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

Optimal therapy for congestive cardiac failure requires identification of correctable factors that aggravate it as well as an understanding of its etiology. Increased sympathetic nervous system activity, reduced renal blood flow, and cardiac hypertrophy and dilation are the main compensatory processes that occur in response to cardiac failure. Although they may be of initial benefit in supporting a reduced stroke volume, they may ultimately prove self-defeating. New drugs for the treatment of severe congestive heart failure include dopamine, which has a selective nonadrenergic dilator effect on the renal vascular bed, and dobutamine, which has potent inotropic effects, lowers the left ventricular filling pressure and does not increase the heart rate or the systemic vascular resistance. By reducing both the resistance to left ventricular ejection and the venous return to the right heart, vasodilators result in improved peripheral perfusion and reduced pulmonary congestion. Optimal therapy for refractory cardiac failure can be rationally determined by characterizing the hemodynamic profile through measurement of the mean arterial pressure, the left ventricular filling pressure, the cardiac output and the systemic vascular resistance. The specific therapy can then be effectively and safely delivered by a careful analysis of the dose-response relation as identified by hemodynamic monitoring.
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PMID:Contributions of hemodynamic monitoring to the treatment of chronic congestive heart failure. 49 82

Reliable, prenatal detection of congenital heart disease has become possible over the past decade with the evolution of fetal echocardiography. We have documented the outcome of 170 cardiac defects diagnosed prenatally since 1984. Of 170 cases, 55 (32%) had major extracardiac malformations and 45 (28%) chromosomal abnormalities (16 had both). Elective termination was chosen in 77 (45%) pregnancies. Of 93 continuing pregnancies 15 were stillborn and 43 died postnatally (48% of these fetuses and infants had extracardiac or chromosomal anomalies, or both). Thirty-five patients survive at 1 to 80 months (mean 36). Aneuploidy or extracardiac defects are present in 20% of survivors. Nonimmune hydrops secondary to cardiac failure was present in 7 continuing pregnancies and none of these patients survived. The prognosis of prenatally diagnosed cardiac lesions is negatively influenced by the presence of cardiac failure, aneuploidy or extracardiac malformations, or a combination of these. Optimal counseling and management requires the identification of these conditions when present.
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PMID:Outcome of prenatally detected cardiac malformations. 159 Feb 38

Optimal metabolic control during the first twelve hours after myocardial infarction may be associated with improved survival in diabetic subjects. A comparison of an intravenous insulin infusion regimen aimed at improving blood glucose levels (n = 35), with 'routine control' (n = 34) in the post infarction period has been carried out in diabetic subjects admitted to four Coronary Care Units over a two year period. However, glycaemic control was similar in both groups (intravenous infusion regimen, mean +/- SD capillary blood glucose 10.3 +/- 2.1 mmol/l, 'routine control' glucose 10.7 +/- 3.6 mmol/l). There were no differences in the rates of arrhythmias (31% v 32%), heart failure (46% v 47%) or mortality (17% v 18%). Mortality in diabetic subjects was lower than that quoted in previous studies but was higher than in non-diabetic subjects admitted to the Coronary Care Unit during the same period. Attempts to improve glycaemic control by means of intravenous insulin infusion were unsuccessful.
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PMID:Metabolic control in diabetic subjects following myocardial infarction: difficulties in improving blood glucose levels by intravenous insulin infusion. 192 6

