Myocardial Oedema and Congestive Heart Failure: One Piece of the Puzzle? Reply

We thank Dr. Arques for showing interest in our paper describing the importance of the right ventricle in heart failure with preserved ejection fraction (HFpEF).1 In this position statement, we review the pathophysiology and potential treatment strategies of right heart failure in HFpEF. Right ventricular dysfunction in acute decompensated heart failure is a major driver of poor prognosis.2 Overt right heart failure leads to systemic venous congestion and multi-organ dysfunction.3 As mentioned by Dr. Arques, increased right-sided filling pressures and concomitant coronary venous hypertension in decompensated heart failure may also lead to passive interstitial accumulation of fluids in the myocardium. This phenomenon has recently been demonstrated by Verbrugge et al.4 Patients presenting with acute decompensated heart failure had more myocardial oedema compared to controls, as visualized by higher T2 values with cardiac magnetic resonance imaging. After treatment, T2 values were significantly reduced—suggesting a reduction in myocardial interstitial oedema—which was coupled with a reduction in central venous pressure.4 Although the direct link between interstitial myocardial oedema and adverse myocardial remodelling in heart failure is unknown, we agree with Dr. Arques this is an interesting topic for research, and myocardial interstitial oedema in decompensated heart failure may indeed be a contributory mechanism of adverse cardiac remodelling. We also agree that we need further research to confirm the potential relevance of myocardial oedema and to develop targeted therapies. This may be especially relevant for HFpEF, because we lack specific therapies to reduce mortality in these patients. A major aspect we stressed in our recent position paper is the importance of adequate volume management in symptomatic patients with HFpEF, especially those with right heart failure, to prevent acute decompensation and further deterioration of right ventricular function.1 New modalities, such as continuous monitoring of pulmonary pressures, may be a useful tool to timely adjust a patient's volume status with diuretics and vasodilators, to prevent excessive central venous hypertension and recurrent hospitalizations for acute heart failure.5 Again, further research should elucidate whether such strategies will be beneficial on the long term.