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

The pathological changes in blood vessels observed in primary (essential hypertension) are similar to those seen in secondary hypertension due to renal disease or other causes. In benign hypertension, the major changes are in the small arteries and arterioles especially in the kidney. Interlobular arteries exhibit intimal thickening and duplication of the elastic lamina (elastosis) and there is hyaline change in the media of many arterioles. In some respects these changes are an accentuation of vessel ageing. Malignant hypertension usually presents in a younger age group (35--50 years) and is characterized pathologically by fibrous endarteritis in the interlobular arteries of the kidney and fibrinoid necrosis in the walls of a proportion of the efferent glomerular arterioles. Similar vessel changes are seen in other organs but many of the pathological changes in the heart and brain of patients with benign hypertension are related to the accentuation of arterosclerosis. There is an increased mortality from cardiac failure, myocardial infarction, cerebral haemorrhage and subarachnoid haemorrhage due to ruptured berry aneurysms in patients with benign hypertension. Although there is ischaemic damage to the kidneys in benign hypertension, death from renal failure is uncommon. Severe ischaemic damage to renal glomeruli and renal failure does, however, occur in malignant hypertension.
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PMID:Vascular pathology in hypertension. 46 85

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.
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PMID:[A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia]. 153 80

A 55-year-old man with a mild fever and sweating developed severe headache for the days before admission. Cerebral computed tomography and selected cerebral angiography on the day of admission revealed subarachnoid hemorrhage due to rupture of an aneurysm of a distal branch of the left middle cerebral artery. Detection of vegetation on the aortic valve by two dimensional echocardiography confirmed the diagnosis of infective endocarditis with a ruptured mycotic cerebral aneurysm. Because of rapid growth of the vegetation on the aortic valve and progression of heart failure despite antibiotic therapy, emergency cardiac surgery was performed. To prevent re-rupture of the aneurysm, the aortic valve was replaced with a bioprosthetic valve, and no anticoagulant was administered postoperatively. Repeated cerebral angiography revealed that the aneurysm was becoming progressively smaller during the next 9 months. No cerebrovascular accident occurred postoperatively. We believe that it is safe to treat a ruptured mycotic cerebral aneurysm without involvement of a hematoma mass in the brain conservatively, and that use of a bioprosthetic valve, if valve replacement is mandatory, and avoidance of anticoagulant therapy during the postoperative period are advisable in the treatment of a patient with infective endocarditis and a ruptured cerebral mycotic aneurysm.
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PMID:[Valve replacement in a patient with infective endocarditis and ruptured mycotic cerebral aneurysm]. 156 43

Catecholamines mediate their effects in the heart through beta 1- and beta 2-receptors. Beta 1-receptors mediate the effects of sympathetic nerve stimulation. Alpha-receptors may have a role but, unlike the beta-receptor mediated responses, act without producing any increase in cyclic AMP. Prolonged receptor stimulation results in a reduction in beta-receptor sensitivity. In contrast blockade with a non-agonist agent is associated with an increase in catecholamine sensitivity which may be responsible for the withdrawal reactions that can occur when beta-blocking drugs are rapidly withdrawn in patients with ischaemic heart disease. Experimentally, prolonged noradrenaline infusions result in ventricular hypertrophy. Catecholamines have been implicated in several pathologies. High and rising catecholamine levels are associated with worsening of prognosis in patients with heart failure. These patients show a decreased beta-receptor number and cellular concentration of catecholamines. On the other hand cardiomyopathy is associated with an increased sensitivity to catecholamines. Catecholamines aggravate cardiac damage in ischaemia. Excessively high catecholamine loads cause myocardial damage in otherwise normal hearts, for example in patients with a phaeochromocytoma and those with various forms of cerebral damage such as subarachnoid haemorrhage, cerebrovascular accidents, and head injury.
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PMID:Heart and catecholamines. 168 38

The effects of hyperdynamic therapy on patients with cerebral vasospasm following subarachnoid hemorrhage (SAH), under normal blood pressure (BP) and normal blood volume conditions, are reported. Forty-four patients, who underwent surgery for aneurysms in acute stage, received hydroxyethyl starch (500 ml/day) postoperatively to prevent dehydration. Twenty-four of the 44 patients with prominent SAH on the computed tomographic (CT) scan, anticipating to develop cerebral ischemia due to vasospasm, were given dobutamine (DOB). The BP was maintained within the normal range, and the heart rate was kept below 130/min. In the 24 patients treated with DOB, cerebral blood flow (CBF) was measured repeatedly by the 133Xe intravenous injection method. In 8 of these 24 patients, the cardiovascular function was monitored with Swan-Ganz (S-G) catheters. Twelve of the 44 patients (27%) developed delayed neurological deficits associated with cerebral vasospasm. The neurological deficits were reversed by the administration of DOB, at a dose of 8-25 (average 12.4) micrograms/kg/min. In 43 patients, the ischemic lesions associated with vasospasm did not appear on CT scan and the patients were of normal condition at discharge. However, one patient showed multiple low-density lesions on CT scan. This was because of the failure of hyperdynamic therapy due to pulmonary complications. No case of pulmonary edema or heart failure due to volume overload was noted. In the 24 patients with prominent SAH, CBF increased significantly by up to 20% following DOB administration, although the BP stayed in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperdynamic therapy for cerebral vasospasm. 169 47

