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

The response to cardiac resynchronization therapy (CRT), which is applied to patients with heart failure (HF) and left bundle-branch block (LBBB), can be predicted from the mechanical dyssynchrony measured on circumferential strain. Circumferential strain can be assessed by either 2D or 3D strain analysis. In this study was evaluated the difference between 2D and 3D circumferential strain using MR tagging with high temporal resolution (14 ms). Six healthy volunteers and five patients with LBBB were evaluated. We compared the 2D and 3D circumferential strains by computing the mechanical dyssynchrony and the cross correlation (r) between 2D and 3D strain curves, and by quantifying the differences in peak circumferential shortening, time to onset, and time to peak of shortening. The obtained maximum r(2) values were 0.97 +/- 0.03 and 0.87 +/- 0.16 for the healthy and LBBB populations, respectively, and thus showed a good similarity between 2D and 3D strain curves. No significant difference was observed between 2D and 3D in time to onset, time to peak, or peak circumferential shortening. Thus, to measure dyssynchrony, 2D strain analysis will suffice. Since 2D analysis is easier to implement than 3D analysis, this finding brings the application of MRI tagging and strain analysis closer to the clinical routine.
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PMID:Quantitative comparison of 2D and 3D circumferential strain using MRI tagging in normal and LBBB hearts. 1732 72

Since the discovery of HFE gene in 1996, considerable progress has been made concerning the iron-metabolism and its major abnormalities. Five types of hereditary hemochromatosis are actually known: type 1 (HFE gene), type 2A (HJV gene), type 2B (HAMP gene), type 3 (TfR2 gene), type 4 (SLC40A1 gene). The HFE C282Y +/+ mutation is responsible for the most frequent type of hemochromatosis in France. Various secondary causes can lead to iron-overload: associated genetic diseases, exogenous iron intake, thalassaemia and refractory anaemia, hepatic siderosis, alcoholic hepatitis, cutaneous porphyria and cirrhosis. The deleterious consequences of iron-overload are due to the interactions of the environmental factors. The role of HFE heterozygote mutations is still discussed. In clinical practice, the interpretation of a serum ferritin increase is a frequent problem that needs a careful evaluation based on the tranferrin saturation measurement. Significant increase of both these factors is in favour of an HFE C282Y +/+ hemochromatosis, after exclusion of a hepatocellular insufficiency or a refractory anaemia. Nevertheless, high ferritin is not always a marker of iron-overload. Thus, there are many disorders increasing the serum ferritin levels without iron overload : cytolysis (hepatic...), inflammatory or infectious syndromes, high alcohol intake, neoplasia... Looking for HFE mutations help to separate type 1 hemochromatosis from other conditions mainly hepatic siderosis (metabolic disorders). The identification of rare types of hemochromatosis (types 2-4) is only required in particular cases. The evaluation of the iron overload is now based on hepatic MRI determination rather than liver biopsy. Repeated phlebotomies remain the essential way to decrease the iron overload in HFE hemochromatosis and to prevent the occurrence of severe and irreversible complications (cirrhosis, arthropathies, cardiac failure, and diabetes). Because of the link established between the amount of iron-overload and the occurrence of complications and the mortality over-risk in HFE C282Y +/+ hemochromatosis, venesections must be started when serum ferritin is higher than 300 microg/l in man and 200 microg/l in woman, whatever the clinical manifestations are and obviously before the symptomatic phase of the disease.
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PMID:[Hereditary and acquired iron overload]. 1737 75

In recent years, Doppler echocardiography has undergone significant technological advances, resulting in spectacular improvements in diagnosis and quantification. This review summarises the advances made in 2006 in fields as varied as cardiac resynchronisation, cardiac failure with preserved systolic function, contrast echocardiography, 3D echocardiography and echocardiographic evaluation of valvular heart disease. Despite growing competition, but mostly complementarity with CT scan and MRI, Doppler echocardiography remains the keystone of cardiological rationale based on non-intensive investigations.
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PMID:[The best of echocardiography in 2006]. 1740 60

In this review, original clinical studies based on scintigraphy, PET or MRI imaging are reported, regarding the main areas of cardiology including ischemia and myocardial infarction, detection of coronary artery disease in various patients subsets, cardiomyopathy and heart failure. A special topic is dedicated to tracers and technical innovations.
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PMID:[The best of nuclear cardiology and MRI in 2006]. 1740 63

We report on a neonatal patient case with a cerebral vascular dilation consistent with a vein of Galen malformation diagnosed on an antenatal doppler ultrasound examination. Antenatal diagnosis was confirmed by fetal MRI scan. After delivery, cerebral MRI scan found the same dilatation and showed no cerebral parenchymal damage. The infant's condition was stable and particularly there was no congestive cardiac failure. Before discharge at ten days of age, clinical examination and particularly cardiac examination was normal. At 14 days of age, symptoms in relation to a congestive cardiac failure appeared. Echocardiography showed a high output cardiac failure with no cardiac malformation. Infectious laboratory tests were normal. Evolution was initially favourable after digitalo-diuretic treatment. Unfortunately, death occurred at 36 days of age due to intractable cardiac failure. This case highlights that, unusually, heart failure can occur long after the first days of life in cases of Galen vein aneurysmal malformation. The optimal time for vascular embolization in neonatal cases of Galen vein aneurysmal malformation is discussed.
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PMID:[Vein of Galen aneurysmal malformation: a neonatal case with unusual evolution]. 1745 18

