Category Archives: Cardiovascular

Benefits of Resistance Exercise

August 29, 2011 Dr. Pullen

In recent years it has become clear that in order to reap the full benefits of exercise that both aerobic exercise and resistance exercise is important. The recommendation of the CDC for adults of all ages is to incorporate strength exercises into the exercise regimen at least 2 days a week. Technically resistance exercise and strength exercise are not synonymous, but for practical purposes the terms are interchangeable. Resistance exercise is exercise where the major muscle groups exert force against a resistance. When the goal of this type of exercise is to increase strength it is strength exercise.

So what are the benefits of resistance exercise? Actually they are multiple, some obvious and others less obvious.

Resistance Exercise Builds Strength: This is one of the obvious benefits, but some aspects may not be appreciated. One aspect that some may not fully appreciate is that this benefit does not go away with age. One study of the elderly (average age 87) showed that an 8 week program of resistance training 3x/ week increased strength by over 100%, increased walking speed by 12%, and reduced the incidence of falls. With the sedentary life style many jobs enforce, and the lack of outdoors physical work by many of us, resistance training can make a huge difference in the way we feel, in our functional capacity to do tasks without hurting ourselves, and in our overall functional capacity.
Resistance Training Builds Bone Strength: Bones are a living tissue, constantly remodeling based on the stress loads placed upon them. Resistance training while bearing weight can lead to increased bone strength and help prevent the fractures of osteoporosis as we age.
Resistance Training Helps Lower Mild Hypertension: Aerobic exercise is the backbone of maintaining cardiovascular health, but resistance training also helps reduce blood pressure to at least some degree.
Resistance Training can Increase Metabolic Rate: Aerobic exercise is again the mainstay of weight control and maintenance, but there is considerable evidence that resistance training when combined with aerobic training leads to higher metabolic rate and more weight loss than aerobic training alone.
Improved Self Image: This is just my opinion and experience, but I believe that maintaining strength, physical capability and muscle mass is has a positive effect on self-image. I know I feel better about myself when I feel strong and fit. Resistance exercises are a key to this for me.

If you believe in the benefits of resistance exercise how should you go about setting up a program? First be real with yourself. Set goals that you believe are possible, sustainable and affordable. You can go to a gym, buy free weights or machines for home, or simply do exercises using your own body weight like pushups, pull-ups, and squats. Rubber band type resistance equipment is inexpensive and very effective. Secondly aim for 3 days a week for resistance exercise. Taking a day between training sessions gives the muscles exercised time to recover and grow. Third learn from Milo of Croton in that progressive overload is the principle behind steadily increasing strength. You don’t need a calf to carry every day until it has grown. Just start with exercises where 8-15 repetitions lead to fatigue. Once this is easy, slightly increase the resistance. Keep increasing the resistance as the exercise becomes easy. Last if a certain exercise leads to persistent pain, change something rather that thinking you can work through the pain. Often some minor change may avoid an overuse injury.

Add resistance training to your regular exercise to reap the full benefits of exercise. Enjoy.

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Xarelto: Now for Post-Op DVT prevention, A-fib, and Soon Maybe Routine Post Acute MI

August 26, 2011 Dr. Pullen

The recent FDA approval of Xarelto (generic name rivaroxiban) as the first direct factor Xa inhibitor for prevention of deep vein thrombosis and pulmonary embolism in patients undergoing hip and knee replacement caught my eye as a family physician who anticipates outliving at least one of these joints. In my community the standard of care for DVT prophylaxis with hip and knee replacement is post-op treatment with low molecular weight heparin in the hospital and short term oral anticoagulation with warfarin. Use of warfarin requires careful monitoring of coagulation times to avoid either under treatment and risk of DVT or over treatment and risk of bleeding. Xarelto is approved to use at a fixed dose and does not require blood testing to monitor its effects. Sounds good but as Paul Harvey always said stay tuned for the “rest of the story.”