We determined serum atrial natriuretic peptide (ANP) and anti-diuretic hormone (ADH) on a time course basis in cases of subarachnoid hemorrhage and studied their influence on the development of hyponatremia. Twenty six cases of subarachnoid hemorrhage were admitted to our hospital in the past 1 year, and by the site of ruptured aneurysms, there were Acom 6 cases, ICA 6 cases, MCA 5 cases and VA BA 4 cases. Serum ANP and ADH levels were determined in the acute phase on Day 1-4, in the hyponatremia phase on Day 5-14 and in the chronic phase on Day 15 downward. Levels of not more than 130 mEq/l were regarded as hyponatremia. Cases showing other evident causes such as heart failure and renal insufficiency were excluded. In the normal control group (n = 20) which was admitted to this hospital for a close check-up, serum ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of more than 50 pg/ml were regarded as being abnormally high. 1) Hyponatremia was observed in 7 cases (26-9%); the day of onset was 11.9 hospital day. The duration was 5.0 days and the minimum serum Na level was 126.4 mEq/l. 2) The serum ADH level was high regardless of whether or not there was the development of hyponatremia in the acute phase but tended to decrease gradually and became normal in the hyponatremia phase. 3) The serum ANP level in the cases of hyponatremia was 40.7 +/- 9.1 pg/ml in the acute phase, 69.0 +/- 25.7 pg/ml in the hyponatremia phase and 40.2 +/- 21.5 pg/ml in the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum ANP and ADH after subarachnoid hemorrhage and hyponatremia]. 183 72

Although much has been written on the response of the heart to various intracerebral events including seizures, ischemia, intracerebral, and subarachnoid hemorrhage, less is known of the cerebral response to altered cardiac rhythm, cardiac failure, and cardiac arrest. The latter may alter central neuronal activity, cerebral blood flow, or cause ischemic damage. Such changes in cerebral function may lead to loss of consciousness, seizures, and focal neurologic deficits at the clinical level.
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PMID:Neurologic manifestations of cardiac disease. 267 32

Fifteen children and adolescents with intracranial arteriovenous malformations are reviewed and their data analyzed; their ages varied between 1 day and 15 years and there was a slight predominance of males (9 male and 6 female patients). In this series, the arteriovenous malformations appeared clinically as cerebral hemorrhage in 9 cases, epilepsy in 3, mental retardation with epilepsy in 1, subarachnoid hemorrhage in 1, and cardiac insufficiency at birth in the other. The diagnostic procedures used were computerized transmission tomography (CTT) of the cerebrum in 14 cases, cerebral panarteriography in 15, and EEG in 4 cases. Treatment took the form of surgery, radiation therapy, or medication. The last was administered to patients with epilepsy, either as a complement to other modes of treatment or as the only treatment. In all, 4 cases died, 2 for reasons to do with their operations, 1 from a lesion of the brain stem in a hematoma of the cerebellum that had not been surgically treated, and the other from an intraventricular hemorrhage 4 months after surgery. In the last patient, necropsy revealed remnants of the arteriovenous malformation. The overall mortality was thus 26% and the surgical mortality, 12.6%. Of the 11 surviving patients only 3 received anticonvulsant drugs; each of them had a good I.Q. and good marks at school, as did the other 8 survivors.
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PMID:Intracranial arteriovenous malformations in infancy and adolescence. 270 71

One of the most common problems in emergency anesthesia for cerebral aneurysm surgery is clinically significant ECG abnormalities. We had a 58 year old patient with severe subarachnoid hemorrhage and diffuse lung edema leading to fatal outcome probably due to catecholamine myocardial injury. During the operative intervention with enflurane and oxygen anesthesia, ST elevation on ECG suddenly appeared and heart failure developed in this patient. Intraoperative ECG suggested the development of acute myocardial infarction of the anterior and inferior wall, but echocardiography revealed a discrepant result; the wall motion abnormality was confirmed in the apex only. The serum CPK in this patient increased a little over the normal limit perioperatively. Overall results suggested that a cause of this patient's death was myocardial injury due to the excessive release of catecholamine. Therefore, we urge the need of through cardiac examinations as well as the administration of preventive drugs for catecholamine myocardial injury in the perioperative management of patients with severe subarachnoid hemorrhage.
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PMID:[Anesthetic management of a patient with severe subarachnoid hemorrhage and diffuse lung edema]. 281 Jul 5

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29


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