The American Society for Preventive Cardiology 30 Years and Counting

ASPC CVD PREVENTION

July 30, 2015 marks the start of the ASPC’s Annual meeting, taking place once again at the spectacular Boca Raton Resort. This year, in addition to our world-class faculty, new elements will be added to the meeting – poster presentations to be published in Clinical Cardiology as well as a Level 1 Expert’s Course in Preventive Cardiology. Over the next three months I will certainly write more about the conference and I hope many of you will avail yourselves of its offerings. (For more complete information please visit www.aspconline.org).

Today however, on the heels of the Dallas Cardio-Metabolic Health Congress (CMHC) I am compelled to write this brief note about the ASPC. The reason is simple. As I sat in the speaker’s row with my friends and colleagues Drs. Jamie Underberg, Amit Khera, and Michael Miller it became clear that the thirty-year-old organization is now firmly entrenched in mainstream education. You see, Dr. Underberg sits on the ASPC’s Board of Directors while Dr. Khera is the Secretary; I am the President Elect, and Dr. Miller is a Past President. It was truly heartwarming to have us all gathered together for the sole purpose of helping to educate our colleagues about issues such as Familial Hypercholesterolemia (FH), Hypertriglyceridemia, Lipid and Cholesterol Guidelines, and the future of HDL research and therapies.  The ASPC is growing at a gratifyingly rapid rate, as more and more physicians, ARNPs, and other healthcare practitioners embrace the doctrine that cardiovascular disease prevention must preempt intervention in order for our nation and the world at large to be able to truly enjoy optimal health. If you are not already a member of the ASPC, please consider becoming one. Also, I encourage everyone interested in prevention to join us in July. I promise you will not be disappointed.

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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The Joyful Luxury of Bringing Home a Puppy

The world is under siege.  Muslim extremists in Iraq are “cleansing” the hijacked country of the world’s most ancient Christians. Men, women, and children are being slaughtered, after they’ve been tortured and raped. Jewish teenagers are being kidnapped and executed by similar extremists; people are being beheaded in city streets. These are the same missionaries of terror that pierced our false sense of security, destroying our towers and the thousands of innocents within. Our civilized world is unequivocally in peril. A return to the dark ages is at our doorstep.  Some say there is nothing to fear; it’s a minority who are at the source of this evil. Yet a minority can create catastrophic consequences. Witness the horror of Nazi Germany. And, a “minority” in the world of Muslims is likely well upwards of 200 million people. This is a minority in truth, but one demanding our unwavering attention and concern.  So how does a puppy fit in this story?

Yesterday my wife fell in love with a nine-week-old puppy. We had recently lost a dog to a sudden splenic rupture from cancer and in truth I believed it would be a long time coming before my wife would open herself up to another similar love. But I was mistaken. She informed me of her find and I immediately knew another dog would be coming home. I was sold on this notion with a simple question, “Isn’t this what life is supposed to be about?” Irrefutable. Life should be about love and puppies and the luxury and freedom to enjoy both. As a Preventive Cardiologist I couldn’t deny both the emotional and physical salutary impact of smiles and laughter engendered by the presence of a simple pup. Then I considered those in other parts of the world; Christians, Jews and non-radicalized Muslims fleeing and dying at the hands of terrorists. These individuals cannot enjoy the American luxuries of which I speak. We are a nation of fortune; but this fortune was built on the selfless sacrifices of our fathers and forefathers. Freedom is not an easy thing to gain but I fear it is quite easy to lose. Understanding this, we must be hyper-vigilant about safeguarding it. Yet its nemesis nips at our heels. Political correctness aside, when critically and honestly examining the world one must acknowledge there is but a single group that seeks to dominate all others. Yes, a minority threatens us, and most of the world abhors the actions of this minority. The minority, however, is fierce, brutal, enormous, powerful, determined, and patient. They will have their way if we do not face and stop them. If we fail, love and puppies, and other often-unappreciated freedoms will become our memories, and the dreams of future generations.

