Understanding Heart Attacks and Heart Disease

compiled by John G. Connor, M.Ac., L.Ac., edited by Barbara Connor, M.Ac., L.Ac.

Table of Contents
Plaque Formation
Myocardial Infarction
Reperfusion, Reactive Oxygen Species and Apoptosis
Mechanical Support – Stents
Natural Compounds that Reduce the Risk of Heart Attack or Benefit Heart Health
Benefits of Diet and Exercise & Life Style Changes in Reducing the Risk of Heart Attack or Heart Disease
Blood and Other Tests in Heart Attack and Heart Disease
Cholesterol, Statins and Heart Disease
Natural Compounds Which Can Be Used to Reduce the Dependency on Statins
Natural Compounds Which Can Help to Lower Blood Pressure

Nearly 70% of adult Americans are overweight or obese; the prevalence of visceral obesity stands at 53% and continues to rise. At any one time, 55% of the population is on a weight-loss diet, and almost all fail. Fewer than 15% of adults or children exercise sufficiently, and over 60% engage in no vigorous activity. Among adults, 11%–13% have diabetes, 34% have hypertension, 36% have prehypertension, 36% have prediabetes, 12% have both prediabetes and prehypertension, and 15% of the population with either diabetes, hypertension, or dyslipidemia are undiagnosed. About one-third of the adult population, and 80% of the obese, have fatty livers. With 34% of children overweight or obese, prevalence having doubled in just a few years, type 2 diabetes, hypertension, dyslipidemia, and fatty livers in children are at their highest levels ever. Half of adults have at least one cardiovascular risk factor. Not even 1% of the population attains ideal cardiovascular health. (Kones R 2011)

Coronary heart disease affects 7.6% of the population in the United States, where > 900,000 myocardial infarctions (MIs) — commonly known as heart attacks — occur annually. Approximately half of all MIs have an identifiable clinical trigger. Myocardial ischemia, MI, sudden cardiac death, and thrombotic stroke each occur with circadian variation and peak after waking in the morning. In addition, physical exertion and mental stress are common precipitants of MI. Waking in the morning, physical exertion, and mental stress influence a number of physiologic parameters, including blood pressure, heart rate, plasma epinephrine levels, coronary blood flow, platelet aggregability, and endothelial function. (Schwartz et al 2010)

Upregulation of sympathetic output and catecholamines (epinephrine, norepinephrine and dopamine) increase myocardial oxygen demand and can decrease myocardial oxygen supply and promote thrombosis. Ischemia (restriction of blood supply to tissues causing a shortage of oxygen and glucose) ensues when myocardial oxygen demand exceeds supply. Increases in blood pressure and ventricular contractility increase intravascular shear stress and may cause vulnerable atherosclerotic plaques to rupture, forming an origination point for thrombosis that can precipitate MI. (Schwartz et al 2010)

Myocardial infarction (MI) is an atherothrombotic disease determined by the interplay between an individual’s genetic background, lifestyle and environment. Atherothrombosis, in turn, is the result of a complex pathological process that is characterized by endothelial (thin layer of cells on the inner surface of blood vessels) dysfunction, atherosclerosis, and finally thrombus formation as the key event of acute MI. Monocytes and platelets are the principal cells involved in these events. Platelets, produced by the cytoplasmicافضل اكشن على fragmentation of bone marrow megakaryocytes (MK), are essential for primary hemostasis, to repair microvascular damages and to initiate physiological thrombus formation. Calcium mobilization is required for stable platelet incorporation into the developing thrombus. Platelets therefore play a pivotal role in the thrombus formation, as well as in the plaque development from the very beginning of atherosclerotic disease. (Czrubbi et al 2012)

Heart diseases are the most common cause of mortality among adults in developed western countries which often are associated with coronary artery diseases. Acute myocardial infarction (AMI) causes early on and risky complications such as ventricular fibrillation, free wall rupture, intraventricular rupture and papillary muscle rupture. (Pourmoghaddas et al 2012)

The development of cholesterol-rich plaque within the walls of coronary arteries (atherosclerosis) is the pathological process which underlies ‘coronary artery disease‘. However, the clinical manifestations of this generic condition are varied. When the atherosclerotic process advances insidiously the lumen of a coronary artery becomes progressively narrowed and the blood supply to the myocardium is compromised (ischaemia) and the affected individual will often develop predictable exertional chest discomfort, or ‘stable’ angina. However, at any stage in the development of atherosclerosis, and often when the coronary artery lumen is narrowed only slightly or not at all, an unstable plaque may develop a tear of its inner lining cell layer (intima), exposing the underlying cholesterol rich atheroma within the vessel wall to the blood flowing in the lumen. This exposure stimulates platelet aggregation and subsequent clot (thrombus) formation. (National Clinical Guideline Centre (UK) 2010)

If the volume of thrombus is sufficient to occlude the lumen of the artery, and this is persistent, then acute ST-elevation (an abnormality of the electrocardiogram) myocardial infarction or ‘STEMI’ ensues, with progressive death (necrosis) of heart muscle tissue. If the volume of thrombus is insufficient to occlude the artery or does so only temporarily then shortage of blood supply to the affected heart muscle (myocardium) is less severe or is intermittent. In these circumstances there is often some myocardial necrosis, as evidenced by a rise in the cardiac specific serum biomarkers such as troponin (a regulatory protein); this syndrome is described as ‘non-ST elevation myocardial infarction‘ (NSTEMI). When myocardial ischaemia is present, but without evidence of actual myocardial necrosis (normal serum troponin level), the clinical syndrome is described as unstable angina (UA). (National Clinical Guideline Centre (UK) 2010)