Xarelto has been used in Canada and Europe for about 3 years so it is not expected that huge unexpected aftermarket risks will show up. The original studies compared Xarelto to a fairly low dose of low molecular weight heparin The studies generally show that Xarelto is more effective at preventing DVT than the low dose enoxaparin (Lovenox). In the U.S. the FDA approved dose for DVT prophylaxis is 30 mg twice daily of enoxaparin twice daily, not the 40 mg once daily used in the comparison trials. It is not unexpected that Xarelto leads to less DVTs and more bleeding than the low dose enoxaparin. I would like to see a study comparing warfarin use with Xarelto in prophylaxis of DVT post lower extremity total joint replacement. If I were having my hip replaced tomorrow I’d pass on Xarelto given what I can see from the current studies. I’ll keep an eye on future studies and clinical experience as my opinion may change with more studies and broad clinical experience.

Potentially more exciting is the very recent August 10, 2011 study in the NEJM where a very large cohort of patients with atrial fibrillation was treated with either Xarelto 20 mg daily or variably dosed warfarin. The results were very promising; with clear cut non-inferiority of Xarelto when compared to warfarin, and a fair probability that Xarelto is superior at preventing stroke. For the statisticians among readers the p-value for non-inferiority was <0.001 and the p-value for superiority was 0.12. The 95% range of confidence is 0.74-1.03. Total bleeding risk was equal at about 14-15% annual risk of bleeding annually in both treatment arms, and the risk of serious intracranial bleeding or death from bleeding significantly lower with Xarelto. This sounds promising and when FDA approved for prevention of stroke in a-fib, which seems very probable, Xaralto is going to give Pradaxa a run for its money in the non-valvular a-fib market. Xarelto promises to have similar benefits as Pradaxa in that it requires no anti-coagulation monitoring. This is a big deal for a-fib patients where the duration of treatment is often many years. The long-term hassle of constant blood monitoring of a condition where treatment is likely to go on indefinitely is significant. The issue of monitoring coagulation status for just 10-35 days post operatively is much less onerous. I anticipate a much higher level of excitement for xarelto for atrial fibrillation than for post operative DVT prophylaxis. (Since this post was published Xarelto has recieved FDA approval for stroke prevention in atrial fibrillation at a dose of 20 mg once daily. Even more exciting was a study presented at a large cardiology meeting showed in a large clinical trial that low dose Xarelto at 2.5 mg twice daily reduced death by 30% in the year post an acute coronary event like a heart attack. This could change the standard care from just anti-platelet therapy to anti-platelet therapy plus low dose Xarelto if it holds up to careful review. The risk of bleeding in this study was only modestly higher and overall death reduction was significant. )

It appears that there may be more drug interaction issues with Xarelto than with Pradaxa. Xarelto is extensively metabolized through the CYP 3A4 pathway, whereas Pradaxa has far less extensive hepatic metabolism and so less likelihood of patients being on drugs with the likelihood of interactions. That alone may make Pradaxa easier to use in this group of patients who are often subject to polypharmacy.

Of further note there are multiple other novel anticoagulant drugs that are likely to be brought to market in the next year or two, and it is likely that each will find a niche.

Update: Today, 9-8-2011, the FDA advisatory committede voted to recommend to the FDA against approval of Xarelto for use in stroke prevention in patients with atrial fibrillation. It looks like Xarelto is not likely soon to be added to Pradaxa as FDA approved new directly acting drugs for use in A-fib for stroke prevention. Apixaban is likely to get FDA approval soon.

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Multaq: Does it Still Have a Role in Atrial Fibrillation?

