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)

Valve repair is often required to maintain haemodynamic performance in patients with infectious endocarditis. Localizations on the aortic valve are frequent and lead to rapid, often severe, deterioration, especially when the valve ring and the septum are also infected. Conduction disorders and rupture of the abscess into the heart cavities are formal indications for surgery. Mitral regurgitation requires surgical repair less often and has a slower clinical course. The tricuspid valve generally tolerates infection well and surgery is only exceptionally indicated. An emergency situation due to heart failure occurring simultaneously with valve damage (ruptured mitral chordae) and moderate regurgitation, can most often be managed medically. Inversely, surgery is required when blood cultures are persistently positive and sepsis remains uncontrolled after 8 days of adapted antibiotics. Surgery is entertained when the risk of emboli is established echographically, although growth on valves is not in itself sufficient. Most operated cases also involve an initial embolic event. Conservative surgery (mitral or tricuspid plasty) should always be performed to avoid the long-term complications of prostheses: valve dysfunction (disinsertion or thrombosis), bacterial resistance, risk of embolism especially for mechanical valves, risk of brain haemorrhage related to anticoagulant therapy. When endocarditis develops on a prosthesis early after implantation reoperation is usually required, especially when certain organisms (yeasts, Staphylococcus aureus) are involved. Haemodynamic performance and bacterial resistance dominate the decision making processes which must be adapted to each individual case. Once the decision for surgery has been made, the operation should not be delayed in the hope a longer antibiotic course will be effective since prognosis worsens rapidly if the haemodynamic situation is allowed to deteriorate.
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PMID:[Infectious endocarditis: the right time for surgery]. 789 43

The treatment of familial amyloid polyneuropathies (FAP) is complex and requires a neurological and cardiological multidisciplinary coverage. It includes specific treatments to control the progression of the systemic amyloidogenesis, the symptomatic treatment of the peripheral and autonomic neuropathy (digestive, urinary, sexual, postural hypotension) and the treatment of organs severely involved by amyloidosis (heart, eyes, kidneys). First line specific treatment of met30 TTR-FAP is liver transplantation (LT) which allows to suppress the main source of mutant TTR, to stop the progression of the neuropathy in 70 % of cases at long-term (with an experience of 18 years) and to double the median survival. In case of severe renal or cardiac insufficiency, a double transplant kidney-liver or heart-liver can be discussed. The tafamidis (in temporary authorization of use in France) is a stabilizing medicine of the tetrameric TTR which showed in very early stages of met30 TTR-FAP short-term capacities to stop the progress of the peripheral neuropathy in 60 % of the cases versus 38 % with placebo. It should be proposed in case of contraindication of TH (age>70 years [20 % of the cases]), of very early stages (very low NIS-LL score), or for the period of wait of LT. Other innovative medicines issued from biopharmaceutical companies have been developed to block the hepatic production of both mutant and wild TTR which are noxious in the late forms NAH (>50 years old) (RNAi [RNA interference] therapeutics, AntiSens oligonucleotids), for removing the amyloid deposits (monoclonal antibody anti-SAP), or to slow down the formation of deposits of TTR and amyloidosis (combination of doxycycline-TUDCA). Clinical trials should be first addressed to the patients with a late onset of FAP or non-met30 TTR-FAP who are less responding to LT and patients with contraindications in the LT. Initial cardiac assessment and periodic cardiac investigations are important for the FAP according to the frequency of cardiac impairment which is responsible of high rate of mortality. Conduction disorders (atrio-ventricular blocks) require the implantation of a pacemaker in about one third of the cases during the evolution of the disease. A myocardial infiltration is detected in two third of the cases and is for a long time latent; it remains often limited to a diastolic dysfunction which can be responsible for hemodynamical difficulties during the LT; it evolves sometimes, late, towards a systolic dysfunction of bad prognosis. A combined liver-heart transplantation is proposed in cases of severe cardiac involvement which are contraindication to the LT only, essentially in forms "not met30". In every case of FAP, a regular cardiological follow-up is required for life, because of the progress of the cardiac involvement, which is not always stopped by the liver transplantation. The symptomatic treatments are indispensable to improve the quality of life of the patients: neurogenic pains, urinary disorders, liqueurs, sexual impotence, postural hypotension. The familial screening of the carriers of the TTR gene mutation and their regular follow-up by appropriate clinical examination and complementary investigations are major to detect early the onset of the disease to start as soon as possible specific therapy.
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PMID:[Treatment of familial amyloid polyneuropathy]. 2234 49

Researchers and clinicians have discovered several important concepts regarding the mechanisms responsible for increased risk of arrhythmias, heart failure, and sudden cardiac death. One major step in defining the molecular basis of normal and abnormal cardiac electrical behavior has been the identification of single mutations that greatly increase the risk for arrhythmias and sudden cardiac death by changing channel-gating characteristics. Indeed, mutations in several genes encoding ion channels, such as SCN5A, which encodes the major cardiac Na(+) channel, have emerged as the basis for a variety of inherited cardiac arrhythmias such as long QT syndrome, Brugada syndrome, progressive cardiac conduction disorder, sinus node dysfunction, or sudden infant death syndrome. In addition, genes encoding ion channel accessory proteins, like anchoring or chaperone proteins, which modify the expression, the regulation of endocytosis, and the degradation of ion channel a-subunits have also been reported as susceptibility genes for arrhythmic syndromes. The regulation of ion channel protein expression also depends on a fine-tuned balance among different other mechanisms, such as gene transcription, RNA processing, post-transcriptional control of gene expression by miRNA, protein synthesis, assembly and post-translational modification and trafficking. The aim of this review is to inventory, through the description of few representative examples, the role of these different biogenic mechanisms in arrhythmogenesis, HF and SCD in order to help the researcher to identify all the processes that could lead to arrhythmias. Identification of novel targets for drug intervention should result from further understanding of these fundamental mechanisms.
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PMID:Identifying potential functional impact of mutations and polymorphisms: linking heart failure, increased risk of arrhythmias and sudden cardiac death. 2406 25

We present a case of takotsubo cardiomyopathy (TTC) with ventricular stand still and atrioventricular block. TTC can mimic ST elevation myocardial infarction and heart failure, but in this case resulted in a severe cardiac conduction disorder and ventricular standstill. This is a recognised but unusual presentation and serves as a lesson to those undertaking anaesthetics to be vigilant for TTC.
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PMID:Takotsubo cardiomyopathy with severe bradyarrhythmia following epidural insertion. 2779 40

Coronavirus disease 2019 (COVID-19) has become a global pandemic. It is still uncontrolled in most countries and no therapies are currently available. Various drugs are under investigation for its treatment. The disease is known to have worse outcomes in patients who have underlying cardiovascular disease. Chloroquine/hydroxychloroquine, azithromycin, remdesivir and lopinavir/ritonavir are currently being studied in trials and show some promise. Conduction disorders, heart failure, and mortality have been reported with the use of these drugs. It is important to have knowledge of potential cardiotoxic effects of these drugs before using them for COVID-19 patients for better allocation of healthcare resources and improvement in clinical outcomes.
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PMID:Cardiovascular Safety of Potential Drugs for the Treatment of Coronavirus Disease 2019. 3262 92