Farley ex rel. Farley v. United States (98 F. Supp. 3d 299, 2015)

MEMORANDUM AND ORDER

LANDYA McCAFFERTY, District Judge.

In October of 2010, Michael Farley experienced symptoms including the loss of his peripheral vision and a painful headache. A veteran of the United States Navy, Mr. Farley sought treatment at the Veterans Administration Medical Center in Manchester, New Hampshire (“Manchester VA”). There, Mr. Farley was examined and given a series of tests, and he learned that he had suffered a stroke.

It is a basic principle of medicine that a patient who has suffered a stroke is generally at an elevated risk of suffering a second stroke. Therefore, doctors who are treating stroke patients must be cognizant of this risk, and they must take steps to prevent a second stroke from occurring. As such, the established standard of care requires that a stroke patient undergo a thorough diagnostic evaluation to determine thé cause of his stroke, and it requires that the patient be prescribed certain medication to treat the underlying condition that caused the stroke to occur.

Unfortunately, Mr. Farley’s doctors at the Manchester VA did not adhere to this standard of care. They failed to provide him with an adequate diagnostic evaluation, and as a result, they carelessly prescribed him the wrong medication. In the words of one of the expert witnesses, Mr. Farley was “medically abandoned” by his doctors.

Approximately six weeks after his initial visit to the Manchester VA, Mr. Farley suffered a second stroke. This second stroke was massive, and it left Mr. Farley with “locked-in” syndrome, meaning that he remains fully conscious, but has no voluntary muscle movement other than the very limited ability to move his eyes and his head.

Now, Mr. Farley’s wife, Jeanice Farley, has brought suit on his behalf under the Federal Tort Claims Act (“FTCA”), 28 U.S.C. §§ 2671 et seq. The court held a four-day bench trial from October 21 to October 24, 2014. After considering the trial testimony and the record evidence, it is the finding of this court that two of Mr. Farley’s doctors at the Manchester VA committed medical malpractice and are legally responsible for failing to prevent Mr. Farley’s second stroke from occurring. This memorandum and order will more fully set forth the court’s findings of fact and rulings of law. See Fed.R.Civ.P. 52(a).

Findings of Fact

I. The Expert Witnesses

The court’s understanding of the complex issues involved in this case was aided by expert testimony offered by both parties. The following expert witnesses testified on behalf of the Farleys regarding liability:

• Dr. Bruce Charash, a cardiologist at the Lenox Hill Hospital in New York City.

• Dr. James Frey, a stroke neurologist at St. Joseph’s Hospital in Phoenix, Arizona.

• Dr. Kenneth Stein, an emergency room doctor at St. Anthony’s Medical Center in St. Louis, Missouri.

• Dr. J. Neal Rutledge, a neurointerventional surgeon from Austin, Texas.

The following expert witnesses testified on behalf of the government:

• Dr. David Greer, a neurologist and the director of the stroke service at Yale University Hospital in New Haven, Connecticut.

• Dr. Warren Manning, the section chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center in Boston, Massachusetts.

• As will be discussed below, the Farleys also offered the testimony of two damages experts.

• Dr. Louis Caplan, a neurologist and senior member of the stroke service, also at Beth Israel Deaconess Medical Center in Boston.

• Dr. Anthony Kim, a stroke neurologist and the medical director at the University of California San Francisco Stroke Center.

At points throughout this memorandum and order, the court has included specific credibility findings pertinent to individual expert witnesses. However, the court notes that, on many occasions, the expert witnesses testified regarding issues, beyond their immediate fields of specialty. For example, several of the neurologists testified regarding cardiovascular issues, and several of the cardiologists testified regarding neurological issues.

Nevertheless, the evidence, established that the treatment of stroke patients is very much an interdisciplinary practice, and requires a working knowledge of both cardiovascular and neurological issues. Thus, while the court gave more weight to testimony that directly related to an expert’s field of specialty, the court acknowledges that these specialties often overlap in the treatment of stroke patients, and the court assigned weight to the testimony accordingly. In assessing the credibility of the expert witnesses, the court has also considered, among many other factors, the witnesses’ backgrounds and areas of expertise, curricula vitae, and publication histories.

II. General Stroke Principles

Broadly speaking, there are two types of stroke. An “ischemic,” or “dry” stroke occurs when the arteries leading to the brain become narrowed or blocked, resulting in reduced blood flow. A “hemorrhagic,” or “wet” stroke occurs when a blood vessel in the brain leaks or ruptures. In this case, the parties agree that Mr. Farley’s first stroke was an ischemic stroke.

With rare exceptions, ischemic strokes can be further categorized as either “thrombotic” strokes, or “embolic” strokes. In this case, while the parties agree that Mr. Farley suffered an ischemic stroke, there is disagreement over whether the stroke was thrombotic or embolic.

A thrombotic stroke occurs when a blood clot forms in the arteries that supply blood to the brain. Most commonly, these blood clots result from deposits of a substance known as atherosclerotic plaque, which can accumulate in the arteries. The plaque deposits can break away and travel through the blood stream to the brain, where they can cause a stroke. Approximately 80% of ischemic strokes are thrombotic in nature.

An embolic stroke occurs when the blood clot responsible for causing the stroke forms in another part of the body, and sweeps through the bloodstream, ultimately making its way to the brain and causing a blockage. Approximately 20% of ischemic strokes are embolic in nature and the vast majority of embolic strokes involve “cardioembolic” blood clots, or blood clots that form in the heart.

The evidence established that there are five potential causes of a cardioembolic blood clot: a tumor in the heart known as a myxoma; an infection of the heart valve called endocarditis; a hole in one of the walls of the heart; a disorder known as atrial fibrillation; and the development of a blood clot in the left ventricle attributable to an irregular heartbeat. The parties appeared to agree that Mr. Farley did not have myxoma, endocarditis, or a hole in the wall of his heart. And, as will be discussed below, the weight of the evidence established that Mr. Farley did not suffer from atrial fibrillation. Thus, the vast majority of the trial testimony relevant to cardioembolic blood clots focused on whether Mr. Farley had developed a clot in his left ventricle.

Dr. Charash, the Farleys’ expert cardiologist, explained the process through which blood clots may form in a patient’s left ventricle. Dr. Charash explained that, in a normally functioning heart, blood flows in a smooth, laminar fashion as the heart contracts in an efficient and symmetrical fashion. Dr. Charash drew an analogy to rushing water, explaining that “[i]f you take a river or rapids and throw a plastic cup in, it’s going to go flying down the river. The chance of it just sticking on the side in the rapids is very low because the momentum of the fluid drives it downstream.”

