Paul Hauptman

Should we be measuring wedge pressures in patients with decompensated heart failure?

Despite a lot of historical baggage including the ESCAPE trial, which showed that use of a pulmonary artery catheter to titrate therapy aimed at lowering pulmonary capillary wedge pressure did not affect mortality or days hospitalized during the next 6 months, compared with therapy guided solely by clinical assessment (JAMA 2005;294:1625-33), I think so.

The procedure should be done sparingly, of course, but there remains a role for invasive hemodynamics, both from a diagnostic standpoint and for monitoring response to therapy.

And therein lies the conundrum for a pharmaceutical company looking to develop a drug for acute decompensated heart failure.

Here’s a thought experiment: You have a drug that has performed well in the preclinical model. You perform a hemodynamic study and show that the wedge pressure declines (and maybe right atrial and mean pulmonary pressures, too). Will that pass muster at the Food and Drug Administration?

It will not.

Now let’s say that you did all that the FDA requested of you (which makes this more than a thought experiment; it’s a miracle), but you do not have any hemodynamic data. Would clinicians adopt the new drug?

I suspect not.

We still like to have the reassurance that something positive is going on from the standpoint of hemodynamics, even if the drug relieves dyspnea, improves quality-of-life and reduces mortality.

So whither the wedge? Clinically, it can be useful in a limited subset of patients for whom dyspnea is unexplained or low output is suspected. In drug development, it may shed light on mechanism of action and inform dose selection.

As a consequence, we still have a relationship with pulmonary artery catheterization, but it’s no longer a marriage, and it’s not a divorce. Maybe it’s a friend with whom an occasional reunion makes sense?

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at St. Louis University and director of heart failure at St. Louis University Hospital. He is associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

Should we be measuring wedge pressures in patients with decompensated heart failure?

Despite a lot of historical baggage including the ESCAPE trial, which showed that use of a pulmonary artery catheter to titrate therapy aimed at lowering pulmonary capillary wedge pressure did not affect mortality or days hospitalized during the next 6 months, compared with therapy guided solely by clinical assessment (JAMA 2005;294:1625-33), I think so.

The procedure should be done sparingly, of course, but there remains a role for invasive hemodynamics, both from a diagnostic standpoint and for monitoring response to therapy.

And therein lies the conundrum for a pharmaceutical company looking to develop a drug for acute decompensated heart failure.

Here’s a thought experiment: You have a drug that has performed well in the preclinical model. You perform a hemodynamic study and show that the wedge pressure declines (and maybe right atrial and mean pulmonary pressures, too). Will that pass muster at the Food and Drug Administration?

It will not.

Now let’s say that you did all that the FDA requested of you (which makes this more than a thought experiment; it’s a miracle), but you do not have any hemodynamic data. Would clinicians adopt the new drug?

I suspect not.

We still like to have the reassurance that something positive is going on from the standpoint of hemodynamics, even if the drug relieves dyspnea, improves quality-of-life and reduces mortality.

So whither the wedge? Clinically, it can be useful in a limited subset of patients for whom dyspnea is unexplained or low output is suspected. In drug development, it may shed light on mechanism of action and inform dose selection.

As a consequence, we still have a relationship with pulmonary artery catheterization, but it’s no longer a marriage, and it’s not a divorce. Maybe it’s a friend with whom an occasional reunion makes sense?

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at St. Louis University and director of heart failure at St. Louis University Hospital. He is associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

Should we be measuring wedge pressures in patients with decompensated heart failure?

Despite a lot of historical baggage including the ESCAPE trial, which showed that use of a pulmonary artery catheter to titrate therapy aimed at lowering pulmonary capillary wedge pressure did not affect mortality or days hospitalized during the next 6 months, compared with therapy guided solely by clinical assessment (JAMA 2005;294:1625-33), I think so.

The procedure should be done sparingly, of course, but there remains a role for invasive hemodynamics, both from a diagnostic standpoint and for monitoring response to therapy.

And therein lies the conundrum for a pharmaceutical company looking to develop a drug for acute decompensated heart failure.

Here’s a thought experiment: You have a drug that has performed well in the preclinical model. You perform a hemodynamic study and show that the wedge pressure declines (and maybe right atrial and mean pulmonary pressures, too). Will that pass muster at the Food and Drug Administration?

It will not.

Now let’s say that you did all that the FDA requested of you (which makes this more than a thought experiment; it’s a miracle), but you do not have any hemodynamic data. Would clinicians adopt the new drug?

I suspect not.

We still like to have the reassurance that something positive is going on from the standpoint of hemodynamics, even if the drug relieves dyspnea, improves quality-of-life and reduces mortality.

So whither the wedge? Clinically, it can be useful in a limited subset of patients for whom dyspnea is unexplained or low output is suspected. In drug development, it may shed light on mechanism of action and inform dose selection.

As a consequence, we still have a relationship with pulmonary artery catheterization, but it’s no longer a marriage, and it’s not a divorce. Maybe it’s a friend with whom an occasional reunion makes sense?

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at St. Louis University and director of heart failure at St. Louis University Hospital. He is associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.