I’ve met so many people over so many years who would far prefer not to have to take any medication to resolve some of their health issues, and would rather fix the problem “naturally”. It is actually a fairly common attitude when dealing in areas of preventative medicine. The two usual areas that I find these attitudes to exist are in the arena of Hypertension or high blood pressure, and the other, in the arena of Lipidology, or high cholesterol.
Today I thought I’d address some thoughts about high blood pressure:
 
High blood pressure exists when BP is > (greater than) 140/90, though there are ranges of normal ranging from 100/60 to 130-135/80 depending upon which medical society articulates their ranges of normal.
 
It affects 1.5 billion people world-wide, about 1/3 of the world’s population.
(40 to 50 million Americans: 40% of African Americans vs. 25% of Caucasians and Hispanics) It accounts for about 54% of strokes and 47% of coronary events worldwide. Therefore, about half of cardiovascular events are specifically related to hypertension, and another large percentage related to pre-hypertension. Thus, high BP remains the leading cause of death worldwide and is one of the world’s great public health problems.
 
So exactly what is it? It is pressure in the arteries, initially observed with a vertical column of mercury to measure by millimeters the pressure generating in the artery of the arm!
 
Your arteries are tubes of muscle, just like your garden hose is a tube of plastic or rubber. When the water is pouring through the hose and gushes out the end, the hose is more flacid. When the nozzle is turned tight, and the water “jets” out, the hose is considerably stiffer. That is because of the tension in the walls of the hose generated by the flow of water and the volume of water passing through.
 
The arteries in your body are way more complicated. They are the muscle tubes that go through all areas of your body to deliver the volume of blood being pumped out of the left ventricle of the heart with every heart beat. For simplicity, figure the heart is beating 60 beats per minute, and it pumps out 100 cc’s of blood per beat. Therefore cardiac output would be 6000cc’s or 6 liters of blood per minute…and it can increase 5 or 6 fold with exercise, or intense activity by increases in heart rate and the increased amount of volume blood ejected with each heart beat.
Thus, into the muscle tubes pumps the blood, at high “spurting” velocity! Therefore, the upper number, Systolic BP (ie.120 to 140 range) is the tension in the wall of the artery when the 100 cc. amount of blood is moving through that measurement area, (thus the dynamic range), and …the Diastolic BP is the remaining, resting tension in the artery wall after the blood has passed by, (the passive range).
 
Now, I want you to start to think about all the many variables that come into play in setting these numbers of your blood pressure:
First is the number, the diameter, and the muscle thickness of all the arteries. The principle artery is the Aorta, and it may vary in caliber size from 20 to 25 mm (about an inch in diameter) up to over 40 plus mm. Every other artery branches off of the aorta (like other rivers coming off the Mississippi) and these arteries may have caliber sizes (diameters) ranging from 2 to 4 mm (like the coronary arteries) to 10 mm or more (like the carotids) to 15 plus mm like the iliac and femoral arteries. 
 
In addition to the changing diameters of the arteries, there is also the substance of the 3 layers of muscle that make the arterial wall. How thick are these layers? How toned are the muscle layers? How pure are they in terms of muscle cell integrity, vs. are they infiltrated with problems of aging and atherosclerotic disease such as displaced muscle cells with inflammatory cells, cholesterol products, fibrin, disrupted collagen, calcium, clotting debris, etc.
 
Now think of the fluid going through the arteries, Blood, right? How thick or thin is it, how much volume is there? Is the body high in body water, and fluid volume, or is it depleted? Is the intravascular compartment (the circulation) dry, and dehydrated, or is there too much fluid, and salt, going through?
 
Then, what about the pump itself? How strong or weak is the heart? What is the size of heart, of the left ventricle? Does it contract normally and strongly, or is it weak and tired and impaired? Are the walls of heart normal, or are they thickened, making filling of the ventricles more difficult? Are the valves tightened down and lessening the flow of blood per heart beat, or are they leaking to the extent that there is back flow, interfering with forward flow?
 
These are just some of the mechanical issues which are complicated enough! What about everything else? What about you: your soul, your mind, your inner world, your struggles, your frustrations, your stresses? Yes, the cortex of your brain, which houses everything that makes you the unique soul that you are, plays a huge role in the dynamic settings of your body!
 
What about the pathways from your brain cortex to your inner brain centers that you DO NOT DIRECTLY CONTROL… but are the churning engines that make everything work in your body… like your pituitary gland, your hypothalamus and your pineal gland. These and other mid-brain areas are the control centers for your neuro-chemicals like serotonin, vasopressin, oxytocin, dopamine. These are the control centers for your autonomic nervous system- the Sympathetic system which releases, adrenalin, epihpehrine, nor-epinephrine, and its opposite, and the Parasympathetic system, which controls the Vagus nerve.
 
