Cardiovascular disease (CVD) risk factors, primarily atherosclerosis and hypertension, were the focus of last month’s heart health article, including research on nutritional ingredients that can improve lipid health and curb development of early forms of heart disease.

However, CVD has a knack for slipping through the best nets of prevention, especially in cases involving late detection of disease factors, as well as various powerful genetic predispositions. Inconsistent compliance with preventive diet and lifestyle regimens can further advance the disease to dangerous stages. As the heart and vascular system sicken, the body becomes highly susceptible to many debilitating cardiac events, and risk of mortality increases; more than 900,000 Americans die each year from CVD, according to the American Heart Association (AHA).While nutrition may exact its best science in prevention of CVD, various natural health ingredients can help limit the occurrence and devastation of cardiac events such as heart attack, stroke and heart failure, and can even promote recovery and overall survival.

In a healthy cardiovascular system, the heart pumps oxygen- and nutrient-rich blood throughout the body. Under normal conditions, depleted blood flows from the body into the right chambers of the heart via two main veins, the superior and inferior vena cava. The right atrium and ventricle then pump the blood out through the pulmonary arteries to the lungs, where carbon dioxide is exchanged for oxygen. The pulmonary veins then guide the replenished blood back into the heart’s left atrium and ventricle, which then pump the oxygen-rich blood out through the aorta for delivery to the rest of the body.

The rhythm and pace of this pumping action composes the heartbeat, which relies on a unique electrical system inside the heart. A node in the right atrium initiates an electrical signal that triggers atrial contractions, causing blood to fill the ventricles. The signal then continues to the ventricles, which contract and pump blood out of the heart. The contraction phase is called systolic, and the period of rest following this series of contractions is called diastolic. The rhythm of these contractions and rests can be monitored by EKG machines, which measure the heart system’s electrical waves. Any disruption to this electrical system can cause a cascade of problems downstream.

Heart rate can become alarmingly faster (tachycardia) or slower (bradycardia) than normal pace, which is roughly 60 to 90 beats per minute. In either case, the rhythm can be regular or irregular, called arrhythmia. Also called fibrillation, this disorganized, irregular rhythm can cause a rapid, chaotic quivering in either the upper two (atria) or lower two (ventricles) chambers of the heart. However, atrial fibrillation is considered by far the most common, occurring in 2.2 million Americans, according to AHA.

Atrial fibrillation involves a circular, chaotic rhythm that is inefficient and cannot pump blood out of the atria. When this happens, blood pools and can form clots, called cardio emboli. These emboli can break apart, travel throughout the body and become lodged in smaller arteries and capillaries resulting in blockages (called embolisms). This causes a stroke when the blockage occurs in vessels that feed the brain. According to AHA, 5.5 million people experience a stroke every year, and 15 percent of these stroke victims also experience atrial fibrillation. A stroke can also be caused by a blockage in other vessels resulting from atherosclerotic plaques that promote clotting.

Atrial fibrillation can involve severe tachycardia in which the heart rate accelerates to between 300 and 600 beats per minute. This weakens the heart, which stretches, thickens and can no longer pump blood efficiently. When the heart can no longer pump, cardiac output is depleted and heart failure occurs.

Congestive heart failure (CHF)—which kills more than 57,000 Americans each year—can occur in any of the four chambers and usually results in a back-up or congestion of blood, called edema.The left ventricle, the last chamber visited by nourished blood before it is pumped out of the heart via the demanding aorta, must create the most pumping power and is thus the largest, most muscular of the chambers. When the left ventricle is damaged it can lose its ability to contract (systolic failure) or to relax (diastolic failure). Either way, blood can back-up into the lungs causing pulmonary edema.

Failure of the left side can ultimately lead to failure of the right side, which means blood cannot be pumped into the heart. This causes a back-up of fluid in the veins that feed the heart, often leading to fluid swollen legs and ankles.

