474 research outputs found
Age, left atrial dimension and arterial stiffness after external cardioversion of atrial fibrillation. A vascular component in arrhythmia maintenance? Results from a preliminary study
Diastolic function measurements and diagnostic consequences: a comparison of pulsed wave- and color-coded tissue Doppler imaging
Tissue Doppler imaging (TDI) plays an important role in assessing diastolic function using echocardiography. However, two different methods [pulsed wave (PW-TDI) and color-coded (CC-TDI)] are currently used. We aimed to compare both measurements. We included 114 patients that were referred to our echocardiography department for evaluation of diastolic left ventricular function. In these patients, we sequentially measured tissue velocities of basal lateral and septal myocardium of the left ventricle in an apical four-chamber view with both PW-TDI and CC-TDI. Our cohort consisted of a heterogeneous group of patients with and without a history of cardiac disease. Mean age of the patients was 52 +/- A 16.7 years, and 62% were males. We found a strong correlation between PW-TDI- and CC-TDI-derived myocardial velocities (r = 0.93; p = 0.001). However, E' (mean of lateral and septal) velocities measured with PW-TDI were consistently higher compared to CC-TDI values [PW-TDI E' 10.3 +/- A 3.9 (SD) cm/s vs. CC-TDI E' 7.7 +/- A 3.1 cm/s; p <0.001]. From these data, we calculated that the relation between E' measured with PW-TDI and CC-TDI can be described as: E' (PW-TDI) = 1.25 + 1.17 x E' (CC-TDI). Consequently, E/E' measured with PW-TDI was consistently lower compared with CC-TDI (9.1 +/- A 3.1 vs. 12.5 +/- A 5.7; p <0.001) From these data, we calculated that the relation between E/E' measured with PW-TDI and CC-TDI can be described as: E/E' (PW-TDI) = 2.13 + 0.56 x E/E' (CC-TDI). Despite a strong correlation, tissue velocities measured with PW-TDI will yield higher values as compared with CC-TDI. This should be taken into account when defining cut-off values for the evaluation of diastolic function
Prenatal hypoxia induces increased cardiac contractility on a background of decreased capillary density.
Background: Chronic hypoxia in utero (CHU) is one of the most common insults to fetal development and may be associated with poor cardiac recovery from ischaemia-reperfusion injury,yet the effects on normal cardiac mechanical performance are poorly understood.
Methods: Pregnant female wistar rats were exposed to hypoxia (12% oxygen, balance nitrogen)for days 10–20 of pregnancy. Pups were born into normal room air and weaned normally. At 10 weeks of age, hearts were excised under anaesthesia and underwent retrograde 'Langendorff' perfusion. Mechanical performance was measured at constant filling pressure (100 cm H2O) with intraventricular balloon. Left ventricular free wall was dissected away and capillary density estimated following alkaline phosphatase staining. Expression of SERCA2a and Nitric Oxide Synthases (NOS) proteins were estimated by immunoblotting.
Results: CHU significantly increased body mass (P < 0.001) compared with age-matched control rats but was without effect on relative cardiac mass. For incremental increases in left ventricular balloon volume, diastolic pressure was preserved. However, systolic pressure was significantly greater following CHU for balloon volume = 50 μl (P < 0.01) and up to 200 μl (P < 0.05). For higher balloon volumes systolic pressure was not significantly different from control. Developed pressures were correspondingly increased relative to controls for balloon volumes up to 250 μl (P < 0.05).Left ventricular free wall capillary density was significantly decreased in both epicardium (18%; P <0.05) and endocardium (11%; P < 0.05) despite preserved coronary flow. Western blot analysis revealed no change to the expression of SERCA2a or nNOS but immuno-detectable eNOS protein was significantly decreased (P < 0.001) in cardiac tissue following chronic hypoxia in utero.