The pituitary gland (the Mother Ship) releases the control hormones like Growth Hormone, Anti-diuretic Hormone, Sexual Stimulating Hormone, Thyroid Stimulating Hormone, and others that control the release of all your end organ systems: thyroid, gonads, adrenals, etc.
 
In addition to this, is the flow of blood to your kidneys, as well as the kidneys ability to make urine. These as well as the adrenal glands are responsible for the release of chemicals called angiotensin, and renin coristol, aldosterone , that play a direct role in the maintenance of correct body water, as well as a direct impact on the measured “tone” in your arterial system.
 
I could go on. This type of essay could go on for many pages, and be expanded into chapters in medical text books. My intent here is only to give a very basic appreciation of how complicated biological science is, and how amazing our human bodies are.
 
There is also an effort to help you understand that there is so much that can go wrong, and it’s amazing that more doesn’t!  These are areas of molecular biology, of physiology, of genetics, as well as behavior that are intersected in the most complex ways. It is the unfolding of these many variables that over the decades of our lives, with the interplay of our behavior, our diets, our tensions, our stresses, and our level of activity or inactivity, that can lead us to the place where overt disease expression occurs: Coronary Heart Disease, Heart Attack, Congestive Heart Failure, Arrhythmias, Sudden Death, Stroke!
 
Because the science of hypertension is so complex, there are many different types of medications that are called upon to treat it. About 8 classes of medications: mostly with about 5 to 10 different drugs in each class, and each drug usually has multiple doses to choose from. So, for any individual, it becomes somewhat of a creative recipe. Best to start with one drug at a time, keep the dose low, and work up if needed, and do one thing at a time. Each person is their own unique environment. Two things need to occur: 1) the drug needs to work to achieve goal, and 2) you have to feel well on it. Stay away from side effects!
 
In fact, the importance of reduction of BP is critical for every decade, even into the 30’s. The difference in each decade, is a 2 to 4 time lowering of cardiovascular events when correctly treated. These outcome differences are based on studies done over many decades, involving hundreds of thousands of people cumulatively, so these statistics bear great scientific weight.
 
I’m hoping to surprise you now!
I’m not going to discuss blood pressure medicines! The foundation of management of BP, and CardioVascular risk reduction in general is to work with the patient with life style modification: So folks, if you want to work on these risk factors “naturally”, then go at it!
 
Lifestyle modifications are recommended for just about everybody with high blood pressure:

• Work on your weight.
• Work on your body.
• Work on your soul and your mind.
• Lower your BP, Lower your Cholesterol, Lower your Blood Sugar.
• Lower your stress, get better sleep, do more activity, enjoy your family, find and nurture love.

 
There is so much more to this!
There will be a medication essay, as well as a cholesterol medication essay….BUT:
 My next essay to you will be called: “The Not So Easy Tidbits To Living a
Healthier Lifestyle”
 
Attached is a nice video to help you understand the dynamics of blood pressure.
 
Best wishes!
 
Brian Chesnie, MD.
9/15/16

Many of my patients question the recommendation of taking an oral anticoagulant (blood thinner) when they have been given the diagnosis of atrial fibrillation. The most common discussion is the risk of stroke by not taking the medication vs. the risk of bleeding taking the medication.
 
This has always been a very complicated decision making process in atrial fibrillation. I am writing this to share with all of you that I don’t arbitrarily just prescribe drugs. Taking care of a patient and the decision making that goes into each patient is complex and individual.  The tools that we as physicians have to use to make our decisions are complex. So I thought I would give you a glimpse into the complexities regarding “guidelines” for treatment with anticoagulation in atrial fibrillation.
 
Back when I was in cardiology training in the late 70’s / early 80’s, the text books would state that if the patient was in atrial fibrillation for longer than 48 hours, then warfarin (Coumadin) should be started.
Over the years, that time frame gradually shrunk down to the point that when atrial fib lasted longer than 12 hours, we would consider initiating therapy.
 
