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

This report dealt with a rapidly growing ball thrombus floating in the left atrium in a case with mitral stenosis detected by serial two-dimensional echocardiography and confirmed at operation. A 45-year-old female was admitted to our hospital on January 7, 1982 because of dyspnea, orthopnea and fever. On admission she had typical auscultatory signs of mitral stenosis, and her chest roentgenogram revealed slight pulmonary venous congestion and marked left atrial enlargement. Laboratory findings including complete blood counts, coagulation studies and blood chemistry were normal except a positive CRP test. Two-dimensional echocardiography performed on January 8 revealed a tight mitral stenosis with the mitral orifice area of about 0.9 cm2, and a floating ball thrombus in the left atrium, which was 2.5 X 3 cm in size. Fuzzy echoes flowing slowly around the thrombus were also observed. Intravenous administration of heparin was started immediately. In the next morning (January 9), the two-dimensional echocardiography was reexamined, which revealed a markedly growing thrombus which became 4 X 4 cm in size. Several hours after the reexamination mitral valve replacement was performed. The removed thrombus was 5.5 X 7 cm in size and consisted of three laminated structures. This finding was consistent with the echocardiographic observations. Coagulation studies made just before operation showed increased coagulability. Increased stagnation of blood in the left atrium due to heart failure and a transient increase of blood cell aggregation and coagulability induced by preceding infection might be responsible for the genesis of such a thrombus.
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PMID:[Two-dimensional echocardiographic observation of a rapidly growing floating left atrial ball thrombus: report of a case with mitral stenosis]. 667 1

Varying degrees of respiratory distress developed in 3 dogs in which hyperadrenocorticism was diagnosed. The respiratory distress was attributed to pulmonary artery thrombosis. Radiography revealed pleural effusion, increased diameter and blunting of the pulmonary arteries, lack of perfusion of the obstructed pulmonary vasculature, and overperfusion of the unobstructed pulmonary vasculature. Thrombosis was confirmed by nonselective angiocardiography in each case. In 1 case, selective angiocardiography showed marked reduction of the transit time of contrast medium from the right atrium to the aorta. Hypertension proximal to the site of thrombosis was confirmed in 2 cases by showing increases in the right ventricular systolic pressures (80 mm of Hg in one case and 54 mm of Hg in the other case). In 3 cases, there was moderate hypoxemia with hypocapnia, suggesting a ventilation-perfusion mismatch. Clinical findings other than respiratory distress included hepatomegaly, ventral edema, orthopnea, and a jugular pulse. Pulmonary artery thrombosis, as it occurred in these 3 cases, was compared with the disease in man. It was concluded that pulmonary artery thrombosis should be suspected in cases of intractable dyspnea, right-sided heart failure of unexplained origin, and acute unexplainable death.
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PMID:Pulmonary artery thrombosis in three dogs with hyperadrenocorticism. 723 99

A case of timolol-associated heart failure in a 73-year old white man is reported. The patient, with a history of cardiovascular disease and glaucoma, was admitted to the hospital because of complaints of shortness of breath, orthopnea, and reduced exercise tolerance. Chest roentgenogram showed interstitial congestive failure, and an EKG demonstrated sinus bradycardia. The patient's medications before admission included quinidine, isosorbide dinitrate, dipyridamole, aspirin, pilocarpine eyedrops 4%, timolol eyedrops 0.5%, and nitroglycerin ointment and sublingual tablets. On the second day of hospitalization, it was noted that the patient's dyspnea and sinus bradycardia could be related to a recent increase in his timolol dosage. The timolol was discontinued, and the patient's heart rate increased. As the patient's pulse rate increased, the symptoms of congestive heart failure disappeared. This case demonstrated the importance of obtaining complete drug histories from patients. The potential for adverse system reactions resulting from topical medications should be considered.
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PMID:Bradycardia and congestive heart failure associated with ocular timolol maleate. 728 2

Medical therapy often fails to control symptoms of severe heart failure. The possibility of modifying to some degree the global ventricular performance with the implantation of a physiological dual chamber pacemaker, set with a short atrioventricular delay (100 msec), has been adopted in two patients with severe heart failure due to coronary artery disease. The baseline clinical condition of both patients was characterized by leg edema, ascites, dyspnea at rest, or even orthopnea with a functional New York Heart Association (NYHA) class III-IV. Acute measurements of hemodynamic and echocardiographic parameters during stepwise shortening of AV interval guided the pacemaker implantation and setting of AV delay in the chronic phase. Within a few days after pacemaker implantation, both patients considerably improved their clinical status as well as their functional NYHA class, improving to class II in one patient and to class II-III in the other patient. In addition, modification of systolic and diastolic parameters paralleled these improvements functional class and clinical condition. Pacemaker therapy in severe heart failure refractory to medical therapy can be of considerable benefit in patients whose quality-of-life is severely compromised when pharmacological therapy is no longer effective. Acute hemodynamic and echocardiographic testing is useful in assessing the most appropriate AV delay and pacing mode.
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PMID:Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual chamber pacing with shortened AV delay. 751 39

