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)

After myocardial infarction, ventricular geometry and function, as well as energy metabolism, change markedly. In nonischemic heart failure, inhibition of xanthine oxidase (XO) improves mechanoenergetic coupling by improving contractile performance relative to a reduced energetic demand. However, the metabolic and contractile effects of XO inhibitors (XOIs) have not been characterized in failing hearts after infarction. After undergoing permanent coronary ligation, mice received a XOI (allopurinol or oxypurinol) or matching placebo in the daily drinking water. Four weeks later, 1H MRI and 31P magnetic resonance spectroscopy (MRS) were used to quantify in vivo functional and metabolic changes in postinfarction remodeled mouse myocardium and the effects of XOIs on that process. End-systolic (ESV) and end-diastolic volumes (EDV) were increased by more than sixfold after infarction, left ventricle (LV) mass doubled (P < 0.005), and the LV ejection fraction (EF) decreased (14 +/- 9%) compared with control hearts (59 +/- 8%, P < 0.005) at 1 mo. The myocardial phosphocreatine (PCr)-to-ATP ratio (PCr/ATP) was also significantly decreased in infarct remodeled hearts (1.4 +/- 0.6) compared with control animals (2.1 +/- 0.5, P < 0.02), in agreement with prior studies in larger animals. The XOIs allopurinol and oxypurinol did not change LV mass but limited the increase in ESV and EDV of infarct hearts by 50%, increased EF (23 +/- 9%, P = 0.01), and normalized cardiac PCr/ATP (2.0 +/- 0.5, P < 0.04). We conclude that XOIs improve ventricular function after infarction and normalize high-energy phosphate ratio in heart failure. Thus XOI therapy offers a new and potentially complementary approach to limit the adverse contractile and metabolic consequences after infarction.
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PMID:Xanthine oxidase inhibitors improve energetics and function after infarction in failing mouse hearts. 1618 26

Following myocardial infarction (MI), contractile dysfunction develops not only in the infarct zone but also in noninfarcted regions of the left ventricle remote from the infarct zone. Inflammatory activation secondary to MI stimulates inducible nitric oxide synthase (iNOS) induction with excess production of nitric oxide. We hypothesized that the anti-inflammatory effects of selective A(2A)-adenosine receptor (A(2A)AR) stimulation would suppress inflammation and preserve cardiac function in the remote zone early after MI. A total of 53 mice underwent 60 min of coronary occlusion followed by 24 h of reperfusion. The A(2A)AR agonist (ATL146e, 2.4 microg/kg) was administered intraperitoneally 1, 3, and 6 h postreperfusion. Because of the 1-h delay in treatment after MI, ATL146e had no effect on infarct size, as demonstrated by contrast-enhanced cardiac MRI (n = 18) performed 24 h post-MI. ATL146e did however preserve global cardiac function at that time by limiting contractile dysfunction in remote regions [left ventricle wall thickening: 51 +/- 4% in treated (n = 9) vs. 29 +/- 3% in nontreated groups (n = 9), P < 0.01]. RT-PCR, immunohistochemistry, and Western blot analysis indicated that iNOS mRNA and protein expression were significantly reduced by ATL146e treatment in both infarcted and noninfarcted zones. Similarly, elevations in plasma nitrate-nitrite after MI were substantially blunted by ATL146e (P < 0.01). Finally, treatment with ATL146e reduced NF-kappaB activation in the myocardium by over 50%, not only in the infarct zone but also in noninfarcted regions (P < 0.05). In conclusion, A(2A)AR stimulation after MI suppresses inflammatory activation and preserves cardiac function, suggesting the potential utility of A(2A)AR agonists against acute heart failure in the immediate post-MI period.
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PMID:Stimulation of A2A-adenosine receptors after myocardial infarction suppresses inflammatory activation and attenuates contractile dysfunction in the remote left ventricle. 1628 33

Cardiac magnetic resonance imaging (CMR) permits a detailed look at the myocardium in patients with recent onset heart failure. Late-enhancement CMR provides information that is similar to that obtained by the naked eye of a pathologist. Myocardial scarring is endocardial in myocardial infarction, but it is epicardial in myocarditis and intramyocardial in hypertrophic cardiomyopathy. Thus, the distinction between these entities is possible by depicting scar via late-enhancement CMR and observing myocardial function by cine magnetic resonance imaging. Moreover, non-invasive follow-up--and hence observation of the healing or remodelling process--can be achieved using CMR. New CMR pulse sequences also permit depiction of myocardial oedema, which may occur early in patients with myocarditis and may be the only sign of the disease in the absence of necrosis. It is anticipated that cardiac MRI will become a standard diagnostic technique in patients with new onset of heart failure, left-ventricular hypertrophy or clinical symptoms suggestive of myocarditis.
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PMID:New non-invasive approaches for the diagnosis of cardiomyopathy: magnetic resonance imaging. 1632 67

