Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old man was referred to our hospital in June 2014 because of severe heart failure. He was diagnosed with familial dilated cardiomyopathy and was administered oral tolvaptan and amiodarone for atrial and ventricular tachycardia. Since up-titration of carvedilol had failed and he was dependent on dobutamine, a left ventricular assist device (LVAD) was implanted. Tolvaptan and furosemide were both discontinued after LVAD implantation and he was discharged from the hospital. Thirteen months later, he was hospitalized for lethargy and hyponatremia of 108 mEq/L, with an antidiuretic hormone level of 2.5 pg/mL, which suggested syndrome of inappropriate antidiuretic hormone secretion (SIADH). We discontinued amiodarone and administered fludrocortisones. However, hyponatremia persisted for a few more days, eventually resulting in delirium and damage to the LVAD driveline. He received an urgent pump exchange and hyponatremia was gradually improved. We considered the possibility that amiodarone-induced SIADH was masked by tolvaptan therapy before LVAD implantation.
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PMID:Amiodarone-Induced Hyponatremia Masked by Tolvaptan in a Patient with an Implantable Left Ventricular Assist Device. 2915 94

BACKGROUND Influenza viruses induce uncomplicated infections in most cases in individuals with no known predisposing factors. Acute febrile illness is generally limited to upper respiratory symptoms and several constitutional symptoms, including headache, lethargy, and myalgia. However, influenza A virus is a cause of severe morbidity and mortality worldwide. Some patients are at risk for serious and fatal complications. Cardiac involvement is a well-known condition, but, clinically apparent influenza myocarditis is not common. Few reports exist regarding recurrent fulminant influenza myocarditis. CASE REPORT We report here a fatal case of heart failure following myocarditis in a 14-year-old female who had seasonal flu symptoms but was otherwise healthy. H3N2 influenza virus infection was detected by molecular analyses of throat and nasal swabs, suggesting damage to myocardial cells caused directly by the virus. CONCLUSIONS Pericardial effusion myopericarditis may occur during influenza virus infection in young individuals, even those with no known predisposing factors. Physicians need to be aware that acute myopericarditis can be a fatal complication of recent influenza virus infection in all patients with instable hemodynamics. Early diagnosis and treatment could reduce, in some cases, the risk of severe cardiac events. However, this sudden and fatal outcome was difficult to predict in a healthy young female with no known risk factors.
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PMID:Fatal Myopericarditis Following an Influenza A (H3N2) Infection. 2973 62

A 38-year-old gentleman presented with thyroid storm with multiorgan involvement in the form of heart failure (thyrotoxic cardiomyopathy), respiratory failure (respiratory muscle fatigue), hepatic dysfunction, fast atrial fibrillation, pulmonary embolism, and disseminated intravascular coagulation (DIC). His Graves' disease (GD) remained undiagnosed for nearly 8 months because apart from weight loss, he has not had any other symptoms of thyrotoxicosis. The presentation of thyroid storm was atypical (apathetic thyroid storm) with features of depression and extreme lethargy without any fever, anxiety, agitation, or seizure. There were no identifiable triggers for the thyroid storm. Apart from mechanical ventilation and continuous veno-venous renal replacement therapy in the intensive care unit, he received propylthiouracil (PTU), esmolol, and corticosteroids, which were later switched to carbimazole and propranolol with steroids being tapered down. He was diagnosed with thyrotoxic myopathy which, like GD, remained undiagnosed for long (fatigability). A high index of suspicion and a multidisciplinary care are essential for good outcome in these patients.
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PMID:Apathetic Thyroid Storm with Cardiorespiratory Failure, Pulmonary Embolism, and Coagulopathy in a Young Male with Graves' Disease and Myopathy. 3302 36

Takotsubo cardiomyopathy (TC), also recognized as stress-induced cardiomyopathy, is a transient condition of left ventricular (LV) dysfunction, which presents similarly to acute coronary syndrome (ACS) but with normal coronaries. Physical or emotional stressors usually precipitate TC. It is typically a benign condition, with a complete resolution once the triggering cause resolves. There have been a few cases of TC induced by diabetic ketoacidosis (DKA) that have been reported in the literature. A 50-year-old Caucasian female patient presented with lethargy, in addition to hypothermia and hypotension. Further investigation showed hyperglycemia with metabolic acidosis and ketonemia. Eventually, she was diagnosed with diabetic ketoacidosis (DKA). On Day 2 of the admission, the patient's condition further deteriorated despite appropriate treatment of DKA. An electrocardiogram (EKG) showed ST-segment elevation in inferior leads, and troponin levels were elevated. Cardiac catheterization showed non-obstructive coronary arteries but a severely reduced cardiac index. Echocardiography showed an ejection fraction (EF) of 25% with global hypokinetic LV. Eventually, the patient was diagnosed with TC or stress-induced cardiomyopathy. TC should always be suspected in any patient presenting with acute heart failure during DKA treatment. TC is a transient syndrome; however, it can result in dreadful complications, including cardiogenic shock, arrhythmias, or thromboembolic events. Early recognition and timely treatment are pivotal in such cases.
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PMID:A Case of Takotsubo Cardiomyopathy Triggered by Diabetic Ketoacidosis and Hypothermia. 3317 48


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