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

Dimension measurements of the right ventricle are difficult to obtain because of its complex geometry, thus we evaluated a method of right ventricular dimension measurements. Crystals were placed on the ventral and dorsal side of the right ventricular free wall, approximately one-fourth of the right ventricular semicircle away from the septum, in the middle of a cranio-caudal axis of the ventricles. The effects of an increased (infusion of 20 mL/kg of 5% glucose for 3 min into seven rabbits), as well as decreased preload (nitroglycerin, 5 micrograms/kg/min i.v. n = 6) were measured and compared with changes during a placebo infusion (n = 6). The change in shortening of the right ventricle wall segment correlated with changes in both atrial natriuretic factor (ANF) plasma concentration (r = 0.89, p < 0.05) and central venous pressure (CVP) (r = 0.94, p < 0.05), respectively. Both these variables are influenced by right ventricular function and dimensions in healthy animals. Dimension measurements obtained across the free wall of the right ventricle appear to reflect right ventricular function well and should be useful in assessing the effects of drugs intended for the treatment of angina pectoris or heart failure.
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PMID:Assessment of right ventricle dimensions with microsonometry in anesthetized rabbits. 148 88

The risk for cardiovascular complications is already substantially increased in persons with borderline elevation of arterial pressure (141-159/90-94 mmHg and transiently below). It increases progressively with higher grades of hypertension. The main aim of treatment is thus a significant improvement in survival for the patient. Persons with raised blood pressure (BP) have often additional cardiovascular risk factors such as deranged carbohydrate metabolism, dyslipidemia, left ventricular hypertrophy, smoking and others. Treatment of hypertensive patients should thus not only normalize BP but should at the same time reduce associated risk factors or at least not increase them. Conventional antihypertensive treatment based on thiazides in high doses or beta-blocking agents led to marked reduction of strokes and heart failure, but did not satisfactorily reduce coronary heart disease or sudden cardiac death. It has been suspected that other cardiac risk factors are insufficiently influenced or eventually even deteriorated by conventional therapy, thus counteracting partly a beneficial effect of lowered BP. Beta-blockers however have at least a secondary preventive effect after myocardial infarction. Newer antihypertensive drugs such as ACE-inhibitors, calcium antagonists and alpha 1-blockers reduce left ventricular hypertrophy and are at least neutral with regard to metabolism of lipids and carbohydrates. The non-thiazide diuretic indapamide and the serotonin (S2-) blocker ketanserin likewise are neutral with regard to glucose and lipid metabolism. The efficacy of these new drugs regarding long term survival is as yet undetermined. Persisting borderline or established hypertension should as a rule always be approached with basic non-pharmacologic measures: loss of overweight, reduction of alcohol intake, exercise, avoidance of high salt foods, abstention from smoking and withdrawal of BP-raising drugs. If antihypertensive medication is indicated, potential first line drugs are ACE-inhibitors, calcium antagonists, beta-blockers, thiazides at low dose, indapamide, ketanserin, the alpha 1-blocker prazosin and others; initially as monotherapy, if needed in combinations of 2 or 3. Older patients or those will with additional disturbances such as diabetes, hypercholesterolemia, nephropathy, heart failure, ischemic heart disease, arrhythmias, claudication, asthma and others need problem-adjusted modifications of treatment.
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PMID:[Antihypertensive therapy in the nineties]. 153 54

Diabetic patients have an increased mortality following myocardial infarction (MI) due to left ventricular failure rather than larger infarcts or dysrhythmias. As this may be due to diabetic microangiopathy affecting the myocardium, we have examined the case records of diabetic clinic patients admitted to the Coronary Care Unit (CCU) with proven MI and compared the hospital outcome of those with and without retinopathy or nephropathy, i.e. markers for generalised microangiopathy. Sixty four consecutive records were traced, for the period when diabetic treatment policy was standardised in CCU, 24 patients had retinopathy (7 proteinuria). When compared to non-retinopathy patients they had similar ages 67 +/- 12 yr [+/- SD] v 63 +/- 9yr) but were of longer duration of diabetes p less than 0.05). There were no differences between the groups in size or site of infarct, previous infarct or hypertension history, blood glucose on admission or diabetic treatment before or after admission. Death occurred in 29% of retinopathy patients compared to 3% of non-retinopathy patients (p less than 0.01). Cardiac failure complicated 75% of retinopathy patients and 25% of non-retinopathy patients (p less than 0.001). Dysrhythmia occurred in 50% and 33% of patients respectively (P = NS). Nine patients had clinical peripheral vascular disease and five of these died. This study, of a selected group of diabetic clinic attenders admitted to CCU with acute MI, demonstrates that microangiopathy and peripheral vascular disease are important prognostic factors in determining hospital outcome as these patients are at increased risk of cardiac failure and death.
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PMID:Microangiopathy as a prognostic indicator in diabetic patients suffering from acute myocardial infarction. 160 65