The authors present the clinical history of a 70-year-old male with arterial hypertension who sought medical advice because of dyspnea on exertion, orthopnea and episodes of paroxysmal nocturnal dyspnea. The electrocardiogram showed left arterial hemiblock and abnormalities of ventricular repolarization compatible with a left lateral endocardiac lesion. Echocardiography revealed a hypertrophied left ventricle with a small ventricular cavity, compatible with an infiltrative-restrictive myopathy. Blood chemistry showed creatinine 4.9 mg/dl, BUN 133 mg/dl and alkaline phosphatase 204 i.v. The patient expired because of intractable heart failure. The histopathological examination of a piece of myocardium (authorized by the family) stained with Congo red confirmed the presence of abundant, diffuse deposits of amyloid, as had been suspected because of the echocardiographic findings.
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PMID:[Cardiac amyloidosis secondary to multiple myeloma detected by echocardiography]. 774 97

Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
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PMID:Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease. 967 Mar 10

A 45 year old man presented with a five week history of worsening exertional dyspnoea and orthopnoea. He had also noted mild, bilateral ankle swelling. The patient had been diagnosed with stage III Hodgkin's lymphoma in 1968 at the age of 21. During the same year he underwent total nodal irradiation followed by chemotherapy in 1971. He had remained entirely asymptomatic over the course of the next 24 years with no evidence of relapse. Cardiac catheterisation undertaken soon after admission revealed a tight left main stem stenosis with a left dominant system. Left ventriculogram showed severe, global hypokinesia, and raised left ventricular end diastolic pressure (22 mm Hg). Urgent coronary artery bypass graft surgery was carried out. He made an uncomplicated recovery and his condition improved sufficiently to allow discharge eight days following the procedure. His heart failure slowly resolved and repeat transthoracic echocardiogram performed six months after surgery showed an unequivocal improvement in left ventricular function. Left ventricular ejection fraction continued to improve and increased from 23% at two months to 42% at two years. He currently remains entirely asymptomatic off all medication.
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PMID:Hibernating myocardium caused by isolated, radiation induced left main stem coronary artery stenosis. 940 63

The long term impact of pre-hospital thrombolysis in acute myocardial infarction on the subsequent development of heart failure symptoms was investigated in 362 consecutive patients. The pre hospital strategy, used in 61 patients, allowed for very early administration of streptokinase, within 1.2+/-0.6 (mean+/-S.D.) hours from pain onset. In contrast, 294 patients treated in hospital received lytic treatment within 2.0+/-0.9 hours. The pre hospital group showed faster reperfusion, as measured by the time to peak creatine kinase and to ST segment recovery, but only a slightly better ventricular function, as compared to hospital treated patients. Heart failure symptoms were significantly reduced in the pre hospital group during hospitalization and at long term follow up: there were less dyspnea, fatigue, orthopnea, nocturnal dyspnea, nocturia, peripheral edema and episodes of pulmonary edema. Angina was reduced as well. We conclude that the initial benefit of prehospital thrombolysis translates into long term reduction of heart failure symptoms, thus improving quality of life.
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PMID:Prevention of congestive heart failure by early, prehospital thrombolysis in acute myocardial infarction: a long-term follow-up study. 970 26

We report the case of a 57-year old man who was admitted to our department because of worsening dyspnea - orthopnea and whose aortic valve had been replaced 31 years previously, with a Starr-Edwards caged-ball prosthesis. His symptoms' deterioration was due to a recent myocardial infarction which in combination with the chronic mitral regurgitation of rheumatic origin led to heart failure. As assessed by echocardiography the mechanical prosthesis did not show signs of significant dysfunction and except for mild regurgitation, it had a good performance. Despite some valve related complications, such as the recurrent thromboembolic events that our patient had, his Starr Edwards aortic prosthesis demonstrated an excellent long term durability and reliability.
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PMID:Thirty one-year durability of a Starr-Edwards aortic prosthesis. 983 29

An 88-year-old woman was admitted to our hospital because of palpitations, dyspnea, orthopnea and appetite loss. On admission, small crackles were heard on her lower back, and her liver was swollen. Chest rentogenogram showed cardiomegaly (cardio-thoracic ratio 65.5%) and bilateral pleural effusion. Electrocardiograms showed atrial fibrillation with an average heart rate of 95 per minute. Echocardiography revealed mitral stenosis. Because the patient was considered to be suffered from heart failure due to mitral stenosis with atrial fibrillation, furosemide (20 mg per day) and digoxin (0.25 mg per day) was started. After digoxin had been raised to a dose of 0.50 mg per day because of sustained rapid ventricular response on the fourth hospital day, she complained of nausea and vomiting. Serum digoxin concentration was 2.55 ng/ml on the next day, and 1.08 ng/ml 96 hours after discontinuing digoxin. There was no complaint after digoxin was restarted with a dose of 0.05 mg per day. She complained of nausea again on the third day when the digoxin was raised to a dose of 0.083 mg in a blinded study. This observation indicates that digoxin intoxication could occur even in the smaller dose of digoxin than usual in the elderly.
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PMID:[An 88-year-old woman with symptoms of intoxication due to a small dose of digoxin]. 1036 32


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