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 FH Foundation, Turning Hope into Reality

I spent Thursday and Friday in California. No, I wasn’t strolling on the beach or sipping local wines. Instead, I was engaged in strategic conversations during our FH Foundation Board of Directors Annual meeting. FH (Familial Hypercholesterolemia), as you know from prior posts, (if you don’t, please visit www.thefhfoundation.org or see my older blogs and FH/cholesterol articles at www.preventivecardiologyinc.com) is a common yet terribly underdiagnosed genetic disorder that elevates LDL cholesterol which in turn causes early and life-threatening heart disease. Affected patients cover a wide spectrum, having disease from before age ten to as late as 70 or 80 years old. We spent some time examining last year’s accomplishments, but more importantly we determined how to continue the process of converting dreams into reality. I’ve chosen to share this story with you for two reasons: First, FH must be conquered. Second and no less important, the Foundation epitomizes the power of a small group driven by unfettered passion, enthusiasm, and commitment.

Katherine Wilemon, the group’s founder, CEO, and tireless leader, suffered her heart attack shortly after the birth of her daughter. Though she had lifelong high cholesterol, and had experienced symptoms before the event, her genetic disease was initially unrecognized. And, in medicine, to be able to provide appropriate care we usually must know what it is we’re treating. Fortunately for Katherine – and her family –  she survived. Subsequently, wishing to turn a terrible event into a hopeful future, Katherine started the FH Foundation. That was just three years back. Since then, Katherine has not only surrounded herself with a growing group of highly effective and devoted patients, doctors, and businesspeople, she has travelled the world building awareness and interacting with every true FH expert. The FH Foundation has established a National FH Awareness Day. It has created the first and only Registry for FH patients in the US (Cascade FH). The FH Foundation spearheaded the establishment of ICD 10 codes for this disease, and it has initiated protocols to identify every single FH patient in our nation.

Our second Global FH Summit will take place this October in New York City. An array of nations will be represented. The list goes on and on. I recount this litany of achievements not to boast, but to demonstrate how the visions of an individual can burgeon, ultimately impacting the reality of so many. Coming away from two days of inspiring meetings I am certain the Foundation will continue to succeed. In short order FH will entirely emerge from the shadows. FH will become a disease on the tip of every doctor’s tongue, and consequently afflicted patients of all ages will no longer suffer and even die unnecessarily. Millions of people’s lives will be changed for the better. At the risk of being mawkish, I must state that my experience with the FH Foundation illuminated the fact that if more of us would only act with similar commitment and intention, we might just find ourselves in a peaceful and unified world. It’s a tall order I know, but the FH Foundation has given me a glimpse of the possibilities that can be born of the seemingly impossible.

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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An Update From the 2014 American Society for Preventive Cardiology (ASPC) Annual Meetings

Two weeks ago was the ASPC’s Annual meeting in Boca Raton, FL. The event was superb. Internationally recognized experts in a variety of disciplines convened in Boca Raton for the three–day-event. Nearly 200 healthcare practitioners from around the country came to listen to Professors from Northwestern, Harvard, NYU, The Mayo, Columbia University, The Miami Miller School of Medicine, Emory, Ohio State, UCLA…  Topics such as the somewhat controversial 2013 ACC/AHA Cholesterol and Obesity Guidelines, the enormously under-recognized disorder Familial Hypercholesterolemia, and the vast sex differences in CVD presentation and treatment were discussed.

My lecture was entitled, “The Omega-3 Fatty Acids DHA and EPA: Caution when interpreting the Trials. It’s time to get back to the basics.”  The talk highlighted enormous limitations inherent in recent omega-3 studies. It is not only clinicians and laypeople who must understand such issues, but the press as well. Too many reporters – and even physicians in the news – misinterpret clinical studies, oftentimes sending not just misleading messages to the pubic, but potentially damaging ones as well.