Plaque Formation
The coronary arteries are one of the most common vessels affected by the atherosclerotic process. The transformation of a normal coronary artery to a completely occluded vessel is a process developed over years via a series of complex changes. The gradual progression from lipid streaks to complicated unstable plaque is strongly associated with the remodeling of the ECM (extracellular matrix), but the molecular mechanism is not well-explained. (Kong et al 2012)

In the early stages of vessel damage prior to plaque formation, chronic minimal injury caused by shear stress particularly at arterial bi-furcations, narrowing or directional changes leads to intraluminal endothelial damage and dysfunction. Concomitantly, pro-inflammatory intracellular signalling pathways are recruited which lead to transcriptional up regulation of expression of growth factors (e.g. vascular endothelial cell growth factor (VEGF), platelet-derived growth factor (PDGF) and fibroblast growth factor-2 (FGF-2)) cytokines (e.g. tumour necrosis factor-alpha (TNF-alpha) and MCP-1), adhesion molecules (e.g. intracellular adhesion molecule-1 and vascular endothelial cell adhesion molecule (VCAM)) and chemoattractant proteins. (Slevin et al 2012)

Endothelial cell damage, activation and up-regulation of adhesion molecules encourage the attraction of platelets, T-cells, and macrophages which engulf excess cholesterol transforming into foam cells and help to produce fatty streaks — some of the earliest pathological sign of plaque development. Endothelial dysfunction is known to impair the production and bioavailability of nitric oxide (protective against atherosclerosis) and therefore the protection of these cells against damage and/or increasing the circulating nitric oxide levels using pharmacological agents could have clinical benefit for high risk candidates. (Slevin et al 2012)

Barbara and I would prefer to use natural compounds to increase nitric oxide levels.As more platelets and immune cells aggregate at a damaged region, the increased cytokine production leads to local cellular proliferation, and transmission of activating signals to the adventitial (outermost layer of the blood vessel) vasa vasorum which become activated and migrate through the layers of the artery to help feed the now growing plaque.(Slevin et al 2012)

Actively growing plaques often remain stable with thick fibrous caps and contain a high proportion of smooth muscle cells. In these cases, arterial remodeling eventually results in a gradual narrowing of the lumen resulting in, patient symptoms such as angina. The mechanisms responsible for determination of the development of vulnerable unstable plaques rather than stable ones is still unknown although there is evidence for the involvement of a number of key factors, namely, oxidative stress and formation of oxidized low density lipoproteins, diabetes, high or fluctuating blood sugar levels and formation of advanced glycation end-products (AGEs), the process of inflammation and tumour-like angiogenesis. (Slevin et al 2012)

Myocardial Infarction
Subsequent arrhythmias and hemodynamic abnormalities in left ventricular dysfunction are the major causes of mortality along with acute myocardial infarction. The arrhythmias predisposing factors are: autonomic nervous system dysfunction, electrolyte disorders, left ventricular dysfunction, myocardial ischemia and medications. Ventricular tachycardia might occur unstably (less than 30 seconds) or stably (more than 30 seconds or along with hemodynamic disorders) in patients with acute myocardial infarction, due to the underlying problems such as left ventricular dysfunction, hypoxia, electrolyte disorders or toxic effects of digoxin, quinidine or dobutamine. Some studies showed that reduction in potassium level increases the probability of ventricular tachycardia in patients. This study showed that hypokalemia (low serum potassium levels) increased the probability of ventricular tachycardia in patients with AMI. (Pourmoghaddas et al 2012)

A large amount of norepinephrine (NE) is released from sympathetic nerves during acute myocardial ischemia. NE participates in ischemic preconditioning (IPC) during short-term myocardial ischemia, which can reduce myocardial injury induced by long-term myocardial ischemia and the incidence of arrhythmias. However, a large amount of NE released during long-term myocardial ischemia has cardiac and neurological toxicity, resulting in a significant increase in the incidence of arrhythmias. The effect of excessive release of NE on sympathetic nerves and the electrophysiology of myocardial cells after ischemia is not clear. (Wu et al 2012)

Ischemia/reperfusion (I/R)-mediated acute myocardial infarction (AMI) is the leading cause of death in the world. (Reperfusion is the restoration of blood flow to a previously ischemic tissue or organ.) The high mortality is due to poor recovery of hearts from AMI and cardiac remodeling induced by progressive necrotic and apoptotic cells in the myocardium. I/R-induced injury is known to increase the levels of reactive oxygen species (ROS) several-fold which can lead to apoptosis. Various reports suggest that antioxidant therapy after I/R would help the myocardium to recover from ROS-induced damage. The deleterious effects of ROS on cardiac tissue can be blocked by antioxidant enzymes such as superoxide dismutase and catalase. These studies indicated that antioxidants capable of scavenging ROS, including reactive oxygen free radicals such as superoxide, hydroxyl, and peroxyl radicals, could have therapeutic advantages to treat I/R-mediated cardiac injury. (Swaminathan et al 2010)

