Doug celebrates after a race
Doug celebrates by dancing around the yard, singing "I Am the Champion"
after coming in third in his age class in his last race, the grueling Woodstock Memorial 10K.
Nine days later, he died while running.

Two years ago, I had never heard the terms syncope, malignant arrhythmia, or sudden cardiac death. Unfortunately, that is no longer the case.

My husband Doug was an active 52 year old. He played softball, ran 5 miles a day, had completed six marathons, and climbed rock, ice and mountains. In mid- March, 2010, Doug had a syncopal (fainting) episode while jogging. Halfway through their lunchtime run, he and his running buddy (MC) stopped to help a lost motorist. When MC turned to ask Doug's input, he saw that Doug was flat on his back, eyes rolled back in his head.

MC immediately shook Doug a little, slapped him in the face and yelled his name, with no response. MC was prepared to begin CPR, but then felt a pulse. Just as he was demanding the motorist's cell phone to call 911, Doug sat up and said, “where am I,…what happened?” He was disoriented and confused. When MC told Doug that he fainted, he asked, “how long was I out for?” MC told him it was no more than 10 seconds.

Doug did not recall feeling woozy or going down. He did not experience nausea, dizziness or vomiting before or after. He told MC he felt fine and insisted they jog back to the office.

However, I pressed him to see his doctor. I was stumped as to why he fainted. I was also worried he might get hurt falling down. Since he ran in the city, what if he fainted while crossing the road, or was robbed while unconscious? Until he could get an appointment, Doug agreed not to run alone.

The doctor did an ECG in the office, asked several questions, and concluded Doug probably experienced what is called a "vasovagal episode" and may have been dehydrated. A vasovagal response happens when there is a sudden drop in heart rate and blood pressure, which reduces blood flow to your brain and can cause fainting. No further tests were done. The doctor told us not to worry, for Doug to stay hydrated, but did not recommend any changes to Doug's exercise regime.

The afternoon of June 7, 2010, Doug had a full physical in preparation for surgery after dislocating his shoulder while playing softball. The same doctor gave him the green light.

Less than 24 hours later, Doug was dead.

He died suddenly while running in the park during his lunch break. The ER doctor told me that the cause was most likely a malignant arrhythmia - a fatal electrical malfunction in his heart. I had never heard of such a thing.

Doug did have moderate hypertension, which was being treated with Benicar HCT. He had elevated cholesterol, for which he took Crestor. He was also taking a baby aspirin every day.

The autopsy revealed that Doug had severe coronary artery disease. My husband's heart was enlarged (cardiomegaly.) He also had "severe concentric atherosclerotic coronary artery wall thickening, mainly in the proximal left anterior descending artery" (sometimes referred to as a "widow-maker.")

I learned later that these conditions can increase the risk of a fatal arrhythmia. I also learned that Benicar HCT was known to cause arrhythmias, and was implicated in a number of sudden cardiac deaths (SCD) in two large scale clinical trials.

After Doug died, I read of several other runners dying during a run - from heart attacks, hypertrophic cardiomyopathy, stress infarctions or arrhythmias. According to the Cleveland Clinic, "in older athletes (35 years and older), SCD occurs more often while running or jogging – in about one in 15,000 joggers and one in 50,000 marathon runners." Sudden Cardiac Arrest, and 1 in (Cleveland Clinic, Sudden Cardiac Arrest)

Now I know that the second most common cause of fainting (after vasovagal) is cardiac arrhythmia. I also learned the hard way that proper diagnosis is vital, since AN ESTIMATED 24% OF PEOPLE WHO EXPERIENCE CARDIAC SYNCOPE SUBSEQUENTLY DIE FROM SUDDEN CARDIAC DEATH. IN PEOPLE WITH CARDIOVASCULAR DISEASE, DEATH RATES ARE REPORTED TO BE 30% IN THE FIRST YEAR, AND APPROACH 50% IN FIVE YEARS. (Source: Pathogenesis and etiology of syncope Brian Olshansky, MD Christopher S Cadman, MD)

Cardiac caused syncope is considered relatively rare, but it kills an estimated 250,000 to 400,000 people each year in the U.S. About 75% of those who die from it are men. (Source: American Heart Association, Circulation. 1998; 98: 2334-2351 doi: 10.1161/​01.CIR.98.21.2334) Cardiac-caused syncope is also ten times more likely to occur in men than in women. While sudden cardiac death of young athletes during exertion gets a lot of press, it is actually much more common in people over the age of 49, and peaks between the ages of 40 and 55.