Over the past 8 years, “decision guidelines” have been put together by various expert panels. This has condensed into the two predominant recommended guidelines presented here: for stroke and embolic protection is the CHA2DS2VASc score, and for the risk of bleeding is the HAS-BLED score. Let me review them for you:
 
CHADS2VASc (Stroke and Embolic Protection)
 
C    CHF/ LV dysfunction (weak heart)        Points:  1
H    Hypertension (high blood pressure)                   1
A    Age > 75 (and up)                                               2
D    Diabetes                                                             1
S2  Stroke/ TIA                                                          2
V    Vascular Disease                                                1
A    Age (between 65 to 74)                                      1
S   Sex category (female has a higher risk)              1
                                         Maximum Score               9
 
Risk Percentage
0 points      <1%
1                  1.3%
2                  2.2%
3                  3.2%
4                  4.0%
5                  6.7%
6                  9.0%
7                  9.6%
8                 10.7%
9                 15.2%
 
Despite earlier itineration such as CHADS, and CHADS2, this classification has shown to be more sensitive and specific.
In a study published in 2013, looking at Stroke and Systemic Embolism (SSE) rate in 11,414 patient-years, {all of whom were on Aspirin +/- Clopidogrel}, the incidence of SSE was 0.9% in patients with a CHA2DS2-VASc score of 1, and 2.1% with those with a score equal or greater than 2.
This has pretty much become the tipping point: a score of 2 or greater is when oral anti-coagulant drugs would be recommended.
 
In this study as well as the Swedish National Patient Registry of 140,000, [unexposed to anti-coagulant therapy], the incidence of stroke was 0.5% to 0.9% in the score of 1 , and in the score of 2  it was between 2 to 3%. In the 0 score range it was close to 0%. Therefore, the 2 or greater score groups are recommended to proceed with anti-coagulants, and the 0 score group are not recommended to proceed. It is the score of 1 where there is a debate. The tipping point for therapy in several scholarly editorials appears to be at about 1.7% for consideration of warfarin, and about 0.9% for consideration of the New Anti-Coagulant Therapies (NOACs). It is felt that the benefit of treatment may outweigh the risks at these percentages.
 
This sounds confusing so the American College of Cardiology, the AHA, and the Heart Rhythm Society have come up with these guidelines:
 
*CHA2DS2-VASc score is recommended for assessment of stroke risk in nonvalvular AF.
*With prior stroke, TIA, or CHA2DS2-VASC equal/greater than 2, Oral Anti-Coagulation is recommended with either warfarin or NOAC.
*Evaluate kidney function before initiation of NOAC.
*With a CHA2DS2-VASc score of 0, it is reasonable to omit Oral Anti-Coagulant Therapy.
*With a CHA2DS2-VASc score of 1, there is the choice of no anti-coagulant therapy, or treatment with anti-coagulant therapy, or treatment with aspirin.
 
What is interesting, is that in the large Swedish study mentioned above, over 40% of patients with a score of 1 were treated with Oral Anti-Coagulation, which was a higher percentage of those treated than in the higher score groups.
WHY?
 I expect because the doctors were weighing the risks in the higher score groups against the further increased risk of bleeding, and the higher score groups have more illness and tend to be older thus making the risk of bleeding greater.
For example, people with history of GI bleeding, or intracranial bleeding, or elderly people who may be at greater risk for falling and injury, as well as those with cognitive impairment…all of these situations may preclude against giving someone an anti-coagulant.
 
So, what about bleeding?
There is a guideline published in 2013, called the HAS-BLED Score:
 
H  Hypertension                                                  Score    1
A  Abnormal kidney/liver function (1 point each)              1 or 2
S Stroke history                                                                1
B Bleeding history                                                            1
L  Labile INR (difficult to control warfarin levels)             1
E Elderly (age >65 {sorry!}]                                              1
D Drugs or alcohol (aspirin, NSAIDS)                             1
 
Just like the CHA2DS2-VASC score of accumulated scoring increases the incidence of stroke/embolus, accumulation of points in the HAS-BLED guidelines increase the risk of bleeding. For example, a score of 1 is associated with a 1.13% bleed rate, a score of 3 is associated with a 3.74% rate, and a score of 5 is associated with a 12.5% rate, etc.
 
The guidelines are very clear as to the purpose of evaluating bleed risk. It does not specifically state that Anti-Coagulation Therapy should not be used. What the guidelines say are:
1.The HAS-BLED score should be considered as a calculation to assess bleeding risk and if the score is equal or greater than 3, (high risk), some caution and regular review is needed following the initiation of anti-coagulant therapy, or anti platelet therapy.
2. Correctable risk factors for bleeding, such as uncontrolled blood pressure, labile INR’s, the use of other drugs, alcohol, should be addressed.
3. Use of the HAS-BLED score should be used to identify modifiable bleeding risks that need to be addressed, but should not be used on its own to exclude patients from Oral Anti-Coagulant Therapies.
 
The purpose of presenting all of this information to you was not to confuse you or overwhelm you, but to give you some education, and more importantly, how difficult it is to come to conclusions about scientific medical data that is not black and white.
 
We see one patient at a time, and though guidelines that are based on extensive clinical research data are there to “guide” us, the decision making process of how we come to recommend certain medications, therapies, surgeries, etc. is very much an individual thing, and hopefully you have doctors who try to do “right” for you.
 
