UMLS:C0018801 - FACTA Search

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

I report five cases of occlusion of the superior mesenteric artery from one general practice; four of these occurred in one year.THE COMMON CLINICAL FEATURES WERE: acute diarrhoea and vomiting in elderly persons (all over 70) with abdominal pain and distension and shock. All had a previous history of auricular fibrillation and cardiac failure and past episodes of clinical arterial occlusive disorders had been experienced by four. Each diagnosis was confirmed at operation and all five patients died. It is important for general practitioners to recognize this syndrome.
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PMID:Acute superior mesenteric artery occlusion: problems of pre-operative diagnosis. 52 38

One hundred consecutive patients in sinus rhythm and without routinely prescribed antiarrhythmic therapy were investigated for ventricular ectopic beats (VEB) prior to discharge after an acute myocardial infarction. The registration was performed for three hours during the day, including light exercise, and three hours at night. The overall VEB frequency was 70%. 34% had uniform VEBs, 22% multiform VEB'S, ANd 11% paired VEB'S 2% HAD THE R-on-T phenomenon and 1% ventricular tachycardia (VT). Ventricular irritability was more common in patients discharged after reinfarction, an estimated large infarct, if they had shown VT or ventricular fibrillation in the acute phase or when treated with diuretics only because of heart failure. There was no lowering of the VEB incidence at night, 17 patients having had ventricular arrhythmias at night only. In 5 cases the VEB'S were of a higher degree during exercise than at rest.
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PMID:Ventricular arrhythmias prior to discharge after acute myocardial infarction. 126 81

Left ventricular catheterization was carried out in 40 patients with acute myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) was elevated in 85% of the patients studied. In 14 patients with apparently uncomplicated infarcts, LVEDP averaged 15 mm Hg, and cardiac index (2.98 liter/min/m(2)), stroke volume (38.3 ml/m(2)), and stroke work (49.2 g-m/m(2)) were within normal limits. In 12 patients with clinical signs of left ventricular failure, LVEDP averaged 29.9 mm Hg, cardiac index was at the lower limit of normal (2.79 liter/min/m(2)), but stroke volume (31.6 ml/m(2)) and stroke work (37.3 g-m/m(2)) were reduced. In 14 patients with clinical signs of shock, LVEDP averaged significantly lower than in the heart failure group (21.1 mm Hg), but cardiac index (1.59 liter/min/m(2)), stroke volume (16.5 ml/m(2)), and stroke work (11.1 g-m/m(2)) were markedly reduced. A large presystolic atrial "kick" (average amplitude 9.5 mm Hg) was an important factor in the high LVEDP in the patients with heart failure but not in those with shock. The first derivative of left ventricular pressure was significantly lower in shock than in the nonshock group. Although right atrial pressure (RAP) and LVEDP were significantly correlated (r = 0.49), wide discrepancies in individual patients rendered the RAP an unreliable indicator of the magnitude of left ventricular filling pressure. THESE DATA SHOW THE FOLLOWING: (a) LVEDP is usually elevated in acute myocardial infarction, even in absence of clinical heart failure; (b) cardiac output apparently is supported by increased LVEDP and compensatory tachycardia; (c) in patients with shock, left ventricular function usually is markedly impaired, but inadequate compensatory cardiac dilatation or tachycardia could contribute to the reduced cardiac output in some individuals; (d) lower LVEDP in shock than in heart failure may represent differences in left ventricular compliance.
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PMID:Left ventricular function in acute myocardial infarction. 510 78