More than 90% of sudden cardiac deaths occur during recreational sports. (Sources: Maron et. al., JACC 1998, Corrado et al., JACC 2003, Marijon et al, Circulation J 2011) "Exercise-related syncope requires investigation because it may be the only symptom that precedes a sudden cardiac death. Syncope that occurs during exercise tends to be more ominous than that occurring in the post-exertional state." (Source: Syncope and the Runner by Yon D. Ough (

During physicals, Doug had a number of ECGs. Although I did not know it until after his death, those ECGs had indicated Doug had Left Ventricular Hypertrophy (LVH - thickening on the left side of the heart), which was confirmed during the autopsy. LVH doubles the risk of death from cardiac causes. (European Heart Journal (2000) 21, 351–353) When people with hypertension also have LVH, their risk of death is three times higher for people with hypertension alone. (Source: European Heart Journal (1996) 17, 143-14) Some doctor's dismiss LVH in athletes, but it can be a result of heart disease (high blood pressure or Hypertrophic Cardiomyopahthy.)

Doug also had mild sinus bradycardia (pulse of 60 or under), which can either be an indicator of physical fitness OR an indicator of heart disease. In Doug's case, it was probably both. A T-wave inversion also showed up on an ECG. We were never shown the reports or told there was any abnormality until I requested copies after Doug's death.

In November 2010, after going on Benicar HCT, Doug told the doctor he was having trouble getting air into his lungs while running. He had to cut back from 5 miles a day to 3.5. The doctor ordered a simple graded treadmill test. (I did not learn until after his death that no echocardiogram was done - I thought that was standard.) We were told the test results were normal, although there were several premature ventricular contractions (PVCs) during cool down.

However, "A major problem with the use of ambulatory ECG monitoring in the diagnosis of arrhythmia is that symptomatic correlation is rarely found" (4% in Holter monitoring). (Syncope and the Runner, Dr. Yon D. Ough)

Physically vigorous treadmill (treadmill) testing can be used for provoking exercise-induced tachyarrhythmias in exertional syncope. However, this test is rarely useful for arrhythmia detection." (Syncope and the Runner, Dr. Yon D. Ough). "...exercise testing is frequently normal in individuals with coronary artery anomalies, so coronary imaging may be required in athletes with syncope and this clinical possibility." (Athlete's Heart and Cardiovascular Care of the Athlete Scientific and Clinical Update, Circulation. 2011)