The heart is one of the most energy demanding tissues in the body and is totally dependent upon oxidative phosphorylation (a metabolic pathway that uses energy released by the oxidation of nutdrients to produce adenosine triphosphate) to supply the large amount of ATP required for beat-by-beat contraction and relaxation. If the blood flow to the heart is impaired (ischaemia), as occurs when a blood clot occludes a coronary artery (coronary thrombosis), the source of oxygen is removed leading to the cessation of oxidative phosphorylation. This causes tissue ATP and creatine phosphate concentrations to decrease with a concomitant rise in ADP, AMP and Pi (inorganic phosphate) concentrations. Although glycolysis is activated, it is unable to meet the demand of the beating heart for ATP. Consequently, the heart rapidly ceases to beat as the contractile machinery is inhibited by elevated Pi and ADP, combined with the decreasing pH that accompanies the accumulation of glycolytic lactic acid. The heart can usually survive a short period of ischaemia and then recover upon reperfusion. (Halestrap et al 2007)

Thrombolysis is still the most common reperfusion method used in myocardial infarction, and the greatest benefit is obtained when thrombolytic agents are administered within the first hour after myocardial infarction (MI). The efficacy of reperfusion therapies is decreased with the prolongation of the time interval between the onset of symptoms and treatment. It is estimated that the benefit is a reduction of 1% in death, for every hour saved when administering the drug within the first six hours after MI. In addition, it has been demonstrated that 25% of patients treated with thrombolytic agents within the first hour leave the hospital with no evidence of myocardial necrosis, a concept termed aborted MI. (Tabriz et al 2012)

Although the performance of the heart may be impaired initially, given time recovery is complete. However, if the period of ischaemia is too long, the tissue becomes irreversibly damaged. Hence, if the heart is to be salvaged, it is important to restore the blood flow as soon as possible. Yet, paradoxically, such reperfusion can exacerbate the damage occurring during the ischaemic period. This is known as reperfusion injury and is accompanied by enzyme release and morphological changes characteristic of necrosis. The extent of damage can be visualised as an area of necrotic tissue known as the infarct whose area can be determined to provide a quantitative measure of injury. (Halestrap et al 2007)

Quantification of damage may also be provided by measuring the release of intracellular proteins such as lactate dehydrogenase or troponin I. In addition to the necrotic cell death that represents the major damage to the reperfused heart there is also evidence that some myocytes around the periphery of the infarct die by apoptosis. Understanding the causes of reperfusion injury and devising ways of preventing it is of major clinical importance in cardiac surgery and the treatment of coronary thrombosis. (Halestrap et al 2007)

Increases in cellular [Ca2+] and reactive oxygen species (ROS), initiated in ischaemia and then amplified upon reperfusion, are thought to be the main causes of reperfusion injury. Mitochondria are involved both in the production of ROS and as targets for the damaging action of both ROS and calcium. (Halestrap et al 2007)

No-reflow (NR) phenomenon is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed by percutaneous (placing a needle through the skin and into a blood vessel) coronary intervention, thrombolysis and coronary artery bypass grafting. The incidence and extent of NR strongly predict adverse clinical outcomes including persistent contractile dysfunction of left ventricular, malignant arrhythmias and cardiac death. Although the mechanisms of NR are not completely understood, existing evidences from both clinic setting and animal NR model support the involvement of ischemia/reperfusion (I/R) injury, vasospasm, neutrophils plugging, and endothelial swelling. Recently, it was reported that patients with higher C-reactive protein levels and white cell count tend to suffer from NR. This suggests the possibility that inflammatory cells and proinflammatory cytokines cells may directly mediate the occurrence and development of NR. Our data thus suggest that inhibition of NF-κB may reduce I/R-associated myocardial no-reflow through reduction of myocardial inflammation. (Zeng et al 2012)

Reperfusion, Reactive Oxygen Species and Apoptosis
Reperfusion is associated with a burst of reactive oxygen species (ROS) production, but here too the source of the ROS is debated. Although some may be produced by xanthine oxidase and NADPH oxidase, it is probable that most is formed by complex 1 and complex 3 of the respiratory chain. When the respiratory chain is inhibited by lack of oxygen and then re-exposed to oxygen, ubiquinone can become partially reduced to ubisemiquinone. This can then react with the oxygen to produce superoxide that is reduced to hydrogen peroxide by superoxide dismutase. Hydrogen peroxide is removed by glutathione peroxidase or catalase, but if ferrous ions (or other transition metals such as copper) are present it will form the highly reactive hydroxyl radical through the Fenton reaction. (Halestrap et al 2007)

Mitochondrial proteins are especially susceptible to ROS induced damage and this is reflected in the impaired respiratory chain activity of mitochondria isolated from ischaemic hearts. Thus ROS have direct effects on several respiratory chain components, most especially on complex 1 but also on complex 3, and other iron sulphur proteins such as aconitase. ROS can also cause thiol oxidation and inhibition of the ATPase and adenine nucleotide translocase. In addition, ROS cause oxidation of glutathione that may then form mixed disulphides with proteins. Such protein modification is thought to have inhibitory effects on ion pumps and therefore exacerbate the effects of ATP deprivation on ionic homeostasis. ROS also cause peroxidation of the unsaturated fatty acid components of the phospholipids, and especially cardiolipin of the inner mitochondrial membrane, and this leads to further inhibition of respiratory chain activity. Furthermore, lipid peroxidation causes the release of reactive aldehydes such as 4-hydroxynonenal that can modify membrane proteins. (Halestrap et al 2007)

