When investigating bovine congestive heart failure (BCHF), we often expect to find dramatic pathological changes in the heart. To better understand those changes, researchers at Kansas State University purposefully assembled a harvest population spanning the full range of visual heart scores, from normal to severely enlarged hearts. After exclusions, the study included 103 cattle, of which 63 had abnormal heart scores. Despite those obvious differences in heart appearance, only eight animals showed moderate fibrosis in any cardiac section and just four had moderate cardiac necrosis.
The findings, described by Dr. Makenna Jensen, don’t identify a single cause of BCHF. Rather, they suggest that we may need to think about the disease as a broader cardiopulmonary syndrome while continuing to investigate why some feedlot cattle develop severe cardiac remodeling and others do not.
A Disease With More Questions Than Answers
Once considered primarily a disease of cattle raised at high elevations, BCHF is now recognized in feedlots at much lower elevations, indicating altitude alone cannot explain the condition. It is believed that pulmonary hypertension remains central to disease development, but multiple factors — including hypoxia associated with bronchopneumonia, obesity, heat stress and other conditions — have been proposed as potential contributors.
Understanding those mechanisms begins with accurately describing how the heart changes during disease.
To do that, Jensen evaluated the hearts of cattle at harvest. Each heart received a visual heart score ranging from 1 to 5, with higher scores representing progressively greater ventricular enlargement and distortion. These gross findings were then compared with microscopic lesions in the heart, lungs and liver.
The study population intentionally included a broad range of heart scores. Forty cattle (39%) were classified as having normal hearts (scores 1 or 2), while 63 (61%) had abnormal heart scores (3 through 5), including 40 animals with severe remodeling (scores 4 or 5). That distribution allowed Jensen to compare pathology across increasingly abnormal hearts rather than focusing only on clinically obvious disease.
The Strongest Clue Wasn’t in the Heart
Perhaps the most surprising finding involved the lungs.
Jensen identified 39 cattle with abnormal lung deflation, a gross finding previously linked with cardiac remodeling. However, 33 of those 39 cattle had less than 5% gross lung involvement, indicating that failure of the lungs to deflate was usually not accompanied by extensive visible pneumonia or other obvious pulmonary lesions.
Statistical analysis confirmed the relationship. Cattle with abnormal lung deflation had a 76% predicted probability of having an abnormal heart score compared with 52% for cattle whose lungs deflated normally.
The findings don’t establish whether pulmonary changes precede cardiac remodeling or develop as a consequence of it. They do, however, reinforce the idea that the lungs deserve as much attention as the heart when investigating BCHF.
Takeaway: If you’re investigating a suspected case of BCHF at necropsy, don’t focus solely on the heart. Careful evaluation of the lungs may reveal changes that provide additional clues, even when obvious pneumonia isn’t present.
Enlarged Hearts Weren’t Necessarily Scarred Hearts
If the lung findings were unexpected, the cardiac histology was equally surprising.
Despite obvious differences in gross heart appearance, moderate fibrosis was uncommon. Only two septal samples, four papillary muscle samples and two right ventricular free wall samples received moderate fibrosis scores, while no left ventricular samples showed moderate fibrosis. Likewise, only four cardiac sections across the entire study demonstrated moderate necrosis.
Those findings suggest gross cardiac remodeling doesn’t necessarily correspond with extensive microscopic damage.
This is an important distinction. An enlarged, misshapen heart may reflect substantial structural remodeling without widespread fibrosis or necrosis detectable on histopathology.
Takeaway: An enlarged heart doesn’t automatically mean you’ll find extensive microscopic damage. Gross appearance and histopathology don’t always tell the same story.
An Intriguing Hypothesis Doesn’t Always Hold Up
Jensen also explored whether embedded myocardial protozoal cysts, presumed to be Sarcocystis, might be associated with abnormal heart remodeling.
Sixty-seven of the 103 cattle had protozoal cysts in at least one cardiac section, and 57 of those animals had cysts present in all four sections examined. In the harvest study, cattle with cysts were more likely to have abnormal heart scores.
Rather than stopping there, Jensen tested the finding in a second study involving 106 feedyard mortalities. She digitally quantified cyst density within cardiac tissue and compared it with both heart score and confirmed BCHF. This time, the association disappeared. Neither abnormal heart score nor confirmed congestive heart failure was associated with protozoal cyst density.
While the harvest study suggested a possible relationship, the mortality study showed that association wasn’t consistent, leaving the role of protozoal cysts in BCHF unresolved.
Takeaway: Finding myocardial protozoal cysts should be interpreted cautiously. Their presence alone doesn’t indicate they caused the cardiac changes or BCHF.
What We Can Learn From This Research
This work doesn’t provide a new diagnostic test or identify a single cause of BCHF. It does, however, offer several practical insights for investigating suspected cases.
- Evaluate the cardiopulmonary system as a whole. One of the strongest gross associations involved lung deflation rather than microscopic cardiac injury, reinforcing the importance of carefully examining pulmonary changes during necropsy.
- Interpret enlarged hearts in context. Gross remodeling did not consistently correspond with extensive fibrosis or necrosis, suggesting heart size alone cannot fully explain disease severity.
- Remember that BCHF remains a moving target. This research illustrates how standardized heart scoring allows the comparison of findings across studies while systematically testing — and sometimes eliminating — potential explanations for this complex disease.
Rather than solving the mystery of BCHF, Jensen’s work narrows the search. It suggests that understanding how the heart and lungs change together may ultimately prove more informative than focusing on either organ in isolation, providing another piece of a puzzle that the beef industry is only beginning to assemble.
