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Pathophysiological mechanisms in chronic heart failure (data from[3]). RAAS: Renin-Angiotensin-Aldosterone System; SNS: Sympathetic nervous systems.

Pathophysiological mechanisms in chronic heart failure (data from[3]). RAAS: Renin-Angiotensin-Aldosterone System; SNS: Sympathetic nervous systems.

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Heart failure (HF) is a major public health problem with a prevalence of 1%-2% in developed countries. The underlying pathophysiology of HF is complex and as a clinical syndrome is characterized by various symptoms and signs. HF is classified according to left ventricular ejection fraction (LVEF) and falls into three groups: LVEF ≥ 50% - HF with pr...

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... main pathophysiological mechanisms leading to HF are increased hemodynamic overload, ischemia, myocardial dysfunction and remodelling, excessive neurohumoral stimulation -chronic sympathetic nervous system overactivity as one of the key pathophysiological mechanisms (in the acute phase, this upregulated sympathetic activity is an essential compensatory response initiated in order to compensate for reduced contractility, and cardiac output but in the long-term, it contributes to cardiac dysfunction as it leads to cardiac hypertrophy and cell dysfunction), activation of the renin-angiotensin-aldosterone system (RAAS), excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis, and genetic mutations [3][4][5][6] (Figure 1). HF is associated with a variety of complications, such as frequent hospitalizations, fatal arrhythmias, and death in the advanced stage of the disease. ...
Context 2
... main pathophysiological mechanisms leading to HF are increased hemodynamic overload, ischemia, myocardial dysfunction and remodelling, excessive neurohumoral stimulation -chronic sympathetic nervous system overactivity as one of the key pathophysiological mechanisms (in the acute phase, this upregulated sympathetic activity is an essential compensatory response initiated in order to compensate for reduced contractility, and cardiac output but in the long-term, it contributes to cardiac dysfunction as it leads to cardiac hypertrophy and cell dysfunction), activation of the renin-angiotensin-aldosterone system (RAAS), excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis, and genetic mutations [3][4][5][6] (Figure 1). HF is associated with a variety of complications, such as frequent hospitalizations, fatal arrhythmias, and death in the advanced stage of the disease. ...
Context 3
... main pathophysiological mechanisms leading to HF are increased hemodynamic overload, ischemia, myocardial dysfunction and remodelling, excessive neurohumoral stimulation -chronic sympathetic nervous system overactivity as one of the key pathophysiological mechanisms (in the acute phase, this upregulated sympathetic activity is an essential compensatory response initiated in order to compensate for reduced contractility, and cardiac output but in the long-term, it contributes to cardiac dysfunction as it leads to cardiac hypertrophy and cell dysfunction), activation of the renin-angiotensin-aldosterone system (RAAS), excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis, and genetic mutations [3][4][5][6] (Figure 1). HF is associated with a variety of complications, such as frequent hospitalizations, fatal arrhythmias, and death in the advanced stage of the disease. ...

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Background Traditional Chinese eight brocade exercise (TCEBE) with same cycle and frequency and different durations has an effect on patients with chronic heart failure (CHF). However, relevant reports on the topic are lacking. Objective This study aims to explore the differences of rehabilitation effect by conducting TCEBE with the same cycle and frequency and different single exercise time for patients with CHF. Methods A total of 103 patients with CHF were randomly divided into long-time group (LTG), short-time group (STG) and control group (CG). The subjects in the three groups were given corresponding routine treatment. In addition, under the guidance of professional TCEBE coaches and nurses, TCEBE was conducted for 12 weeks (3 times/week) for LTG (60 min/time) and STG (30 min/time). Minnesota living with heart failure questionnaire (MLHFQ) was used, and 6-min walk (6MWK) and brain nautical peptide (BNP) were tested. Results 1) At 12 weeks, the comparison between groups obtained the following results: For the LTG, MLHFQ was less than that of the CG (P < 0.01), 6MWT was greater than that of the CG (P < 0.05), and 6MWT was greater than that of the STG (P < 0.05); for the STG, MLHFQ was less than that of the CG (P < 0.05); no significant difference in BNP was found among the three groups; 2) At 12 weeks and 0 weeks, the comparison obtained the following results: For the LTG, MLHFQ decreased by 37.7 %, and 6MWT increased by 46.7 % (P < 0.01); for the STG, MLHFQ decreased by 31.7 %, and 6MWT increased by 31.5 % (P < 0.01); for the CG, MLHFQ decreased by 14.6 %, and 6MWT increased by 19.7 % (P < 0.05); no significant change in BNP was found in each group. Conclusion TCEBE of two kinds of duration improves the quality of life and 6MWT of patients with CHF but has no positive effect on BNP. Compared with 30-min/time, 60-min/time further improves 6MWT in patients with CHF but has no additional benefit on quality of life.