Overall, it is thought that the combined effects of ROS and elevated [Ca2+] play a critical role in the transition from reversible to irreversible reperfusion injury, and that mitochondria are the major target of these agents. In particular, they lead to the opening of the mitochondrial permeability transition pore, that is now widely accepted to play a critical role in reperfusion injury. (Halestrap et al 2007)

Reactive oxygen species (ROS) have been implicated to play a role in a number of cardiovascular diseases (CVD), including hypertension, atherosclerosis, myocardial ischemia/reperfusion (I/R) injury, and restenosis after angioplasty or bypass surgery. ROS are generated in vascular cells by NAD(P)H oxidases, uncoupled endothelial nitric oxide (NO) synthase, and other enzymatic sources, or as a byproduct of mitochondrial respiration. A host of different species are produced, each having distinct effects and signaling functions that may, if unbalanced, lead to exacerbation of pathophysiological processes. (Levonen et al 2008)

In hypertension, the production of superoxide (O2) (a free radical) in the vasculature and the subsequent inactivation of endothelium-derived NO and decrease in its bioavailability have been shown to be particularly detrimental. Increased O2 production and the loss of bioavailable NO are also critical for restenosis, in-stent restenosis, and vein bypass graft failure. In addition, O2 is the predominant ROS produced either intracellularly or extracellularly by infiltrating inflammatory cells in I/R injury. In addition, other ROS as well as oxidation products of macromolecules such as oxidized low-density lipoprotein (oxLDL) can have their own spectrum of effects accelerating the development of CVD. (Levonen et al 2008)

The pathogenesis of ischemia/reperfusion injury depends on many factors, among them, reactive oxygen species (ROS) is considered as an initiator of the injury. ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. ROS production is physiologically controlled by free radical scavengers such as glutathione peroxidase (GPx), thioredoxin reductases (TrxR), and superoxide dismutase systems. Clinical trials have shown that metabolic therapy can decrease the cellular damage due to oxidative stress. GPx and TrxR are seleno-cysteine dependent enzymes, and their activity is known to be related to an adequate supply of dietary selenium. (Guo et al 2012) Brazil nuts are one of the most concentrated sources of selenium.

Recently, the recognition of a different cell death phenomenon ‘apoptosis’ (programmed cell death) has become a major clinical interest. It accounts for a great proportion of cell loss associated with myocardial infarction (MI) and / or ischemia-reperfusion (IR). Cell loss through apoptosis contributes to the impairment of cardiac performance and also plays an important role in myocardial remodeling processes. Induction of apoptosis is implicated in myocardial I-R injury among other cardiovascular diseases. Various studies have demonstrated that not only reactive oxygen species (ROS) per se, but also their oxidation products and other secondary messenger molecules generated by ROS can trigger the programmed cell death. It has been reported that these programmed cell death pathways can be inhibited by antioxidants. (Mohanty et al 2006)

Prolonged severe ischemia leads to cardiac cell death. Necrosis previously was regarded as the only mode of cell death, whereas, now there is accumulating evidence that in addition to overt necrosis, a subset of cells also die by apoptosis. The relative contributions of necrosis and apoptosis to cell death in ischemia and reperfusion are still open to debate, although necrosis appears to dominate during ischemia, and apoptosis may dominate during reperfusion. There is now evidence that apoptosis occurs during sustained ischemia and when reperfusion follows shorter periods of ischemia. (Mohanty et al 2006)

The progressive loss of cardiomyocytes in a heart that is already compromised leads to further deterioration of cardiac function, conduction disturbances due to degeneration of SA, AV and inter-nodal pathways, cardiac remodeling and cardiomyopathy. The fact that apoptosis plays a role in the tissue damage seen after myocardial infarction has pathological and therapeutic implications. (Mohanty et al 2006)

Mechanical Support – Stents
Drug eluting stents (DES) have been available in clinical practice since 2002 in Europe and 2003 in the USA, where they have been used in up to 90% of percutaneous coronary interventions (PCI) in the following years because of their effectiveness in reducing the rate of restenosis when compared with bare metal stents (BMS). This effect did not result in a reduction of mortality or myocardial infarction within 4 years after the intervention in randomized clinical trials. In observational studies, the results are somewhat conflicting: some confirmed that DES are effective in reducing the need for new revascularisation without affecting the rate of mortality or myocardial infarction whereas others reach contrasting conclusions, that is, DES would favour a reduction in mortality and myocardial infarction with minimal impact on the need for repeat revascularisation. (Olivari et al 2012)

It has been demonstrated that the implantation of the drug-eluting stent (DES) reduces the angiographic restenosis and the need for repeat revascularization compared with the bare metal stent. However, the use of the DES results in a prothrombotic environment, predisposing the patient to late stent thrombosis. Clopidogrel and Aspirin are the major antiplatelet drugs for the prevention of stent thrombosis. The risk of early thrombosis events amongst patients with the DES is remarkably reduced by dual antiplatelet therapy. According to the current guidelines, antiplatelet therapy is needed for at least 9 to 12 months after the implantation of the DES. Extended use of dual antiplatelet therapy (for more than 12 months) was not significantly more effective than Aspirin monotherapy in reducing the risk of myocardial infarction or stent thrombosis, death from cardiac cause, and stroke. (Poorhosseini et al 2012)

