Tag Archives: CAD

What You Should Know About Lipoprotein(a) And Heart Attack Risk

If you have had a heart attack at an early age or one of your parents did but your standard risk factors for coronary heart disease are normal you should consider getting tested for Lipoprotein(a) or Lp(a).

The standard lipid profile that most patients get checks LDL (bad) HDL (good) and total cholesterol along with  triglycerides. While these are useful, I have many patients who have normal standard values but have developed advanced coronary heart disease at an early age despite following a perfect lifestyle (not smoking, regular aerobic exercise, healthy diet.)

The skeptical cardiologist tests such patients for Lp(a) (pronounced LP little a)  and it is quite frequently elevated.

For patients, these are the facts to know about Lp(a)

  1. It is the strongest single inherited (monogenetic) risk factor for the early development of coronary artery disease, heart attacks and strokes.
  2. In addition to increasing risk of atherosclerosis, high Lp(a) is strongly associated with the development of calcific aortic valve disease which can result in narrowing of the aortic valve and aortic stenosis.
  3. Depending on the cut-off used  up to one in five individuals may have elevated Lp(a)
  4. Levels of Lp(a) can be measured with a simple blood test that should cost no more than 50 to 100$. This is not included in standard lipid or cholesterol testing.
  5. Risk for heart attack starts to rise with levels above 30 mg/dl and Canadian guidelines from 2016 (see here)) consider >30 mg/dl to be a risk factor and they recommend measuring Lp(a) in those with a family history of premature CAD or those at intermediate risk.
  6. The European Atherosclerosis Society (EAS, 2010), suggested levels of <50 mg/dl as optimal. The EAS advised measuring Lp(a) once in all patients with premature CVD.
  7. As levels get even higher risk also rises as these graphs show

 

 

 

 

Treatment For High Lp(a)

The lifestyle changes (both exercise and diet) that improve bad and good cholesterol levels have no effect on Lp(a). Our best drugs, the statins, for reducing risk of heart attack and stroke also don’t lower Lp(a) levels.

Only niacin has been shown to reduce Lp(a) across broad populations but there is no evidence that Lp(a) lowering by niacin lowers cardiovascular risk so it cannot be recommended for treatment.(In the AIM-HIGH study niacin did not reduce cardiovascular events in patients with Lp(a) with levels>50 mg/dl, despite achieving a mean Lp(a) reduction of 39%.)

Cholesteryl ester transfer protein inhibitors which raise HDL levels also reduce lipoprotein(a) concentrations, but three such inhibitors have not shown a clinical benefit.

In fact, currently there are no studies showing that lowering Lp(a) with any drug will effectively lower the associated risk of heart attack, stroke and aortic stenosis.

In the not too distant future, effective therapies may emerge. There are promising newer agents (antisense oligonucleotides or ASOs) currently in clinical trials and in limited populations the PCSK9 inhbitors, mipomersen and estrogen have lowered Lp(a) levels.

Why Test For Lp(a)?

If we have no effective therapies that work by lowering Lp(a) why recommend testing for it?

I test Lp(a) for  two reasons.

First, since it is inherited, patients with high levels should consider having first degree relatives tested for Lp(a) to identify those who are going to be at high risk. This provides an early warning of who in the family is most at risk for cardiovascular complications early in life. Such patients should be considered for early screening for subclinical atherosclerosis. In addition, they should be additionally motivated to do everything possible to reduce their elevated risk by lifestyle changes.

Second, I tend to recommend  more aggressive cholesterol lowering in patients who have evidence for early plaque build up for atherosclerotic events early in life than I otherwise would be.     I tend to agree with the approach diagrammed below:

 

With this approach for patients who have had events related to atherosclerosis or advanced CAC for age we work super aggressively on optimizing all risk factors. I try to lower LDL to <70 with statins and with the addition of ezetimibe or PCSK9 inhbitors if needed.

If the patient has more problems with atherosclerotic events despite optimizing risk factors and Lp(a) >60 mg/dl, some experts recommend using apheresis a technique which runs the patient’s blood through a filter which removes LDL and Lp(a). Personally, I have not sent any patients for apheresis and await better studies proving its benefit.

