ACC/AHA Guidelines: Not a Replacement for Clinical Contemplation

On May 19th the Journal of the American College of Cardiology published an illuminating paper by Pant et al. examining the impact of a dramatic change in one of the Cardiac Guidelines. The paper was entitled “Trends in Infective Endocarditis Incidence, Microbiology, and Valve Replacement in the United States from 2000 to 2011”. In 2007 the ACC/AHA Guidelines were radically shifted, advocating an enormous reduction in sub-acute bacterial endocarditis prophylaxis (SBEP) precautions. The rationale for the dramatic shift from an aggressive to a conservative stance emanated from two findings: a lack of RCT evidence for the need for SBEP precautions under most circumstances, and the growing problem of antibiotic resistance. Without claiming prescience or any other such miraculous gift, I will tell you that at the time I predicted a significant future rise in endocarditis. My belief was that the guidelines overshot their intentions. Some individuals, I surmised, have valvular heart disease that predisposes them to developing SBE yet fails to be “significant” enough to make them candidates for the revised SBEP recommendations.

For several years I bucked the system and continued my aggressive prophylaxis. Then I buckled. I followed the guidelines to a tee. Though none of my patients has developed SBE, I now question my decision to cave under the pressure of the guidelines. I have always been one to try to think through issues, to treat patients outside any preordained box and beyond an overly simplified algorithmic construct. But in this case I felt perhaps I should just go with the flow. In truth, it was just easier to do so. My liability was lessened and my decision-making efforts were simplified. Yet, in retrospect, seeing the predictable rise in streptococcal SBE, I have been forced to re-examine my decision. In doing so, once again I am confronted with our current fixation on RCTs as proof positive “evidence,” with all other levels of understanding being “non-evidence”.

The absence of RCTs in this construct is tantamount to a lack of evidence. This paradigm is of course false. Many levels of valid evidence exist and oversimplification, though appealing, is inherently flawed and theoretically dangerous. We see this now in eight years of follow up after the change in ACC/AHA SBEP Guidelines. We also see this in many other aspects of everyday practice. Though I chose an easier and perhaps idler path in this circumstance, I will now reverse my position and once again give greater thought to each SBEP recommendation I render. It will take longer to do so; more complex doctor-patient discussions will be required; and larger liability will fall upon my shoulders. But these are the elements required to be a better physician. I owe it to my patients, and equally importantly to myself, to do so. Having said this, pragmatic issues remain. How do we practice medicine in an efficient, cost-effective, economically sound, intellectually stimulating, personalized, high-level fashion, while adhering to the mounting pressure of regulatory changes and requirements? This is the question that requires our most focused attention yet typically receives short shrift. For modern American Medicine to enjoy the future we all believe it deserves, this question, along with its counterparts, deserves our full and undivided attention.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

For more information about the supplements and vitamins critical to your everyday health visit www.vitalremedymd.com.

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Save the Date: It’s the American Society for Preventive Cardiology’s 40th Anniversary – The July 2015 Conference is Shaping up to be Extraordinary

That’s a long title for this week’s blog, but it’s tough to shorten. Planning a conference is quite a challenge: The venue is chosen; topics are selected; speakers are invited; and the word is disseminated. Many people’s hands are in the mix – in the case of the ASPC, our management company as well as members of the planning and executive committees work tirelessly to create a conference that will meet and exceed its intent. This year’s ASPC meetings, again at the beautiful Boca Raton Resort, will bring together attendees from across the country (and likely outside the US as well) in order to learn from some of our nation’s most renowned experts in genetics, vascular disease, hypertension, diabetes, women’s heart health, inflammation, thrombosis, CVD risk reduction strategies, familial hypercholesterolemia, lipids and lipoproteins, novel medications…

Our goal is to highlight the most cutting edge as well as tried and true approaches for ASCVD prevention so clinicians eager to improve their strategies to combat and prevent the toll of vascular disease among their patients can more effectively do so. Conference attendees are among the most dedicated of our country’s healthcare practitioners – cardiologists, internists, obstetricians, family practitioners, nurse practitioners, physicians’ assistants, pharmacists, dietitians, and many others. The Boca Raton Regional Hospital supports the program and offers its physicians the opportunity to attend this one-of-a-kind meeting. Groups such as WomenHeart, and chapters of the ACC and AHA (and others) typically endorse the meetings as well. This year, in honor of the ASPC’s 40th Anniversary, the meetings will offer its attendees two new opportunities. First, abstracts from trainees across the globe will be evaluated for presentation. Second, we will offer the inaugural Expert’s Course in ASCVD Prevention. Diplomas will be awarded to those who successfully complete the course. So who are our speakers – professors and experts in their disciplines from Harvard, Hopkins, Emory, The Mayo, Columbia, UCSD, Tulane, Minnesota, NYU, and other outstanding institutions. And when is the meeting – July 31 through August 2nd. Put it on your calendar – you and your patients will be very happy you did. See you in July!

