This, the News Page, of the Northwest Tennessee Cardiology Clinic web site is intended to provide interest items to our patient population. Occasionally this will be in editorial format from Dr. Hall in first person. There will be interesting items, important notices, and current event items to be aware of as relates to heart health. It is not intended to replace or supplant medical advice given to the patient by their personal physician.
Salt Guidelines - Outdated ?
The American Heart Association recommendation for 1.5 grams of salt per day has been the guideline since 1980. The hospital "AHA diet" is actually based on 2 grams salt per day. However, recent information has come to light that suggests that there is no basis for this "established" guideline. Most recently, published in the New England Journal of Medicine, several studies addressed this and found some interesting relationships. The expected relationship of rising blood pressure with increased salt intake was evident; however, this relationship was not linear. In fact, blood pressure really only increased when sodium intake exceeded 3.5 - 4 grams per day.
The most striking relationship was that between sodium intake and adverse cardiovascular events. There was a trend to higher cardiovascular events when salt intake was greater than 5 grams per day, but not as much as when the salt intake was less than 2 grams per day. In other words, consumption of too little salt (often measured as sodium excretion in the urine) is as harmful as consuming to much salt ...if not more ! In fact, sticking to the AHA guidelines would lead to a two-fold increase in major adverse events. At this point, however, the American Heart Association has not changed their guideline.
Look forward to hearing more on this in coming studies and in popular media. So what would the best sodium intake level be to reduce cardiovascular risk ? It appears at this time to be approximately 4 grams per day - more than twice the recommended "guideline" !
For added detail on this topic, see the following:
- Moderate Sodium Intake Tied to Lower CVD Events : PURE
- Low-Salt Diets May Pose Health Risks, Study Finds
- Topol on Salt: Time to Shake the Sodium Guidelines ?
- - August 29, 2014 .
Coumadin (Warfarin) and the INR
An often requested question I receive from patients, particularly those prescribed Coumadin, is not only how does it work, but how is it therapeutically followed. Coumadin, which is a trade name for the chemical warfarin, and which is comically called "rat poison" by many of my patients, has been used to prevent thrombosis (clotting) since before I was born. It was originally discovered back in the 1920's in cattle that had died from hemorrhaging after minor procedures. These cattle had been feeding on molded silage consisting of sweet clover which over time was identified as a potent anticoagulant (clot formation inhibitor). Over the following 20 years, the chemistry was worked out and it was known that Vitamin K was the antidote. Coumadin worked not by inhibiting Vitamin K's action, but by limiting its supply. Vitamin K is important in the function of many clotting factors in the body and is prevalent in green leafy vegetables. Now here's where a discussion of coumadin can get quite complex, and my intent is to keep this essay at a level where my patients can understand and conceptualize what is going on without knowledge of human biochemistry. By decreasing vitamin K available to synthesize clotting factors, the ability of the body to thrombose (to form clots) is reduced. And yes, it is still being used as a rodenticide ("rat poison") although much stronger chemicals are now available.
So how did it get from being used as a rodent killer to being used in humans as an anticoagulant ? In the early 1950's, someone tried to commit suicide by ingesting a lot of rat poison. By this time, it was known that Vitamin K is the antidote and this was given. The patient survived. After clinical trials, warfarin was approved for use in humans. President Dwight D. Eisenhower was one of the first recipients after his heart attack in 1955.
Coumadin is often referred to as a "blood thinner" although it does not change or alter the viscosity of blood. It is used to treat thrombosis (clotting) in low flow areas such as veins to reduce the risk of embolism (breaking a piece off of the clot) to other organs where blood supply could be blocked (such as a pulmonary embolus - a clot in the lung). Also, when you have a quivering (fibrillating) heart chamber in the setting of a viscous liquid (blood), gelling or coagulating can occur and increases the risk of stroke by a factor of five. Coumadin is the most often prescribed medication used to reduce the risk of this occurrence. There are now other medications on the market that are being used in this setting, and we'll discuss those at a later time. Also, when an artificial mechanical heart valve is implanted, there are low flow areas and eddy currents behind the new valve that tend to be a coagulation risk, as well as the obvious presence of a metallic foreign object. As with former President Dwight Eisenhower, coumadin is still being used in certain cases after a heart attack, although other medications are now known to be more effective.