August 18, 2011 Dr. Pullen

Multaq has had so much bad news lately that the question whether it should play any role in the prevention or treatment of atrial fibrillation seems timely. Multaq, generic name dronedarone, was brought to the U.S. market about 2 years ago by Sanofi-aventis for the treatment of atrial fibrillation. It had FDA approval for the treatment of paroxysmal atrial fibrillation, permanent atrial fibrillation, and atrial flutter. I had really forgotten about Multaq as I have very few if any patients that local cardiologists have put on the drug. It came back to my attention today when drug reps came detailing it at the office. Somewhat incredulously the reps never even mentioned that the FDA released a warning on July 22, 2011 to physicians not to use Multaq in patients with permanent a-fib because the PALLAS trial was stopped early when patients on Multaq had a two-fold increase in death, stroke and heart failure hospitalization in patients with permanent a-fib.

Since its release Multaq has been in the news frequently as the FDA time after time has released warnings about its use. Not phased the manufacturer pushed ahead with the PALLAS trial. This study was undertaken to see if Multaq would reduce the incidence of major cardiovascular events like stroke, arterial embolization, MI, or cardiovascular death in patients with permanent a-fib. To date no anti-arrhythmic drugs have been shown to improve outcomes in this high-risk group of patients, and there were hints from the initial ATHENA trial of Multaq that it might improve outcomes. The PALLAS trial appears to have turned out to be a disaster for Sanofi-aventis when instead of improving outcomes in patients with permanent a-fib it appeared to double the rate of the very cardiovascular events Multaq was hoping to prevent. This led to the premature halt of the trial and the FDA warning of last month.

Multaq has had a really rough first 2 years with a seemingly never-ending litany of FDA warnings about its use. In early 2010 the FDA warned about the possibility of an increased risk of congestive heart failure (CHF) in patients on Multaq. On Feb 22, 2010 the FDA changed the warning label of Multaq to note that some patients had worsening of CHF on the drug. In the second quarter of 2010 the FDA warned about a possible link of Multaq with Torsades de pointes, a potentially lethal and very difficult to treat cardiac arrhythmia. In the third quarter of 2010 it became apparent that Multaq could interact with warfarin, an anticoagulant used in most a-fib patients to prevent strokes, leading to an increase in the anticoagulation effect and risk of hemorrhage. Near the end of 2010 cases of severe liver damage due to Multaq began to surface, and on Feb 11, 2011 the FDA warned that Multaq should be stopped if there is a suspicion of liver damage.

Now in a blow that I suspect may lead to the demise of Multaq the FDA has told patients on Multaq that they should contact their physicians to see if they should stop Multaq. The warning specifically tells patients not to stop Multaq without consulting their physician, but it appears that with the information we now have that the use of Multaq in patients with persistent atrial fibrillation is contraindicated. The FDA is telling physicians that they should not prescribe Multaq for patients with persistent a-fib and that the PALLAS data, which is preliminary at this point, is being analyzed to see how to apply this new information to therapy of patients with paroxysmal a-fib and flutter.

MULTAQ is a drug whose primary indication is the potential benefit of reducing hospitalization rates in patients with atrial fibrillation by maintaining a sinus rhythm. the concern of potential risks of hepatic failure, worsening of CHF, drug interactions with warfarin and now higher risk of death, stroke and heart failure hospitalization in patients with permanent atrial fibrillation make it seem less than prudent to start almost any patients on Multaq. The primary question remaining is whether patients currently on Multaq who are maintaining a regular sinus rhythm without any or many episodes of intermittent a-fib should continue the medication or be taken off Multaq. My guess is that Multaq will fall into the category of drugs rarely used very quickly if Aventis-sanofi decides to keep the drug on the market at all. As recommended by the FDA if you are taking Multaq you should contact your physician to see if you are better off continuing to take Multaq, or if you are better off to discontinue the medication. Don’t stop on your own.