For more event information visit: aspconline.org

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

For more information more about essential vitamins and supplements visit www.vitalremedymd.com.

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The Approaching Medical Maelstrom

The AHA 2014 Scientific Sessions are over and I have already written twice about IMPROVE IT but I feel compelled to write again. Although the media has been oddly silent about the trial (why is that I wonder???), I predict its fallout will greatly impact the disciplines of Cardiovascular Disease Prevention, Clinical Lipidology, and even the essence of clinical practice. The reasons are manifold. First, the trial proved two critical theories: a lower LDL cholesterol level is better, and statins are not the only way to achieve a clinically relevant LDL reduction. Additional key considerations from IMPROVE IT include:

  •  Lower LDL in properly chosen patients (and probably almost everyone) yields lower rates of stroke and heart attack, the two most formidable foes of modern man. For example, in the trial, an LDL of 53 was significantly better than an LDL of 70. Should we doctors then aim for 40, or perhaps even 25?
  • In our high-risk patients should we consistently and continuously add medications to statins in order to drive cholesterol levels lower and lower? For example, in a patient with a prior heart attack is it now fair to accept 70 for an LDL when we know that 53 would decrease our patient’s chance of having a recurrent and potentially life-threatening event?
  • What do we do with the hotly debated 2013 ACC/AHA Cholesterol Guidelines? They eliminated LDL goals and allowed for the use of Zetia only with individualized – and typically time-prohibitive – clinician/patient discourse, but they did NOT encourage driving LDL lower than 70. The Guidelines advocated for an LDL response to therapy of > 50%. So where does that leave our heart patients who start with LDLs of 180, for example. If they achieve the intended LDL reduction of 50% and thereby remain with an LDL of 90 mg/dL the guidelines surely say all is well – job well done. They state there is no indication to go further. Well now there is an indication. Now we can say with certainty that an LDL of 53 is a far better goal than 90. Having an LDL of 90 leaves significant and now manageable residual risk. So then how can a health care provider in good conscience advocate keeping such a patient at an LDL that clearly conveys greater risk?
  • The Guidelines also strongly advocate our utilization of maximum statin doses prior to adding an agent like Zetia. Knowing that higher dose statins produce more side effects while yielding a diminishing return on cholesterol lowering, wouldn’t it now be more prudent for doctors to prescribe low dose statins in combination with Zetia? This would limit side effects while yielding lower LDL levels than would the Guideline recommended approach. More food for thought.
  • How will insurance providers respond to Improve-It’s results? After the ACC/AHA Guidelines’ release, with lightening speed they downgraded access to add-on therapies such as Zetia. Of course that saved them money. So what now? Will they respond in kind, follow the science, and quickly allow patients access to these medications? We shall see but I have my doubts. Profits it seems oftentimes take precedence over science and health.
  • One more crack at the Guidelines for now: It is true that we do not know what represents the optimal LDL cholesterol level in human beings. Based upon our ever-expanding understanding of lipids including our body’s limited need for extraneous cholesterol however, it is safe to say that that level is probably quite low, perhaps even as low as 25 or 30 mg/dL. And, given the fact that many of us are goal-oriented, wouldn’t it now make sense to join our friends across the pond as well as our very learned friends here at home in the National Lipid Association and simply reinstate LDL goals?
  • As I sit at my desk tapping these keys I am clearly frustrated by the politics and economics woven inextricably into the fabric of medical practice. But I am also comforted and encouraged by the knowledge that many of us have already spent the last decade and beyond practicing the way we felt the science dictated. And by so doing, in the matter of LDL-lowering with Zetia, for every 120 patients we’ve treated in an Improve-It style, we’ve saved 3 from enduring a stroke or heart attack. This fact renders all our struggles worthwhile.