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.
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PMID:Ischemic hepatitis: widening horizons. 848 Jul 56

The lack of success of antihypertensive drug therapy in decreasing cardiovascular events has caused close examination of the influence of antihypertensive drugs on cardiac risk factors. Striking differences exist in the pharmacological profiles of antihypertensive drug classes and subclasses as well as in the influences of the drugs on electrolyte, lipid, and glucose metabolism. Differences also exist in the effects of the drugs on left ventricular hypertrophy. These differences in the effects of antihypertensive drugs on cardiac risk factors may assist in explaining the lack of a favorable effect on cardiovascular events in previous clinical trials. However, prospective trials are necessary to demonstrate that treatment of hypertension with drugs that have a more favorable effect on cardiac risk factors will reduce cardiac events (i.e., myocardial infarction, heart failure, and sudden death).
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PMID:Antihypertensive therapy and cardiovascular risk. Are all antihypertensives equal? 173 Apr 49

Late complications of diabetes mellitus include a variety of clinical pictures, mainly related to the involvement of the arterial wall both of large vessels (macroangiopathy) and small vessels (microangiopathy), and of the peripheral nervous system (neuropathy). Their presence in almost all types of diabetes indicates that there is a common pathogenetic mechanism, which can be substantially identified in high blood glucose levels and related alterations. Hyperglycemia, in fact, leads to some metabolic abnormalities, i.e. non-enzymatic glycosylation of proteins and polyol pathway activity; moreover it can negatively affect the pattern of some hormones, especially GH and sex steroids, and normal rheological and clotting properties of blood. These abnormalities, confirmed by experimental models, play a key role in the development of late diabetic complications. However some evidence indicates that a genetic background may predispose to their development or protect from their onset. The two main forms of diabetic retinopathy, non-proliferative and proliferative, show an incidence which increases with age and duration of diabetes, reaching 100% when diabetes lasts for more than 20 years. The risk of blindness, which is very high for the proliferative form, has been dramatically reduced by laser-photocoagulation. Diabetic nephropathy affects a lesser number of diabetics but, after a silent or preclinical stage, leads to renal failure and subsequent replacement therapy. Strict metabolic control in the silent stage and later rigid anti-hypertensive treatment can prevent or retard the evolution of this complication. A close association has been observed between diabetes and hypertension, which can directly affect the onset and evolution of diabetic nephropathy, probably through a common genetic mechanism. Diabetic neuropathy has a wide variety of clinical manifestations, at somatic, autonomic and central levels and can greatly modify the quality and expectancy of life. However, the major cause of death in diabetic subjects is large vessel disease or macroangiopathy, which is similar to non-diabetic atherosclerosis regarding the main histopathological and clinical manifestations but has a much higher prevalence and severity. Finally, a specific cardiomyopathy has also been described in diabetes mellitus and can account for the high rate of heart failure observed in these patients.
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PMID:The late complications of diabetes mellitus. 174 48

The study was undertaken to examine central hemodynamic and carbohydrate metabolic parameters in patients with coronary heart disease (with or without signs of chronic heart failure, Stages I and IIA). The changes in carbohydrate metabolism in CHD patients were detected earlier than those in central hemodynamics. In patients with Stage I heart failure, who had normal resting hemodynamic parameters, metabolic parameters were indicative of abnormalities in carbohydrate metabolism: there was a reduction in carbohydrate tolerance and red blood cell release of insulin in response to glucose load and an increase in blood immunoreactive insulin, erythrocytic glucose-6-phosphate dehydrogenase activity and greater adrenalin- and insulin-containing erythrocytes. It is suggested that it is advisable to determine the above parameters of carbohydrate metabolism in patients with coronary heart disease.
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PMID:[Correlation of some parameters of carbohydrate metabolism and central hemodynamics in the early stages of circulatory insufficiency in patients with ischemic heart disease]. 175 10

