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)

Heart failure is a severe, disabling disease that portends a short life expectancy. This grave prognosis may be explained by growth-promoting effects of angiotensin II implicated in heart failure that mediate a genetic response called programmed cell death. The effects of angiotensin II are inhibited by angiotensin-converting enzyme (ACE) inhibitors, which improve exercise performance and quality of life, attenuate disease progression, and modestly lengthen survival. Unfortunately, mortality remains exceedingly high and may be partly attributable to augmented production of angiotensin II from a non-ACE chymase pathway. Angiotensin II production may therefore increase despite treatment with ACE inhibitors. The angiotensin II receptor antagonists are a new class of nonpeptide-reversible inhibitors that may offer clinical promise in heart failure through blockade of angiotensin II actions, whether produced from ACE or non-ACE chymase pathways.
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PMID:Angiotensin II receptor blockers: novel therapy for heart failure? 866 7

Infections caused by Mycobacterium avium-intracellulare complex are generally manifested as pulmonary disease, osteomyelitis or lymphadenitis, and cutaneous infection is rare. We describe a case of M. intracellulare infection of the skin in a 79-year-old man without apparent immunologically disabling disease or therapy. He had cutaneous infection of the right hand over 10 years, developing a fistula and, finally, an ulcer and abscess, 2 months before his death from heart failure. Mycobacterium intracellulare was identified by both microbiological characteristics and DNA-DNA hybridization.
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PMID:Infection with Mycobacterium avium-intracellulare with abscess, ulceration and fistula formation. 903 10

Chronic (congestive) heart failure (CHF) is a disabling disease where patients suffer from dyspnoea and exercise intolerance. Peripheral skeletal muscle disorders play a major role in the pathogenesis of these symptoms and also in the progression of the disease. Besides cardiovascular endurance training, strength training should be an important component of cardiac rehabilitation programs in CHF because of its ability to efficiently improve muscle function and muscle mass. Safety of this type of training, while long-time questioned, has been established. Training recommendations for strength training should be based on current research. The positive training effects induced by strength training improve the patients' functional capacity and exercise tolerance and thereby also their quality of life and its widespread use should be promoted.
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PMID:Strength training for patients with chronic heart failure. 1617 71

A 63-year-old Caucasian male, diagnosed with dilated cardiomyopathy in 1993, remained clinically stable for several years. In 2003, a marked increase of N-terminal pro-natriuretic peptide serum level (611 ng/ml to 4926 ng/ml) was observed; left ventricular (LV) septum thickness was 10 mm. In addition, sensorimotor polyneuropathy and autonomic dysfunction occurred. Further progression of heart failure occurred despite unchanged systolic LV function. Endomyocardial biopsy in 2006 revealed transthyretin amyloidosis by Congo red and immunohistochemical staining, as well as Val94Ala substitution by transthyretin gene analysis. Cardiac amyloid deposition was quantified by technetium-99m-3,3-diphosphono-1,2-propanodicarboxylic acid (99mTc-DPD) scintigraphy. Mutational search of the relatives (n = 1) was unremarkable. The transthyretin Val94Ala mutation is characterized by sensorimotor polyneuropathy, autonomic dysfunction, and gastrointestinal and cardiac involvement with amyloid. This mutation is an addition to the growing spectrum of transthyretin mutations with late onset of clinical symptoms, but noteworthy because of progressive, finally disabling disease course. Final clinical assessment of severity of cardiac involvement in the present patient is rendered complex by possible concomitant or preceding idiopathic dilated cardiomyopathy.
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PMID:Transthyretin valine-94-alanine, a novel variant associated with late-onset systemic amyloidosis with cardiac involvement. 1796 88

Heart failure is a progressive and disabling disease. The incidence of heart failure is also on the rise, particularly in the elderly of industrialized societies. This is in part due to an increased ageing population, whom initially benefits from improved, and life-extending cardiovascular therapy, yet ultimately succumb to myocardial failure. A major cause of heart failure is ischemia secondary to the sequence of events that is dyslipidemia, atherosclerosis, and myocardial infarction. In the case of heart failure postmyocardial infarction, ischemia can lead to myocardial cell death by both necrosis and apoptosis. The extent of myocyte death postinfarction is associated with adverse cardiac remodeling that can contribute to progressive heart chamber dilation, ventricular wall thinning, and the onset of loss of cardiac function. In cardiomyocytes, recent studies indicate that myocardial ischemic injury activates the unfolded protein stress response (UPR) and this is associated with increased apoptosis. This paper focuses on the intersection of ischemia, the UPR, and cell death in cardiomyocytes. Targeting of the myocardial UPR may prove to be a viable target for the prevention of myocyte cell loss and the progression of heart failure due to ischemic injury.
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PMID:The Myocardial Unfolded Protein Response during Ischemic Cardiovascular Disease. 2253 6

