<![CDATA[Brian Chesnie, M.D.-Board Certified Cardiologist & Lipidologist Newport Beach - CARDIO TOPICS]]>Tue, 13 Oct 2020 01:32:49 -0700Weebly<![CDATA[DIFFICULT CHOICES IN COVID ERA]]>Thu, 14 May 2020 19:15:01 GMThttps://www.chesniehearthealth.com/cardio-blog/difficult-choices-in-covid-era Hello everyone!

I’d like to thank you all for so many appreciations and positive responses to the letters I’ve been sending out since the Covid-19 virus, the Coronavirus, came into and changed our world.
The feedback has been very positive which I really appreciate, because I’ve been trying to present some realistic perspective, in the midst of so much created bone-chilling fear.

This is now a very difficult time we live in, and for so many different and multi-layered reasons, much of which is also now political!

Some of what I’d like to say may be somewhat politically incorrect, but I would like to try to continue with a realistic and personal perspective.

I’m a doctor and a cardiologist, and this is how I see it:
I checked the CDC website, and asked what the death rate is in the United States over the past 10 years. You can all check it out. The range is about 2,800,000 people dying per year in the United States. (Always less than 3 million.)  I’ve mentioned this before in a previous letter, but the number one cause of death is cardiovascular disease at about 850,000, followed by strokes, (which is also mostly an atherosclerotic, arterial disease). Then, followed by cancer, unexpected deaths, (usually tragedies: murder, car accidents, other accidents, suicides, drug deaths) pneumonia, infectious disease, flu, and “others”!

I’ve also previously presented some information on annual flu season, with the millions of people who get it (DESPITE THE FLU VACCINE!), get hospitalized, and the range of 30,000 to 65,000 who die annually from this viral contagion! Viruses continue to mutate so every flu season is a mutation of a previous influenza virus.
Despite this, no one has previously ceased flying in airplanes (whereby we inevitably get sick from all the sneezing and coughing of those next to us and behind us), and no countermeasures have ever been put in place, EVER, to mitigate behavior during flu season.

This has now been described as a Pandemic, something that we have not apparently faced before, but why? We had the Spanish flu in 1918, with 60 to 80 million further deaths added upon the ravages of WW1, the Asian flu in the 1950’s, Polio, all of which were quite vicious, and obviously over the years, other viral illnesses that have caused great degrees of suffering.

This virus, was possibly leaked out from a lab in Wuhan, China (you should all know the stories around this), and  then manipulated by the Chinese government to keep it hidden, to “lockdown“  travel in China, and to allow up to 500,000 people to travel world- wide.

It appears to be highly contagious, but with quite a low level of high degree illness and death, despite the fear and terror brought upon us by the media.
Yes, many older people have died, in nursing homes, and as well, with chronic morbid illness: over the age of 65, (I’m older than that!) having obesity, diabetes, hypertension, cardiovascular disease, pulmonary disease, and other organ system diseases.

This is indeed a calamity, with so many getting sick and dying, and certainly with so many dying, the sadness is overwhelming to family and friends. Almost always!...
But here’s the hurtful thing: Dying is where we all end up!
We’re only here for a small moment of time, for many it’s never enough, but it is what it is. Many die too young, some die maybe at the right time, (which is never the right time), and some live too long!I’m sorry to say this, but it’s true!

And yes, there are the outliers, the young, the otherwise healthy, who get stricken and succumb in the most sad and unexplainable ways. (You still have to wake up every morning being lucky, because it’s the random chance of life!)

I’m going to try and address some perspective here based on a personal story:
My Mother, Henrietta died last year. She was 96 years old and she had a wonderful, complete, and fulfilling life. She was loved and admired by many, and she was a leader in her community. She was self-sufficient and terrific up to 94. She then had a stroke, she survived, but she then spent the next year and a half diminishing, waking up every morning regretting that she was waking up. She lost her thought processing, (I could no longer speak to her on the phone), she became bed ridden, and she required 24/7 care. If she had a catastrophic event, such as a cardiac arrest, a pneumonia, another stroke, anything that would have taken her, she and the family all agreed that she would die naturally: No Code, no heroic measures, no ventilator, no prolonging her life. Thus, if she got the flu, or if she got the Covid Virus, and if she died from that, then that would have been ok. Most certainly for her! There comes a time for all of us when your time is up! And more often than not, it’s nothing that any of us are in control of.

Certainly sensitivity, correct behavior, well thought out protocols, decency, practicing good medicine and nursing,  should always be present...But when a vicious virus is attacking our biological selves, and the death rates are higher in the elderly and the ill, then perhaps there’s something to be said about the “natural way of things”.

I previously wrote that our experience of “modern medicine” is about 75 years old! Consider the invention of insulin in the 1920’s, and antibiotics (Penicillin) around World War 2). With the unfolding of “modern medicine” there is so much that we can address, take care of, manage, and sometimes cure, so there is a perception that everything must be done, and when the outcome is unsuccessful, and leads to death, all too often, it is someone’s fault! Sometimes that’s true, but way more often, it is the natural end of a life despite everyone’s very good efforts.

A word about public health: I’ve been very impressed by the Presidential Task Force, and the people on it. They were all dealing with an unknown situation!  Look how easy it is to be the arm chair quarterback on Monday morning and find endless criticism as to when and how this was all done wrong. They, including the President, and the Vice-President, and all those participating, have been utterly tireless, not sleeping, presenting information and trying to soothe the public spirit the best they can, and in the face of endless rudeness, criticism and rancor from so many in the media. This was a new thing, and no one even now really knows where it’s going!

All the doctors I know went through medical school, further training, specialization in the medical and surgical fields, and we all take care of people with many, many health problems. Most are practitioners, and many also went into academic medicine, doing basic, and clinical research, writing papers, teaching, etc.
Then there are those who went into public health from various clinical backgrounds, and I must say it’s a different discipline!
Dr. Fauci is getting a lot of heat now, particularly as things are moving so slowly to get back to an acceptable “Normal” I do think he tends to Speculate and Prognosticate more than he should. The job in public health is to create models and trajectories of disease infiltration. The job is to create the “worst case scenario” particularly when you’re working for the President of the United States: because the worst case scenario is a possible outcome, And the Administration needs to plan for that... and no one knows what will really happen until it’s happened!

This is an intellectual discipline about public health policies, behavior, population control, bureaucratic rules, and the input of control and authority: so we’re seeing it blend into various forms of political authoritarianism!
The longer it goes on, the worse it gets, and we are suffering through a huge collapse of our and the world economies.  Two months ago, we had the best employment and the best economy in our country’s history, and now we have the worst since and including the Great Depression of the 1930’s.

I think that our leaders, our writers, our pundits and commentators are lacking the imagination to really articulate how horrible and tragic this is. This circumstance may lead to human destruction and death perhaps more that the virus! The Depression created utter human misery: People starving, the breakdown of law and respect for our institutions (already going on), families being torn apart: parents had to give their children away (go watch the excellent movie, Seabiscuit again!)

Which leads to this:
This is a war with an invisible enemy, which has been the analogy already articulated by the President.
It may not be a geo-political war yet, but this has been a viral attack which has changed our world, with loss of work, identity, health, life, money, school, sports, culture, and everything that we accepted as being normal in our lives

The media and certain politicians are continuing to foment fear. Yet the original advisements still hold: allow for appropriate social separation, stay home if you’re sick with a fever, a cough, a cold, etc. Wear an appropriate mask in the appropriate situations! Wash your hands over and over! And be respectful to others!

We must not cave in to fear, and paralysis. We must look the monster in the eye, and fight back with our good common sense, our need to Make A Living, Support Our Families, Nurture Our Children, and Help Our Elders!

