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

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with substantial cardiovascular morbidity and mortality. The arrhythmia can be initiated and/or maintained by rapidly firing foci, single- and multiple-circuit reentry. Once initiated, AF alters atrial electrical and structural properties (atrial remodeling) in a way that promotes its own maintenance and recurrence and may alter the response to antiarrhythmic drugs. Thus, initial episodes of paroxysmal (self-terminating) AF lengthens to the point where the arrhythmia becomes persistent (requires cardioversion to restore sinus rhythm) and permanent. AF usually requires a trigger for initiation and a favorable electrophysiological and/or anatomical substrate for maintenance. The substrate includes both cardiovascular (coronary artery disease, valvular heart disease, heart failure, hypertension, dilated cardiomyopathy) and non cardiovascular diseases (thyrotoxicosis, pulmonary diseases). Accordingly, the initial step in patients with AF requires a careful assessment of symptoms and identification of underlying reversible triggers and potentially modifiable underlying structural substrate and treat them aggressively. In contrast to other cardiac arrhythmias, antiarrhythmic drugs (ADs) are the mainstay of therapy. Long-term treatment of AF is directed to restore and maintain the sinus rhythm with class I and III ADs (rhythm-control) or to allow AF to persist and ensure that the ventricular rate is controlled (rate-control) with atrioventricular nodal blocking drugs (digoxin, beta-blockers, verapamil, diltiazem) and prevent thromboembolic complications with anticoagulants. However, the long-term efficacy of ADs for preventing AF recurrence is far from ideal, because of limited efficacy (AF recurs in at least one-half of the patients) and potential side effects, particularly proarrhythmia. Thus, the choice of the appropriate AD will depend on the temporal pattern of the arrhythmia, the presence of associated diseases, easy of administration and adverse effects profile, particularly the risk of proarrhythmia. The recent finding that angiotensin converting enzyme inhibitors and beta-blockers reduce the incidence of AF in patients post myocardial infarction with left ventricular dysfunction confirmed the importance of targeting the underlying arrhythmogenic substrate. This review focuses on the mechanisms underlying AF and the mechanism of action and the efficacy and safety profile of the ADs used in the treatment of atrial fibrillation. The advantages and disadvantages of rhythm and rate control, the role pill in a pocket concept and the role of the new ADs are dicussed.
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PMID:Pharmacological approaches in the treatment of atrial fibrillation. 1475 23

Amiodarone-associated thyrotoxicosis (AAT) is often poorly tolerated owing to underlying cardiac disease, and it is frequently refractory to conventional medical treatment. The goal of this study was to describe the patient characteristics, management, and outcomes of all the patients treated surgically for AAT at a single institution. We conducted a retrospective chart review of all patients managed surgically for AAT (April 1985 through November 2002) at the Mayo Clinic in Rochester, Minnesota. Altogether, 29 men and 5 women, ages 39 to 85 years (median 60 years), treated with amiodarone for 3 to 108 months underwent near-total or total thyroidectomy. Frequent symptoms were worsening heart failure, fatigue, weight loss, and tremor. Altogether, 12 patients failed medical management of their AAT, and 21 received no preoperative medical therapy. One patient had been successfully managed medically but required definitive treatment. Common indications for operation were the need to remain on amiodarone, cardiac decompensation, medically refractory disease, and severe symptoms, both hyperthyroid and cardiac, necessitating prompt resolution. The median+/-SD American Society of Anesthesiologists (ASA) classification (1 = healthy through 5 = moribund) was 3.00+/-0.58. A total of 27 specimens had histology consistent with AAT. Complications included death (n = 3), rehospitalization (n = 3), symptomatic hypocalcemia (n = 2), pneumonia (n = 2), cervical hematoma (n = 1), prolonged ventilatorywean (n = 1), and stroke (n = 1); one patient developed hypotension, adult respiratory distress syndrome, and sepsis. Of the 31 surviving patients, 25 (80%) remained on amiodarone postoperatively. The median follow-up was 29 months, at which time all surviving patients were free of hyperthyroid symptoms. Thyroidectomy is an effective treatment for AAT but has a high incidence of perioperative morbidity and mortality. The cardiovascular co-morbidities and high operative risk in this group of patients may account for the increased complication rate.
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PMID:Surgical management of amiodarone-associated thyrotoxicosis: Mayo Clinic experience. 1549 61