On a final note let us not forget that doctors have NO financial incentive to prescribe these medications. Our only “dog in the fight” is protecting our patients from harm. Insurance providers often do have a financial incentive to preclude doctors from prescribing some medicines (typically those that cost them more money). So whom do you, the patients, want to be in control of your medication regimen – the more highly educated and clearly non-conflicted physicians, or the less knowledgeable and often-conflicted insurance carriers? The answer to me seems pretty clear.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

For more information more about essential vitamins and supplements visit www.vitalremedymd.com.

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IMPROVE-IT Trial: the Day of Reckoning Approaches

Tomorrow morning a large crowd will gather here at the AHA meetings in frigid Chicago to learn the findings of the long-awaited IMPROVE-IT trial. The trial will demonstrate whether or not Ezetamibe (Zetia) added to a Simvastatin (Zocor) successfully decreased cardiovascular events in high-risk patients.

Many lipid specialists and cardiologists, myself included, have used Ezetamibe in combination with statins since the drug’s release. We believe wholeheartedly in the “lower LDL is better” hypothesis. Our clinical results, though anecdotal, have been uniformly exceptional. We fully anticipate that – barring confounding circumstances – the trial will be a winner.

Making this prospect even more impactful is the current NEJM publication by Dr. S. Kathiresan, (a brilliant Harvard Cardiologist/Geneticist) describing a novel genetic mutation that decreases LDL cholesterol, and concomitantly reduces ASCVD events. Where is this mutation you might ask: In the same receptor that is blocked by the drug Ezetamibe. Essentially individuals bearing such a mutation are born with the equivalent of continual Zetia use. This experiment of nature surely supports the speculation that Ezetimibe effectively lowers heart disease, even on top of statin therapy.

For now, we can only speculate about IMPROVE-IT’s findings. Tomorrow will bring some hard facts along with an assessment of how the findings will impact not only doctors’ use of Ezetamibe, but equally importantly, how health insurance companies will view the matter as well. Until tomorrow my admittedly unbiased fingers will be tightly crossed.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

For more information more about essential vitamins and supplements visit www.vitalremedymd.com.

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The Emory Symposium on Coronary Atherosclerosis Prevention & Education

Here’s a shoutout to my friend and colleague, Dr. Larry Sperling.

The renowned Emory Heart Center of the Emory University School of Medicine will be holding its 13th annual Emory Symposium on Coronary Atherosclerosis Prevention & Education June 4-8, 2014. This year’s event, which is titled “Emory Escape 2014“, will be held at the OMNI Amelia Plantation on lovely Amelia Island, Florida..

The challenge
Cardiovascular disease remains the number one cause of death of men and women in the United States, and is a major cause of disability. The American Heart Association has a stated goal to reduce deaths from cardiovascular disease and stroke by 20% by 2020. In order to achieve this goal, physicians and clinicians must gain the knowledge, skill and resources to integrate the latest research and clinical guidelines in the context of their own practice.

The event
At ESCAPE attendees will hear nationally renowned speakers discuss the recently released, 2013 ACC/AHA guidelines on hypertension, blood cholesterol, obesity, healthy living and risk assessment. In addition, there will be one day dedicated to lectures on CV prevention in “special population” patients, including patients with HIV, PCOS, breast cancer, connective tissue disease and post renal transplant. There will also be lectures on electrophysiology, interventional cardiology, heart failure, tobacco cessation, and women’s heart health. This conference will close the knowledge gaps between national guideline goals, practice, and research. Physicians and clinicians will have the opportunity to discuss with the speakers and other attendees how these principles can be applied to patient care in the context of their own practice in order to decrease cardiovascular disease risk.

In addition to the extensive educational curriculum, events will include pre-meeting workshops,  an attendee and spouse session and a family social and cookout.

Who should attend
Cardiologists, internists, family practitioners, emergency medical personnel, primary care physicians and nurses can all benefit from this conference.

Register online at www.eccri.emory.edu/escape – registration deadline May 4th

Call 1-800-THE-OMNI to make room reservations.

Hosted by: Emory University School of Medicine Department of Medicine Division of Cardiology.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

Learn more about essential vitamins and supplements at www.vitalremedymd.com.