The three-phase opening brought forth by the Task Force is rational and well thought out, and some politicians are proceeding with it, while others are holding back and continuing with rules to continue to control human behavior. There must be a process of moving forward! Europe is doing it, some states are doing it, some regions in some states are doing it. WE MUST PROCEED! We must not let our economy, our culture, our world, our well- being collapse because of this. We must be brave and have the commitment that we will not be defeated; WE MUST AND WE WILL PREVAIL!

Because at the end of the day, we will come to an end! And what we take with us, is hopefully the realization that we did our best!


<![CDATA[COVID 19- THE POWER OF WORDS]]>Thu, 02 Apr 2020 19:43:27 GMThttps://www.chesniehearthealth.com/cardio-blog/covid-19-the-power-of-wordsI wanted to say something about Dr. Fauci’s comments yesterday. Yes he is a brilliant scientist and as well a great infectious disease epidemiologist.

His words yesterday were jarring: that we would see millions of cases of patients with Coronavirus and the surge would see between 100,000 to 275,000 deaths!


Some of you may know that after my cardiology fellowship training at the University of Toronto, I became a Lown Fellow at Harvard School of Public Health. My mentor was Dr. Bernard Lown, who was also renowned as a great scientist, and also a great clinician. If some of you think that I do a good job as a clinician and in “taking care of people”, I learned most of those skills from him.

He said something once that got my attention:


That means, watch out what you say to patients about their future!

You can heal and you can hurt, and the words, though often based on experience, are nonetheless, “SPECULATIVE”.

In Cardiology, we’re really good with it:

“You’re next heart beat may be your last one!”

“You’re a walking time bomb!”

“You have the ‘widow maker’!”

“Most of your heart is dead!”

“Your heart virtually exploded!”

I’ve heard it all!

There are times I have said the wrong thing to a patient and I kick myself afterwards!

From my teaching I have always tried to teach patients about their problems, and to try and create optimism and educational choice making.

In Medicine, words can “hex” and damage, or they can be used as tools for healing!

The old adage stands true:

“Hope for the best”, “Plan for the worst”.

I’d like to say, as a humble clinical cardiologist who does his best to “take care of people”, that perhaps Dr. Fauci was planning for the worst! We don’t yet know how many millions of people will get this contagious virus, and currently we know that the mortality in the US is less than 1.5 %, but to state on an interview with CNN that there could be between 100,000 to 275,000 deaths is a speculative statement that only sows more fear.

Again, try to hold on to “PERSPECTIVE”!

<![CDATA[COVID 19- FEAR MONGERING]]>Thu, 02 Apr 2020 19:31:49 GMThttps://www.chesniehearthealth.com/cardio-blog/covid-19-fear-mongering
​I’m finding it distressing that the news outlets are showing the “daily counts” every moment of the day!

Worldwide and US daily numbers of new cases of Coronavirus and daily death counts! And the percentage increase daily!

This does nothing but create further fear!

If only they would post next to this information the US year to date influenza rates, the total number of cases (greater than 20,000,000), the number of hospitalizations,  (greater than 500,000), the number of deaths  (greater than 20,000).

This would help create perspective!

To help create further perspective, the 2019 death rate in the US from all of heart disease was about 840,000). Of these, about 366, 000 were from Sudden Cardiac Death.

There were about 750,000 myocardial infarction (heart attacks ) in the US last year. Of these, about 400,000 die from the heart attack and from heart failure.

There were over 140,000 deaths from stroke.

We are biological and we’re on the planet for a only a limited period of time.

I just spoke to a life long friend in Toronto yesterday. He is a notable physician there.

Both he and his wife tested positive for the Coronavirus and they have been quarantined at home the past 2 weeks. They both had a sore throat, fever, mild flu like illness, and they are better.

We should all be respectful of this illness and yes people have died and will die, but I hope that this information provides some perspective and helps lessen “the Fear Count”!

<![CDATA[NY TIMES ARTICLE ON EVOLUTION AND HEART DISEASE]]>Thu, 08 Aug 2019 21:17:25 GMThttps://www.chesniehearthealth.com/cardio-blog/ny-times-article-on-evolution-and-heart-diseaseI had two patients send me this article from the New York Times written by Dr. Haider Warraich, M.D., who is a cardiologist. I found it interesting and wanted to share it with you. Click the button below!
<![CDATA[HEART ATTACK!! (WORSE THAN A ROOT CANAL)]]>Thu, 25 Apr 2019 19:36:21 GMThttps://www.chesniehearthealth.com/cardio-blog/heart-attack-worse-than-a-root-canal
​As I’ve previously mentioned in earlier essays, coronary artery disease caused by the underlying disease of ATHEROSCLEROSIS is by far and away the Number One cause of dying per year in the United States. Death occurs most commonly by Ventricular Fibrillation with over 400,000 people dying suddenly, most of them with underlying coronary artery disease. Another million people will have heart attacks, which may or may not kill them, and they may also end up with Congestive Heart Failure, which can be treated, but can also lead to significant incapacity and death. (I refer you back to my earlier essay on HEART DISEASE which explains the underlying disease process of Atherosclerosis and how it can suddenly create a sudden event causing a Heart Attack (Myocardial Infarction). In fact, most of our efforts as Cardiologists, are based around, not only taking care of these emergency- based problems, but also trying to thwart the progress and ongoing development of Atherosclerosis so that it doesn’t cross over to the clinical expression of coronary artery disease).

So, this topic, is Public Health Enemy Number One!

An actual heart attack is referred to in medical language as a Myocardial Infarction, (or MI), and is divided into 2 subtypes: Acute STEMI (ST Segment Elevation Myocardial Infarction), or NON-STEMI.

    This type of heart attack is the big 500-pound gorilla. A STEMI heart attack brings on a "full court press" at the hospital. When a patient arrives in the emergency room of any hospital with chest pain, they are triaged very quickly and evaluated if there is a heart problem. When an EKG is done- usually immediately-, and the EKG shows an ST elevation MI, very quick emergency protocols are triggered. This is all based on a concept called “ Door to Balloon Time”.
    This means, that if a person is having an acute heart attack (myocardial infarction, or MI, with the findings of ST elevation in the ER, certain medications are immediately given, the interventional cardiologist is called as is the heart catheterization lab team, and everyone gets to the Cath Lab as quickly as possible!
The time sequence of entry into the hospital to the moment the artery is “ballooned” open is measured and must be initially under 90 minutes, and is now expected to be under 60 minutes. This is a national health policy and something every hospital is assessed on.
We at Hoag, on a quarterly basis, are usually at the 100% level!
The reason why this time interval is so important, is because “Time Saves Heart Muscle”.
In other words, when a total blockage of an artery occurs, there is no flow of blood going down the artery and the area of heart muscle cells that are fed oxygen and nutrients are suddenly deprived. As time goes by, heart cells start to get injured and begin to die off. The longer the time, the more degree of injury and eventual cell death.
If the blockage is high up towards the source of the artery, the greater the area of heart muscle at risk. The farther down the blockage is, the area would become relatively smaller, so the damage to the heart may not be as big an area of injury and cell death.


A non-STEMI MI, is also known as an Acute Coronary Syndrome (ACS). The presentation of the patient may be the same with chest pain and other symptoms, but the EKG does not show the ST segment elevation. It will show other EKG changes, but the bottom line is that this type of presentation does not usually suggest an acute blockage of a specific artery, and is not considered as being the same type of immediate emergency as the acute STEMI MI is.
In this regard, we would usually observe and stabilize the patient first with a variety of heart medications. Certain tests may follow including further EKG’s, lab tests, echocardiogram and nuclear imaging tests, or special CT angiograms, and if necessary, a heart catheterization study to do an angiogram.  This may lead to further intervention with angioplasty and stenting, or even bypass surgery... or none of the above, and the patient is taken care of with the use of long-term medications. The reason for this is that the artery in this context is not usually completely blocked, and there may be various degrees of limited flow going through, and there may also be more complex coronary issues involving narrowing of other arteries.

