1,721,601 research outputs found
Considerations on safety and treatment of patients with chronic heart failure at high altitude
Full text linkConsiderations on safety and treatment of patients with chronic heart failure at high altitude. High Alt Med Biol 14:96-100, 2013. - Prognosis and quality of life of chronic heart failure (HF) patients have greatly improved over the last decade. Consequently, many patients are willing to spend leisure time at altitude, usually <3500 m, but their safety in doing so is undefined. HF is a syndrome that often has relevant co-morbidities, such as pulmonary hypertension, COPD, unstable cardiac ischemia, and anemia. HF co-morbidities may per se impede a safe stay at altitude. Exercise at simulated altitude is associated with a reduction in performance, which is greater in HF patients than in normal subjects and greater in patients with most severe HF. In normal subjects, the reduction in performance is ∼2% every 1000 m altitude increase, whereas it is 4% and 10% in HF patients with normal or slightly diminished exercise capacity and in HF patients with markedly diminished exercise capacity. On-field experience with HF patients at altitude is limited to subjects driven to altitude (3454 m) for a few hours. The data showed a reduction in exercise capacity similar to that reported at simulated altitude. "Optimal" HF treatment in patients spending time at altitude is likely different from optimal treatment at sea level, particularly as regards β-blockers. Carvedilol, a β1-β2-α- blocker, reduces the hypoxic ventilatory response through a reduction of the chemoreflex response, and it reduces alveolar-capillary gas diffusion, which is under control by β2-receptors. These actions are not shared by selective β1-blockers such as bisoprolol and nebivolol, which should be preferred for treatment of HF patients willing to spend time at altitude. In conclusion, spending time at altitude (<3500 m) is safe for HF patients, provided that subjects are free of co-morbidities that may directly interfere with the adaptation to altitude. However, HF patients experience a reduction of exercise capacity in proportion to HF severity and altitude. Finally, HF patients should undergo a specific "altitude-tailored treatment" to avoid pharmacological interference with altitude adaptation mechanisms
Cardiopulmonary exercise testing for heart failure patients : a hodgepodge of techniques, parameters and interpretations. In other words, the need for a time-break
Full text linkExertional dyspnoea in cardiorespiratory disorders : The clinical use of cardiopulmonary exercise testing
Full text linkComparing losartan with enalapril in congestive heart failure
No full textWe compared the effects of losartan and enalapril on exercise oxygen uptake, diffusing capacity of lung for carbon monoxide, and evaluated the consequences of cyclo-oxygenase and prostaglandin inhibition in 16 patients with congestive heart failure and 8 controls. In patients, but not in controls, losartan and enalapril similarly improved exercise tolerance and oxygen uptake. This effect was inhibited, however, by cyclooxygenase blockade with aspirin while patients were taking enalapril and not losartan. Our findings suggest that because losartan's effect is dissociated from prostaglandin activation, it may be an advancement for the treatment of patients with congestive heart failure and coronary artery disease in whom aspirin is indicated
Surfactant protein B : From biochemistry to its potential role as diagnostic and prognostic marker in heart failure
No full textGrowing interest raised on circulating biomarkers of structural alveolar–capillary unit damage and very recent data support surfactant protein type B (SP-B) as the most promising candidate in this setting. With respect to other proteins proposed as possible markers of lung damage, SP-B has some unique qualities: it is critical for the assembly of pulmonary surfactant, making its lack incompatible with life; it has no other known site of synthesis except alveolar epithelial cells different from other surfactant proteins; and, it undergoes a proteolytic processing in a pulmonary-cell-specific manner. In the recent years circulating SP-B isoforms, mature or immature, have been demonstrated to be detectable in the circulation depending on the magnitude of the damage of alveolar capillary membrane. In the present review, we summarize the recent knowledge on SP-B regulation, function and we discuss its potential role as reliable biological marker of alveolar capillary membrane (dys)function in the context of heart failure
Exhaled nitric oxide and exercise performance in heart failure
No full textIn heart failure abnormalities of pulmonary function are frequently observed particularly during exercise, which is characterized by hyperpnea, low tidal volume, early expiratory flow limitation and reduced lung compliance. Exhaled nitric oxide (NO) is increased in asthma. We evaluated whether a correlation between exhaled NO and lung mechanics exists during exercise in heart failure
Matrix metalloproteinase and heart failure : is it time to move from research to clinical laboratories?
No full textPrognostic implications of heart failure with preserved ejection fraction in patients with an exacerbation of chronic obstructive pulmonary disease
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