Dr. Charash testified that certain abnormalities in a patient’s heart may allow blood clots to form. This is particularly true, Dr. Charash explained, when the patient’s heart is beating in an asymmetrical fashion. An example of such asymmetry, Dr. Charash testified, would be if certain walls of the patient’s heart were contracting faster or slower than other walls. Dr. Charash and other experts described this condition as a “segmental wall motion abnormality.”

This distinction between symmetrical and asymmetrical weakening of the heart is important. Symmetrical weakening, Dr. Charash testified, refers to a uniform weakening of the heart. A patient will be said to be suffering from symmetrical weakening when his heart is pumping blood with diminished efficiency, but when the mechanics of the heartbeat are otherwise normal. Dr. Charash explained that this global weakening might occur, for example, as a result of prolonged alcohol abuse, chronic high blood pressure, or a viral disease.

Asymmetrical weakening, on the other hand, refers to a scenario where a patient’s heart exhibits signs of weakening in some areas but not others. Dr. Charash testified that symmetrically weakened hearts are less likely to produce blood clots, while asymmetrically weakened hearts are at much higher risk. Dr. Charash explained as follows:

The global [weakening] group, even though [the heart is] weakened, has symmetric contraction, and that somewhat lessens the risk of forming a blood clot____[A] segmental wall motion abnormality [ ] is the one that carries the greatest risk of clot formation.

In a symmetrically weakened heart, Dr. Charash explained, the blood continues to move in a smooth and uniform fashion. In an asymmetrically weakened heart, however, the blood has an opportunity to form eddies or pools because the heart is not expanding and contracting in a uniform fashion. This disrupts the flow of blood and can lead to areas of stagnation where blood clots are likely to form. Dr. Char-ash again invoked the same rushing water analogy, explaining that “a blood clot will typically form on a wall of the heart because that’s where the most stagnant flow is, just like in a rapids. The speed is quickest in the center, where on the side it’s slower.”

The evidence established that a cardioembolic blood clot that forms in a patient’s left ventricle is likely to be ejected from the heart into the blood stream. Once in the blood stream, the clot can travel anywhere in the body, but may make its way to the brain and cause a stroke.

III. The Standard of Care

The standard of care applicable to the treatment of ischemic stroke patients is well-settled.

A. Secondary Stroke Prevention

The evidence conclusively established that patients who have suffered a stroke are at elevated risk of having another stroke, and that the standard of care calls on a doctor treating a stroke patient to take steps to reduce this risk. This process is generally referred to as “secondary stroke prevention.” Counsel for the Farleys used a demonstrative exhibit that set forth five “rules” for doctors in the capacity of treating stroke patients. ' The first of these rules stated that a doctor should try to prevent a second stroke in a patient who presents with a stroke. Over the course of the trial, every single expert witness stated that he agreed with this rule.

B. The Diagnostic Process

Often, as here, the first physician to encounter a patient following a stroke is an emergency room doctor. To successfully engage in secondary stroke prevention, the emergency room doctor must orchestrate a diagnostic process (often referred to by the expert witnesses as a diagnostic “workup”) to identify the cause of the patient’s stroke. The standard of care calls on the doctor to utilize a series of tests and to involve a series of specialists in this process.

As an initial matter, the doctor should order a computed tomography scan (“CT scan”) to obtain imaging of the patient’s brain. This imaging will allow the doctor to assess whether a stroke has occurred and whether the stroke was ischemic or hemorrhagic. It will also allow the doctor to identify the severity of the stroke, as well as the location of the stroke within the brain. Finally, a CT scan may allow the doctor to identify the approximate period of time that the stroke took place.

The standard of care also calls on the doctor to order an imaging study known as a computed tomography angiogram (“CTA”). A CTA is a scan designed to evaluate the arteries in a patient’s head and neck to look for the presence of atherosclerotic plaque. The presence of atherosclerotic plaque may be an indication to the doctor that the patient has suffered a thrombotic stroke.

The doctor should also order a series of tests to assess the patient’s heart. An abnormally functioning heart may be an indication to the doctor that the patient has suffered an embolic stroke resulting from a cardioembolic blood clot. The first of these tests is known as electrocardiogram (“EKG”). An EKG measures the electrical impulses in the heart and can detect the occurrence of a recent heart attack or other anomaly.

The second test of the heart is known as an echocardiogram. Two types of echocardiograms were discussed at trial: a transthoracic echocardiogram (“TTE”), and a transesophageal echocardiogram (“TEE”). The TEE and the TTE are both echocardiograms, and they share similar acronyms, but they are significantly different tests. A TEE is an invasive procedure that involves sedating the patient and using a probe, inserted orally and into the esophagus, to view the heart from the interior of the chest cavity. Because a TEE views the heart from the rear, it tends to produce superior imaging of the posterior portions of the heart. A TTE, on the other hand, is an echocardiogram that uses technology similar to an ultrasound, and is administered by holding a transducer above the patient’s chest, which produces a visual image of the heart. Unlike the TEE, the TTE views the heart from the front, and therefore tends to produce superior imaging of the anterior portions of the heart. The parties dispute whether the TEE or the TTE is the superior test, but the evidence clearly established that the standard of care calls on doctors to order at least one of these echocardiograms promptly following the patient’s first stroke.

Next, the standard of care calls on the doctor to assess the patient for atrial fibrillation, which, as noted previously, is a disorder that can lead to blood clots forming in a patient’s heart. Atrial fibrillation occurs when electrical signals to the heart are disrupted, causing the upper chambers of the heart to quiver, instead of beating normally and rhythmically. This can result in decreased circulatory efficiency and may put the patient at risk of a cardioembolic blood clot.

To test patients for atrial fibrillation, doctors often prescribe the use of a device known as a Holter monitor. A Holter monitor is a portable heart monitoring device that a patient may wear continuously for extended periods of time. The use of a Holter monitor over a period of several days (or even several weeks) is important. There was much discussion at trial about the difficulty of diagnosing atrial fibrillation. The evidence established that this difficulty stems from the fact that atrial fibrillation is often episodic, meaning that a patient may exhibit symptoms at one point in time, but not another. One of the Farleys’ expert witnesses, Dr. Rutledge, drew an analogy to a set of railroad tracks. Dr. Rutledge testified that simply because a passerby does not happen to see a train at one point in time does not mean that a train did not pass by previously, or that one would not pass by in the future. Thus, the extended use of the Holter monitor increases the likelihood that it will detect evidence of atrial fibrillation.