(The current NOACs {New Oral Anti-Coagulants} are:

1. Pradaxa,  (dabigatran) 75 or 150 mg, twice daily
2. Eliquis,  (apixaban)  2.5 or 5 mg, twice daily
3. Xarelto,  (rivaroxaban)  15 or 20 mg, once daily
4. Savaysa, (edoxaban) 30  or 60 mg, once daily)

I would like to try and clarify the misunderstanding that exists, even among health care professionals, of how the blockage of a coronary artery (which creates a heart attack, or “Myocardial Infarction”) relates to the smoldering underlying disease of “Atherosclerosis”. The tragedy of Coronary Artery Disease is that it is essentially an “after the fact” diagnosis. This means that a clinical event has had to have happened: anginal chest discomfort, acute coronary syndrome, heart attack, placement of a stent, or having a coronary bypass operation. Once any of these have occurred, you now have the diagnosis of Coronary Artery Disease.
 
The actual blockage in the artery, or the limitation of blood flow in the artery is NOT the actual disease. It is a consequence of the disease. The underlying disease, the root cause is a disease process called Atherosclerosis. This disease is an insidious culprit, located within the wall of the artery, smoldering over decades until it may unpredictably disrupt through the wall into the Lumen (where the blood flows) and compromise the flow of blood.
 
Lets begin this way: the ventricles are the pumps of the heart (the lower chambers) that pump the “fuel” to all the cells in the body. The “fuel” is oxygenated blood, as well as nutrients, vitamins, hormones, chemicals, enzymes, proteins, amino acids, etc.  that are carried by a series of tubes, getting smaller and smaller to where the blood may be transferred into organs and into cells. These tubes are the arteries, the largest of which is the aorta (the diameter is about 20 to 30 millimeters), to the smallest which are the first 2 that come off the aorta above the aortic valve and left ventricle: the coronary arteries (diameter of 2 to 4 millimeters). The right and left coronary arteries and their branches sit on the surface of the heart and wrap around the heart, delivering oxygenated blood and other substances to the heart muscle.
 
An artery is like a hose. It is circular, and the structure like the plastic of the hose is actually a three- layered muscle. The inner wall where the blood flows, is called the endothelium which is the lining into the artery, like your skin is the lining into your body.  The inner layer of muscle is called the “intima”, the middle layer is called the “media”,  and the outer most layer is called the “adventitia”. Think of the lining, or endothelium, as the bricks and mortar, though this “mortar” is permeable, meaning that “things” such as cells, proteins, cholesterol, etc. can pass through the lining into the inner arterial structure.
 
The arteries do not maintain the same diameter, nor the same direction. They vary in caliber size, they change direction, and they have bifurcating branches that twist and turn as well; and the flow of blood is by no means constant! With the contraction of every heart beat from the left ventricle, there is a sudden, rapid, bolus amount of blood ejected through the artery.
 
(When your blood pressure is checked, this is what the upper number is, the systolic number of your blood pressure: the bolus (amount) of blood traveling through the artery against the tension in that muscular tube, while the lower number, the diastolic number, is the absence, or relaxation phase of wall tension in that muscular tube.)
 
Therefore, arteries, particularly coronary arteries, which are smaller size arteries, are subject to great stresses throughout life; High velocity spurts of blood shooting into tubes that twist and change direction, changing diameter size, with branches  that bifurcate, and a lining that is vulnerable to penetration into the interior of the arterial structure… and the penetration of substances includes good things as well as bad things! If a person lives to 80, there will be about 4 billion heart beats!
 
I like to explain the insidious nature of atherosclerosis with the analogy of termites penetrating into the wood structure of your home. Termites penetrate into the wood structure and eat the wood from the inside out. Much the same with the atherosclerotic process…and the atherosclerotic process often begins in childhood and in some cases, in infancy! There have been studies of autopsies on babies who have died, demonstrating the presence of fatty streaking and infiltration of cholesterol onto the coronary artery wall. These babies were born to overweight mothers in poor areas of the country who ate poor food very rich in saturated fats.
 
The science of atherosclerosis is extremely complicated. It involves biochemical pathways, molecular and cellular biology, histological changes of cells, physiological pathways of food absorption and pathways through the liver. It simply cannot be realistically communicated in “sound bites”. I can tell you that I have practiced cardiology now for over 30 years, and in the last 10 years undertook intense study, writing of exams, and became board certified in clinical lipidology, which is the science of atherosclerosis, and I can tell you that it is staggering in its complexity and variability.
 