Antiproatherogenically Yours,

-ACP

For those patients seeking more detailed information and references I recommend Dr. Siggurdson’s excellent post on Lp(a)

There is a Lipoprotein(a) Foundation with reasonably informative and accurate website you can peruse here for more information.

Finally, if you want to delve deeply into the data check out this recent JACC review here.

The graphs above and this figure
showing the proposed pro-inflammatory, pro-atherogenic and pro-thrombotic pathways of Lp(a) are from that article.

 

Skeptical Thoughts From The Dental Chair: Part 2, Are Routine Dental Cleanings Beneficial?

In Part I of this series we listened to the skeptical cardiologist’s seemingly paranoid thoughts questioning the risk/benefit ratio and value of things that dentists do.

One such thing is the routine 3, 6, or 12 month visit for teeth cleaning that has been recommended by every dentist I’ve ever seen, and was vigorously defended by my current dentist (actually, he deferred the defense to his assistant). Exactly what is done at these sessions apparently varies widely and has widely varying names.

A 2015 review of the topic in The Journal of Clinical Periodontology likes to use the term  professional mechanical plaque removal for the various processes involved:

“This may include scaling or polishing teeth (or both) at supragingival locations, subgingival sites or a combination of each. Oral hygiene instructions (OHI) for personally performed mechanical plaque control may be an integral aspect of this intervention. Thus, the term PMPR covers a heterogeneous group of procedures but excludes deliberate root planning or root surface debridement.”

The lead author, one Ian Needleman, works at the Unit of Periodontology, UCL Eastman Dental Institute, UCL, London, UK.

After reviewing the best evidence available (from randomized controlled trials, RCTs), the authors concluded:

The strongest findings from this review are that professional mechanical plaque removal (PMPR) when combined with oral hygiene instructions (OHI) results in a greater reduction in plaque and gingival bleeding than no treatment. However, there is no evidence of a difference in the effect on plaque and gingival bleeding comparing PMPR combined with OHI versus OHI alone when OHI is both thorough and repeated, that is there is no additional effect of PMPR on plaque and gingival bleeding above that gained from OHI where PMPR has initially been provided.

Yep, you heard that right. The dental cleaning you’ve been suffering through all your life adds nothing to the oral hygiene instructions (brush your teeth twice a day, floss once a day) and presumably the home daily oral hygiene that results from those instructions.

Furthermore :

A striking further key finding for these comparisons remains the lack of data investigating prevention of periodontitis.

Correct. There are no studies that PMPR prevents periodontitis.

A brief discussion from the NIH website on gum disease is helpful here:

Periodontal-Disease-Trailhead-DentalWhen gingivitis is not treated, it can advance to “periodontitis” (which means “inflammation around the tooth”). In periodontitis, gums pull away from the teeth and form spaces (called “pockets”) that become infected. The body’s immune system fights the bacteria as the plaque spreads and grows below the gum line. Bacterial toxins and the body’s natural response to infection start to break down the bone and connective tissue that hold teeth in place. If not treated, the bones, gums, and tissue that support the teeth are destroyed. The teeth may eventually become loose and have to be removed.

The periodontal review paper concludes:

  • There is most likely no value in providing PMPR without oral hygiene instruction. Repeated, thorough oral hygiene instructions for personally applied plaque control appear as influential as PMPR on periodontal health.

  • PMPR might achieve greater patient satisfaction with treatment. The impact on adherence to care might be important.

  • Although more frequent PMPR favours greater health gains for surrogate outcomes of prevention, there is little to guide the frequency of PMPR applications. This should therefore be judged by a needs and risk assessment although such an approach should be tested in a rigorously designed study.

A 2013 review by the Cochrane Collaboration came to similar conclusions (Cochrane review periodontal PDF), finding only one acceptable study comparing “scale and polish” of the teeth to no “scale and polish” and concluding:

This study showed no evidence to claim or refute benefit for scale and polish treatments for the outcomes of gingivitis, calculus and plaque.

A search of the website of the American Dental Hygienist Association, including the section entitled “evidence-based practice recommendations,” fails to find any support for routine dental cleaning.