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Mayo Clinic Cardiovascular Disease Prevention Conference – a Testament to the Dedication of Healthcare Practitioners

Okay. You read the title and immediately imagined a bunch of doctors and scientists lounging on the spectacular Mexican beaches while you – if you live pretty much anywhere in the US – dig yourself out from yet another snowfall. It is true that the beach is pristine. And yes, the weather is unbeatable. But, truth be told, every speaker and attendee spent days and evenings continually holed up in a windowless conference room discussing issues ranging from exercise and diet, to Familial Hypercholesterolemia (FH), to even the impact of COPD on CVD. The meeting was excellent. Great discussions, proposals for future collaborations, some colleagues reuniting while others being introduced to a new group of associates. The ACC/AHA Cholesterol and Risk Assessment Guidelines as well as the new BP Guidelines were hotly debated.

In all, it was a wonderful weekend that enabled us to exchange ideas, consider alternate approaches to our patients, and simply grow as doctors, nutritionists, and scientists. So while American Medicine continues to be a target of mostly criticism, rest assured there are many who continue to do their part to ensure the viability and continuation of truly top-notch healthcare and research.

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New AHA / ACC Cholesterol Guidelines – Controversial but not to be Feared

Last week four guidelines were released by the AHA and ACC. A tremendous amount of controversy surrounded the Cholesterol Guidelines as they deviated in fundamental ways from prior standards. The writers of the guidelines took a strict Evidence Based Medicine (EBM) slant, limiting extrapolation and thereby altering the traditional approach to cholesterol management. For example the format of all prior clinical trials did not specifically address cholesterol goals. Thus they were excluded from the guidelines. That does not, however, mean that it is wrong to continue to try to “get our patients to goal”. It simply means that in the strictest view of EBM, there is insufficient evidence to do so. The American Society for Preventive Cardiology (ASPC, of which I am Treasurer) and several other organizations endorsed the document. The National Lipid Association (NLA) did not. It is critical for practitioners to understand two things when trying to utilize this document as effectively as possible. First, the guideline was meant to be a living work, one that will be updated at regular intervals. Second, and perhaps far more consequential, it is essential that practitioners ardently adhere to a single paragraph from the guidelines which follows:

“Guidelines attempt to define practices that meet the needs of patients in most circumstances and are not a replacement for clinical judgment. The ultimate decision about care of a particular patient must be made by the healthcare provider and patient in light of the circumstances presented by that patient. As a result, situations might arise in which deviations from these guidelines may be appropriate.”

In sum, we most always remember that guidelines are just tools to help practitioners understand the most recent evidence in medicine. They are not laws. Clinical judgment must always reign supreme.

Please read more about preventive cardiology at www.preventivecardiologyinc.com.

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Familial Hypercholesterolemia – a Common Yet Life-Threatening Genetic Disorder

This article was originally published on HomeCareforYou.com.

You or someone you love might be harboring an undetected threat called Familial Hypercholesterolemia (FH). As genetic disorders go, FH is quite common. In fact, the condition occurs five times as frequently as Cystic Fibrosis. FH victims typically have severely elevated cholesterol; their disorder frequently remains undetected; and most patients develop vascular disease very early in life. These people often die from heart attacks in their forties and fifties. One consequence of the explosion in our understanding of genetics has been the discovery of more than 1600 genetic mishaps that can lead to FH. In the general population this disorder occurs in one out of every 500 people. Specific populations called founder groups (groups of people who are descendants of a genetically similar small population) such as French Canadians, Christian Lebanese, and South African Ashkenazi Jews have a prevalence of this malady that can be as high as one in sixty-seven people.

So what is FH and how does it harm so many?
cholesterol meterIn order to understand this ailment we must first review a few basic elements regarding cholesterol and its main transporter, LDL (Low Density Lipoprotein). Cholesterol is the building block for many key components in our body. LDL is a spherical lipoprotein particle that carries cholesterol. Think of it as a floating bubble that carries its freight— cholesterol and triglycerides—from one part of our body to another. This LDL “bubble” serves as a barrier “protecting” us from what would otherwise be the consequence of cholesterol floating freely in the blood. The result of that scenario would be instant death; free cholesterol would form razor-sharp crystals shredding anything in its path. LDL particles obviously provide a valuable function as our body’s dominant cholesterol transporters, but they have been dubbed the “bad cholesterol” because overly-abundant levels of these lipoproteins clearly lead to heart attacks and strokes. Thousands of studies have proved this; it is one of the few “facts” we have in modern medicine. As a result of our understanding of the detrimental consequences of high LDL, medications such as the statins have been created to lower LDL levels and in turn diminish our chances of experiencing a heart attack or stroke.

