                IN THE SUPREME COURT OF THE STATE OF IDAHO

                                   Docket No. 39039-2011

JOSEPH HENRY,                       )
                                    )                        Boise, November 2012 Term
   Claimant-Appellant,              )
                                    )                        2013 Opinion No. 9
v.                                  )
                                    )                        Filed: January 23, 2013
DEPARTMENT OF CORRECTION,           )
Employer, and STATE INSURANCE FUND, )                        Stephen W. Kenyon, Clerk
Surety,                             )
                                    )
   Defendants-Respondents.          )

       Appeal from the Industrial Commission of the State of Idaho.

       The order of the Industrial Commission is affirmed.

       Richard S. Owen, Nampa, argued for appellant.

       Bridget A. Vaughan, Special Deputy Attorney General, Boise, argued for
       respondents.




EISMANN, Justice.
       This is an appeal from a decision of the Industrial Commission finding that the claimant
had failed to prove that the heart attack he suffered while at work was an industrial accident
because his cardiologist could not determine whether the plaque rupture that caused the heart
attack was triggered by events occurring before or after the claimant arrived at work. We hold
that the Commission’s findings of fact are not clearly erroneous and affirm its order denying
compensation.


                                             I.
                                    Factual Background.

       On November 15, 2009, Joseph Henry (Mr. Henry) suffered a heart attack shortly after
arriving at his place of employment with the Idaho Department of Correction where he worked
as a prison guard. He was transported by ambulance to the hospital and was diagnosed by a
cardiologist as having an “acute posterolateral myocardial infarction due to a blockage of the
right circumflex obtuse marginal artery.” The cardiologist performed emergency surgery to
place a stent in the occluded artery. Ten days later, Mr. Henry suffered another cardiac event
while undergoing a cardiac stress test, and the following day he underwent triple bypass surgery.
       In April 2010, Mr. Henry filed a complaint with the Industrial Commission in which he
contended that his heart attack on November 15, 2009, constituted an industrial accident. He
also contended that the triple bypass surgery was related to the heart attack and that his heart
attack exacerbated his preexisting anxiety disorder, rendering him totally and permanently
disabled.
       The parties had an evidentiary hearing before a referee, and on June 24, 2011, the referee
issued proposed findings of fact and conclusions of law that Mr. Henry had failed to prove that
his employment caused or contributed to his heart attack. The Commission adopted the referee’s
proposed findings and conclusions and issued an order that Mr. Henry had failed to prove he
suffered an industrial accident. Mr. Henry then timely appealed.


                                          II.
    Did the Industrial Commission Apply the Wrong Burden of Proof as to Causation?

       The issue in this case was the cause of Mr. Henry’s heart attack. It is undisputed that he
had preexisting medical conditions and activities that increased the likelihood that he would
suffer a heart attack. His preexisting condition certainly would not preclude him from being
awarded benefits under the worker’s compensation law. “Compensation is recoverable where an
employee’s work . . . causes an accident which aggravates or accelerates a previous disease
condition of the employee, and an employee must establish his employment caused or
contributed to his injury—here the myocardial infarction.” Horner v. Ponderosa Pine Logging,
107 Idaho 1111, 1114, 695 P.2d 1250, 1253 (1985). Mr. Henry argues that the Commission
misapplied the law by requiring him to prove that his industrial accident was the sole cause of his
heart attack and that his preexisting conditions were not a cause. As will be shown when
discussing the sufficiency of the evidence to support the Commission’s conclusion, Mr. Henry’s
assertion is incorrect. The Commission did not require that Mr. Henry prove that his heart attack
was caused solely or even primarily by his employment. Rather, it found that he “failed to




                                                2
establish to a reasonable medical probability that his heart attack was triggered by his activities
at work on November 15, 2009.”


                                            III.
                      Are the Commission’s Findings of Fact Supported
                          by Substantial and Competent Evidence?

       “When this Court reviews a decision of the Industrial Commission, it exercises free
review over questions of law, but reviews questions of fact only to determine whether substantial
and competent evidence supports the Commission’s findings.” Eacret v. Clearwater Forest
Indus., 136 Idaho 733, 735, 40 P.3d 91, 93 (2002). Substantial and competent evidence is
relevant evidence that a reasonable mind might accept to support a conclusion. Id. Because the
Commission is the finder of fact, its conclusions on the credibility and weight of the evidence
will not be disturbed on appeal unless they are clearly erroneous. Id. This Court does not weigh
the evidence or consider whether it would have reached a different conclusion from the evidence
presented. Id. Whether the Commission correctly applied the law to the facts is an issue of law
over which we exercise free review. Combes v. State, Indus. Special Indem. Fund, 130 Idaho
430, 432, 942 P.2d 554, 556 (1997).
       It is undisputed that prior to his heart attack, Mr. Henry had preexisting medical
conditions that increased his risk of a heart attack. At the time of the heart attack, Mr. Henry was
54 years of age. He had suffered from chronic anxiety for about 14 years, and in 2004 he had
been instructed to resume taking medication for hypertension that he had been prescribed in
2003. In 2001 he was diagnosed with sleep apnea and was subsequently prescribed a C-Pap
device. In 2004 he was diagnosed with hypercholesterolemia with a total cholesterol level of
298; he was prescribed medication for that condition in 2006; and he had a cholesterol level of
328 on March 21, 2008. At the time of his heart attack, he had been smoking cigarettes for about
38 years and was smoking one and one-half packs a day.
       On the day of his heart attack, Mr. Henry had preexisting atherosclerosis, with three
different coronary arteries having some degree of stenosis due to the buildup of plaque. His right
coronary artery was occluded, but it was being supported by collaterals from the obtuse marginal
branch system. The occlusion of the right coronary artery was not then causing any symptoms.
Mr. Henry’s heart attack occurred when the obtuse marginal branch of the circumflex coronary