Acute myocardial infarction (AMI) is a frequent and disabling disease, which is the first cause of cardiovascular mortality worldwide. Infarct size is a major determinant of myocardial functional recovery and mortality after AMI. Limitation of infarct size thus appears as an appropriate strategy to prevent post-ischemic heart failure and improve survival. Reperfusion is the only treatment recommended to reduce infarct size but despite obvious benefits, it may also have deleterious effects called ischemia-reperfusion (IR) injury including myocyte cell death. Proteins involved in the apoptosis cascade generally interact over large surfaces lacking well-defined pockets. Therefore, inhibitory peptides are optimal biomolecules to target these large protein surfaces, they are often more selective to their target than conventional small organic molecules, and they can be tailored for optimal affinity or desired metabolic property. Since peptides do not cross freely biological membranes, they are generally administered in association with cell penetrating peptides (CPPs) and with homing peptides (HPs) for selective organs or tissues targeting. As a first approach in vivo, we made use of the already known BH4 peptidic inhibitor of the mitochondrial apoptotic pathway, which showed cardioprotective properties in a murine model of AMI after a single bolus of intravenous administration. More importantly, similar peptidic strategies and tools are likely to be adaptable to many other situations in which cells have to be protected from apoptosis such as stroke or organ transplantation.
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PMID:CPP-conjugated anti-apoptotic peptides as therapeutic tools of ischemia-reperfusion injuries. 2314 Apr 57

Heart failure is a common and disabling disease with high mortality that carries substantial societal costs. Current therapeutic strategies are aimed at relieving symptoms, avoiding hospitalization, and prolonging life, but disease progression is ultimately inevitable. MicroRNAs (miRNAs) are short, non-coding RNA molecules with pervasive roles in eukaryotic biology, annealing to complimentary sites on target mRNAs, and repressing gene expression. The fact that miRNAs are dysregulated in many human disorders, including cardiovascular disease, and the relative ease with which endogenous miRNA expression can be altered using synthetic antisense oligos has stirred enthusiasm for these molecules as potential drug targets. The aim of this review article was to summarize the current knowledge on the roles of miRNA in the pathophysiology of heart failure as well as the use of miRNAs as therapeutic targets and diagnostic tools for the disease.
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PMID:MicroRNAs in the failing heart--novel therapeutic targets? 2537 81

Pompe disease (PD) is a rare, inherited autosomal recessive metabolic disorder caused by the deficiency of the lysosomal acid alpha-glucosidase (GAA) enzyme described in 1932 by the Dutch pathologist Joannes Cassianus Pompe. The prevalence of PD ranges from 1:40,000 to 1:300,000 births and depends on geographic and ethnic factors. Clinical manifestations may vary from a rapidly progressive disabling disease with cardiomegaly, hepatomegaly, weakness, generalized hypotonia, and death within the first year of life, to a mild presentation characterized by slowly progressive myopathy predominantly involving the skeletal muscles. The laboratory diagnostic gold standard is represented by the determination of the alpha-glucosidase activity. However, the muscle histology may also yield the diagnosis by evaluating the tissular glycogen accumulation. Until recently, supportive measures constituted the unique available therapy. Currently, the administration of the recombinant GAA is being used with promising results. The authors present the case of a 5-month-old boy, previously diagnosed with hypertrophic cardiomyopathy since the age of 2 months, who presented acute heart failure accompanied by biventricular dilation followed by refractory shock and death. The autopsy findings confirmed the glycogen-accumulation disease.
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PMID:The infantile-onset form of Pompe disease: an autopsy diagnosis. 2689 45

Heart failure with reduced ejection fraction (HFrEF) is a deadly and disabling disease. A key derangement contributing to impaired exercise performance in HFrEF is decreased nitric oxide (NO) bioavailability. Scientists recently discovered the inorganic nitrate pathway for increasing NO. This has advantages over organic nitrates and NO synthase production of NO. Small studies using beetroot juice as a source of inorganic nitrate demonstrate its power to improve exercise performance in HFrEF. A larger-scale trial is now underway to determine if inorganic nitrate may be a new arrow for physicians' quiver of HFrEF treatments.
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PMID:Dietary nitrate's effects on exercise performance in heart failure with reduced ejection fraction (HFrEF). 3026 Dec 90

Constrictive pericarditis is a disabling disease of the heart, which causes cardiac diastolic dysfunction. We present a case of a 44-year-old gentleman with a history of blunt chest trauma who presented with constrictive pericarditis with right-sided heart failure. Imaging studies revealed a calcified pericardium. He underwent an uneventful pericardiectomy. Calcification is common yet rare if it involves the pericardium. It normally occurs following fibrosis and adhesion which are associated with the chronicity of the disease, hence creating more challenge to the operating surgeon in the pericardiectomy procedure.
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PMID:Trapped heart in heavily calcified pericardium. 3313 17


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