DHA and EPA are the essential fatty acids found in fish, NOT flax, Chia, or olive/canola oil. These fatty acids have been studied in a variety of disorders ranging from heart attacks to dementias, ADHD, eye disease, inflammatory bowel disorders, and Rheumatologic ailments. The list is actually even more extensive than this. Their benefits are legion – anti-inflammatory, anti-oxidant, anti-arrhythmic, and anti-thrombotic to name a few. Scientists across the globe are spending their entire careers evaluating the myriad biological effects of these fatty acids. Although we still do not know precisely how DHA and EPA will fit into our medicinal armamentarium, we do know that they have an important role to play. More studies and clinical trials are needed. One thing is clear however. DHA and EPA are here to stay. They represent a component in our diets that should be emphasized, not neglected. Nearly daily fatty fish or fish oils should be a part of most people’s dietary habits.

Beyond the value of DHA and EPA is an even more important message though. The media, in their unbridled attempt to produce quick and enticing stories, often critically misses the mark. Consequently we all must be very careful about how we interpret what we read or hear. We must always be vigilant when drawing conclusions about our health as well as other consequential matters.

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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February 28 is “Rare Disease Day” – FH is a Rare Disease That’s Just Not That Rare

Familial Hypercholesterolemia (FH) is a genetic disorder of LDL cholesterol handling which can lead to heart attack and stroke at very young ages. You may be shocked to learn that afflicted children as young as four years old have required bypass surgery or even perished from heart attacks. More surprising still is the fact that we now recognize that FH is far more common than previously believed. Some studies indicate that one in 200 people has a “milder” form of the disease, while one in 160,000 suffers from its most severe variant. It’s all FH though, and even in mild cases the risk of heart attack can be 20 times that of a “normal” individual.cholesterol meter Heart attacks in such cases occur much earlier in life than would ordinarily be anticipated. Here’s an example to which everyone can relate. 20% of patients who have heart attacks under the age of 45 have FH. Consider all the young people you know who’ve had heart attacks. One fifth of them probably have this genetic disorder. That is a huge number. The most recent estimate puts the number of FH patients in the US at 1 to 2 million. So that is certainly not rare! The number of extraordinarily severe cases is probably between 2 and 3 thousand, qualifying for the definition of a rare disease – being fewer than 200,000 in the US. Distressingly, only about 10% of FH patients have been identified as having the disease. That leaves 90% unrecognized, undertreated, and at great risk. We must change this pattern.

It is imperative on this Rare Disease Day that we all do our part to spread the word about FH. If you or someone you love has an LDL-C greater than 190 mg/dL you very likely bear this genetic malady. That means every one of your first-degree relatives – parents, siblings, and yes, even your children – has at least a 50% chance of also having the disease. Early treatment is key to improving outcomes. That’s why we recommend all children with a family history of premature heart disease or very high LDL cholesterol have their initial cholesterol level checked at the age of 2. By identifying family members with FH we can then treat them accordingly. Early recognition saves lives, sparing families the agony of losing a young, vibrant relative in the prime of her life. The good news is that there is much we can offer patients with FH. Novel medications and procedures such as LDL apheresis can dramatically lower LDL levels.

To learn more about such treatment strategies, please visit the FH Foundation at thefhfoundation.org.  If you believe you might have FH, please join our National Registry, the CASCADE FH Registry and become one of the many people who will help us curtail the terrible toll FH often takes. We look forward to hearing from you!

To learn more about LDL apheresis treatment options visit preventivecardiologyinc.com. Explore more preventive health issues at fpim.org.

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From the Ivory Tower to the Trenches: A Practical Approach to the 2013 ACC/AHA Cholesterol and Risk Assessment Guidelines

The distillation of well over one hundred pages of two guidelines into a pragmatic and accessible tool for the practicing clinician is of course a monumental task. It is essential to do so though. Clinicians require clear guidance in helping them manage patients in harmony with scientific developments. To think though that science is simply and solely a regurgitation of large randomized double blind placebo-controlled trials would be foolhardy to say the least. Science – especially medical science – is so much more. The fast-paced evolution of science keeps us all on our toes. And there are so many levels to consider: clinical trials of all forms, basic science of multiple disciplines, clinical acumen borne of clinical experience, and of course good old-fashioned common sense. So the Guidelines’ authors’ use of just a single facet of science, the Randomized Clinical Trial (RCT), a priori limits the utility of the recent guidelines. Still, they must be addressed and reckoned with. Indeed like most other things in life, they are not “all bad.” Before distilling the Guideline’s into a practical approach that I personally intend to follow, let’s first put the premise of the RCT as “King” in a real-world context by examining a typical doctor’s approach to patients.

