#1 CAUSE OF ADULT DEATH IN THE U.S. FOR EACH OF THE PAST 100 YEARS:
Heart disease is not a Lipitor, Crestor or even an anacetrapib deficiency. It is a complex end result of multiple factors driven by our diet, fitness level, stress and other lifestyle factors such as smoking, social connections and, increasingly, environmental toxins.” ~Dr. Mark Hyman, M.D.
More than 650,000 Americans die annually from heart disease (or over 1,700 a day). Add stroke deaths to this total and the number of annual U.S. deaths directly related to the cardiovascular system (heart and blood vessels) climbs to over 790,000. The annual number of Americans dying from heart disease has been between 600,000 and 700,000 since the mid-1950s. 
Put another way, heart disease (>1,700 deaths/day) kills about the same number of Americans every day as died due to Hurricane Katrina in 2005 (when an estimated 1,800 lives were lost).
Image Source: https://slate.com/human-interest/2014/06/death-map-the-most-common-causes-of-death-in-each-state-of-the-union.html
Financially speaking, about one out of every six U.S. healthcare dollars is spent on heart/cardiovascular disease. For the person with heart disease and no other chronic conditions, average annual medical expenses are over $7,000 (or more than $580 a month). For the person with heart disease and at least one other chronic condition, average medical costs are over $14,000 (or more than $1,160 a month). What about heart attacks and strokes you say? Americans suffer 1.5 million heart attacks and strokes each year. For heart attacks, the average hospital stay is around 5 days and costs over $21,000. [8-10]
CAN WE AVOID OR EVEN EFFECTIVELY COMBAT MOST CASES OF CARDIOVASCULAR DISEASE?
YES! THROUGH A SMART HOLISTIC, INTEGRATIVE APPROACH
Below are some of my top tips/strategies for making progress against the top cause of adult death in the U.S. and the world- cardiovascular disease. As cardiovascular disease can be driven by numerous lifestyle and physiological factors, an all-encompassing holistic strategy to prevent or effectively combat CVD is often best...
* Try to avoid a chronic sleep deficit, which is defined as a long-term habit of <6 hours of quality sleep a night (which doubles risk of heart attack or stroke). 
* Try to make progress against sleep apnea, especially severe sleep apnea, which increases risk of congestive heart failure 58%. 
* Most research agrees that a habit of 7-9 hours of quality sleep a night is ideal for health, and chronically poor sleep quality (including lack of deep, lack of restful sleep and/or frequent waking) increases risk of CVD. 
Image Source: http://blog.lcwa.com/2017/03/aasm-promotes-heart-impacts-of-sleep.html
EXERCISE & PHYSICAL ACTIVITY-RELATED FACTORS
* Stay active, as little to no exercise and/or physical activity increases risk of CVD. 
* Avoid a regular habit of high-intensity exercise (especially high-intensity, long-duration exercise), which, perhaps surprisingly to some, is a CVD risk factor, particularly when coupled with an otherwise sedentary lifestyle and/or other CVD risk factors. [38-39]
* Avoid a habit/lifestyle of sitting >6 hours a day (especially prolonged, uninterrupted sitting), which can increase risk of blood clots & DVT. [40-42]
Image Source: https://www.safetyandhealthmagazine.com/articles/17906-sitting-or-standing-too-much-at-work-new-video-addresses-ways-to-lower-associated-health-risks
STAYING HYDRATED + DIGESTIVE & RENAL SYSTEM SUPPORT
* Stay hydrated. A healthy goal here might involve trying to drink at least 1/2 your weight, in ounces, of water every day. Clinical data links chronic dehydration or under-hydration to increased risk of CVD. 
* Support intestinal/gut health. Strategies here may include utilizing probiotics, prebiotic fiber, psyllium fiber, and consuming a hypo-allergenic diet. This may also include avoiding/restricting use of antibiotics, NSAIDs & opioids (especially chronic use), as impaired gut health & altered microbiome has been linked to CVD. [44-45]
* Support liver & gallbladder health. Strategies here may include utilizing various choline supplements, TUDCA, TMG, taurine, milk thistle/silymarin and bitter greens. Avoiding/restricting excess carbs, acetaminophen/Tylenol use, and no to moderate alcohol consumption are also good ideas, as impaired liver health has been tied to CVD. [45-46]
* Support kidney health & healthy blood pressure. Strategies here include staying hydrated, using ACV, and consuming proper amounts of dietary potassium & magnesium. Avoiding/restricting use of PPI's, ACE inhibitors, radiocontrast agents, and other nephrotoxic substances is suggested, as impaired kidney functioning (including Chronic Kidney Disease) is a risk factor for CVD. 