Let me mention the immense skill, training, knowledge, and trouble-shooting capabilities of the Interventional Cardiologist, and the Cath Lab Team.
Firstly, because of the urgency to get to the hospital as fast as possible to “Get That Artery Open”, is a whole different story when an emergency occurs during the day , during regular “business hours” versus evening, night time, holidays and weekends. The stress level is very high. The On-Call Phone is always at your side, even if you’re going to the bathroom, or having a shower, or you’re trying to sleep in the middle of the night. When the call comes, you go, and you go as quickly as you can.

The doctor and the team are walking into a completely unknown situation, each and every time. Some of the issues are:  how much time went by before the patient even showed up? What is the clinical stability of the patient? What is the intensity of their pain? What is the extent of the damage and the degree of heart failure? Is the blood pressure stable, or are they in cardiogenic shock? Are they having arrhythmias? Which ones? Are they having cardiac arrest and ventricular fibrillation? Do they need balloon pumps and other heart augmentation devices? (On many occasions we don’t even know who the patient is, or what the story was.)
Where is the culprit blockage? Which vessel? How complex is it? Does it involve one artery, or is it at a bifurcation of 2 arteries? How long is it? How many other narrowings are present? Can we get the wire passed? Can we get it through the blockage? How do we prevent the wire from perforating of dissecting the artery which can lead to death? How can we stabilize the heart rhythm when recurrent cardiac arrest keeps continuing?
Now I bet you are wondering WHAT IS AN ANGIOGRAM, ANGIOPLASTY, AND STENT? Click on the link provided to watch this video at your convenience (FYI- Skip the Ads)!. It does a good job of demonstrating what we do as cardiologists in the cath lab.

Here’s a Little Joke:
A mechanic is working on the engine of a cardiologist’s nice car. He had to change a valve. It took several hours. He was complaining to the doctor that he only made $75 an hour, and given the car he was driving, the doctor must obviously make more an hour than he did. Whereupon, the cardiologist said, yes I understand, but when I work on an engine, it’s running! (This is obviously an old joke because in this era, I think plumbers and mechanics are now actually earning more per hour than we are! LOL)

Coronary artery disease does not necessarily always unfold with gradual plaque buildup to the point of blood flow compromise and then the artery finally blocks off.  This does happen to many people and their presentation is often one of recurrent exertional ANGINA chest discomfort, and/ or the stress tests and echoes and scans will show abnormalities that will lead to an angiogram and then stenting or bypass surgery. These plaques that compromise coronary blood flow are fixed, rigid, and calcified.

However, the majority of people having an acute Myocardial Infarction do not have these very high grade obstructive narrowings causing that specific event.
These people have plaques that are not fixed, rigid, and calcified. They may not be impairing coronary blood flow at all. They may narrow the artery by 20% to 50% which is not sufficient to cause flow impairment. BUT they are VULNERABLE and INFLAMED and SOFT, and may become UNSTABLE. 
I compare these plaques to “Creme Brûlée” because they have a “hard cap” filled with cholesterol and inflammatory products and they can unexpectedly and unpredictably FRACTURE or RUPTURE and when this occurs, the artery is acutely blocked and heart attack has begun.
Here are 2 stories where 2 people survived: One who got to the hospital quickly, and had restoration of blood flow through a blocked artery, and his heart function got back to normal, and he was given a new lease on life.
The other, did not get to the hospital quickly because he didn’t even know he was having a heart attack. Unfortunately, he has been left with a permanently damaged heart. However, with good medical care, he is still alive and doing pretty well, and he realizes how lucky he has been.
Both of these patients had “ruptured plaque”.

Patient # 1 is a 66-year-old man. He considers himself to be in very good shape and goes to the gym a lot and does a lot of weight lifting. He also rides his bicycle several times a week from the Newport Pier to the Huntington Beach Pier. However, he was noticing a sharp and aching pain to his left chest muscle area when he would lift himself into his bed. (It is a bed that is fairly high up off the ground, so he has to face the bed backwards, and use his arms to lift himself up). He also noticed the same pain when he moved his arms across his chest. He did not have any chest discomfort when working out, or when riding his bicycle.

I felt that he was having pain from strained pectoral chest muscles, from his weight lifting, and provoking it with his various movements and body positions. He did not have any pain or discomfort that sounded like angina when he was exerting himself.

However, this patient has risk factors including diabetes and high cholesterol numbers. He was not paying attention to his diet, and he was not on the correct doses of medications- when he took them. I referred him to a different endocrinologist, and I changed his cholesterol medications to get his levels into the correct range. I had him do a treadmill, and he exerted well, without discomfort, however, he did have non diagnostic stress test with non-specific abnormalities on the EKG. Therefore, we went on with a more precise study, called a nuclear imaging study.
All of his heart testing was perfectly normal.
Interestingly, right after he finished his study (which was normal showing no perfusion abnormalities that would indicate blockage), he went to have lunch with some friends. While eating he had the sudden onset of a heavy, crushing, quite severe central chest discomfort, associated with sweating. He never had anything like this before. His friends did not ignore this and drove him immediately to the hospital. His EKG showed an Acute STEMI.

He was taken immediately to the Cath Lab and the angiogram showed a total blockage of his major left coronary artery (left anterior descending artery). Though it may sound straight forward, the artery was successfully opened with a very good door to balloon time and it was successfully stented.

He went home 2 days later, and went on to full recovery (His initial left ventricular function was diminished due to the acute injury, but when we repeated his echocardiogram 6 weeks later, it was perfectly normal).
Though he initially blamed us for missing something, he demonstrated no insight into the fact that he never took his medications in a committed way and the control of his diabetes and cholesterol was, in fact, quite inadequate. He also had a hard time understanding the concept of plaque rupture!  But many people have trouble understanding this.

Patient # 1 has not had a recurrence. He is still exercising, and is now on correct medical management involving good diabetes treatment, cholesterol numbers are very good with LDL driven well below 70, and he is on appropriate combination of anti-platelet medications (blood thinners).

Patient # 2 is a 70-year-old man. He was sent over to my office by his family doctor because he was short of breath, weak, tired, loss of appetite and energy, and he was in atrial fibrillation but was not at all aware of his heart beat. His heart rate was moving along appropriately, not too fast. His EKG was very abnormal, showing an anterior wall Myocardial Infarction, though he wasn’t aware that he had ever had a heart attack!
However, on questioning, he recollected that 8 days before, he was walking through the airport and he had upper mid abdominal and upper left abdominal pain that was quite severe. He actually went to a local Emergency Room and was found to have kidney stones. Because it was felt that the pain he was having was due to the kidney stones, no heart work up was done.
I explained to him that the EKG in our office showed he had had a heart attack, and that he was in CONGESTIVE HEART FAILURE, which was completely astonishing to him. He came back the next day for an echocardiogram which confirmed the story: profound weakening of the left ventricle! We measure the performance of the left ventricle which is called the EJECTION FRACTION (EF).  A normal EF is from 50% to 75%.

His EF was only 16%!  This means he was really in bad shape with very, very weak heart performance, and also with significant leakage of the Mitral Valve.

So he now had a completed event with full and terrible damage done to his heart. He was now in severe Congestive Heart Failure, by which he could die, and he was also at significantly increased risk of dying of SUDDEN DEATH by Ventricular Fibrillation.

He was immediately admitted to the hospital and started on all the appropriate medications for correction of heart failure, protection of life-threatening arrhythmias, as well as treatment for his atrial fibrillation, and appropriate lowering of his cholesterol.

He also had a heart catheterization (angiogram), and interestingly, we found that he had a single blockage of the left anterior descending artery (LAD) which had spontaneously reopened with what was now a 50% to 60% narrowing, so he did not need a stent.
What apparently happened, was that he had a plaque rupture blocking the artery causing the heart attack, likely when he was going through the airport, and by good luck, at some point the artery re-opened! However, not before very serious damage was done to his left ventricular function.