                                                 3
artery became occluded. He was transferred to the hospital, where he underwent a cardiac
catheterization procedure and an angioplasty stent procedure. He spent two days in the hospital
and fully recovered from that heart attack. A stress test conducted ten days after the heart attack
revealed the right coronary artery occlusion, for which he underwent triple bypass surgery.
       Mr. Henry’s preexisting condition is not a bar to receiving benefits. “An employer takes
an employee as it finds him or her; a preexisting infirmity does not eliminate the opportunity for
a worker’s compensation claim provided the employment aggravated or accelerated the injury
for which compensation is sought.” Spivey v. Novartis Seed Inc., 137 Idaho 29, 33, 42 P.3d 788,
792 (2002). “Aggravation of a preexisting condition may constitute an injury if it is precipitated
by an accident.” Painter v. Potlatch Corp., 138 Idaho 309, 312, 63 P.3d 435, 438 (2003). An
“accident” is defined as “an unexpected, undesigned, and unlooked for mishap, or untoward
event, connected with the industry in which it occurs, and which can be reasonably located as to
time when and place where it occurred, causing an injury.” I.C. § 72-102(18)(b). “The claimant
must prove to a reasonable degree of medical probability that the injury for which benefits are
claimed is causally related to an accident occurring in the course of employment.” Stevens-
McAtee v. Potlatch Corp., 145 Idaho 325, 332, 179 P.3d 288, 295 (2008).
       In this case, Mr. Henry’s cardiologist was the only medical expert who testified regarding
the causation of the heart attack. He explained that the heart attack was caused when preexisting
atherosclerotic plaque in Mr. Henry’s artery ruptured, which was the inciting event of a coronary
thrombosis. The issue with respect to causation was whether the plaque rupture was causally
related to Mr. Henry’s employment.
       The cardiologist testified that mental stress, anxiety, exercise, and cold weather can cause
blood pressure to go up, which puts hemodynamic stress on the artery, and that “the
hemodynamic stress and probably other factors that are hormonal related release of certain
hormones during stress and anxiety can cause an atherosclerotic plaque to rupture.” Prior to the
hearing, Mr. Henry’s attorney sent a letter to the cardiologist asking whether certain specified
conditions that existed with respect to Mr. Henry’s employment could have caused his heart
attack. The conditions included mental stress, anxiety, physical exertion, and being in cold
weather. The attorney described them in the letter as follows:
               Mr. Henry arrived for work on the morning of November 15, 2009, very
       early, about 6:30 a.m. Mr. Henry tells me that it was below freezing, dark and
       windy out at the state prison south of Boise.

                                                4
                Mr. Henry was late to work and got out of his car and walked quickly to
       the first building which Mr. Henry tells me is approximately 75 yo [sic] 100 yards
       away from the parking lot. By the time Mr. Henry got to the first administration
       building he did not feel very good, kind of had a general feeling of malaise, but
       had no specific symptoms.
                Mr. Henry went in to the administration building where it was nice and
       warm and went through a check through process required by his employer. He
       then went back outside and walked as fast as he could another 450 yards to a
       second building. Mr. Henry tells me that he was late to work, worried about his
       job, and walked as fast as he could this last 450 yards in the cold weather.
                By the time Mr. Henry got to the front door of the second building, he was
       sweating profusely and his co-workers immediately asked if he was alright. Mr.
       Henry indicates that he was taken to a break room and sat down. Over the next
       half hour, he continued to sweat profusely, his heart was racing, and these
       symptoms continually and gradually got worse. By 7:00 a.m., Mr. Henry notified
       his boss that he was pretty certain that he was having a heart attack and asked to
       be transported to the hospital.

The cardiologist responded by stating that “the temperature, the time of day, the activity level
and the mental stress he was under, I think it is quite likely that those factors contributed to his
myocardial infarction that day.”
       In his later deposition, the cardiologist explained that mental stress, anxiety, physical
exertion, and being in cold weather were circumstances that could trigger a heart attack. He
stated that the heart attack could have happened without such triggers and that one could never
be certain that these circumstances were the trigger. However, he explained that “you can only
make the conclusion that because the heart attack occurred on that day, and those activities were
occurring at that time, and those events were occurring, that there has to be some contribution to
that heart attack on that day.” He added that the triggers were not the sole cause of the heart
attack, but in his opinion they were contributors which were 50% responsible for causing the
heart attack.
       Respondents’ counsel then asked the cardiologist to consider factors that were occurring
prior to Mr. Henry’s arrival at work. They were that Mr. Henry was aware he was running late
before leaving his home in Caldwell, that he was anxious about getting to work on time, that his
car was parked outside all night in the cold weather, and that he started the car and left for work
without allowing it to warm up first. The attorney asked whether the cardiologist thought that
any of those factors may have triggered the onset of the heart attack that morning.             The
cardiologist answered that those factors should have been considered, but he could not tell

