with the renin-angiotensin-aldosterone system. Recent research has focused on more complete blockade of the renin-angiotensin system than that achieved with ACE inhibitors alone with the addition of direct angiotensin II receptor blockers. This new class of drugs may become not only a reasonable alternative to ACE inhibitors in patients intolerant of the drug but also a possible addition to ACE inhibitors in the battle to prevent progression of remodelling and disease. beta-blockers are the most exciting new class of drugs used to combat heart failure. They appear not only to combat the remodelling process that occurs in the progression of disease but also other pathological events such as apoptosis and cellular oxidation. New medical therapies currently being investigated include novel agents such as endothelin antagonists, natriuretic peptides, vasopressin antagonists and anticytokine agents--all part of a new era in drug management of heart failure that has evolved with continued advances in the understanding of chronic heart failure (CHF).
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PMID:New advances in the pharmacological management of chronic heart failure. 1124 47

We report the case of a 70-year-old hypertensive man with a solitary kidney and chronic renal insufficiency who developed two episodes of transient anuria after losartan administration. He was hospitalized for a myocardial infarction with pulmonary edema, treated with high-dose diuretics. Due to severe systolic dysfunction losartan was prescribed. Surprisingly, the first dose of 50 mg of losartan resulted in a sudden anuria, which lasted eight hours despite high-dose furosemide and amine infusion. One week later, by mistake, losartan was prescribed again and after the second dose of 50 mg, the patient developed a second episode of transient anuria lasting 10 hours. During these two episodes, his blood pressure diminished but no severe hypotension was noted. Ultimately, an arteriography showed a 70-80% renal artery stenosis. In this patient, renal artery stenosis combined with heart failure and diuretic therapy certainly resulted in a strong activation of the renin-angiotensin system (RAS). Under such conditions, angiotensin II receptor blockade by losartan probably induced a critical fall in glomerular filtration pressure. This case report highlights the fact that the angiotensin II receptor antagonist losartan can cause serious unexpected complications in patients with renovascular disease and should be used with extreme caution in this setting.
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PMID:Repeated transient anuria following losartan administration in a patient with a solitary kidney. 1125 25

Hospital admission for congestive heart failure is extremely common and quite expensive, although it is frequently preventable. New drugs and therapies have been reported to reduce admissions, decrease morbidity and mortality, and improve the quality of life for these patients. Patients with an ejection fraction less than 40 percent (decreased systolic function) should be treated with medication to improve symptoms and prevent progression of heart failure. Angiotensin-converting enzyme (ACE) inhibitors are a mainstay of treatment in patients who can tolerate them; in patients who cannot take these drugs, angiotensin II receptor blocking agents offer an alternative. Patients with New York Heart Association class II or III heart failure should also receive a beta blocker (metoprolol, carvedilol or bisoprolol). Recent research has shown that treatment with spironolactone improves mortality and hospital readmission rates. An exercise program should also be recommended for all patients with heart failure unless their condition is unstable.
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PMID:Reducing readmissions for congestive heart failure. 1132 25

Clinical trials of beta blockers in heart failure have generally required that patients be receiving optimal drug therapy before randomization to the study medication. Therefore, because beta blockers are used in addition to conventional drug therapy, review of the standard drug therapy of mild-to-moderate heart failure before the advent of beta blockade is essential to understanding the role of beta blockers in the treatment of heart failure. The conventional medical management of systolic heart failure includes angiotensin-converting enzyme (ACE) inhibitors, which should be used as first-line therapy; diuretics, for the management of body fluid-volume excess; digoxin; and some other vasodilators. These therapies have been evaluated in large-scale, randomized, controlled trials. ACE inhibitors have been shown to significantly attenuate disease progression and improve outcome (ie, morbidity and mortality) in patients with mild-to-moderate systolic heart failure. Controversial or unproven therapies include nonglycoside inotropic agents, angiotensin II receptor antagonists, antiarrhythmic agents, anticoagulants, and calcium channel blockers. The pharmacologic management of diastolic heart failure is largely empirical and is directed at reducing symptoms. Symptoms caused by increased ventricular filling pressures may be treated with diuretics and long-acting nitrates. Some calcium channel blockers and most beta blockers prolong diastolic filling time by slowing heart rate, thereby potentially improving the symptoms of diastolic heart failure. Calcium antagonists, beta blockers, diuretics, and ACE inhibitors may also promote regression of left ventricular hypertrophy and thus improve ventricular compliance, possibly preventing the development of diastolic dysfunction. Because randomized controlled trials of diastolic heart failure are lacking, this review focuses on the conventional management of mild-to-moderate systolic heart failure before the advent of beta blockade.
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PMID:Medical management of mild-to-moderate heart failure before the advent of beta blockers. 1133 76

Renin-angiotensin-aldosterone systems play a critical role in the development and progression of cardiovascular diseases, and inhibitors of angiotensin-converting enzyme have proven effective for the treatment of these diseases. Since angiotensin II receptor antagonists can inhibit the effects of angiotensin II via ACE-independent pathways, e.g., chymase, they were considered to be more effective than ACEIs. On the other hand, ACE inhibitors can increase bradykinin, and thus, nitric oxide, which may cause potent cardioprotection, inhibition of smooth muscle proliferation and attenuation of inflammation mechanisms. It appears that angiotensin II receptor antagonists and ACEIs may mediate cardioprotection in different ways. This is the rationale to explore the possibility of a combined administration of both drugs for the treatment of chronic heart failure and other cardiovascular pathology. In this review we try to analyze the role of ACE, kinins and chymase inhibition in the pathophysiology and treatment of cardiovascular diseases.
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PMID:Interactions of angiotensin-converting enzyme, kinins and nitric oxide in circulation and the beneficial effects of ACE inhibitors in cardiovascular diseases. 1134 78