By inhibiting NF-kappaB activation, the up-regulation of cardiac proinflammatory genes can be ameliorated, and the activation of MMPs can be decreased during CPB (cardiopulmondary bypass), thereby lessening the severity of cardiac mechanical dysfunction after global cardiac ischemia/reperfusion injury. (Yeh et al 2005)

Natural Compounds that Reduce the Risk of Heart Attack or Benefit Heart Health
Herbal extracts, by virtue of being comprised of a mixture of active compounds, could act through more than one mechanism, and hence could potentially exert multiple beneficial effects. (Wang et al 2011)

Metabolic therapy involves the administration of a substance normally found in the body to enhance a metabolic reaction within the cell. By improving cellular energy production, metabolic therapy has the potential to benefit cardiac function during the stress of cardiac surgery, myocardial infarction and cardiac failure. Coenzyme Q(10) is a lipid-soluble antioxidant that plays a crucial role in cellular ATP production. Magnesium orotate, a key intermediate in the biosynthetic pathway of glycogen, has been shown to improve the energy status of the cell and improve recovery from cardioplegic arrest. The amino acid aspartate plays an important role in providing energy substrates for oxidative phosphorylation in the myocyte. (Hadj et al 2003)

Acanthopanacis Senticosi could improve T wave elevation and decrease of heart rate in the rabbit myocardial ischemia model subjected to pituitrin injection, and promote regeneration of the surface cells. In such a model, rat myocardial ischemia was significantly improved with a preserved SOD activity and a reduced malondialdehyde (MDA) production. (Yuan & Jing 2011)

Alpha-lipoic acid (ALA) was originally identified as an obligatory cofactor for mitochondrial α-ketoacid dehydrogenases and was found to play an important role in mitochondrial energy metabolism. ALA enhances glucose utilization in isolated rat hearts. Growing evidence suggests that ALA maintains the cellular antioxidant status by either enhancing or inducing the uptake of antioxidant enzymes. ALA administration reduces aortic AGEs (advanced glycation end-products) content, cardiac mitochondrial superoxide production, and insulin resistance in diabetic animal models. (Lee et al 2012)

Alpha-lipoic acid – Administration of lipoic acid significantly up-regulated cellular ALDH2 activity concomitantly with a reduction in apoptosis, production of reactive oxygen species, 4-HNE and MDA, these effects were reversed in the presence of ALDH2 or PKCε inhibitors. Our results suggest that the cardioprotective effects of lipoic acid onischemia-reperfusion injury are through a mechanism involving ALDH2 activation. The regulatory effect of lipoic acid on ALDH2 activity is dependent on PKCε signaling pathway. (He et al 2012)

Andrographis paniculata Present studies on Andrographis paniculata concentrate on Andrographolide and the flavonoid component API0134. This flavonoid component API0134 could improve canine heart function, decrease the extent of myocardial infarcted area, alleviate the extent of myocardial injury, and decrease the occurrence of arrhythmias. (Yuan & Jing 2011)

Angelica sinensis extract may improve anti-oxidant capacity, activate ERK signaling transduction pathway, and enhance the expression of endothelial NOS. Radix angelica sinensis could upregulate the expression of Bcl-2 and downregulate the expression of Bax, causing a decreased Bax/Bcl-2 ratio, so that apoptosis of the myocytes could be inhibited, and left ventricular function and ventricular remodeling improved. (Shangguan et al 2008)

Arjuna – Many experimental studies have reported its antioxidant, anti-ischemic, antihypertensive, and antihypertrophic effects, which have relevance to its therapeutic potential in cardiovascular diseases in humans. Several clinical studies have reported its efficacy mostly in patients with ischemic heart disease, hypertension, and heart failure. (Maulik & Talwar 2012)

Arjuna – Experimental studies have revealed the bark of Terminalia arjuna Wight & Arn exerting significant inotropic and hypotensive effect, increasing coronary artery flow and protecting myocardium against ischemic damage. It has also been detected to have mild diuretic, antithrombotic, prostaglandin E(2) enhancing and hypolipidaemic activity. There is ample clinical evidence of its beneficial effect in coronary artery disease alone and along with statin. (Dwivedi S 2007)

Astragalus – Total flavonoids of Astragulus and Astragaloside A work as inotropic agents by way of increasing cAMP contents of the myocardium, and inhibiting the activity of the Na+-K+-ATPase on the myocardial cellular membrane, while Astragalosides act as free radical scavengers. Astragaloside IV is a leading active ingredient with inotropic effect, not only improving heart function of the experimental rats, but also avoiding an increase of the oxygen consumption of the myocardium. (Yuan & Jing 2011)

Bacopa monniera — Histopathological studies and myocardial creatine phosphokinase content further confirmed the cardioprotective effects of B. monniera in the experimental model of ischaemia-reperfusion injury. The study provides scientific basis for the putative therapeutic effect of B. monniera in ischaemic heart disease. Interestingly, B. monniera also restored the antioxidant network of the myocardium and reduced myocardial apoptosis, caspase 3 and Bax protein expression. (Mohanty et al 2010)

Baicalin is a flavonoid compound extracted from Scutellaria baicalensis Georgi. Baicalin significantly improved the SOD activity of the hypoxic myocytes of neonatal Sprague-Dawley rats inhibited NO secretion. When baicalin was given to the rats 5 mins before ligation of the coronary artery, the post-infarction heart function improved with decreased malondialdehyde content and increased SOD activity (Liu et al 2003).