                                                 5
whether the heart attack was triggered by them or by the circumstances that occurred after Mr.
Henry arrived at work. He testified as follows:
               So is there a time when he’s been exposed to the scenario that you
       described, is that leading up to or helping prepare for this occlusion, is this a
       contributor to it, it really becomes into fine points that are so difficult to be factual
       or scientifically based that you just can’t distinguish that exact degree of
       contribution.
               We don’t know what’s going on inside that artery. Was that artery—had a
       small plaque rupture during that time when he first got in the car? Was it
       happening as he was driving? Was it little bits of splitting of that atherosclerotic
       cap? Were things beginning to develop back then?
               With any scientific certainty you can’t answer that question. You can’t
       say that you know that that was happening. What scientifically you can say is
       when the onset of symptoms occurred, the artery at that time did close, and the
       heart attack began at that time.
               But can you say where along the day or the day before what was the
       stressing his system, when was this—when was the inevitable day that this thing
       was going to happen? You have to look at it, I think, major stressors and minor
       stressors.
               And if you look at things, you know, the cold car, the cold steering wheel,
       the driving through traffic, were those stressors that were contributing? They
       likely could have been, should have been, you know, considered. But can you—
       how far can you dissect that down? That’s where I get in trouble of dissecting
       down all those, you know, minute events that begin to occur.
               And I can’t go that fine for you as you’d like me to be discerning which
       was the one, was it the cold car, the steering wheel, the traffic, the getting out?
       Certainly in his perception, at the time of my history taking with him, during the
       time of it and then subsequently going into more depth afterwards, he didn’t relate
       to me those events. . . .
               So I can’t pin that down to you in a certainty the preceding—earlier in
       the—preceding events earlier in the day what contributed to that, what percent.
       Very difficult for me to give you a discrete, scientifically based answer.
               ....
               For you to ask me what’s the contribution of the cold morning getting in
       the car and the drive to Boise is for me too fine a point to be so accurate to give
       you an opinion on what contribution—I just can’t give that.

       The Commission interpreted the cardiologist’s testimony as being able to identify when
the blockage of the artery occurred because there was an onset of symptoms, but being unable to
identify whether the plaque rupture that caused the blockage occurred as a result of stressors
prior to Mr. Henry arriving at work or after he had arrived at work. The Commission stated:
               The sense that emerges from the quoted testimony is that blockage of the
       artery immediately leads to symptoms typically associated with a myocardial

                                                  6
        infarction. Therefore, one can determine when the blockage occurred by looking
        to the onset of symptomatology. However, [the cardiologist] was much more
        circumspect about identifying the event or events which made the occurrence of
        the blockage inevitable. It is impossible, in other words, to say whether the
        inciting events that led to the plaque rupture occurred prior to Claimant’s arrival
        on the premises, or subsequent thereto.

        “The Industrial Commission, as the factfinder, is free to determine the weight to be given
to the testimony of a medical expert.” Eacret, 136 Idaho at 737, 40 P.3d at 95. “When deciding
the weight to be given an expert opinion, the Commission can certainly consider whether the
expert’s reasoning and methodology has been sufficiently disclosed and whether or not the
opinion takes into consideration all relevant facts.”               Id.    The Commission found that the
cardiologist “was unable to opine which of these [pre-arrival at work or post-arrival]
activities/events made it inevitable that Claimant would suffer the November 15 thrombosis
when he did.”
        Mr. Henry argues that the Commission erred because the cardiologist was clear and
unequivocal in his testimony that the artery blockage occurred after Mr. Henry’s arrival at work.
Mr. Henry points to the following testimony: “I don’t think that artery closed when he was
getting in the car that morning or when he drove from Caldwell to Boise. I think it closed when
he was walking up those stairs, and it hit him very suddenly.” However, the issue of causation is
not when the artery became blocked. It is when the plaque rupture occurred that ultimately
caused the blockage.
        In its opinion, the Commission stated that a pivotal issue of causation was “ascertainment
of when the thrombosis actually occurred” because “if the circumflex artery blockage occurred
prior to Claimant’s arrival at the workplace, it is impossible to associate that event with his post-
arrival activities.” The Commission then discussed evidence that it stated suggested an onset of
symptoms prior to Mr. Henry’s arrival at work. 1 Mr. Henry contends that the Commission erred
by relying upon such evidence to discount the cardiologist’s opinion as to when the occlusion
occurred.




1
  Mr. Henry testified that when he arrived at work an unnamed coworker had stated that he did not look well.
Another coworker testified that after the heart attack, Mr. Henry told him that he was not feeling well when he came
to work that day and that he should have paid attention to how he was feeling.

                                                         7
       As stated above, the issue of causation hinges upon when the plaque ruptured, not when
the occlusion ultimately occurred. Although the Commission stated that “there is also testimony
of record which would suggest an onset of symptomatology prior to Claimant’s arrival on the
premises,” it did not base its decision upon such testimony. After discussing it, the Commission
stated, “Considering the totality of the evidence, even the fact of Claimant’s worsened post-
arrival condition ultimately fails to establish that the injurious event which ultimately caused the
blockage occurred after Claimant arrived at the worksite.” (Emphasis added.)
       In this case, Mr. Henry had the burden of proving that the event which ultimately caused
the blockage of his artery was work related. The Commission found that he had failed to do so
because the cardiologist could not state that the plaque rupture—the event that ultimately caused
the blockage—occurred at work. The Commission concluded its analysis by stating:
       In the final analysis, [the cardiologist’s] testimony is insufficient to establish that
       Claimant’s post-arrival activities were responsible for causing or contributing to
       the occurrence of Claimant’s myocardial infarction. The evidence just as easily
       supports the proposition that it was something that happened prior to Claimant’s
       arrival at the worksite that made his heart attack inevitable and caused it to occur
       when and how it did.