Although acute heart failure can be caused by a heart attack and results in severely declined breathing due to pulmonary edema, heart failure can become chronic and worsen over a longer period of time. In addition to arrhythmias, numerous other cardiovascular disease factors can cause CHF, including hypertension (strains heart muscles), heart valve malfunctions/diseases, hyperthyroidism (increased body metabolism demands increased cardiac output), anemia (less red blood cell content requires more output), cardiomyopathy (damage to the heart myocardium) and coronary artery disease—which can cause blockages that starve the heart.

Ironically, the heart does not get the oxygen-rich blood it needs to function from the fluid flowing through it, but instead is fed by coronary arteries branched off from the aorta. Any blockage in these coronary arteries can result in less oxygen supplied to the heart. In early, small blockages, angina occurs. People often mistake the chest pains of angina for a heart attack, but angina is not as severe and might never worsen to unstable angina or heart attack. Also called myocardial infarction, a heart attack involves the halt of oxygen to the heart (called myocardial ischemia), causing some cell death in the myocardial muscle tissue. The amount of muscle damaged and the odds of recovery of that muscle are dependent upon how soon blood flow to the heart is restored after an infarction.

A heart attack, which AHA reported occurs in more than 7 million Americans annually, can also result in arrhythmias, due to the damage to the myocardial muscle. While atrial fibrillation from an infarction can increase risk of stroke, ventricular fibrillation is the real concern during or directly following infarction. With this type of arrhythmia, the lower chambers quiver and can not effectively pump blood out of the heart to the rest of the body, causing death within minutes. In fact, most heart attack victims who die before reaching the hospital fail to get acute treatment for ventricular fibrillation—an Electrical shock from a defibrillator that restores normal rhythm.