Coumadin has a narrow therapeutic window - meaning that the amount of anticoagulation between 'too much' and 'not enough' is quite small ... and is different for different patients. On top of that, many other medications, medical conditions, and foods can either make anticoagulation 'too much' or 'not enough'. So how is this measured ? Again, without getting too technical, it is measured by the blood test known as the "pro time", which is short for Prothrombin Time (PT). Although not technically accurate, you can think of this as roughly the time it takes for blood to clot. A normal "pro time" is roughly 12-13 seconds. During routine anticoagulation, we would strive to reach a "pro time" of roughly 1 1/2 to 2 times this value. As it turns out, however, during the time I was in training in the early 1980's, it was noted that there was a significant variation in "pro times" depending on how it was measured. Yes, this gets technical, but here's the bottom line - in order to "normalize" these variations, the patient's measured "pro time" is compared to a "normal" patient's "pro time" in a mathematical ratio. And it is this ratio, known as the International Normalized Ratio or INR, that we now measure.
A normal INR would of course be 1.0 and so standard anticoagulation would strive to a value of 2-3. The practitioner always personalizes this depending on the patient's case history and can sometimes range lower (1.5 - 2.0) or, in the case of metallic heart valves, higher (2.5 - 3.5). Nowadays, a simple finger stick in the doctor's office is all it takes to measure this INR. Once the dose is established for that individual patient, it is most often measured monthly. Coumadin does not establish itself quickly in the body, often taking 3 - 5 days to reach therapeutic levels, and as a result also takes the same amount of time to wash out once the patient stops taking it. Giving Vitamin K only accelerates this a small bit and in emergency cases, plasma is often given to quickly replenish clotting factors. For elective surgery on patients taking Coumadin, stopping the Coumadin 3 - 5 days is the norm with the resumption of dosing very soon after surgery. Again, it takes 3 - 5 days to reestablish therapeutic effect. If it is critical that anticoagulation be maintained during this interval, often a low-molecular weight (or regular) heparin is given subcutaneously.
Again my goal is not to be exhaustive in explaining the pharmacy of warfarin. The study of clotting in the human body is not for the faint of heart ! The goal is to allow my patient population an understanding of what Coumadin is, how it works, and how its effect is measured and therapeutically followed with the INR.
For added detail on this topic, see the following:
- - July 6, 2013.
Grapefruit Interaction with Medications
One of the more interesting questions I've gotten from some of my patients is the question of interaction of many prescribed medications with, strangely enough, grapefruit. This was accidentally discovered by a Canadian research group back in 1989 when they were researching the effect of alcohol (ethanol) on the effect of a common and popular blood pressure medication, Plendil (felodipine). In order to hide the taste of ethanol, it was mixed with grapefruit juice. In many of the study individuals, it was noted that the blood pressure was dramatically lower than could be predicted. As it turned out, it wasn't the fault of the alcohol - it was the grapefruit juice ! The grapefruit is a hybrid of the Jamaican orange and the Indonesian pomelo and the "Ruby Red" variant from Texas is the most popular commercially.
This "grapefruit juice effect" is due to a plant chemical called furanocoumarin. The effect is incompletely understood but basically it increases the bioavailability of many medications. Many medications pass through the intestines with very little of it making it to the bloodstream and this is calculated in its proper dosage. However, the furanocoumarin in grapefruit juice interacts with an enzyme that causes many medications to 'hang around' longer, making it more available. This has the effect of substantially increasing the dose of medication - a setup for an overdose ! Even small amounts of grapefruit (or grapefruit juice) consumed hours before taking these medications can be detrimental.
Further studies are being performed to identify how some medications are more prone to this effect than others and to what extent different patients can be effected. Many popular medications used for blood pressure, heart arrhythmias, and cholesterol management ('statins') are on a growing list of interactors with grapefruit juice. But why, for example, Plendil (felodipine) interacts more than Norvasc (amlodipine) or Zocor (simvastatin) reacts more than Crestor (rosuvastatin) or Pacerone (amiodarone) reacts more than Betapace (sotolol) is simply not known at this time. Additionally, as I frequently state to my patients, "different people are different" ! That is some are more sensitive to the effect of grapefruit juice.