(Citation to the record omitted.)
       The Commission determined that Mr. Henry had failed to prove that he suffered an
industrial accident.   An industrial accident is defined as “an unexpected, undesigned, and
unlooked for mishap, or untoward event, connected with the industry in which it occurs, and
which can be reasonably located as to time when and place where it occurred, causing an injury.”
I.C. § 72-102(18)(b).     The plaque rupture certainly was “an unexpected, undesigned, and
unlooked for mishap, or untoward event” and it certainly caused an injury—the blockage of the
right circumflex obtuse marginal artery. However, to be an industrial accident, the accident must
be one “arising out of and in the course of any employment covered by the worker’s
compensation law.” I.C. § 72-102(18)(a). “The words ‘out of’ have been held to refer to the
origin and cause of the accident and the words ‘in the course of’ refer to the time, place, and the
circumstances under which the accident occurred.” Dinius v. Loving Care and More, Inc., 133
Idaho 572, 574, 990 P.2d 738, 740 (1999). The Commission ultimately determined that Mr.
Henry had failed to prove that the plaque rupture arose out of and in the course of his
employment. It concluded that he “has failed to establish to a reasonable medical probability



                                                 8
that his heart attack was triggered by his activities at work on November 15, 2009.” Its finding
in that regard is not clearly erroneous.
       The dissent tries to play cardiologist and provide testimony that Mr. Henry’s cardiologist
was unable to provide. The issue in this case is not when the heart attack occurred. The heart
attack is the injury, and for Mr. Henry to be entitled to compensation there must have been an
industrial accident that caused that injury. In this case, the accident would have to have been the
rupture of atherosclerotic plaque. As the cardiologist testified: “When an atherosclerotic plaque
ruptures, that is the inciting event of a coronary thrombosis. So anxiety, cold weather, physical
activity, you have all the milieu in place to cause a coronary thrombosis to occur.”
       A thrombosis is the “intravascular coagulation of the blood in any part of the circulatory
system,” http://dictionary.reference.com/browse/thrombosis (accessed: January 17, 2013). The
cardiologist did not testify as to how long after the plaque rupture it would have taken for the
blood clot to form to the extent that it blocked the artery.
       The cardiologist’s opinion as to the cause of the heart attack was based upon the temporal
relationship between known stressors and the occurrence of the heart attack. As to the cause of
the heart attack, he testified that “you can only make the conclusion that because the heart attack
occurred on that day, and those activities were occurring at that time, and those events were
occurring, that there has to be some contribution to that heart attack on that day.” When      the
cardiologist was informed that some of the stressors he identified occurred prior to Mr. Henry’s
arrival at work and was asked whether they could have triggered the heart attack, he said he
could not answer that question with any scientific certainty. All that he could say is that the
heart attack occurred after Mr. Henry arrived at work. His testimony was as follows:
               We don’t know what’s going on inside that artery. Was that artery—had a
       small plaque rupture during that time when he first got in the car? Was it
       happening as he was driving? Was it little bits of splitting of that atherosclerotic
       cap? Were things beginning to develop back then?
               With any scientific certainty you can’t answer that question. You can’t
       say that you know that that was happening. What scientifically you can say is
       when the onset of symptoms occurred, the artery at that time did close, and the
       heart attack began at that time.

       What the cardiologist did not say after being informed of the stressors that existed prior
to Mr. Henry’s arrival at work is significant. The cardiologist did not exclude as a possible cause
of Mr. Henry’s heart attack the stressors that were occurring prior to Mr. Henry’s arrival at work.

                                                  9
He did not state that those stressors occurred too long before the onset of symptoms to have
precipitated the plaque rupture. He did not, as asserted by the dissent, reaffirm his prior opinion
that the cause of the heart attack was work-related. All he could say with any scientific certainty
was that the heart attack occurred after Mr. Henry arrived at work.
          The hearing officer was not required to determine the cause of Mr. Henry’s heart attack.
Mr. Henry was required to prove the cause by producing expert testimony showing that the
plaque rupture was an industrial accident. His cardiologist did not so testify after he was
informed of the stressors that existed prior to Mr. Henry’s arrival at work. Although the dissent
is willing to read between the lines and infer opinions not actually rendered by the cardiologist,
the hearing officer was not required to do so.


                                               IV.
                                            Conclusion.

          We affirm the order of the Industrial Commission, and we award respondents costs on
appeal.


          Justices W. JONES and HORTON CONCUR.


          J. JONES, Justice, dissenting.
          I dissent from the Court’s opinion for two reasons―the Commission erred in
disregarding the uncontradicted testimony of Dr. Parent as to the cause of Henry’s heart attack
and the Commission’s findings on the issue of causation are clearly erroneous. Dr. Parent
testified as to the factors that can precipitate a heart attack and how those factors precipitated
Henry’s heart attack while he was at work. The Commission’s referee stepped out of her role as
fact-finder and dabbled in medical diagnosis.
          In the usual worker’s compensation case, the causation issue generally comes down to a
battle of the experts―the claimant’s expert testifying that the injury was work-related, and the
employer/surety’s expert testifying to the contrary. In those situations, the Commission must
parse through the evidence and determine which expert’s testimony is the more reliable. That did
not happen in this case. Here, the only expert who testified on the issue of causation was Henry’s
cardiologist, Dr. Parent, who testified that the heart attack was precipitated when Henry was