Berberine (goldenseal) – had positive inotropic action and improved heart function of heart failure patients. (Cui 2006)

Carnitine, taurine and coenzyme Q(10) – Our results support the potential cardioprotective impact of carnitine, taurine and coenzyme Q(10) during myocardial ischemia. In contrast to carnitine supplementation alone, carnitine, taurine and coenzyme Q(10) improved survival as well as cardiac function, gene expression and delayed remodeling. (Briet et al 2008)

Cilantro (coriander) – Our results show that methanolic extract of CS (Coriandrum sativum L.) is able to preventmyocardial infarction by inhibiting myofibrillar damage. It is also concluded that, the rich polyphenolic content of CS extract is responsible for preventing oxidative damage by effectively scavenging the Isoproterenol generated ROS. (Patel et al 2012)

Coenzyme Q(10) (CoQ(10) – Patients with chronic heart failure have low plasma concentrations of CoQ(10), an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ(10) is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. (Molyneux eet al 2008)

Coenzyme Q(10) – Long-term treatment with ubiquinone increases plasma and myocardial CoQ content and this can improve the survival of myocardial cells during ischemia and limit postinfarct myocardial remodeling.(Kalenikova et al 2007)

Coenzyme Q(10) – appears to be involved in the coordinated regulation between oxidative stress and antioxidant capacity of heart tissue. When the heart is subjected to oxidative stress in various pathogenic conditions, the amount of CoQ10 is decreased, which triggers a signal for increased CoQ10 synthesis. It has been reported that in patients with cardiac disease such as chronic heart failure, the myocardium becomes deficient in CoQ10and CoQ10reductase. CoQ10 level is also reduced in other cardiovascular diseases such as cardiomyopathy. CoQ10 can protect human low-density lipoprotein (LDL) from lipid peroxidation, suggesting its role in atherosclerosis. Several reports exist in the literature indicating cardioprotective effects of CoQ10 against ischemia-reperfusion injury. (Maulik et al 2000)

Coenzyme Q(10) – (1) Serum and myocardial levels of CoQ can be raised acutely by iv liposomal CoQ. (2) Myocardial CoQ levels correlate best with I/R (ischemia and reperfusion) protection. (3) Acute iv CoQ improves function and efficiency and decreases oxidant injury after I/R. Intravenous CoQ may be effective clinically for acute cardiac ischemic syndromes. (Niibori et al 1998)

Creatine – A large amount of experimental evidence shows that pretreatment with Creatine is capable of reducing the damage induced by ischemia or anoxia in both heart and brain, and that such treatment may also be useful even after stroke or myocardial infarction has already occurred. (Perasso et al 2011)

Curcuma longa (Turmeric) In the present investigation it was observed that subsequent to ischemia and reperfusion injury, Curcuma longa treated group demonstrated significant anti-apoptotic property, which might contribute to the observed preservation in cardiac function and cardioprotective effects. Furthermore, the myocardial salvaging effects of Curcuma longa were supported by histopathological studies. (Mohanty et al 2006)

Curcumin, an inhibitor of NF-kappaB, ameliorated the surge of pro-inflammatory cytokines during cardiopulmonary bypass and decreased the occurrence of cardiomyocytic apoptosis after global cardiacischemia/reperfusion injury. (Yeh et al 2005)

Dan-Shen-Yin (DSY) – is a traditional Chinese formula comprising Salvia Miltiorrhiza, Sandalwood and Fructus Amomi. The results of this study show that DSY exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, possibly through its anti-inflammatory and anti-oxidant properties, and may thus be used as a potential therapeutic reagent for the treatment of coronary heart disease. (Yan et al 2012)

DHA & EPA – The most compelling evidence for the cardiovascular benefit provided by omega-3 fatty acids comes from 3 large controlled trials of 32,000 participants randomized to receive omega-3 fatty acid supplements containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or to act as controls. These trials showed reductions in cardiovascular events of 19% to 45%. These findings suggest that intake of omega-3 fatty acids, whether from dietary sources, fish oil, vegan supplements (those interested may wish to look at sites similar to https://cleanwellness.com/clean-vegan-omega-3.html), or in any other form should be increased, especially in those with or at risk for coronary artery disease. Patients should consume both DHA and EPA. (Lee et al 2008)

Dioscin exists extensively in Dioscoreaceae – In the rat models of myocardial ischemia-reperfusion injury, either a high dose dioscin (300 mL/kg/day) or a low dose dioscin (150 mL/kg/day) may lead to a smaller myocardial infarction size and better cardiac function comparing to the control (Zhao et al., 2008).

EGCG – the results of our study shows that EGCG protects the lysosomal membrane against ISO-induced cardiac damage. The observed effects might be due to the free radical scavenging and membrane stabilizing properties of EGCG. (Devika & Prince 2008)

Ginkgo biloba extract (Egb761) – has shown an antagonistic action on platelet-activating factor, a key point ofmyocardial injury. (Zhang and Gao, 2008).