Finally, the standard of care calls on an emergency room doctor treating a stroke patient to engage the services of both a cardiologist and a neurologist to assess the patient. These specialists bring to bear particularized knowledge of the brain and the cardiovascular system to ensure that the patient receives an accurate diagnosis of the cause of his stroke, and to ensure that he receives appropriate preventative treatment. Separately, the emergency room doctor should take steps to ensure that the patient’s primary care provider (“PCP”) is made aware of the stroke and is integrated into the patient’s treatment.

The involvement of a cardiologist, a neurologist, and the PGP is relevant to a concept known as “continuity of care.” The treatment of stroke patients generally requires a team approach, involving the emergency room physicians who initially treat the patient, a cardiologist, a neurologist, and the patient’s POP. There was widespread agreement among the expert witnesses that the involvement of all of these doctors increases the likelihood that the patient will be treated properly, that a single physician will coordinate his care, and that, consequently, the patient will have a better outcome.

Because the stroke diagnostic process involves the administration of multiple tests, and the involvement of multiple doctors, the standard of care generally calls for stroke patients to be admitted to the hospital. Multiple expert witnesses testified that doing so serves to facilitate the information-gathering process by ensuring that test results are gathered efficiently, and that experts are promptly engaged and consulted.

In sum, when a patient presents to the emergency room after suffering an ischemic stroke, the standard of care calls on the treating physician to promptly order the following tests (in no particular order): a CT scan, a CTA, an EKG, and an echocardiogram (whether a TTE or a TEE). The doctor should also consider the use of a Holter monitor to test the patient for atrial fibrillation. In addition, the doctor should promptly engage the services of a cardiologist and a neurologist to evaluate the patient, and the doctor should contact the patient’s PGP to make him aware of the stroke and to ensure the continuity of the patient’s care. To facilitate this diagnostic process, the doctor should have the patient admitted to the hospital.

C. Treatment

In most cases of ischemic stroke, the treating physician will be able to determine the cause of the patient’s stroke by using the diagnostic process outlined above. As noted, except in rare cases, the stroke will either have been a thrombotic stroke resulting from atherosclerotic plaque in the arteries leading to the brain, or an embolic stroke resulting from a blood clot that formed in the patient’s heart and swept through the bloodstream to the brain. 'The thoroughness and accuracy of the diagnostic process is critical, because a physician’s prescribed course of treatmént for secondary stroke prevention will differ significantly based on the cause of the patient’s first stroke.

i. The Basics of Aspirin Versus Coumadin

Two drugs, Aspirin and Coumadin, are commonly used in secondary stroke prevention. Aspirin belongs to a class of drugs known as antiplatelet agents. Aspirin works to “thin” the blood by preventing blood platelets from binding to one another. As a general matter, Aspirin is considered to be effective as a means of preventing blood clots from forming in the arterial circulation. Thus, if a patient is deemed to be at risk of a thrombotic stroke (meaning a stroke resulting from atherosclerotic plaque in the arteries), the patient may be prescribed Aspirin.

Coumadin belongs to a class of drugs known as anticoagulants. Coumadin prevents clotting proteins in the blood from binding together. As a very general matter, Coumadin is considered to be effective at preventing blood clots from forming in the heart in certain circumstances. Thus, a patient deemed to be at risk of a cardioembolic stroke may be prescribed Coumadin, depending on the situation and a longi list of patient-specific risk factors.

Although Coumadin and Aspirin • are both used in secondary stroke prevention, they function differently and are intended to treat different causes of stroke. Thus, the decision to treat a patient with Aspirin versus Coumadin is an important one. Several of the Farleys’ expert witnesses offered helpful and persuasive testimony about the science underlying the formation of blood clots in the arteries and in the heart, and about how Aspirin or Coumadin can alleviate these problems.

ii. How Aspirin Works

Dr. Stein testified that when an individual has atherosclerotic plaque in the arteries leading to the brain, it raises the potential for blood clot formation. Dr. Stein explained that a small piece of the plaque may become slightly detached, causing blood platelets to flock to this area in order to seal the newly-formed opening. These platelets can bind together and form a blood clot, which may then break away and travel through the bloodstream to the brain.

Dr. Stein explained that Aspirin is generally the accepted treatment for patients who have suffered strokes resulting from atherosclerotic plaque. Aspirin works to “thin” the blood by preventing blood platelets from binding to one another, and thus it prevents clots from forming in areas where a piece of atherosclerotic plaque has broken away.

iii. How Coumadin Works

Coumadin is intended to serve a very different function. There was widespread agreement among the expert witnesses that Coumadin is ineffective at preventing strokes caused by atherosclerotic plaque. Rather, Coumadin is intended to treat blood clots that can form inside the heart in certain circumstances. Several of the Farleys’ expert witnesses explained how Coumadin can remedy this situation.

Above, the court outlined the process through which asymmetrical weakening of a patient’s heart can prompt the formation of blood clots in areas of slow or stagnant blood flow. Dr. Charash explained that Coumadin prevents, blood clots from forming by suppressing the “chemical chain reaction” that occurs in these areas.

Dr. Stein added further detail by explaining the chemical processes through which pooled or stagnant blood will prompt the formation of blood clots. Dr. Stein testified regarding the role of .clotting proteins. These proteins serve a vital function. ' For example, when an individual suffers a cut to the skin, clotting proteins serve to seal the cut, preventing further blood loss and infection. However, Dr. Stein explained that clotting proteins can also bind together and cause a blood clot in areas where there is stagnation or pooling of blood.

Dr. Frey offered similar testimony. He testified regarding the presence of 13 types of protein molecules in the blood that interact to form what he described as a “spiderweb net” in areas where blood flow has slowed. Dr. Frey explained that this spiderweb will often form the basis of a blood clot.

Drs. Charash, Stein, and Frey offered persuasive testimony that Coumadin is highly effective in blocking the chemical process that causes the clotting proteins to bind together. Thus, Coumadin is the preferred drug to treat patients who have a blood clot in the heart, or who are at risk of forming a clot in the heart, because Coumadin will dissolve existing clots and prevent new ones from forming.

iv. The Widely-Accepted, Medical- Guidelines Recommend Coumadin for Ischemic Stroke Patients At Risk of Cardioembolic Blood Clots

For patients who have suffered an ischemic stroke, there is a set of widely-used guidelines on which doctors rely in deciding whether to treat the patient with Aspirin or Coumadin. These so-called Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack (“Guidelines”) were a central focus of the trial testimony.

The Guidelines are promulgated by the American Heart Association and the American Stroke Association. The evidence offered by both parties established that the Guidelines are the definitive source of information for doctors treating ischemic stroke patients, and the court views the Guidelines as important in understanding the applicable standard of care.