  • A book that changed my life - literally
  • Runner's World: Can you prevent sudden death?
  • Sudden Cardiac Death Foundation - Middle-aged Runners at Higher Risk of Sudden Cardiac Death during Marathons
  • Syncope and the Runner, Dr. Yon D. Ough
  • Syncope in Athletes, The Journal of Family Practice, 2007 - "Prompt diagnosis of syncope in athletes is essential as it may be a marker for sudden cardiac death." (The article recommends a series of cardiac tests)
  • "Ventricular arrhythmias are the most common cause of sudden cardiac death, both bradyarrhythmias and the usually more benign supraventricular arrhythmias can lead to syncope or sudden death." (Source: American Heart Association, Circulation. 1996; 94: 1147-1166 doi: 10.1161/​01.CIR.94.5.1147,
  • "...hypertrophic or enlarged heart can cause electrical instability in the heart which can in turn cause lethal arrhythmias. In addition, any enlarged heart places a person at a “significantly increased risk” of sudden cardiac death" Source: Moqeet v. Angel View Care Homes,
  • "Syncope or loss of consciousness is the direct result of a transiently inadequate of supply of blood to the brain. Such reduction of cerebral perfusion may occur because of lowered cardiac output due to arrhythmias, and in such cases may be referred to as a Stokes-Adams attack. By far the most common form of syncope, however, is that associated with abnormal autonomic regulation of blood pressure and/or heart rate, and it is then called vasovagal syncope." (American Academy of Neurology, March 16-23, 2013 annual meeting, Chapter 7, Episodic Disorders):
    • "True cardiac syncope, formerly known as Stokes-Adams attack, consists of transient loss of consciousness due to reduction of cerebral blood flow directly due to abrupt, reduced cardiac output secondary to arrhythmia. Cardiac syncope usually occurs in older patients with a history of other forms of heart disease such as coronary artery disease or angina. Cardiac syncope is typically recurrent, and is potentially lethal when due to cardiac arrhythmia such as ventricular tachycardia. Accurate diagnosis is vital. ... patient with cardiogenic syncope may have physical signs of heart disease such as cardiomegaly ....
    • Diagnostic tests. No diagnostic tests are necessary when a diagnosis of vasovagal syncope is made because of a typical history and circumstances. If cardiac syncope is suspected, a 12-lead EKG followed by a 24-hour Holter monitor is indicated. An (M-mode 2D) echocardiogram ($600) will look for valvular disease such as aortic stenosis. If all of these tests are normal, it is unlikely that further tests will be required because the diagnosis of cardiogenic syncope is unlikely. Recurrent episodes in the face of normal initial cardiac evaluation warrant referral to a cardiologist.
    • Tilt-table testing does not usually contribute to the diagnosis of vasovagal syncope, and is indicated only in cases when diseases of the autonomic nervous system causing orthostatic hypotension are suspected. Such conditions may be accompanied by other autonomic symptoms or signs, and if they are suspected a neurological consultation would be more cost-effective and appropriate.
    • Dehydration, such as that following heavy alcohol use, may be a contributing factor, lowering the "safety factor" for adequate cerebral perfusion. Postprandial diversion of blood flow to the splanchnic blood vessels, which do not contribute significantly to sustaining systemic blood pressure, increases vulnerability to orthostatic hypotension.
    • Cardiac syncope, in contrast, may occur in any situation, is unrelated to postural change or circumstance. It is related directly to abrupt insufficiency of cerebral blood flow due to reduce cardiac output, as from severe bradycardia, heart block, or a systole.
    • Premonitory Symptoms. 
      • Vasovagal syncope rarely happens without characteristic premonitory symptoms: fading of vision, nausea, sweating, weakness, tinnitus, or a feeling of an impending faint are the most common. Such symptoms may last several seconds to a half-minute or so before consciousness is lost. The person with syncope usually slumps limply to the ground and does not fall stiffly or assume a rigid position. Twitching or myoclonic movements of the limbs may occur briefly, and may suggest to on-lookers that a seizure is occurring. Unlike the clonic movements of a seizure, however, which lasts 30–60 seconds, in so-called "convulsive" syncope the jerks last only a few seconds. Urinary incontinence may occur, and should not automatically suggest a diagnosis of seizure. Patients awaken quickly, usually within 15–30 seconds, and are immediately oriented. Vomiting may occur on awakening, and pallor or sweating persisting for some minutes may be noted by witnesses.
      • Cardiac syncope, on the other hand, characteristically occurs without warning; the patient loses consciousness abruptly. Occasionally brief palpitations preceding the attack or at other times may be reported, but this is by no means invariable.