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PB2: I Tried It and I Like It

August 15, 2011 Dr. Pullen

I just heard about a product called PB2 made by Bell Plantation and was really excited to see if it is as good as it was described by a good friend Kelly Aversa on her blog daily homemade. Kelly is a terrific cook and I’ve never tasted anything she prepared that I didn’t like, so if she “loves PB2’ I suspected I would too. I was so anxious to try it out that I borrowed a jar from Kelly to try while my order is being shipped. PB2 is really quite good. I found that when mixed by the directions it is a bit runny, but by adding a bit less water it is good enough to eat on crackers or in a sandwich and feel like you are eating peanut butter. It lacks a bit of the mouth feel from the oil in regular peanut butter, but for about 1/4 the calories it is a great option if you love peanut butter but need to watch your caloric intake. In recipes it is a great alternative.

Kelly posts the Weight watchers WW pts+ information on each of her recipes, and the PB2 Thai Chicken recipe looks great and has just +1 WWpts+ for the sauce. I don’t think you can smell traditional peanut butter without a higher score. (actually a 2 tbsp. helping of traditional peanut butter has 5 WWpts+ and a 2 tbsp. serving of PB2 has 1 WWPts+) I’m not in weight watchers but do try to watch my weight so I’m jazzed. PB2 is essentially peanut butter powder that can be reconstituted with water for use. I read the nutritional information about PB2 and it appears that PB2 has most of the protein goodness or peanut butter without the high fat calories. Here is a brief comparison of nutritional info for a 2 tablespoon serving of Adams No Stir peanut butter and PB2:

2 Tablespoon Helping Nutritional Information	Adam’s No-Stir Peanut Crunchy Peanut Butter	PB2	Chocolate PB2
Calories	190	45	45
Calories from Fat	130	13	13
Sugars	1 gram	1 gram	1 gram
Total Fat	17 grams	1.5 grams	1.5 grams
Saturated Fat	3 grams	0 grams	0 Grams
Sodium	130 mg	94 mg	70 mg
Protein	7 grams	5 grams	5 grams

The first thing I noted on this nutritional information is that PB2 appears to be a lower calorie food that does not try to make up for the fat by adding sugar and salt. The whole question comes down whether you think PB2 tastes good enough to substitute for regular peanut butter as a snack or sandwich with jelly. I think it is clearly going to be a great substitute in recipes. Either way for a peanut butter lover like me the thought of avoiding the extra calories of peanut butter and still getting the PB taste I love makes using PB2 a solid option. If your are as excited as I am consider checking out the

Bell Plantation Store and maybe try some yourself.

So far I’ve found great recipe sources. Great examples of these are on daily homemade and include:

PB2 Chocolate Chip Cookie Bar

There are hundreds of recipes for use of PB2 in cooking on the Bell Plantation site. I found 38 entrees, 47 side dishes, 67 deserts, 10 beverages, 10 no-bake recipes and others under the category of “healthy.” I suspect all of the recipes will fall under at least “healthier” than real peanut butter when used for cooking.

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Pradaxa: Better, Safer and Simpler than Warfarin?

July 22, 2011 Dr. Pullen

Pradaxa, generic name dibigatron, has the potential to change the way we manage atrial fibrillation to prevent stroke. Stroke is one of the most feared medical problems for many patients, and atrial fibrillation is one of the biggest risk factors for stroke. Stroke is the third leading cause of death in the U.S. and the leading cause of long term disability. Having atrial fibrillation increases a person’s risk of having a stroke about five fold and is the cause of 15-20% of strokes in America, over 100,000 strokes a year. Most patients with atrial fibrillation are candidates for long-term anticoagulation, and until Pradaxa was approved by the FDA in October, 2010 patients were either treated with oral warfarin, injectable low molecular weight heparin, or with less effective anti-platelet medications like aspirin.

