Expert cardiologists discuss the progressive nature of heart failure and the associated risk factors of diabetes on HF.
Neil Minkoff, MD: One of the things that we have difficulty with as an industry in health care is working on the progressive nature of heart failure. Could those who are still currently practicing share with us some of the complexity and complications they see, and how those complications and the progressive nature of heart failure tend to impact their patients?
Nihar Desai, MD, MPH: Neil, the way you described it is right on. Heart failure, unfortunately, is a chronic progressive disorder. It is characterized, as Steve alluded to, by this complex interplay between heart function, kidney function, and other organs. What seemingly happens is that our patients are along this general trajectory, and it’s characterized by acute decompensations, generally leading to hospitalization. During hospitalization, they get acute therapies and acute treatments to try and bring them back up to that curve. Unfortunately, all too often they are on this downward decline. Despite our best therapies—of which there is now an expansive array—the downward decline of heart failure continues. Ultimately, you’re left with a situation of needing a definitive therapy for heart failure, of which there are only a couple: heart transplant, a ventricular assist device, or palliation and redirecting goals of care. What we see so often in heart failure is this continued pattern of hospitalization, decline, and trying to get people back to a stable functional status. But it is this ongoing myocardial damage, kidney damage, and that interplay that then continue to get us into trouble with our patients.
Steven Nissen, MD: One of the things I see is that often, the treatment early on in the disease is suboptimal. Every time a patient comes in, they get their treatment escalated, and you can make a very strong case for earlier intervention. We do have an array of effective drugs, but they’re not always used effectively. They’re not always used early in the disorder, but rather, after a patient has severe functional impairment. At that point, we can certainly benefit the patient, but the disease is less reversible. I would give you an example of someone who is undertreated, gets enlargement of the left ventricle, and now has functional mitral regurgitation. That’s further exacerbating their ability to have good forward flow.
You mentioned transplant and LVAD [left ventricular assist device], but 1 thing I would add is that recent data on using interventions like the mitral clip to reduce the regurgitant flow show they can be quite effective in certain patients who have poor coaptation. We have a lot of tools in the tool chest. I wish we were using them better. I work primarily in the coronary intensive care unit, so I see these people. They come in and they’ve had progressive symptoms for years, but they’re maybe just on a low dose of an ACE inhibitor or not even on beta-blockers. They’re certainly not on mineralocorticoid receptor antagonists, and I find it frustrating. With a lot of tools in the tool chest, including—as we’re going to talk about—SGLT2 inhibitors, a question that always comes up is, can we intervene earlier and prevent that progressive and late deterioration?
Neil Minkoff, MD: Dr Desai, I’d like to build on what we were just hearing, in terms of moving upstream. But I also want to understand, as we start to look at the SGLT2 inhibitors, the connection that might be occurring between diabetes and heart failure, and how diabetic patients are dealing with cardiovascular disease and heart failure as a complication.
Nihar Desai, MD, MPH: Neil, it’s a really important point. Jaime Murillo and Steve have already raised several of the important points. It’s worth highlighting again the important interplay between a constellation of conditions—diabetes, obesity, metabolic syndrome, chronic kidney disease, and heart failure—and how those often travel together. You can think about all the various pathways that relate those, from diabetes and coronary artery disease, to people having accelerated atherosclerosis or more aggressive forms of atherosclerosis, to having heart attacks and then systolic heart failure, all the way to obesity and heart failure or kidney disease and heart failure, and all of the interplay between kidneys, the endocrine organs, and heart function.
We know that the most likely cause of death for a diabetic patient will be cardiovascular disease. Too often, that is either a heart attack and then ultimately heart failure, or some interplay between those 2. While we’ve always appreciated the interplay between these different clinical conditions, it’s been in part because the SGLT2 inhibitors have catapulted this discussion around how we best think about the biology. That includes the pathobiology between diabetes, obesity, metabolic syndrome, heart failure, and kidney disease. But also, as Steve and Jaime have been very eloquently talking about, how can we move to a preventive mindset? How do we aggressively treat risk factors, whether that is diabetes, kidney disease, hypertension, or other things, to try to prevent that ultimate occurrence of heart failure? The SGLT2 inhibitors have really stimulated a lot of good discussion in that arena as well.