Ginseng Radix Ginseng is from Panax Ginseng, a herbaceous plant of the Araliaceae. The chemical components include ginsenosides, ginseng polysaccharides, and active peptides, etc. Ginsenosides can limit myocardial infarction size, regulate metabolism of arachidonic acid, and increase the 6-Keto-PGF1α/TXB2 ratio (Li et al 2006). The optimal concentration of ginsenosides for myocardial protection was 20–80 mg/L, however, this drug may show a harmful effect on the myocardium when the concentration was 160 mg/L (Chen et al 1994). (Yuan et al 1997) obtained a similar result in a cardiac concordant xenotransplantation rat model where the proper concentration of the drug was 40 mg/L; whereas the protective effect diminished and it may jeopardize the myocardium when the concentration was 320 mg/L. (Yuan & Jing 2011)

Grape seed proanthocyanidins extract – The study suggests that grape seed proanthocyanidins extracts (GSPE) has a protective effect on myocardial ischemic reperfusion arrhythmias, which may be mediated by inhibiting the degradation of connexin 43 (Cx43) and enhancing gap junctional conductance. (Liang et al 2009)

Grape seed proanthocyanidins – have cardioprotective effects against reperfusion-induced injury via their ability to reduce or remove, directly or indirectly, free radicals in myocardium that is reperfused after ischemia. (Pataki et al 2002)

Hawthorn – The study confirms the protective effect of alcoholic extract of the berries of Crataegus oxyacantha against isoproterenol-induced inflammation and apoptosis-associated myocardial infarction in rats. (Vijayan et al 2012)

Hawthorn – The results suggested that Crataegus oxycantha extract attenuated apoptotic incidence in the experimental myocardial ischemia-reperfusion model by regulating Akt and HIF-1 signaling pathways. (Jayachandran et al 2010)

Hawthorn – Several studies have shown that Crataegus oxycantha (COC) extract is effective in quenching ROS, particularly free radicals. Human subjects treated with COC extract after myocardial infarction have shown improvements in heart rate, reduction in blood pressure, and an increase in the left-ventricular ejection volume. Moreover, meta analysis of a randomized trial with COC extract showed its beneficial role as an adjunctive treatment for chronic heart failure. The results of this study suggested that the COC extract may reduce the oxidative stress in the reperfused myocardium, and play a significant role in the inhibition of apoptotic pathways leading to cardioprotection. (Swaminathan et al 2010)

L-arginine and L-lysine – The protective effect of L-arginine and L-lysine on lysosomal enzymes and membrane bound ATPases was examined on isoproterenol induced myocardial infarction in rats. Lysosomal enzymes play an important role in the inflammatory process. The rats given isoproterenol intraperitoneally for 2 days showed significant changes in the marker enzymes, lysosomal enzymes and membrane bound phosphatases. Histopathological studies also confirmed the induction of myocardial infarction in isoproterenol administered rats. Prior oral treatment with L-arginine (250 mg kg(-1) daily) and L-lysine (5 mg kg(-1) daily) for 5 days significantly prevented these alterations and restored the enzyme activities to near normal. These findings demonstrate the protective effect of L-arginine and L-lysine in combination against isoproterenol induced cardiac damage. (Ebenezar et al 2003)

L-Carnitine – treatment initiated early after acute myocardial infarction and continued for 12 months can attenuate left ventricular dilation during the first year after an acute myocardial infarction, resulting in smaller left ventricular volumes at 3, 6 and 12 months after the emergent event. (Iliceto et al 1995)

Magnesium – Mg++ is beneficial in acute Myocardial Infarction, protection during open heart surgery and treatment and prevention of heart rhythm disturbances. (Akhtar et al 2011)

Magnesium – Hypomagnesemia is common in hospitalized patients, especially in the elderly with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with an increased incidence of diabetes mellitus, metabolic syndrome, mortality rate from CAD and all causes. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially gives magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel. The data regarding its use in patients with acute myocardial infarction (AMI) is conflicting. Although some previous, relatively small randomized clinical trials demonstrated a remarkable reduction in mortality when administered to relatively high risk AMI patients, two recently published large-scale randomized clinical trials failed to show any advantage of intravenous magnesium over placebo. Nevertheless, there are theoretical potential benefits of magnesium supplementation as a cardioprotective agent in CAD patients, as well as promising results from previous work in animal and humans. These studies are cost effective, easy to handle and are relatively free of adverse effects, which gives magnesium a role in treating CAD patients, especially high-risk groups such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as Torsades de Pointes and intractable ventricular tachycardia. (Shechter M 2010)

Olive leaf extract – In vitro, oleuropein and its major metabolite, hydroxytyrosol (which are polyphenols contained in olive leaf extract), exhibited a range of pharmacological properties beneficial for the cardiovascular system. These actions included enhanced nitric oxide production by mouse macrophages, antiinflammatory effects,protection against oxidative myocardial injury induced by ischemia and reperfusion, decreased blood pressure, inhibition of platelet aggregation and eicosanoid production, and scavenging of free radicals in addition to inhibition of 5- and 12-lipoxygenases . Oleuropein reduced infarct size, plasma lipid concentrations, and plasma markers of oxidative stress in cholesterol-fed rabbits. In vivo, olive leaf extract lowered blood cholesterol and lipid concentrations in cholesterol-fed rats and lowered blood pressure in nitro-L-arginine methyl ester-induced hypertensive rats as well as in normotensive rats. (Poudyal et al 2010)

N-acetyl cysteine (NAC) – Pretreatment with NAC showed protective effects on adenosine triphosphatases, minerals, and lipid peroxidation. The in vitro study confirmed the reducing property of NAC. The observed effects are due to the membrane-stabilizing and antioxidant effects of NAC. The results of this study will be useful for the prevention of myocardial infarction. (Meeran & Prince 2012)