Simply put, it is an infiltration process with cholesterol products, mainly LDL, penetrating through the lining and into the interior of the artery wall. This is associated with the attachment of inflammation cells, called macrophages, that enter the vessel wall and displace and disrupt the integrity of the muscle cells. Associated with this displacement is also a leaking out of “poisonous toxins” that further cause degradation and destruction to the architectural integrity of the arterial wall. This interior disruption eventually breaks through the arterial lining and causes bleeding and further inflammation of the vessel wall, into the lumen where the blood flows. The bleeding of the vessel wall, as well as the inflammation process, causes clotting products to accumulate with the creation of “Plaque” which is a combination of clotting products, fibrin and thrombin, and cholesterol products, and inflammatory cells. It is not a “linear process” but accumulates sporadically and unpredictably with shear stress, flow stress, and variable plaque rupture.
 
This may lead to a gradual growth of plaque that becomes hardened and calficifed and may block the interior lumen to 70, 80, 90 percent and interfere with the flow of blood through the artery.
 
These are the types of plaques and narrowing that we look for in cardiology practices, and these will often be associated with the onset of chest discomfort, often with exertion (angina), or with the presentation of an abnormal exercise stress test, or an abnormal nuclear stress test. When angiography is done we will see one or more narrowing in the coronary arteries, and depending on location, number, degree of narrowing, it will usually lead to opening up the vessel ( angioplasty) and placement of a stent, or possibly the consideration of coronary artery bypass surgery. Interestingly these plaques are firm, rigid, and calcified and they tend to be stable. I compare them to the Rock of Gibraltar: they are not going anywhere! They certainly interfere with fuel delivery to the engine, and if the heart is working hard and not getting enough fuel delivery, terrible things can happen including sudden death. But they tend not to completely close off, and tend not to cause acute heart attack (myocardial infarction).
 
The task at hand with these very significant narrowing that interfere with coronary blood flow, is to utilize medications that improve flow, that stabilize the heart, and slow or stop the process of further plaque accumulation. The procedures discussed above do NOT AT ALL cure the disease, or control the development of the disease, but restore flow through or around the artery (stent of bypass) to deliver the appropriate amount of blood to the heart muscle and protect it.
 
However, there is even more of an insidious problem to atherosclerotic coronary disease! A plaque may be present that is small and “mushy”. It may encroach into the artery lumen by 20 or 30 percent, not interfering with flow delivery at all. And it is not at all like the Rock of Gibraltar, it is much more like Creme Brûlée!… A soft mushy plaque filled with fatty cholesterol and toxic byproducts covered by a thin cap, that can unpredictably rupture and then clot off and block the artery. In fact, these insidious smaller plaques are considered to be “vulnerable” or “unstable” and their unpredictable rupture causes about 60 to 70 percent of acute coronary syndromes, or heart attacks (myocardial infarction)
 
These plaques do not present with chest discomfort, or abnormal exercise stress tests, or abnormal nuclear stress tests. And if an angiogram is done, a stent is not provided, nor is a bypass operation because the narrowing does not interfere with blood flow delivery.
 
The task at hand is to either slow the further build up of plaque, stop the process of plaque build-up, or even reverse the process and try to aim for plaque regression.
 
This is the domain of clinical lipidology, or preventative cardiology.
The placement of stents, particularly within the context of rushing the patient to the cath lab to open the artery during an acute heart attack is hard, stressful, heroic work. To try and prevent that from happening at all, so that a person never knows what it means to rush to the hospital in the throes of an acute heart attack, or to be brought in, in cardiac arrest, or to end up with severe heart failure, is what the goal is of preventing all of this from happening.
 
This is an initial conceptual overview of the topic.  The next discussion will be to talk about the issues of lifestyle, and diet, and medication to prevent the tragedy of coronary artery disease.
 
Remember: this is an “after the fact diagnosis”. This means that a clinical event has had to have happened: anginal chest discomfort, heart attack, stent, bypass. When this has happened the person is labeled as having Coronary Artery Disease.
The underlying disease before clinical presentation is the insidious “termite infested” hidden disease process call Atherosclerosis, and this is what we in Preventative Cardiology work so hard on trying to control. 
 

My first essay a few weeks ago was on the causes and the physiology of atrial fibrillation: more or less, identifying the problem.
Today I will write about the options for treatment.