Plasmapheresis, also known as therapeutic plasma exchange, is used in the treatment of several disorders. Temporary improvement after plasmapheresis in cases with thyrotoxicosis has been reported. A 55-year-old woman presented with agranulocytosis induced by propylthiouracil and clinical signs of heart failure. Three sessions of plasmapheresis were performed. We observed an improvement of thyroid hormone levels and clinical findings as well. Plasmapheresis can be an option when drug treatment of thyrotoxicosis fails.
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PMID:Plasmapheresis in the treatment of hyperthyroidism associated with agranulocytosis: A case report. 1549 48

In this study three problems concerning interactions between thyroid and cardiovascular system are discussed. Cardiac arrhythmias, congestive heart failure, pleural effusion, hyperlipidaemia, arterial hypertension may be consequences of thyroid disorders leading to inappropriate hormone secretion. During such illnesses as heart failure, myocardial infarction and in patients undergoing coronary artery bypass surgery profound changes may occur in thyroid hormone metabolism known as sick euthyroid syndrome. Treatment with amiodarone may lead to changes in thyroid tests results and to development of hypothyroidism or thyrotoxicosis.
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PMID:[Thyroid and cardiovascular disorders]. 1551 16

A 39-year-old white man was referred to our hospital for evaluation of his jaundice and pruritus. The patient was treated with I for diffuse toxic goiter prior to his referral to our hospital. Clinical examination and laboratory investigations excluded viral hepatitis, autoimmune hepatitis, granulomatous disease, primary biliary disease, extrahepatic biliary obstruction, and heart failure. Liver biopsy showed severe intrahepatic and canalicular cholestasis with minimal inflammatory changes. The patient's jaundice promptly resolved with therapy for hyperthyroidism and thyroid storm as bilirubin levels decreased from 35 mg/dL (normal: 0.5-1.2 mg/dL) to 0.4 mg/dL. Thyrotoxicosis can be an uncommon cause of profound cholestasis. Our case differs from all other reports in the literature because of the severity of the cholestasis and its prompt resolution with treatment for thyrotoxicosis.
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PMID:Severe cholestatic jaundice in hyperthyroidism after treatment with 131-iodine. 1559 31

Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone. The cardiovascular symptoms of thyrotoxicosis were described more than two hundred years ago and remained the basis of diagnosis in modern medicine. Myocardium, peripheral circulation and sympathetic nerve system, all affecting cardiovascular hemodynamics, are influenced by thyroid hormones in many ways. Sub-clinical hyperthyroidism is characterized by suppressed thyroid stimulating hormone and normal free triiodothyronine and free thyroxine levels. Cardiovascular symptoms: elevation of heart rate, myocardial contractility, stroke volume, myocardial oxygen consumption, systolic blood pressure and reduction in systemic vascular resistance and diastolic blood pressure can be often seen even in case of subclinical hyperthyroidism. Thyrotoxicosis exacerbates the symptoms of a preexisting heart disease, but it can also cause complaints in case of a structurally normal heart. The most common cardiac complications are arrhythmias (mainly atrial fibrillation), heart failure and hypertension. Amiodarone is used for the treatment and prevention of several arrhythmias. It is safely applicable even in case of left ventricular dysfunction. The more common application is limited by its side effects that can develop even at low doses and may involve several organs (thyroid gland, lungs, liver, heart, nerve system among others). The complex effect of amiodarone on thyroid function ranges from mild abnormalities of thyroid function tests to overt thyrotoxicosis or hypothyroidism.
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PMID:[Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone]. 1563 34

