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”.

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Cholesterol and Vascular Disease Part 6: LDL-Apheresis and Novel Cholesterol Strategies on the Horizon

Today’s final post in this six-part series describes one FDA approved non-medication treatment for severely elevated LDL cholesterol, and three novel medications on the horizon.

LDL-Apheresis is a non-drug therapy for patients with vascular disease and LDL-C > 200. It is reserved for patients with a genetic disorder called Familial Hypercholesterolemia (FH), or those individuals who cannot tolerate standard medications but still have very high LDL levels. Therefore, this treatment is clearly not for everyone. In a manner similar to dialysis, patients are connected to a filtering machine through two IV lines. Blood is withdrawn from one arm, circulated through a series of filters and returned to the body through the other arm. Typically the procedure is performed every other week. Each treatment results in a 60% to 80% reduction in LDL particles. After treatments, the LDL will rise steadily until it can be lowered once again with another therapy. Although LDLs do increase after a treatment, studies have demonstrated a nearly 75% reduction in cardiovascular events when patients are treated with LDL-Apheresis. Thus, LDL-Apheresis is a viable option for high risk patients. I am very fortunate to be able to run one of the forty or so centers in the USA, and I am happy to say that not only is the procedure extraordinarily well tolerated, but also the lipid effects are nothing short of remarkable.

As for the medications on the horizon, three deserve immediate recognition: Mipomersen, Lomitapide, and REGN727. These are all currently “experimental” but deserve mention not just because they will likely soon be on the market, but because each one represents a truly fresh way to lower LDL.

  • Mipomersen, licensed by Genzyme, is a second generation antisense oligonucleotide that is administered weekly by injection. It dramatically lowers LDL. The English translation is that this drug thwarts our body’s LDL production mechanism at the DNA level. DNA’s job is to produce mRNA in order to translate DNA’s protein-producing knowledge into the actual creation of proteins. Mipomerson binds and inactivates the mRNA that carries the code for the essential protein in every LDL particle, apoB. Without apoB, LDL cannot be created. Mipomerson does not block cholesterol production; it stops our body from producing too many LDL particles. Very different from the way statins work!
  • Lomitapide – owned by Aegerion – works differently. The first step in normal LDL particle construction is the merger of apoB (a protein) with triglycerides (fats). Even within cells, fats do not float freely; they must be chaperoned from one place to another. (Remember, water – blood – and fat do not mix!) The chaperone for triglycerides in the intestinal and liver cells is called MTP, or Microsomal Triglyceride Transfer Protein. Lomitapide inhibits MTP; it is our first MTP inhibitor. By blocking the transfer of enough triglycerides to the essential apoB protein, defective LDL precursors are produced. Our bodies don’t like out-of the-ordinary substances, and so these precursors are rapidly destroyed. The result, dramatically decreased LDL (and triglyceride) levels.
  • Finally, there’s REGN727, a drug that is too young to bear a proper name. This agent utilizes yet another innovative approach to diminish LDL. If you recall from Part 4 of this series, LDL receptors bring LDL into cells. When we have a lot of LDL receptors on our liver cells, LDL levels fall, and our blood vessels are far better off. Our bodies produce a substance called PCSK9 whose role is to bind and inactivate LDL receptors. When PCSK9 levels are out of control, we destroy too many receptors and develop dangerously high levels of LDL. REGN727 is an antibody against PCSK9, so it stops our bodies from inappropriately destroying valuable LDL receptors. By doing so, it too lowers LDL. Of the three novel agents, this one is furthest from the market. It needs more thorough testing before it can be released. At this point though, confidence is high. Hopefully within a few years we will see all three of these agents helping millions of patients avoid experiencing heart attacks and strokes.

I hope you’ve enjoyed reading this series on Cholesterol and Vascular Disease as much as I’ve enjoyed writing it. Thanks for tuning in. Next week…

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Cholesterol and Vascular Disease Part 4: The Great Statin Debate

It has been unequivocally established that high levels of LDL can lead to heart attacks and strokes. Parts 1- 3 of this blog described the history of cholesterol, the superiority of LDL particles over LDL cholesterol, and the pathophysiology associated with an overabundance of LDL particles. In addition to our understanding of the biological process whereby LDL particles cause vascular disease, we also have a plethora of clinical trials demonstrating the efficacy of lowering LDL.

Everyone–lay people, physicians, and scientists–is plagued by the overabundance of clinical trials involving all aspects of health and medicine, many of which clearly contradict one another. In order to practice medicine in a fashion that appropriately considers the outcomes of these clinical trials, one must find a way to make sense of them. My approach has been to evaluate the clinical trials not just individually, but as a whole. I look for trends. When studies repeatedly reach the same conclusions (especially when they pathophysiologically “make sense”) I feel much more comfortable concluding that they are correct. In the case of LDL we find a commonality that is indisputable. The studies repeatedly demonstrate that statins–a class of cholesterol lowering medications I will momentarily describe–uniformly decrease the risk of cardiovascular events by about 30%. This event reduction is consistent among patients in the setting of both primary and secondary prevention. And so we must listen to the studies and lower our patients’ LDLs accordingly.

Statins are the class of medication for cholesterol management that unequivocally possess the greatest amount of science supporting their use. These medications work by blocking a critical enzyme in our body’s production of cholesterol. In response to lower levels of cholesterol within our cells, the cells increase surface receptors to bring in more LDL particles. The result is a diminution in the number of LDL particles – as well as the LDL cholesterol – in our bloodstream. Read More…

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Vitamin D – an Important Daily Vitamin

Hands and Sunset

I’ve felt for quite some time that vitamin D — and D3 in particular — should be an important component of a healthy individual’s daily vitamin intake, often in the form of supplementation.

