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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular diseases including heart failure represent a common disease in patients referred for anesthesia. In most cases, heart failure is caused by left ventricular dysfunction due to coronary heart disease. The aims of the treatment of chronic heart failure are the relief of symptoms, the improvement of prognosis and the prevention of the progression of heart failure. The first-line treatment involves the underlying heart disease such as myocardial revascularisation procedures in coronary heart disease or the correction of valve diseases. The pharmacological therapy depends on the stage of heart failure and symptoms of the patient. Heart failure therapy includes ACE-inhibitors, betablockers, diuretics und digitalis. Nitrates can be prescribed in patients with symptomatic heart failure despite adequate therapy but calcium antagonists are not recommended. Repeated or prolonged treatment with positive inotropic agents like phosphodiesterase inhibitors or beta-adrenergic drugs increases mortality but this is commonly used in acute stages of heart failure refractory to treatment. Interactions of ACE-inhibitors or AT1- antagonists with anesthetic agents can lead to severe hypotension especially in hypovolemic patients. Whether those drugs should be continued perioperatively or not has been controversially discussed. The use of betablockers has a positive impact on cardiac morbidity and mortality during and early after surgery. Chronic treatment with diuretics can be associated with hypovolemia and an imbalance of electrolytes leading to hypotension and arrhythmia during anesthesia but careful evaluation prior to anesthesia can avoid such complications. The continuation of digitalis during anesthesia has been controversially discussed due to the various interactions with anesthetics.
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PMID:[Current treatment of chronic heart failure]. 1289 47

Cardiac remodeling is a complex process, which involves genetic, molecular and cellular changes in cardiomyocytes and the interstitium, leading to progressive structural and functional alterations, including cardiac dilatation, interstitial fibrosis, and a reduction in contractility and relaxation. As cardiac function worsens, ventricular dysfunction, heart failure and end-stage heart disease are the ultimate consequences. Underlying mechanisms include myocardial stretch and neurohormonal and cytokine activation. Consequently, therapies aiming counteracting these mechanisms have proven successful in attenuating or even preventing cardiac remodeling. In particular, ACE inhibition, beta-blockade and aldosterone antagonism have proven to be effective in modulating the process of remodeling and in reducing the occurrence of adverse events in heart failure. Of interest, although several other antagonists of neurohormonal, including endothelin, or of cytokine activation have been shown to effectively modulate remodeling, studies thus far have been negative in terms of event reduction in heart failure. Whereas insight in cardiovascular remodeling has already significantly contributed to existing management strategies in heart failure, further studies in different mechanisms may provide additional therapeutic measures.
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PMID:Pharmacological modulation of cardiovascular remodeling: a guide to heart failure therapy. 1461 97

Diabetes mellitus is one of the significant risk factors for many cardiovascular diseases. Diabetes mellitus is 3-4 times more frequent in patients with heart failure compared to patients without heart failure. Prognosis of patients with heart failure and diabetes mellitus is worse than prognosis of non-diabetic patients with the same left ventricular dysfunction. The term diabetic cardiomyopathy refers to a relation between diabetes mellitus and heart disease, but it probably isn't a separate morphology unit. In treatment of patients with diabetes mellitus general rules apply to heart failure management. The effect of ACE inhibitors was in majority of studies stronger in diabetics than in non-diabetics, the effect of beta blockers was comparable or smaller. Treatment is based on good compensation of metabolic parameters, blood pressure, titration of ACE inhibitors into recommended doses, and an optimal dose of a beta blocker. Type II diabetics with heart failure will, due to decreased resorption and metabolism, need insulin more often than diabetics without heart failure.
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PMID:[Diabetes mellitus and chronic heart failure]. 1504 Jan 57