Recipe for Survival

Managing and limiting atherosclerosis, smoking, obesity and diabetes can not only ward off development of CVD, but can also help heart disease patients back away from the edge of serious heart crisis, including arrhythmia, CHF, stroke and heart attack. Thus, there is an obvious overlap of dietary ingredients researched for atherosclerosis, hypertension and cardiac events.However, additional ingredients appear in research on cardiac events as aids for recovery and adjuncts to post-event treatments. Most importantly, some trials have indicated serum levels of certain nutrients correlate to life or death from CVD. Heart health starts with the diet, as does overall CVD survival. Much attention has been focused on the dietary foods common to the many countries in the Mediterranean region, where heart disease is less prevalent than in North America. The Mediterranean diet is praised for its high consumption of fruits and vegetables, whole grains, beans, nuts, fish, wine and unsaturated fats, such as olive oil. Utilizing validated food questionnaires, researchers from the University of Athens Medical School, Greece, examined the relationship between diet adherence and survival in more than 1,300 Greek men and women diagnosed with coronary heart disease (CHD).¹ Increased adherence to the diet was associated with significantly reduced mortality, especially cardiac death, among persons with prevalent CHD. Accordingly, many of the dietary supplement ingredients indicated as beneficial for reduced risk of CVD, cardiac events and mortality are major components in the Mediterranean diet. Nuts, grains, legumes and plant foods dominating the Mediterranean diet and similar heart health diets are tremendous sources of dietary fiber. While insoluble fiber helps bowel function, soluble fiber helps manage cholesterol and decrease risk of CVD. According to a Tulane University, New Orleans, study involving more than 9,700 subjects and lasting 19 years, increased intakes of soluble fiber can significantly reduce risk of not only CVD and CHD, but also cardiac events.² A similar reduction of CVD events was indicated in a trial involving more than 2,500 men and women consuming cereal fiber.³ Those with the highest fiber intakes experienced a 21-percent reduction in events, especially stroke and other cardiac ischemia. Confirming these findings, a review of cohort studies, involving a combined 336,244 men and women, found each 10 g/d increment increase in total dietary fiber intake correlated to a 14-percent decrease in risk of all coronary events and a 27-percent reduction in risk of coronary death.⁴ In addition to being rich in fiber, nuts and legumes are rich in vegetable protein, which can serve as a healthy replacement for animal protein that is increasingly associated with increased ischemic heart disease. A Boston-based collaborative cohort study from Harvard School of Public Health, Harvard Medical School, the Channing Laboratory and Brigham and Women’s Hospital examined protein intake and risk of ischemic disease.⁵ After controlling for other risk factors, they found decreased risk of ischemic heart disease in women was associated with increased protein intake, both animal and vegetable. However, they noted western diets rich in animal protein might contribute an unhealthy amount of saturated fat and cholesterol. Fellow Harvard School of Public Health experts stress the importance of protein variety, in order to achieve the complete protein profile of amino acids. Nuts, poultry and fish are good sources of the “conditionally essential” amino acid arginine, an immediate precursor to nitric oxide (NO), which promotes vasodilation—the opening up of blood vessels. NO presence and synthesis can be reduced following heart attack or stroke; thus, scientists have investigated L-arginine supplementation as a post-infarction treatment in these cases. Citing conflicting results on arginine in stroke trials, researchers from the University of Nottingham, United Kingdom (U.K.), conducted a Cochrane review and found arginine and NO reduced total cerebral infarct (stroke lesion) volume in both permanent and transient models of ischemia.⁶ However, they noted the narrow window for this benefit following a stroke may be limiting. Adding to these benefits, research from Japan showed L-arginine supplementation reduced thrombotic (blood clotting) tendency in cerebral microvessels.⁷ Oral L-arginine also improved blood flow in induced forearm ischemia in a University of Colorado, Denver, trial involving diabetic women.⁸ Reduced NO in the brain following a heart attack might contribute to the sympathetic nervous system reaction that can lead to CHF. Japanese scientists discovered increased arginine-NO in mice following heart attack helped control this dangerous sympathetic drive.