While campaigning in Las Vegas last October, Vermont Senator Bernie Sanders began experiencing tightness in his chest. He was rushed to a hospital where he was diagnosed with a heart attack and had two stents implanted to open blocked arteries.
Despite little details about his cardiac condition, the event cast a cloud over his candidacy.
At the time I asked (and answered) a few questions): Is it appropriate for voters to lose confidence in Sanders at this point? He was already the oldest candidate in the race at age 78 years. Would he survive a 4 year term in the grueling position of head of the free world?
We now have more details to better answer these questions.
On December 30 of 2019, a letter from Brian P. Monahan, MD MACP on a letter head which reads in all caps “THE ATTENDING PHYSICIAN:Congress of the United States” to The Honorable Bernard Sanders was released.
This letter summarized Sanders’ “general health history and current medications” as Sanders had requested
Monahan, an oncologist by training, examined Sanders on 12/19/2019 at which time he found the senator was:
” 6 feet tall and 174 pounds. His blood pressure was 102/56, with a pulse of 62 beats per minute. His total cholesterol was 117 milligrams per deciliter of blood, HDL cholesterol (or “good” cholesterol) was 32 milligrams, and LDL cholesterol (or “bad” cholesterol) was 58 milligrams.”
With the exception of the low HDL these are good numbers and they indicate that Sanders LDL/bad cholesterol was at the appropriate goal post MI of <70 mg/dl. I would be a little concerned about the lowish BP of 102/56 in a 78 year old man but this likely reflects to some extent medications he is receiving to strengthen and protect his heart muscle.
Past Medical History
Next, Monahan summarizes Sanders’ past medical history
Over the years you have been treated for medical conditions including gout, hypercholesterolemia, diverticulitis, hypothyroidism, laryngitis secondary to esophageal reflux, lumbar strain, and complete removal of superficial skin lesions. Your colorectal cancer screening is up to date. Your past surgical history consists of repair of left and right-side inguinal hernias by laparoscopic technique and a right true vocal cord cyst excision. In November 2019, a follow-up ENT evaluation of your vocal cords for hoarseness was stable. You have no history of tobacco use, exercise regularly, and seldom drink alcohol.
Now we know some Bernie’s characteristic voice is due to a vocal cord cyst and that he is following a healthy lifestyle with regular exercise and no cigarette smoking.
What Happened In Vegas: The Myocardial Infarction
Monahan’s description of the heart attack (myocardial infarction or MI) Sanders suffered in Las Vegas gives more information than I had seen previously but is still lacking in details which I felt were important to know: troponin level and ejection fraction
The most significant event in your recent health was your admission to the Desert Springs Hospital in Las Vegas Nevada on October 19 2019. You experienced myocardial infarction due to an acute blockage of a coronary artery. In the initial hours of your evaluation, you were found to have an elevation of cardiac muscle proteins in your blood accompanied by diminished heart muscle strength and chamber wall motion reduction as determined by echocardiogram. You underwent prompt cardiac catheterization with identification of the narrowed segment of the midportion of the left anterior descending coronary artery. The narrowed segment was re-opened followed by the placement of two drug-eluting stents, a procedure that is referred to as primary percutaneous coronary intervention (Per). You received standard treatment with medications to improve your heart function and provide antiplatelet therapy required by your stents. You were released from the hospital three days later and returned home.
The exact elevation of the cardiac muscle protein, aka troponin, level is not reported.
He indicates “diminished heart muscle strength” determined by an echocardiogram and this is the ejection fraction (EF) but the exact percent EF is not given.
In my previous post on Senator Sanders I wrote
The size of Sanders’ heart attack is an important determinant of his prognosis. The more myocardial cells that died the larger the damage. We can detect and quantify heart attacks with a blood test using a cardiac specific protein called troponin.
Some heart attacks are tiny and only detected by very slight increases in the troponin in the blood whereas larger ones result in large increases in the troponin. What kind did Sanders have?
The more damage to the main pumping chamber of the heart, the left ventricle, the weaker the pumping action as measured by the ejection fraction. The lower the ejection fraction the more likely the development of heart failure. What is Sanders ejection fraction? Does he have any evidence of heart failure?
Heart Failure?: Signs Or Symptoms?
Later in his letter Monahan indicates
You have never had symptoms of congestive heart failure
This is an interesting turn of phrase. The doctor is not stating clearly that Sanders did not have congestive heart failure (CHF)
We diagnose CHF by eliciting certain symptoms such as shortness of breath or fatigue and observing certain signs such as crackles in the lungs, distention of the jugular veins, or swelling in the legs. These findings are combined with lab tests (BNP or pro BNP) and imaging studies (chest x-ray, echocardiography).
Given Monahan’s phrasing I suspect there were signs and/or abnormal labs that suggested CHF on his presentation with chest pain. The good news is that subsequent testing indicates no CHF.
Monahan goes on to describe current medications:
Your current daily medications include atorvastatin, aspirin, clopidogrel, levothyroxine, and lisinopril
The aspirin and clopidogrel are anti-platelet agents which are standard after implantation of drug-eluting stents like the two Sanders received at the time of his MI. They help keep the stents from stenosing or clogging up.