Chronic heart failure is a prevalent condition associated with high morbidity, high mortality and reduced quality of life. Chronic heart failure is the end-stage of various forms of heart disease. The prognosis is poor, worse than for patients with various forms of cancer. The diagnosis of heart failure is made in the presence of multiple symptoms and signs combined with objective evidence of cardiac dysfunction. Treatment consists of pharmacological as well as non-pharmacological approaches. ACE inhibitors and beta-blockers are the basis of treatment, while diuretics and other medications are given on an individual basis. The aim of treatment is to reduce progression of the underlying disease and to reduce mortality and morbidity.
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PMID:[Modern diagnosis and treatment of heart failure]. 1511 90

During pregnancy cardiac output rises by 40-50%. At first stroke volume in particular increases, with the heart rate rising mainly in the second part of the pregnancy. More and more women with congenital heart disease are reaching adulthood and want to become pregnant. The haemodynamic changes during pregnancy are an additional burden for women with heart disease. Risk factors for occurrence of important cardiac problems during pregnancy are: previous cardiac events, lower functional class, cyanosis, left-sided heart obstruction or a diminished systolic function of the systemic ventricle. Pregnancy is contraindicated in pulmonary hypertension, in Marfan syndrome with an ascending aorta diameter of > 50 mm and in severe mitral or aortic valve stenosis. The recurrence risk for children varies between 3 and 50%, depending on the nature of the congenital heart disease. Foetal outcome is depending on the haemodynamic situation and medication use of the mother. ACE inhibitors are contraindicated during pregnancy.
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PMID:[Congenital heart disease and pregnancy]. 1583 34

Current evidence favors the view that regardless of etiology, there is a predictable sequence of neuroendocrine activation that operates in most dogs and cats with progressive heart disease and that it is largely, but not entirely, independent of etiology. The natriuretic peptides and sympathetic nervous system seem to be early responders to developing cardiac and hemodynamic perturbations in both species. BNP plays a particularly prominent role in cats, possibly as a reflection of disease etiology. Shortly thereafter, plasma endothelin concentrations rise, reflecting the impact of the hemodynamic alterations on the vasculature. Endothelin and the natriuretic peptides directly suppress plasma renin release but have divergent effects on aldosterone. Activation of the tissue RAAS may operate early on to further the progression of heart failure, but evidence of plasma RAAS activation occurs comparatively late and near the time of development of overt CHF. Finally, in animals with severe CHF that are prone to hypotension,vasopressin levels may also rise, contributing to the retention of free water and congestion that is refractory to diuretics. Although oversimplified, this scenario seems to be consistent with data obtained in human, canine, and feline patients. These observations provide some impetus for evaluating ACE inhibitors in cats and beta-receptor-blocking drugs in dogs and cats. Perhaps we are also a little closer to identifying useful biochemical markers that can aid in the diagnosis of heart disease, guide therapy, and improve our understanding of the biologic processes occurring in our patients.
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PMID:Neuroendocrine evaluation of cardiac disease. 1532 72

Pimobendan is an oral inodilator compound available in many countries for use in canine heart failure. It combines calcium-sensitizing effects with PDE III inhibition, resulting in positive inotropic effects and veno- and ergic signal transduction pathway in the failing heart, the calcium-sensitizing effects may assume greater importance in patients with heart failure. Clinical studies in human patients have shown sustained improvement in hemodynamics and exercise tolerance, with favorable neurohormonal effects. One study showed a nonsignificant trend toward increased mortality [20], but proarrhythmic effects have not ben observed. Studies in naturally occurring canine heart failure suggest that pimobendan's effects are at least comparable to those of ACE inhibitors, if not superior. Pimobendan is likely to play an increasing role in the future in the treatment of canine heart disease.
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PMID:Use of pimobendan in the management of heart failure. 1532 74

Advanced heart failure, also be defined as stage D heart failure, characterized by advanced structural heart disease and marked symptoms of heart failure at rest despite dietary modification, salt restriction and maximal medical therapy including ACE inhibitors, angiotensin II receptor blockers, digitalics, diuretics and beta blockers. These patients require frequent hospitalizations and specialized interventions such as heart transplantation, implantation of mechanical assistance devices, continuous intravenous inotropic therapy to palliate symptoms, or continued terminal care.
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PMID:[Management of advanced or refractory heart failure]. 1568 Jan 39