Warfarin has been the choice of most physicians and patients for prevention of stroke in patients with atrial fibrillation because it works well. The annual risk of stroke in patients with atrial fibrillation is 4.5% without warfarin anticoagulation, and 1.4% with warfarin treatment. This risk varies a great deal from individual to individual depending on associated risk factors like coexisting hypertension, diabetes, congestive heart failure, prior TIA or stroke and age over 75. A scoring algorithm called the CHADS2 score is often used to better assess an individual’s risk. For most patients the absolute reduction in risk of stroke is high enough that most physicians have encouraged most of their atrial fibrillation patients to take warfarin. Warfarin therapy is no small undertaking though and has very significant bleeding risks. Several major problems are involved with use of warfarin as an anticoagulant:

A patient has to wait several days for the anticoagulation effects of warfarin to take effect. During this time the patient needs to be tested frequently, sometimes daily, to assess whether the prescribed dose of warfarin is just right.
It often takes one to several weeks to get the dose just right. Then after the INR is just right they will still need monthly blood tests to assure they remain adequately but not overly anticoagulated. If this sounds like a big hassle and expense you are very perceptive. It is.
Many drugs interfere with warfarin metabolism and so drug interactions are notoriously difficult to manage in patients on warfarin.
Because Warfarin is a vitamin K antagonist dietary variation in vitamin K content can have a significant effect on the anticoagulation effect of warfarin.
The therapeutic window for warfarin dosage is quite narrow, meaning the difference in dose between not enough and too much can be quite small. It is very difficult to predict what dose an individual patient will need.

Pradaxa is approved by the FDA for treatment of atrial fibrillation at a single fixed dose for most patients. It is dosed at 150 mg twice daily, and is effective within hours of taking the first dose. It works at least as well as warfarin to prevent stroke in patients with non-valvular atrial fibrillation, and overall the Pradaxa side effects profile is generally lower than with warfarin. In addition Pradaxa has far fewer drug interactions than warfarin which is notoriously affected by both diet changes and innumerable other medications. Bleeding risks with Pradaxa seem to be about the same overall as with warfarin. There may be a minimally lower risk of major cerebral hemorrhage and a higher risk of gastrointestinal bleeding with Pradaxa vs. warfarin.

The big issue holding back the widespread use of Pradaxa seems to be its cost. In a recent cost effectiveness analysis in the Annals of Internal Medicine for use in patients age >65 with non-valvular heart disease, assuming a daily cost of Pradaxa at $13.60 the conclusion was that Pradaxa has incrememtally higher costs and incrementally higher added years of life. Currently Pradaxa costs $230./ 60 doses , ie. 30 days supply or $7.66/day at Costco.com. With this lower cost than assumed in the study it seems like Pradaxa may win in the cost effective analysis.

I believe this study takes into consideration the lower risk of cerebral hemorrhage complications that can often lead to very expensive hospitalizations and long term nursing home care with Pradaxa. When I talk with other physicians they generally tell me that they would rather deal with GI bleeding, which is slightly more common with Pradaxa, than with intracranial bleeding which is slightly more common with warfarin. I’ll be interested to see more post marketing cost analysis comparisons as they become available, and to see how many patients are switched from warfarin to Pradaxa, and how many new patients are started on each of these medications.

I will not be surprised if as more physicians gain experience with Pradaxa, and more cost analysis is done, that Pradaxa will become the standard of care for treatment of atrial fibrillation for stroke prevention in patients at high enough risk of stroke to warrant the risks of therapy.

While you’re here be sure to follow @DoctorPullen on Twitter and subscribe (at the right) so you don’t miss a post and get the between-post random thoughts, new ideas as they happen.

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Simvastatin vs. Lipitor – New Restrictions Make it a Different Equation

June 10, 2011 Dr. Pullen

Simvastatin vs. Lipitor: Now a whole new decision based on the recent FDA restrictions on simvastatin 80 mg dosing.

Yesterday I posted a brief article about the new announcement of the FDA restrictions on the use of simvastatin 80 mg. Some patients, especially those with diabetes or preexisting atherosclerotic vascular disease, have LDL goals that are really low. There is some evidence that pushing LDL levels as low as 70 or lower can prevent progression or even possibly reverse this vascular disease. For many patients in order to achieve these levels a reduction of 40-50% or more in their baseline LDL cholesterol level is needed. In order to achieve this degree of LDL lowering one of the more potent statin regimens is often needed.

