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

Although tissue Doppler (TD) imaging of the left ventricle is now commonly used in clinical settings, TD imaging of the right ventricle (RV) is not routinely practiced. Yet, there are significant data on clinical uses of RV TD imaging, including established normal values using both color and spectral TD. In acute left ventricular (LV) inferior wall myocardial infarction, depressed RV TD velocities have been shown to correlate with the presence of RV impairment, and with patient outcome. In patients with LV heart failure, TD imaging has been correlated to RV ejection fraction by radionuclide angiography, and is an independent predictor of outcome. In patients with congenital heart disease, RV TD has been especially valuable for assessing RV function, and has been correlated to invasive hemodynamic indices, and RV ejection fraction by magnetic resonance imaging. The RV performance (Tei) index has been calculated and validated using TD-derived, rather than conventional pulsed Doppler time intervals. RV TD indices have been shown to be useful in the detection of subclinical and clinical disease in morbid obesity, chronic pulmonary, and systemic disease. TD-derived RV strain imaging can detect segmental myocardial dysfunction, overcoming limitations to conventional TD imaging resulting from tethering. For both TD velocity and strain imaging, however, appreciation of the limitations of these techniques is necessary for their appropriate use. Given its rapid acquisition times, reproducibility, and ease of addition to standard transthoracic echocardiographic protocols, RV TD and strain imaging are important additional modalities in the comprehensive echo-Doppler assessment of RV function.
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PMID:Right ventricular tissue Doppler and strain imaging: ready for clinical use? 1745 72

To this day the aetiology of sarcoidosis continues to elude definition. Partially as a consequence of this, little in the way of new therapies has evolved. The enigma of this condition is that, unusually for a disease with the potential for devastating consequences, many patients show spontaneous resolution and recover. Cardiac involvement can affect individuals of any age, gender or race and has a predilection for the conduction system of the heart. Heart involvement can also cause a dilated cardiomyopathy with consequent progressive heart failure. The most common presentation of this systemic disease is with pulmonary infiltration, but many cases will be asymptomatic and are detected on routine chest radiography revealing lymphadenopathy. Current advances lie in the newer methods of imaging and diagnosing this unusual heart disease. This review describes the pathology and diagnosis of this condition and the newer imaging techniques that have developed for determining cardiac involvement.
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PMID:Sarcoid heart disease. 1791 69

Diuretics are pharmacological agents that increase natriuresis through inhibition of tubular re-absorption of sodium. The mechanisms and site of this inhibition differ with each drug class, accounting for their additive effects on natriuresis increase and their hydroelectrolytic side effects. The response to a given diuretic dose depends on the diuretic concentration on the urine at its action site. This concentration may be decreased by pharmacokinetic factors such as encountered in renal insufficiency or in nephrotic syndrome. These resistance mechanisms of diuretics may be corrected by dose increase, previous diuretic fixation on albumin or warfarin administration. Once these mechanisms are opposed, the diuretic concentration for maximal efficacy is reached at is action site and the natriuresis obtained as the normal maximal plateau. This is not the case when an oedematous systemic disease with effective hypovolemia is present, like in heart failure or cirrhosis, or when chronic use of loop diuretics has induced a hypertrophy of the more distant part of the tubule. In theses cases, a pharmacodynamic resistance exists, resulting in a lower maximal natriuresis plateau in spite of adequate concentration of the diuretic at its action site, even in the absence of pharmacokinetic resistance factors. The main indications of diuretics are systemic oedematous disease and hypertension. In the oedematous diseases, diuretics indication is both straightforward and sufficient only if effective hypervolemia is present. The therapeutic approach is discussed according to the various clinical conditions and pathophysiological background. In uncomplicated hypertension, diuretics are the cornerstone of the therapy. The most suitable diuretic treatment for hypertension is an association of low doses thiazide (12.5-50 mg/day) with potassium sparing diuretics. Rare indications of diuretics are also reviewed.
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PMID:[Diuretic-based therapy]. 1791 42

Heart diseases resulting in heart failure are among the leading causes of morbidity and mortality in the Western world and can result from either systemic disease (e.g., hypertensive heart disease, ischemic heart disease) or specific heart muscle disease (e.g., dilated cardiomyopathy/DCM). Subproteome analysis of such disease subsets affords a reduction in sample complexity, potentially revealing biomarkers of cardiac failure that would otherwise remain undiscovered in proteome wide studies. Label-free nanoscale LC-MS has been applied in this study to validate a Triton X-114-based phase enrichment method for cardiac membrane proteins. Annotation of the subcellular location combined with GRAVY score analysis indicates a clear separation between soluble and membrane-bound proteins with an enrichment of over 62% for this protein subset. LC-MS allowed confident identification and annotation of hydrophobic proteins in this control sample pilot study and demonstrates the power of the proposed technique to extract integral membrane-bound proteins. This approach should be applicable to a wider scale study of disease-associated changes in the cardiac membrane subproteome.
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PMID:Nonionic detergent phase extraction for the proteomic analysis of heart membrane proteins using label-free LC-MS. 1871 67

