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Category Archives: Cardiovascular

Is Your Cough a Lisinopril Cough?

Lisinopril was the third most prescribed medication United States in 2010 and lisinopril cough is the most common lisinopril side effect seen in everyday practice. (In this article I will refer to lisinopril cough rather than angiotensin converting enzyme inhibitor cough as a matter of convenience because lisinopril is by far the most commonly prescribed medication the class.)  Since it is so common you would expect that making a diagnosis of  lisinopril cough should be quite simple, and sometimes it is. Other times differentiating lisinopril cough from other causes of cough can be pretty complicated. Most of the time in the office we can suspect lisinopril cough because the patient  did not have the cough prior to starting lisinopril and it tends to be a dry twitchy cough that just will not go away. The problem lies in fact that lisinopril cough often doesn’t stop immediately on discontinuation the medication and that many of the patients using lisinopril have other potential causes of cough.

I used to think that lisinopril cough always started in the first month or so of using lisinopril, but it’s clear that a small minority of patients will develop a lisinopril cough months or longer after starting lisinopril. In addition although most patients find their lisinopril cough decreasing shortly after stopping lisinopril and resolving within a few weeks, there are patients where the cough can persist for many weeks or even months.

Although most people think of cough as a symptom of a respiratory infection or an allergic problem like asthma or hay fever, it is becoming increasingly clear that esophageal acid reflux is a common cause of cough. Cough related to reflux can either be due to occult minor aspiration of gastric contents into the trachea or from irritation of the esophagus leading to cough without aspiration. Reflux related cough is another type of cough can take a long time to resolve even on aggressive anti-reflux therapy, and so be difficult to diagnose with certainty. If a patient is also on lisinopril the sorting out which problem is causing the cough can be a challenge.

Lisinopril is used primarily for the treatment of high blood pressure and congestive heart failure. It is also used for prevention of kidney disease in patients with diabetes. All of these conditions are seen more often in older adults, obese patients and often in patients with multiple complex medical conditions. This can make physicians reluctant to discontinue lisinopril because every medication change in a complex patient can upset a delicate balance, so if a patient is doing well except for the cough it is tempting to now want to make any medication changes.  Thankfully now switching to an angiotensin receptor blockers is a fairly easy medication alternative, especially with losartan now available as an inexpensive generic ARB with losartan soon to follow.

Lisinopril cough is felt to happen because the site of action of lisinopril is in the lungs where it prevents the conversion of angiotensin I into angiotensin II.  It is not completely clear what causes the cough but the known fact that angiotensin converting enzyme inhibitors function at a cellular level in the lung seems to be the key. Angiotensin I is produced in the kidney and released to the circulation. The angiotensin I in the bloodstream circulates through the lungs where it is converted into angiotensin II in a process requiring an enzyme called angiotensin converting enzyme. ACE inhibitors like lisinopril block the site where angiotensin I fits at the angiotensin converting enzyme therefore blocking the production of angiotensin II which is the active form of angiotensin. Angiotensin II works in the peripheral arterioles to cause constriction of the tiny arteries and therefore elevation of blood pressure. The angiotensin receptor blockers (ARB) function at this receptor in the peripheral arterioles and so ARB medications are much less commonly associated with cough.  Unfortunately cough is an occasional but very infrequent cause of cough which can further complicate trying to decide whether the cough was related to lisinopril if it doesn’t resolve quickly and switching medications.

The incidence of lisinopril cough is almost certainly higher than the incidence noted in the original studies of lisinopril quoted at 1% for patients with congestive heart failure 3.5% for patients with hypertension, but the exact incidence of lisinopril cough is really unclear.

When I see a patient on lisinopril with cough I first try to put the cough into perspective. If the cough started as part of a typical upper respiratory infection with congestion, fever or chills, sore throat or other similar symptoms I will tend to advise the patient that the cough will likely resolve as the illness passes.  Problems like post-bronchitic bronchospasm, where cough persists for weeks or months after an episode of acute bronchitis can be a challenge sometimes, but usually this approach works. On the other hand if the cough is a fairly mild cough that persists or gradually progresses to be much more annoying then I usually suggest that we stop the lisinopril and use an alternative medication, usually a generic ARB like losartan.  Then we wait and see if cough resolves over the next few weeks. If cough persists more than a few weeks it comes a bit trickier. If the cough seems to be gradually diminishing I usually try to convince the patient with a longer.  If the cough is not improvingat all we need to look harder for another cause.