To be clear, the question asked is: is there any benefit to performing the PMPR on patients with no evidence of gum disease?  If you have chronic periodontitis, then a  2015 review from the American Dental Association (ADA ) concludes that there is moderate evidence that scaling and polishing is helpful, improving the amount of clinical attachment of gum to teeth by 0.35 mm. There are no studies showing that it prevents tooth loss.

Screen Shot 2016-03-26 at 9.31.56 AMIf your gums are fine and you want to start skipping the “scale and polish” two Cochrane reviews suggest that powered toothbrushes do better than manual toothbrushes at plaque removal.  I promise, that is all the oral hygiene instruction I am providing.

periodontal-disease-systemic
Misinformation in a graphic from NJSmiles of Ramsey. This theory is no longer believed valid but it makes for nice scare tactics. If losing your teeth doesn’t worry you, how about heart attacks and chronic kidney disease?

Finally, the theory my dentist put forth that gingivitis or periodontitis causes heart disease or coronary artery disease has not been proven. Check out this NPR story or this statement from the American Heart Association for more discussion on this topic.

Stay tuned for Parts III and IV of the skeptical questions about dentistry in which we examine the risks of disease transmission and the role of dental radiography.

Gingerly Yours,

-ACP

 

The Incredibly Bad Science Behind Dr. Esselstyn’s Plant-based Diet

txorito pamplona
Txorizo Pamplona. This delightful sausage of Navarra in the basque region of Spain is right out in Esselsystn’s plant-based diets.

The skeptical cardiologist has heard a few cardiologist colleagues rave about the movie “Forks Over Knives” and promote the so-called “whole-foods, plant based diet.”

One of the two major physician figures in the movie is Dr. Caldwell Esselstyn, a former surgeon and now a vegan evangelist.

salad
You’ll be eating a lot of this on the Esselstyn diet but do not, under any circumstances add a salad dressing containing any oil of any kind to attempt to make it palatable or satiating.

Esselstyn, along with T. Colin Campbell (of the completely discredited “China Study” (see here for a summary of critical analyses of that data), Dean Ornish, and Nathan Pritikin, are the leading lights of a dying effort to indict any and all fat as promoting heart disease and all the chronic diseases of western civilization.

Esselstyn, in his book, “Preventing and Reversing Heart Disease” lists the following rules:

  • you may not eat anything with a mother or a face (no meat, poultry, or fish)
  • you cannot eat dairy products
  • you must not consume oil of any kind
  • generally you cannot eat nuts or avocados

What? No Fish or Olive Oil? You Cannot Be Serious!

oil
Whatever oil this might be (?sunflower) is right out even though it comes from a plant. According to Esselstyn, using his brilliant ‘logic and intuition” all fats, whether saturated or unsaturated are going to damage the lining of your arteries.

The best randomized controlled trials we have for diet to prevent coronary artery disease (CAD, the cause of heart attacks) have shown that supplementing diet with olive oil and nuts substantially lowers CAD.

Every observational study in nutrition has demonstrated that fish consumption is associated with lower cardiovascular disease.

Esselsstyn’s Really Bad Science

While working at the Cleveland Clinic, Esselstyn developed an interest in using a plant-based diet to treat patients with advanced CAD. He says he had an epiphany one rainy, depressing day when he was served a slab of bloody roast beef.

In his own words:

“my original intent was to have one group of patients eating a very-low fat diet and another receiving standard cardiac care and then compare how the two groups had fared after three years.”

If he had followed his original intent, and randomized patients entering the study, he could claim that he had performed a legitimate, important scientific study. Twelve of the 24 would be allocated by lottery to the Esselstyn diet and 12 to whatever was the standard recommended CAD diet at the time. Unfortunately this approach, due to a “lack of funding, was not practical.”

So instead, 24 patients were sent to him, “all suffering from advanced CAD” and began the horrifically strict dietary program he had developed based on his “logic and intuition.”

Interestingly, patients not only were put on Esselstyn’s incredibly low fat diet, but they were also given cholesterol lowering medications and were “switched to statin as soon as these became available in 1987.”

In addition, 9 of the 18 patients who stuck with the program had previously undergone coronary bypass surgery and two had undergone angioplasty of a coronary artery.

6 of the 24 original patients “could not comply with the program” and were sent back to their regular cardiologists. This gives you an idea of how difficult it was to follow this diet.