In medical schools, residencies, and fellowships all physicians are trained how to diagnose and manage patients. Take a hypothetical case. A new patient awaits your expertise as you enter the exam room. The patient has dutifully completed a multi-page questionnaire, the modern-day equivalent of a Review of Systems (ROS), Past Surgical History (PSH), Past Medical History (PMH), List of Allergies and Current Medications, and History of Present Illness (HPI). You’ve read the document prior to entering the room but you spend time clarifying the issues and creating this patient’s cohesive medical story. Then you examine him; from his right, just as you were taught in medical school. Your exam has morphed of course, emphasizing those aspects relevant to your particular specialty but still incorporating features from other areas of interest. After all, it is a whole person you are seeing, and ailments oftentimes breach systems’ boundaries as they are not constrained by artificial barriers. You examine his blood work as well as any other pertinent tests that have been performed prior to the visit. Then you think. You place the pieces of his particular puzzle in an orderly fashion; you make diagnoses; and then you create a plan. Reflecting on every single aspect of this fundamental, age-old doctor-patient interaction, consider how much of it is truly based upon solid RCT evidence. I will spare you the agony of this exercise as I’ve already done it countless times. The answer is essentially none. Where are the RCTs validating our ROS, HPI, examination from the right…? They simply do not exist. Yet, this is how we all practice medicine. And, it has worked out rather well for our patients. None of us should be handcuffed by RCTs when we evaluate and treat patients; we are all free to use any and all of the countless tools at our disposal. And frankly, the more tools in our chest, the better off are our patients. So, rule number one in addressing the guidelines is, “Remember that they are not rules.” Guidelines are not a part of the Ten Commandments. Even the authors of the 2013 ACC/AHA Guidelines acknowledge this when they state, “Guidelines attempt to define practices that meet the needs 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.” Translation: You the doctor should treat each and every individual patient in the manner you deem most appropriate. You must not feel shackled by these or any other “Guidelines.” With this in mind, I will now review the Cholesterol and Risk Assessment Guidelines to present an approach I will utilize in my practice. The views that follow emanate from experience garnered through practicing Clinical Lipidology and Preventive Cardiology, in addition to my personal interpretation of the literature as a whole.

Four groups qualify for statin therapy in the new guidelines, and I agree; they should all be treated. They are:

  1.  Patients with clinical atherosclerotic cardiovascular disease (ASCVD), defined as acute coronary syndromes (ACS), myocardial infarction (MI), stable or unstable angina pectoris, coronary or other arterial revascularization, stroke, transient ischemic attack (TIA), or peripheral arterial disease (PAD) presumed to be of atherosclerotic origin. These patients are to receive high-intensity statins.
  2. Primary elevations of LDL-C > 190 mg/dL (consistent with Familial Hypercholesterolemia, or FH). These patients are to receive high-intensity statins.
  3. Diabetic patients between the ages of 40 and 75 with LDL-C 70 to 189 mg/dL and no history of ASCVD. Patients with 10 year risk > 7.5% receive high-intensity statins while others receive moderate-intensity statins.
  4. Patients without clinical ASCVD or Diabetes Mellitus between the ages of 40 and 75, having an LDL-C 70 to 189 mg/dL and 10 year ASCVD risk of > 7.5%. These patients are to receive moderate-to-high intensity statins.