The Guidelines contain a section titled “Medical Treatments for the Patient with Cardiogenic Embolism.” This section advises doctors on whether to treat stroke patients with Aspirin or Coumadin depending on the nature of the stroke and the other symptoms that the patient may be exhibiting. The introductory language of this section is extremely important. In relevant part, this language states:

In general, patients with cardiac disease and [stroke] face a high risk of recurrent stroke. Because it is often difficult to determine the precise mechanism [of the patient’s first stroke], the choice of a platelet inhibitor [Aspirin] or anticoagulant drug [Coumadin] may be difficult. Patients who have suffered an ischemic stroke who have a high-risk source of cardiogenic embolism should generally be treated with anticoagulant drugs to prevent recurrence.

See Pl.’s Ex. 43 at 12 (emphasis added).

Following the introductory language, there is a series of subsections specific to particular symptoms that a stroke patient may be exhibiting. Each subsection gives a specific recommendation as to whether the patient should be treated with Aspirin or Coumadin. The first three subsections, A, B, and C, were frequently discussed at trial. At later points, this memorandum and order will return to a discussion of the Guidelines and the specific subsections. For present purposes, however, the court notes the importance of the introductory language, which plainly directs doctors treating ischemic stroke patients at high risk of cardioembolic blood clot formation to treat the patient with Coumadin.

v. The Relevant Studies Show the Effectiveness of Coumadin Over Aspirin in Preventing Cardioembolic Stroke

The Guidelines reach their recommendations by distilling the latest medical 'data and research. The available clinical trials are reviewed and compiled to provide specific recommendations and to inform best practices.

The Farleys introduced into evidence a series of studies and clinical trials that are cited in the Guidelines. These studies and trials attempted to draw conclusions about the effectiveness of Aspirin and Coumadin by tracking stroke patients and recording their incidences of death and stroke recurrence. Most all of these studies and trials concluded that Coumadin is more effective than Aspirin at improving outcomes for stroke patients at risk of cardioembolic blood clots.

The following table summarizes the relevant studies and their outcomes:

Study Conclusion

Anticoagulants in the Secondary Prevention of Events in Coronary Thrombosis Study (“ASPECT I”) “We conclude that the long-term anticoagulation treatment after [heart attack] in low-risk patients has a limited effect on mortality but achieves substantial benefit by reducing the risk of cerebrovascular events and recurrent [heart attack].”

Anticoagulants in the Secondary Prevention of Events in Coronary Thrombosis Study-2 (“ASPECT II”) “In patients with recently admitted acute coronary events, treatment with high-intensity oral anticoagulation or aspirin with medium-intensity oral anticoagulation was more effective than aspirin on its own in the reduction of subsequent cardiovascular events and death.”

Warfarin/Aspirin Study in Heart Failure (“WASH Study”) “There were trends to a worse outcome among those randomized to aspirin for a number of secondary outcomes. Significantly more patients randomized to aspirin were hospitalized for cardiovascular reasons, especially worsening heart failure.”

Warfarin Versus Aspirin for Reduced Cardiac Ejection Fraction (“WARCEF Study”) “In the entire patient population, there was a constant and significant benefit with [Coumadin] as compared to aspirin with respect to rate of ischemic stroke.”

Warfarin, Aspirin or Both After Myocardial Infarction “In this study, we found a statistically significant superiority of [Coumadin] in combination with aspirin, as well as [Coumadin] alone as compared with aspirin for the reduction in the composite end point.”

Ventricular Dysfunction and the Risk of Stroke After Myocardial Infarction “Our study suggests that the beneficial effects of anticoagulation on the rate of stroke after [heart attack] is evidenced not only in patients with moderate to severe decreases in left ventricular ejection fraction, but also patients with relatively well-preserved left ventricular function.”

vi. The Expert Testimony Also Suggested that Coumadin is More Effective than Aspirin in Preventing Cardioembolic Stroke

The weight of the expert testimony affirmed the recommendation set forth in the Guidelines that ischemic stroke patients who are at high risk of cardioembolic blood clots should be treated with Coumadin. Dr. Charash offered uncontroverted testimony that when these patients are placed on Coumadin therapy, the risk of stroke drops by approximately 50% in 48 hours, and by about 95% within four days.

D. The Standard of Care in Review

To briefly summarize, the standard of care applicable to the diagnosis and treatment of ischemic stroke patients is generally well-settled. The doctor treating the patient must initiate a comprehensive diagnostic “workup” to determine the cause of the patient’s stroke. The thoroughness and accuracy of the workup is essential to ensure effective secondary stroke prevention. This workup will typically entail a CT scan, a CTA, an EKG, and an echocardiogram. It may also involve the use of a Holter monitor. The treating emergency room physician is responsible for involving a cardiologist, a neurologist, and the patient’s PCP, in order to ensure continuity of care. Depending on the nature of the facility at which treatment is taking place, completing the diagnostic workup may require admitting the patient to the hospital.

If it is determined that the patient’s first stroke was a thrombotic stroke, meaning a stroke resulting from the buildup of atherosclerotic plaque in the arteries leading to the brain, Aspirin is generally the appropriate course of treatment. If, however, it is determined that the patient is at high risk of a cardioembolic blood clot, the patient should generally be treated with Coumadin. Treating such a patient with Coumadin will significantly improve the likelihood of a positive outcome.

IV. Mr. Farley’s Treatment at the Manchester VA

A.Preliminary Background Information

Mr. Farley, presently 60 years old, is a veteran of the United States Navy. Mr. Farley sustained service-related injuries to his left arm in 1974. In January of 2000, he was deemed permanently and totally disabled by the United States Department of Veterans Affairs based on these injuries.

Mr. and Mrs. Farley married in 1982. They have three children: George Farley (age 31); James Farley (age 25); and Kimberly-Rae Farley (age 23). Mr. and Mrs. Farley had been separated for approximately six years at the time of Mr. Farley’s strokes because of discord related to Mr. Farley’s use of narcotics. For at least a portion of this period, Mr. Farley lived with his sister in Bennington, New Hampshire. Mr. Farley also may have had a girlfriend at some point during this time. Nevertheless, the evidence suggested that Mr. and Mrs. Farley did not have plans to divorce, and were hoping to reconcile. Despite his separation from Mrs. Farley, Mr. Farley maintained relationships with his children during this time.

Since the late 1990s, Mr. Farley had sought treatment at the Manchester VA for an assortment of medical issues, including issues related to the service injury to his left arm. In recent years, Mr. Farley’s care was principally overseen by Dr. Armando Del Rio, his PCP.