                                                 10
climbing a set of stairs at work. Neither the employer nor the surety produced an expert to
contest Dr. Parent’s opinion testimony. Rather, the Commission’s referee played devil’s
advocate, discrediting his opinion for lack of foundation but then relying on snatches of his
testimony to posit that the heart attack was likely precipitated by events that occurred prior to
Henry’s arrival at work. In doing so, the referee appears to have transgressed from a finder of
fact to somewhat of a medical diagnostician.
       It should be observed that Dr. Parent was not a medical hired gun, who glances at an
injured worker’s medical records and then provides an erudite diagnosis. Dr. Parent is a board
certified cardiologist who has been practicing in Boise since 1988. He began treating Henry on
November 15, 2009, the date of his heart attack, and continued treatment thereafter. Thus, when
his deposition was taken on March 4, 2011, he was quite familiar with Henry and the factors that
affected Henry’s cardiac health.
       One thing that stands out in Dr. Parent’s deposition testimony is the significant role that
anxiety played and plays in Henry’s cardiac well-being. Dr. Parent had an opportunity to observe
this first-hand during the course of a stress test conducted ten days after the heart attack. He
testified that Henry had trouble―experienced chest pain―during the stress test:
       He had trouble for sure. When the stress test was performed, he had reduced
       exercise capacity, the onset of chest discomfort and symptoms, he had EKG
       abnormalities that told us that he was threatening to have future heart attacks
       under stress conditions, and that he had ventricular tachycardia, which is an
       unstable life-threatening rhythm often provoked in patients with recent heart
       attacks, previous heart attacks, and ongoing ischemia.

                                                 * **

       And I believe that chest pain occurred because he became so anxious and so
       emotional that he was running a very fast heartbeat, very rapid blood pressure, he
       was in distress. It was sort of self-inflicted, you might say, from his anxiety state.
       Not ‘cause anything new had happened to his coronary arteries.

As a result of the foregoing, Dr. Parent recommended immediate bypass surgery, which was
performed that same day.
       Dr. Parent testified that Henry “is one of the most anxious people I’ve ever treated. And I
think that anxiety is a major contributor to ongoing symptoms, recovery, and functionality in a
patient.” Dr. Parent said that Henry’s work at the prison was a significant source of his anxiety.



                                                11
The following exchange occurred at Dr. Parent’s deposition with respect to the time that Henry
was released to return to work:
       Q.     [Henry’s counsel] Okay. The reason I ask is if Mr. Henry said when he
       was released to return to work he had a lot of anxiety trouble, it scared him to be
       around inmates and he thought that his blood pressure was affected, and I
       wondered if you have any recollection of his reaction to returning to work?

       A.     [Dr. Parent] I would concur with your statements about his returning to
       work. It caused him high anxiety, yes.

       As to the cause of Henry’s heart attack, it is important to consider Dr. Parent’s predicate
deposition testimony:
       Q.      [Henry’s counsel] All right, sir. You’ve indicated in letters to myself and
       to counsel that when Mr. Henry was late to work, he was hurrying in from a warm
       building to the cold outside; that the physical stress of that exercise triggered his
       heart attack.

       Can you explain, Doctor, the effect of cold weather on the efficiency of a heart
       and how that works? What I’m thinking, Doctor, is we always hear in the winter
       of people who are out shoveling snow and have heart attacks, and I was
       wondering if you could help us understand why.

       A.      We know that the arteries are very dynamic in their size and under certain
       stimuli they will constrict. And cold weather and anxiety cause constriction of the
       artery size so it narrows the channel.

       We also know that mental stress, anxiety, exercise, and cold weather, blood
       pressure goes up, which puts a hemodynamic stress on the artery, increases the
       need for oxygen to the heart muscle. So at the same time flow needs to be
       augmented, there’s now a reduction of flow because of constriction.

       We also know that the hemodynamic stress and probably other factors that are
       hormonal related to release of certain hormones during stress and anxiety can
       cause an atherosclerotic plaque to rupture.

       Q.      I’m sorry?

       A.      An atherosclerotic plaque to rupture.

       Q.      Thank you.

       A.      When an atherosclerotic plaque ruptures, that is the inciting event of a
       coronary thrombosis. So anxiety, cold weather, physical activity, you have all the
       milieu in place to cause a coronary thrombosis to occur.


                                                12
       Q.      Okay. Let me see if I can summarize that in a way that I understand,
       Doctor. And please correct me if I’m wrong. The way I understand it is, if Mr.
       Henry was anxious or in cold weather, the veins actually constrict some because
       of the cold weather and the anxious condition.

       The anxiety and cold weather also requires―the body’s telling the heart to pump
       faster to supply more blood, but the veins are constricted, so it’s more difficult for
       the heart to do that, and that causes the blood pressure to go up. Am I right on
       that?

       A.    The blood pressure goes up because of anxiety and stress, not because of
       ―not as you had stated.

       Q.      Okay.

       A.     The causality there would be anxiety and increased workload, blood
       pressure rising.

       Q.     All right. Do you continue to believe, Dr. Parent, that Mr. Henry’s
       physical exertion against the setting of his underlying personality was the factor
       and the cause of his heart attack on the morning of November 15 of 2009?

       A.      I believe it was a factor.

(emphasis added). In other words, a rupture of atherosclerotic plaque can result from a physical
cause (narrowing of the artery related to cold weather and anxiety and consequent increase in
blood pressure which puts greater stress on the artery, which can dislodge plaque) or chemical
cause (anxiety-related release of certain hormones that can rupture the plaque), or a combination
of the physical and chemical causal factors. Dr. Parent opined that these factors precipitated
Henry’s heart attack when he began climbing the stairs, which was somewhat over 30 minutes
after he arrived at work.
       The referee discounted Dr. Parent’s medical opinion based solely on her conclusion that
Dr. Parent had failed to consider Henry’s activities prior to arriving at work on November 15 and
was unaware that Henry was unwell upon arrival at work. According to the referee, “[b]ecause
Dr. Parent failed to consider this evidence, his opinion lacked foundation.” However, the referee
clearly failed to read Dr. Parent’s deposition carefully. When Dr. Parent was asked about factors
that contributed to Henry’s heart attack on November 15, 2009, the following exchange
occurred:



                                                13
Q.     [Respondents’ counsel] And do you have an opinion as to the extent of the
contribution?

A.      [Dr. Parent] Well, I stated on the letters before, I think, that 50 percent
likelihood that these―there’s a 50 percent causality of the activities of that day in
triggering the heart attack.