DIALING IN PROTEINS/AMINOS, FATS/FATTY ACIDS & NET CARBS
* Consume moderate amounts of protein (habitual very high or very low protein diets have been linked to increased CVD risk). 
* Consider foods & supplements that boost nitric oxide levels and/or otherwise support healthy circulation. Items here include supplements like citrulline and cayenne, and sources of dietary nitrates like beets, celery and spinach. [49-50]
Image Source: https://www.atisavpharma.pt/genisav/
* Increase your omega 3 intake, especially from sources like wild-caught salmon and high EPA & DHA fish oils. A diet low in omega 3 fatty acids is a risk factor for CVD [51-53]
* Don't be afraid of healthy sources of dietary fat (including saturated fat and cholesterol). A diet low in total fat is a CVD risk factor. [54-55]
* Avoid/restrict your intake of artificial trans fats (i.e. industrial trans fats). Trans fats are a type of unsaturated fat. There are two types of trans fats- natural (like CLA & VA [vaccenic acid], found in high amounts in grass fed beef & dairy) and industrial/artificial (created in an industrial process that adds hydrogen to liquid vegetable oils to make them more solid). The primary dietary source for artificial or industrial trans fats is hydrogenated and/or partially-hydrogenated oils. Industrial TFAs may be positively related to CVD whereas natural (or ruminant) TFAs are not. 
* Moderate or restrict your carbohydrate intake (ex. ketogenic diet or "quasi keto"). This is especially cardioprotective if you're also significantly overweight and/or have other CVD risk factors (including CVD itself). A diet high in carbohydrates is a risk factor for CVD (compounded if carbohydrate sources regularly include significant amounts of refined grains, cane sugar, low-quality refined sweeteners and/or alcohol). [57-58]
[see the end of the article for more data on high carb diets being linked to CVD]
THE IMPORTANCE OF MICRONUTRIENTS & OTHER CV-SUPPORTING NUTRIENTS
* Consider nicotinic acid (a form of vitamin B3), which can help dyslipidemia (abnormal cholesterol levels) and improve circulation. Nicotinic acid is particularly effective at raising low HDL levels. [59-61]
* Consider vitamin B12 (methylcobalamin form), gentle iron (ferric pyrophosphate or ferrous bisglycinate forms) and folate (folate or 5-MTHF forms), to support red blood cell activity and healthy oxygen levels (which is vital for heart health). Note that excess iron in the blood may be a risk factor for CVD. 
* Consider antioxidants such as vitamin C (ascorbic acid, sodium ascorbate, acerola cherry, etc.), natural vitamin E and CoQ10 (ubiquinol or ubiquinone), all of which help reduce oxidative stress/damage caused by excess free radical production in the cellular mitochondria (note that cholesterol found in arterial plaque is almost always oxidized, indicating damage from excess free radical production). [63-64]
* Consider vitamin K2 and/or EDTA supplements, both of which work to keep calcium in bones and out of cardiovascular tissue (calcification of cardiovascular tissue being a driving factor in the development of many types of CVD). Note that more caution is needed with EDTA use. [65-67]
* Consider supplements like magnesium and potassium, which work to relax soft tissue and promote healthy blood pressure levels and cardiac functioning. [68-72]
* Don't be afraid of unrefined sea salt (i.e. the minerals sodium and chloride), as salt by itself is not a risk factor for CVD (salt can spike blood pressure when consumed by a person with kidney dysfunction and potassium or magnesium deficiencies). [73-74]
* Consider heart-healthy, collagen-building, anti-microbial supplements and foods that contain sulfur (ex. MSM, garlic). 
* Consider supplements like turmeric extract/curcumin, which help to keep systemic inflammation in check (chronic inflammation being a driving factor in progression of CVD). [76-77]
* Consider a proteolytic enzyme supplement like nattokinase, to help reduce excess levels of fibrin/fibrinogen, which are often found in vascular plaque and fibrotic cardiac tissue. [78-80]
* Safely & effectively treat underlying and/or systemic infections (parasitic, bacterial, fungal and/or viral). Infections and various microorganisms have been recognized as significant causes of cardiac diseases for many decades. All components of the heart can be adversely affected by infectious agents. Elevated WBC/leukocyte counts are indicative of infection and are associated with CVD morbidity and death. Arterial plaque often contains activated macrophages as well as T lymphocytes and mast cells- all indicative of infection. [81-84]
[see the end of the article for more data on how factors like food allergies, portion control, caloric restriction and intermittent fasting affect cardiovascular health]
ENVIRONMENTAL HEALTH FACTORS (SPECIFICALLY, AIR QUALITY)
* Reduce your exposure to air pollution and respiratory irritants. Several studies have demonstrated an increased risk for cardiovascular events in relation to both short & long-term exposure to modern-day concentrations of particulate matter in the air. 