Primary pulmonary hypertension (PPH) is a rare disease, which almost inevitably leads to right-sided heart failure and death. This is to our knowledge the first report of ophthalmological complications. A 43-year-old woman in the late stage of PPH who had been continuously treated with oxygen developed an uveal effusion syndrome, which manifested as bilateral central serous retinal detachment and ciliochoroidal swelling. The serous detachment improved promptly after interruption of the oxygen therapy and again worsened when it was resumed because of massive dyspnea. Systemic blood pressure was 115/95. Right-sided cardiac catheterization revealed a systolic pulmonary arterial pressure of 110 mmHg. Pulmonary function tests showed a normal PO2 with oxygen and a light hypoxia without therapy. We came to the following conclusions: First, the central serous retinal detachment and peripheral choroidal swelling were induced by the striking increase in pulmonary arterial pressure, which almost equaled the systemic arterial pressure. Although the same ophthalmological findings have been reported in experimental animals after exposure to pure oxygen, pulmonary function tests disproved high oxygen concentration as the causative agent in our patient. Second, the improvement of pigment epithelial function after the interruption of oxygen therapy could be explained by the following hypotheses. Hypoxia induced a dilation of the choroidal arteries, followed by an improved supply of nutritive material for the pigment epithelium. There is experimental evidence that glucose might be the limiting metabolite of pigment epithelial function.
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PMID:[Serous retinal detachment in O2 therapy of primary pulmonary hypertension]. 178 18

This study was to search if captopril (C) reduces albuminuria in a group of type II diabetics with diabetic nephropathy (DN). Eleven type II diabetics with DN and hypertension, with albuminuria over 0.30 g/L/24th, fasten blood glucose under 250 mg/dL, serum albumin over 3 g/dL, without infection, cardiac failure or diuretic treatment, were treated with C for six months, as the only treatment for hypertension and albuminuria. Every month, albuminuria in a 24h urinary collection, medium arterial pressure (MAP), serum creatinine and fasten blood glucose were measured. Ten women and one man with 60 (50-70) years of average age (0 to 100th percentile), with 18 (8-35) years of diabetic disease, and 4 (1-7) years of clinic hypertension were studied. Before the treatment with C they had albuminuria of 6.9 (0.7 to 12.5) g/L/24h, MAP of 119.7 (93.2 to 139) mmHg, serum creatinine of 2.2 (0.7 to 7.5) mg/dL and glucose of 168 (78 to 250) mg/dL. After 6 months with C, they had albuminuria of 3.5 (0.2 to 9.6) g/L/24h (p less than 0.01), MAP of 113.4 (92.9 to 132.4) mmHg (p = 0.5), serum creatinine of 2.3 (0.5 to 6.4) mg/dL (p = 0.23) and glucose of 133 (87.5 to 239) mg/dL (p = 0.32). The MAP showed a predictive relation over albuminuria (p = less than 0.004). During the six months of study, C reduced albuminuria in type II diabetics with hypertension and diabetic nephropathy.
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PMID:[Captopril reduction of albuminuria in type-II diabetics with diabetic nephropathy]. 180 Feb 20

Enoximone, a new phosphodiesterase-inhibitor with positive inotropic and vasodilating activities is available for intravenous use in patients with severe heart failure. A review of the current knowledge regarding the adverse effects of this substance reveals that they are characterized by cardiovascular, central nervous, and gastrointestinal side effects. Adverse effects occurred in 20% of patients and were mostly due to the pharmacological properties of enoximone. Cardiovascular side effects (10%) were the most frequent; ventricular and supraventricular arrhythmias were most common. Two to three percent of the patients experienced hypotension due to the vasodilator activity of enoximone. Headache, insomnia, and anxiety were the most frequent adverse effects on the central nervous system. Three percent of the patients treated experienced vomiting, nausea, abdominal pain, and diarrhea. An increase of liver enzymes and serum glucose could be observed, mostly in patients with previous liver disease or diabetes. Pharmacokinetic drug interactions are not known; possible pharmacodynamic interactions result from the pharmacological properties of the drugs. Intravenous therapy with enoximone causes a few serious side effects that can only be controlled by careful observation of the patients treated.
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PMID:[Tolerance of enoximone in patients with heart failure]. 183 4


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