All components of the renin-angiotensin system have been demonstrated in the brain and AT1 receptors have been localized in brain areas involved in central cardiovascular regulation. It is currently unclear whether AT1 receptor antagonists, which are increasingly used in the treatment of arterial hypertension and chronic heart failure, have the potential to mediate action via the central renin-angiotensin system. Therefore, we tested the in vivo access of the non-peptide AT1 receptor antagonist, eprosartan (30 and 60 mg per kg of body weight (BW) for 4 weeks, i.p. administered by osmotic minipumps), to angiotensin II receptors in the rat brain by in vitro autoradiography with 125I- (Sar1- Ile8) angiotensin II as a ligand. Eprosartan significantly increased plasma renin activity by four-fold and six-fold at doses of 30 and 60 mg x kg(-1), respectively (P< 0.05 vs CTRL). In the brain, eprosartan produced a dose-dependent inhibition of AT receptor binding in the median cerebral artery ( 850 +/- 249 and 650 +/- 106 vs 1072 +/- 116 dpm x mm(-2) of CTRL; P< 0.05). Furthermore, eprosartan inhibited angiotensin II receptor binding in discrete brain areas, which express exclusively, or predominantly, AT1 receptors both outside and within the blood-brain barrier, such as the paraventricular nucleus ( 180 +/- 47 and 130 +/- 18 vs 545 +/- 99 dpm x mm(-2)of CTRL; P< 0.05), the subfornical organ ( 106 +/- 26 and 112 +/- 17 vs 619 +/- 256 dpm x mm(-2)of CTRL; P< 0.05), and the organum vasculosum laminae terminalis ( 461 +/- 110 and 763 +/- 136 vs 1033 +/- 123 dpmx mm(-2)of CTRL; P< 0.05). These results emphasize that eprosartan readily crosses the blood-brain barrier in vivo and selectively inhibits binding to AT1 receptors in specific brain nuclei. The modulation of central regulatory mechanisms might contribute to AT1 receptor antagonists overall therapeutic efficacy in cardiovascular disease.
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PMID:Central inhibition of AT1receptors by eprosartan--in vitro autoradiography in the brain. 1140 17

Prognosis in congestive heart failure is directly linked to neurohormonal activation. Angiotensin II through the activation of the renin angiotensin aldosterone system has been the principal focus therapy over the last 2 decades. New agents that target selective blockade of the angiotensin II receptor have been introduced in clinical trials for the treatment of heart failure. Aldosterone has been identified as a critically important neurohormone with direct detrimental effects on the myocardium. Aldosterone antagonists have been used in clinical trials to improve mortality in patients with chronic heart failure.
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PMID:Angiotensin receptor blockers and aldosterone antagonists in chronic heart failure. 1140 5

The combination of an angiotensin II receptor antagonist and a thiazide has been used extensively in the treatment of patients with overt heart failure. The effect of this combination on the vascular wall early in the disease, however, has not been investigated. To evaluate this effect, the vascular status of 3-month-old cardiomyopathic hamsters was assessed after daily administration of a combination of losartan (25 mg/kg, p.o.) and hydrochlorothiazide (6.5 mg/kg, p.o.) over an 8-week period. Age-matched golden hamsters were used as healthy controls. The contractile response of aortic rings to endothelin-1 was significantly higher in cardiomyopathic hamsters than in control animals. Concentration-response curves for the endothelin-1-induced contraction were displaced to the right after hydrochlorothiazide+losartan treatment (toward the curves for healthy controls); however, E(max) from treated hamsters was significantly reduced when compared to E(max) from untreated cardiomyopathic animals (1.016+/-0.073 vs. 1.346+/-0.153 g, P<0.05, n=6). No significant differences in the EC50 values from these curves were observed between hydrochlorothiazide+losartan treated and untreated cardiomyopathic animals (2.90+/-0.95 vs. 1.10+/-0.85 nM, P>0.05). The acetylcholine-induced relaxation observed in cardiomyopathic animals was not improved after treatment with hydrochlorothiazide+losartan or hydrochlorothiazide alone, but the combination of these drugs increased significantly the basal production of nitric oxide (NO). Angiotensin-converting enzyme activity increased in plasma (from 29.9+/-1.23 to 41.16+/-1.82 nmol x mg(-1) x min(-1), n=8, P<0.05) but decreased in the aorta (from 0.33+/-0.02 to 0.25+/-0.017 nmol x mg(-1) x min(-1), n=6, P<0.05) after treatment with hydrochlorothiazide+losartan. In addition, the combination of these drugs reduced the heart-to-body mass ratio (3.96+/-0.07 for treated vs. 5.01+/-0.20 mg/g for untreated animals, n=7, P<0.05), and the thickness of the aortic media (0.076+/-0.003 for treated vs. 0.149+/-0.009 mm for untreated animals, n=8, P<0.05). Although hydrochlorothiazide alone lowered systolic blood pressure to the same level achieved with both drugs in combination (from 166+/-10 for untreated cardiomyopathic animals to 84+/-1 mm Hg for hydrochlorothiazide+losartan, and 80+/-5 mm Hg for hydrochlorothiazide alone, P<0.05), no significant reduction in heart-to-body mass ratio was observed in animals treated with the diuretic alone (P>0.05). In conclusion, in this model of heart failure, chronic hydrochlorothiazide+losartan administration normalizes the vascular responses to endothelin-1, improves basal vascular tone, and prevents the development of cardiac and vascular hypertrophy.
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PMID:Chronic administration of losartan plus hydrochlorothiazide improves vascular status in young cardiomyopathic hamsters. 1140 35


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