The cornerstone of atrial fibrillation management is divided into 2 categories: rate control and rhythm control. In other words, if the person is in persistent or permanent atrial fibrillation, are we able to control heart rate in the normal range both with rest, inactivity, and activity, or not. Heart rates tend to be on the high side with atrial fibrillation, so that we usually need to control heart rate with certain drugs that slow the ventricular rate, (the heart beat) into the normal range. Sometimes people may have heart rates that are too fast as well as too slow, so  medications are required to slow the "too fast" side, and a pacemaker is required to maintain the heart beat from going too slow. As well, because of the increased risk of blood clot developing in the left atrial appenda ge, anti-coagulation is also a cornerstone of management to prevent a clot from traveling to the brain and causing a stroke.
The other strategy of management is called rhythm control: Are we able to provide the person with medication, or procedural work, to establish and maintain normal heart rhythm?
In order to decide which may be the best option (there are always choices), we need to assess the pattern of atrial fibrillation: how many times does it occur, the frequency, how long is the person in it for, or is it persistent, (or permanent), what is the underlying nature of the heart problem, and how symptomatic or asymptomatic are they? If a person is exquisitely symptomatic, the approach to the problem would be quite different from another person who has no symptoms at all! The first person would certainly require a strategy that could hopefully establish and maintain normal rhythm, and the second person could pursue both that option as well as consider rate control as the o ther option.
Restoration of normal sinus rhythm may improve heart function, exercise tolerance, and quality of life and these considerations must be assessed to determine which direction may be best suited.
An important study was presented in the New England Journal of Medicine in 2002 called the AFFIRM Study which looked at 4,060 patients all over age 65. In all patients, the atrial fibrillation was paroxysmal ( they were in and out of it) and they were divided into 2 randomized groups: Rhythm control with anti-arrhythmic drugs and if necessary, cardioversion, and Rate control, using drugs that slowed the heart rate down. There was a very subtle trend of increased mortality in the rate control group that was NOT statistically significant, and there was NO evidence that the rhythm control strategy protected patients from stroke more than the rate control strategy.
In terms of Risk Management decision making, a Major Decision is determining the risk of stroke and the appropr iate anti-coagulant for low, intermediate, and high risk patients.
15 to 25%  of all strokes in the US can be attributed to atrial fibrillation. Risk factors that elevate stroke risk in AF are: male sex, valvular heart disease, cardiomyopathy and weak heart function, congestive heart failure, diabetes, smoking, advanced age, advanced coronary disease.
For each anti-coagulant, the benefit in terms of stroke reduction must be weighed against the risk of serious bleeding. If a person is younger, and healthy, with a healthy heart, their risk of stroke is in the 2 to 4% / year level. The older the person is, and adding up additional co-morbidities such as those mentioned above, increase the stroke risk to 6%, 8%, 10% and upwards to 15% per year. The risk of stroke or bleeding on an anti-coagulant, whether it be warfarin, or one of the new oral anti-coagulants is in the range of 2 to 2-1/2%. Therefore the argument holds that if you are young, well and healthy with recurrent and iso lated atrial fibrillation, perhaps you don't need to take an oral anti-coagulant  because there is no risk/gain improvement. Then, an aspirin would be recommended. However, if you are older and you start adding on the various health issues described above, and your risk goes up per year of a stroke to 8-10-12-15%, and your risk of stroke or bleed is 2 to 3%, then I would ask you, what would you choose? It becomes more complicated with other circumstances as well. What if the person is elderly and has dementia? What if they are  a significant fall risk? What if they have had a hemorrhagic stroke or a GI bleed or have a hematology problem that makes bleeding issues greater? With these issues, a clinical decision may be made with the patient and family that perhaps the risk of taking the anti-coagulant is greater than the reward.
The cornerstone of medical management for heart rate control involves 3 different types of drugs. The first is digitalis (digoxin, Lanoxin, Digitek). The second is the family of drugs called beta-blockers (propranolol, metoprolol, atenolol, etc.). The third is a group of drugs called calcium channel blockers ( diltiazem, verapamil, etc.) These drugs may also be used in combination, and it should be understood that every person is a unique human being and therapy must be careful individualized. If heart rates remain too fast despite these, or side effects are too great, then a procedure may be done called an AV node ablation with the addition of a pacemaker. This ablation seals off the AV node which is the relay switch transmitting electrical impulses from the atria down through to the ventricles. By ablating it, or sealing it off, the impulses don't go through, so the atrial fibrillation chaos in the upper chambers does not communicate to the ventricles. Therefore a pacemaker is put in place to drive the heart beat in the ventricles at a nice regular controlled rate. This eliminates the need for the above medications, except for the anti-coagulant, which would be continued.
To try and maintain normal sinus rhythm, there is a whole family of completely different drugs (sometimes used in combination with the above mentioned drugs) that are called anti-arrhythmic drugs and their job, once sinus rhythm is re-established, is to maintain the continuation of sinus rhythm. These drugs are more complicated, and they require a whole lot of finesse to use properly. It is pretty much the standard of care today that the only doctors who prescribe these medications are cardiologists and electrophysiologists (heart rhythm specialists). These drugs are pretty much beyond the domain of internal medicine specialists and family practitioners. These drugs only work so well, about a 50 to 70% overall success rate, though when successful on a given person can be 100% effective. These drugs need to be assessed carefully because they can sometimes cause a worsening of arrhythmia that can be dangerous. Therefore, when I am starting a new drug such as this with a patient, I will observe them for 2 or 3 days in the hospital, or I will have them take the first dose in my office and observe them for several hours and do repeated EKG's and then bring them back a few days later for a treadmill stress test.
The other topic of discussion is about atrial fibrillation ablation which has been in existence now for about 15 years. The technology has improved over the years and the experience of the ablation specialists has increased so that today it is a very acceptable option for people, particularly when one or two of the medications have been tried and haven't worked, either because of side effect problems or drug failure. I will not discuss this further on this essay, as it requires it's own essay.
A very interesting study was presented at the annual Heart Rhythm Society convention in 2014, from Adelaide Australia, called the "Aggressive Risk Factor Reduction Study: Implications for AF (ARREST-AF)"
They hypo thesized that the late recurrence of atrial fibrillation after ablation is due to progression of pathology of the underlying atrial environment, and that aggressive risk factor intervention would improve ablation outcomes.
Therefore they asked patients if they would like to participate in a more intensive post- procedure program, or just receive the usual advice about "eat better and exercise more"!
The active treatment group participated in an intense lifestyle modification program in a dedicated clinic with doctors, and nurses, guiding them on diet, exercise, weight management, sleep apnea management, cholesterol and blood pressure treatment, smoking cessation and alcohol reduction: ALL THE USUAL STUFF WE ALL KNOW ABOUT AND DON"T DO!!!!
After the first ablation 61 accepted, and 88 refused and the follow-up was for 2 years.
Here's the difference:
After 1 year, 62% of those who participated were free of atrial fibrillation after a single ablation, and only 26% of the non-participating group were free of atrial fibrillation.
For those who then went on to have an additional ablation, 87% of the participating group were free of atrial fibrillation, whereas 48% of the non-participating group were free of atrial fibrillation. All of this achieved a high degree of statistical significance.
Additionally, those who participated in the risk factor medication arm had statistically significant improvements in blood sugar control, cholesterol levels, blood pressure with reduction in medications, sleep apnea, and an overall global improvement in well-being.
To conclude, I would suggest that atrial fibrillation, like so many health conditions, can be well managed with a variety of treatment options. The task at hand is to assess and work with one person at a time and treat each patient as a unique individual. Personal responsibility also plays a role! Yes you can take this or that medication for slowing the rate, or maintaining normal rhythm, or you can go to the electrophysiology lab and have an ablation, which may or may not work, but the underpinning is to try and live a healthy life with a healthy attitude and do yourself what is right as regards nutrition, good sleep, good activity, less alcohol, stop smoking, and take the right medications to improve your cholesterol numbers and your blood pressure numbers...and by doing all of this, the problems of atrial fibrillation may indeed resolve.
I hope that you found the first part of my atrial fibrillation discussion helpful, as well as this second part. Obviously there is so much more that I could have included, but I did want to deliver an educational and pragmatic overview. ​

