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)

It is generally accepted that myocardial ischemia, and its extreme consequence, acute myocardial infarction, can result from transient or permanent disproportion between myocardial oxygen demand and coronary artery blood supply. Insufficient coronary artery blood supply may have many reasons. The aim of the study is to point to the clinical features of the coronary vasculitides as well as to the diagnostic and therapeutic possibilities. Coronary artery involvement in infectious angiitis, in Takayasu's arteritis, in granulomatous giant cell arteritis, in thromboangiitis obliterans, in polyarteritis nodosa, in Wegener's granulomatosis and in Churg--Strauss syndrome is discussed. The diagnosis of coronary vasculitis must be supposed in every patient with primary or secondary vasculitis in whom chest pain or cardiac failure appear. In young patients with clinical, electrocardiographic or laboratory signs of coronary artery disease, especially in absence of risk factors for atherosclerosis, the diagnosis of coronary vasculitis must be considered in differential diagnosis. (Fig. 4, Tab. 1, Ref. 32.).
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PMID:[Vasculitides of the coronary arteries]. 862 Mar 25

We report a case of a male teenager with severe heart and acute renal failure as the dominant clinical manifestations of renovascular hypertension (RVH) caused by atypical giant cell arteritis (GCA). Unrecognized RVH and treatment of the consequent heart failure by angiotensin-converting enzyme inhibitors (ACEI) probably contributed to progression of renovascular disease to bilateral renal artery occlusion. Recurrent "flash" pulmonary edemas could not be prevented until surgical revascularization of the only functioning right kidney was achieved by an aortorenal bypass. Prompt post-operative normalization of heart function and arterial hypertension occurred despite the histopathological finding of the resected renal artery compatible with GCA and 4-year duration of significant renovascular disease. At the last check-up, the patient was asymptomatic, with normal arterial pressure on the prescribed treatment: carvedilol, hydrochlorothiazide, prednisolone 20 mg daily and aspirin. Subsequent follow-up is necessary to observe the evolution of GCA as an exceptionally rare cause of RVH.
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PMID:Heart and renal failure in renovascular hypertension caused by giant cell arteritis--case report. 1726 2

Giant cell arteritis occurs mainly in the cranial arteries, especially in the temporal area, and rarely in the coronary arteries. Here, we present a case of coronary artery giant cell arteritis in a 51-year-old woman who complained of atypical chest pain. Radionuclide angiography showed dilated left ventricle with global hypokinesia. Despite medical treatment, she suffered progressive heart failure and finally was given a heart transplant. The pathologic examination revealed myocardial infarction due to coronary giant cell arteritis. Unusual giant cell arteritis should be considered in the differential diagnoses of myocardial infarction.
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PMID:Myocardial infarction due to giant cell arteritis: a case report and literature review. 1739 68

Giant cell arteritis (GCA) is a well-known entity, creating aortic valve regurgitation secondary to dilatation of the aortic wall. No direct involvement of the aortic valve leaflets has yet been documented. A 75-year-old woman with a history of polymyalgia rheumatica and Horton disease was admitted to the authors' institution with acute cardiac failure, severe left ventricular systolic dysfunction and grade III aortic valve insufficiency. The aortic valve was excised and replaced in the usual manner with a pericardial tissue heart valve. Histopathological examination revealed a non-bacterial granulomatous inflammation with giant cells, strictly limited to the valve leaflets. The present case appeared to be the first with isolated involvement of the valve leaflets by GCA, creating acute aortic valve insufficiency.
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PMID:Acute aortic valve insufficiency and cardiogenic shock due to an isolated giant cell inflammation of the aortic valve leaflets: case report and review of the literature. 1859 33

Cardiogenic flash pulmonary oedema is a common and potentially fatal cause of acute respiratory distress. Although it often results from acute decompensated heart failure, abrupt-onset aortic regurgitation can sharply rise cardiac filling pressure and, consequently, pulmonary venous pressure, leading to rapid fluid accumulation in the interstitial and alveolar spaces. We report a case of a 64-year-old woman admitted to the emergency department with a flash pulmonary oedema; a careful clinical investigation subsequently revealed a rare aetiology for this 'common' presentation. After a detailed auscultation that unmasked a diastolic cardiac murmur, an acute severe aortic insufficiency was further confirmed by echocardiography, showing inflammation and thickening of the entire aorta wall. The patient was submitted to valve replacement surgery, and histological examination, to our surprise, showed features of aortitis, remarkable for the presence of giant cells. A diagnosis of idiopathic aortitis versus inaugural giant cell arteritis was proposed and treatment started with corticosteroids.
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PMID:Pulmonary oedema in the emergency room: what is hidden beyond an apparently common presentation. 2479 26

Cardiovascular toxicities associated with immune checkpoint inhibitors (ICIs) have been reported in case series but have been underappreciated due to their recent emergence, difficulties in diagnosis and non-specific clinical manifestations. ICIs are antibodies that block negative regulators of the T cell immune response, including cytotoxic T lymphocyte-associated protein-4 (CTLA-4), programmed cell death protein-1 (PD-1), and PD-1 ligand (PD-L1). While ICIs have introduced a significant mortality benefit in several cancer types, the augmented immune response has led to a range of immune-related toxicities, including cardiovascular toxicity. ICI-associated myocarditis often presents with arrhythmias, may co-exist with myositis and myasthenia gravis, can be severe, and portends a poor prognosis. In addition, pericardial disease, vasculitis, including temporal arteritis, and non-inflammatory heart failure, have been recently described as immune-related toxicities from ICI. This narrative review describes the epidemiology, diagnosis, pathophysiology, and treatment of cardiovascular toxicities of ICI therapy, highlighting recent developments in the field in the past year.
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PMID:Cardiovascular toxicities associated with immune checkpoint inhibitors. 3095 59