A few problems with this construct are:

  1. The Risk calculator is still shrouded in uncertainty. Many issues remain to be resolved, not the least of which is the fact that a strong Family History of premature ASCVD fails to impact risk in this system. Also, only 24,000 patients were evaluated to construct this tool which sits at the center of these guidelines and is meant to be used to determine therapy for hundreds of millions of people. Therefore, for now, when I opt to do a 10 year risk assessment I will still use Framingham Risk Scoring. I do so with the understanding of the limitations of this scoring system and the concomitant need for methods to further risk reclassify patients.
  2. The intention is to treat patients with high-intensity statins and assume an LDL-C reduction of > 50%, and moderate intensity statins to achieve a reduction of 30 to 50%. LDL-C goals are now passé in this paradigm. However, we all know that each patient is unique. Some respond very well to statin therapy; others do not. I will therefore continue to measure LDL-C (as well as LDL-P) on drug and I will continue to get my patients to goals at least as stringent as those in ATP3. There are ample data supporting the “lower is better” hypothesis. For example, the Cholesterol Treatment Trialists (CTT) study showed in both phases one and two that lower is better. The fact that we do not have RCTs that have used titration of statins to LDL goals as a primary endpoint in no way negates the overwhelming body of literature showing better outcomes at lower LDL-C , apo B, and LDL-P levels across a range of different statins. I will continue treat to targets.
  3. The high-dose-statin-absent-adjunctive-therapy (or-even lipid/lipoprotein-follow-up) concept is to me “pie in the sky.” We all know that from an LDL-C – but even more so LDL-P or apo B – standpoint by prescribing statins alone we will fall woefully short of what we have been accustomed to achieve. We also know that lower is better. Thus, by adhering to the guidelines’ advice we will very possibly see worse future outcomes. Additionally, we know from several trials that statin-related Diabetes Mellitus is dose related. JUPITER found that 20 mg of Rosuvastatin reduced 2.5 ASCVD events or deaths for every one excess in DM. Thus there is a trade-off for uptitration of statins. For me, I will use statins as a base and other therapies such as cholesterol absorption inhibition and bile acid sequestration as adjunctive therapy.
  4. ASCVD includes the presence of PAD but it does not include the presence of subclinical disease in the coronary or carotid arterial trees. This is counterintuitive. There is ample evidence that the presence of a high Coronary Artery Calcium score (CAC) or age-and sex-inappropriate Carotid Intimal Media Thickness (CIMT) predicts higher risk of ASCVD events. Even absent the copious data we have accumulated, doesn’t it make physiologic sense to ascribe as much value to disease in the vascular beds that are direct culprits for the very events we are attempting to thwart as we do to distant arteries in the legs? I will continue to use CIMT and CAC (and coronary CT angiography) in intermediate risk patients as tools to risk reclassify patients.
  5. The age limits of 40 to 75 are problematic. What do we do with a 35 year old woman with no other ASCVD risks except an LDL-C of 180 mg/dL and a powerful family history of premature ASCVD? Her 10 year risk is only 1.6% but she is too young to be treated by the new guidelines regardless of her risk score. I would unequivocally treat this woman.
  6. The absence of a significant lipoprotein and triglyceride discussion relegates the guidelines to be strictly statin/LDL-C documents. They do not attempt to be comprehensive and the authors acknowledge this fact. Thus, we should not be misled to believe that lipoproteins and triglycerides are suddenly unimportant. They are not. I will continue to assess them and manage them in a patient-centric, individualized manner. Again, every patient is different. Each one deserves his or her unique assessment and management. “One size fits all” has no place in modern medicine.
  7. Biological markers like Lipoprotein Associated Phospholipase A2 (LpPLA2), myeloperoxidase (MPO), oxidized LDL, Lp(a), and urine microalbumin have numerous studies either validating their position as ASCVD risk factors or at least implicating them in ASCVD. Though de-emphasized in these guidelines, biological markers are helpful tools in understanding our patients’ risks as well as motivating our patients to adjust their lifestyles and take their medications. I will continue to utilize them in my practice of “Interventional Prevention.”