Simvastatin was the third of the currently used statins to lose its patent and become available as a generic drug. First generic was lovastatin, generic for Mevacor. Mevacor was the first statin medication to gain FDA approval in the U.S. It was somewhat slow to gain widespread use as it took some time for data to become available about the benefits of statin use to lower LDL cholesterol. By the time statin used became widespread statins with greater effect on LDL reduction became available. Pravachol (Pravastatin) and Zocor (simvastatin) followed Mevacor to market. Shortly after Zocor became available Lipitor came to market. Lipitor zoomed to become the market leader based on a number of factors. One of the factors was the greater LDL reduction available with Lipitor. In head to head comparison of simvastatin vs. Lipitor, Simvastatin has a considerably more modest LDL reduction. See the table below. In addition Lipitor was featured in several high profile studies which vaulted the popularity of statins for both secondary and primary prevention of coronary artery disease.

Lipitor, a Pfizer product, is the number one grossing drug in the world, with over $10 billion in sales in 2010. Simvastatin reclaimed a huge portion of statin sales in 2009 when generic simvastatin became available, in part because at the top dose of 80 mg simvastatin’s LDL reduction approaches the LDL reduction possible with lower doses of Lipitor. The news this week that the FDA is limiting the use of simvastatin 80 mg is going to make the simvastatin vs. Lipitor/atorvastatin choice lean much more toward Lipitor/atorvastatin. On Nov 30, 2011 a generic for atorvastatin is going to become available. Despite this I anticipate another 6 months, when multiple generic companies can market atorvastatin before generic atorvastatin prices drop to the range of the other generic statins. The apparent lack of an abnormally high incidence of myopathy as a lipitor side effect is going to drive this change.

Still that’s only a year from now, and the simvastatin vs. Lipitor choice is now one I can realistically entertain, knowing that the price excess of Lipitor is soon to disappear. I’ll consider changing my simvastatin 80 mg patients to Lipitor now, and generic atorvastatin when it becomes available unless they have been stable and symptom free for a long period of time. The FDA recommends change unless a patient has tolerated simvastatin 80 mg for over a year. This is because most cases of myopathy and rhabdomyolysis from simvastatin 80 mg happen in the first year of use. I’ll still consider low dose simvastatin for patients who need only a more modest reduction in LDL reduction, but I expect atorvastatin to quickly become the most widely used statin after it competes in price with simvastatin.
In the long run the simvastatin vs. Lipitor choice looks like one that Lipitor, soon to be generic atorvastatin, is going to win by a runaway. I’ll report back in a couple of years to let you know if I’m right.

Expect 30-40% LDL Reduction	Simvastatin 20 mg	Atorvastatin 10 mg
Expect 40-45% LDL Reduction	Simvastatin 40 mg	Atorvastatin 20 mg
Expect 45-50% LDL Reduction	Simvastatin 80 mg	Atorvastatin 40 mg
Expect 50-55% LDL Reduction		Atorvastatin 80 mg

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Simvastatin 80 mg and New FDA Restrictions

June 8, 2011 Dr. Pullen

I’ve been pretty aggressive over the last few years at getting patients onto generic statins when their cholesterol can be controlled appropriately and have a number of patients on simvastatin 80 mg. The branded statins, like Lipitor and Crestor are at least as effective as simvastatin 80 mg, but cost far more, and simvastatin has seemed to be the most potent of the available inexpensive generic statins. Pravastatin and lovastatin are generic alternatives, but are considerably less effective at lowering the LDL cholesterol in patients who need a major LDL lowering drug.

As with any individual physician my “n” or number of patients treated is small enough that it is not possible from personal experience to detect issues like the increased incidence of myopathy and rhabdomyolysis noted with simvastatin 80 mg, or with lower doses used in patients on meds like amlodapine, diltiaziem, and others.