The bottom line is DON'T consume ANY grapefruit or grapefruit juice while taking ANY medication on this growing list.
For further information on this topic, see the following:
- More New Drugs a Bad Fit With Grapefruit
- Drugs that Interact with Grapefruit on the Rise
- Mayo Clinic - Grapefruit Juice: Beware of Dangerous Medication Interaction
- - February 10, 2013 .
Heartscore™ - worth it ?
Also known as a heart scan or coronary artery calcium (CAC) scan, this is a computed tomographic (CT) scan used to look for calcium deposits in the coronary arteries of the heart. This test attempts to stratify risk of coronary events (e.g. heart attacks) in asymptomatic (meaning no symptoms of chest pain) individuals considered to be at intermediate risk. This risk gives the probability of a coronary event at between 10 to 20% over a 10 year period. Coronary artery disease is caused by plaque formation within the walls of the coronary arteries. This plaque is made up of fat, cholesterol, and calcium. It is this calcium that can be detected by a CT scan.
The use of heart scans has been controversial primarily due to the concept of intermediate risk. A heart scan is not useful for those patients at either low risk for a heart attack or high risk for a heart attack. For example, if you are less than 55 years old, with normal cholesterol and blood pressure and don't smoke, your risk of heart attack can be calculated to be less than 10% in the next 10 years. A heart scan done in this population will likely not tell you more than you or your doctor already know. If you are greater than age 65, smoke, have high cholesterol and blood pressure, you are at high risk for a coronary event in the next 10 years. Again a heart scan won't do you much good as you and your doctor already know you are at high risk due to the presence of significant coronary risk factors. You can calculate your own coronary heart disease (CHD) risk and read more about coronary risk at the Framingham Heart Study site. Additionally a heart scan will not provide any information about how your condition should be treated. The American Heart Association and the American College of Cardiology do not recommend routine heart scans be performed in patients without signs or symptoms of heart disease.
It is in the intermediate risk area where a heart scan might show benefit. In other words, if you are between the age of 55 and 65, have borderline high cholesterol or high blood pressure, or smoke, your risk of a coronary event can be calculated to be between 10% and 20% over the next 10 years. If you have had chest pains, stress testing would be my choice above a heart scan because it measures function. In other words, besides measuring exercise tolerance, the stress test measures the hemodynamic significance of any occlusive plaque. If you have some plaque, it may not be significant and the stress test can guide treatment or suggest further testing.
The theory behind the coronary artery calcium (CAC) score is that the more calcium that is measured in the coronary arteries, the more likely it is you have coronary heart disease. However, having calcium in your coronary arteries does not necessarily mean you have coronary heart disease (CHD). Additionally, by degree, you could have severe CHD, but have very little or no calcium on the heart scan. This is because the plaques that cause coronary artery disease start off as soft and non-calcified and only harden (calcify) with time.
To the degree that the heart scan has any benefit at all, it may be in the behavioral aspects of patient treatment. The target group for those obtaining heart scans are those that are worried that they have a particular disease even if they have no symptoms and no risk factors for the disease. It is often advertised as a walk-in procedure, not requiring a doctor's order. Many insurances do not cover this procedure. Once the CAC score is obtained, a copy of it should be presented to your doctor. Realizing that the patient may have increased risk for CHD, usually increases compliance with lifestyle changes necessary to lower risk - low cholesterol diet, losing weight, quitting smoking, proper blood pressure management. With these measures, coronary heart disease risk can be lowered even though coronary artery calcium may progress over time.
For further information on the heart scan, see the following:
- Mayo Clinic - Heart Scan (Coronary Calcium Scan)
- WebMD - Coronary Calcium Scan
- The St. Francis Heart Study Randomized Clinical Trial
- U.S. Services Preventive Task Force - Using Nontraditional Risk Factors in Coronary Heart Disease Risk Assessment