He went home on all of his new medications and he was given a LIFE-VEST that he had to wear all the time because of the increased risk of having a sudden cardiac arrest.
The Life-Vest is an external defibrillator that you wear for several weeks before we are allowed to put in an Implantable Cardioverter Defibrillator (ICD). In some people we will see an improvement in heart function over a 6-week period, so they do not require a permanent ICD, whereas other people continue to have problems with weak hearts and heart failure and they require an ICD for hopeful prevention of sudden death, and in some cases further therapy for correction of heart failure. The ICD detects life-threatening arrhythmia and will shock the patient hopefully back to normal rhythm if the arrhythmia reaches predetermined thresholds that indicate a life-threatening situation.
(The topic of Sudden Death and the development of the Implantable Cardioverter Defibrillator (ICD) is an entirely separate essay as is the topic of Congestive Heart Failure)

He continued to have problems with breathing, exhaustion, weakness and his heart function over this period did not improve, so he, in fact, received a very special device which is a Bi-Ventricular ICD. This ICD not only treats and terminates life threatening arrhythmias such as Ventricular Tachycardia, and Ventricular Fibrillation, but also paces the heart in both left and right ventricles, and may improve heart contractility and improve the clinical problem of congestive heart failure.

Two years later, he is alive and doing pretty well. He is able to walk now without shortness of breath, and in fact, says he feels pretty well. His heart function has improved but not up to normal range. He still has some weakness of his heart, but his life quality is quite good and he is extremely grateful.

Each patient who has a heart attack is unique and each one is an individual human story. I have given you a picture of the enormity of what we face with CORONARY ARTERY DISEASE and MYOCARDIAL INFARCTION. Heart Attack can be a devastating HEALTH ATTACK and can completely change your life or take your life.
 Please refer back to my earlier essays on Heart Disease, Lifestyle, Hypertension, and Statins. These essays will explore many of the topics touched upon in this essay, and will give you further insight into the importance of what we do for disease prevention, as well as provide encouragement for good health.
<![CDATA[OVERVIEW OF BIO-IDENTICAL HORMONES]]>Thu, 07 Jun 2018 18:25:30 GMThttps://www.chesniehearthealth.com/cardio-blog/overview-of-bio-identical-hormonesMost of you are aware that for many years, I have been interested in practicing preventive cardiology. This dates back to over 10 years ago when I got board certified in Clinical Lipidology. Thus, in addition to taking care of many people with active and serious heart problems, I have also worked hard in trying to prevent these problems from happening, and to give people the potential of living better lives.

About 4 years ago, I became increasingly interested in the medicine of hormones and how they work in your body, particularly as we age: the question being, “How can we maximize our potential as human beings, in terms of good health, vigor, energy, and mindfulness, as we age?”

In 2017 I studied extensively and participated in 4 courses, over a total of 100 hours of course material, on the subject of “Mastering the Protocols for Optimization of Hormone Replacement Therapy”, taught by Dr. Neal Rouzier: a fascinating learning experience.

I would like to present here, an overview of the concepts of natural hormone replacement therapy. I won’t be discussing specific hormone literature, as I have previously done with testosterone, and also vitamin D. There will be further essays written on estrogen and progesterone, and thyroid at later times. 

This essay will be predominantly a series of passages from Dr. Rouzier’s booklet of “Bioidentical Hormone Replacement Therapy” and should give you very good insight into what this is all about.

“Conventional medicine has always held the belief that aging is inevitable and that the progressive deterioration that occurs in our adult years cannot be altered. This is simply not true. We have also been lead to believe that the diseases of aging, such as heart disease, stroke, cancer, and senility, are all a part of the normal aging process. The downward spiral of physical and mental decline that we have come to accept as a natural part of growing older is becoming recognized as somewhat controllable and preventable. The most effective  solution of any disease process is prevention of that disease. We are now in an era where mainstream medicine is now focusing on slowing down the aging process with the science of genomics, telomeric application and optimal hormonal supplementation. Research is showing that maintaining our hormone levels in a youthful state can help prevent the debility and illness that accompany the aging process. Hopefully this will lead to increased longevity by preventing the illnesses that usually lead to our demise, and more importantly is the possibility that our quality of life in our later years may be significantly enhanced.”

“Over the last 50 years research in the fields of endocrinology and immunology has improved our knowledge as to how and why we age. The rate and incidence of disease formation as well as the rate of aging are partially controlled by our endocrine and immune systems. The endocrine system regulates our body’s temperature, reproduction, growth, aging and immune system. Communication between the nervous system, the endocrine system and the immune system makes it possible for us to adapt and survive in our environment. It is through hormones that these systems interact with each other. Hormones are molecules that are released into the blood stream and exert biochemical effects on distant organs and cells. Hormones can affect every cell in the body by activating receptor sites on the cell and thereby cause an internal activation of protein synthesis and activity. The hormone’s effect is determined by a specific receptor site on the target cell. Hormones exert different actions on different cell types in different tissues. A decrease in the production of hormones begins in middle age and continues to diminish in a linear fashion until old age.”

“Hormones are either proteins or derivative of cholesterol. These molecules are manufactured in endocrine glands, which include the adrenal glands, the testes, ovaries, pancreas, thyroid, pituitary gland and pineal gland. When there is degeneration and aging of the organs, the levels of hormones diminish. In addition, the specific receptor sites on the cells tend to change and deplete and become less interactive with hormones as they once were in our younger years. Whether  the problem is low hormone levels or hormone resistance, the solution is optimal hormone replacement.”


“For many years, medicine has recognized the health benefits of replacing these waning hormones. For most physicians, synthetic hormones were the only option. Now it is possible to produce natural hormones that in every way match those produced by the body. Most hormones can be derived from plants, such as soy and yams. What is most important is that the end product is a molecule identical to the hormone molecule found naturally in the body. This applies to all hormones—thyroid, estrogen, progesterone, testosterone, DHEA. We have come to understand that synthetic hormones, which are chemically different that those naturally found in the body, can cause a whole host of side effects and even cancer. it does not make sense whatsoever to replenish with chemically different hormones when bio-identical hormones, to which our bodies are accustomed, are available.”

“You might ask, ‘if there are hormones available that are natural to my body, who do doctors prescribe synthetic hormones?’ The explanation involves the powerful pharmaceutical industry in the United States, politics and economics.



“Where does one fill prescriptions for natural hormones? There is a special type of pharmacy known as a compounding pharmacy. These are regular licensed pharmacies that are capable of providing you with any drug from pharmaceutical companies. But compounding pharmacies are able to do more. They are able to use the pure pharmaceutical grade hormone and compound it into the specific dose and form ordered by the physician. They can produce pills, capsules, liquids, and creams. This type of program is highly customized and personalized.”


“More people are beginning to realize that they no longer have to accept the fact that their health, appearance and function must deteriorate. They no longer want to accept growing frail and feeble...Science is creating a new paradigm of preventive medicine by allowing our bodies to remain stronger, healthier, and more vigorous...

"Hormone replacement therapy, however, is not a panacea. It will not reverse aging. It will not keep us permanently at one age. We will still continue to age and lose cells secondary to a process that is regulated genetically. With hormones we may be able to slow the precipitous decline that occurs after midlife; no sudden falling off in our physical and mental health. We hope to stay resilient. We aim for a gradual transition that will be less noticeable that it would be without hormone replenishment. The purpose is to simply replenish the hormones that already occur naturally in our body and boost them back up to the appropriate medically sound levels necessary to maintain youthful health and vigor. Which hormones to replenish, how much to replenish and how to adjust the hormones so that they have a synergistic effect is the art and science of the specialty of natural hormone replacement medicine, which is a key aspect to preventive medicine.”