⁹ A study conducted in Russia reported an 80-percent survival rate among heart attack animals taking L-arginine, compared to 33 percent in control animals.¹⁰ They further noted arginine can deliver a cardioprotective effect independent of NO. In 2005, the first large-scale, randomized, double blind, placebocontrolled trial investigating the ability of L-arginine and NO to alleviate the course of infarction measured mortality, re-infarction, edema or recurrent ischemia in 792 patients heart attack patients randomized to receive oral arginine or placebo in addition to routine therapy.¹¹ There was a slight benefit of reduced clinical events recorded in the arginine group, compared to controls, and researchers noted arginine was well tolerated. However, a comparable trial conducted at Johns Hopkins University, Baltimore, and published in early 2006 reported arginine supplementation added to standard post-infarction therapies did not improve vascular stiffness or cardiac output and might even be associated with increased post-infarction mortality.¹² Vasodilation from nitric oxide production is also attributed to supplementation with L-carnitine, a derivative of the amino acid lysine. Like arginine, carnitine is considered conditionally essential, as demand for the nutrient sometimes exceeds the body’s ability to synthesize it. In a Spanish animal study, carnitine supplementation led to more aortic relaxation in hypertensive rats than in normal, healthy rats.¹³ The benefits were even more acute in a Canadian animal trial, in which treatment with propionyl-L-carnitine, a carnitine derivative, improved left ventricle function rats with induced heart attack and failure.¹⁴ An infusion of this derivative, along with L-carnitine and acetyl-L-carnitine, given to rats prior to induction of ischemic infarction significantly improved heart function recovery, in addition to reducing the size and death of heart damage.¹⁵ A review of carnitine revealed treatment with carnitine (up to 6 g/d for as much as a year) in patients with heart attack, angina and CHF can reduce post-infarction death and recurrent failure.¹⁶ The reviewers noted carnitine also appears to improve exercise tolerance and oxygen consumption in cases of moderate to severe CHF. One of the important functions of carnitine is in the transport of fatty acids into the mitochondrial matrix, where they can be metabolized for energy. Scientists have linked defects in this carnitinefatty acid transport system to increased cardiomyopathy, which can be reversed with oral carnitine supplementation.¹⁷ Fatty acids have a wide range of heart health benefits. While their effects on lipid health and CVD risk are well documented, essential fatty acids (EFAs) have demonstrated numerous other heart benefits, including decreased risk of cardiac arrest and reduced CVD mortality, especially sudden cardiac death.¹⁸ Most research in this area has centered on marine polyunsaturated fatty acids (PUFAs), namely fish oil. In fact, long-term fish intake has been associated with reduced incidence of atrial fibrillation,¹⁹ as well as decreased risk of both stroke and thrombotic infarction.²⁰ Based on these epidemiological findings, researchers have studied fish oil supplementation in numerous areas of advanced CVD. The well-known GISSI-Prevenzione trial showed 1 g/d of marine EFA supplementation in 11,324 heart attack survivors significantly reduced the risk of recurrent MI and stroke, decreasing both overall cardiovascular mortality and sudden cardiac death.²¹ A major component of fish oil’s cardiac benefits may be its impact on arrhythmias. In a randomized, double blind, placebo-controlled trial conducted at six medical centers, scientists from Oregon Health and Sciences University, Portland, concluded fish oil supplementation did not reduce risk of ventricular tachycardia (VT) or ventricular fibrillation (VF), and may be pro-arrhythmic in some patients.²² However, researchers from Harvard Medical School, Boston, reported their double blind study showed regular daily ingestion of fish oil in people at high risk of ventricular arrhythmias may significantly decrease potentially fatal ventricular arrhythmias.²³ Dutch scientists studying the effect of fish oil on premature ventricular complexes (PVC)— common arrhythmias that can lead to more dangerous arrhythmias— found supplementation of 1.5 g/d fish oil did not decrease PVCs in patients with recurrent PVCs, but it did significantly decrease heart rate, indicating a lower risk of sudden cardiac death.²⁴ This benefit to heart rate was confirmed in an Emory University School of Medicine, Atlanta, trial, in which 58 elderly patients randomized to receive either 2 g/d fish oil or 2 g/d soy oil for six months experienced improved heart rate variability, with more pronounced benefit in the fish oil group.²⁵

