You Gotta Have Heart

Ya gotta have heart!
by Lana Kaiser, D.V.M.

     Several years ago I had a calf born dead, right in front of my eyes. He was alive when I
saw his head and feet, but by the time he hit the ground he was deader than a doornail.
The pathologist at Michigan State University said the cause of death was a large a trial
septal defect (ASD). I figured it was just bad luck, or the phase of the moon, so I shipped
the cow. All was well until the exact same thing happened to another cow. It was then
time to investigate – we turned a farm problem into a research study! Breeders from
across the country called, wrote, sent us hearts and filled out questionnaires. If you have
been waiting for the results of the study, here they are!

Heart disease in cattle
     Unlike humans, and many other species including dogs and cats, heart disease in cattle
is not considered a big issue. In fact, it is not often thought about when people consider
sick cattle. Heart problems in cattle are basically 2 types, those associated with infection
and congenital heart disease.
     Infection is usually associated with “hardware,” which results when a cow eats a wire,
nail or some other sharp metal object. The sharp object generally ends up in the
reticulum, where strong contractions push it through the wall. The direction it goes
determines the kind of problem that results, but if it pierces the heart you can end up
with a variety of heart problems, including infection of the valves (bacterial endocarditis).
Magnets are a useful way to prevent hardware disease. Cattle can also develop
bacterial endocarditis from a systemic bacterial infection (septicemia), where bacteria
circulates in the blood stream and lodges and grows in various places. This type of heart
infection may be seen in calves with scours, from a virulent Salmonella infection.
The other type of heart disease in cattle is called congenital – the calves are born with it,
and it is usually an anatomic change or abnormality – the architecture isn’t quite right.
Some congenital heart problems are lethal, meaning the calf is born dead. Some are
very mild, meaning they may be discovered incidentally on necropsy of an adult animal.
The clinical disease then ranges from dead to nothing!
     Congenital heart disease generally results from a hole in the heart where it should not
be, an abnormal valve, abnormal blood vessels coming from the heart, or less
commonly, a combination of defects. A hole in the heart results in shunting of blood in an
abnormal direction, somewhat like diverting a river. Both ASD and VSD (ventricular
septal defect) are examples of holes in the wall of the heart resulting in abnormal blood
flow. Abnormal valves can be “stenotic” (opening too small), blocking the forward motion
of the blood, (like damming a river) or “regurgitant” (valve doesn’t shut right) causing the
blood to go backwards.

The normal heart
     The hearts job is to move blood. It moves blood from the lungs to the body, and then
from the body back to the lungs. The blood gets oxygen in the heart, which is essentially
fuel the body needs to function. The normal heart is an exquisite system of pumps,
valves and pipes. The left side of the heart is a high pressure system pumping blood to
the body. The right side is a low pressure system pumping blood to the lungs. If you
were a red blood cell containing oxygen, your journey would be from the lungs to the
pulmonary veins (PV), to the left atrium (LA), through the mitral valve (MV), to the left
ventricle (LV), through the aortic valve (AV), into the aorta (Ao), to the body. Your return
trip would be from the body, to the vena cava (VC), to the right atrium (RA), through the
tricuspid valve (TV), to the right ventricle (RV), through the pulmonary valve (PV), into
the pulmonary artery (PA), and to the lungs. Then, you would start all over again! Any
abnormality along that route would lead to abnormal blood flow.

The normal heart in utero
     In the calf, before birth, there is no need to send blood to the lungs because fetal blood
obtains oxygen from the placenta. The fetal heart has a series of detours that normally
close after birth. One big impetus for these changes is when the calf takes his first
breath – this results in changes in pressure and closing off the detours. In utero there is
a hole in the atrial septum, letting blood flow from the right atrium to the left atrium,
bypassing the lungs. Normally, this hole has a big, floppy membrane covering it so when
blood flows from right to left it poofs out like a wind sock. After the calf is born, the hole is
covered by the membrane and blood cannot go left to right. Think of it like a 10 foot gate
on a nine foot opening – cattle can push the gate open to get out, but they cannot move
back when the gate is closed. After birth, the membrane eventually scars and forms part
of the atrial septal wall.

What is an ASD?
     An ASD is a hole in the atrial septum that has an abnormal membrane and
consequently, blood can flow through the hole in either direction. Also, because the
electrical system of the heart goes through the atrial septum, any abnormalities of the
septum can lead to abnormal electrical activities called “arrhythmias.” Clinical signs of
ASD range from minimal to severe. The calf may appear totally normal, have labored
breathing, exercise intolerance (can’t keep up with the herd), fail to gain weight and look
unthrifty. You may think the calf has pneumonia. On a physical exam, the calf will likely
have a heart murmur (caused by the abnormal movement of blood), both the heart rate
and respiratory rate may be increased and there may be abnormal heart rhythm.

OK, so what about the study??
Calf heart study:
     We received many calls and letters from producers and veterinarians who were interested in
the study, and who thought they may have seen a case of heart disease in calves or adult
cattle. We received 27 hearts from beef producers in Michigan (19), Ohio (3), Colorado (1),
Washington (1), Minnesota (1), Illinois (1) and Nebraska (1). Twenty-four of the 27 hearts
were from Maine-Anjou or Maine-cross cattle; there was one Angus, one Chi and one
Shorthorn. We also received hearts from 20 Holsteins, from newborn to 5 months of age.

