Dr. Joel Brock DNP, DC, APRN, NP-C
It is heart disease month, and I cannot help but reflect on when I was 12 years old. Sadly, I lost my father to heart disease after he suffered a series of heart attacks. I always wondered what happened to him? When would medical science catch up so early treatment or prevention measures would help intervene, or even prevent such catastrophes? Could a model of care be created to support self-preservation and wellness by addressing heart disease risk from every direction possible? This topic has engaged me to the point of doing a Ph.D. over heart disease as there are so many more ways to monitor, treat, and support people who are suffering or at risk-not just monitoring standard cholesterol markers.
Read on to learn more about additional blood markers and genetics that can help you live a long and heart healthy life. I have been passionate about educating myself, colleagues, and our clients on the latest research and advances in heart health, particularly from an integrated model supporting the whole person, physically, emotionally, and spiritually. Stay tuned for information about our upcoming podcasts and webinars this month to take a deeper dive!
Beyond Medications- A Whole Systems Heart Health Approach
Heart medications such as those for blood pressure and/or statins are often critical but not the end of the story related to treatment and wellness. Understanding and modulating the risk factors for cardiovascular disease has moved far beyond just measuring traditional cholesterol markers and administering stand-alone pharmacological intervention. Unfortunately, many conventionally trained practitioners are not aware of the latest information on the importance of a whole systems approach. An integrative model of care includes advanced blood markers along with the use of vital nutrients, lifestyle modification, stress transformation, and supporting behavioral change to optimize longevity and well-being. This is especially important for those with a strong family history of cardiac disease.
Medications May Not Always be the Answer
Besides the standard cholesterol lipid panel and measuring “bad” cholesterol (LDL), there are many other biomarkers for diagnosing and monitoring heart disease. Studies have shown a number of blood markers of equal importance, if not more predictive, of cardiovascular risk than cholesterol. For example, compelling literature reveals that people taking statin drugs may not have the anticipated prevention or protection from cardiac events as once thought and other supportive treatment may be vital. There are those who should never take various medications from a genetic standpoint (read more below). There may also be involvement with issues tied to inflammation, autoimmunity, gut function, blood sugar, insulin regulation, genetic susceptibility, and hormonal imbalance. These clinical factors are often critical in the overall picture of cardiac disease. Unfortunately, these factors are often not addressed in our traditional disease-care model.
Additional Cardiovascular Health Markers You Should Be Aware Of
Many individuals could be saved, helped, guided, or given secure medical advice if advanced tests were considered standard tests. Along with a standard lipid panel, these are the additional markers we consider for those at risk (continue reading below for a more detailed explanation).
- Small dense LDL (sdLDL) percentage – Additional risk and stand-alone marker
- Lipoprotein(a) (Lp(a)) Lp(a) – Familial and genetic connection to disease
- apoB- the backbone of LDL particles
- Oxidized phospholipids on apoB (OxPL-apoB) – Arterial calcification risk
- Apolipoprotein A-I (apoA-I) – Lipid control and balance
- Very Low-Density Lipoprotein Cholesterol (VLDL-C) – Obesity link
- Lipoprotein-Associated Phospholipase A2 Activity (LpPLA2) – Indicates growing plaque and risk for an immediate event
- Myeloperoxidase (MPO) – A cytokine that indicates possible plaque rupture
- High Sensitivity C-Reactive Protein (hs-CRP) – Inflamed tissue in the blood vessels
- Fibrinogen – Link to arterial narrowing
- Homocysteine – B vitamin need and Artery wall damage and clotting
- C-Peptide – High blood sugar and insulin link
- Heart Statin Induced Myopathy (SLCO1B1) Genotype Test – Statin tolerance
Many more markers could be discussed, but this is the basis of what many experts now consider as a new standard in routine screening and as a start for monitoring methods, along with a detailed history and physical exam.
STAY TUNED TO UPCOMING PODCAST, WEBINAR and NEWSLETTER
There is much to discuss about other clinical markers related to cardiovascular health including good fats, gut-based pathology, detoxification, hormones, stress, exercise, diabetes, diagnostics, referral needs, and supportive nutrient as well as medication information for a complete package to help support the need for our mission of comprehensive and integrated care! Please follow us over the next several weeks for an entire conversation over what is crucial when looking at comprehensive cardiovascular health, evaluation, and management. Our team of providers is always here to help at Carpathia Collaborative.
ADDITIONAL DETAILS on BLOOD MARKERS
- The percentage of small dense LDL (sdLDL): Low Density Lipoprotein (LDL) is a measurement of the protein that acts like a boat carrying around the cholesterol. Yet the size and type of boats are critically important. The number of small boats or “sdLDL” particles is an independent marker for cardiac risk. Standard LDL may be normal, but if the percentage and level of small dense LDL markers are elevated, the risk of a cardiovascular event can still be present. If not measured, it could lead an individual into having a false sense of security.
- Apolipoprotein B. ApoB is the backbone of the LDL protein and allows the cholesterol molecule to enter in cells. Elevated levels of apoB are significant predictors of heart disease and are a more meaningful indicator of cardiovascular disease than the standard LDL measurements done on routine labs.
- Lipoprotein(a) (Lp(a)) Lp(a): This is a genetically determined, independent marker that can be associated with a doubled risk of a complex disease. This is an LDL-like particle and is a protein made in the liver and intestines and then attached to the cholesterol. When LP(a) and ApoB are elevated together, things get even worse.
