Pulmonary Congestion: Who is at Risk?

Abstract

Previous heart failure hospitalization identifies patients at very high risk for re-congestion, up to 50% at 6 months, with the highest risk in those with recent hospitalizations. Even without hospitalization, patients with current signs and symptoms of congestion are still at high risk for heart failure events, for which an increase in outpatient diuretic dose is a harbinger. People who have chronically elevated pulmonary artery pressures are at risk even if they are not currently aware of symptoms. As for systemic hypertension, pulmonary hypertension can be a silent killer as it progresses to right heart failure, which is often the final common pathway for patients who have been compensated for years with low left ventricular ejection fraction. Congestion is the intersection of clinical HFrEF versus HFpEF, so therapy for both populations is better guided by pulmonary artery pressure information. Where the two phenotypes differ is in the causes and therapies for congestion. Neurohormonal activation play a large part in congestion for HFrEF, as the neurohormonal antagonists have had such a large cumulative benefit to decrease hospitalizations. The benefit of managing pulmonary artery pressures in HFrEF is highest when combined with the fundamental therapies of ACEI and blockers. These agents have at best minor effects to decrease hospitalizations with HFpEF. The impact of ambulatory pulmonary pressure-guided therapy is consistently shown for preserved EF. This impact extends to patients with severe obesity, in whom it may be even more helpful as other signs of congestion are unreliable. Advanced renal disease with refractory diuretic resistance confers the highest risk, which is not decreased by knowledge of pulmonary pressures. These patients usually have a persistently cold and wet profile or a profile of disproportionate right heart failure, on the way to end-stage D disease. On the other hand, patients who follow and maintain lower pulmonary artery pressures are empowered in their own care, describing increased sense of control and decrease impact of HF on their lives. It is our hope that the combination of this patient engagement and the protection of the right ventricle can map a new trajectory for patients that does not accept failure. Previous heart failure hospitalization identifies patients at very high risk for re-congestion, up to 50% at 6 months, with the highest risk in those with recent hospitalizations. Even without hospitalization, patients with current signs and symptoms of congestion are still at high risk for heart failure events, for which an increase in outpatient diuretic dose is a harbinger. People who have chronically elevated pulmonary artery pressures are at risk even if they are not currently aware of symptoms. As for systemic hypertension, pulmonary hypertension can be a silent killer as it progresses to right heart failure, which is often the final common pathway for patients who have been compensated for years with low left ventricular ejection fraction. Congestion is the intersection of clinical HFrEF versus HFpEF, so therapy for both populations is better guided by pulmonary artery pressure information. Where the two phenotypes differ is in the causes and therapies for congestion. Neurohormonal activation play a large part in congestion for HFrEF, as the neurohormonal antagonists have had such a large cumulative benefit to decrease hospitalizations. The benefit of managing pulmonary artery pressures in HFrEF is highest when combined with the fundamental therapies of ACEI and blockers. These agents have at best minor effects to decrease hospitalizations with HFpEF. The impact of ambulatory pulmonary pressure-guided therapy is consistently shown for preserved EF. This impact extends to patients with severe obesity, in whom it may be even more helpful as other signs of congestion are unreliable. Advanced renal disease with refractory diuretic resistance confers the highest risk, which is not decreased by knowledge of pulmonary pressures. These patients usually have a persistently cold and wet profile or a profile of disproportionate right heart failure, on the way to end-stage D disease. On the other hand, patients who follow and maintain lower pulmonary artery pressures are empowered in their own care, describing increased sense of control and decrease impact of HF on their lives. It is our hope that the combination of this patient engagement and the protection of the right ventricle can map a new trajectory for patients that does not accept failure.