ACTIONS OF THE SYMPATHETIC NERVOUS SYSTEM: The sympathetic nervous system is an important cardiovascular regulator, particularly during stress and exercise; its sympathetic nervous activity is regulated in centers in the brain stem and transmitted to organs and blood vessels that are innervated by sympathetic nerve endings. In the heart, the sympathetic nervous system increases heart rate and contractility. The effect of the sympathetic nervous system in different vascular beds depends on the degree of innervation, the distribution of postjunctional receptors and the effect of local mediators. Overactivation of the sympathetic nervous system may lead to hypertension and is involved in heart failure. The degree of sympathetic activation determines prognosis in heart failure. Hence, vasodilators ideally should also blunt sympathetic activity, or at least avoid activating it. DIFFERENCES AMONG CALCIUM ANTAGONISTS: Calcium antagonists are widely used for the treatment of hypertension and coronary artery disease. Their main mechanism of action is inhibition of L-type Ca2+ channels. Short-acting nifedipine leads to a marked increase in heart rate, sympathetic nerve activity and plasma catecholamines, similar to those induced by a cold pressor test. With long-acting nifedipine heart rate does not increase, but sympathetic nerve activity does increase. Other calcium antagonists have been less thoroughly investigated, but indirect evidence suggests differences between the different classes. Verapamil and diltiazem lower heart rate. Plasma noradrenalin measurements suggest that verapamil does not stimulate the sympathetic nervous system, but tends to suppress it. Second-generation dihydropyridines with longer duration of action do not increase heart rate; their effects on peripheral sympathetic nerve activity are not clear. Thus, in summary, the different classes of calcium antagonists differ with regard to their effects on sympathetic nerve activation. A decrease in heart rate and nerve activity might be beneficial for long-term prognosis, particularly in hypertension and heart failure.
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PMID:Calcium antagonists and sympathetic nerve activation: are there differences between classes? 953 92

SYMPATHETIC NERVOUS SYSTEM AND HYPERTENSION: Biochemical, electrophysiological, pharmacological and haemodynamic findings support the existence of sympathetic nervous system activation in primary human hypertension. Analysis of regional sympathetic nervous system function, using both neurophysiological methods for measuring sympathetic nerve firing rates, and neurochemical techniques for quantifying regional noradrenaline spillover to plasma has demonstrated activation of the sympathetic nervous outflows to the heart, the kidneys, and skeletal muscle vasculature, particularly in younger patients. The initiating cause of this sympathetic nervous stimulation is unknown, but estimation of central nervous system noradrenaline turnover in hypertensive patients, using measurements of the washout of noradrenaline and its lipophilic metabolites into the internal jugular veins, indicates that activation of forebrain pressor noradrenergic nuclei is the probable underlying mechanism. CONSEQUENCES OF INCREASED SYMPATHETIC ACTIVITY: The sympathetic activation present in human hypertension no doubt contributes to the blood pressure elevation, and is a legitimate target for therapeutic intervention with imidazoline receptor-binding agents such as rilmenidine. In addition, the sympathetic nervous activation seems to have adverse consequences in hypertensive patients beyond initiating the blood pressure elevation. There is evidence that neural vasoconstriction has metabolic effects, in skeletal muscle impairing glucose delivery to muscle, causing insulin resistance and hyperinsulinaemia, and in liver retarding postprandial clearing of lipids, contributing to hyperlipidaemia. Cardiac sympathetic activation is demonstrably a cause of sudden death in heart failure patients; a comparable arrhythmogenic effect is probable in hypertension. A trophic effect of sympathetic activation on cardiovascular growth is also likely, contributing to the development of left ventricular hypertrophy. Rilmenidine, through its central nervous system actions, has been demonstrated to powerfully reduce sympathetic nervous activity in essential hypertension patients. INHIBITING THE SYMPATHETIC SYSTEM: As the clinical consequences of sympathetic nervous activation in essential hypertension appear to go beyond that of hypertension pathogenesis, extending to a causal influence in atherosclerosis development, cardiovascular hypertrophy and cardiac arrhythmias, it is possible that, of all antihypertensive drugs, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk. This remains to be tested.
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PMID:High blood pressure management: potential benefits of I1 agents. 974 6