The development of heart failure (HF) after acute myocardial infarction (MI) is recognized as a major complication that leads to a significant increase in morbidity and mortality. Given the availability of effective treatments for improving both quality of life and survival for patients at increased risk for developing HF after MI, early identification of these individuals is critical. Noninvasive cardiac imaging offers a detailed characterization of two important pathophysiological processes related to the development of HF post-MI: left ventricular (LV) remodeling and LV functional recovery. Cardiovascular MRI has recently emerged as the preferred noninvasive imaging modality because of its ability to provide the most comprehensive and informative evaluation of these processes. In addition to allowing for an accurate and reproducible longitudinal follow-up of LV volumes and mass, MRI also offers information on infarct size, the presence of microvascular obstruction, and the transmural extent of infarct scar, all of which are valuable parameters that can assist in identifying patients at risk for developing HF after MI.
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PMID:Cardiac imaging to identify patients at risk for developing heart failure after myocardial infarction. 1633 11

Current patient selection criteria for Cardiac Resynchronization Therapy (CRT), an efficacious treatment for heart failure, include no measure of disconjugate cardiac contractility other than prolonged QRS on electrocardiogram. Using cardiac magnetic resonance imaging, we examined the roles of cardiac asymmetry, asynchrony, and circumferential strain in DCC with the principal aim of generating a robust numerical index for use in future trials of CRT. Standard cardiac magnetic resonance imaging was done on a GE 1.5 Tesla Signa LX MRI clinical scanner (GE Healthcare, Milwaukee, WI, USA) and analyzed by MASS Analysis (MEDIS, Leiden, The Netherlands). The methods were evaluated in eleven patients with advanced heart failure due to ischemic and non-ischemic cardiomyopathy, who did not qualify under current criteria for CRT, five CRT candidates pre-op and eleven normal subjects. Using t-test and standardized differences (SD = sd/diff, Power (N) = number of patients to reach p < .05) we determined efficacy. Indices of asymmetry and asynchrony (Ism and Isn, respectively) could be measured with accuracy and provided excellent statistical power when used as surrogate markers to delineate heart failure and CRT patients from control subjects. Asymmetry and asynchrony in heart contraction are both critical components of dilated cardiomyopathy that can be improved by CRT. Magnetic resonance asynchrony is efficacious in screening patients and should now be compared with recently published echocardiography data to improve outcome for this costly but valuable therapy.
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PMID:Magnetic resonance criteria for future trials of cardiac resynchronization therapy. 1635 44

We report a case of recurrent craniopharyngioma in the third ventricle with obstructive hydrocephalus, which was successfully treated by placement of the Ommaya reservoir by neuroendoscopic procedure. A 72-year-old male with disorientation and gait disturbance was admitted to our hospital. He had been suffering chronic heart failure and arrhythmia due to mitral valve insufficiency, and panhypopituitarism after the first craniotomy for craniopharyngioma. MRI demonstrated obstructive hydrocephalus at the foramen of Monro by the cystic tumor. Cyst decompression and placement of Ommaya reservoir were successfully performed in local anesthesia. Postoperatively, his disorientation and gait disturbance were improvement, and no chemical meningitis developed. Neuroendoscopic management for cystic craniopharyngioma with obstructive hydrocephalus was effective procedure for elderly patient with systemic risk factor.
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PMID:[Neuroendoscopic placement of the reservoir in an elderly patient with recurrenced craniopharyngioma: case report]. 1635 32

In an established swine model of severe left ventricular (LV) hypertrophy (LVH), the bioenergetic and functional consequences of transplanting autologous mesenchymal stem cells (MSCs) overexpressing vascular endothelial growth factor (VEGF-MSCs) into the LV were evaluated; transplantation was accomplished by infusion of VEGF-MSCs into the interventricular cardiac vein. Specifically, the hypertrophic response to aortic banding was compared in seven pigs treated with 30 million VEGF-MSCs, eight pigs treated with 30 million MSCs without VEGF modification, and 19 untreated LVH pigs. Eight pigs without banding or cell transplantation (normal) were also studied. Four weeks postbanding, LV wall thickening (MRI), myocardial blood flow (MBF), high-energy phosphate levels ((31)P magnetic resonance spectroscopy), and hemodynamic measurements were obtained under basal conditions and during a catecholamine-induced high cardiac workstate (HCW). Although 9 of 19 untreated banded pigs developed clinical evidence of biventricular failure, no MSCs-treated animal developed heart failure. MSCs engraftment was present in both cell transplant groups, and both baseline and HCW MBF values were significantly increased in hearts receiving VEGF-MSCs compared with other groups (P < 0.05). During HCW, cardiac inotropic reserve (defined as the percent increase of rate pressure product at HCW relative to baseline) was normal in the VEGF-MSCs group and significantly decreased in all other banded groups. Additionally, during HCW, the myocardial energetic state [reflected by the phosphocreatine-to-ATP ratio (PCr/ATP)] of VEGF-MSCs-treated hearts remained stable, whereas in all other groups, PCr/ATP decreased significantly from baseline values (P < 0.05, each group). Myocardial von Willebrand factor and VEGF mRNA expressions and myocardial capillary density were significantly increased in VEGF-MSCs-treated hearts (P < 0.05). Hence, in the pressure-overloaded LV, transplantation of VEGF-MSCs prevents LV decompensation, induces neovascularization, attenuates hypertrophy, and improves MBF, myocardial bioenergetic characteristics, and contractile performance.
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PMID:Bioenergetic and functional consequences of stem cell-based VEGF delivery in pressure-overloaded swine hearts. 1638 94