  • Exercise-Related Syncope: "collapse occurring before the finish line is a much more ominous event than that occurring after the finish line....Echocardiography ... should
    precede exercise stress testing
    ...." (Source: Exercise-Related Syncope in the Young Athlete: Reassurance, Restriction or Referral? Am Fam Physician. 1999 Nov 1;60(7):2001-2008,
  • "Athletes presenting with syncope should be carefully evaluated to uncover underlying cardiovascular disease or rhythm disorder....Athletes with serious symptoms should cease competition while cardiovascular abnormalities are being fully evaluated." (ACC/AHA/ESC 2006 Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)
    • Management of Syncope in Athletes. Note that Slide 21 is of particular interest in
      terms of distinguishing between arrhythmic and neuorocariogenic or
      nonarrhythmic syncope. Doug reported no prodrome, only one episode, it was
      exertional, and he had no post syncope symptoms - these were all red flags. (Source:
  • The 2006 ACC/AHA/ESC Guidelines present recommended tests in prioritized order.
    Note that Doug's doctor did an ECG in the office before and AFTER the syncope, but
    the treadmill test was done BEFORE the syncope in response to Doug
    complaining about inability to get air in his lungs and having to cut down
    running from 5 miles/day to 3.5 miles per day.
    • GENERAL EVALUATION OF PATIENTS WITH DOCUMENTED OR SUSPECTED VENTRICULAR ARRHYTHMIAS, Section 5.1, History and Physical Examination, "Palpitations, presyncope, and syncope are the 3 most important symptoms
      requiring further characterization in patients suspected of having
      ventricular arrhythmias. Palpitations are usually of a sudden onset/offset
      pattern and may be associated with presyncope and/or syncope. Sudden
      episodes of collapse with loss of consciousness without any premonition that
      usually last for a few seconds must raise the suspicion of conduction
      defects or ventricular arrhythmias." ( - 2006
      ACC/AHA/ESC Guidelines)
  • "Older adults are more likely to have orthostatic, carotid sinus hypersensitivity, or cardiac syncope, whereas younger adults are more likely to have vasovagal syncope.... (Am Fam Physician. 2011 Sep 15;84(6):640-50. Evaluation of syncope. Gauer RL,
  • Useful clinical rules to assess the short-term risk of death and the need for immediate hospitalization include the San Francisco Syncope Rule and the Risk Stratification of Syncope in the Emergency Department rule. Guidelines suggest an algorithmic approach to the evaluation of syncope that begins with the history and physical examination. All patients presenting with syncope require electrocardiography, orthostatic vital signs, and QT interval monitoring. Patients with cardiovascular disease, abnormal electrocardiography, or family history of sudden death, and those presenting with unexplained syncope should be hospitalized for further diagnostic evaluation. .... In cases of unexplained syncope, further testing such as echocardiography, grade exercise testing, electrocardiographic monitoring, and electrophysiologic studies may be required. Although a subset of patients will have unexplained syncope despite undergoing a comprehensive evaluation, those with multiple episodes compared with an isolated event are more likely to have a serious underlying disorder....Cardiac syncope is the second most common type of syncope. [Vasovagal is the most common.] It results from arrhythmias, mechanical abnormalities, or structural abnormalities, and is generally seen in older adults....[San Francisco Syncope Rule] Predictors of serious outcomes were systolic blood pressure less than 90 mm Hg, shortness of breath, history of congestive heart failure, abnormal electrocardiography (ECG), and hematocrit level less than 30 percent.... Risk Stratification of Syncope in the Emergency Department (ROSE),...indicators...includes brain natriuretic peptide (BNP) levels of 300 pg per mL (300 ng per L) or greater; bradycardia of 50 beats per minute or less; rectal examination with positive fecal occult blood test; anemia (hemoglobin of 9 g per dL [90 g per L] or less); chest pain with syncope; ECG with Q waves; and oxygen saturation of 94 percent or less on room air. Patients are considered high-risk if any of the seven criteria are present." (Am Fam Physician. 2011 Sept 15;84(6):640-650, Evaluation of Syncope,
  • "Approximately 80% of patients who suffer sudden cardiac death (SCD) have underlying coronary artery disease. About 15% have valvular disease, dilated cardiomyopathy (enlarged heart), or left ventricular hypertrophy (enlarged left ventricle.) Risks factors include male sex (70% of sudden cardiac deaths occur in men) and vigorous activity, which increases the risk approximately 17 fold over normal daily activities. Additional factors include race (more prevalent in African Americans) and diabetes mellitus, as well as hypertension, tobacco use, and high serum cholesterol. Many sudden cardiac arrest investigators also believe that certain medications such as .... diuretics, and angiotension converting enzyme inhibitors can precipitate sudden cardiac death.(Inside Surgery, Michael Jackson's Sudden Cardiac Arrest,
  • "The presence of left ventricular hypertrophy in hypertensive patients, diagnosed by electrocardiographic criteria, is associated with a risk of mortality from cardiovascular disease three times greater than the risk associated with hypertension alone." In this study, LVH was found in 14%/20% (men/women) in normotensives and 25%/26% in hypertensives. (Prevalence of left ventricular hypertrophy in a hypertensive population, European Heart Journal (1996) 17, 143-14,
  • Doug's doctor assumed LVH was associated with being athletic. However, a paper published in the European Heart Journal noted: "We are uncomfortable with the currently accepted view that athletic left ventricular hypertrophy is a purely physiological adaptation with no pathological consequences, for several reasons. Firstly, although sudden cardiac death in competitive athletes under the age of 35 years is rare, up to 18% of post-mortems of athletes dying during sport suggest a condition which has been termed idiopathic left ventricular hypertrophy, where no clear reason has been found for the increase in left ventricular mass....The following, which may be associated with an adverse prognosis, should be measured: (a) left ventricular mass/mass index, (b) brain natriuretic peptide, (c) QT dispersion and (d) ACE genotype." (European Heart Journal (2000) 21, 351–353 Article No. euhj.1999.1783, available online at on Athletic left ventricular hypertrophy: long-term studies are required,
  • Left ventricular hypertrophy, whether established by ECG or by cardiac echo, is a strong independent risk factor for cardiovascular deaths and, in particular, sudden cardiac death in patients who also had a history of hypertension. (AHA Clinical Cardiology: New Frontiers Sudden Cardiac Death, Circulation. 1998; 98: 2334-2351 doi: 10.1161/​01.CIR.98.21.2334,
  • "Sudden death is a major health problem; about 250,000 sudden cardiac deaths occur each year among U.S. adults....Sudden cardiac death occurs at an average age of about 60 years, claims many people during their most productive years and devastates unprepared families." (Arrhythmias and Sudden Cardiac Death, A Publication of the American Heart Association,
  • Bradycardia is often associated with damage to heart tissue from some type of heart disease. (Mayo Clinic,
  • People with hypertrophic cardiomyopathy (HCM) may have LVH, and can succumb to sudden cardiac death (SCD). Death is sometimes the first symptom. Treatment with diuretics "will exacerbate symptoms in hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance." (We don't know if Doug had HCM, but he did have LVH and was on a diuretic (Benicar HCT) for high blood pressure."Traditional risk factors for sudden death in individuals with HCM include unexplained syncope, family history of SCD, marked left ventricular hypertrophy (≥ 30 mm), ventricular tachycardia, and a decrease or subnormal (< 20mmHg) increase in systolic blood pressure on exercise testing. Non-traditional riskf factors include specific mutations in the genes encoding for troponin T and myosin and bradyarrhythmias (slow rhythms of the heart). (Wikipedia, often not a reliable source,
  • AHA article, Athlete's Heart and Cardiovascular Care of the Athlete Scientific and Clinical Update, Circulation. 2011; 123: 2723-2735 doi: 10.1161/​CIRCULATIONAHA.110.981571)
  • Neurocardiogenic (Vasovagal) Syncope, Comprehensive Cardiovascular Care Group. "Neurocardiogenic syncope cannot be detected in the office with a routine blood pressure or heart rate screening."