As we learn more and more about the promising role of vitamin D, additional patients with D deficiencies are being identified. Unfortunately, vitamin D is not found naturally in many foods, so most of our vitamin D is produced in our bodies by the action of sunlight on the skin.

Aging decreases our synthesis of vitamin D
Most vitamin D is produced in our bodies when ultraviolet rays from sunlight strike the skin and trigger vitamin D synthesis. As humans age, however, we often lose the ability to manufacture adequate amounts of vitamin D.  Research indicates that vitamin D is important not only for proper absorption of calcium and the maintenance of bone health, but also for maintaining healthy joints, a healthy cardiovascular system and healthy moods. In addition, vitamin D plays an important role in regulating cell division and differentiation and supports immune system function through its effects on macrophages, natural killer cells (NK), and T cells. Scientific data indicate that vitamin D also has a role in helping to maintain breast, prostate, colon, and kidney health. In other words, its impact in our bodies is far-reaching.

Vitamin D3 more effective than D2
A recent study published in The American Journal of Clinical Nutrition* further supports my evidence-based belief that vitamin D3 is more effective than D2 (it can raise blood levels of vitamin D up to 70% better than D2). AJCN’s first-ever systematic review and meta-analysis comparing the effectiveness of the vitamin D forms supports the findings of many other researchers and studies.  (Note: vitamin D is found in two forms D3 or Cholecalciferol and D2, or Ergocalciferol. In contrast to Cholecalciferol, Ergocalciferol is not natural; it is a byproduct of irradiated fungi).

Check your vitamin D level
Ask your doctor to do a simple blood test for 25-hydroxyvitamin D [25(OH)D] that will provide the best measure of your vitamin D status. A 25(OH)D level of 40-50 ng/ml is currently thought to be optimal. If necessary, supplement with a daily multivitamin with adequate levels of vitamin D3 and then additional vitamin D3 as needed. A general rule of thumb is that your vitamin D level will rise 10 points for every 1,000 IU D3 taken daily.

Read that label
Look for the terms vitamin D3 or cholecalciferol on supplement labels. The D2 form of the vitamin (ergocalciferol) though widely used in fortification and supplements, is less potent and artificially derived.

*Study: “Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis1–3” — Laura Tripkovic, Helen Lambert, Kathryn Hart, Colin P Smith, Giselda Bucca, Simon Penson, Gemma Chope, Elina Hyppo ̈nen, Jacqueline Berry, Reinhold Vieth, and Susan Lanham-New

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Innovative Heart Failure Discovery: Heart Failure’s Effects in Cells May be Reversed Via Rest

Our hearts might not be so different from our skeletal muscles after all. Researchers at the Imperial College London  have found that structural changes in heart muscle cells after heart failure can be reversed by allowing the heart to rest. Findings from a study conducted on rats published today in the European Journal of Heart Failure show that the condition’s effects on heart muscle cells are not permanent, as has conventionally been believed by scientists and physicians. The discovery could open the door to new treatment strategies and procedures.

Heart failure means the heart can no longer pump enough blood to meet your body’s needs. It is commonly the result of a heart attack; it can occur with other disorders; or it can occur as a result of simply aging. Around 750,000 people in Britain are living with heart failure and it is estimated that it affects nearly 5 million Americans. Severe heart failure carries a substantial risk of death within one year, which is worse than the prognosis associated with most cancers. Clearly we need new heart failure treatments and preventive measures.

In 2006, researchers at Imperial College led by Professor Magdi Yacoub showed that in some individuals resting the heart using an LVAD (Left Ventricular Assist Device) fitted for a limited time can help the heart muscle to recover. The LVAD is a small pump that boosts the function of the heart and reduces strain on the left ventricle, the most important pumping chamber of our heart. The new study is a major step in understanding the mechanisms for improving muscle recovery at the level of heart muscle cells.

The Imperial researchers studied whether “unloading” the demands on heart muscle cells can reverse the changes and damage that occurs during heart failure in rats.

“If you injure a muscle in your leg, you rest it and this allows it to recover,” said Dr Cesare Terracciano, from the National Heart and Lung Institute (NHLI) at Imperial, who supervised the study. “The heart can’t afford to rest – it has to keep beating continuously. LVADs reduce the load on the heart while maintaining the supply of blood to the body, and this seems to help the heart recover. We wanted to see what unloading does to heart muscle cells, to see how this works.”

Researchers transplanted a failing heart from one rat into another rat alongside that rat’s healthy heart, so that it received blood but did not have to pump. After the heart was able to rest, several changes in heart structure that impair heart contraction were reversed in the damaged heart.

“This is the first demonstration that this important form of remodelling of heart muscle cells induced by heart failure is reversible,” said Michael Ibrahim, also from the NHLI at Imperial, who conducted the research for his PhD funded by the British Heart Foundation. “If we can discover the molecular mechanisms for these changes, it might be possible to induce recovery without a serious procedure like having an LVAD implanted.”

The most profound cellular effects observed in this study concerned structures called t-tubules. These allow electrical signals to travel deep into the muscle cells so that all of the fibers contract simultaneously. T-tubules become sparse and irregular after heart failure. Unloading the heart led to the t-tubules returning to normal.

original press release via:

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