* Avoid unnecessary stress and manage other stressors in healthy ways. Chronic high stress levels can lead to dysfunction in the hypothalamus-pituitary-adrenal/thyroid axes, which can lead to excess cortisol, which can contribute to excess inflammation, which contributes to CVD. [86-87]
* Don't smoke. Cigarette smoking contributes to the production of oxidizing chemicals, inflammation, reduced nitric oxide (NO) bioavailability and increased adherence of platelets and macrophages (turning into foam cells), ALL of which contribute to CVD. [88-90]
* Avoid anabolic steroids (or if using, use with extra caution). Long-term use in particular (>2 years) has been linked to heart disease. 
* Avoid cocaine- its use increases CVD risk. 
MEDICAL FACTORS: MEDICATIONS & SURGERIES
* Several non-cardiovascular medications have been implicated as increasing the risk of CVD or of causing/contributing to a cardiovascular event [heart attack, stroke]. For every one of the conditions for which these drugs are used there exists safe, effective alternatives. Drugs here include...
-Corticosteroids (ex. prednisone, hydro-cortisone, etc.)
-Diabetes meds (including metformin & thiazolidinediones)
-Amphetamines (including ADD/ADHD meds like Adderal, Vyvanse, etc.)
-TCAs (class of anti-depressants)
-Clozapine (an atypical anti-psychotic med)
-Respiratory meds like albuterol
-Certain cancer drugs
Most cardiovascular drugs, by and large, do not safely & effectively address the underlying root issues driving the progression of CVD and should be avoided or weaned off of, in favor of safe & effective lifestyle, dietary and healthcare interventions. Drugs here include...
* Statins. Statins lower CoQ10 levels by up to 40%, contribute to fatigue, muscle pain/myalgia, nerve damage [those who use statins for >2 years have 4-14 fold increased risk of neuropathy], cause cognitive & memory problems in 90% of users, drastically increase the risk of developing diabetes and, ironically, increase the risk of heart failure. [100-110]
* Blood thinners like warfarin/coumadin. A 2014 study by Quest Diagnostics found that warfarin only had the desired effect 54% of time. Warfarin carries a black box warning, which implies the drug or device has side effects that may cause serious injury or death. For warfarin, side effects include bleeding (including internal hemorrhaging), abnormal and/or large bruising, coughing up or vomiting blood or materials that look like coffee grounds, death of skin tissue (necrosis/gangrene), calciphylaxis (a buildup of calcium in small blood vessels) and death. A 2007 study in the American Journal of Medicine estimated that nursing home residents suffer 34,000 serious, life-threatening or fatal events related to warfarin each year. And a 2011 report in the New England Journal of Medicine found that warfarin accounted for 33,000 emergency hospitalizations among the elderly from 2007-2009 (this was more than twice as many as the next drug).
* Blood thinners like Xarelto. Xarelto “works” by inhibiting the enzyme Factor Xa, which is essential in the body’s natural formation of blood clots. As of late 2018 more than 20,000 lawsuits were pending against Johnson & Johnson and Bayer, the makers of Xarelto, with plaintiffs contending that the drug manufacturers failed to sufficiently warn people about the severe risk of uncontrollable bleeding and the inability to reverse these side effects during the first few years the drug was on the market.
* Blood thinners like Eliquis. Like Xarelto, Eliquis is a Factor Xa inhibitor. According to FDA reports from 2014 to September 2018, over 47,000 people reported side effects when taking Eliquis, including more than 2,500 deaths.
* Blood thinners like Pradaxa. An anticoagulant like Xarelto and Eliquis, Pradaxa “works” in a slightly different way, by blocking thrombin, an enzyme produced by the body that plays a primary role in the natural clotting process. After only 2 years on the market Pradaxa was formally linked to more than 500 deaths. That number is now in the thousands. Accordingly, thousands of lawsuits have been filed against Pradaxa-maker Boehringer Ingelheim over severe bleeding injuries allegedly caused by the drug. In 2014 the drug maker paid $650 million to settle 4,000 of these lawsuits.