Esselsstyn’s “data” then consists of following 18 patients, 9 of whom had already undergone coronary bypass surgery, all of whom were taking statin drugs with his diet without any comparison group.

This group of 18 did well from a heart standpoint, of course. It is impossible to know if the diet had anything to with their outcome.  Most of them had already undergone the “knife” or had had angioplasties that took care of their most worrisome coronary blockages. They were all taking statin drugs . They were all nonsmokers and they were all highly motivated to take good care of themselves in all lifestyle choices.

Any patients who were not intensely motivated to radically change their diet would have avoided this crazy “study” like the plague.

This “study” is merely a collection of 18 anecdotes, none of which would be worthy of publication in any current legitimate medical journal.

Three of the 18 patients have died, one from pulmonary fibrosis, one presumably from a GI bleed, and one from depression. Could these deaths be related to the diet in some way? We can’t know because there is no comparison group.

Should Anyone Eat Ultra-low Fat Diets?

It is possible that the type of vegan/ultra-low fat diets espoused by Esselstyn and his ilk have some beneficial effects on preventing CAD, but there is nothing in the scientific literature which proves it.

Scientific reviews of the effect of diet on CAD in the last 5 years have concluded that the evidence is best for the Mediterranean diet, which emphasizes fish consumption, olive oil and nuts. These reviews dismiss ultra-low fat diets because of a lack of evidence supporting them, and an inability to get people to follow them.

If you have ethical or philosophic reasons for only eating things with no mother or face, then by all means follow your conscience.

Too often, however, I find that those who choose veganism for philosophic reasons want to find health reasons to support their diet and mix the bad science and philosophy into a bland evangelical stew they recommend for all.

I remain, therefore, in favor of cioppino, paella, butter and all the glories of the omnivore that make life so rich.

Omnivorously yours,

-ACP


I have updated this post with comments from readers and my response along with analysis of the latest “data” from Dr. Esseslstyn’s “study” at my post entitled:

more-incredibly-bad-science-from-dr-esselstyns-plant-based-vegan-diet-study


For an amazingly complete (and surprisingly entertaining) dissection of the scientific inaccuracies of “Forks Over Knives” with humorous overtones, I recommend Denise Minger’s post “Forks Over Knives: Is the Science Legit? (A Review and Critique). Be prepared for lots of graphs!

Dealing With The (Cardiovascular) Cards You’ve Been Dealt

The skeptical cardiologist was in Atlanta recently  visiting  his Life Coach (LCOSC). Oddly enough, the wife of the LCOSC (who I’ll call Lisa) had just undergone a coronary calcium scan  and it came back with a high score.  Most women her age (58 years old) have a zero score but hers came back at 208 .

What is the significance of a calcium score of 208 in this case?

The CT scan for calcium (discussed by me in more detail here) focuses entirely on quantifying the intense and very specific kind of x-ray absorption from calcium. The three-dimensional resolution of the scan is such that the coronary arteries which supply blood to the heart can be accurately located and the amount of calcium in them very accurately and reproducibly added up. Calcium is not in the arteries normally and only accumulates as atherosclerotic plaque builds up over time. The build up of fatty plaque (atherosclerosis) is the major cause of coronary artery disease (CAD, sometimes termed coronary heart disease (CHD)) which is what causes most heart attacks and most death in both men and women in the U.S.

We can enter Lisa’s numbers into the online MESA calculator to see how she compares to other white 59 year old women. The calculator tells us that 72% of her peers have a zero calcium score and a score of 208  is higher than 95% of her peers. Although the 95th percentile is a good place to be for SAT scores it is not for atherosclerosis. This means substantial amount of fatty atherosclerotic plaque has built up in the arteries and puts the individual at significantly greater risk for heart attack and stroke. A calcium score of 100-300 confers a 7.7 times increased risk compared to an individual with similar risk factors with a zero calcium score.

Most of the risk factors that we can measure to assess one’s risk of heart attack (blood pressure, diabetes, smoking) were absent in Lisa. Her cholesterol levels had risen in the last 10 years but when I entered her numbers (total cholesterol 221, HDL 68) into the ASCVD risk estimator her 10 year risk came back at 2.5%. This is considered low and no treatment of cholesterol would be advised by the new guidelines.