Most of the time lisinopril cough is usually fairly simple problem to diagnose and manage because most physicians recognize cough as among the most common of lisinopril side effects, but like almost everything in medicine things are sometimes more complicated than they appear and cough is a symptom that can be a diagnostic and therapeutic challenge.

 

 

 

Obesity, Smoking, Death and Medication Use




Somehow I was not in the least surprised when I came across a Huffington Post article showing which states in the US have the highest rates of medication use.  Why am I not surprised?   Intuitively I suspected that these are the states with the highest rates of obesity and smoking.  Look back to a prior post on how obesity has surpassed smoking as the leading preventable cause of death in America. Every one of the top 9 most medicated states is in the highest tier of rates of obesity.  What medical conditions lead inexorably to the use of multiple medications?  Think diabetes, hypertension and chronic pain.  All of these conditions are directly related to obesity in many cases.  Also think heart and lung diseases like asthma, COPD and coronary artery disease, all well documented to be related to both smoking and obesity.  Here are the 9 “most medicated states” from the Huffington Post article with the CDC 2011 rate of obesity in parentheses.  For interest I’ve also put the state’s rank in terms of smoking incidence from the CDC data.
State (Retail Rx per capita)         Rate of obesity             Smoking Rate (national rank)

  1. West Virginia (18.4)                      >30%                               25% (tie for 8th highest)
  2. Tennessee (16.9)                          >30%                              25% (tie for 8th highest)
  3. Alabama (16.9)                             >30%                              25% (tie for 8th highest)
  4. Kentucky (16.5)                             30%                               29% (alone w/top rate)
  5. Arkansas (16.4)                            >30%                              26% (6 way for 2nd)
  6. South Carolina (16.3)                     25%-29%                        24% (4-way tie for 12th)
  7. Mississippi (15.9)                            >30%                             26% (6-way tie for 2nd)
  8. Iowa (15.3)                                  25%-29%                        22% (3-way tie for 17th)
  9. Missouri (15)                                 >30%                              26% (6-way tie for 2nd)

For reference there are nine states with 2009 rates of obesity > 30% of which 7 are here in the top 9 most medicated states. The national average rate of smoking is 21% and all 9 of the states with the highest rates of medication use are in the top 17 states for rates of smoking.

I cannot access the SDI data to see what the rates of obesity are in the states with the lowest incidence of obesity are  but here are some other health related statistics and their relationship to a relative lower obesity rate.

1)      Colorado is alone as the only state in the US with a 2009 rate of obesity at <20%.   Why doesn’t Colorado rank at the very top for the lowest for death rates in adults?  Possibly because of a smoking rate of 20% (tie for 28th highest leaving it pretty good but with  a death rate of 709/100,00 (11th best).

2)      The fifteen states with obesity rates from 20-25% (the best except for Colorado) are listed below in alphabetical order:

                                                      Death rate (rank)                             Smoking Rate (rank)

a)      Alaska                               742 (2oth)                           24% (Tie for 12th highest)

b)      California                         660 (4th)                                15% (50th highest, i.e. 2nd lowest)

c)       Connecticut                   691 (8TH)                               18% (tie for 38th highest)

d)      Hawaii                               590 (1st)                                16% (49th, i.e. 3rd lowest)

e)      Idaho                                 723 (16th)                             18% (tie for 38th highest)

f)       Minnesota                        675 (5th)                                17% (tie for 44th highest)

g)      Montana                           786 (33rd )                            20% (tie for 29th highest)

h)      New Jersey                     717 (14th)                             18% (tie for 38th highest)

i)        New York                        676 (6th)                                19% (tie for 32nd highest)

j)        Oregon                              748 (22nd)                             18% (tie for 38th highest)

k)      Rhode Island                   749 (23rd)                             20% (tie for 28th highest)

l)        Utah                                    659 (3rd)                               11% (51st highest, i.e. lowest)

m)    Vermont:                           721 (15th)                             18% (tie for 38th highest)

n)      Virginia                              762 (25th)                             19% (tie for 32th highest)

o)      Wyoming                           773 (29th)                             21% (tie for 21st highest)

Looking at this data you may note that 4 of the 5 states with the lowest death rates are in the 15 states with the lowest rates of obesity, and that none of them are worse than the 44th highest smoking rates. (only Arizona is missing, in the next 25%-29% obesity rate and at a tie for 21st in rate of smoking)  You may also note that the only two states in the top 15 for lower obesity rates ranking in the bottom half for death rates have smoking rates ranking at 21st and 29th.

