Navegando por Palavras-chave "Diastolic dysfunction"

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    Heart failure with preserved ejection fraction induces molecular, mitochondrial, histological, and functional alterations in rat respiratory and limb skeletal muscle
    (Wiley-Blackwell, 2015-03-01) Bowen, T. Scott; Rolim, Natale P. L.; Fischer, Tina; Baekkerud, Fredrik H.; Medeiros, Alessandra [UNIFESP]; Werner, Sarah; Bronstad, Eivind; Rognmo, Oivind; Mangner, Norman; Linke, Axel; Schuler, Gerhard; Silva, Gustavo J. J.; Wisloff, Ulrik; Adams, Volker; Optimex Study Grp; Univ Leipzig; Norwegian Univ Sci & Technol; Universidade Federal de São Paulo (UNIFESP)
    AimsPeripheral muscle dysfunction is a key mechanism contributing to exercise intolerance (i.e. breathlessness and fatigue) in heart failure patients with preserved ejection fraction (HFpEF); however, the underlying molecular and cellular mechanisms remain unknown. We therefore used an animal model to elucidate potential molecular, mitochondrial, histological, and functional alterations induced by HFpEF in the diaphragm and soleus, while also determining the possible benefits associated with exercise training.Methods and resultsFemale Dahl salt-sensitive rats were fed a low (CON; n = 10) or high salt (HFpEF; n = 11) diet of 0.3% or 8% NaCl, respectively, or a high salt diet in combination with treadmill exercise training (n = 11). Compared with low-salt rats, high-salt rats developed (P < 0.05) HFpEF. Compared with CON, the diaphragm of HFpEF rats demonstrated (P < 0.05): a fibre type shift from fast-to-slow twitch; fibre atrophy; a decreased pro-oxidative but increased anti-oxidant capacity; reduced proteasome activation; impaired in situ mitochondrial respiration; and in vitro muscle weakness and increased fatigability. the soleus also demonstrated numerous alterations (P < 0.05), including fibre atrophy, decreased anti-oxidant capacity, reduced mitochondrial density, and increased fatigability. Exercise training, however, prevented mitochondrial and functional impairments in both the diaphragm and soleus (P < 0.05).ConclusionOur findings are the first to demonstrate that HFpEF induces significant molecular, mitochondrial, histological, and functional alterations in the diaphragm and soleus, which were attenuated by exercise training. These data therefore reveal novel mechanisms and potential therapeutic treatments of exercise intolerance in HFpEF.
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    Left Atrial Volume and Function in Patients With Obstructive Sleep Apnea Assessed by Real-Time Three-Dimensional Echocardiography
    (Elsevier B.V., 2008-12-01) Oliveira, Wercules [UNIFESP]; Campos, Orlando [UNIFESP]; Lira-Filho, Edgar Bezerra [UNIFESP]; Cintra, Fatima Dumas [UNIFESP]; Vieira, Marcelo; Ponchirolli, Andrea [UNIFESP]; De Paola, Angelo de [UNIFESP]; Tufik, Sergio [UNIFESP]; Poyares, Dalva [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Albert Einstein Hosp
    Background: Studies have suggested that obstructive sleep apnea (OSA) contributes to the deterioration of left ventricular diastolic function. This may lead to atrial myocardial overstretching and enlargement, which could be associated with increased cardiovascular risk. the aim of this study was to evaluate left atrial (LA) volume and function in patients with OSA compared with controls without OSA and their associations with any left ventricular diastolic abnormalities using real-time 3-dimensional echocardiography (RT3DE).Methods: Fifty-six patients with mild to severe OSA and 50 controls of similar age and with similar body mass indexes, blood pressure, and frequency of hypertension were analyzed. All subjects underwent polysomnography and RT3DE.Results: A larger 3-dimensional maximum LA volume indexed for body surface area, larger volume before atrial contraction, and higher active atrial ejection fraction were found in patients with OSA (P < .01 for all). Mitral annular early diastolic velocity (E') was reduced in patients with OSA (P = .03), whereas late diastolic velocity (A') and the ratio of mitral valve early diastolic velocity to mitral annular early diastolic velocity (E/E') were increased in the same group (P < .05 for both). in addition, a lower E'/A' ratio was also found in the OSA group (P = .02). An increase in 3-dimensional maximum LA volume indexed for body surface area was observed, depending on OSA severity. the apnea-hypopnea index and E/E' ratio were independent predictors of an increase in 3-dimensional maximum LA volume in a multiple regression model.Conclusion: Using RT3DE, this study demonstrates that OSA induces a functional burden on the left atrium, resulting in remodeling. These functional and structural changes are related to the impairment of diastolic function in this population. (J Am Soc Echocardiogr 2008; 21: 1355-1361.)