Research Looks at Congestive Heart Failure in Feedlot Cattle

By: Heather Smith Thomas

Some cattle at high elevations suffer pulmonary artery hypertension, which leads to congestive heart failure, but more cattle are susceptible to bovine congestive heart failure (BCHF), showing up in feedlot animals. BCHF is an untreatable, fatal condition involving pulmonary hypertension that culminates in right ventricular failure, but may begin with left-heart dysfunction. This makes it different from right heart failure at high altitudes because BCHF affects both sides of the heart.

Dr. Milt Thomas, Colorado State University says the heart problem at high altitudes occurs much earlier in the animal’s life, while BCHF generally occurs in the finishing phase in the feedlot.

“We’re doing a USDA-funded project to try to understand feedlot heart disease. We have a feedlot facility in Akron, Colorado (Eastern Colorado Research Center, at 4100 feet elevation) and a client who feeds 500-plus commercial Angus-type steers there every year, with high incidence of feedlot heart disease. That client allowed us to buy 107 steers for our research,” says Thomas.

“We treated those steers like any other steers in the feedlot, and have now taken them to slaughter, and have our initial data—and found feedlot heart disease,” he says.

“We did PAP (pulmonary arterial pressure) testing like we do in high-altitude cattle, to know which ones were tolerating the process of getting fat and which ones were not. These steers had never been above 6000 feet elevation but we found a lot of high-PAP cattle. There were so many that we created a high-PAP and a low-PAP group to study, evaluating their feed intake in our Grow-Safe Feed Intake Unit,” he says.

“Out of those steers, death loss was 5.5%. One died early in the feeding phase—which may have been related to stress of shipping fever. The others died late in the feeding period when they should have been past the early risks, and they all died from feedlot heart disease.”

All steers were slaughtered at the Global Food Innovation Center (GFIC) on the CSU campus. “Even though some of them died, we still had 12 high-PAP and 12 low-PAP steers we slaughtered and we are studying their heart and lung tissues and performance data,” says Thomas.

“All the low-PAP animals had normal-looking hearts and the high-PAP steers had severely malformed hearts. These were the steers that made it to slaughter. All the steers that died in the late feeding period had severely malformed hearts,” he says.

“With feedlot heart disease, they often perish near the end of the finishing phase—very expensive losses. One hypothesis is that some of these cattle are highly stressed by fattening because they are high-PAP cattle, and when they get a secondary challenge like respiratory disease or heat stress it pushes them over the edge,” he says.

“The high-PAP steers had poor average daily gain in the final phases of feeding and feed conversion was terrible. By contrast, the low-PAP steers had very good average daily gain, very good feed conversion. The closer we got to finishing, the more the performance declined on the high-PAP steers,” he explains.

Some people wonder if this is occurring because we’ve selected cattle for fast growth and easy fattening. “The only way we can know would be to find some old semen and create some 1950-era cattle to compare with today’s cattle,” he says.

“We find this problem in every breed but there are genetic differences in the high-altitude problem—some breeds and some family lines are less susceptible. In general, cattle have high PAP, however, so anything that stresses them could be a problem.”

There are correlations between obesity and heart disease. “If an animal already has fairly high PAP plus some of the issues that arise from fattening, we see more heart failures,” he says.

Some people wonder if it’s the kind of feed, amount of gain, or the breed. “I think we can say that it is none of the above and all of the above. There are many factors–not just any one cause,” says Thomas. For a feedlot producer, or cow-calf producer retaining ownership through feeding, it’s crucial to know more about this.

Greta Krafsur, DVM is a pathologist who did her PhD work on congestive heart failure in feedlot cattle. She is now assistant professor in the Department of Veterinary and Biomedical Sciences at South Dakota State University and also employed by the University of Colorado Denver Anschutz School of Medicine Cardiovascular Pulmonary Research Lab where she works with human physicians whose expertise in pulmonary hypertension and heart disease have influenced her thinking regarding the complex problem of bovine congestive heart failure.

For several years she’s been working with Milt Thomas. “As a pathologist I was in charge of the tissue harvest to make sure we got all the tissues needed for this study. We have many collaborators in this research. We’re not only collecting tissues for the cattle industry but also for human medicine,” says Krafsur.

“I’m now in the process of trimming all tissues so they can go to the lab to be made into slides. I also collected fat from around the heart, as well as visceral abdominal fat, and now analyzing the proteomic, metabalomic and lipidomic signatures, because I suspect that these cattle have a unique inflammatory metabolic condition. The ones that develop pulmonary hypertension and congestive heart failure have this unique signature that is pro-inflammatory and have glycolytic metabolism and also tend to have a lot of heart fat. I think the cattle that suffer from this condition have a genetic variance when it comes to how lipids are transported and metabolized,” she says.

“We put a high premium on marbling, and some of these hearts are well marbled but this is not where we need marbling! My research is looking at the influence of heart fat and inflammation in the heart and if it’s setting these cattle up for this problem.”

“We’ve also looked at grass-fattened animals versus grain-fed. Microscopically the grass-fat cattle hearts do not look any healthier than the corn-fed conventionally-fattened animals. Many people think these problems are due to what we feed them and the way we feed them, but I’m not sure,” says Krafsur. It may be a factor, but the animal’s own metabolism may be the bigger key.

“Researchers at the Genetics, Breeding, and Animal Health Research Unit at the USDA, ARS, U.S. Meat Animal Research Center in Clay Center, Nebraska and at the Great Plains Veterinary Educational Center at Clay Center say this problem is now happening earlier in the feeding period, with the cattle they have studied. In this last group of cattle that we did with our USDA grant, I would agree,” she says.

If these animals could be pinpointed earlier, they could be taken out of the typical feedlot program and managed differently. They might be fed differently and slaughtered earlier. “I’m trying to determine what’s going on with them, but at the same time trying to verify certain biomarkers used in the human medical population to classify and predict human heart failure with pulmonary hypertension patients. A couple biomarkers that are very prognostic with humans are significantly different in cattle that develop pulmonary hypertension and congestive heart failure. These are promising biomarkers that we could also use in cattle—where we could just take blood samples and measure them,” she says.

“Unhealthy fat is very pro-inflammatory, and sets up an environment for fibrosis in the heart, and more inflammation. Some of these genes have something to do with lipid metabolism. It’s been shown in human patients with congestive heart failure that many of them go on to develop pulmonary hypertension and ultimately right heart failure. Those patients do worse than any other class of pulmonary hypertension patients. Heart fat is a key player in the whole complex pathophysiology of that disease. I need to look at this in the cattle and see if it is a similar issue.”

Although management and feeding regimens in feedlots are similar across the industry, there’s a subset of cattle that develop BCHF for reasons unknown. “I think some cattle do not respond favorably to the high demands imposed by excess calories, aggressive growth and fat body condition during feeding/fattening. This subset of cattle seem to experience systemic inflammation and metabolic and lipid dysfunction that lead to cardiopulmonary remodeling and dysfunction. This condition is invariably fatal and we need to find biomarkers predictive of disease that can be used to assess risk and inform management decisions,” she says.

Why do we see this problem in the feedlot but not in adult cows and bulls? Is it because we’re not pushing them to grow so fast? Mature cattle are larger frame size than several decades ago yet we’re not seeing BCHF except for high altitude disease in certain bloodlines. Perhaps it’s because we develop heifers and bulls slower—for longevity rather than swift fattening for slaughter–but we don’t know.

“Perhaps there is an underlying genetic problem, and certain things about the environment—what and how we feed—and when the two come together there may be a subset of cattle that don’t respond favorably. Under different conditions you might never see the problem,” she says.

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