Contrast this with the five states with the highest death rates:

  1. West Virginia with >30% obesity and 25% smoking rate (tie for 8th highest)
  2. Mississippi with > 30% obesity and 26% smoking rate (tie for 2nd highest)
  3. Oklahoma with >30% obesity and 26% smoking rate (tie for 2nd highest)
  4. Alabama with > 30% obesity and 25% smoking rates (tie for 8th highest)
  5. Louisiana with >30% obesity and 26% smoking rate (tie for 2nd highest)

In contrast the states with the lowest death rates have the opposite statistics for obesity and smoking rates:

  1. Hawaii with 20-24% obesity and 16% smoking rate (3rd lowest).
  2. Arizona is the exception in these states with 25-29% obesity and a smoking rate of 21% (right at the national average and ranking in a 6 way tie for 20th highest in the U.S.
  3. Utah with in the 20-20% obesity and the lowest smoking rate in the U.S. at 11%.
  4. California with 20-24% obesity and 16% smoking, second only to Utah.
  5. Minnesota with 20-24% obesity and in a tie for 4th lowest smoking rates at 17%.

It appears that states where citizens choose not to smoke and trend to be less obese have both lower rates of medication use and lower death rates. My guess is that the observation of lower death rates and lower rates of medication use are the result of lower rates of diabetes, hypertension, COPD, cardiovascular disease in these same states.   Yes these other health markers also trend directly with obesity and smoking rates.

So what can you as an individual learn from this?  Get fit, avoid obesity and don’t smoke.  No surprises here.

You may also enjoy:

Belly Fat is Bad for Our Health

Just How Fat are Americans?

CDC Widgets  - Go Here to calculate your own BMI and see other cool calculators

Some states have taken measures to reduce tobacco use, you can use this CDC widget to see how your state is doing, and what other states have done.

Tobacco Control State Highlights 2010

Tobacco Control State Highlights 2010 Widget. Flash Player 9 is required.
Tobacco Control State Highlights 2010 Widget.
Flash Player 9 is required.

 

One Nation – Under Pressure

By Brooke Douglas, RD, CD

High blood pressure. The words don’t exactly strike fear into most American’s hearts. After all, it’s not painful, like cancer. It doesn’t sound deadly, like heart disease. But it’s literally a time bomb in our blood vessels that threatens our heart, brain and kidneys. Make no mistake – it’s a killer! So what makes our blood pressure rise? Too much salt, extra body weight and spending too much of your time sedentary. But wait! Don’t blame it all on the salt shaker. Only 7% of the excess salt in the average American’s diet comes from the salt shaker. The remaining 93% comes from all the processed and convenience foods we buy at the vending machine, at the local corner store, at the grocery store (for quick dinners) and at fast food and dine-in restaurants.

If your doctor has told you to cut back on your salt intake…you will have to do more than put the salt shaker away.

As for extra body weight (lose weight) and inactivity (begin a modest exercise program and spend less of your day sedentary), applying the following tips may help you on your quest to lower your blood pressure.

Here are some sodium-cutting tips you can try today:

Introduce additional flavor to your foods with herbs and spices like garlic, oregano, basil, pepper, thyme and sesame. These all add flavor without the extra sodium. If a recipe calls for salt, cut the amount called for in half and taste it before adding more.

Make healthy choices at the grocery store. Processed foods (anything in a box or bag) tend to be high in sodium because it helps preserve foods longer and increase flavor. Always read labels for the foods you buy, including the sodium content on the nutrition facts label and the ingredients list.

Remember that “low-fat” or “low-calorie” doesn’t mean healthy. These diet foods can also be higher in sodium because manufacturers hope that added sodium, a flavor-enhancer, will bring back the flavor that is missing since fat and other higher-calorie ingredients are removed. This is especially true for frozen dinners, which are often loaded with extra salt.

Choose low-, no- or reduced-sodium versions of your favorite soups, frozen meals, canned foods, and snacks. Even butter is available without added salt!

Choose fresh or frozen veggies over canned varieties, which often contain added salt to help increase shelf life. If you can’t find sodium-free varieties of canned vegetables, rinse the can’s contents in a colander under water before cooking to remove excess salt.