Osteoprotegerin, a member of the tumor necrosis factor receptor superfamily, has pleiotropic effects on bone metabolism, endocrine function, and the immune system. Myocardial expression and circulating levels of osteoprotegerin are increased in heart failure. The relationship between osteoprotegerin levels in the general population and indices of left ventricular structure and function is unknown. Plasma osteoprotegerin levels and cardiac MRI indices of left ventricular structure and function were available in 2715 subjects (median age: 44 years; 45% male) enrolled in the Dallas Heart Study. The associations between osteoprotegerin concentration and indices of left ventricular structure and function were assessed by linear regression analysis, adjusting for possible confounders. By gender-specific linear regression analysis, higher osteoprotegerin levels were significantly associated with higher left ventricular mass, left ventricular wall thickness, left ventricular concentricity index, and lower left ventricular ejection fraction (P<0.001 for all). After adjustment for age, race, fat-free mass, fat mass, hypertension, diabetes, coronary artery disease, estimated glomerular filtration rate, hypercholesterolemia, smoking status, hormone replacement therapy, coronary artery calcium score >10, and presence of aortic plaque, osteoprotegerin remained significantly associated with each of these left ventricular indices among male subjects (P<0.05 for each). Among female subjects, higher osteoprotegerin was independently associated with higher left ventricular end-systolic volume and lower ejection fraction (P<0.0001 for each) but not with indices of left ventricular hypertrophy. These findings are compatible with the theory that osteoprotegerin may play a pathophysiological role in the development of left ventricular hypertrophy and systolic dysfunction.
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PMID:Plasma osteoprotegerin levels in the general population: relation to indices of left ventricular structure and function. 1747 Jul 18

Heart failure has a high prevalence and it has a poor prognosis despite the advances in pharmacological treatment. Cardiac resynchronization therapy with biventricular pacemaker has a clinically proven efficacy in the treatment of heart failure with intraventricular dyssynchrony. Conventionally the therapy is indicated in severe drug refractory heart failure (NYHA III-IV) with optimal drug treatment, increased QRS duration (> or = 120 ms), echocardiographic parameters (left ventricular ejection fraction at most 35%). Implementation of new methods (tissue doppler echocardiography, CT, MRI, electroanatomical mapping) can help to select potentially responding patients. Individual optimization of therapy can be performed with non-invasive and invasive methods, the efficacy can be improved even in responding patients. Due to the outstanding efficiency widening the indications is a must. Currently, the efficacy is being investigated in mild heart failure and patients with narrow QRS. Several other questions (transvenous or surgical implantation, need of an implantable defibrillator) will be answered in future trials.
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PMID:[Resynchronization therapy of heart failure]. 1747

Heart failure (HF) is a common syndrome related to varied pathophysiologic processes. Individualization of care according to the patient's pathologic and modifiable substrate is of increasing importance. The use of modern cardiovascular MRI (CMR) provides for the centralization of diagnostic testing with the ability to assess cardiac morphology, function, flow, perfusion, acute tissue injury, and fibrosis in a single setting. This offers the potential for a paradigm shift in the noninvasive diagnosis and monitoring of patients with HF. This article outlines a diagnostic approach for the primary use of CMR in the phenotypic characterization, risk stratification, and therapeutic management of patients with HF.
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PMID:The role of cardiovascular MRI in heart failure and the cardiomyopathies. 1797 91

Mammalian myocardial infarction is typically followed by scar formation with eventual ventricular dilation and heart failure. Here we present a novel model system in which mice constitutively expressing cyclin A2 in the myocardium elicit a regenerative response after infarction and exhibit significantly limited ventricular dilation with sustained and remarkably enhanced cardiac function. New cardiomyocyte formation was noted in the infarcted zones as well as cell cycle reentry of periinfarct myocardium with an increase in DNA synthesis and mitotic indices. The enhanced cardiac function was serially assessed over time by MRI. Furthermore, the constitutive expression of cyclin A2 appears to augment endogenous regenerative mechanisms via induction of side population cells with enhanced proliferative capacity. The ability of cultured transgenic cardiomyocytes to undergo cytokinesis provides mechanistic support for the regenerative capacity of cyclin A2.
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PMID:Cyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure. 1749 21

We report a case of neonatal dural sinus malformation already visible on antenatal ultrasound. This is a rare disease entity in infants and children. Clinical diagnosis was made by demonstrating a cranial murmur on auscultation; macrocrania and signs of progressive cardiac failure. Imaging studies as cerebral ultrasound, postnatal MRI scan and MR angiography demonstrated a large dural sinus malformation originating from the sagittal sinus with extensive arteriovenous fistulae. Due to the extent of the lesion, the existing ischemic brain damage and involvement of the torcular, no therapeutic options were available and the child died of irreversible cardiac failure. The diagnosis was confirmed with autopsy. We discuss the clinical presentation, imaging and neuropathological results and relate our findings to embryological data and the existing literature.
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PMID:A case of neonatal dural sinus malformation: clinical symptoms, imaging and neuropathological investigations. 1753 53


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