* Blood thinners like Plavix. In November 2015 the FDA determined that using Plavix does not increase OR decrease risk of death, calling into question its general efficacy. In that same year, the FDA issued a warning suggesting that Plavix patients had been put at risk of bleeding unnecessarily, even though the drug had already been on the market nearly 20 years! Since Plavix was approved for human use in 1997, thousands of people have claimed that the drug caused them gastrointestinal bleeding, severe bleeding from minor cuts, and even brain damage. In September of 2016 there were more than 5,000 lawsuits filed nationwide against Bristol-Myers Squibb (BMS), the makers of Plavix. [111-120]
* Blood pressure meds like pharmaceutical diuretics. One of the primary risks of pharmaceutical diuretics center around worsening kidney function and even kidney failure. The website www.GoodRx.com lists pharmaceutical diuretics as one of the top 10 worst medications for kidneys. Worsening kidney functioning can increase uric acid levels, which can exacerbate gout in some patients. Other side effects include rashes (again, usually brought on by worsening kidney functioning), abnormal electrolyte levels (electrolytes include 6 essential minerals: calcium, magnesium, potassium, phosphorus, sodium and chloride), metabolic alkalosis (due to increased excretion of chloride in proportion to bicarbonate), hypokalemia (i.e. low potassium, which can cause cramps and, more seriously, precipitate cardiac arrhythmias and sudden death) and a cluster of symptoms including fatigue, muscle weakness, headache and/or dizziness (all of which can increase fall risk for older adults, and are likely due to lower levels of sodium, chloride and/or potassium).
The Multiple Risk Factor Intervention Trial (MRMIT) was a large study performed in 1985 that looked at men with high blood pressure. One group received standard drug therapy while the other received a treatment that involved pharma diuretics. In the diuretic group, there was an increase in the onset of cardiac arrhythmia AND the death rate increased, EVEN THOUGH THEIR BLOOD PRESSURE WAS LOWER THAN THE OTHER GROUP. The researchers hypothesized that this may have been due to substantial mineral loss due to the diuretics. Mineral deficiency can lead to irregular heartbeat, stroke, heart attack and death. [121-122]
* Blood pressure meds like beta blockers. Beta blockers like propranolol (active ingredient in Inderal, InnoPran, Pronol), metoprolol (active ingredient in Lopressor, Toprol) and atenolol (active ingredient in Tenormin) are known to cause a 5-7lb weight gain during the first few months of use. Some research suggests that hypertensive drug-related weight gain may be, at least in part, related to fluid retention as a result of drug-induced damage to the kidneys. Other side effects of beta blockers include fatigue, dizziness, headaches; nausea, vomiting; metabolic acidosis (calcium naturally drives up pH levels, so it makes sense that reducing bioavailable calcium might drive down pH levels, leading to acidosis), water retention/edema in the extremities; low blood pressure (hypotension), slow heart rate and arrhythmia, due to a reduced ability for the heart to contract. [123-136]
* Blood pressure meds like calcium channel blockers. The use of calcium channel blockers has been strongly linked to blood sugar imbalances. The beta-islet cells in the pancreas depend on an influx of calcium through L-type calcium channels in order to release insulin. CCBs reduce bioavailable calcium, which leads to a subsequent reduction in the release of insulin, which can lead to hyperglycemia. The “insulin blockade” here also impairs the myocardial cells ability to uptake glucose, which further decreases the hearts ability to contract, compounding hypotension. One study analyzed the results of 9 separate clinical trials, collecting data from over 27,000 patients accounting for nearly 120,000 years of treatment. In total, more than 12,000 patients were on calcium channel blockers and another 15,000 were taking other hypertensive meds (including diuretics, beta blockers and ACE inhibitors). While the calcium channel blockers seemed as effective as the other drugs in lowering blood pressure, they were significantly worse at preventing heart attack and heart failure. In the patients treated with calcium channel blockers, the risk of heart attack was 27% higher and the risk of heart failure was 26% higher. [123-136]
* Blood pressure meds like ACE inhibitors. The side effects of ACE inhibitors (ex. lisinopril) include hypotension (excessively low blood pressure), headache, dizziness, chronic cough, fainting, kidney problems including edema/swelling and rash (GoodRx rates ACE Inhibitors as one of the top 10 worst medications for kidney health), and an increase in bradykinin (BK) levels, leading to increased inflammation, pain and tissue damage. According to FDA reports, over 210,000 people have reported adverse side effects from taking lisinopril from 2003-2018. From 2003 to Sept 2018 more than 4,000 deaths were attributed to lisinopril, including more than 250 every year from 2011-2018. [123-136]