Olives, pickles and other items packed in brine are saturated in salt, as are many smoked and cured meats, like salami and bologna. Limit your intake of these high-sodium foods and be on the lookout for lower-sodium varieties.

Fast foods are high in more things than just fat. Many of these meals, sandwiches and fries contain more than your daily recommended intake of sodium in just one serving. When consulting restaurant websites to make healthy choices, pay attention to sodium levels as well. By keeping your portions in check (order a junior burger or small French fry instead of the big burgers and super fries) will help control your sodium (and caloric) intake.

Thanks much to Brooke for returning as our first-of-the-month guest contributor.  She does a great job with nutrition advice, so if you are concerned about your or a loved one’s blood pressure give her a call. Did you know that your insurance might cover several visits with a Registered Dietitian? Let Brooke help you navigate the insurance maze to determine whether your insurance will pay for you to having some nutrition coaching with a Registered Dietitian. You can find her at Nutrition Authority.

You may also enjoy this CDC widget:

Periodontal Disease and Atherosclerosis: Another Observational Study Conclusion Disproved

Another widely accepted dogma that comes from observational studies alone was shown to be just our eyes fooling us when surprisingly this week the American Heart Association released an unusual scientific statement with the conclusion that the evidence does not support gum disease as a risk factor or as a cause of cardiovascular disease.  For over 20 years it has been widely believed that periodontal gum disease is a risk factor and a cause of coronary heart disease and stroke.  The story of how the dogma that poor oral health became nearly universally accepted as a risk factor of cardiovascular disease is worth looking at because it exposes the risks of accepting data from an observational study as true just because it seems to make sense and conform to what we also see in practice.

Essentially all of the evidence used to support the belief that gum disease is a risk factor or a cause of atherosclerosis was from observational studies.  In an observational study it is observed that condition A is present more often in people with condition B than in persons without condition B.  Many studies showed that patients who had heart attacks are more likely to have bad oral health than patients who have not had heart attacks.  This is far different from saying that gum disease causes heart attacks.  In an extensive evaluation of all of the studies showing a relationship between gum disease and cardiovascular disease a panel including both dentists and physicians concluded that the evidence simply does not support the conclusion that there is a causative relationship. The problem appears to be that several other risk factors for cardiovascular disease are also put patients at risk for gum disease.  These include tobacco use and low socioeconomic status, as well as age and diabetes mellitus.  In a controlled study these confounding variables would be considered and “controlled” for in any analysis.  In an observational study this is much more difficult to take into account

The association of periodontal disease and atherosclerosis was so in synch with our bedside observations that it was intuitive to accept the association as dogma. For me at least it never occurred to seriously question the relationship. This was in part because of the widespread acceptance of the test hsCRP (highly sensitive C-reactive protein), a test for low-grade systemic inflammation as an independent risk factor for coronary disease.  It was easy to infer that because periodontal disease is a chronic inflammatory condition, can lead to bacteremia, and is a potential cause of systemic inflammatory marker elevation, that is “just made sense” that it is a cardiovascular risk factor.

I hope this 20 year walk down the path of least resistance is one I and others will remember when presented with an observational study purporting to show a relationship. Although I tell patients frequently that just because one factor precedes or coexists with another that it does not automatically follow that one causes the other, I too am obviously guilty of falling into this trap.

Sometimes as a medical community we are criticized for insisting on controlled, randomized, blinded studies to prove efficacy of our treatments, tests and procedures. It can be an expensive, time consuming and sometimes frustratingly tedious process.  Still, without solid scientific controlled studies we will be at risk of taking what seems to make sense as factual.  Bleeding sick patients was accepted as dogma in centuries prior to use of the scientific method, and we need to beware believing everything we see.

What is Inflammation?

My latest in a series of my favorite Khan Academy health related videos is on inflammation.  I expected this video to be more scientific, teaching about the process commonly called the inflammatory cascade, a process where once something happens to start the inflammation process how the body responds with a series of chemical reactions leading to the cardinal signs of inflammation:  dolor(pain), calor(heat), rubor(redness) and tumor(swelling).  Actually the video is an interview with a physician about the long term vs. short term effects of inflammation and methods used to reduce inflammation.

Certainly don’t go out and start using all the drugs mentioned in the interview, but it is fun to watch and get you thinking.  Enjoy.

You may also like these previous posts:

Aspirin:  Should You Take One a Day?

