J. Thomas Heywood, MD, FACC, reviews five important things to remember about Pulmonary Hypertension.
Back to Symposium Page » well again. Thank you. Thank you all. And thank you for the wonderful talks today, uh, hoping to clarify, you know, harmony, hypertension. There's been a lot of progress and just a few short years. And every year this is changing, so we have new things to discuss. So I wanted to end this just some up. Some, you know, there is such a complicated area. I wanted to make sure that people left with really some key points firmly, firmly intact. I don't see there we go. My disclosures again. Remember the types of pulmonary hypertension, pulmonary venus or post capillary? This is left heart disease. Wedge pressure greater than five. Would units less than three Pulmonary arterial hypertension, pre capillary called wedge low Would units usually more than five. So pulmonary vascular resistance is increased. But there are these mixed forms where there's a little bit of both and those are more complicated because, you know, why would it be simple when it can become complicated? The would units are just the media pressure divided by the cardiac output. MPA pressure is the mean pressure minus the wedge. So number one thing to remember patients with P pressures greater than 45 or 50 on eco most likely have pulmonary hypertension in need evaluation. Pulmonary hypertension is defined by means of a pressure greater than 20. So a systolic pressure of 50 on echo or even 45 high probability of pulmonary hypertension. Don't ignore this finding. Whether you need a cath or not depends on the clinical context. You know this is just the pressure. There's a patient connected to the pressure, but often the ideology is clear. There's low E f or severe might trigger agitation. But if there isn't, um, start to explore why they have hypia pressures. And if you need help, give us a call. Number two. Most patients with pulmonary venous hypertension have left heart disease clues. They're older. There's clear evidence of hard left heart disease, aortic stenosis or mitral regurgitation, low ejection fraction left ventricular hypertrophy or atrial fibrillation. A key feature is increased left atrial size. Uh, most of the time, when you have pulmonary hypertension and you have a big left atrium. Uh, it's pulmonary venous disease. Not always, Uh, sometimes we need a heart cath or a C t to sort this out, but that that is useful way over 90% of the time. So after you see Hae papa pressures, look at the left atrial size. Number three. Pulmonary arterial hypertension is less common but important to find number one because it's treatable, often in women and women often get a short shrift. Some women wait two or three years for their diagnosis of pulmonary hypertension, unfortunately, and so if a woman, especially young woman, describes shortness of breath with exertion, be sure to get an echo to exclude pulmonary hypertension. Sometimes it's curable, as you've heard. Often it's treatable. So if they have some forms of congenital heart disease, if they have retained pulmonary embolism and glide can be curable but almost always treatable. And I have patients that have had pulmonary hypertension from idiopathic pH. I've been treating for more than 10 years, and they do very well. Usually, people with pulmonary arterial hypertension are in Sinus rhythm. That's a clue, and again, they have a normal left atrial size. Number four FPF is probably the most common form of pH that you'll see. There's over three million cases in the US most often older women majority have pulmonary hypertension pressures anywhere from 40 to 50 to 62 higher. As Dr Shrivastava said, diuretics are critically important in this. If you can adequately directs the patient, the pressures will go down. But we now have other ways of treating them. SGL t two inhibitors The sodium glucose transport inhibitors for that were first created for diabetes, but we use now more and more in heart failure. Selected patients with uh half path, who have an EF less than 60% but greater than 40% may be able to get sick uber travel, sardine or entrust Oh, and then cardio memes for these patients with persistently high elevated pressures and and then just to end on the future, some questions Can't hype pressures be measured as easily as systemic blood pressure? Think you've seen from these talks that hype pressures are terrible and are associated with very high mortality? But many patients never have their pressures measured. They have elevated pressures for years and are not treated now. It's easy to measure systemic blood pressure. It's or it has been hard to measure P a pressures. We do have the echo, but we can't get echoes all the time. What if we could measure p A pressures as easily as systemic blood pressure. Would that change? Things we knew Papa pressures all the time. When we do a better job at controlling them, what difference would it make and new therapy? We talked about cardio members. This is this device that we put into the pulmonary artery. There is a large trial that's just finishing. Called the Guide HF trial. This is 3600 patients with no criteria either elevated, uh, BNP or prior hospitalization. The randomized arm has been completed, and we'll hear the answer to this part next month. But basically we're looking at if patients we put in a cardio memes in these 1000 patients and monitored half of them for a year and the other half after a year, would we see a mortality benefit in terms of mortality, heart failure, hospitalization and er visits? And this is, uh, cardio memes, either in low effort. Normally, f in the low e f standard therapy was used. So why is guide so important? Because it's all ejection. Fractions does not require prior hospitalization. And if this trial shows that measuring pH pressures in patients with heart failure improve survival, then this would become common therapy for almost all patients with heart failure, and so this would really revolutionize the field. And what we'd like to do is not just prevent subsequent heart failure hospitalizations, but prevent the first hospitalization, which could alter the clinical course of the disease. And finally, there is now an implantable pump that holds a prosthesis. Cyclone re module in, uh, this pump goes in the abdomen, and then there's a a catheter that's tunneled under the skin to the superior vena cava where the module in is infused. Uh, this pump has a reservoir that would last between 1 to 3 months, depending on how much how fast you get the re module. And and this would be a very easy way to give I v therapy to patients. You could refill the pump just by putting a needle across the skin and refilling the pump. Uh, the I V therapies are very powerful, but they do have complications when you have to give a chronic catheter that's in the skin. But this would be would take the infection out of the picture, so this may allow us to use I V therapy much earlier and maybe in more patience. And this therapy is very powerful. So this may help to treat pulmonary hypertension patients. Pump exists hasn't been approved yet, but might be approved this year. We will see. So again, Thank you for spending, uh, your morning with us again. Here's my phone number. If you have questions. Uh, I don't know if there's a other questions for me, but, uh, you know, whether you do this now or later, be happy to answer them. But can I please go to the app, fill out your, um, the questions about the course and, uh, tell us what we did, right? Tell us what we did wrong in order to get your cmi credit for this, uh, procedure for this course today.