* Blood pressure meds like ARBs. In a meta-analysis of 24 clinical trials involving ARBs, more than 25,000 patients with heart failure were randomly assigned to take either an ARB or control substance (placebo or ACE inhibitor). The results? ARBs were found to be no better than a placebo or ACE inhibitors in reducing the risk of death, disability or hospital admission for any reason. However, more patients stopped treatment early with ARBs than with placebo due to adverse side effects. ARBs have also been associated with a modestly increased risk of new cancer diagnosis. Speaking of cancer, one popular ARB, valsartan (brand name Diovan) was in the news a lot in late 2018 and early 2019, after the FDA issued a major recall on the drug. This only happened after the drug regulating authorities in 22 other countries had already issued recalls. The recall was due to the presence of n-nitrosodimethylamine (NDMA) in a large number of valsartan batches. NDMA is classified as a probable human carcinogen (i.e. cancer-causing substance). [123-136]
* Cardiovascular surgeries like heart bypass. More than 7 million cardiovascular surgeries are performed in the U.S. every year, which is the most by specialty type. Of those, about a quarter million are heart bypass surgeries. More specifically called coronary artery bypass graft surgery or CABG for short (pronounced “cabbage”), the commonly stated goal of heart bypass surgery is to improve blood flow to the heart. The surgery is generally recommended for individuals who have moderate to severe coronary heart disease (CHD), a condition where plaque builds up inside the coronary arteries that supply oxygen-rich blood to the heart. If CHD progresses, hardened plaque can narrow the coronary arteries, thereby reducing the flow of oxygen-rich blood to the heart. This is often a cause of chest pain (angina). If the condition progresses further, blood flow to the heart can be mostly or completely blocked off, especially if a large blood clot forms in the area or travels to the blockage. This is one of the most common causes of a heart attack.
CABG was first performed on humans in the late 1960s. Bypass surgery would grow in popularity through the 1970s, 80s and 90s to a peak in the year 2000, when more than 500,000 procedures were performed in the United States. Since then that number has dropped significantly, in part due to advancements made with stents (angioplasty) and perhaps due to the impact that certain clinical studies have had (such as the on-going STICH study, started in 2002). Still, approximately 250,000 bypass surgeries are performed in the U.S. every year.
The late Harvard cardiologist Dr. Thomas B. Graboys estimated that 90% of coronary artery bypass surgeries are unnecessary. Two relatively well-known clinical studies seem to indicate that heart bypass surgery isn’t worth the trouble for the vast majority of those who undergo it. An early study published in 1983 called the CASS (coronary artery surgery study) followed 780 patients under 65 years old who were allocated to either drug treatment (n=390) or heart bypass surgery (n=390) for coronary heart disease from 1975-1979. The difference in 5-year survival rate between the two groups was not statistically significant, nor was there a significant difference in likelihood of heart attack or ventricular functioning between the two groups. Two other relatively well-known studies during the same time period, the Veterans Affairs Cooperative Study (VA) and the European Surgery Study (ECSS) echoed the general findings of the CASS.
Another more recent study, the on-going STICH study, began in 2002 and had study results first presented in 2011. In this study, more than 1200 patients were assigned to either drug treatment or bypass surgery for CHD. Nearly 5% of patients who underwent bypass surgery died within the first 30 days after surgery. In the STICH study, 41% of patients assigned to drug treatment died during the 5 year follow up period, whereas the mortality rate for those who received bypass surgery plus medication was 36% for the same period, a relative reduction in risk of 14% (this difference did not reach statistical significance). According to most of the research I looked at, the primary physical benefit associated with heart bypass surgery centers around a reduction in angina (chest pain).
General efficacy aside, cardiac bypass surgery is a serious and highly invasive procedure with a lengthy recovery time and some significant and relatively common adverse side effects. Most CABG patients can expect to spend 3-10 days in the hospital after the surgery and another 6-12 weeks recovering at home. Some of the more common adverse side effects include cognitive impairment (problems with general cognition, memory loss, etc.) and even additional surgery to address issues like infection in or around the surgical wound. The days immediately after surgery generally carry the highest mortality risk, and around 2-5% of all patients who receive heart bypass surgery will die sometime in the first 30 days after the procedure. After that time, the risk of death due to surgical complications usually drops significantly. Still, only 75% of CABG patients will live for at least another 10 years post-surgery. For those who do live that long, the risk of death again increases dramatically (by 60-80%) around the 8-10 years mark (this is according to a Danish study that looked at the life expectancy of 51,000 Danes who’d undergone CABG).