- Oxidized phospholipids or Phospholipids on apoB (OxPL-apoB): Oxidation is a process where a molecule of Oxygen interacts with a substance to alter it. For example: iron + oxygen creates rust! Oxidized or “rusty” phospholipids are found on various lipoproteins, namely, LDL, VLDL, and especially Lp(a). When the arterial wall takes up these oxidized phospholipids, they can accelerate the hardening of arteries, thereby increasing the risk of myocardial infarctions, strokes, and calcific aortic valve narrowing (stenosis). Oxidized phospholipids are highly pro-inflammatory and contribute to many diseases of aging. Clinicians can use OxPL-apoB levels to reclassify patients into higher or lower risk categories allowing better-personalized care. Shouldn’t something of this significance be mandatory?
- Apolipoprotein A-I (apoA-I): ApoA-I is a protein produced in the liver and intestine. It helps provide the structure to HDL particles (mostly good cholesterol). It activates enzymes that add a fatty acid to cholesterol (esterifies cholesterol) and allows it to enter the core of HDL for appropriate control. Low levels are associated with higher cardiovascular risk. Not adding this biomarker is a chance for missing disease severity.
- Very Low-Density Lipoprotein Cholesterol (VLDL-C): VLDL is a lipoprotein made in the liver and carries harmful triglycerides. This test is often used with the general lipid profile to screen for cardiovascular disease (CVD). High levels of VLDL cholesterol and triglycerides in your blood may mean you are at risk for CVD. People who are obese also have higher levels of VLDL cholesterol. If this is a link to obesity and heart attack, why is it not used more in various patient populations?
Additional Inflammatory Biomarkers That Should be Considered.
- Lipoprotein-Associated Phospholipase A2 Activity (LpPLA2): LpPLA2 is an enzyme produced by monocytes/macrophages in the blood and various tissues that break down phospholipids. Increased blood levels of LpPLA2 are associated with soft, active growing plaque. This biomarker predicts CVD risk independent of LDL-C and other inflammatory markers associated with a 2-fold increased risk for coronary events and a 2-fold increased risk for stroke. Inflammatory markers prime even normal cholesterol levels as dangerous. Why are inflammation and specific markers not considered as standard?
- Myeloperoxidase (MPO): MPO is a cytokine enzyme found in circulating white blood cells (neutrophils) and is also produced by white blood cells (monocytes) in the foam cells that develop within the artery wall that generates plaques. Elevated levels of MPO may indicate the presence of unstable plaque or buildup in the arterial wall and an increased risk of plaque rupture. In patients with high levels of MPO, careful evaluation of CVD risk should be considered by practitioners. Elevated MPO levels are a significant independent risk factor for a critical adverse cardiac event (MACE) over the ensuing one to six months. If that is the supportive information on this marker, why is it not used in high-risk patients?
- High Sensitivity C-Reactive Protein (hs-CRP): CRP is an acute-phase inflammatory cytokine synthesized by the liver. It tells us about inflammation inside the blood vessels. The “high sensitivity” CRP tells us about systemic inflammation that can turn cholesterol into a pathological state.
- Fibrinogen: Fibrinogen is an acute-phase inflammatory plasma protein synthesized by the liver and is an essential component in clotting mechanisms. It accelerates the narrowing of arteries significantly if present in elevated levels, and is associated with inflammation. Every 100 mg/dL increase in plasma fibrinogen level > 370 mg/dL has been associated with a 1.8 fold increased risk of CVD. It is the cherry on top of the cake for vascular damage if other markers are causing damage and inflammation.
- Homocysteine: High homocysteine is a marker for the utilization of certain B Vitamins such as B6, B12 and Folate. It is an important risk factor for ischemic heart disease, fatal and nonfatal myocardial infarction, sudden cardiac death, premature coronary artery disease, extracranial carotid-artery stenosis, venous thrombosis, stroke, and peripheral vascular disease. Why is this not used as a tool to screen for the possibility of multiple conditions?
- C-Peptide: Elevated C-peptide levels are associated with high insulin, insulin resistance, diabetes, obesity, renal insufficiency and can elevate aldosterone to create high blood pressure, as well as the inflammatory cytokine interleukin-6, along with triglycerides which can harm the cardiovascular system and skew the balance of good versus bad cholesterol along with glucose levels. Why is it not measured if a marker can help link blood sugar irregularities and blood pressure with cardiovascular disease?
Important Genetic Marker
- Heart Statin Induced Myopathy (SLCO1B1) Genotype Test: Boston Heart Diagnostics. The SLCO1B1 gene is critical to the body’s uptake and metabolism of statins drugs. Statin-associated muscle symptoms include the onset of muscle aches, spasms, weakness, and muscle pain, which are the most frequent adverse events associated with statins. Up to 60% of patients stopped taking a statin due to muscle pain as the primary reason for discontinuation. About 25% of people carry either one or two copies of the SLCO1B1 variant. This increases their risk up to 4.5-fold – or 17-fold, respectively for developing significant statin-induced myopathy or muscle pain due to statins drug usage. This test helps healthcare providers identify patients at higher risk for such adverse side effects and prescribe the right statin type and dose with the most negligible probability of causing myopathy. If statins are so prevalent and prescribed constantly, why is this safety measure not in place for all prescriptions due to its prevalence?
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