As I noted in an earlier post generic Lipitor is expected to lose its patent this year, and generic atorvastatin should be available. This is likely to obviate the need for higher doses of simvastatin for lipid control in patients with very high cholesterol. Since the earlier warnings I’ve been using lower dose simvastatin and avoiding simvastatin 80 mg in most patients, but this recent evidence presses the need to avoid simvastatin 80 mg even more. For the press release by the FDA see:

FDA Drug Safety Communication: New restrictions, contraindications, and dose limitations for Zocor (simvastatin) to reduce the risk of muscle injury

Safety Announcement

Additional Information for Patients
Additional Information for Healthcare Professionals
Data Summary
Simvastatin Dose Limitations
Relative LDL-lowering Efficacy of Statin and Statin-based Therapies
References

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Psyllium Husk

May 16, 2011 Dr. Pullen

I’m writing another post on psyllium, because the prior post Psyllium Husk Benefits has been so popular. I first learned about psyllium as a family practice resident in the early 1980’s when due to a suboptimal diet and harried lifestyle I developed hemorrhoids. My residency director recommended I start on psyllium, and the results were terrific. Instead of spending 15 minutes reading the paper and hoping for a bowel movement, I spent 15 seconds, no straining, and within days the hemorrhoids stopped bothering me.

This led me to investigate psyllium properties and benefits. I was pleased to find the psyllium is different from most of the other available fiber supplements available then, or available today. The biggest difference is that psyllium husk is a water soluble fiber that binds bile salts. Bile salts consist in significant part of cholesterol, and by binding the bile salts it prevents the reabsorption from the gut of the cholesterol and lowers LDL cholesterol. This technique of lowering LDL cholesterol was the mechanism of action of the primary LDL lowering drug available in the early 1980’s called cholestyramine. The problem with cholestyramine was that it causes significant constipation. This is often severe enough to prevent compliance with the four daily doses needed to be effective. Metamucil on the other hand is often used to prevent or treat constipation, and helps promote regular, soft, easy bowel habits. See the psyllium husk benefits post for lots of details on the cholesterol benefits of psyllium husk.

Psyllium also slows the absorption of simple carbohydrates from the gut when consumed with a meal. This has the benefit of lowering blood sugar levels after the meal, and can be helpful in patients with glucose intolerance. It’s not really considered a treatment for diabetes, but may be slightly helpful in this regard.

Psyllium is available for consumption in multiple forms. The most commonly used and popular form is as a powder that can be mixed with water or juice to drink. This is an inexpensive and simple way to take psyllium. The trick to this is to mix and drink it quickly, as it tends to form a gel if left in the liquid for more than a few seconds. I recommend mixing in just 4 ounces of water and the drinking a large glass of water immediately afterwards to dilute the mixture in the stomach. The usual dosing is 1-3 large heaped teaspoons daily. This can be all in one dose, or split into 2-3 doses a day. It’s best to gradually increase to a full dose, because if you start on a high dose initially it can cause gas and bloating.

Psyllium is also available in capsules that range from 100-500 mg in dosing. The problem with these is that to get a useful dose you need to take so many capsules. A heaping teaspoon has up to 4 grams (4000 mg) so to take the equivalent in capsules would be 8 of the 500 mg capsules. This would cost a lot more and just be a lot of very large capsules to take.

Psyllium can be consumed as crackers or wafers. Metamucil makes a psyllium wafer in apple crisp and cinnamon flavors, but I cannot find good nutritional data on these to assess dosing and calorie content. There are many online recipes for making psyllium into crackers.

Since 1989 psyllium has been an ingredient in several cereals available commercially. These vary in the amount of psyllium and the other nutritional values. A good review is available here.

Overall I recommend just using the less expensive and very effective psyllium powders like Metamucil, Konsyl, or multiple other brands. I use branded sugar free orange flavored Metamucil as I find the texture of some of the slightly less expensive generics to be less palatable, but any of them should be equally good water soluble fiber sources.