Fifty consecutive elderly (> 60 years) patients admitted to our department with congestive heart failure (CHF) entered a prospective database, to define their main clinical, instrumental and cognitive characteristics. In addition we evaluated the patterns of drug therapy in this aged population. Eighty percent of this sample had been previously hospitalized for CHF. Two or more associated diseases were present in 92%. Heart disease was ischemic or hypertensive in etiology in 80% of patients. Acute dyspnea was the most common presenting symptom. Atrial fibrillation or flutter were found in 38% of patients. Ultrasound evaluation evidenced left ventricular dysfunction of a systolic type in 49% and of a diastolic type in 28.6% of subjects. Diuretics and cardiac glycosides were the most widely administered drugs, followed by ACE-inhibitors, nitrates and dobutamine. Older ( >or= 75 years) patients were treated with more agents, with a trend to a lesser use of dobutamine. Moderate to severe mental deficit was present in 20.8% of our sample, while significant depression was more common (54.2%). The main implications of the clinical profile of the elderly patient hospitalized for CHF are discussed.
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PMID:Congestive heart failure in the elderly requiring hospital admission. 1537 42

The primary aim of this study was evaluation of the efficacy of telmisartan (angiotensin II receptor blocker- AT(1) blocker) on blood pressure in 10 patients with renal impairment in moderate or advanced stages of renal insufficiency and not dependent on haemodialysis. Its effect on proteinuria, renal function (represented by serum urea, creatinine, glomerular filtration), evaluation of overall therapy compliance in comparison with a previously prescribed angiotensin converting enzyme inhibitors (ACEI) were secondary aims. Considering the presence of left ventricle hypertrophy in all patients as a marker of hypertensive cardiopathy, the effect of telmisartan therapy on non-invasive cardiovascular parameters (ECG, echocardiography, and assessment of heart rate variability-HRV) was also evaluated. The study group involved 10 hypertensive patients (6 women, 4 men) with diabetic and non-diabetic renal impairment, proteinuria above 1 g/24 hours, hypertensive cardiopathy and intolerance of ACEI (cough). Telmisartan was added to their long-term antihypertensive combination therapy in a dose of 40 mg for the first 14 days, after which the dose increased to the maximal of 80 mg. The average initial daytime systolic blood pressure (SBP) was 149 +/- 19.7 mm Hg, average night-time SBP 145 +/- 23.0 mm Hg, average initial daytime diastolic BP (DBP) 90.6 +/- 2.5 mm Hg, night-time DBP 88.9 +/- 13.5 mm Hg. Average initial serum creatinine was 207.2 +/- 48.5 micromol/l, urea 15.1 +/- 4.4 mmol/l, GF 0.5 +/- 0.1 ml/s. Echocardiography revealed left ventricular (LV) hypertrophy with well preserved systolic and moderately impaired diastolic LV function. Also the HRV assessment revealed impaired neurovegetative (e.g. sympathovagal) balance. After 1 year of combination therapy with telmisartan, there was a clearly significant reduction in both SBP and DBP in both day and night-time (SBP daytime 149.6 vs.116.6 mm Hg, night-time 145.8 vs. 129.5 mm Hg; DBP daytime 90.6 vs. 83.5 mm Hg, night-time 88.9 vs. 79.3 mm Hg) and proteinuria (2.37 vs. 1.27 g/24 hour, p < 0.05). There were no significant changes in serum creatinine, urea values, and LV functions. On the other hand, further progression of the sympathovagal balance impairment was noted (continuing reduction of HRV in 9 from 10 patients), which can be described as the priority finding. The total compliance of telmisartan therapy was very good and without adverse clinical side effects. In conclusion - telmisartan reduces blood pressure and proteinuria safely and effectively in patients with various types of nephropathy in moderate or advanced stages of renal insufficiency.
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PMID:Telmisartan in the treatment of hypertension in patients with chronic renal insufficiency. 1552 50


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