And then there’s the financial cost. For a coronary artery bypass graft surgery, the general price range in the U.S. is between $70,000 and $125,000 per procedure (although it can be as low as $40,000). Cost variance often hinges on factors like the complexity of the procedure and where the procedure is performed. [137-150]
* Cardiovascular surgeries like angioplasty. Angioplasty is more formally known as percutaneous cardiac intervention (or PCI for short). During the procedure, a long, thin plastic tube called a cardiac catheter is inserted into an artery (the entry site is usually either the groin area of the leg [most common] or the arm [less common]). Using x-ray, video and radioactive dyes, the catheter is then guided by a cardiologist through the blood vessels on its way to the heart. Once the catheter reaches the coronary artery, a tiny balloon on the catheter is inflated, in an attempt to increase the opening of the artery so that blood flow is improved. As a result, any arterial plaque present is compressed against the wall of the artery. This is called a balloon angioplasty. Around 80% of the time a metal stent is also placed at the site of the blockage, in an attempt to reinforce the opened blood vessel and prevent a re-narrowing of the artery (called restenosis). In balloon angioplasty without a stent, it’s estimated that restenosis will happen in about 30% of cases. Some data shows that bare metal stents reduce the chance of restenosis to around 15% and drug-eluting stents (stents that emit medication) reduce the risk to around 10%.
Compared to bypass surgery, angioplasty recovery time is minimal and usually consists of 1 night in the hospital followed by a few days of recovery. As with all invasive procedures, angioplasty presents risks. Common adverse side effects include restenosis and blood clots that form around stents, as well as bleeding, bruising or infection at the entry site (often the groin area of the leg). Other dangers include an increased risk of heart attack, stroke and coronary artery damage during the angioplasty procedure, as well as adverse reactions to the dye and medication used during the procedure. It’s important to note that cardiac stents cannot be removed once implanted, and many angioplasty patients are encouraged to take blood thinning medications indefinitely post-procedure.
Angioplasty was first performed on humans in the 1970s. Since that time the procedure has grown in popularity, to the point where an estimated 660,000 angioplasties are now performed every year in the United States (as of 2018). What’s made angioplasty even more popular than coronary bypass surgery? Likely factors include its minimally-invasive nature, shorter recovery time, lower cost, advances in drug-eluting stent technology, and even the impact of recent studies like the STICH (the results of which called to question the general effectiveness of bypass surgery).
One particularly influential study, the 2007 COURAGE trial (COURAGE stands for Clinical Outcomes Utilizing Revascularization and Aggressive druG Evaluation) examined more than 2200 patients with coronary heart disease who were assigned to either drug therapy or angioplasty (PCI). At 2.7-7 years follow up there were no statistically significant differences between the two groups for a number of important factors, including the end point of death, incidence of stroke, incidence of heart attack or of hospitalization due to acute cardiac event. According to the COURAGE authors’ findings, 8 of 10 patients who undergo angioplasty are inappropriate candidates who’d be better served by more conservative therapy. [151-160]
[note that the use of supplemental oxygen (21-100% oxygen) for various cardiovascular disease conditions is a hotly debated topic within the field, and various studies have come to conflicting conclusions]
COMORBIDITY FACTORS: OTHER DISEASES THAT INCREASE RISK OF CVD
* Obesity/excess weight [161-162]
* Diabetes (type 2) [163-164]
* Arthritis (and other joint pain conditions) 
* Various gut/intestines, liver and kidney diseases [166-168]
* Hyperparathyroidism (parathyroid gland helps regulate calcium levels; excess parathyroid hormone increases blood calcium, which can accumulate in cardiovascular tissues) 
LAB & MEDICAL TESTS TO MONITOR CVD RISK FACTORS
As far as lab testing for cardiovascular disease goes, while the standard lipid panel has been elevated by mainstream medicine for several decades now, it doesn’t even make my list of the top lab tests for CVD, which includes…
CMP-14 (includes markers for several blood proteins, major minerals and blood sugar, as well as liver & kidney markers)
Organic Acids Test (OAT) (includes a large number of analytes, including yeast & fungal markers, bacterial markers, oxalate metabolites, glycolytic cycle markers, mitochondrial markers, neurotransmitter markers, folate (vitamin B9) metabolism markers, ketone & fatty acid oxidation markers, other B vitamin markers (B2, B5, B6, B7/biotin & B12), vitamin C, CoQ10, glutathione markers, an ammonia marker, an aspartame marker, a dozen or so amino acid markers, a phosphoric marker, and creatinine.