B. The First Stroke — Initial Symptoms

.On the morning of October 20, 2010, Mr. Farley called the Manchester VA and reported that, for the past two days, he had been suffering from a migraine headache and loss of right-sided peripheral vision in both eyes. The Manchester VA scheduled Mr. Farley for an appointment to see an optometrist that afternoon.

Shortly thereafter, Mr. Farley called back to report that he could not attend the appointment because he could not get a ride from his home to the Manchester VA. Mr. Farley indicated that he would report to the Manchester VA the following day.

C. October 21, 2010 Visit

i. Preliminary Evaluation

At 10:35 a.m. on the morning of October 21, 2010, Mr. Farley presented to the Manchester VA, where he again reported that he was suffering from a severe headache and that he had lost right-sided peripheral vision in both eyes. Mr. Farley described the headache as occurring in recent days, and reported that it was causing him pain on a scale of eight out of ten.

Mr. Farley was seen by Dr. Gary Lamphere in the Urgent Care Clinic. Mr. Farley explained that, approximately four days earlier, he had been attempting to move a 50-pound télevision when it slid and struck him in the head, causing his neck to hyperextend. At trial, Dr. Lamphere testified that Mr. Farley’s symptoms, a severe headache and loss of right-sided peripheral vision, were consistent with someone who had suffered a recent stroke.

Dr. Lamphere first referred Mr. Farley for an optometry consultation. A Manchester VA optometrist diagnosed Mr. Farley as suffering from new onset incongruous right homonymous hemianopsia (or a loss of the right half of the visual field), a finding typically associated with the occurrence of a stroke.

ii. CT Scan

Convinced that Mr. Farley had suffered a stroke, Dr. Lamphere then ordered a CT scan of Mr. Farley’s brain. The CT scan revealed “poor gray-white discrimination and decreased attenuation with effacement of the sulci in the posterior medial left occipital lobe consistent with a subacute infarct.” In other words, the CT scan showed that Mr. Farley had suffered a stroke in the rear, lower-left portion of his brain. That the stroke was deemed to be “subacute” meant that it had likely occurred several days prior. Dr. Lamphere testified that he was also able to glean from the CT scan that Mr. Farley’s stroke was an ischemic stroke.

As noted, the CT scan revealed that Mr. Farley’s stroke had occurred in the rear, lower-left portion of his brain. A series of arteries carries oxygenated blood from the heart to the brain. The vertebral arteries and the basilar artery run up the back of the neck and supply blood to the rear portions of the brain. The carotid arteries run up the front of the neck and supply blood to the front portions of the brain. The CT scan revealed to Dr. Lamphere that a blood clot had traveled through the arteries in the back of Mr. Farley’s neck and had become lodged in the basilar artery, blocking the flow of blood to the rear, lower-left portion of Mr. Farley’s brain, and resulting in an ischemic stroke,

iii. CTA Exam

Next, Dr. Lamphere ordered that Mr. Farley undergo a CTÁ. Mr. Farley’s CTA revealed that the vertebral arteries and the basilar artery were generally normal in appearance. The CTA did reveal, however, “a small amount” of atherosclerotic plaque in Mr. Farley’s left carotid artery.

Dr. Lamphere testified at trial that the results of the CTA convinced him that the arteries in Mr. Farley’s head and neck were “most likely” not the source of the stroke. Although the CTA did reveal a “small amount” of atherosclerotic plaque in the carotid artery, Dr. Lamphere testified that he was “fairly convinced” that atherosclerotic plaque was not the cause of the stroke. Dr. Lamphere noted that this level of atherosclerotic plaque in a man of Mr. Farley’s age was not surprising.

iv. Contemplated Transfer to the West Roxbury VA

During the course of the afternoon on October 21, 2010, Dr. Lamphere contemplated transferring Mr. Farley from the Manchester VA to the Veterans Administration Medical Center in West Roxbury, Massachusetts (“West Roxbury VA”). The West Roxbury VA is a tertiary care facility capable of admitting patients for monitoring and treatment. The evidence established that had Mr. Farley been transferred to the West Roxbury VA, he likely would have been admitted to the hospital, and likely would have been evaluated by a neurologist.

In preparing to transfer Mr. Farley, Dr. Lamphere completed an inter-facility transfer form and spoke with Dr. Natasha Frank, a physician employed by the West Roxbury VA. Dr. Lamphere obtained Dr. Frank’s approval and Mr. Farley’s consent to complete the transfer. An ambulance was en route to transport Mr. Farley to Massachusetts when, for reasons that are unclear, Dr. Lamphere cancelled the transfer.

The evidence suggested that the decision to cancel the transfer was made amidst confusion at the Manchester VA. Dr. Lamphere testified that he received a telephone call from Dr. Frank advising him that- if Mr. Farley’s CTA produced normal results, the transfer would be unnecessary. However, the parties stipulated that Dr. Frank has no memory of this conversation, and that it would not have been her usual practice to advise against a transfer in those circumstances. Furthermore, Dr. Lamphere conceded that his receiving such a call from Dr. Frank was a “very unusual situation.” Ultimately, it is unclear why Dr. Lamphere elected to cancel the transfer.

v. EKG

Finally, later in the afternoon on October 21, 2010, Dr. Lamphere ordered an EKG for Mr. Farley. The EKG produced normal results.

vi. Dr. Lamphere Did Not Determine the Cause of Mr. Farley’s Stroke

Dr. Lamphere’s treatment notes from the October 21, 2010 visit state as follows: “Subacute left occipital CVA [cerebral vascular accident],? etiology .., R/O [rule out] cardiac source of embolic [cerebral vascular accident].” These notes suggest that Dr. Lamphere had reached the conclusion that Mr. Farley had suffered a subacute stroke in the left, rear portion of his brain, but that Dr. Lamphere was uncertain as to its etiology, or cause. The notes further imply that Dr. Lamphere suspected that the stroke might have resulted from a blood clot that had formed in Mr. Farley’s heart.

The treatment notes comport with Dr. Lamphere’s testimony at trial. Dr. Lamphere testified that despite running the CT scan, the CTA, and the EKG, he was uncertain about the cause of Mr. Farley’s stroke. Dr. Lamphere was “fairly convinced” that the arteries in the head and neck had not been the source of the stroke. Dr. Lamphere suspected, but was not sure, that Mr. Farley’s stroke had resulted from a cardioembolic blood clot. Indeed, he testified that a cardioembolic blood clot was “high” on his list of potential causes.