Q.       Would your opinion with respect to causation change under a slightly
different factual scenario, if the facts established that Mr. Henry commuted from
Caldwell to his work; that on the morning in question he was aware he was
running late while still in Caldwell prior to reporting for work at the correctional
facility; that he entered a vehicle that he had not been warmed up, that had been
parked outside, presumably was exposed to the same temperatures in Caldwell, or
close to the same temperatures, and on route to Boise, although in a vehicle, and
was aware he was late during that commute, do you think any of those factors
may have caused the onset of the myocardial infarction that morning?

                                                ***

A.     It’s a little bit like bending a stick and saying, when is the breaking point
going to occur? You hear it crack, you hear it pop, you see some splinters, you see
some fibers, and then the thing breaks.

So is there a time when he’s been exposed to the scenario that you described, is
that leading up to or helping prepare this artery for this occlusion, is this a
contributor to it, it really becomes into fine points that are so difficult to be factual
or scientifically based that you just can’t distinguish that exact degree of
contribution.

We don’t know what’s going on inside that artery. Was that artery―had a small
plaque rupture during that time when he first got in the car? Was it happening as
he was driving? Was it little bits of splitting of that atherosclerotic cap? Were
things beginning to develop back then?

                                          ***

But can you say where along that day or the day before what was stressing his
system, when was this -- when was the inevitable day that this thing was going to
happen? You have to look at it, I think, major stressors and minor stressors.

And, if I look at things, you know, the cold car, the cold steering wheel, the
driving through the traffic, were those stressors that were contributing? They
likely could have been, should have been, you know, considered. But can
you―how far can you dissect that down? That’s where I get in trouble of
dissecting down all those, you know, minute events that begin to occur.



                                           14
(emphasis added). Dr. Parent was then asked:
       Q.       [Respondents’ counsel] Would your opinion at all be affected by evidence
       which suggested he appeared to be ill when he went through the check-in station,
       the first building he entered that day after coming from the parking lot?

       A.      [Dr. Parent] I think a nonmedical person looking at someone who’s late to
       work and who’s under stress might easily make a judgment on somebody’s health.
       Mr. Henry is an anxious person who displays that anxiety on his sleeve and you
       see that in him.

(emphasis added). So, Dr. Parent was filled in as to all the activities that allegedly occurred
before Henry arrived at work and of all evidence relating to feelings of unwellness that may have
existed prior to the heart attack. It is apparent that Dr. Parent evaluated what he considered
“major stressors and minor stressors” in considering the pre-arrival activities and that he
considered the unwellness observations made by “nonmedical” persons in giving the following
critical testimony:


       I don’t think that artery was closed when he was getting in the car that morning or
       when he drove from Caldwell to Boise. I think it closed when he was walking up
       those stairs, and it hit him very suddenly.”

So, even considering all of the factors that the referee thought should have been taken into
account, Dr. Parent did take them into account in reaffirming his opinion. 2
       It might have been helpful if someone had asked Dr. Parent what he meant by the artery
closing―whether it was the constriction or narrowing of the artery that resulted in a rupture of
the plaque or whether it was the plaque actually occluding the circumflex artery. However,
neither the referee nor this Court has the medical expertise to second-guess Dr. Parent’s opinion.
Presumably, a board-certified cardiologist is aware of the time it typically takes for a rupture to

2
  The referee also found Dr. Parent’s testimony insufficient and flawed “because he failed to rule
out the early morning activities.” In forming and stating his opinion that Henry’s heart attack was
precipitated when he began climbing the stairs, Dr. Parent was not required to “rule out” any
particular factors. Rather, he was required to consider Henry’s history, the factors that affected
Henry’s heart health, and the activities that Henry engaged in both before and after arriving at
work. Dr. Parent did so in reaffirming his initial opinion during the taking of his deposition. He
considered major and minor stressors and apparently ruled out minor stressors that may have
been “minute events,” in reaching his determination. Based on his experience and expertise, he
unequivocally testified that the heart attack was precipitated at that time and place. This is not a
situation where the cause is unknown, requiring that other possible causes be ruled out.

                                                15
result in an occlusion and it was his opinion that it occurred suddenly. Dr. Parent was certainly
aware of the major stressors affecting Henry, particularly his high anxiety, the anxiety Henry’s
workplace environment caused him, the role anxiety can play in causing a plaque rupture, and
the confluence of these factors as Henry began climbing the stairs at work on November 15. 3 In
any event, the referee intermingles plaque rupture, blockage, and thrombosis in her findings. For
example:
       34.     In addressing the question of causation in this case, a pivotal issue is
       ascertainment of when the thrombosis actually occurred. Obviously, if the
       circumflex artery blockage occurred prior to Claimant’s arrival at the workplace,
       it is impossible to associate that event with his post-arrival activities. Since it is
       the blockage of the artery that produces symptomatology, it should be possible, as
       Dr. Parent has noted, to ascertain when the blockage occurred, by determining
       when the symptomatology began.