Much appreciation to Neal Rouzier, MD, with whom I studied extensively to learn this very interesting area of medicine.

<![CDATA[VITAMIN D]]>Tue, 29 May 2018 16:43:04 GMThttps://www.chesniehearthealth.com/cardio-blog/vitamin-dMany people ask me on a daily basis about Vitamin D and what is its importance.

Despite its name, vitamin D is not a vitamin, but a steroid hormone made in the skin, (from cholesterol). The normal range is pretty wide, from 30 to 100, and it’s better to work up to the higher levels than maintain at the lower levels. It’s usually pretty easy to get to “normal” levels by taking up to 50,000 units of vitamin D3 a week for up to 8 weeks and then maintain at 1000 to 5,000 units daily. 

57% of patients in once study were judged to be vitamin D deficient, including 37% who consumed more than the recommended amount of vitamin D (at least 800 IU/ day). Although vitamin D can be obtained through the diet, most foods contain very small amounts, so humans are dependent on skin production to maintain normal levels ( or, with the addition of daily supplements.)

Vitamin D deficiency is important to understand in age-related morbidities. 

Meta-analysis of double-blind randomized trials showed that vitamin D reduced the risk of falling by 22%.

Low Vitamin D levels play a role in bladder incontinence, because there is poorer coordination of the muscles used to control urination. Low levels also play a role in age-related macular degeneration as well asl cognitive decline.

The lower the vitamin D, the greater the incidence of sarcopenia, or bone loss. Men and women with baseline levels less than 25 no LVH/L were more than twice as likely to develop sarcopenia.

Increasing the levels of serum vitamin D regardless of age, may reduce the risk of breast cancer. Vitamin D level of 35 ng/ml has associated with a 20% reduction in the risk of breast cancer. In another study, average  levels of 52 ng/ml had 50% lower risk of breast cancer than those with serum vitamin D of less than 13 ng/ml. Vitamin D intake of 2,000IU/day has been associated with vitamin D levels of 32 ng/ml. The higher level noted above corresponded to an intake of 4,000 IU of vitamin D per day.

Vitamin D may provide greater health benefits than previously thought, benefits that include not only improved bone health, but other effects as well. Increased vitamin D levels may decrease the risk of cancer, especially that related to colorectal adenomas. Elderly adults may even benefit from higher doses such as 2000 IU to 5000 IU daily. Vitamin D levels of 82 nmol/L and higher were also associated with a 50% lower risk of developing colorectal cancer. Some researchers are advocating even higher doses, up to 10,000 IU per day.

Lower levels of Vitamin D are associated with a higher risk of heart attack in a graded manner. High levels of vitamin D among middle-age, and elderly populations are associated with a substantial decrease in cardiovascular disease, type 2 diabetes and metabolic syndrome.

Vitamin D has been traditionally related to bone metabolism, although several studies in the last decade have suggested its role in muscle strength and falls, cardiovascular and neurological disease, malignancies, autoimmune diseases and infections. Vitamin D appears to be a hormone with several actions and is fundamental for many biological systems including bone, skeletal muscle, brain and heart. It helps to maintain physical strength in the elderly and is protective against falls.

Additionally, a study demonstrated that women with moderate to severe depression had substantial improvement in their symptoms of depression after they received treatment for Vitamin D deficiency. Both the presence and severity of depression were associated with decreased serum levels of vitamin D and increased levels of parathyroid hormone in older patients.

In a paper called Vitamin D for cancer prevention: Global Perspective, higher levels of vitamin D were associated with substantially lower incidence rates of colon, breast, ovarian, renal, pancreatic, aggressive prostate and other cancers. It was projected that raising the minimum year- around levels to 40 to 60 ng/ml would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three fourths of deaths from these diseases in the United States and Canada.

I hope that this little essay helps you understand and appreciate further the role of vitamin D.]]>
<![CDATA[TESTOSTERONE AND THE PROSTATE]]>Mon, 26 Mar 2018 18:54:46 GMThttps://www.chesniehearthealth.com/cardio-blog/testosterone-and-the-prostate This is a lecture that I prepared and I thought it would be enjoyable to read in this “slide show” format. It gives really good information regarding testosterone and how it interacts with the prostate. However, this is not fully accepted in the Urology community. I guess I’ve always been somewhat iconoclastic, but I sure have enjoyed the dozens and dozens of hours I’ve spent in studying these and other topics in great depth to learn what many docs don’t know.
Click the link below to download the presentation. I hope you enjoy reading through this!
Brian Chesnie, M.D.
File Size: 163 kb
File Type: pdf
Download File

<![CDATA[Testosterone: Cardiovascular Myths and Benefits]]>Thu, 11 Jan 2018 21:42:02 GMThttps://www.chesniehearthealth.com/cardio-blog/testosterone-cardiovascular-myths-and-benefits
I enjoy writing educational essays in this website to hopefully provide interesting reading material to my patients. 
I have previously written essays that include an overview of issues pertaining to prevention and how to achieve well-being. Included was an introductory essay of how your body’s natural hormones play important roles throughout life in maintaining the strength and well- being of your body. 
Over the past year I have taken a number of educational seminars and study in the area of optimizing your own body’s hormones to help improve health and well-being.
I’d like you all to know that I have recently written the exam and passed with flying colors and am now certified in this interesting area.
Following is an essay overviewing the benefits as well as the myths pertaining to testosterone therapy. This essay is derived from numerous peer review papers in the medical literature which convey significant benefit of testosterone therapy, and this essay will also touch upon some of the negative papers that achieved much media attention and conveyed significant misperceptions about this subject. 
I recently gave this talk at Cardiovascular Conference to the Department of Cardiology at Hoag Memorial Hospital.
 Testosterone is a hormone secreted by the ovaries, the adrenal glands, and the testes. The “Normal Range” is portrayed at about 250 to 900 pg/ml. This is an arbitrary setting based on up to 20 men in the 50 to 80 year old range. The ranges would be considerably higher in the healthy 20 to 30 year old group: consider about 500 to 2000!
Depletion of testosterone with aging (testosterone deficiency) includes symptoms of diminished libido, sense of vitality, erectile dysfunction, reduced muscle mass and bone density, mood change, depression, and anemia.
There are 2 papers in the medical literature written in 2013, and 2014 that received enormous media attention. These have determined to be very flawed papers, written with very faulty statistical design and flawed methods and conclusions. They both initially suggested that there was an increase in cardiac events such as heart attacks and strokes, but further analysis demonstrated incorrect interpretation of the numbers and incorrect conclusions. In fact 29 societies and 50 international experts have called for the retraction of these papers. One paper has had to make 3 corrections with apologies, and when re-done it actually showed that testosterone lowered the percentage of adverse cardiovascular events. The second paper had no control group, and in fact, it was based on merely handing out a testosterone prescription and did not assess whether the men were actually taking it!
One of the big confusions is that doctors think that testosterone increases the risk of clotting and what it does to the blood. This is simply not true.
The confusion is many doctors think that testosterone can cause a blood disorder called Polycythemia, which can increase the risk of clotting. This is because Polycythemia causes an increase in hemoglobin and hematocrit, (red blood cells) as well as an increase in white blood cell count and increase in platelets. It is the increase in platelets that causes the increase risk of clotting. 
Testosterone at high levels may increase the level of hemoglobin and hematocrit (red blood cells which carry oxygen to your cells)! This is something called “erythrocytosis”. Testosterone does not increase the level of white cells nor platelets and therefore does not increase the risk of clotting.
 In fact, over 200,000,000 people on the Planet Earth may have “erythrocytosis” because they live at over 7,000 feet above sea level and they don’t have an increased risk of clotting. In fact, the US Olympic athletes often train in Colorado at elevation in order to boost their hemoglobin and hematocrit!  It is not uncommon for the Sherpas who carry heavy loads in the Himalayas to have very elevated hemoglobin and hematocrit. They do not have an increased risk of blood clots.
Since those two studies, more than a dozen clinical trials and observational studies have provided additional information, with none demonstrating increased cardiovascular risk. On the contrary, several of these studies have suggested that testosterone therapy may be cardioprotective. Following are some examples:
A recent paper published in the Journal of Cardiovascular Pharmacology and Therapeutics by Traisch in 2017 compared a group of higher cardiovascular risk men treated with testosterone versus placebo: 360 men treated versus 296 on placebo;  a 10 year follow-up. The treated group had a significant lower incidence of death, heart attacks and stroke than the placebo group. Also noted was a reduction in waist circumference, and body weight, improvement in lipid profile and reduction of blood glucose.
In fact, the placebo group had 26 nonfatal heart attacks and 30 nonfatal strokes and the testosterone treated group had none. There were 21 deaths in the placebo group: 19 cardiovascular events including 5 heart attacks, 4 strokes, 7 heart failures, 2 thromboembolism, 1 Pulmonary embolism. There were 2 deaths in the testosterone treated group: 1 person died after a surgical procedure, and 1 person died in a car accident.
A series of papers called the Testosterone Trials showed at 2 year of follow up, 8 heart attacks in the placebo group, and 1 heart attack in the testosterone treated group. There were improvements in cholesterol levels, blood sugar levels, blood pressure, heart rate, weight, waist circumference...and these were added benefits in addition to the presence of statins.
Another paper showed an 8 year weight loss of 17-24% with testosterone therapy comparing favorably to the 10 year weight loss of 14%-25% seen with bariatric surgery.
The Testosterone Trials were published in the New England Journal of Medicine in 2016. They were a set of 7 double blind placebo-controlled trials at 12 sites. The studies were built around inclusion criteria of sexual function, physical function and vitality in 790 men over the age of 65. These men had issues of obesity, high blood pressure, diabetes, some were smokers, and a number even had previous heart attacks: they were considered to be a high risk group. 
Androgel, a fairly weak commercial product was used and more or less doubled the testosterone levels from around 230 to 250 to about 500 ng/dL (nothing stellar!).
The testosterone group versus placebo group showed improved sexual desire, increase in sexual activity, and improved erectile function. There was improvement in walking distance and duration. There was an improvement in energy, mood, reduction in depression; improved muscle strength and bone density. Over 2 years, cardiovascular events including heart attack, stroke, and death due to cardiovascular cause were 9 in the testosterone treated group and 16 in the placebo group. (3 deaths in the testosterone group, 7 in the placebo group.)