Red palm oil

is a lesser known source of PUFAs, as well as carotenes and vitamin E. In one South African trial, red palm oil protected against consequences of ischemic heart injury in an rat heart model.²⁶ The scientists noted total myocardial PUFA content increased in hearts supplemented with red palm oil, which appears to improve reperfusion function (restoration of blood flow), possibly via the NO-cGMP pathway.²⁷

Carotenoids and vitamin E are abundant in various fruits and vegetables, as are numerous other vitamins, minerals and flavonoids. Drawing on the link between increased fruit and vegetable intake and decreased rates of coronary heart disease, scientists from Institut Pasteur de Lille, France, undertook a meta-analysis of observational studies on fruit and veggie intake and stroke.²⁸ Among the more than 230,000 men and women in the seven trials reviewed, risk of stroke decreased by 11 percent in those consuming more fruit, by 3 percent in those eating more vegetables, and by 5 percent in those ingesting higher amounts of both fruits and vegetables. Carotenoids are fat soluble phytochemicals responsible for the bright colors in fruits, vegetables and other plants. Plasma levels of various carotenoids, including beta-carotene, alpha-carotene and lycopene, have been inversely associated with risk of ischemic stroke.²⁹ Recent research from Chei-Mei Foundation Hospital, Taiwan, reported plasma concentrations of alpha- and beta-carotene (provitamin A) are lower in patients with acute ischemic stroke than in healthy controls, and are negatively correlated with high sensitivity C-reactive protein (hs- CRP) and neurological deficits.³⁰ A study of various carotenes and vitamin E revealed increased beta-carotene intake is inversely related to risk of heart attack.³¹ A 2003 Japanese study found lycopene-rich tomatoes possesses anti-thrombotic effects both in vitro and in vivo, hinting tomato and lycopene might be useful in disease marked by thrombosis (blood clotting), such as heart attack and stroke.³² Further evidence of lycopene’s benefit to cardiac survival was found in data from the Kuopio Ischaemic Heart Disease Risk Factor Study, in which men with the lowest serum lycopene levels had a 3.3-fold risk of acute coronary events, including stroke.³³ One of the non-provitamin A carotenoids, lycopene has also been linked to reduced risk of MI in person with higher adipose concentrations of the nutrient.³⁴ Another non-provitamin A carotenoid, astaxanthin, has also limited stroke, exhibiting neuroprotective actions in ischemic mice in a Japanese trial, which suggested a possible antioxidant mechanism.³⁵ Further cardiac benefits were observed in a Medical College of Wisconsin, Milwaukee, trial, in which astaxanthin given to rats prior to heart attack significantly reduced the area infarction/damage.³⁶ Astaxanthin has also shown promise as a inhibitor of cardiac muscle damage, possibly via antioxidant protection against oxidative damage in the heart.³⁷ Antioxidant vitamins, primarily vitamin C and vitamin E, have garnered mixed results in research on cardiac events and mortality. The conclusions on vitamin E have been varied, at best, as some controversial trials concluding vitamin E does not benefit cardiac mortality rates³⁸ and may even increase risk of heart failure,³⁹ yet other trials have shown tocotrienols can protect against neurological damage from stroke.⁴⁰ While Greek researchers concluded vitamin C was the most promising antioxidant inhibitor of oxidative damage in heart failure,⁴¹ British scientists from University of Sheffield found treatment of 500 mg/d vitamin C and 800 IU/d alpha-tocopherol in 48 acute ischemic stroke patients not only increased plasma total antioxidant capacity, but also reduced both post-stroke lipids and inflammation.⁴² Similar results were reported in a Slovakian trial involving combined supplementation of 100 mg/d vitamin C, 100 mg/d vitamin E, 6 mg/d beta-carotene and 50 mcg/d selenium given to 28 heart attack survivors for three months.⁴³ The antioxidant treatment limited genetic damage compared to controls, with the most pronounced benefit in smokers. In fact, low serum levels selenium, a trace mineral, have been linked to increased homocysteine levels and risk of cardiac death.⁴⁴ Other mineral deficiencies appear to indicate cardiac catastrophe, as low magnesium levels have been linked to hypertension, CHF, arrhythmia and infarction,⁴⁵ and calcium intake has been inversely related to mortality from stroke, both ischemic and hemmorhagic.⁴⁶ Similarly, low toenail chromium concentration was inversely associated with risk of initial myocardial infarction in men,⁴⁷ and long-term copper deficiency can lead to heart malfunction, including systolic and diastolic dysfunction, indicative of cardiomyopathy.