  • Micah True, ultra runner, died while running alone in the desert in 2012. The autopsy report indicated that True probably suffered a cardiac dysrhythmia during exertion due to unclassified cardiomyopathy. The left ventricle of his heart was concentrically thickened and dilated, and mild dehydration. According to the Associated Press, “While medical examiners couldn’t point to the cause of the heart disease, they said True’s left ventricle, the chamber of the heart that pumps oxygenated blood to the rest of the body, had become thick and was dilated. That can result in an irregular heartbeat during exertion." (Runner's World)
  • Ryan Shay, 2007, age 28. The autopsy report indicated he died of an irregular heartbeat caused by an enlarged heart (cardiac hypertrophy). There was also evidence of scar tissue (patchy fibrosis) in his heart, possibly from an old infection.
  • A 48 year old Dept. of Energy security force subcontractor died on 06/11/2007, right after running on a treadmill on an interval training routine. He had passed an annual physical on 06/22, and had a stress EKG and stress echocardiogram in May 2006, which provided no indication of coronary artery disease. CPR was administered immediately, and other resuscitation efforts by paramedics were ineffective. He did have hypertension, high blood pressure, was overweight, and a family history of heart disease. An autopsy revealed cardiomegaly, acute coronary insufficiency and severe coronary atherosclerosis. See investigation report.
  • Jim Fixx, 1984, age 52. The author of "The Complete Book of Running" was found dead alongside the road. An autopsy found severe blockages in all 3 of his coronary arteries, so he probably either died of a heart attack or cardiac sudden death. ....a setup for heart attack or sudden death. He had not had a physical in years, had a history of obesity and smoking, and also had a strong family history of coronary artery disease in his family: his father had a heart attack at age 35 and died of his second one when he was 43. (Source: Athlete's Heart Blog)
  • Daniel Langdon, 36 and Jonathan Fenlon, 26 died in 2009 during the Detroit Half-Marathon. The autopsy results for both listed cardiac dysrhythmia as the cause of death. 65 year old Rick Brown also died from "heart disease." Langdon and Brown collapsed between the 11- and 12-mile markers. Fenlon collapsed just after finishing the 13.1 mile race.





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