A decrease in the supply of ATP from the creatine kinase (CK) system is thought to contribute to the evolution of heart failure. However, previous studies on mice with a combined knockout of the mitochondrial and cytosolic CK (CK(-/-)) have not revealed overt left ventricular dysfunction. The aim of this study was to employ novel MRI techniques to measure maximal myocardial velocity (V(max)) and myocardial perfusion and thus determine whether abnormalities in the myocardial phenotype existed in CK(-/-) mice, both at baseline and 4 wk after myocardial infarction (MI). As a result, myocardial hypertrophy was seen in all CK(-/-) mice, but ejection fraction (EF) remained normal. V(max), however, was significantly reduced in the CK(-/-) mice [wild-type, 2.32 +/- 0.09 vs. CK(-/-), 1.43 +/- 0.16 cm/s, P < 0.05; and wild-type MI, 1.53 +/- 0.11 vs. CK(-/-) MI, 1.26 +/- 0.11 cm/s, P = not significant (NS), P < 0.05 vs. baseline]. Myocardial perfusion was also lower in the CK(-/-) mice (wild-type, 6.68 +/- 0.27 vs. CK(-/-), 4.12 +/- 0.63 ml/g.min, P < 0.05; and wild-type MI, 3.97 +/- 0.65 vs. CK(-/-) MI, 3.71 +/- 0.57 ml/g.min, P = NS, P < 0.05 vs. baseline), paralleled by a significantly reduced capillary density (histology). In conclusion, myocardial function in transgenic mice may appear normal when only gross indexes of performance such as EF are assessed. However, the use of a combination of novel MRI techniques to measure myocardial perfusion and mechanics allowed the abnormalities in the CK(-/-) phenotype to be detected. The myocardium in CK-deficient mice is characterized by reduced perfusion and reduced maximal contraction velocity, suggesting that the myocardial hypertrophy seen in these mice cannot fully compensate for the absence of the CK system.
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PMID:Multimodal functional cardiac MRI in creatine kinase-deficient mice reveals subtle abnormalities in myocardial perfusion and mechanics. 1641 75

In most cases inflammatory changes of the myocardium are asymptomatic. If inflammatory changes of the myocardium manifest with clinical symptoms, the condition is termed myocarditis. Myocarditis is regarded as a major cause for sudden death of young adults and accounts for up to 20% of the cases. In Europe viral infections represent the most important cause of myocarditis. In chronic myocarditis, viremia is often absent and myocardial fibrosis and dilated cardiomyopathy (DCM) resulting in heart failure can occur. The role of cardiac MRI in chronic myocarditis is not yet well understood. MRI is a sensitive tool detecting myocardial fibrosis on late images after application of paramagnetic contrast agents. The region of contrast accumulation is defined as "late enhancement" (LE). Data are available now suggesting that differentiating fibrosis due to myocardial infarction from inflammatory causes is facilitated using MRI late images. Fibrosis after ischemic infarction includes the subendocardial layer of the myocardium. If the subendocardial layer of the myocardium is not involved in the fibrosis, infarction is unlikely and can be reliably excluded as an important differential diagnosis in the vast majority of affected patients.
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PMID:[MRI in chronic myocarditis]. 1641 74

Idiopathic infantile arterial calcification (IIAC) is a rare condition characterized by extensive calcification and stenosis of large and medium-size arteries. The etiology of the disease is unknown. However, the inheritance pattern has been shown to be autosomal recessive. The clinical presentation is variable, including cardiac failure (most common clinical finding), hypertension, and respiratory failure. Plain radiography, sonography and MRI can aid in the diagnosis. We present a case in which contrast-enhanced MR angiography with breath-hold and cardiac gating techniques allowed complete evaluation of the extent of this disease.
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PMID:Idiopathic infantile arterial calcification: imaging evaluation and the usefulness of MR angiography. 1642 73


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