3 research outputs found
Mechanisms and Management of Breathlessness in Chronic Heart Failure
Background: The pathophysiology of dyspnoea (‘breathlessness’) is poorly understood and
treatment options limited. This is particularly true for heart failure in which dyspnoea is a
cardinal symptom, even when the heart failure is optimally managed. This thesis aims to
untangle mechanisms and utilise this knowledge to optimise heart failure management. It
focuses on the potential of nebulised furosemide as an adjunct treatment, given its excellent
safety record and existing evidence that it modulates dyspnoea via direct action on lungs.
Methods: A multi-dimensional questionnaire was used to survey the prevalence of dyspnoea
in the heart failure community. A randomised, double blind, placebo-controlled crossover trial
(RCT) was then performed in healthy participants to determine the specific components of
dyspnoea that are relieved by the action of furosemide on the lungs. This study led to the
design of a feasibility RCT in patients with heart failure using the visual analogue scale (VAS)
ratings of the ‘air hunger’ (AH) component of dyspnoea as the primary outcome measure. The
RCT itself; i) addressed other issues that could account for variability in relief seen in previous
studies, ii) explored blood biomarkers of heart failure in relation to dyspnoea and iii) provided
guidance for future definitive clinical trials.
Results: 1) 47% of patients experienced dyspnoea in the community. Dyspnoea-12 scores
correlated with New York Heart Association class, with many in class III experiencing dyspnoea
at rest. 2) Nebulised furosemide specifically relieved AH induced in healthy participants but did
not affect the 'work/effort' component. Relief was only with nebulised, not intravenous
furosemide. 3) Breathing furosemide quickly or slowly did not alter dyspnoea relief, but
ventilation was not matched. 4) Cardiopulmonary exercise testing (CPET) produced an average
VO2peak of 54±15% predicted, with a measurable anaerobic threshold in 73% of tests and
raised dyspnoea to 42±19%VAS. 5) Nebulised furosemide resulted in no significant
improvements in exercise capacity. 6) Cardiac biomarkers increased appropriately and returned to baseline within 1 hour of exercise. The maximal absorption efficiency of nebulised
furosemide was 2%.
Conclusion: 1) Dyspnoea is a prevalent symptom in heart failure, comparable to chronic
obstructive pulmonary disease. The NYHA classification may require clarification regarding
presence of breathlessness at rest. 2) Relief of dyspnoea with nebulised furosemide occurs via
a mechanism within the lungs and should be targeted at those in whom ‘air hunger’
predominates. 3) CPET is a feasible method for dyspnoea assessment in heart failure. 4) Fully
powered RCT of nebulised furosemide in heart failure are warranted taking on board the
preliminary information gathered in this thesis to optimise treatment effect
Debating pharmacological options for dyspnoea relief: The need for full, accurate and balanced critical appraisal of the evidence
Specialist intervention is associated with improved patient outcomes in patients with decompensated heart failure: evaluation of the impact of a multidisciplinary inpatient heart failure team
Objective. The study aimed to evaluate the impact of a multidisciplinary inpatient heart failure team (HFT) on treatment, hospital readmissions and mortality of patients with decompensated heart failure (HF).
Methods A retrospective service evaluation was undertaken in a UK tertiary centre university hospital
comparing 196 patients admitted with HF in the 6 months prior to the introduction of the HFT (pre-HFT) with all 211 patients seen by the HFT (post-HFT) during its first operational year. Results. There were no significant differences in patient baseline characteristics between the groups. Inpatient mortality (22% pre-HFT vs 6% post-HFT; p<0.0001) and 1-year mortality (43% pre-HFT vs 27% post-HFT; p=0.001) were significantly lower in the post-HFT cohort. Post-HFT patients were significantly more likely to be discharged on loop diuretics (84% vs 98%; p=<0.0001), ACE inhibitors (65% vs 76%; p=0.02), ACE inhibitors and/or angiotensin receptor blockers (83% vs 91%; p=0.02), and mineralocorticoid receptor antagonists (44% vs 68%; p<0.0001) pre-HFT versus post-HFT, respectively. There was no difference in discharge prescription rates of betablockers (59% pre-HFT vs 63% post-HFT; p=0.45). The mean length of stay (17±19 days pre-HFT vs 19±18 days post-HFT; p=0.06), 1-year all-cause readmission rates (46% pre-HFT vs 47% post-HFT; p=0.82) and HF readmission rates (28% pre-HFT vs 20% post-HFT; p=0.09) were not different between the groups. Conclusions. The introduction of a specialist inpatient HFT was associated with improved patient outcome. Inpatient and 1-year mortality were significantly reduced. Improved
use of evidence-based drug therapies, more intensive diuretic use and multidisciplinary care may contribute to these differences in outcome