The term 'cardiorenal syndrome' (CRS) has increasingly been used in recent years without a constant meaning and a well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the CRS today includes 5 subtypes whose etymology reflects the primary and secondary pathology, the time frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can generally be defined as a pathophysiological disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical derangements, to make the rationale for management strategies and to design future clinical trials with accurate selection and stratification of the studied population.
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PMID:The cardiorenal syndrome. 1916 27

The term cardiorenal syndrome (CRS) has increasingly been used in recent years without a constant meaning and a well accepted definition. To include the vast array of interrelated derangements, and to stress the bi-directional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome includes today five sub-types whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal co-dysfunction secondary to systemic disease. The cardiorenal syndrome can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischaemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness.
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PMID:[Cardiorenal syndrome, current understanding]. 1955 20

Sarcoidosis is a systemic disease which affects many organs, including the heart. Cardiac sarcoidosis has a reported incidence of about 25 % and carries a poor prognosis. It can occur in the form of conduction abnormalities, pericardial and valvular heart disease, congestive heart failure, arrhythmias and sudden cardiac death. The diagnosis of cardiac sarcoidosis is difficult, requiring a high index of suspicion and the use of electrocardiography, echocardiography, nuclear medicine imaging, myocardial biopsy and magnetic resonance imaging. Corticosteroids have been the cornerstone of treatment of cardiac sarcoidosis, but other immunosuppressives have also been used, along with standard heart failure therapy, antiarrhythmic medications, pacemakers and implantable defibrillators. Cardiac transplantation is an option for patients who do not respond to medical treatment. We briefly review the current armamentarium for the diagnosis and treatment of cardiac sarcoidosis.
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PMID:Cardiac sarcoidosis. 1967 Jan 8

Rheumatoid arthritis (RA) is a systemic disease of unknown etiology characterized by a chronic inflammatory process mainly leading to destruction of synovial membrane of small and major diarthrodial joints. The prevalence of RA within the general adult population is about 1% and female subjects in fertile age result mostly involved. It's an invalidating disease, associated with changes in life quality and a reduced life expectancy. Moreover, we can observe an increased mortality rate in this population early after the onset of the disease. The mortality excess can be partially due to infective, gastrointestinal, renal or pulmonary complications and malignancy (mainly lung cancer and non-Hodgkin lymphoma). Among extra-articular complications, cardiovascular (CV) involvement represents one of the leading causes of morbidity and mortality. Every cardiac structure can be affected by different pathogenic pathways: heart valves, conduction system, myocardium, endocardium, pericardium and coronary arteries. Consequently, different clinical manifestations can be detected, including: pericarditis, myocarditis, myocardial fibrosis, arrhythmias, alterations of conduction system, coronaropathies and ischemic cardiopathy, valvular disease, pulmonary hypertension and heart failure. Considering that early cardiac involvement negatively affects the prognosis, it is mandatory to identify high CV risk RA patients to better define long-term management of this population.
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PMID:[Cardiac involvement in rheumatoid arthritis]. 2014 1

The concept of COPD as a systemic disease has been widely accepted in the past several years. In parallel, it has been emphasised that COPD morbidity and mortality is strongly related to co-morbid conditions. This review summarises some recent studies showing that in patients with COPD, the prevalence of cardiac failure is manifested in 10%-46% of the patients, and that up to 40% of patients with cardiac failure show evidence of COPD, about half of them not earlier diagnosed. Recent data also show an increased risk for arteriosclerotic manifestations in COPD patients, and cardiac complications are common causes of death in COPD patients. Other manifestations of the metabolic syndrome, as diabetes, are also over-represented in patients. It is also a well-established fact that a low FEV(1) is a risk factor for cardiovascular diseases and events. Mechanistically, a systemic inflammation in COPD could be a link to cardiovascular events. COPD raises inflammatory parameters and local anti-inflammatory treatment seems to have a potential to decrease the systemic inflammation and also to decrease cardiovascular events.
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PMID:COPD and co-morbidities, with special emphasis on cardiovascular conditions. 2029 51

To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome (CRS) includes today five subtypes whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys, whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type 3 CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/ or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical disorders and to design future clinical trials.
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PMID:Cardiorenal syndromes: definition and classification. 2042 91


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