A 26-year-old man presented with high output heart failure and severe systolic left ventricular dysfunction. The underlying cause was determined to be thyrotoxicosis. With aggressive treatment of the hyperthyroid state, near-normalization of the patient's left ventricular systolic function was achieved. Unfortunately, he succumbed to pancreatitis, followed by multiple ICU complications. A brief review of the literature is provided.
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PMID:Thyrotoxicosis-an uncommon cause of heart failure. 1571 Feb 88

Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. Palpitations, caused by sinus tachycardia and occasionally by atrial fibrillation, are the most frequent cardiovascular symptom. As atrial fibrillation may be the only manifestation of thyrotoxicosis, thyroid hormone excess should routinely be excluded in patients with this rhythm disturbance. Heart failure occurs mostly in the presence of underlying heart disease or tachycardia-induced cardiomyopathy in patients with long-standing atrial fibrillation. On occasion, long-standing hyperthyroidism may lead to heart failure even in the absence of concomitant cardiac conditions. Beta-blockers offer symptomatic relief and at the same time slow the ventricular response in patients with atrial fibrillation. Amiodarone, and occasionally iodinated contrast agents, may cause iodine-induced thyrotoxicosis. Clinical suspicion is essential in the diagnosis of amiodarone-induced thyrotoxicosis (AIT), because the antiadrenergic effect of the drug may conceal symptoms. AIT should be considered in any patient on amiodarone in the presence of new-onset or recurrent atrial arrhythmias or unexplained weight loss. Beyond discontinuation of amiodarone, treatment options include propylthiouracil or methimazole, potassium perchlorate, steroids, lithium and, if pharmacological treatment fails, surgery. Amiodarone may potentially be used less frequently in the future since recent studies have shown that this drug is inferior to implantable cardioverter defibrillators in prevention of sudden cardiac death in patients with severe heart failure. In addition, non-iodinated amiodarone analogues are currently in advanced phase of clinical testing.
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PMID:Thyrotoxicosis and the cardiovascular system. 1598 1

A 53-yr-old previously healthy man was admitted to our hospital for thyrotoxicosis without ophthalmopathy. Initial therapy with propylthiouracil caused an acute elevation of liver enzymes. Then, he received a first course of 131I therapy (20 mCi). At the end of 6-mo follow-up after 131I, he was still thyrotoxic and developed moderately severe ophthalmopathy. The patient refused thyroid surgery and decided to undergo second course of 131I therapy (30 mCi). Concomitantly with the 131I, we opted to give high-dose pulse glucocorticoid therapy (PGT) to prevent further deterioration of GO. The patient was started on intravenous methylprednisolone pulse therapy 1 g daily in a cycle (one cycle every 2 wk, each cycle comprising two infusions on alternate days). After the end of the second day of PGT administration, he suddenly developed onset of acute pulmonary edema and hypertension. There was no previous history of cardiac disorder or conditions predisposing to cardiac failure other than thyrotoxicosis. A presumptive diagnosis of fluid overload and/or hypertension- induced acute heart failure was made. After prompt investigations excluding cardiogenic causes, we thought that this condition was triggered by PGT that was superimposed on thyrotoxicosis-related hemodynamic instability. Graves' patients with uncontrolled thyrotoxicosis should be under careful surveillance when PGT is planned. To our knowledge, this is the first reported case of life-threatening acute pulmonary edema caused by PGT in GO.
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PMID:New-onset acute heart failure after intravenous glucocorticoid pulse therapy in a patient with Graves' ophthalmopathy. 1694 91

Subacute thyroiditis is a possibly viral, inflammatory thyroid disorder which can cause thyrotoxicosis. Ventricular arrhythmias are uncommon in thyrotoxicosis and usually occur only in those with marked heart failure or associated cardiac disease. In this case, we present a 52-year-old woman having incessant ventricular tachycardia due to subacute thyroiditis without underlying cardiac disease.
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PMID:Incessant ventricular tachycardia due to subacute thyroiditis. 1713 71


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