  1. Numerous studies have shown that testosterone therapy reduces waist circumference, body fat mass, blood pressure, and blood glucose. It increases lean body mass, insulin sensitivity, and improvement in the lipid (cholesterol) profile. Since obesity, dyslipidemia (bad cholesterol numbers), insulin resistance, metabolic syndrome, hypertension, and diabetes are well established cardiovascular risk factors, ANY therapeutic modality that improves these risk factors should be expected to reduce cardiovascular risk.
  2. Testosterone administration results in increased muscle mass, strength endurance, and exercise tolerance. There a decrease in subcutaneous and visceral fat. There is enhanced psychological status and enhancement of well-being. There is an increase in lean muscle mass, and improvement in bone density. There is improvement in skin tone. There is improvement in libido and sexual performance.
  3. Testosterone offers protection to the cardiovascular system, the neurological system, the musculoskeletal system, the vascular system, the immune system. It prevents against deterioration of muscle, ligaments, joints, tendons, bones and skin. It protects against insulin resistance, metabolic syndrome, and diabetes by decreasing visceral fat
  4. It decreases pro-inflammatory proteins that cause further deterioration of atherosclerosis. It protects against dementia.
In fact, testosterone is banned in the Olympics and professional sports due to the fact that it improves strength, it increases muscle mass, it increases endurance, and it may therefore improve athletic performance.
 Testosterone for women has the same beneficial effects as it has for men.
It improves well-being, energy, strength and endurance. It improves body composition, decreases visceral and subcutaneous fat, and improves bone density. It maintains muscle mass which helps maintain better metabolism. This is beneficial for prevention of diabetes and heart disease. It may improve sexual function and increases orgasmic ability. It increases collagen in skin with increased skin thickness, improved texture, decrease in wrinkles and decrease in fat deposition and cellulite. 
It is indicated for any woman who wants to improve health, wellness, strength, confidence aesthetics, metabolism, fat loss, sexual function, and breast cancer protection.
It is contraindicated in pregnancy, planned pregnancy, breast feeding, and physician resistance!
  1. There are commercial creams that tend to be lower in delivery capability because the percentage mixed in cream is of a lower concentration.
  2. There are compounded bioidentical creams that may be applied to skin that deliver higher concentrations.
  3. There are injections that deliver higher concentrations but there is a peak and trough effect with levels that go up and down.
  4. There are pellets that are surgically placed under the skin that can last for over 3 months.
My preference is with the compounded creams because they are well absorbed, maintain higher and consistent levels without a “peak and trough” effect.
 When the full literature is reviewed and studied, the overwhelming trend is very much in favor that testosterone at a minimum does not harm in terms of cardiovascular risk, and indeed there is an abundance of evidence that it offers significant benefit to cardiovascular risk factors, and outcomes. The 2 papers that suggested a negative interaction have been highly criticized and found to be flawed in their presentation, analysis, and conclusions. There are several dozen papers in the literature that show significant benefit. Additionally, are the added benefits of well-being, energy, libido, sexual function, muscle mass, diminished fat, skin tone, improved bone density. 
This is a hormone that is intrinsic to both males and females. It offers benefits to both.
However, only males have prostates and this is another area where misinformation and confusion abound in the relationship of testosterone to prostate cancer. I will next go into a full discussion of this topic-something the medical community at large does not know much about- in my next blog, which will follow shortly.