⁴⁸ A common method to address broad vitamin and mineral deficiency or reduced fruit and vegetable intake is supplementation with a multivitamin. Epidemiological evidence supports such supplementation to reduce risk of CVD and cardiac events. The Stockholm Heart Epidemiology Program (SHEEP), a large population-based case-control study conducted in Sweden—where fruit and vegetable consumption is historically low and foods are not fortified with folic acid—concluded low-dose multivitamin supplements may aid in the primary prevention of MI.⁴⁹ Folic acid and other B vitamins have been investigated for their ability to lower homocysteine levels, but as with other nutrients, the results on reduced cardiac events have been mixed. Chinese research has shown CHD patients typically have increased homocysteine and decreased serum folate,⁵⁰ and a Spanish study reported subjects with the lowest intakes of folate had twice the risk of MI.⁵¹ Similarly, a review of data from the Vitamin Intervention For Stroke Prevention (VISP) trial concluded higher does of vitamin B12 (cobalamin) lower homocysteine levels and significantly reduce the risk of ischemic stroke, CHD and death.⁵² In a University of Sheffield, England, trial, daily supplementation with a B-complex (5 mg folate, 5 mg B2, 50 mg B6, 0.4 mg B12) increased plasma vitamin B levels and reduced plasma anti-inflammatory markers in acute ischemic stroke patients.⁵³ And Swiss research found six months of supplementation with a combination—folate, B12 and B6—lowered homocysteine and decreased incidence of MI and cardiac-related death.⁵⁴ Many nutrient-rich foods have demonstrated cardiac benefits in both epidemiological and clinical trials. Joint research from the University of South Florida College of Medicine, Tampa, and the National Institute on Drug Abuse, Baltimore, found treatment with antioxidant-rich blueberries, spinach and spirulina reduced ischemia and reperfusion injury in cerebral infarction.⁵⁵Tea drinkers appear to avoid such infarction altogether, exhibiting lower risk of both CHD and stroke.⁵⁶ Focused on tea’s antioxidant catechins, Dutch National Institute of Public Health scientists reviewing cohort data reported increased catechin intake might reduce risk of ischemic heart disease mortality, but not of stroke and MI;⁵⁷ however fellow Dutch researchers found an inverse correlation between tea consumption and risk of heart attack.⁵⁸ Considering the substantial role of oxidative damage in ischemia, studies have hinted at potential benefits of other antioxidants on parameters of cardiac events. In one trial, pre-ischemic administration of alpha lipoic acid and vitamin E helped reduce post-embolism lipid peroxidation, brain damage volume and neurological deficit.⁵⁹ The vitamin-like antioxidant coenzyme Q10 (CoQ10) has multiple actions in heart health. CoQ10 (as Q-Gel® from Tishcon Corp.) has been shown to uptake in the heart,⁶⁰ where it can be useful in a range of cardiac events. Reviewers from Virginia Commonwealth University, Richmond, noted CoQ10 benefits CHF patients by increasing cardiac output, and can also reduce stroke volume.⁶¹ Similar results emerged from a University of Kentucky, Lexington, review, which found limited evidence the coenzyme might beneficially address the oxidative stress and depressed CoQ10 levels common in CHF, improving left ventricular ejection fraction (output) and diastolic volume.⁶² Similar functional benefits were discovered in a Brazilian case-study involving a CHF patient treated with 150 mg/d of CoQ10.⁶³ The researchers observed gradual improvement in left ventricle function, including fractional shortening and ejection fraction during supplementation, noting that systolic function decreased three months after supplementation ended. CoQ10 is also known for its role in mitochondrial ATP (adenosine triphosphate) synthesis, a crucial aspect of energy production on a cellular level. Subjects in a human study showed decreased atherosclerotic activity following acute myocardial infarction, but those also taking statin drugs, which might lower bodily CoQ10 stores, reported higher incidence of fatigue.⁶⁴ Fellow energizer ribose, a naturally occurring pentose carbohydrate and component of ATP, enhances high-energy phosphates and improves diastolic dysfunction following myocardial ischemia, according to recent research presented at a meeting of the Heart Failure Society of America in Boca Raton, Fla. In the study, University of Utah, Salt Lake City, scientists examined ribose (as CORvalen™, from Bioenergy) in patients with advanced CHF and compromised ventilatory efficiency, which limits exercise ability. Following eight weeks of ribose supplementation (5 g/d), subjects showed improved ventilatory efficiency and oxygen uptake efficiency. Additional research conducted at the same university facility demonstrated supplementation with ribose (as CORvalen) in ischemic-based CHF patients can also boost myocardial performance scores while maintaining maximum exercise capacity, as well as improve CHF survival.