CBC (includes indicators for red blood cells/RBCs, white blood cells/WBCs, and platelets.
GI Map Test (comprehensive stool test with several GI bacterial, fungal, viral & parasitic markers)
Omega 3 & 6 fatty acid test (or EFA test)
Cardio IQ panel (not the standard lipid panel; includes LDL subfractions markers including lipoprotein(a))
A1c (measures blood sugar levels over past 2-3 months)
Micronutrient panel (spectracell)
B12 test (shows up on OAT)
Vit C (shows up on OAT)
Vit D 25 hydroxy
Magnesium RBC test
Compete iron panel (serum iron, transferrin, ferritin, hem.)
CoQ10 (shows up on OAT)
Glutathione (glutathione markers are on OAT test)
Hs CRP (inflammation test; should be on cardio IQ panel as well)
Blood culture (to test for systemic/blood infections)
Fibrinogen activity blood test
Mitochondrial markers (on OAT test)
Of all the above I would emphasize these 9: CMP (which includes calcium, blood sugar & kidney markers), OAT (which includes mitochondria, vit C, CoQ10 & glutathione markers), CBC, GI MAP, Cardio IQ Panel (which includes CRP), A1c, vitamin D, magnesium RBC and iron panel.
As far as other cardiovascular medical tests are concerned, I recognize that angiograms (cardiac, peripheral, CT) can offer extremely helpful digital imaging of the CV system, but I think there are some potentially serious side effects associated with the radioactive contrast agents used (as some clinical data documents).
I also prefer exercise-induced stress tests that monitor blood pressure and use EKG and ultrasound/echo to drug/chemical-induced stress tests and those that use radiocontrast agents (called nuclear stress tests).
NOTABLE WEBSITES & BOOKS
* Dr. Stephen Sinatra, Integrative Cardiologist (www.drsinatra.com)
* The Great Cholesterol Myth (2012) by Jonny Bowden, PhD and Dr. Stephen Sinatra, M.D. (cardiologist)
* Cholesterol Clarity (2013) by Jimmy Moore and Dr. Eric C. Westman, M.D.
* The Sinatra Solution: Metabolic Cardiology (2015) by Dr. Stephen Sinatra, M.D. (cardiologist)
ADDENDUM 1: ADD'L RESEARCH ON HIGH CARB DIET INCREASING CVD RISK
* A 2009 review of data from >2900 participants from the Framingham study found high glycemic index diets unfavorably affected CVD risk. 
* A 2016 review of scientific literature on saturated fat & sugar found high sugar/carb diets induced abnormalities associated with CVD while sat fat intake did not. 
* A 2017 review that found added sugars drive coronary heart disease. 
* A 2018 large review of diet and CVD risk, including a review of the PURE study [>135,000 participants] found total fat intake had beneficial effects on CV health and higher carb intake [>60% of diet] increased CVD risk. 
ADDENDUM 2: THE FOOD ALLERGY-CVD LINK
* A 2008 review of the data on allergies [including food allergies] and the cardiovascular system showed how food allergies drive gut inflammation, and gut inflammation adversely impacts immune response, systemic inflammation and cardiovascular health. 
* 2011 review highlighted the link between allergies, inflammation & cardiovascular disease. 
* 2018 review of the clinical literature emphasized the role that inflammation, not cholesterol, plays in driving CVD. 
ADDENDUM 3: THE BENEFITS OF PORTION CONTROL & CALORIC RESTRICTION ON CV HEALTH
* A 2009 study highlighted caloric restriction's positive effects on CV functioning. 
* A 2009 review of clinical literature highlighted the benefits of caloric restriction on CV health. 
* A 2011 review showing caloric restriction's benefits on CV health. 
* A 2016 review of the effects of caloric restriction [including eating to 70-80% full] found positive impacts on longevity & other health markers, including CV markers. 
ADDENDUM 4: INTERMITTENT FASTING'S BENEFITS ON CV HEALTH
Technically-speaking, a fast is abstaining from food for at least 8 hours. Over the last few years, “intermittent fasting” has become a health buzz phrase, usually indicating a person is practicing a habit of abstaining from food (or calories) for at least 12-16 hours before eating. Twenty-four hour fasts have also grown in popularity, as have extended fasts of 2 days or more.