In summation let us remember that these guidelines are not law. They are based entirely upon a mere 25 “highest level” clinical trials, ignoring thousands of “lower level” trials, human biology and physiology, and clinical acumen. To some extent I would say they are so limited in scope by inappropriately-stringent data-entry criteria that they have become Ivory Tower, clinically-blind advice. Their very construct diminishes their real world relevance.  Ironically the system suggested in the guidelines has itself never been validated by the very type of RCT evidence demanded by the guideline authors. Something is surely wrong with that. Yet on a positive note the new guidelines are simpler than ATP3. Reliance more upon Global (Total) Risk rather than individual risk factors makes it easier for clinicians to make recommendations. Still, simple is not always good. As outlined above, I intend to use the guidelines as a foundation upon which to build a more dynamic and plastic way to approach the patients in my clinical practice. I refuse to await trials that may never appear. Instead, I will continue to avidly follow the literature, eagerly learn from my colleagues, and diligently incorporate a wide gamut of data to render the well-considered recommendations I ultimately share with my patients.

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

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Interventional Prevention – Taking Cardiovascular Disease Prevention to a New Level

In the November 27, 2013 JAMA issue, my letter, “The Pitfalls of Population-based Prevention was published with a very favorable response from Dr. Harvey Fineberg, the head of the Institute of Medicine (IOM). I was elated to see not only the letter’s publication and my introduction of the term, “Interventional Prevention” – a modern-era approach to risk reduction – but Dr. Fineberg’s forward-thinking reply as well. Interventional Prevention is after all a departure from “standard” prevention practices. We typically think of prevention in two facets, primary and secondary.

Primary prevention entails thwarting events before they have occurred while secondary prevention is the system wherein doctors utilize strategies to stop adverse events from occurring AFTER a first event has taken place. For example, hypertension and tobacco abuse are both well-established risks for heart attack and stroke. Our goal as health care practitioners is to lower blood pressure and help patients stop smoking in order to prevent heart attacks and strokes. In patients who have already had one of these events, this is termed secondary prevention; while it is primary prevention in those who have never suffered such an outcome. This describes the established approach to prevention.

Interventional Prevention is a much more proactive process. In this construct, doctors use cutting-edge predictors of risk such as biological markers in our blood and urine and imaging of different vascular beds (carotid and coronary arteries for example) to diagnose “hidden” disease or biologic perturbations and motivate patients to make significant lifestyle and medication changes in order to reduce their risk. Then we can evaluate these same markers and actually see improvements. We can do this in patients who have never had heart attacks and strokes, ostensibly decreasing their risk of ever experiencing such an adverse outcome. In Interventional Prevention, doctors identify and expose novel risks, make changes in patients’ regimens, and then facilitate improvement in what would otherwise have been “hidden” risk factors. Essentially we illuminate the invisible thereby affording patients and doctors the opportunity to heal aspects of our bodies before these perturbations cause irreparable harm. For example, with appropriate interventions we can demonstrate improvement in inflammatory blood enzymes such as LpPLA2. High levels of LpPLA2 predict both heart attacks and strokes while low levels predict the opposite. Through proper interventions we can witness the normalization of this and many other blood and urine biomarkers, clearly demonstrating on an individual basis the improvement in health and concomitant diminution of risk. This is truly patient-centric medicine. The medicine of the future has already arrived.

Learn more about comprehensive preventive cardiology at 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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Freedom through the Eyes of a Preventive Cardiologist

As an Interventional Cardiologist turned Preventive Cardiologist I understand all too well how much better it is to prevent a disease before it ever has the opportunity to strike. After all, what would you rather experience – a heart attack, angioplasty, stroke, or bypass surgery – or simply a modification of your lifestyle – eating better, exercising regularly and perhaps taking a medicine or two? Most of us would opt for the latter. I’ve yet to meet anyone who has enjoyed the experience of a major cardiac event, but most everyone likes being lean, fit, and energetic. Recently I was struck by the application of “prevention” to politics.