<![CDATA[STATINS]]>Mon, 07 Aug 2017 18:51:39 GMThttps://www.chesniehearthealth.com/cardio-blog/statinsPicture
On a daily basis I encounter patients who refuse to take statin medications. The Internet provides so much information and misinformation that mythologies abound and it is very hard to sift through what is meaningful and what is not. This blog contains a lot of information: it is everything you wish to know or don't want to know about the importance of statin therapy.
The class of drugs known as statins was discovered by Dr. Akira Endo at Sankyo in Japan in the early 1970’s.
 It inhibits the enzyme 3-hydroxy-methylglutaryl-coenzyme A (HMG-CoA) reductase. Merck&Co. launched the first statin made available to the public, lovastatin (Mevacor) in 1987.
Lovastatin and the other statins that followed have resulted in a substantial reduction in virtually all clinical manifestations of atherosclerotic vascular disease, including coronary events, strokes, and revascularization procedures, and have prolonged the lives of millions of people.
Of the 6 most commonly used statins, 3 are derived from fungi (lovastatin, simvastatin, and pravastatin, and 3 are synthetic (fluvastatin, atorvastatin, and rosuvastatin). As mentioned, statins block or “inhibit” HMG-CoA in the liver and this blocks a protein called mevalonate,
which then suppresses the manufacture of cholesterol; the stronger the statin, the more mevalonate that is inhibited. Additionally, the more this occurs (with the stronger statins) more LDL receptors are manufactured in the liver cell to go to the cell surface to remove circulating LDL into the hepatocyte (liver cell) and degrade the LDL into bile acid.
Statins have a significant lipid lowering effect and have significantly lessened the event rates of coronary artery and other arterial diseases. It must be noted that though 1/3 to 1/2 of those who take statins have benefit in outcome, 1/2 to 2/3’s do not.
Though the reduction of cholesterol and LDL levels are proposed as the primary principle for arterial protection, it is not the sole mechanism for benefit. There are several actions that are independent of cholesterol lowering:
1)Statins improve inflammation in the artery wall and can improve features associated with plaque stability.
2)Blood C-reactive protein (CRP), a marker of inflammation is reduced by statins independently of the amount of cholesterol lowering.
3)Statins improve endothelial function rapidly, before any appreciable reduction in serum cholesterol can be detected. (The endothelium is the lining into the artery wall).
4)Statins reverse endothelial dysfunction in young smokers with normal LDL levels.
5)Regression of coronary atherosclerosis, and improvement in clinical outcomes with intensive statin therapy are related equally to reduction of CRP and other inflammatory markers as well as LDL cholesterol regulation.
If statins offer benefits that are independent of cholesterol lowering, how does this occur?
 There are a group of complicated protein interactions  (the rho proteins), that influence cellular membrane metabolism. This process triggers much of the atherosclerotic process: reduction of nitric oxide, acceleration of vascular inflammation, increased levels of inflammatory proteins, increased vascular smooth muscle proliferation, increased levels of thrombotic (clotting) factors. (Plus many more very complex cellular and biochemical interactions).
Statins interact with and reduce these Rho proteins . This produces a decrease or even a complete reversal of most of the atherosclerotic cellular processes listed previously. This is a very important arena of science and clinical research.
Lipid Effects:
The evidence that lowering LDL cholesterol reduces cardiovascular events is very strong!:
Statins are the preferred first line treatment of choice for coronary disease risk reduction within the context of pharmacological therapy. The concept of “lower is better” is supported by a lot of data.
The statins differ in their LDL lowering capability. This was demonstrated in the STELLAR trial (Statin Therapies for Elevated Lipid Levels Compared Across Doses to Rosuvastatin). This was a randomized, parallel -group, open label, comparator-controlled trial of 2431 hypercholesterolemia adults to compare lipid  changes after 6 weeks for all of the statins and doses tested: Rosuvastatin lowered LDL cholesterol across its 10 to 40 mg dose range by 46% to 55%, compared with 37% to 51% for atorvastatin 10 to 80 mg dose range, 28% to 46% for simvastatin 10 to 80 mg dose range and 20% to 30% for the pravastatin 10 to 40 mg dose range. This LDL lowering effect is reflected in their ability to attain the earlier National Cholesterol Education Program Adult Treatment  Panel 111 (NCEP ATP111) LDL goals.
Again, from STELLAR, the percentage of coronary heart disease patients who achieved treatment goal of less than 100 mg/dl with Rosuvastatin 10 mg, Atorvastatin 20 mg, Simvastatin 40 mg and Pravastatin 40 mg were 55%, 43%, 31% and 11% respectively.
Another example of statin effectiveness to achieve LDL lowering to less than 100 mg/dl was studied with Rosuvastatin in a group of patients with very high LDL levels from 190 to 240 mg/dl (this group has heterozygous familial hypercholesterolemia). Rosuvastatin 10 mg lowered LDL to less than 100 in 37% of patients, and 20 mg lowered LDL to less than 100 in 66%.
Statins also lower triglycerides, generally in the range of 15 to 30%, also in relation to the strength of the statin in lowering LDL. Generally, the greater the baseline triglyceride , the greater the lowering. Patients who have triglycerides of greater than 200 tend to have a more aggressive lipid atherosclerotic pattern. This goes along with metabolic syndrome which is a pre-diabetes picture: High levels of triglycerides, low levels of HDL, increased VLDL particles, and LDL particles that are smaller, more dense, and greater in number which are more aggressive in the atherosclerotic profile.
Statins have been shown to be effective in improving all of these parameters. By their very mechanism of action, statins remove VLDL and LDL particles from the circulation. There is not only reduction in concentration of particle number of LDL and VLDL but also a preferential removal of smaller dense LDL particles. In one study, atorvastatin removed 44% of small dense LDL particles and 10% of larger particles and 31% of all LDL particles. By contrast, niacin, a drug used for patients with this more aggressive atherosclerotic profile, shifted small LDL particles to larger ones and reduced particle number by 14%. Niacin does have a beneficial effect on increasing HDL levels by 10% to 15%. Rosuvastatin may raise HDL to 8% to 10%.
Impact on Morbidity and Mortality
Statins have been evaluated in more than 100,000 individuals participating in randomized, controlled clinical event end point trials: over 18 large population studies, both primary risk prevention studies (no coronary or arterial event has occurred yet) and also secondary risk prevention studies ( the event has occurred, and we’re trying to prevent the next one).
The conclusion for all of these studies is that all outcomes of atherosclerotic vascular disease is reduced with statin therapy including coronary artery disease death, non-fatal MI, coronary revascularization, acute coronary syndrome, unstable angina, stroke, peripheral vascular disease, cardiac arrest, and heart failure.
Reductions in total mortality have been specifically documented in 4S, LIPID (Long Term Intervention with Pravastatin the Ischemic Heart Disease), and HPS (Heart Protection Study).
Several of the Primary Prevention studies include:
1.the ALLHAT Study with 10,335 adults double blinded to placebo or Pravastatin 40 mg/day. There was an average of LDL lowering of 17% and a lowering of coronary or stroke events by 9% over 4.8 years.
2.the ALERT study with 2100 adults on placebo or Fluvastatin 40 mg/day showed an average lowering of LDL of 32% and a lowering of coronary events of 35%. The average reduction of cardiac death, nonfatal MI and revascularization was 17%. Followup was 5.1 years.
3.the ASCOT trial included 14,350 adults treated with placebo or Atorvastatin 10 mg. the LDL     average  lowering was 35% and reduction  in CHD events was 31% with followup of 3.3 years.
4.SPARCL with 4731 adults treated with placebo or Atorvastatin 80 mg had LDL lowering of  45% and a reduction of coronary events of 35% over 4.9 years.
5.WOSCOPS trial with 6595 men, treated with placebo or Pravastatin 40 mg daily. LDL lowering was averaged at 26% and coronary events lowered by 31% over 4.9 years.
6.AFCAPS/TEXCAPS study had 66065 adults treated with placebo or Lovastatin 20 to 40 mg day . LDL lowering averaged 25%, and coronary event lowering averaged 40% over 5.2 years.
Secondary Prevention studies are studies where a coronary vascular event has already occurred. Some of these studies are:
1.4S: 4444 adults treated with placebo or Simvastatin 40 mg daily. LDL lowering was 35%, coronary event reduction was 34% over 5.4 years.
2.LIPID: 9014 adults treated with placebo or Pravastatin 40 mg. LDL lowering was 25% and coronary event reduction was 24% over 6.1 years.
3.CARE: 4159 adults treated with placebo or Pravastatin 40 mg. LDL lowering was 32% and coronary event reduction was 24% over 5 years.
4.HPS: 20,536 adults treated with placebo or Simvastatin 40 mg. LDL lowering was 32% and coronary event reduction was 27% over 4.9 years.
5.TNT: 10,000 adults treated with placebo, or Atorvastatin 10 mg vs. Atorvastatin 80 mg. Further drop in LDL lowering of 24% and a further reduction in coronary events of 22% over 4.9 years.     
It is important to comment that all of the above dramatic percentage drops in LDL lowering and disease event rates are not percentages based on the total number of patients. These reductions are called relative risk reductions and an example would be the following:
Of 10,000 patients, 200 patients taking placebo had a cardiovascular event, and 100 patients taking statin had a cardiovascular event. That would represent a 50% reduction based on RELATIVE RISK criteria which in clinical double blind randomized studies MUST achieve statistical significance by at least 0.05%. This is based on the numbers in the study, the percentage of people responding, and the length of time of the study. It would be a mistake to think that in a 10,000 person study, 7000 had coronary events on placebo and 3000 had events on statin. That is something that never occurs in these types of studies.
The statins are effective at reducing cardiovascular event rates in patients with existing vascular disease (secondary prevention) as well as those with only risk factors (primary prevention). Statins are equally effective in reducing risk and events in men and in women, irrespective of age. Statins are effective in reducing events in diabetic patients. Patients with diabetes or metabolic syndrome often have atherogenic dyslipidemia with only modestly increased LDL. In spite of this, statins are excellent treatments of choice in these patients because they effectively  reduce small dense LDL particles, cholesterol-enriched remnant particles and overall particle number as discussed above. The Collaborative Atorvastatin Diabetes Study (CARDS) specifically studied type 2 diabetic patients and reported a  37% relative event reduction which was so robust that the trial was stopped prematurely.
In 2012, there was a departure from the original NCEP ATP111 recommendation of driving LDL to less than 100 in intermediate risk patients and to less than 70 in higher risk patients. Though the National Lipid Association and several European cardiovascular societies have maintained this recommendation, the American College of Cardiology presented a new recommendation of achieving a 30% lowering of LDL from baseline in intermediate risk patients and a greater than 50% reduction in the higher risk groups. Though there is considerable debate amongst the various professional groups, the primary caveat is the importance of LDL lowering through diet and exercise programs and then utilizing pharmacologic tools with statins as the primary recommendation.
Alzheimer’s Disease.
Alzheimer’s Disease is a neurodegenerative disorder that leads to cognitive decline and neuropsychiatric symptoms and diffuse structural abnormalities in the brain. It is characterized by the deposition of amyloid plaques and neural fiber tangles that may be related to cholesterol synthesis.
Evidence that links cholesterol and Alzheimer’s Disease has come from observational studies. It has been observed that an elevated cholesterol level in mid-life increases the risk of Alzheimer’s Disease to 2 to 3 fold in later life. Conversely it has been observed that people who take statins and other lipid-lowering agents have a 60% to 75% reduction in the future risk of Alzheimer’s Disease.
Elevation of liver enzyme blood tests to greater than 3 times normal with statin therapy are rare. In one meta analysis of 74,102 patients the incidence of this was 1.4% in statin treated patients and 1.1% in placebo control patients. It appears to be more related with the intensity of the statin dose rather than the degree of LDL lowering. It also tends to be transient. In an analysis of 180,000 people it was reported that 300 in 90,000 treated with a statin had elevations of 3 times normal. Of the 300, only 110 had consecutive elevations with another repeated blood test.
The incidence of actual liver failure is extremely rare. In the FDA Adverse Event Reporting System (AERS), it was calculated that there was 1 case in 1.4 million patient-treatment-years. In fact the incidence of 1 case per million is the same in patients taking a statin as well as with people NOT taking a statin.
In the context of a 3 fold increase in liver enzyme blood tests it is considered prudent to interrupt statin therapy for a brief period of time and reassess lab values and then resume therapy. It is recommended that the clinician evaluate clinical symptoms and signs of liver dysfunction ( malaise, fatigue, loss of appetite, weight loss, jaundice). It the blood tests normalize or if the blood tests are only mildly elevated, then the statin therapy may be resumed, or in the latter case, not interrupted.
The position of the National Lipid Association is that interruption of statins with mild elevation of liver blood tests (<3 times normal) to avoid a very remote risk of liver failure, the patient will be exposed to a disproportionally higher risk for cardiovascular events.
Patients with nonalcoholic fatty liver disease have a significantly increased cardiovascular risk and are candidates for statin therapy. Statins are actually safe in these patients. Statins do not further elevate baseline liver enzyme abnormalities, and in fact may actually improve liver function.
The 2 more serious muscle problems are myopathy (muscle discomfort, pain, weakness, with an elevation of creatine kinase (CK) to greater than 10 times upper limit of normal, and rhabdomyolysis ( the above with associated kidney failure and higher risk of death).
These serious muscle-related adverse effects are rare.  In an analysis of 21 randomized clinical trials with 180,000 person-years of followup on statin therapy or placebo, myopathy occurred in 5 patients per 100,000 person-years, and rhabdomyolysis in 1.6 patients per 100,000 person-years. The AERS database reported a rate of 0.3 to 2.2 cases of myopathy and 0.3 to 13.5 cases of rhabdomyolysis per 1 million statin prescriptions.
Muscle toxicity with statins is a class effect but there appears to be a difference between weaker and stronger statins. Pravastatin was not associated with a case of rhabdomyolysis in 19,768 people studied for 5 years. Simvastatin produced rhabdomyolysis in 0.1% of 2265 patients on 80 mg in the A to Z trial.
The more common adverse effect of statins is myalgia, which is muscle soreness, pain, or weakness.  This is not associated with the above serious complications of myopathy or rhadbomyolisis. The incidence of myalgia varies between 5% to 15% in the literature. There tends to be some misinformation as to the accuracy because there is often confusion about what constitutes statin related myalgia, versus a localized sore muscle or joint, related to activity or arthritis. Reports of myalgia with statins in clinical trials are the same as, or only slightly more than, those reported in patients receiving placebo. However, this complaint is the most common reason for patients to discontinue therapy.
A specific gene has been discovered that affects liver uptake of statins. This gene (rs4363657) occurs in about 15% of the population. With this gene, statins would not be taken up as freely into liver cells thus elevating statin blood levels. Also higher statin doses, and drug interactions may also increase the statin blood level and thereby increase the risk of muscle achiness.
Some investigators have related the cause of myalgia and myotoxicity to a drop in ubiquinone levels. This is also known as coenzyme Q10 (CoQ10).  Ubiquinone plays a role in cellular energy and cell membrane activity. It is carried in LDL particles and thus, with lowering of LDL levels there is also a lowering of CoQ10 levels. There is some conflicting data as to the measurement of CoQ10 levels in muscle cells, and the lowering effect related to dosage of statin. There have been conflicting results on the benefits of giving CoQ10 to patients to prevent or to treat muscle-related symptoms. In one study that used high doses of lovastatin, supplementation with CoQ10 240 mg daily did not reduce the frequency of myalgia compared to those not receiving it. In another study, statin-taking patients who had myalgia had their pain assessed on a 10 point grid. Those given 100 mg daily CoQ10 had reduction of 5 to 3 with the addition of this: Somewhat equivocal!
However, there are no known risks associated with taking CoQ10. Giving patients CoQ10 may be tried in patients who develop myalgia and cannot otherwise tolerate statin therapy.
The clinician should also be aware of anything that can elevate statin blood level. This would include higher dosage, older age, frailty, female gender, renal insufficiency, hepatic dysfunction, hypothyroidism, and use of other pharmaceutical agents that have interaction with statins.
I’ve addressed before the complexity of the disease called “Atheroscelerosis”. I’ve discussed how it can smolder and develop over decades and then how it can suddenly erupt: with a ruptured plaque causing an acute coronary event.
In preventive cardiology, we are committed to impacting this mysterious and complicated process. There are 3 objectives: first is to try to slow down the atherosclerotic process, second is to stop it, and third is to reverse it.
When people are unable or unwilling to engage in the science of pharmacology, they are removing very important ammunition to engage this unrelenting disease. Obviously there are many facets that are called into play: appropriate nutrition, exercise, weight management, avoidance of diabetes, hypertension and smoking. Most people know what to do as regards these behavioral issues, how many are successful in conquering these issues? I’ve learned that optimization of your body’s hormones plays an exceptional role as well, but when overt bias exists that is oppositional to the gift that the science of pharmacology has given us, why would you put yourself in a position whereby you are not giving yourself the best opportunities to counter this difficult and unpredictable disease?
The bibliography to the above essay is obviously very extensive and is not listed here. However, much of the essay was synthesized from the chapter on Statins, written by James McKenney, Peter Ganz, Barbara Wiggins, and Joseph Saseen in the textbook of Clinical Lipidology, edited by Christie M. Ballantyne.