Prof. Theresa McDonagh,
This session addressed several issues pertinent to the current and future treatment of acute heart failure (AHF)-one of the last areas of great unmet need within the heart failure family of syndromes. Dr Gad Cotter (Durham, US) started off the session by considering the importance of dyspnea as a treatment target in AHF. The first take home message was that patients want to feel less breathless; data from the EuroHeart Failure Survey and the Adhere Registries confirm this. Dyspnoea is also important and it is directly related to one of the main pathophysiological mechanisms in heart failure i.e congestion. Data from the Protect Study confirm that relief of congestion and dyspnoea are associated with weight loss in AHF. Lack of improvement in dyspnea also predicts adverse outcomes in AHF. It was associated with an increase in 14 day and 30 day mortality in the Protect Study. However about 30% of patients do not get relief of dyspnea during a heart failure admission. Dyspnoea can be relieved effectively by many of our treatments for AHF. Diuretics do reduce breathlessness. Interestingly, recent evidence suggests that higher doses of furosemide are not significantly better in this regard that lower doses. Levosimendan improved dyspnea in the REVIVE trial, however outcomes worsened; hence this drug is not available in many countries. In the Unload Trial, ultrafiltration did not improve dyspnea. Tolvaptan, however, does improve breathlessness and has a neutral effect on mortality in AHF. There is clearly a need for future trials to address dyspnea reduction in AHF; hopefully the ongoing study with relaxin will result in an improvement in this important symptom without adverse effects on heart failure mortality. Dr Gheorghiade (Chicago, IL) discussed the importance of end organ protection in AHF. He outlined the main end organ problems encountered in AHF: cardiac injury (troponin release) and worsening renal function, as well as some of the entities related to target organ damage, namely, abnormal haemodynamics, fluctuating neurohormonal profiles and changes in electrolyte balance. He pointed out that a hospitalization for heart failure is associated with a worse prognosis. The hypothesis underlying this phenomenon is that each hospitalization results in myocardial and renal damage. This then leads to progression of heart failure. Ischaemia is a major factor in causing that cardiac damage in AHF patients with coronary artery disease. This can be worsened by use of some inotropes, e.g milrinone which is known from the OPTIME study to be associated with a higher mortality in patients with coronary artery disease. Deterioration in renal function also results in poorer outcomes in AHF. However he stressed the point that it important to treat the heart in AHF and not concentrate too much on the kidneys. They merely reflect the fact that there is a severer cardiac problem. Kidney function early after discharge is an important predictor of adverse events following an AHF admission. Future therapies with novel cardiac and renal protective agents are needed to try and improve AHF outcomes. Dr Grinfeld from Argentina focussed on therapies for preventing rehospitsalisations in AHF patients. Readmission rates after AHF vary. In the US they are about 25% at 30 days and around 50% at one year. Rehospitalisations are independent predictors of subsequent death. Strategies to reduce hospitalization should include inititation and uptitration of evidence based pharmoacotherpy including ACE inhibitors, beta-blockers and aldosterone antagonists and device therapy as appropriate. Consideration should be given to the need for revascularization in selected patients. Heart Failure Disease management programmes play a crucial role in prevention of rehospitalisations. She also focused on whether rehospitalisation should be a Quality Outcome measure for AHF because of the complex relationship between length of stay and rehospitalisation rates. The session was ended with Professor Marco Metra (Brescia, IT) reviewing treatment strategies in AHF which reduce mortality. This is an important endpoint as the in-hospital and post-discharge mortalities are still high at between 4-9% and 9-15% respectively. Drugs we commonly use for AHF have variable effects on mortality. In particular, loop diuretic and inotrope use are associated with an increased mortality rate. Newer drugs which have recently been subjected to randomised controlled trials in AHF have shown variable effects on mortality. Levosimendan reduced it at 180 days in the LIDO trial whereas in a meta-analysis of trials with nesiritide, mortality was increased. Larger trials adequately powered to address mortality with levosimendan (SURVIVE) and Nesiritide (ASCEND) showed no survival benefits in AHF patients. So the quest to find drugs in AHF which reduce mortality still goes on. To date, many trials in AHF have had limitations in terms of their design and in their recruitment of too heterogenous a group of patients. Future trials of newer intotropic agents (Isataroxime and Cardiac Myosin Activators) and vasodiltaors (Relaxin) will hopefully provide clearer answers to the problem.
Treatment targets in acute heart failure
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