Myocardial relaxation is an energy-dependent process. Indeed, adenosine triphosphate (ATP) is required to pump free myoplasmic calcium back into the sarcoplasmic reticulum. It is also necessary to extrude the calcium ions which enter the cell during the plateau phase of the action potential. The calcium-sodium exchange mechanism does not seem to require energy in itself, but sodium exchanged for calcium eventually needs to be extruded via sodium/potassium ATPase and there is also an ATP-dependent calcium pump. Thus, when ATP production is limited, calcium may remain fixed to troponin for part or for the whole of diastole, resulting in a slower rate of isovolumic relaxation and reduced distensibility of the myocardium. Alterations in diastolic function caused by inadequate energy production occur in the high-demand type of myocardial ischaemia. There is also growing evidence that most forms of heart failure are accompanied by a state of energy depletion. Alterations in mitochondrial density and enzymatic activity are common in the failing myocardium and may partially explain the reduction in ATP production. Inadequate growth of the capillary network in hypertrophied myocardium, impaired subendocardial perfusion due to increased diastolic wall stress and/or coronary artery disease, probably also contribute to an imbalance between energy production and utilization. As relaxation is intrinsically a much slower process than activation and since changes in ATP concentration may also affect calcium efflux by allosteric effects, impaired relaxation and reduced diastolic distensibility are almost universal in chronic congestive heart failure. Optimal therapy of heart failure should, therefore, also aim at improving this phase of the cardiac cycle.
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PMID:Diastolic dysfunction and myocardial energetics. 218 40

Hypertension increases cardiovascular morbidity and mortality two- to fourfold. The chief hazards are now atherosclerosis and coronary disease. Risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensive patients with a high total/high-density lipoprotein (HDL)-cholesterol ratio, impaired glucose tolerance, high fibrinogen, electrocardiographic (ECG) abnormalities, and who are cigarette smokers. Evidence of organ involvement such as left ventricular function are hallmarks of impending cardiovascular sequelae. Electrocardiogram-left ventricular hypertrophy (ECG-LVH) behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, infarction, cardiac failure, and stroke. Consideration of cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, set goals, and determine the efficacy of treatment. Awaiting evidence of organ involvement is dangerous since the first such evidence is often a sudden death, stroke, or myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure.
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PMID:Risk factors in hypertension. 246 76

Hypertension increases cardiovascular morbidity and mortality two to four-fold. The chief hazards are now atherosclerosis and coronary disease. The risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of the blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensives with a high total/high density lipoprotein (HDL) cholesterol ratio, impaired glucose tolerance, high fibrinogen, those with ECG abnormalities and cigarette smokers. Evidence of organ involvement such as left ventricular hypertrophy, proteinuria or impaired left ventricular function are hallmarks of impending cardiovascular sequelae. The presence of ECG-LVH behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, myocardial infarction, cardiac failure and stroke. Consideration of all cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, and set goals and determine the efficacy of treatment. Waiting until there is evidence of organ involvement is dangerous since the first such evidence is often sudden death, a stroke or a myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure. This can be achieved by hygienic (dietary) measures or pharmacological therapy in those who do not respond to diet alteration, weight control and exercise.
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PMID:An integrated view of hypertension. 260 26

Patients with advanced heart failure may be candidates for mechanical circulatory support, heart transplantation, or both. Optimal medical therapy in such patients, who are frequently unstable clinically, is focused on traditional and newer methods of inotropic support. Accordingly, the response to intravenous and oral enoximone, an experimental compound with phosphodiesterase inhibitory properties, was examined in 25 patients with unstable, severe chronic heart failure as a result of ischemic or myopathic heart disease. Eight hospitalized patients had far-advanced failure and were dependent on dobutamine, dopamine, or both to support their cardiocirculatory status (group 1). Seventeen patients had severe failure and were hospitalized electively because of their clinical instability despite digoxin, diuretics, and vasodilators (group 2). Intravenous (1 to 2 mg/kg) and oral (1 to 2 mg/kg) enoximone significantly (p less than 0.05) improved right and left heart function, and the salutory hemodynamic response was sustained for 6 to 8 hours. In group 1, catecholamines were discontinued and clinical stability was reestablished on oral enoximone; stability was also restored in group 2. Nevertheless, 19 patients died on long-term enoximone therapy with approximately half succumbing to their heart failure. Thus enoximone, a compound with inotropic and vasodilator properties, was useful in the acute and short-term management of unstable, chronic heart failure and had an additive hemodynamic benefit to dobutamine, dopamine, or both. Enoximone may therefore be a useful adjunct to stabilizing these patients before mechanical circulatory support or transplantation. The advanced degree of myocardial failure in these patients, however, precludes enoximone together with standard medical therapy from having a more favorable impact on clinical outcome in these patients.
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PMID:Enoximone (MDL 17,043), a phosphodiesterase inhibitor, in the treatment of advanced, unstable chronic heart failure. 295 97