ALTERATIONS OF THE ENDOTHELIUM: Because of its anatomic position between circulating blood and smooth muscle cells, the vascular endothelium is a prime target for cardiovascular diseases such as hypertension, hypercholesterolemia, diabetes or ischemia. The morphological changes occurring in the endothelium have been known for many years, but it was only recently that the functional alterations have been described. IMPACT OF NO: Under physiological conditions, the vascular endothelium plays a protective role by secreting relaxation factors. In the disease state, the synthesis and release of NO may be reduced or even abolished. The exact significance of endothelium-dependent vasodilatation disorders remains a topic of research, but the properties of NO strongly suggest it is involved in several diseases. For some diseases it is still a question as to whether the observed anomalies are the cause or the consequence of the underlying disease. DISEASE-SPECIFIC CHANGES: NO is known to be reduced in atherosclerosis, either because of less synthesis or accelerated degradation. In different experimental modules of hypertension, the baseline level of NO release appears to be decreased. Conversely, NO release can be normal, reduced or increased in diabetes. In heart failure, there appears to be not only a permanent alteration in NO secretion, but also an increase in factors stimulating vascular contraction, contributing to an altered capacity for vascular adaptation in these patients.
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PMID:[Nitric oxide (NO), vascular protection factor. NO related cardiovascular diseases]. 976 31

AIM OF THE STUDY: Heart failure is the final clinical presentation of a variety of cardiovascular diseases, such as coronary artery disease, hypertensive, toxic, and inflammatory heart disease. However, the cellular mechanisms responsible for the progressive deterioration of myocardial function observed in heart failure remain unclear and may result from cell death (programmed or not) and from an increase in number of nuclei and in the degree of their ploidy. METHODS: We examined thirty-eight explanted hearts obtained during transplantation for DNA content in the myocytic population. All thirty-eight patients had severe chronic heart failure: 23 had idiopathic dilated cardiomyopathy, and 15 had ischemic cardiomyopathy. Ten hearts of people whose death was not due to primary heart disease or as a consequence of major risk factors of coronary artery disease, including hypertension, diabetes, obesity, or severe atherosclerosis, were used as controls. DNA content in the myocytic population was evaluated using Image Cytometry. RESULTS: The DNA content per nucleus and per myocyte in cardiomyopathic hearts are characterized by: a) a decrease of the diploid DNA content of myocytic nuclei; b) an increase of DNA ploidies higher than 4c; c) a decrease in mononucleated myocytes; d) an increase in binucleated and multinucleated myocytes. The changes are more prominent in dilated cardiomyopathy. e) The total ploidy index, used to calculate the total DNA content, is related to heart weight and ventricular weight. CONCLUSIONS: Ischemic and dilated cardiomyopathies result in reduction of ventricular mass-to-chamber volume ratio and in discrete foci of myocyte cell death, leading to an elevation in systolic and diastolic stress on the remaining viable cells. Therefore mechanical stimuli generated by global and local loading abnormalities associated with end-stage failure may contribute to activate genes implicated in cell proliferation. Observations in this investigation are consistent with recent results documenting that in the presence of overload conditions the myocytes may retain their capacity to proliferate throughout life and this growth reserve mechanism may become operative in response to severe myocardial dysfuntion and overt failure. Polyploidization and multinucleation are prominent phenomena in the end-stage of ischemic and dilated cardiomyopathy in humans.
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PMID:DNA Content in End-Stage Heart Failure. 1035 69