^65,66 Ribose may also be a useful adjunct to coronary artery bypass surgery following acute MI, helping to reduce time between infarction and surgery which would also lower hospital stay costs. In one trial, twenty-four MI patients at Saddleback Memorial Medical Center in Orange, Calif., received ribose (as CORvalen) upon admittance to the hospital, while 20 control patients received no ribose.⁶⁷ Those in the ribose group showed 49-percent greater increases in post-operative cardiac index than controls. Researchers concluded revascularization with off-pump bypass surgery combined with ribose preloading improved cardiac function to a greater degree than traditional techniques. Exercise capacity and fatigue in CHF has also been improved by the herb hawthorn (Crateagus oxyacantha L.). In a Swiss study, a standardized extract of fresh hawthorn significantly enhanced exercise tolerance and maximum load in 143 CHF patients.⁶⁸ In a German trial, another hawthorn extract (as WS 1442 from Schwabe GmbH) reduced clinical progression of fatigue, stress dyspnea (shorteness of breathe) and palpitations in 952 patients.⁶⁹ And, reviewers from the Universities of Exeter and Plymouth, England, found hawthorn treatment in CHF patients from eight different trials was more effective than placebo in decreasing pressure heart rate product and improving maximum workload.⁷⁰ Vasodilatory herb ginkgo biloba is also beneficial in ischemic cardiac disease, although researchers note possible contraindication in patients also taking anti-coagulant and anti-platelet medications.⁷¹ A French trial showed ginkgo extract can attenuate myocardial stunning following a brief ischemic insult in the pig heart, possibly due to the actions of both its non-ginkgolide and ginkgolide constituents.⁷² In Japanese research, ginkgo extract administered to hypertensive rats decreased blood pressure and contributes strong anti-thrombotic and antioxidant benefits in cerebral thrombosis.⁷³ However, a Cochrane Review revealed no convincing evidence from trials of superior quality and design to support ginkgo use to promote post-stroke recovery, although researchers noted ginkgo extract was associated with a significant number of improved patients.⁷⁴ The various biological activities of an extract of French maritime pine bark (as Pycnogenol®, from Horphag Research, supplied in the United States by Natural Health Sciences) results in different mechanisms of action in protection against cardiac events. According to a German review, Pycnogenol protects against oxidative stress in several cell systems, including the cardiovascular system, by doubling the intracellular synthesis of anti-oxidative enzymes and by acting as a potent scavenger of free radicals.⁷⁵ The researchers further concluded Pycnogenol is active in the protection and regeneration of heart healthy vitamins C and E, in addition to inhibiting the process of vasoconstriction, via increased endothelial NOS activity. Pycnogenol can also inhibit dangerous vasoconstriction by decreasing endothelial levels of endothelin- 1, an amino acid peptide that can cause hypertrophy (excessive organ thickening or enlargement).⁷⁶ A recent research collaboration by Chieti-Pescara University and the San Valentino Vascular Screening Project, Italy, reported Pycnogenol is effective in controlling edema, particularly in the legs.⁷⁷ More recently, an herbal extract from bamboo leaf has shown potential in improving vascular health via various mechanisms of actions. As UniBEX™, from Unigen Pharmaceuticals, bamboo leaf extract has demonstrated vascular repair activities, and its phenylpropanoids were shown as potent antioxidants in proprietary vascular studies. Addressing the duality of NO in human health, two proprietary flavone compounds in UniBEX have limited harmful NO production in immune cells (iNOS), but increased helpful NO production in endothelial/vascular cells (eNOS), according to unpublished research. However, researchers from China, where bamboo leaf has been used historically as traditional medicine, reported orientin—a flavonoid found in bamboo leaves—was responsible for an observed vasorelaxtant effect on animal aortic rings, via eNOS control.78 Further, independent in vitro studies have revealed bamboo leaf can help stabilize atheromas (plaques) and protect against thrombosis, by suppressing vascular adhesion molecule (VCAM) expression and IL-6 in endothelial cells. There are numerous CVD risk factors, including atherosclerosis and hypertension, to consider in addressing the progression of heart disease to dangerous cardiac events and even death. Management of heart health begins and ends with dietary factors, as various foods and their biochemical components have delivered significant epidemiological and clinical results against causes and consequences of arrhythmia, heart attack, stroke and CHF. When combined, the growing scientific knowledge bases on lipid/vascular health, cardiac events and mortality can provide a powerful list of cardioprotective ingredients for use in heart healthy natural products. by Steve Myers