Atrial fibrillation is the most common of abnormal heart rhythm disturbances. Fibrillation, or a fibrillating heart chamber does not contract to pump the blood, it quivers much like a choppy sea in a storm with waves and wavelets colliding into each other and fractionating into even more chaotic and colliding waves. Therefore if the ventricles (the lower heart chambers and the power pumps of the heart ) fibrillate, that is sudden death which is the most common cause of dying in North America. Yes , ventricular fibrillation is Sudden Cardiac Death.
Atrial Fibrillation IS NOT. In fact, many people may have atrial fibrillation and they may be completely asymptomatic and not know that they have it. 
Therefore, instead of the upper chambers of the heart (the atria) contracting in a timed relationship prior to the lower chambers of the heart (the ventricles) the upper chambers of the heart are quivering and bombarding the electrical relay switch to the lower chambers (the AV node) at about 600 times a minute and it is the job the AV node to block these impulses so that a life sustainable heart beat can occur (figure about 60 to 120 beats per minute).

About 2.2 million people in the United States have atrial fibrillation and it is age dependent. The older you become, the more likely it becomes. Less that 1% have it under the age of 50, and over 8% have it over the age of 60, and over 15%, over the age of 80. Men tend to predominate over women...and up to 15% have wha t we would call "Lone Atrial Fibrillation" meaning that there is no discernible underlying heart problem. However, it is most associated with a variety of underlying heart ailments such as general cardiovascular disease, atherosclerotic coronary artery disease, valvular heart disease, hypertensive heart disease, cardiomyopathy, and diabetes.
The greatest problem that people face with atrial fibrillation is the stoke risk. This is because blood is not dynamically squeezed out of the atria before the atrial-ventricular valves shut, but merely passes through passively from the atria to the ventricles. Therefore, some of the blood around the edges and in the appendage may stagnate and thus clot. The overall stroke risk is about 5% per year, ranging from 2% in those with "healthy" hearts and up to 10-15% in hearts that are not healthy. The overall risk ranges from 2 to 7 times in those who have atrial fibrillation versus those without atrial fibrillation.