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PSVT

March 28, 2011 Dr. Pullen

PSVT, or paroxysmal supraventricular tachycardiaia, is one of the cardiac conditions where over the last few decades researchers have made tremendous progress in diagnosis, treatment, and even cure of the condition. PSVT is a common medical condition in which sudden paroxysms or attacks of very rapid heart rate seem to arise out of nowhere. They can be brief, just a few seconds or a minute or two, or can last hours and lead to circulatory compromise.

When everything is working normally in our heart, each heartbeat is triggered by the sinoatrial node in the right atrium. This node starts causing heart muscle fibers in the heart to depolarize, an amazing electrical/chemical reaction that rapidly spreads to all adjacent heart muscle cells. Special heart muscle cells called Purkinje cells, that connect to form Purkinje fibers, are able to incredible quickly transmit this depolarization from cell to cell and through the atria until they reach the atrioventricular node (AV node) where after a momentary pause, the depolarization races through bundles of Purkinje fibers in the ventricles called bundle branches out to the ventricular heart muscle. In the perfectly formed heart there is a fibrous tissue that separates the atria and the ventricles so that the depolarization of heart muscles can only pass from the atria to the ventricles through the AV node.

In most patients with PSVT there is an aberrant group of muscle cells that goes through this connective tissue separator allowing the depolarization to get from the atria to the ventricles, or backwards, other than through the AV node. When this is present sometimes a circular movement of the depolarization can occur, leading to a very rapid heart rate. This very rapid heart rate, often at rates as high as 190-200 beats/ minute is called PSVT.

Some patients with PSVT have a resting EKG that shows a specific abnormality where the PR interval is very short and there is a “slur” on the QRS wave. This specific type of PSVT is called Wolfe-Parkinson-White syndrome.

Treatment of PSVT can be with medications to slow the ability of the heart to beat, and make PSVT less rapid and so better tolerated. The biggest breakthroughs though in PSVT management have been the ability to use cardiac catheters along with tiny instruments to map the conducting ability of the heart and find the aberrant tissue that connects the atria to the ventricles. If this can be located the cardiologist can then destroy the aberrant fibers usually using thermal probes and so effectively cure PSVT. In patients with frequent, prolonged, or very rapid PSVT this has revolutionized therapy, and been life-changing and at times lifesaving therapy.

Experienced cardiology electophysiologists have rates of success with PSVT ablation of 95% or higher. It has become a standard of therapy for many patients where PSVT is not easily controlled medically. Newer cryoablation procedures are being developed to allow treatment of the few PSVT patients who cannot have radiofrequency ablation. The cryotherapy procedures allow treatment of aberrant pathways in areas too close to key structures like the AV node to treat with radiofrequency.

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A Fitness Gene?

March 18, 2011 Dr. Pullen

Our individual genetic makeup seems to play a role in just about everything about us, and so this probably should come as no surprise. There is proving to be a genetic explanation for why some people seem to get really fit when they exercise, and others just don’t. An interesting article in the NY Times Health section outlines a recent genetic study of aerobic capacity improvement with exercise. I found it an interesting read:

March 16, 2011, 12:01 am

Is Fitness All in the Genes?

By GRETCHEN REYNOLDS

Why do some people respond to an aerobic workout routine by becoming incredibly fit, whereas others who exercise just as hard for months end up no fitter than when they began?

That question has bedeviled countless people who’ve started exercise programs. It has also motivated a major new study of the genetics of fitness. Scientists long have known that when any given group of people faithfully follows the same aerobic workout routine, some increase their cardiorespiratory fitness substantially, while an unfortunate few seem to get no benefits at all. But what, beyond the fundamental unfairness of life, makes one person’s body receptive to exercise and another’s resistant? According to the new study, which will soon be published in The Journal of Applied Physiology, part of the answer may depend on the state of specific genes. Read more

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