Yet, despite his uncertainty regarding the cause of Mr. Farley’s stroke, Dr. Lamphere did not pursue a series of diagnostic steps called for by the standard of care which could have helped him narrow the possibilities. First, Dr. Lamphere could have prescribed the use of a Holter monitor to evaluate Mr. Farley for atrial fibrillation. Dr. Lamphere also could have promptly ordered an echocardiogram to assess Mr. Farley’s heart. Dr. Lamphere admitted at trial that he did nothing to determine whether Mr. Farley might have been able to undergo an echocardiogram that day. Instead, Dr. Lamphere arranged for Mr. Farley to undergo the test at a much later date.

Dr. Lamphere could have promptly engaged a cardiologist in Mr. Farley’s care. Dr. Lamphere conceded at trial that a doctor treating a stroke patient should attempt to rule out the heart as the source of the patient’s stroke. As Dr. Lamphere explained, a patient who has suffered a stroke resulting from a cardioembolic blood clot is generally at high risk of a subsequent stroke because the ongoing conditions in the patient’s heart may cause another clot to form. Dr. Lamphere admitted at trial that he was aware as of October 21, 2010, that the Manchester VA had a cardiologist on staff. Indeed, Dr. Lamphere acknowledged that this cardiologist, Dr. Daniel Lombardi, had an office “literally just a hallway down from [ ] the Urgent Care Clinic” where Dr. Lamphere was practicing. Nevertheless, despite both his concern that the source of Mr. Farley’s stroke was cardioembolic and the ease of promptly engaging a cardiologist, Dr. Lamphere testified that he did not consult with Dr. Lombardi, nor did Dr. Lamphere arrange for Dr. Lombardi to examine Mr. Farley that day.

Likewise, Dr. Lamphere could have arranged for Mr. Farley to be seen by a neurologist. Dr. Lamphere testified that a neurologist was on staff and available at the Manchester VA on October 21, 2010. Nevertheless, Dr. Lamphere did not engage the neurologist’s services for Mr. Farley.

Finally, Dr. Lamphere could have arranged for Mr. Farley to be admitted to the hospital. Dr. Lamphere testified that had he done so, Mr. Farley likely would have been seen by both a cardiologist and a neurologist. These specialists, Dr. Lamphere conceded, have specific expertise treating stroke patients.

Despite not knowing the precise etiology of Mr. Farley’s stroke, but strongly suspecting a cardioembolic cause, and despite not pursuing the various diagnostic avenues available to him, Dr. Lamphere discharged Mr. Farley in the late afternoon on October 21, 2010. Mr. Farley was instructed to take two baby Aspirin daily to prevent stroke and to return to the Manchester VA if his symptoms worsened. He was told that the Manchester VA’s cardiology department would contact him to schedule an echocardiogram.

Later that day, Dr. Lamphere ordered a TEE for Mr. Farley. A series of mishaps related to the TEE ensued. As an initial matter, Dr. Lamphere testified that his usual practice under the circumstances would have been to order the TEE to take place within one week. However, Dr. Lamphere failed to note this timeframe on the TEE order, and the TEE was scheduled for November 18, 2010, almost one month after Mr. Farley initially sought treatment. Dr. Lamphere candidly conceded at trial that the timing of the TEE was the result of an “apparent mistake” on his part.

Then, for reasons that are not entirely clear, Dr. Lamphere cancelled the TEE. Dr. Lamphere theorized at trial that the TEE may have been inadvertently can-celled due to a mistake he may have made in entering the order through the Manchester VA’s computer system. The TEE was only later rescheduled for November 18 when Mr. Farley brought the issue to the attention of a Manchester VA nurse.

D. November 18, 2010 Visit

Mr. Farley arrived at the Manchester VA on November 18, 2010, for the TEE. As instructed, Mr. Farley had not eaten that day, and had arranged for a driver to take him to and from the appointment because he would be sedated for the procedure. However, after Mr. Farley arrived, it was determined that the probe necessary to conduct the TEE was not functioning properly. Instead of administering the TEE, Dr. Lombardi, the Manchester VA cardiologist, administered a TTE, the echocardiogram conducted by holding a transducer above the patient’s chest.

The TTE revealed that Mr. Farley’s heart was functioning abnormally. Specifically, it found that Mr. Farley’s left ventricle was dilated, that Mr. Farley was suffering from hypokinesis with severe hypokinesis of the inferior and basal inferolateral walls of his heart, and that Mr. Farley’s ejection fraction was 30-35%.

To briefly summarize, the left ventricle is one of four chambers of the human heart and it is responsible for pumping oxygenated blood to the body. Mr. Farley’s TTE showed that his left ventricle was dilated, or enlarged, and that two of the walls of the left ventricle — the inferior wall and the basal inferolateral wall — were exhibiting signs of a recent heart attack in that they were moving abnormally. In other words, Mr. Farley was suffering from asymmetrical weakening of his heart because these two walls were significantly weakened relative to other areas of the heart. Finally, the ejection fraction is a measure of the percentage of blood in the heart that the heart ejects with each beat. An ejection fraction of 65-70% is considered normal, so Mr. Farley’s ejection fraction of approximately 30-35% was abnormally low.

Dr. Lombardi testified that he called Dr. Del Rio, Mr. Farley’s PCP, with the results of the TTE shortly after it was performed. Dr. Lombardi testified that “[he] contacted [Dr. Del Rio] that afternoon and [] made him aware of the findings and particularly the fact that [Mr. Farley’s] ejection fraction was found to be reduced.” Dr. Lombardi testified further that Dr. Del Rio told him that he planned to relay the results of the TTE to Mr. Farley at their next appointment. According to Dr. Lombardi, Dr. Del Rio indicated that he preferred to discuss the results with Mr. Farley in person.

There is no evidence in the record to corroborate Dr. Lombardi’s testimony that any such conversation occurred. Dr. Lombardi conceded at trial that'he did not make a written note of the conversation with Dr. Del Rio in the medical records. Incredibly, when asked why he had not done so, Dr. Lombardi disavowed any responsibility for Mr. Farley’s care, explaining that he opted not to make a written note of the telephone call “because [he] really wasn’t in the capacity of treating Mr. Farley.” The court finds that Dr. Lombardi’s testimony about speaking with Dr. Del Rio was not credible, and that no such conversation took place.

Despite having gathered and reviewed the troubling results of Mr. Farley’s TTE, Dr. Lombardi discharged Mr. Farley, and did not schedule him for any further care.

E. December 1, 2010 Visit

Mr. Farley next visited the Manchester VA nearly two weeks later, on December 1, 2010, for a routine visit with his PCP that had been scheduled prior to his stroke. He was first seen in the urgent care center for seemingly unrelated pain in his right hand. Afterward, Mr. Farley was seen by his PCP, Dr. Del Rio.