       35.     Dr. Parent has supposed that the blockage occurred after Claimant arrived
       on the premises, and there is evidence in the record to support the proposition that
       Claimant’s symptoms worsened considerably following his arrival at the
       workplace. Specifically, Dr. Parent considered Claimant’s exertional activities
       after he arrived at work including walking 75 yards from his car to a security
       checkpoint, walking another 25 yards into the Administration Building, waiting
       while his belongings were inspected, walking through the Administration
       Building where he passed through another security checkpoint, when walking as
       fast as he could for 450 yards until he reached Unit 15, where he climbed stairs.

       36.     However, there is also testimony of record which would suggest an onset
       of symptomatology prior to Claimant’s arrival on the premises. In this regard,
       recall that Mr. Kimmel testified that Claimant reported feeling unwell during his
       drive to the prison and a coworker commented that he looked unwell on arrival at
       the Administration Building. Further, Dr. Parent did not consider Claimant’s pre-
       work exertional activities, although he agreed they were likely contributory. In
       fact, Dr. Parent neither discounted nor quantified any other of the morning’s
       activities in terms of their contribution to the closure of the affected artery at that
       point in time. At one juncture, Dr. Parent even implied that activities from the day
       before could have put processes in motion that made Claimant’s heart attack on
       November 15 inevitable.

3
  The role that stress and anxiety played, as opposed to the cold temperature, is heightened by the
referee’s finding that “the evidence is insufficient to establish that Claimant was actually
exposed to any risk of vasoconstriction due to cold temperatures.” One might question the
medical qualifications of the referee to make such a finding but, nevertheless, it is a finding
placed on the record by the referee and approved by the Commission. If the cold did not
contribute, then the role of stress and anxiety becomes preeminent. And, this nicely coincides
with Dr. Parent’s testimony.

                                                 16
       37.    Considering the totality of the evidence, even the fact of Claimant’s
       worsened post-arrival condition ultimately fails to establish that the injurious
       event which ultimately caused the blockage occurred after Claimant arrived at the
       worksite.

There are a number of glaring errors in the foregoing findings. First, although Henry’s counsel
advised Dr. Parent in his April 6, 2010 letter that by the time Henry got to the Administration
Building “he did not feel very good, kind of had a general feeling of malaise,” he also reported
that Henry “had no specific symptoms.” It is true that Henry told a co-worker that he was feeling
“unwell” and that Mr. Kimmel testified Henry told him that when he had come in to work that
day “he wasn’t feeling well” and “during the drive and things like that he should have kind of
paid attention to, I guess, his own feeling of,” but there is absolutely no evidence in the record to
support a finding that Henry had “an onset of symptomology” prior to arriving at work, or that he
had any pre-arrival “symptoms” that could considerably worsen after arrival. There is no
evidence indicating how or why Henry felt “unwell,” what the cause of the malaise was or that it
was symptomatic of anything, or to what Henry should have paid attention during his drive to
work. There is no evidence in the record that any of these factors were symptomatic of a heart
attack. Dr. Parent knew that Henry had a general feeling of malaise when he initially formed his
opinion. The doctor was advised of that and the other pre-arrival factors during his deposition,
prior to the time that the doctor gave his testimony reaffirming his initial opinion. It appears the
doctor was not much impressed by the reports of “nonmedical” persons, particularly where there
were no reports of symptomology. It is understandable that a board-certified cardiologist might
feel his own experience is more important than the general, uninformed observations of lay
persons in formulating a medical diagnosis. Yet, the Commission placed great store in the
layperson unwellness reports in discounting Dr. Parent’s testimony.
       The referee also asserted that Dr. Parent did not consider Henry’s pre-work exertional
activities in developing his opinion. As shown above, however, Dr. Parent considered those
activities in unequivocally reaffirming his opinion. The referee claims Dr. Parent “agreed they
were likely contributory.” That is not correct. In his deposition, Dr. Parent testified they should
be “considered” (“They likely could have been, should have been, you know, considered.”) And,
he did just that in reaffirming his opinion. The referee apparently concluded that all of Mr.
Henry’s pre-arrival and post-arrival activities were equal-value stressors. In other words, getting


                                                 17
into a cold car in Caldwell or being late for work were entitled to equal weight with climbing a
set of stairs at a workplace that caused Henry a great deal of anxiety. That isn’t necessarily the
case. As Dr. Parent testified, after having been advised of all of the pre-arrival activities asserted
by Respondents, “you have to look at . . . major stressors and minor stressors.” There is no
indication that Dr. Parent did not give greater weight to major stressors, such as Henry’s unusual
anxiety about his workplace, in forming his opinion. And, there is no indication in the record that
the referee had the qualifications or was better positioned to weigh the various stressors or to
form a medical opinion as to what precipitated the heart attack. Had the Respondents wished to
question or rebut Dr. Parent’s opinion testimony, they certainly had it within their power to hire
their own expert for the purpose of doing so. It was not up to the referee to second-guess or rebut
Dr. Parent’s opinions.
       In a 1937 worker’s compensation case, this Court stated:
       The rule applicable to all witnesses, whether parties or interested in the event of
       an action, is, that either a board, court, or jury must accept as true the positive,
       uncontradicted testimony of a credible witness, unless his testimony is inherently
       improbable, or rendered so by facts and circumstances disclosed at the hearing or
       trial. Manley v. Harvey Lumber Co., 174 Minn. 489, 221 N.W. 913, 914. In
       Jeffrey v. Trouse, 100 Mont. 538, 50 P.2d 872, 874, it is held that neither the trial
       court nor a jury may arbitrarily or capriciously disregard the testimony of a
       witness unimpeached by any of the modes known to the law, if such testimony
       does not exceed probability. And, in Arundel v. Turk, 16 Cal.App.2d 293, 60 P.2d
       486, 487, 488, the rule is stated thus: “Testimony which is inherently improbable
       may be disregarded, * * * but to warrant such action there must exist either a
       physical impossibility of the evidence being true, or its falsity must be apparent,
       without any resort to inferences or deductions.”