Statin Side Effects:  Add Type 2 Diabetes

 

Understanding What Causes Heart Disease

In order to help readers understand what causes heart disease here is another in my Monday series of selected Khan Academy Health related videos will focus on coronary artery disease and heart attacks.  This video is quite helpful in laying out the basics of heart disease, and should answer most of the answers as to what causes heart disease. A few clarifying points may make it a bit more helpful.  First when they talk about an atherosclerotic plaque rupturing and leading to a clot that causes a heart attack they don’t mention that the mechanism of the clot’s initial formation is the aggregation of platelets at the site of the ruptured plaque.  That’s why we often recommend taking low dose aspirin to inhibit platelet aggregation, so that if a plaque ruptures platelets are less effective at aggregating at the site and causing complete coronary artery blockage.  In addition medications like the statins and possibly the ACE inhibitors or ARB medications probably function at least in part by stabilizing the lining cells of arteries and reducing the chances of plaque rupture.

One other comment is that the video implies that only if a large heart attack occurs is cardiac arrest likely.  Actually even small heart attacks, and likely even episodes of coronary ischemia not severe enough to cause actual death of cardiac tissue can lead to cardiac rhythm disturbances, a.k.a. cardiac arrhythmias that may cause cardiac arrest and sudden death.

The key to preventing coronary artery disease, heart attacks, heart failure and cardiac arrest is to lower your risk of developing atherosclerosis.  The primary risk factors are tobacco use, high blood pressure, diabetes, lipid abnormalities like high LDL cholesterol and low HDL cholesterol, obesity and sedentary lifestyle. In some cases other familial factors play a role, but most often a strong family history of heart disease is because of a hereditary tendency to one or more of these risk factors.

So what do you do? In order of importance in my opinion:

  • Don’t smoke.  If you do smoke quit now.
  • If you have high blood pressure be sure it is well controlled.
  • If you have diabetes do everything you can to control your blood sugars.
  • If you have high LDL cholesterol and other risk factors discuss use of a statin or other lipid lowering medications with your doctor.
  • Stay fit.  Exercise regularly, reduce your dietary animal fat intake, and lose weight if you are overweight or obese.
  • If you already have atherosclerotic vascular disease, i.e. if you have had a heart attack, stroke, or peripheral artery disease even more aggressive treatment of risk factors like high cholesterol, high blood pressure, obesity, and diabetes is important.  Ask your doctor about how to accomplish these things.
  • Ask your doctor about taking an aspirin daily.

Why Patient’s Don’t Have Advance Directives?

I was reading my American Family Physician at the YMCA this weekend, and found an article “Implementing Advance Directives” that prompted me to come home and write this post. I have to admit that I should need to more often and earlier with many of my patients. I need to have a better plan for helping patients successfully and confidently choose to complete both a living will and a durable power of attorney.  A living will outlines you preferences for decisions you want made on your behalf in various circumstances if you are unable to verbalize you own preferences.  A durable power of attorney legally authorizes someone to make health care decisions for you in the circumstances where you are unable to make them for yourself.  These two documents complement each other.  I’ve too often tried to maneuver the minefield of coming to decisions for a patient’s care when they have failed to make their preferences clear and implement a durable power of attorney giving one individual the power to execute those choices. Then an out of town relative shows up to save the day, or a sibling dispute over how to deal with Dad’s terminal illness care happens.  This type of thing is all too common, and makes a stressful time for everyone.  Making your preferences known, putting it in writing, and designating a legal power of attorney helps your loved ones avoid this unnecessary messy and at times ugly scenerio. Both of these documents are crucial to both you and your family to assure that your wishes for decision making about your health are carried out according to your wishes.

Why don’t I do a better job?  I suspect it is a combination of factors.  I think the first is that this is rarely high on a patients list of topics they want to discuss at an office visit.  It is easy to put off this discussion when seemingly more pressing issues are the patient’s expressed reason for the office visit.  Even at physical exam visits, or in the medical coding lingo “preventative care” or “health maintenance” visits, it is alluring to focus on topics that lead to a longer or healthier life rather than a better death experience.  Here is the list of the physician-related barriers to completion of an advance directive listed in the AFP article:

  • Discomfort with the topic.
  • Lack of institutional support.
  • Lack of reimbursement.
  • Lack of time.
  •  Waiting for the patient to initiate the discussion.