To determine what occurred at the December 1, 2010 visit, the court must necessarily rely on Dr. Del Rio’s treatment notes, as well as a written transcript of Dr. Del Rio’s deposition offered in evidence by the government. This is because Dr. Del Rio was unavailable to testify at trial. Based on the parties’ representations, it appears that Dr. Del Rio was aware of the dates of the trial, but nevertheless scheduled an international trip during the same period of time.

Having viewed a portion of Dr. Del Rio’s deposition, and having read the full deposition transcript, the court concludes that Dr. Del Rio was generally not a credible witness. His deposition testimony is often nonresponsive and evasive, an impression enhanced when considered in light of Dr. Del Rio’s decision to render himself unavailable to appear at trial.

Dr. Del Rio’s notes from the December 1 visit suggest that he discussed with Mr. Farley the troubling results of the TTE. The notes also suggest that Mr. Farley told Dr. Del Rio that he had not been taking Atenolol and Crestor, medications previously prescribed to him to lower his blood pressure and cholesterol levels, because Mr. Farley did not believe that he needed them. It is not apparent from Dr. Del Rio’s notes whether Mr. Farley indicated that he was, or was not, taking the Aspirin that Dr. Lamphere had prescribed. However, Dr. Del Rio did write that “education [was] given about importance of takng (sic) meds regulalry (sic) and also to ake (sic) asa (sic) daily.”

At this appointment, Dr. Del Rio issued Mr. Farley new prescriptions for Atenolol, (blood pressure), Crestor (cholesterol), Vitamin B12, and Aspirin. He also scheduled Mr. Farley for a further cardiology workup, which was to take place on December 16, 2010.

Dr. Del Rio’s notes give no indication that he was aware that Mr. Farley had suffered a stroke. The notes do mention Dr. Del Rio’s belief that the TTE results were indicative of a recent “cardiac event,” but Dr. Del Rio makes absolutely no mention of a stroke. And, as noted previously, Dr. Del Rio took the position during his deposition that he was entirely unaware that Mr. Farley had suffered a stroke at all.

One of the government’s .own expert witnesses, Dr. Manning, concluded that Dr. Del Rio was wholly unaware that Mr. Farley had suffered a stroke. Dr. Manning testified that, based on his review of the record, there was no indication that Dr. Del Rio was aware of the stroke as of Mr. Farley’s December 1, 2010 appointment.

The court finds that, incredibly, Dr. Del Rio was unaware as of December 1, 2010, that his patient, Mr. Farley, had suffered a serious stroke approximately six weeks earlier. Although the Farleys do hot seek a finding that' Dr. Del Rio violated the standard of care, the court notes that Dr. Del Rio bears much of the blame for his own ignorance. A cursory review of Mr. Farley’s recent medical records prior to the December 1, 2010 visit would have revealed the details of Mr. Farley’s treatment at the Manchester VA on October 21, 2010.

What is more, Dr. Del Rio’s electronic signature was recorded on a nurse’s note on October 20, 2010, the day on which Mr. Farley first called.the Manchester VA to report his symptoms of headache and loss of peripheral vision. The nurse’s note on which Dr. Del Rio’s electronic signature appears indicates the nurse’s belief that Mr. Farley was at risk of a stroke. At a bare minimum, signing this note should have called Dr. Del Rio’s attention to Mr. Farley and the potential that he had suffered a stroke.

F. December 2, 2010 — The Second Stroke

On December 2, 2010, the day after his appointment with Dr. Del Rio, Mr. Farley was found unresponsive in his home. Mr. Farley was taken to the Elliot Hospital in Manchester, New Hampshire, where he was diagnosed as having suffered a massive stroke in the basilar artery, the same region of the brain in which his first stroke had occurred. As a result of this second stroke, Mr. Farley is paralyzed and suffers from locked-in syndrome, meaning that he is fully cognizant, but has the ability to control only minor movements of his eyes and head.

Since his second stroke, Mr. Farley has required extensive medical treatment, and has resided at several different assisted-living facilities in Massachusetts and New Hampshire. The evidence established that Mr. Farley has received suboptimal care at these facilities. For example, at one of the facilities, Mr. Farley developed grade-four pressure sores, meaning that the sores extended through skin, fat, and muscle, all the way to the bone. Mr. Farley has also not been given adequate range-of-motion physical therapy, resulting in the painful shortening and constricting of the muscles in his arms, legs, and hands (a condition known as “contractures”).

V. Findings Regarding the Cause of Mr. Farley’s First Stroke

Based on the expert testimony and the medical records, the court finds it more likely than not that Mr. Farley’s first stroke was caused by a cardioembolic blood clot, meaning a blood clot that formed in his heart, and traveled through his blood stream to the brain. The court bases this finding on the following facts.

A. Mr. Farley’s CTA Ruled Out Atherosclerotic Causes of the First Stroke

To begin, Mr. Farley’s first stroke was almost certainly either a thrombotic stroke caused by atherosclerotic plaque in his arteries, or an embolic stroke caused by a blood clot that formed in his heart. The court finds that Mr. Farley’s CTA was sufficient to rule out a thrombotic stroke.

The specific results of Mr. Farley’s CTA are contained in the medical records. They state in relevant part:

.Each vertebral artery is normal in appearance. The basilar artery is normal. Each common carotid artery is normal in appearance. There is a small amount of atherosclerotic plaque at the left carotid bulb.

Both of Mr. Farley’s strokes occurred in the rear portion of his brain, which receives oxygenated blood from the heart via the vertebral and basilar arteries. The carotid arteries, on the other hand, transport blood to the front portions of the brain. Thus, to be clear, the atherosclerotic plaque that was detected on the CTA was in a different artery (the carotid artery) than the rear arteries (the vertebral and basilar arteries) that supply blood to the posterior portions of the brain where Mr. Farley’s strokes occurred.

Although Mr. Farley’s CTA did reveal “a small amount of atherosclerotic plaque” in the left carotid artery, the Farleys’ expert witnesses all adamantly concluded that atherosclerotic plaque was not the cause of Mr. Farley’s first stroke. Dr. Charash testified that “[w]ithin a reasonable medical certainty [the CTA] showed there was no primary disease in the [] blood vessels ... going to the brain, which meant that this was not a primary brain circulation stroke.” Dr. Frey concurred. He testified that the CTA revealed that “[Mr. Farley’s] arteries were clean and it was a good study....” Dr. Stein testified that the CTA “came back normal....”