Lowering LDL with statins
Most of us know that the fundamental medication in cholesterol management is the statin. Statins work by blocking a critical enzyme in the multi-stepped process of cholesterol synthesis. This enzyme is present in every cell in the body. In response to the statin-induced cholesterol decline within our cells, affected cells deliver a greater number of LDL receptors to their surface. Think of receptors as adhesive-coated indentations in the cell membrane. These receptors capture the LDL “bubbles” as they float by in the blood. The receptor with its bonded LDL particle is then brought inside the cell. Within the cell, the cholesterol contained within the LDL particle can be utilized in any way the cell deems fit. For instance, it can be a building block for Vitamin D in the skin, bile acids in the liver, or testosterone in the testes. Once a cell has acquired enough cholesterol to serve its manufacturing needs, it stops overproducing LDL receptors. All cells engage in this process, but our liver is the organ that manufactures the majority of LDL receptors, thereby most meaningfully diminishing the content of LDL within our blood. To maintain a healthy balance of LDL within our bodies it is essential for our cells – particularly within our liver – to be able to produce LDL receptors, position them on their surface, and capture their prey—LDL particles.

The Malady of FH
Patients with Familial Hypercholesterolemia possess a genetic defect that disrupts their LDL receptors. In some cases the patient manufactures too few receptors; in others, the receptors themselves are defective. Even though they capture LDL, faulty receptors are unable to successfully bring their cargo into the cell. This defect results in a situation wherein the cell “effectively” lacks LDL receptors. There are two types of FH patients, those who have inherited one faulty gene from one parent (the common variety – 1 in 500) and those who have inherited one faulty gene from both parents (the extraordinarily rare form – 1 in 1,000,000). When an individual receives an abnormal gene from only one parent, he or she is known as heterozygous for the particular genetic flaw involved. An individual is homozygous for a disorder when both parents contribute abnormal genes. Because of the nature of the FH genetic defect, heterozygous individuals–those possessing only one genetic error from one parent–will experience the disorder, albeit in a less aggressive form than their homozygous counterparts. As this defect causes suboptimal LDL receptors, patients develop extraordinarily high LDL cholesterol levels. A typical heterozygous patient will have LDL cholesterol in the 200s. Homozygotes have LDL cholesterols over 500! So here is the problem. From conception on, FH patients’ bodies are bombarded with excess LDL cholesterol. Their arteries, tendons, eyes… everything is soaked in cholesterol. In contrast to patients who do not have this disorder, afflicted individuals have a markedly prolonged burden of high LDL. They bathe in cholesterol their entire life. That is why these individuals develop premature cardiovascular disease. In fact, patients with FH have a 12-fold higher risk of coronary artery disease compared with their own unaffected relatives. FH patients have a fifty percent mortality by the age of sixty if they are inadequately treated. And even more frightening, FH patients typically live their lives in the dark, undiagnosed and untreated. With- out being properly recognized, appropriate and life-saving care cannot possibly be rendered. Thus, our charge is crystal clear: Doctors must improve our ability to identify these patients early on in life and by so doing treat them appropriately and diminish their risk of dying young.

The FH patient
Let’s truly “look at” the patient with FH. In order to be able to recognize and appropriately treat these individuals, doctors and patients must be familiar with what this disorder looks like. First it’s critical to know that LDL cholesterol levels fluctuate throughout our lifetimes. We are born with our lowest levels, and after puberty LDL steadily rises throughout the rest of our lives. So pediatricians must appreciate that an LDL cholesterol of 160 might indicate the presence of FH, whereas in an adult this same LDL cholesterol level would be considered only moderately elevated. It is also important to understand that men and women have very different cholesterol levels. Until menopause, women have lower total cholesterol, LDL cholesterol, and triglyceride levels; and higher HDL cholesterol levels than men. Unfortunately, after menopause each of their lipid parameters deteriorates. Thus, physicians need to have a solid grasp of the influence that gender and age have on all lipid values (my lecture on this can be found at (http://aspconline.org/resources/ highlights.php). You can see that there is often great complexity in interpreting lipid and lipoprotein values; it is therefore important at times for patients to see lipid specialists in order to receive more refined therapy (To find a lipid specialist near you, visit www.lipid.org). We know what FH patients’ lipids look like, and we know that their vascular tree is severely diseased by an overabundance of LDL, but what other manifestations result from such high lifetime LDL levels? In addition to vascular disease, there are also disfiguring non-arterial consequences of FH. A life-time of markedly elevated LDL cholesterol can lead to an accumulation of fat in unusual parts of our bodies. Our tendons are often affected where fatty deposition can lead to palpable lumps called xanthomas. The Achilles tendon is a frequent target of this aberrant fat accumulation. Tendon xanthomas can easily be seen by the naked eye. Our palms can also be affected, with an abnormal yellowish discoloration in their creases called palmar xanthomas. Another area for physicians to focus their attention is our eyes. In the corner of the eye, adjacent to the nose, we can at times see yellowish deposits called xanthelasmas. In the eye itself, we sometimes see light-toned fatty deposits called corneal arcus. These tend to occur on the bottom and top of the cornea at the edge of the iris (the-colored part of the eye) because that is where the density of blood vessels is greatest. Seeing tendon and palmar xanthomas, or corneal arcus in patients under the age of forty-five, essentially confirms the diagnosis of FH.