     Six bull calves and one 18 month-old-heifer had atrial septal defects. In addition, one 5-
month-old Holstein had an ASD, meaning there was a hole in the wall between the left and
right atrium. The hole was covered by an abnormal membrane, which was insufficient to
cover the hole.

     Of the six bull calves with ASD, three were purebred Maines (three different sires); one was a
Maine cross, sired by a Red Angus; one was a Maine-cross, sired by a Maine; and the sixth
was a Shorthorn.

     Four of six calves with pathological ASD were born dead or lived less than 24 hours. These
four Maine calves were male and had mean birth weights of 94.4 lbs, which was heavier than
the breed average of 86.5 lbs. With the exception of one two-headed calf, all other hearts
from the other calves born dead, or who lived less than 24 hours, were normal.

     After the study was “complete,” we received three additional hearts from calves born dead, or
calves that lived less than 24 hours: two normal hearts (Maine calf & Hereford calf) and one
Maine calf with multiple congenital defects. We also received word of an additional Maine calf
born dead with multiple congenital heart defects.

     Of the animals that lived a week or more, three had normal hearts, one had bacterial
endocarditis and one 70-day-old calf had multiple congenital defects.

What does this data mean?
     ASD is a problem in many species, including humans, and is
believed to have a genetic component. The exact inheritance is not clear in humans, or cattle
for that matter! Finding ASD in breeds other than Maines, and in crossbred cattle, suggests
that it is a cattle problem, not a breed problem. Finding ASD, in both bulls and heifers,
suggests that it is not a sex linked recessive type of inheritance. ASD in cattle from birth to 18
months of age suggests a continuum of disease. Finding ASD in calves from four different
unrelated sires suggests no one sire is responsible for the defect.

Producer survey of calving outcomes
A survey was sent to all members of the American Maine-Anjou Association (AMAA). A total
of 341 questionnaires were returned from Maine-Anjou breeders from 32 states. Ohio (11%),
Michigan (9%), Texas (9%), Indiana (8%) and Oklahoma (7%).

     For 1998 and 1999, producers reported they calved out an average of 48 (+/- 76; range 0 to
550) cows annually. The total number of calves born during this period was 16,513. The total
number of calves reported born dead was 291 (1.8%). The number of calves born dead per
producer per year ranged from zero to three, with a mean of 0.04.

     Producers that reported the sex of calves, 5,541 male calves and 5,826 female calves were
born (total 11,367). The calves identified by gender, 1.92% were born dead (137 males and
81 females, total 228).

What does this data mean?
     Birth weights for the Maine calves born dead were greater than
the breed average for bull calves, further suggesting that dystocia could be involved in
exacerbating the problems associated with ASD during birth. Producers reported 1.8 % loss
due to calves born dead and 11% of calvings requiring assistance. These figures are not
different from the USDA NAHMS 1997 survey of 2,713 producers from 23 states, suggesting
our sample was representative of US cow-calf producers, and Maine cattle do not suffer
greater death loss at birth than other breeds. This further supports the notion Maine-Anjou
breeders have taken a proactive role in preventing dystocia by sire selection, and dystocia is
not a greater problem in Maine cattle than other breeds.

Necropsy?
     While 23% of producers routinely necropsied calves born dead, 77% did not.
Interestingly, 90% were willing to submit hearts for this study. A significant correlation
was found between the number of calves born dead and having the dead calf
necropsied. Only 10% of producers reported they were told by their veterinarian they
had an animal with a heart defect.

What does this data mean?
     This suggests most of us are likely to believe one dead
calf can be chalked up to bad karma, but after that people want to know what happened.

More producer info
     Average number of producers was 44. Number of acres averaged was 696 (range 6 to
20,000). In addition to Maine cattle, 14 other breeds were reported to be owned,
including Longhorns, Brahman, White Park, Braunvieh, Pinzgauer, as well as Hereford,
Angus, Simmental, Chi, Charolais, Shorthorn, Limousin, Red Angus and Salars.
Average herd size was 77 head (range = 4 - 980 head). Producers reported an average
of 22 Maine cows (range 1 to 350) with an average of 2.3 bulls per herd (range 0 to 60).
Almost half reported growing crops including corn, beans, beats, wheat, milo, barley,
cotton, rye, grapes, apples, pickles and trees. A small number reported other species of
livestock including hogs, dairy, poultry and “other.”

What does this data mean?
     Maine breeders are a diverse group!
The bottom line? Unlike some other breed associations that may have ignored potential
genetic problems in their breed, the AMAA (and much to the surprise of many
researchers) helped to fund this study. Although the study didn’t tell us everything, it
gave us some good information.

-Not all calves born dead, die of “bad karma” – some die from congenital defects.
Necropsy can tell you that.

-ASD appears to be a cattle problem, not a breed problem.

-Cattle appear to get a variety of congenital heart diseases.

-Sometimes what looks like pneumonia in cattle is actually heart disease.