The use of helical CT, infusing pump and non-ionic contrast media has enabled the evaluation of different hepatic circulatory phases during contrast injection. Starting the acquisition of scans 20 to 30 seconds after the injection at a rate of 3 to 4 ml/sec the arterial enhancing of the liver is depicted. THROMBOSIS OR COMPRESSION OF THE PORTAL VEIN: Hypervascular triangle-shaped was with peripheral base can be seen, secondary to the increased arterial flow to compensate for the diminished portal flow. ARTERIOPORTAL SHUNTS: This condition can be caused by tumors such hepatocellular adenocarcinomas and hemangiomas, trauma, interventional procedures, cirrhosis, AVMs and surgery. INFLAMMATORY LESIONS: Hypervascular areas can be seen during the arterial phase in abscesses or cholecystitis, returning to their normal condition in the arterial phase. ANATOMIC VARIANTS: Third veins coming from the periphery (capsular veins, accessory cystic vein and an aberrant gastric vein) supply enhanced blood earlier than the portal circulation. OTHER CAUSES: In liver cirrhosis diffuse hyperattenuated areas can be seen during the arterial circulation. In right-sided heart failure, pericardial disease and Budd-Chiari Syndrome, "mosaic areas" can also be noted. In other patients these perfusion disorders were considered unknown. TUMORS: The well-differentiated hepatocellular carcinoma is a lesion with a predominant arterial blood supply, thus appearing in general hyperdense in this phase. Hemangiomas may appear as highly hyperdense lesions in the arterial phase and can be misinterpreted as HCC if smaller than 2 cm. (30% of cases). Focal nodular hyperplasia is a benign lesion (vascular malformation associated with focal nodules of hepatocellular hyperplasia) with increased arterial blood supply. Hepatic adenomas show an important hypervascularity during the arterial phase and, if large, they may present a small central scar and or capsule. Low or high-grade dysplastic nodules can sometimes be seen as hypervascular areas during the arterial phase. Although most metastasis are depicted as hypodense lesions sometimes they can show arterial hypervascularity such as carcinoid and pancreatic islet cell metastasis.
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PMID:[Liver hyperdensity during arterial phase on CT exams]. 1147 23

FROM A CLINICAL POINT OF VIEW: Diagnosis of dysthyroidism in the elderly is particularly difficult because of the lack of sensitivity and specificity of classical symptoms and examinations. Neuro-mental and cardiovascular signs are frequent: dysthyroidism should always be searched for in the presence of dementia, depressive syndrome, heart failure or tachyarrhythmia. BIOLOGICAL DATA: Simple screening must therefore be widely proposed and relies on complete thyroid stimulating hormone (TSH) assay, further completed by free thyroid hormone assay. Biological diagnosis is easy in the healthy elderly patient, but interpretation of the assays is delicate in the case of intercurrent diseases or treatment with amiodarone. THE CAUSES TO BE LOOKED FOR: The detection of hypothyroidism does not require etiological exploration, other than the search for iodine overload. In cases of hyperthyroidism, scanning usually reveals a nodular goitre. THERAPEUTIC REGIMENS: In most cases treatment is simple. Replacement therapy is used for hypothyroidism. Patience and cardiovascular monitoring are essential. In the absence of iodine overload or compressive goitre, radioactive iodine is the treatment of choice. These simple treatments avoid the loss of physical and mental autonomy and cardiovascular complications. The importance of screening of these so-called "profitable" diseases in the elderly is obvious.
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PMID:[Dysthyroidism in elderly patients. Clinical characteristics]. 1181 26

TODAY: The management of heart failure (HF) has considerably progressed over the last two decades. Treatment today relies on prevention and treatment of congestion (limited salt intake, diuretics, converting enzyme inhibitors) and limiting neurohormone stimulation (converting enzyme inhibitors +/- aldactone, beta-blockers). IN THE YEARS TO COME: Based on new concepts, several therapeutic strategies are interesting: blocking over vasoconstrictor systems which have not been taking into account; stimulation of vasodilator and natriuretic systems; modulation of cardiac remodelling; modulation of the immune and inflammatory systems; modification in intrinsic contractility; prevention of rhythm disorders. Among these differing strategies and molecules, it is not easy to predict those that will change the HF prognosis. In any event, their efficacy and safety remain to be demonstrated with large cohort randomised studies. THE PRINCIPLES: To reduce the number of drugs administered, two options appear particularly interesting: measurement of hormone levels (BNP) in order to adjust treatment and administration of molecules with greatest efficacy and safety profiles; limit cardiac remodelling by using new imaging techniques to detect it more precisely and select the molecule(s) exerting the required effect. To target the new molecules better, patients should be classified according to their etiology, stage and progressive profile of their disease, cardiac remodelling, expression of principle endocrine systems and pro-inflammatory cytokines, expression of inflammatory and immune systems and inherent genetic characteristics and response to treatment. This would permit the adaptation of treatment to each individual patient with heart failure.
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PMID:[Future molecules in heart failure]. 1182 85

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