* A 2019 review of the clinical data on I.F. and CVD found that I.F. lowered total cholesterol, triglycerides, and LDL cholesterol and inhibits the development of atherosclerotic plaque by reducing the concentration of inflammatory markers such as IL-6, homocysteine, and CRP. 
* A 2012 study of Intermittent Fasting with a liquid diet found that it favorably modulates visceral fat and adipokines in a way that may confer protection against CHD. 
* A 2008 review of the clinical data on fasting and CVD found that fasting was associated with lower risk of CAD. Fasting was also associated with lower diabetes prevalence. 
ADDENDUM 5: THE POSITIVE IMPACT OF BREATHING EXERCISES ON CV HEALTH
While not mentioned above, there is a fair amount of clinical data on the health benefits of breathing exercises, particularly for the cardiovascular, respiratory and autonomic nervous system. [184-187]
ADDENDUM 6: ADD'L NUTRIENTS/SUPPLEMENTS TO SUPPORT MITOCHONDRIAL HEALTH (CRUCIAL FOR CV HEALTH)
In addition to CoQ10 and other antioxidants mentioned above, the supplements L-carnitine, D-ribose and ALA are also often used to support healthy mitochondrial functioning, which can positively impact CVD, especially in cases where notable mitochondrial dysfunction is present. [188-191]
44 www.scielo.br/scielo.php?pid=S0066-782X2012000300011&script=sci_arttext&tlng=en (gastro changes associated with heart failure)
45 http://circ.ahajournals.org/content/circulationaha/133/17/1696.full.pdf (gastro & liver issues in heart failure)
46 www.ncbi.nlm.nih.gov/pmc/articles/PMC5437502/ (NAFLD linked to CVD)
47 http://circ.ahajournals.org/content/108/17/2154 (kidney disease as risk factor for CVD)
50 www.ncbi.nlm.nih.gov/pmc/articles/PMC3575935/ (2013; vascular effects of dietary nitrates)
56 www.nature.com/articles/ejcn201134 (artificial/industrial transfat vs ruminant/natural transfat)
59 https://www.ncbi.nlm.nih.gov/pubmed/17705685 (2008)
60 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4523006/ (2015)
61 https://www.ncbi.nlm.nih.gov/books/NBK541036/ (2019)
71 www.bmj.com/content/346/bmj.f1378 (potassium intake & CVD)
72 https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1524-6175.2002.01728.x (potassium intake & CVD)
75 www.altmedrev.com/archive/publications/7/1/22.pdf (2002; sulfur's applications in medicine)
78 https://www.nature.com/articles/srep11601 (2015)
79 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372539/ (2017)
80 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6043915/ (2018)
85 https://www.ahajournals.org/doi/10.1161/01.CIR.0000128587.30041.C8 (2004)
92 http://www.onlinejacc.org/content/70/1/101 (2017 review of adverse CV effects of cocaine)
98 https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/216932 (2003/04)
99 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6033155/ (2018)
161 https://ahajournals.org/doi/10.1161/circulationaha.106.171016 (2005)
162 https://www.acc.org/latest-in-cardiology/articles/2018/07/06/12/42/cover-story-obesity-and-cardiovascular-disease-risk (2018)
166 www.clinsci.org/content/132/1/85 (gut-CVD link)
167 https://www.nature.com/articles/s41575-018-0010-0 (liver-CVD link)
168 https://heart.bmj.com/content/103/23/1848 (kidney disease-CVD link)
169 https://academic.oup.com/eurheartj/article/25/20/1776/497057 (2004)
181 www.ncbi.nlm.nih.gov/pmc/articles/PMC6471315/ (2019; intermittent fasting in cardiovascular disorders)
182 www.ncbi.nlm.nih.gov/pmc/articles/PMC3514278/ (2012; I.F. and CVD)
183 www.ncbi.nlm.nih.gov/pmc/articles/PMC2572991/ (2008; benefits of fasting to lower CVD risk)
184 www.ncbi.nlm.nih.gov/pmc/articles/PMC5909014/ (2018 study on breathing's health benefits)
185 www.ncbi.nlm.nih.gov/pmc/articles/PMC5769199/ (2018 study on breathing's health benefits)
186 www.ncbi.nlm.nih.gov/pmc/articles/PMC5709795/ (2017 study on breathing's health benefits)
187 www.ncbi.nlm.nih.gov/pubmed/23076942 (2012 study on breathing's health benefits)
188 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4566449/ (2014 review on supplements for mito dysfunction)