In my case it is certainly not discomfort with the subject, and I am not intentionally waiting for the patient to bring up the subject, but lack of time and reimbursement undoubtedly play a role.

 

In addition most patients really don’t need my help in working through this decision process if they address the issue before there is a crisis. Although there are cultural, personal and ethnic variables that shape our decision making, most of my patients can  really quite quickly and easily work through the process of completion of both a very functional living will and a durable power of attorney without my assistance.  So why doesn’t everyone just do it themselves?  Here are the barriers listed in the AFP article that are patient related:

  • Fear of burdening others, i.e. family or friends.
  • Health Literacy
  • Lack of interest or knowledge of the subject.
  • Spiritual, cultural or racial traditions.
  • Waiting for their physician to initiate the discussion.

So how can you just “Do it yourself?” It’s really easy.  Obvoiusly since you are reading this article you have access to the internet, and everything you need is just a few clicks away.  I encourage you, if you have not already completed these documents, to DO IT NOW:

 

  1. Down load your state’s Advance Directives at the caringinfo.org site.  This is really easy and you can get everything you need by selecting your state from the list here.
  2. Many states have a form called a POLST form.  This stands for physician orders for live sustaining treatment.  If you use a search engine like Google, and you type in your state + POLST form you will easily find a form to download if your state has a POLST form.  You can get the Washington State form to download easily at WA POLST download.  Many physician offices have these available, just ask your doctor.
  3. For some people a form to help you ascertain your values on this subject and to make your values clear to the individual you choose to have your medical power of attorney is helpful.  The University of New Mexico  Institute for Ethics has published online a non-copyright protected form for you to download.  Some patients will find it helpful to attach this to their advance directive as guidance to their proxy in making decisions in line with their values.

There you have it.  You have no more valid excuses to keep you from completing your own advance directive and living will.  Once you complete it be sure to not keep it a secret.  Give a copy to your physician, to the person you choose as your DPA, and keep a copy handy at your home.   Don’t be a victim of your own procrastination or discomfort with this topic.  If you find it helpful ask questions on the subject up with your personal physician.  Be sure to let them know you have these documents completed.

In my best cheer-leading mantra:  You can do it!  Go – Go – Go!

 

 

 

Belly Fat Is Bad For Our Health

Is I took my shower this morning and once again looked down at my post-middle age belly, I am reminded that belly fat is bad. This is not news. We have known for years that belly fat is not just a problem because it hangs over the belt and many of us dislike the way it looks, but because it is an indicator of intraabdominal fat that is a risk factor for atherosclerotic heart disease.  Having a big derriere or big thighs seems to be less of a health concern.

Look at both the subcutaneous fat and the fat inside the abdominal cavity in this overweight patient at laparotomy.

My cadaver for dissection  in medical school was an old man, who was quite thin and had very minimal visceral fat, and when I saw my first few general surgical abdominal cases I was impressed by the amount of fat in the epiploical fat in the omentum and around the mesentery of many patients. I somehow had thought that most of our belly fat was just between the skin and the abdominal cavity, i.e. subcutaneous fat. In obesity a part of out abdominal girth is made up of intraperitoneal (inside the abdominal cavity) fat.

A Nov. 2008 NEJM article reported on a very large study of biometric measurements and showed that the rates of death were clearly related to “abdominal adiposity.” The study showed that increasing abdominal circumference and an increased ratio of abdominal circumference to hip circumference were both significantly related for a higher death rate. This correlation held up even when controlled for BMI, a general measure of height for weight. In other words if you have more belly fat that is a bigger health risk factor than if you carry your weight in your thighs, buttocks or breasts. Those of us with belly fat as opposed to having a fat in other places have long been known to be at higher risk of heart attacks, and recent research suggests correlation of belly fat with diabetes, and possibly some cancers.

So why does increased intra-abdominal fat, also called visceral fat, correlate with heart disease. Animal studies in mice show that increased visceral fat leads to higher rates of inflammation. There is considerable evidence that measures of low-grade inflammation, like highly sensitive C-reactive protein (h-CRP) are indicators of higher risk of coronary heart disease. A condition called metabolic syndrome is defined by having increased belly fat, an abdominal circumference of more than 40 inches (measure the smallest abdominal circumference, usually just above the umbilicus while standing at rest) along with borderline or high blood pressure, low HDL cholesterol and borderline or slightly high fasting blood sugar. Metabolic syndrome is felt to be a pre-diabetic condition and is a risk factor for the same types of cardiovascular conditions as diabetes.