The only clue that her cardiologist would have that Lisa has advanced premature atherosclerosis is that her mother had coronary heart disease at an early age, something we call premature CAD. Her mom at the age of 62 suffered a heart attack and had a stent placed in one of her coronary arteries. The occurrence of significant premature CAD in a parent or sibling  substantially increases the chances that a patient will have premature CAD and the earlier it occurred in the parent or sibling the higher the risk.

Some of this excess risk is transmitted by measurable risk factors such as hypertension and hyperlipidemia and some through lifestyle factors but the majority of it is through genetic factors that we haven’t fully identified.

How much of an individual’s risk for heart attack  is determined by genetics versus lifestyle?

A large Swedish study found that adopted men and women with at least one biological parent with CHD were 1.5 times more likely to have CHD than adoptees without. In contrast, men and women with one adoptive parent were not at increased risk.

Since 2007 an intense project to identify genetic factors responsible for CAD has been underway at multiple academic centers. Thus far 50 genetic risk variants have been identified. According to Dr. Robert Roberts

” All of these risk variants are extremely common with more than half occurring in >50% of the general population. They increased only minimally the relative risk for coronary artery disease. The most striking finding is that 35 of the 50 risk variants act independently of known risk factors, indicating there are several pathways yet to be appreciated, contributing to the pathogenesis of coronary atherosclerosis and myocardial infarction. All of the genetic variants seem to act through atherosclerosis, except for the ABO blood groups, which show that A and B are associated with increased risk for myocardial infarction, mediated by a prolonged von Willebrand plasma half life leading to thrombosis”

 How well do the standard risk factors capture the individuals risk for heart attack?

The standard approach to estimating risk fails in about 25% of individuals as it does not accurately convey the high risk of the patient with family history and it overestimates risk in many elderly individuals who have an excellent family history.

It is in these patients that testing for the actual presence of atherosclerosis, either by vascular screening or coronary calcium is helpful.

Reducing The Excess Risk of Premature CAD

For many individuals there are clear-cut lifestyle changes that can be implemented once advanced CAD is identified: cigarette smoking cessation, weight loss through combinations of diet and exercise with resulting control of diabetes, However, many patients like Lisa, are non-smokers, living a good lifestyle, eating an excellent diet with plenty of fresh fruit, vegetables, fish and healthy oils and  without obesity or diabetes. There is no evidence that modifying lifestyle in this group is going to slow down an already advanced progression of atherosclerosis.

Patients like Lisa have inherited predisposition to CAD, it is not due to their lifestyle.

Lisa’s cardiologist  suggested she get a copy of Dr. Esselstyn’s book “Prevent and Reverse Heart Disease”. This book, based on the author’s experience in treating 18 patients with advanced CAD espouses an ultra low fat diet. The author declares that “you may not eat anything with a face or a mother (meat/poultry/fish)” and bans  full fat dairy products and all oil (“not even a drop”)

Such “plant-based diets” (codeword for vegan or vegetarianism) lack good scientific  studies supporting efficacy and are extremely hard to maintain long term. There is nothing to suggest that Lisa’s long term risk of heart attack and stroke would be modified by following such a Spartan dietary regimen.

Her cardiologist did recommend two things proven to be beneficial in patients with documented advanced CAD: statins and aspirin.

Taking a statin drug will arrest the atherosclerotic process and reduce risk of heart attack and stroke by around 30% as I’ve discussed here and here.

An aspirin is now indicated since significant atherosclerosis has now been documented to be present as I’ve discussed here.

We can blame a lot of heart disease on lifestyle: poor diets and lack of exercise are huge factors leading to obesity, diabetes, hypertension and hyperlipidemia, but in many patients I see who develop heart disease at an early age, lifestyle is not the issue, it is the genetic cards that they have been dealt.

Until we develop reliable genetic methods for identifying those at high risk it makes sense to utilize methods such as vascular screening or coronary calcium to look for atherosclerosis in individuals with a family history of premature CAD.

Once advanced atherosclerosis is identified, we have extremely safe and effective medications that can help  individuals like Lisa deal with the cardiovascular cards they have been dealt.