Dr. Rutledge’s testimony on the CTA findings was particularly persuasive. In describing the CTA results, Dr. Rutledge testified as follows:

[Mr. Farley] has minimal plaque ... the origin of the great vessels are clear. There’s no significant atherosclerotic disease in the aorta that would be a contributing factor to [the] stroke.... [B]ased on the imaging findings we know it’s not the vessels in the head or neck.. :. All those are normal.

This testimony was compelling not only because it was detailed and unequivocal, but also because Dr. Rutledge was arguably the most qualified of any of the expert witnesses to interpret the CTA results. Dr. Rutledge is a neurointerventional surgeon, meaning that he specializes in image-guided surgeries of the head and neck. He is also board certified in a field known as neuroradiology, which is a subspecialty of diagnostic radiology, and which deals specifically with imaging of the head and neck. Thus, the court was highly convinced by Dr. Rutledge’s testimony that the CTA effectively eliminated atherosclerotic plaque as the cause of Mr. Farley’s first stroke.

While the Farleys’ expert witnesses were all on the same page regarding the CTA findings, the government’s expert witnesses were far less consistent. As an initial matter, Drs. Kim and Greer appeared to agree with the Farleys’ experts that the CTA revealed a low probability that the clot resulted from atherosclerotic plaque. Dr. Kim stated during his deposition that the CTA “revealed no narrowings of arteries in the head or neck that would explain his symptoms. So his neck vessels were patent.... It made the possibility of atherosclerotic disease less likely.” Dr. Greer took a similar position. He testified on direct examination that it was reasonable to assume based on the results of the CTA that “there was no significant pathology in the arteries of the neck and the head that might explain the stroke[.]”

Dr. Manning disagreed. Dr. Manning testified that while the CTA “essentially cleared” the arteries in Mr. Farley’s head and neck, it was still possible that there was atherosclerotic plaque in Mr. Farley’s aorta — the main artery leaving the heart— that would not have been detected on the CTA. Dr. Manning based this opinion on the fact that atherosclerotic plaque had been detected in Mr. Farley’s left carotid artery. Dr. Manning opined that “[w]hen you have plaque in one place ... you’d find plaque in many different places.” According to Dr. Manning, because Dr. Lamphere had not obtained imaging of Mr. Farley’s aorta, it was impossible to rule out atherosclerotic causes of Mr. Farley’s first stroke.

Dr. Caplan seemed to agree with Dr. Manning. On cross examination, Dr. Ca-plan was asked whether the CTA results were sufficient to rule out atherosclerotic causes of Mr. Farley’s first stroke. Citing the fact that the CTA did not visualize the aorta, Dr. Caplan replied that no, “I don’t think you could rule it out.” Further questioning revealed, however, that Dr. Caplan had testified during his deposition that the CTA did, in fact, rule out atherosclerotic causes. Dr. Caplan is, of course, entitled to change his mind, but the inconsistency undermined his credibility on this particular issue.

In sum, six of the eight expert witnesses testified that the CTA ruled out atherosclerotic plaque as the cause of Mr. Farley’s first stroke. The dissenters were Drs. Manning and Caplan. Importantly, neither of them took the position that the CTA indicated an atherosclerotic cause. Rather, they merely suggested that the CTA could not conclusively rule out atherosclerotic plaque as the cause of the stroke because Dr. Lamphere had not also obtained imaging of Mr. Farley’s aorta. And, as noted, Dr. Caplan had previously opined that he believed that the CTA did, in fact, rule out atherosclerotic causes.

Further supporting the conclusion that the CTA was sufficient to rule out atherosclerotic causes of Mr. Farley’s first stroke is the fact that the government essentially stipulated to this effect. Prior to the start of trial, in accordance with the local rules of this court, the parties each submitted a final pre-trial statement. See LR 16.2(b)(2). Both final pre-trial statements contained identical versions of what the parties described as a “brief statement of the case,” which contained a series of stipulated facts. In relevant part, the parties stipulated that “[a CTA] of the head and neck showed all arteries essentially normal in appearance. This suggested to Dr. Lamphere that restriction of the blood flow was most likely not from atherosclerotic blockage of the head and neck arteries or a clot originating from such plaque____” See Def. United States of America’s Final Pre-trial Statement, doc. no. 17 at 12; see also Pl.’s Pre-trial Statement, doc. no. 18 at 2.

For all of these reasons, the court finds that the results of Mr. Farley’s CTA indicate that his first stroke was not a thrombotic stroke resulting from atherosclerotic plaque. The overwhelming weight of the expert testimony, coupled with the government’s own pre-trial stipulation, support this finding.

B. The TTE Findings Indicated a Cardioembolic Source

As described above, Mr. Farley underwent a TTE on November 18, 2010, which was administered by Dr. Lombardi. Dr. Lombardi’s written findings are contained in the medical records, and state in relevant part:

The left ventricle is mild to moderately dilated in the end-diastolic and systolic dimensions. The ejection fraction is visually estimated to be 30-35%, and there is global hypokinesis with severe hypokinesis of the inferior wall and basal inferolateral wall.

As noted previously, the left ventricle is the chamber of the heart that is responsible for pumping oxygenated blood to the body. Mr. Farley’s TTE revealed that his left ventricle was dilated, or enlarged.

The ejection fraction measures the percentage of blood that the heart ejects with each beat. A normal ejection fraction is approximately 65-70%. Thus, Dr. Lombardi’s estimation of Mr. Farley’s ejection fraction at 30-35% suggests that Mr. Farley was well below the normal range.

Finally, Dr. Lombardi noted that Mr. Farley’s heart was exhibiting “global hypokinesis” with “severe hypokinesis” of two of the walls of the left ventricle. The term hypokinesis refers to “diminished or slow movement.” Stedman’s Medical Dictionary 934 (28th ed.2006). Thus, Dr. Lombardi’s note indicates that Mr. Farley’s heart was generally exhibiting diminished or slow movement, and that this diminished or slow movement was particularly pronounced in two.of the walls of the left ventricle.

The weight of the evidence established that these conditions put Mr. Farley at heightened risk of cardioembolic blood clot formation. On this issue, Dr. Charash’s testimony was particularly helpful and persuasive.

Dr. Charash was unequivocal in his belief that the TTE findings conclusively established that Mr. Farley’s stroke was cardioembolic in nature. On direct examination, Dr. Charash stated the following:

[W]hen you’re doing an echocardiogram on a patient who had a stroke and you are trying to figure out the mechanism and you ... find to your surprise that the patient has a 30-35% ejection fraction from a previously silent heart attack with a segmental wall motion abnormality, that’s as close to medical certainty as you can have that the heart had a clot in it that broke off because that’s the mon-. ey shot. That’s a gigantic finding. It has major repercussions.

The court