The atorvastatin is a statin/cholesterol lowering drug which should be given post MI in high dosages (40 to 80 mg daily) to reduce the risk of progression of the atherosclerotic plaque in Bernie’s coronaries which caused his MI. The atorvastatin has lowered his LDL to <70.
Lisinopril is an ACE inhibitor which is likely being utilized in this case to help strengthen and protect his heart muscle after the MI. Typically this would be used in conjunction with a beta-blocker however later in the letter, Dr. Monahan indicates Sanders was taken off a beta-blocker:
Several of the medications you initially required (blood-thinner, beta blocker) were stopped based on your progress. Your heart muscle strength has improved
Why Was The Beta-Blocker Stopped?
I see two possibilities, one portending a good prognosis and the other a bad prognosis.
Beta-blockers have been shown to significantly improve outcomes post MI in patients with depressed EF. The normal EF is >55%. Did Sanders’ EF improve to the point where the doctors felt beta-blockers would no longer be beneficial? This would be a good prognostic sign.
The other possibility is that Sanders’ blood pressure was so low on the beta-blockers that he was weak or dizzy. This would be a bad prognostic sign.
A third possibility seems less likely to me: excessive heart rate slowing on a beta-blocker. Given his resting heart of 62 bpm on no beta-blocker he should have been able to tolerate at least a low dose of beta blocker.
Cardiac Testing Post MI
After Sanders returned to his home in Vermont he saw his personal cardiologist Martin LeWinter and underwent further testing which according to Monahan showed the following
The heart chamber sizes, wall thickness, estimated pressures, and heart valves are normal.
I’m presuming this information comes from an echocardiogram. One of the key pieces of information that would come from this same echocardiogram is the ejection fraction. Why doesn’t he mention the EF?
Several 24-hour recordings of your heart electrical activity indicated no significant heat rhythm abnormality.
So Senator Sanders had at least two Holter monitors. This is not the norm post MI and I have to think he must have had some significant arrhythmias on telemetry while hospitalized to prompt these investigations. What rhythm abnormalities prompted multilple Holter monitor studies?
Sanders also underwent a treadmill stress test in December which is the norm post MI. Findings were summarized by Monahana
a successful graded exercise treadmill examination monitoring your heart function, muscular exertion, and oxygen consumption that indicated a maximal level of exertion to 92% of your predicted heart rate without any evidence of reduced blood flow to your heart or symptoms limiting your exercise performance. Your overall test performance was rated above average compared to a reference population of the same age. The cardiac exercise physiologist who evaluated your results determined that you are fit to resume vigorous activity without limitation.
A letter from Dr. Phillip Ades indicates this was a cardiopulmonary exercise test and it appears maximal aerobic capacity was measured directly but this number is not revealed.
However, this type of stress test is not capable of monitoring “heart function” and Monahan’s statement that there was no “evidence of reduced blood flow to your heart” can only mean there were no EKG changes as blood flow to the heart was not directly measured.
Fitness To Continue Campaigning And Serve As President
Senator Sanders’ doctors conclude based on all the evidence they have that he is fit and able.
In addition to the letters referenced above, Mr. Sanders’s personal cardiologist, Martin LeWinter wrote a letter (which I can’t locate) which states that Mr. Sanders had experienced “modest heart muscle damage” but that his heart function was now “stable and well-preserved.”
Once more, the two things I would like to know are not being precisely described.
Heart muscle damage would be precisely assessed by the maximal troponin level during his MI. Modest is defined as “not large” in the Cambridge English dictionary.
Heart function would be precisely assessed by the ejection fraction. Well-preserved is most frequently used to describe older things or people that are in good condition or don’t appear as old as they really are. It’s often used to describe left ventricular function but is vague. Why not just state the ejection fraction?
It would also be nice to know what coronary artery was stented and what was the status of the other coronary arteries that weren’t stented.
“At this point, I see no reason he cannot continue campaigning without limitation and, should he be elected, I am confident he has the mental and physical stamina to fully undertake the rigors of the presidency,”
I have a lot of confidence in Dr. LeWinter’s (see below) integrity and judgement and therefore would agree with his conclusions. I’d feel even more confident if I had access to all of Senator Sanders’ relevant data.
N.B. I recognized Dr. LeWinter’s name as he has been a prominent figure in the area of pericardial disease and heart failure research.
His CV is very impressive.
Dr. LeWinter is Professor of Medicine and Molecular Physiology and Biophysics and Director of the Heart Failure and Cardiomyopathy Program at the University of Vermont. He received his undergraduate degree from Columbia University, his M.D. from New York University and sub-specialty training in Cardiovascular Disease at University of California, San Diego. In addition to heart failure, cardiac hypertrophy and myocardial dysfunction Dr. LeWinter has had a longstanding interest in pericardial disease. Dr. LeWinter has received continuous research support from the NIH for over 35 years and is the author of over 190 original research papers, over 60 book chapters and review articles, and the Editor of two books. He is a Fellow of the American Heart Association, the American College of Cardiology, the Cardiovascular Section of the American Physiological Society and the International Academy of Cardiovascular Sciences, and a member of the Association of University Cardiologists. Dr. LeWinter has served on numerous Editorial Boards and research review committees and is an Associate Editor of the journals Circulation and Coronary Artery Disease.