Pierstorff v. Gray’s Auto Shop, 58 Idaho 438, 447−48, 74 P.2d 171, 175 (1937). See also
Dinneen v. Finch, 100 Idaho 620, 626−27, 603 P.2d 575, 581−82 (1979); Wood v. Hoglund, 131
Idaho 700, 703, 963 P.2d 383, 386 (1998).
       Furthermore, this Court has held that when the findings of the Commission “are not
supported by substantial, competent evidence, they are not binding or conclusive, and upon
appeal will be set aside.” Dean v. Dravo Corp., 97 Idaho 158, 161, 540 P.2d 1337, 1340 (1975).
Whether the findings are supported by substantial, competent evidence is a question of law to be
determined by the Court. Id. In Dravo, the Court was considering a case where the worker’s
compensation claimant’s physician provided the only testimony pertaining to causation. Id. The
Court concluded that “contrary to the determination by the Commission, the testimony of Dr.

                                                 18
Colburn as to the causation is consistent and uncontradicted,” despite the fact that on cross-
examination the doctor “conceded it was impossible, medically speaking, to state without some
conjecture” that a subsequent injury was related to an earlier work-related injury. Id. The Court
looked to an Oregon worker’s compensation case, Clayton v. State Compensation Dep’t., 454
P.2d 628 (Or. 1969), for guidance on reliability of medical testimony. Id. According to the Court,
the principal issue in the Clayton case was “whether the stress and fatigue sustained in the
decedent-husband’s work was a causal factor in producing his heart attack.” Id. The only medical
testimony was presented by a doctor “who was unable to find a probability of causation in that
particular case.” Id. Our Court approvingly quoted the following from the Clayton court’s
opinion:
       In making a diagnosis the doctor draws upon the conclusions of medical science
       demonstrating that certain diseases can be traced to certain causes. These
       conclusions are not stated in absolutes; they are expressed in terms of
       probabilities. From the empirical study of many cases medical science can say
       that if certain symptoms are present there is a probability that certain disease is
       present. The probability is stronger in the identification of some diseases that it is
       in others, depending upon what has been learned about the causes for the
       particular disease. The diagnosis in a particular case involves the reasoning that
       since this probability has been established in cases in general the probability
       exists in the particular case being diagnosed. In the absence of evidence showing
       that the particular case in issue is distinguishable from cases in general it must be
       accepted that where medical science finds a probable causal relationship for the
       general group probable legal cause is established for the particular case being
       litigated. 454 P.2d at 631.

Dravo, 97 Idaho at 161−62, 540 P.2d at 1340−41. The Oregon court reversed the finding of no
causation made by the lower court. Clayton, 454 P.2d at 632−33. In other words, absolute
certainty is virtually unattainable in determining causality in the heart attack arena, but
competent medical experts can establish medical probabilities based on their expertise.
       In Dravo, we concluded:
       Dr. Colburn’s testimony that in his opinion there was a probable relationship
       between the October 1969 injury and the ultimate necessity for the operation
       stands uncontradicted. There is a lack of competent, substantial evidence to
       sustain the Commission’s finding to the effect that the doctor’s testimony was
       changed on cross-examination, as the question asked of him dealt with an issue
       immaterial to principal question.




                                                19
Dravo, 97 Idaho at 162, 540 P.2d at 1341. In other words, a competent physician’s testimony as
to causation, when consistent and uncontradicted (or, as stated in Pierstorff, not “inherently
improbable”), is not subject to being disregarded, simply because the physician asserts, as Dr.
Parent did here, that you can’t say with certainty exactly when a stick will break when it is bent,
that you can’t go inside an artery to see exactly when a plaque ruptures, and that you can’t say
for certain when a minor stressor might play some minute part in contributing to a heart attack.
Dr. Parent stated his opinion that Henry’s artery closed when he was climbing the stairs, causing
him to very suddenly experience a heart attack and he reaffirmed that opinion after being fully
briefed of all of the pre-work factors and activities. The Respondents were fully aware of what
Dr. Parent’s testimony would be, yet they failed to bring in their own expert to try to pick his
opinion apart. Anyone who has tried a case involving medical causality knows that it is unwise
to try to prevail upon cross-examination in such a case.
       In this case, Dr. Parent had an intimate knowledge of the workings of Henry’s heart, what
it responded to, how stress and anxiety played a large part in its well-being, and what factors
might precipitate a thrombosis in that heart. Indeed, ten days after the heart attack, Dr. Parent had
the opportunity during the stress test to see a virtual replay wherein Henry came close to a heart
attack brought on largely because of his unique anxietal state. With this knowledge and his
unquestioned expertise, he was by far in the best position of all of the players to determine what
precipitated Henry’s heart attack. Neither the referee, nor the Commission which relied upon the
findings of the referee, nor anyone else, was in a better position to make that determination.
There is absolutely no grounds to disregard or reject Dr. Parent’s opinion and the Commission
erred in doing so. I would reverse the Commission’s decision.


       Chief Justice BURDICK CONCURS.




                                                 20