Unfortunately we don’t really get to choose where we become obese. Don’t believe the headlines or web sites promising a secret fix to lose your belly fat, or any other particular fat you dislike. There is no believable evidence to support specific exercises to lose weight in specific areas. We can get stronger muscles in areas we exercise, but cannot specifically lose our belly fat, or any other fat by any means other than overall reduction of body fat, i.e. weight loss. Weight loss is not easy, and maintaining weight loss is arguably even harder than losing weight. I have patients who truthfully assure me that they have lost hundreds of pounds, they have just gained it all back and more.  Still reduction of total body fat is the only way to reduce belly fat, so I know I need to keep up my exercise and my efforts to eat better to lose my belly fat. Wish me success in my ongoing fight to lose my belly fat.

Pradaxa Bleeding Side Effects

The possible increased incidence of pradaxa side effects of serious bleeding have become newsworthy since my post on Pradaxa in July, Pradaxa side effects especially bleeding complications have dominated the news on this new anticoagulant. I think it is hard to put these pradaxa bleeding side effects in perspective. The use of Pradaxa has been quite popular in the treatment of patients with atrial fibrillation for the treatment of stroke. In the initial study of approximately 18,000 patients that led to the FDA approval of Pradaxa the incidence of bleeding complications was fairly similar to the incidence of bleeding on warfarin therapy. Between the FDA approval of Pradaxa in October 2010 through August 2011 the FDA reports approximately 1.1 million Pradaxa prescriptions dispensed in the US and over 3 to 70,000 individual patients treated with Pradaxa from outpatient retail pharmacies. This is a lot of patients and with the known bleeding complication rates of both warfarin and Pradaxa significant number of major bleeding side effects would’ve been expected. This is been the case and the FDA is currently reviewing aftermarket use of Pradaxa using a process called The Mini-Sentinal surveillance program to see if the bleeding complication rate in newly started patients on Pradaxa is comparable to warfarin or maybe better or worse. Certainly the Pradaxa side effects of major bleeding are dramatic and can be life-threatening, just as the same as these complications with warfarin use can be. Still the benefit of stroke prevention in atrial fibrillation patients is generally felt to be enough higher than the risk of bleeding complications that anticoagulation therapy with either warfarin, Pradaxa,  apixaban  or one of the other anticoagulants on the market is felt to be indicated for many patients.

I’ve heard from patients and red in the news about the fact that Pradaxa cannot be reversed with vitamin K like warfarin can. I think this is a seriously flawed argument. The Pradaxa half-life is short enough that requires twice daily dosing (12-17 hours) and within about 36 hours after the last dose of Pradaxa it’s anticoagulation effect should be largely gone in patients with normal renal function. When using vitamin K as an antidote warfarin it takes a day or two for significant hepatic metabolism of the coagulation factors inhibited by warfarin and I seriously doubt if use of vitamin K leads to a reversal of the anti-coagulation in warfarin patients any faster than or even as fast as simply discontinuation of Pradaxa therapy. It’s true that in major emergencies either fresh frozen plasma or other coagulation factor products can be used as an infusion to reverse the quite neuropathy in warfarin use. Pradaxa works directly as an inhibitor of coagulation, so its anticoagulation effect should be less responsive  to this type of therapy. Still I suspect that the argument that there’s no antidote for Pradaxa is less important clinically than it sounds in newsprint.

It will be interesting to see how the aftermarket evaluation of Pradaxa and the other newer anticoagulants bears out. Patients taking Pradaxa seem to certainly appreciate not needing to have frequent coagulation clinic visits to monitor their quite elation status necessary with warfarin use, and so far thankfully I’m not aware of any of my patients who have had bleeding complications from Pradaxa. I seem to see the current local cardiologists still prescribing Pradaxa fairly frequently and my expectations are that as more data comes to bear on the situation Pradaxa will be found to have a bleeding complication rate fairly similar to warfarin. Stay tuned for more updates regarding Pradaxa side effects and efficacy as they become available.

Doctors Die Too, but Maybe Differently

I stumbled across this terrific article titled:

How Doctors Die by Ken Murray a FP at USC.  

It is largely anecdotal, but is a really an interesting perspective on how at least some physicians choose to forgo futile end-of-life treatments because they know the limits of modern medicine first hand.

Also Enjoy:

Octogenerian’s Letter to Santa