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

A young woman presented with rapidly progressive dyspnea and clinical findings strongly suggestive of primary pulmonary hypertension or possible pulmonary embolism (or both). She died of acute right-sided heart failure. A diagnosis of pulmonary veno-occlusive disease was made at autopsy. Approximately 100 cases of this disease have been reported previously in the literature. We describe a patient with a particularly florid progression of this unusual disease. Death occurred within six weeks of the onset of symptoms.
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PMID:Florid pulmonary veno-occlusive disease. 220 15

The limiting of the reporting of maternal deaths to those that are included in the criteria of the World Health Organization excludes deaths which yield useful information for further improvements in clinical performance. In this series of 22 maternal deaths, six deaths would have been excluded from reporting: one "direct" obstetric death of pre-eclampsia; one "indirect" death as a result of renal and cardiac failure; two deaths as a result of postnatal depression which led to suicide three and four months postpartum, respectively; and two deaths of cancers, where diagnostic delay may have been a result of the coexistent pregnancy. The importance of primary pulmonary hypertension, cardiomyopathy and psychiatric illness is emphasized. We endorse the recent recommendation of the International Federation of Gynaecology and Obstetrics (FIGO) that all maternal deaths that occur more than 42 days after the end of a pregnancy should be assessed for possible relationships with childbirth, and suggest that a time limit of one year would include all deaths that are worthy of scrutiny.
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PMID:When is a maternal death a maternal death? A review of maternal deaths at the Mercy Maternity Hospital, Melbourne. 259 8

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

Clinical and pathologic findings in seven patients who died of severe pulmonary artery hypertension due to toxic oil syndrome are assessed. These cases correspond to a late stage of evolution of the disease characterized by progressive deterioration in clinical features--increasing dyspnea, chest pain, syncope, and death (in low-output heart failure). The main pathologic pulmonary vascular findings consisted of plexiform lesions, thromboses, and venous lesions. Endothelial damage induced by the toxic agents is suggested as an initial causative mechanism, perpetuated by intimal proliferation and in situ thrombosis. Plexiform lesions appear late and active histologically. This new cause of pulmonary artery hypertension, with pathologic findings similar to those found in primary pulmonary hypertension, may help in understanding the pathophysiology of this unknown disease.
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PMID:Pulmonary hypertension due to toxic oil syndrome. A clinicopathologic study. 291 83

Cardiac transplantation has emerged as a standard mode of clinical therapy for end-stage heart failure, while heart-lung transplantation is still an experimental rather than a standard mode of clinical therapy for end-stage heart and lung disease. Since clinical application of heart-lung transplantation began in March 1981, there has been continual improvement in donor care, surgery, post-operative management, and the diagnosis and treatment of lung and heart rejection. According to our 6-year clinical experience, both patients with Eisenmenger's physiology and patients with primary pulmonary hypertension are considered suitable candidates for heart-lung transplantation. In the future, our recipient population will include small children and patients with cystic fibrosis. Suitable candidates must have good liver and kidney function, and freedom from previous major pulmonary emboli, systemic diseases, and previous thoracic surgery. Patients must maintain their functional and emotional status to pass successfully the difficult postoperative period. Proper donor and recipient selection in connection with improved heart-lung preservation has resulted in excellent operative survival (100%) following the last ten operations, and only the lack of suitable donors can limit the number of heart-lung transplantations in the future.
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PMID:Recipient selection for heart-lung transplantation. 314 9

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

The present study was undertaken to clarify the natural history of primary pulmonary hypertension (PPH) from a hemodynamic point of view. The subjects consisted of 83 patients (18 men and 65 women), whose ages ranged from 14 to 69 years and averaged 33 years. They were contacted through a nationwide survey. All patients underwent right-sided cardiac catheterization; cardiac output was measured in 52 patients and pulmonary capillary wedge pressure, in 40 patients. The following results were obtained. 1. The patients who died within three months of their cardiac catheterization were in severe right ventricular failure as shown by their elevated right atrial pressures and decreased cardiac indices. 2. The patients who died suddenly within two years of their cardiac catheterization had the same degree of right ventricular failure. The only difference was severe hypoxia in the patients with cardiac failure (54 +/- 21 vs 66 +/- 4 mmHg, p less than 0.05). 3. The patients who survived more than two years had normal right ventricular function. 4. Among the hemodynamic variables used to estimate prognosis; namely, pulmonary artery diastolic pressure, pulmonary capillary wedge pressure, cardiac index, pulmonary vascular resistance and pulmonary to systemic vascular resistance ratio, the cardiac index was the best predictor of prognosis.
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PMID:[Natural history of primary pulmonary hypertension elucidated by pulmonary hemodynamics]. 324 88

An 8 year old girl with primary pulmonary hypertension and signs of heart failure was given 17.5 mg of verapamil injected into the pulmonary artery over 25 minutes to test for the reversibility of pulmonary arteriolar obstruction. Pulmonary artery pressure fell from 70/50 to 35/25 mm Hg. Treatment with 40 mg verapamil by mouth four times daily was started, and she was discharged. She gradually became asymptomatic and resumed the activities of a normal child of school age. On recatheterisation seven months later her pulmonary artery pressure was 30/10 mm Hg. She was still doing well 12 months after the start of treatment.
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PMID:Verapamil in primary pulmonary hypertension. 397 Jul 93

Despite the high incidence of sudden death in pregnant patients with primary pulmonary hypertension (PPH) and heart failure, no data are available that thoroughly elucidate the peripartum hemodynamic alterations occurring in these patients. The present report describes the clinical course of a pregnant patient with PPH and provides data regarding peripartum hemodynamic alterations. Hemodynamic parameters were stable during labor and delivery, but pulmonary vascular resistance rose gradually while cardiac output fell after parturition. Dobutamine caused a modest but unsustained increase in cardiac output. Nitroprusside produced a significant sustained augmentation of cardiac output from 3.5 to 5.0 liters/min due to reduction of systemic and pulmonary vascular resistances, and permitted restoration of hemodynamic stability and resolution of heart failure. The authors believe that pregnant patients with PPH and severe heart failure in whom abortion is not possible should have complete hemodynamic monitoring during parturition and for several days thereafter. Segmental epidural anesthesia and lateral positioning of the patient minimize hemodynamic alterations during labor and delivery. Nitroprusside and dobutamine may be effective for treatment of congestive heart failure.
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PMID:Peripartum heart failure due to primary pulmonary hypertension. 687 14

The results of the medical treatment of primary pulmonary hypertension are usually very poor. A case of severe primary pulmonary hypertension in chronic heart failure was treated with the calcium antagonist nifedipine, a powerful vasodilator which acts directly on vascular smooth muscle. Nifedipine, administered in a dose of 20 mg sublingually, caused a pronounced fall in pulmonary and systemic vascular resistances (54 and 49%, respectively) and a rise in cardiac output (90.3%). Improvement was maintained over a three-month period. These data suggest that nifedipine can be used in the treatment of this condition.
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PMID:Primary pulmonary hypertension: effects of nifedipine. 742 94


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