Conclusion: These data offer potential mechanisms for poor recovery following ischaemia, including decreased coronary flow reserve and impaired angiogenesis with subsequent detrimental effects of post-natal cardiac performance
Relationship between tei index and left ventricular geometric patterns in a hypertensive population: a cross-sectional study
High frequency of diastolic dysfunction in a population-based cohort of elderly women - but poor association with the symptom dyspnea
Myocardial tissue Doppler echocardiography and N-terminal B-type natriuretic peptide (NT-proBNP) in diastolic and systolic heart failure
Study on the evaluation of the clinical effects of traditional chinese medicine in heart failure by complex intervention: protocol of SECETCM-HF
<p>Abstract</p> <p>Background</p> <p>Experts in Traditional Chinese Medicine (TCM) have studied the TCM subject of the pathogenesis of heart failure (HF) for several decades. As a result, the general idea is <it>ben </it>deficiency and <it>biao </it>excess. However, the clinical evaluation system which combined the TCM and western medicine in HF has not been developed yet. The objective is to establish the evaluation index system for the integration of TCM and western medicine. The evaluation indexes which include TCM items will specify the research design and methods.</p> <p>Methods</p> <p>Nine medical centers in different cities in China will participate in the trial. A population of 340 patients with HF will be enrolled through a central randomized system for different test groups. Group A will be treated with only western medicine, while group B with western and Chinese medicine together. The study will last for 12 months from the date of enrollment. The cardiovascular death will be the primary outcome.</p> <p>Discussion</p> <p>By putting the protocol into practice, the clinical effects of TCM for HF will be identified scientifically, objectively as well as rationally. The proper index system which built in the study will be helpful for the clinical effect expression of HF by integrated medicine in future.</p> <p>Trial Registration</p> <p>ChiCTR-TRC-00000059</p
Aortic stiffness as a marker of cardiac function and myocardial strain in patients undergoing aortic valve replacement
Background: Cardiac function and myocardial strain are affected by cardiac afterload, which is in part due to the
stiffness of the aortic wall. In this study, we hypothesize that aortic pulse wave velocity (PWV) as a marker of aortic
stiffness correlates with conventional clinical and biochemical markers of cardiac function and perioperative
myocardial strain in aortic valve replacement (AVR).
Methods: Patients undergoing AVR for aortic stenosis between June 2010 and August 2012 were recruited for
inclusion in this study. PWV, NYHA class and left ventricular (LV) function were assessed pre-operatively. PWV was
analysed both as a continuous and dichotomous variable according to age-standardized reference values. B-type
natriuretic peptide (BNP) was measured pre-operatively, and at 3 h and 18-24 h after cardiopulmonary bypass (CPB).
NYHA class, leg edema, and LV function were recorded at follow-up (409 ± 159 days).
Results: Fifty-six patients (16 females) with a mean age of 71 ± 8.4 years were included, with 50 (89%) patients
completing follow-up. The NYHA class of PWV-norm patients was significantly lower than PWV-high patients both
pre- and post-operatively. Multiple logistic regression also highlighted PWV-cut off as an independent predictor of
NYHA class pre- and post-operatively (OR 8.3, 95%CI [2.27,33.33] and OR 14.44, 95%CI [1.49,139.31] respectively). No
significant relationship was observed between PWV and either LV function or plasma BNP.
Conclusion: In patients undergoing AVR for aortic stenosis, PWV is independently related to pre- and post-operative
NYHA class but not to LV function or BNP. These findings provisionally support the use of perioperative PWV as a
non-invasive marker of clinical functional status, which when used in conjunction with biomarkers of myocardial strain
such as BNP, may provide a holistic functional assessment of patients undergoing aortic valve surgery. However, in
order for PWV assessment to be translated into clinical practice and utilised as more than simply a research tool, further
validation is required in the form of larger prospective studies specifically designed to assess the relationship between
PWV and these functional clinical outcomes
Who fans the flames of Alzheimer's disease brains? Misfolded tau on the crossroad of neurodegenerative and inflammatory pathways
Neurodegeneration, induced by misfolded tau protein, and neuroinflammation, driven by glial cells, represent the salient features of Alzheimer's disease (AD) and related human tauopathies. While tau neurodegeneration significantly correlates with disease progression, brain inflammation seems to be an important factor in regulating the resistance or susceptibility to AD neurodegeneration. Previously, it has been shown that there is a reciprocal relationship between the local inflammatory response and neurofibrillary lesions. Numerous independent studies have reported that inflammatory responses may contribute to the development of tau pathology and thus accelerate the course of disease. It has been shown that various cytokines can significantly affect the functional and structural properties of intracellular tau. Notwithstanding, anti-inflammatory approaches have not unequivocally demonstrated that inhibition of the brain immune response can lead to reduction of neurofibrillary lesions. On the other hand, our recent data show that misfolded tau could represent a trigger for microglial activation, suggesting the dual role of misfolded tau in the Alzheimer's disease inflammatory cascade. On the basis of current knowledge, we can conclude that misfolded tau is located at the crossroad of the neurodegenerative and neuroinflammatory pathways. Thus disease-modified tau represents an important target for potential therapeutic strategies for patients with Alzheimer's disease
- …