Treatment Options
In 2011, initiating an FH call to action, the National Lipid Association released guide- lines to improve the identification and treatment of these patients. The NLA guidelines emphasize early detection; we now know that under appropriate circumstances very young children (even two years old in some cases!) should be screened. Once a patient has been diagnosed with FH, it is important not to stop there, but to perform “cascade” testing. This is a rigorous search of the patient’s relatives to determine who among them might also have the disease. Through proper cascade testing, doctors can discover many additional patients who would otherwise have been left untreated. Along with the National Lipid Association, other organizations such as the American Society for Preventive Cardiology and The FH Foundation are doing their part to raise FH awareness. Pharmaceuti- cal companies such as Genzyme and Aegerion are also help- ing out. Pharmaceutical companies frequently sponsor scientific educational conferences, enabling doctors to remain current with the ever-changing landscape of medical knowledge. They build websites devoted strictly to educating the lay public, allowing all people to more effectively become their own advocates. And of course they also create the medications, such as statins, that lower our risk of heart attack and stroke. In the case of FH, Gen- zyme has fashioned a novel medication, Mipomerson, in order to more effectively manage patients with extraordinarily high LDL levels. Aegerion has created Lomitapide another unique LDL-lowering agent. Other innovative agents are in the works. Those of us who specialize in the management of severe lipid disorders are thrilled to have access to ground-breaking medications that will hopefully make an even greater dent in the damage inflicted by FH. Finally, let’s examine the state-of-the-art management of FH individuals.

First and foremost, diet and exercise are always paramount in maintaining optimal cardiovascular health. For FH patients though, more aggressive treatment is always needed. To “get them to goal”, combination therapy is uniformly required, which means using a statin as the foundation and then adding two, three, or even four other medications. Novel agents such as Lomitapide (Aegerion) and Mipomerson (Genzyme) were recently FDA-approved for the treatment of severely afflicted FH patients. These medications represent a new and welcome addition to Lipidologists’ medical armamentarium. Even still, many of these patients require more aggressive interventions. One of the best modalities available is LDL-Apheresis. In a manner similar to dialysis (minus the fatigue and potential side-effects), patients are connected to a filtering machine through two IV lines. Blood is withdrawn from one IV, circulated through a series of filters, and returned to the body through the other IV. Typically the two-hour procedure is performed in an outpatient- setting once every other week. Each treatment results in a 60 percent to 80 percent reduction in LDL (other pro-atherogenic substances are also removed). Over the ensuing two weeks, the LDL rises steadily until it can be lowered once again with another treatment. Despite the fact that LDL gradually increases between treatments, studies have demonstrated a nearly 75 percent reduction in cardiovascular events when patients are treated with LDL-Apheresis. Thus, LDL-Apheresis is a viable option for difficult-to-treat heterozygotes and mandatory for all homozygotes. (To find a center near you, visit www.lipid. org) Familial Hypercholesterolemia is a frequently undiagnosed genetic disorder adversely affecting patients’ lipids and leading to premature heart attack, stroke, and death. A solid understanding of age and gender associated lipid fluctuations, physical signs of FH, and the nuances of cholesterol management is essential for doctors to diagnose and treat this disease. Somewhere between 600,000 and one million Americans suffer from FH. Consequently we must do our best to understand, manage, and perhaps most important of all, “spread the word” about this insidious but conquerable threat. It is a mission that can be accomplished only through the coordinated efforts of doctors, scientists, medical associations, industry, and patients themselves. Fortunately, this is what we find taking place today.

Please read more about preventive cardiology at www.preventivecardiologyinc.com.

Images courtesy of HomeCarForYou.com

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