The reasons why atrial fibrillation occurs is because of what happens to atrial cells as well as atrial electrical integrity due to a whole variety of circumstances. The autonomic nervous system plays a huge role, both the sympathetic nervous system (the release of adrenaline, epinephrine, norepinephrine)...which influences electrical traffic with exercise, stress, excitement, anxiety, and also the parasympathetic nervous system ( the vagus nerve and release of acetyl-choline) which occurs during deeper sleep, and digestion. 
Other issues pertain to cellular changes such as stretch, change of shape, fibrosis and inflammation and are related to ischemia, endocrine gland interaction, alcohol and drugs, genetics, and aging.
Therefore, people may have a triggering initiating event in a permissive atrial environment. The triggers are usually found inside the pulmonary veins where they enter into the left atrium. These pulmonary triggers can fire at about 500 to 600 times a minute, and under the influe nce of many things: (consider emotion, stress, sleep, high blood pressure, alcohol, certain drugs, heart failure, ischemia, thyroid and cortisol levels) atrial fibrillation may occur because of the cellular changes occurring in the atria itself.

It is important to not only have an appreciation of what may contribute to the phenomena of atrial fibrillation but also to identify it clinically.
Is it"Paroxysmal", whereby it starts and stops on its own, or is it "Persistent" whereby it starts on its own, but needs help to get back to normal rhythm, either by medication interaction or with cardioversion, or is it "Permanent", which means that you are in it and you live life with it! (Not necessarily a bad thing!)
One must also appreciate the clinical spectrum. People may be either completely asymptomatic and not know they have it, or they may have disabling symptoms and be very and unpleasantly aware that they are in it...and everything in between...and the way the person pre sents themselves allows for different options of how to take care of it. For example, a person who is completely asymptomatic does have the danger and risk of presenting as their very first presentation with a devastating stroke, or with congestive heart failure, Because they had now awareness or knowledge of having atrial fibrillation so therefore they were not on any therapy to take care of it.

Therefore, when I encounter someone with atrial fibrillation, I have to inquire the type: paroxysmal, persistent, permanent; the frequency, the duration, the heart rate, the symptoms, the intensity of the symptoms, the precipitating factors such as exertion, stress, sleep, digestion and bowel function, caffeine, alcohol. I have to appreciate their age. I have to do a full workup to understand what type of heart problems may exist. I have to assess for hypertension, diabetes, cholesterol, thyroid, sleep patterns, etc. An echo, a treadmill, sometimes a stress nuclear imaging study, a h olter monitor all need to be done to provide a thorough understanding of the status and nature of that person's heart functionality.

I need to assess the risk of stoke, and determine whether anti-coagulation should be recommended. Is the risk low, intermediate or high. Does the risk of anti-coagulation warrant the benefit. If someone is younger, and has a normal heart structurally and does not have high blood pressure, or diabetes, the risk of stroke is in the 2 to 2-1/2 % range per year. The risk of having a stroke on an anti-coagulant as well as the risk of having a bleed is in the range of 2 to 2-1/2% per year, so you are trading one evil off as equal to the other evil. But if you are older, and have high blood pressure or diabetes, and you have had prior heart or vascular events, and your heart is weaker, the risk of stroke may be up to 10 to 15%. Therefore, being on an anti-coagulant would be considered beneficial because you lower that risk to 2 to 2-1/2 %, an obvious a dvantage! But what if you are more elderly, and you have a tendency to fall, or you have had a hemorrhagic stroke, or a GI bleed, or a hematology problem  that enhances bleeding risk...quite a different story!

This is the first half of what I would like to present to you as regards the phenomenology of atrial fibrillation. Consider it an overview of presentation, problems and causes. The next essay will address aspects of treatment and management. How can you live life well with atrial fibrillation? Can you achieve old age with well being and otherwise good health? What are the choices? Is heart rate control a way to go if you have it? What about restoration and maintenance of Normal Sinus Rhythm? How possible is that? How is that done? What are the medication choices? How well do the medications work? When is a pacemaker appropriate? What about the procedure of an atrial fibrillation ablation? Is is safe? Is it dangerous? How successful is it? Are there things I can do in m y lifestyle that may be of benefit to not getting it?
These are the things I will address in my next "address"! ​