Americans are in the throes of controversy regarding freedom. Daily I listen to my patients as they express their worries that we might be on the road to socialism. Most people would reject such a notion, saying, “it’s impossible; America will always be the land of the free.” Yet, the patients who fret the most are those who actually lived through times of dramatic social change – Cubans, concentration camp survivors, former Eastern Europeans… These individuals have had the misfortune of going from freedom to “captivity”. And what’s truly most terrifying is the unwavering commonality of their views. They all echo the same sentiment declaring, “This is exactly what it looked like before Castro, or Hitler”, or whomever it was that led the movement that ultimately stole their freedom. By “exactly what this looked like “ these patients tell me they mean gun control, governmental intervention in business, loss of certain freedoms of religious expression and the like. They uniformly speak of the insidious nature of freedom’s ebb. Citizens of their former nations had decried the possibility that terrible social change was in the winds believing such a thing could not possibly occur. Listening to them intently I have concluded that freedom is much easier to lose than it is to gain.

Now I understand the need for us all to listen closely to what is happening in Washington as well as wherever we live. We must critically evaluate what we hear on the news, and steadfastly maintain open and circumspect eyes. Everyone would agree our country is in the midst of dramatic change. The question of course remains as to what direction we will take. As in the case of medical prevention it is time for us all to make perhaps our most important decision. Are we willing to do what it takes to prevent the loss of something our forefathers fought so bravely to attain? Will we sit back lazily and let the chips fall where they may? Or, will we get in the game, keep up with national and international events, maintain open but cautious minds, and speak loudly if we believe our freedom to be in jeopardy?  Remember the example of medicine – no one wants a bypass. The best way to avoid a bypass is to be proactive. The same, I believe holds true for remaining free.

Visit vitalremedymd.com for more preventive healthcare solutions.

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The Fiscal Cliff: Lessons Gleaned from Preventive Cardiology

Cardiovascular prevention requires a team effort with the doctor at the helm but the patient a necessary, eager, and deeply involved participant. The goal of prevention is to identify risks and then diminish them before a crisis ensues. Success demands identification of potential problems followed by a collaborative effort between doctor and patient to minimize those risks. Only through both proper identification and risk reduction can heart attacks and strokes be prevented. As I reflect on what I do for a living I am struck by the similarity we are all experiencing as we walk steadily toward the fiscal cliff. And I find myself perplexed by the fact that although our elected leaders have identified the problems they have been unable to work collaboratively to correct the issues. An analogous scenario would be this. I, the physician, identify a severe cholesterol problem in a patient. I then perform a coronary CT angiogram and demonstrate multiple plaques within the patient’s arteries feeding her heart. I recommend a medication to lower her risk and show her all the copious data supporting my recommendation. She turns to me and replies, “No thank you; I think I’ll just take my chances.” I of course counter with a litany of references to literature and clinical experience. Although I understand this is the best option for her, I fail to offer “lesser” alternatives. I am intransigent. She too is adamant; refuses therapy; and six months later sustains a fatal heart attack. The heart attack could have been avoided, but to do so required the joint efforts of doctor and patient. I should have been more open to “alternative” – albeit probably less successful – possibilities, and she should have been more willing to consider my well-considered recommendation.

Now we find ourselves in an economic and political game of “chicken”. Who will flinch first? Unfortunately the stakes are unbearably high. All our futures hang in the balance. Our president, recently elected by a narrow margin in the most contentious presidential battle many of us have ever witnessed blames the Republican Congress for the standoff. The Republicans blame the President. It appears their current mode of “working together and reaching across the aisle” is at best a pipedream and at worst an impossibility. Surely the Republicans must bend. But so too should the president. He represents the entire country, even the nearly 50% who did not vote for him. He was appalled by Romney’s 47% comment yet he seems to be enacting the very principle he condemned.  And, he is our leader. The buck does stop with him. He must find the way to compromise. And if he does ultimately reach across the aisle the Republicans in turn must be willing to compromise as well. If not, we will like lemmings drop over the fiscal cliff. And we all know how that ends for the lemmings. Let’s hope Congress and our President find the way to diminish the risk that they’ve so clearly identified. Let’s hope we do not experience the unnecessary, potentially fatal, but certainly avoidable “heart attack”.

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

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