Late changes are frequent in saphenous vein grafts. About 10 to 12 years after bypass, about one-third are occluded, one-third have wall irregularities and narrowings attributed to atherosclerosis and one-third are seemingly intact. These changes are associated with recurrence of angina and other deleterious clinical events such as unstable angina, acute myocardial infarction, heart failure and death. Intimal fibrous hyperplasia may be a precursor of these changes, which could be minimized by appropriate surgical technologies and perhaps antiplatelet therapy. These late changes appear related to serum hyperlipidemia and smoking. Optimal control of these risk factors may retard their development and subsequent clinical deterioration. Although internal mammary artery (IMA) graft is the conduit of choice because of its apparent immunity to premature atherosclerosis, and hence its longer durability, saphenous vein grafts are still placed in many old patients and others, when a short operation time is a priority, and above all in combination with IMA grafts in order to obtain complete revascularization.
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PMID:Late changes in saphenous vein coronary artery bypass grafts and their implications in clinical practice. 350 31

In the International Prospective Primary Prevention Study in Hypertension, electrocardiographic changes before and during 3- to 5-year antihypertensive treatment were investigated in a cohort of 5819 men and women aged 40 to 64 years with entry diastolic blood pressures of 100 to 125 mm Hg. They were randomly allocated to treatment regimens that either included or excluded the slow-release beta-blocker oxprenolol. Electrocardiograms (ECGs) were assessed using the Minnesota Code and assigned to groups of normal ECGs or ECGs with pressure-related, ischemic, "intermediate," or "other" abnormalities. Antihypertensive treatment was associated with a decrease (mainly in men) of pressure-related and (mainly in women) of intermediate abnormalities. Ischemic abnormalities increased, particularly in men. Inclusion of the beta-blocker resulted in a greater reduction in intermediate abnormalities and in a lesser increase in ischemic abnormalities. Better blood pressure control was associated with a lesser increase in ischemic abnormalities and in a regression of pressure-related abnormalities. The presence of ST segment depression and of a complete left bundle branch block in the entry ECG was associated with a significant risk for sudden death and myocardial infarction. Optimal blood pressure control prevents pressure-induced cardiac target organ damage and, hence, heart failure, and may delay the progression of ischemic abnormalities. This tallies with the lower critical cardiac event rate associated with lower blood pressure that was observed in the same study.
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PMID:Electrocardiographic changes during antihypertensive therapy in the International Prospective Primary Prevention Study in Hypertension. 359 89

Optimal timing of surgery in infective endocarditis (IE) depends mainly on the haemodynamic tolerance of the patient. Emergency surgery is required in cases of refractory heart failure due to valvular lesions, intracardiac fistulas and high grade cardiac conduction abnormalities caused by septal abscesses. Surgery must be considered in all patients who have undergone a transient episode of heart failure such as a pulmonary oedema and it must be early--within 2 or 3 weeks of starting antibiotic therapy in patients with aortic regurgitation. Bacteriological indications are less frequent: persistent sepsis beyond the first week in spite of medical therapy, mycotic IE or prosthetic valve endocarditis caused by Gram-negative or staphylococcal organisms. Some complications may swing the argument in favour of surgery: detection of root abscesses or mycotic aneurysms using transoesophageal echocardiography, and systemic embolisms with persistent, large and mobile vegetative lesions. Mortality rate depends on the haemodynamic status but also on the severity of anatomical lesions, on the type of endocarditis (native or prosthetic valve), on the type of surgery and on bacterial aetiologies. It varies between 5% and 30%. The late postoperative outcome is good. The actuarial survival rate at 8 years was 70% in our series of 31 patients with aortic regurgitation and early surgery. In mitral regurgitation, conservative surgery is possible in most cases. In our department, 48 patients with mitral bacterial lesions have been operated on with conservative surgery without operative mortality. IE was active in 14, recent in 12 and had occurred earlier in 22.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surgical treatment of infective endocarditis. 767 34


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