N-3 PUFAs (n-3 polyunsaturated fatty acids) – Low levels of circulating n-3 PUFA are associated with decreased HF-free survival in post-acute myocardial infarction patients. (Hara et al 2012)

N-3 PUFAs – These results demonstrate that the increase in the dietary omega-3 PUFA, at the expense of omega-6 PUFA, reduces infarct size and helps to inhibit apoptosis in the limbic system after myocardial infarction in the rat. (Rondeau et al 2011)

N-3 PUFAs or probiotics – These results indicate that a high-PUFA n-3 diet or the administration of probiotics, starting after the onset of reperfusion, are beneficial to attenuate apoptosis in the limbic system and post-myocardial infarction depression in the rat. (Gilbert et al 2012)

N-3 PUFAs – A beneficial role of fish consumption on the risk of myocardial infarction (MI) has been reported and is mostly ascribed to n-3 (omega-3) fatty acids. The biomarker results indicate a protective effect of fish consumption. No harmful effect of mercury was indicated in this low-exposed population in whom Ery-Hg and P-EPA+DHA were intercorrelated. (Wennberg et al 2011)

N-3 PUFAs – Treatment with n-3 fatty acids after myocardial infarction exerts favorable effects on levels of platelet- and monocyte-derived microparticles, thus possibly explaining some of the anti-inflammatory and anti-thrombotic properties of these natural compounds. (Del Turco et al 2008)

Panax Notoginseng saponins could improve the Ca2+ pump activity on the membranes of myocardial sarcoplasmic reticulum, reduce myocardial intracellular Ca2+, and inhibit left ventricular remodeling. (Deng, 2007)

Panax quinquefolium total saponins could decrease the left ventricular load, and decrease myocardial oxygen consumption, and increase the blood supply to the ischemic myocardium. (Liu et al 2001).

Polygonum multiflorum — Its ability to enhance myocardial anti-oxidant status under the conditions of ischemia reperfusion-induced oxidative stress has been proved (Yim et al, 2000).

Potassium – Hypokalemia increased the probability of ventricular tachycardia in patients with acute myocardial infarction. Thus, the follow up and treatment of hypokalemia in these patients is of special importance. (Pourmoghaddas et al 2012)

Potassium – Among inpatients with acute myocardial infarction , the lowest mortality was observed in those with postadmission serum potassium levels between 3.5 and <4.5 mEq/L compared with those who had higher or lower potassium levels. (Goyal et al 2012)

Resveratrol – Our results show that resveratrol improved left ventricle diastolic function, endothelial function, lowered LDL-cholesterol level and protected against unfavourable hemorheological changes measured in patients with coronary artery disease (CAD). (Magyar et al 2012)

Resveratrol – Previous studies have established that resveratrol can exert significant cardiovascular protective effects in various models of myocardial injury, hypertension, and type 2 diabetes. Recent studies provide clear evidence that resveratrol treatment can also confer vasoprotection in aged mice and rats, attenuating ROS production, improving endothelial function, inhibiting inflammatory processes and decreasing the rate of endothelial apoptosis. The mechanisms underlying the cardiovascular protective action of resveratrol are likely multifaceted. Resveratrol was shown to up-regulate eNOS and increase NO bioavailability. Resveratrol can also induce major cellular anti-oxidant enzymes (e.g. glutathione peroxidase, heme oxygenase, superoxide dismutase) in cardiac and vascular cells, which result in a marked attenuation of oxidative stress. Resveratrol both down-regulates vascular and cardiac expression of TNFα and inhibits NADPH oxidases in the vasculature. It is significant, that resveratrol was also shown to inhibit mitochondrial production of reactive oxygen species in the vasculature. In addition, resveratrol both in vivo and at nutritionally relevant concentrations in vitro was shown to inhibit inflammatory processes, including NF-κB activation, inflammatory gene expression and attenuation of monocyte adhesiveness to endothelial cells, all of which may contribute to its cardioprotective effects in aging. (Csiszar A 2011)

Schisandrae chinensis The protective effects of this agent were experimentally observed as to increase SOD activity of erythrocyte, markedly lowered the lipid hydroperoxide content of the venous blood, and lessen the myocardial infarct extent (Guo et al 2006)

Selenium – Dietary selenium intake influences post-infarct cardiac remodeling even when provided within the range of physiological values. Our data suggest that the cardioprotective effect of selenium might be mediated by a reduced oxidative stress, a lower connexin-43 dephosphorylation, and a decreased TNF-α expression. (Tanguy et al 2011)

Selenium – Glutathione peroxidase and the thioredoxin reductase are selenocysteine dependent enzyme systems, and their activity is known to be dependent upon an adequate supply of dietary selenium. Moreover, various studies suggest that the supply of selenium as a cofactor also regulates gene expression of these selenoproteins. As such, dietary selenium supplementation may provide a safe and convenient method for increasing antioxidant protection in aged individuals, particularly those at risk of ischemic heart disease, or in those undergoing clinical procedures involving transient periods of myocardial hypoxia. (Venardos et al 2007)

Vitamins C and E – The results suggest that early administration of antioxidant vitamins C and E in patients withacute myocardial infarction and concomitant diabetes mellitus reduces cardiac mortality. (Jaxa-Chamiec et al 2009)

Vitamins C and E – This randomized pilot trial shows that supplementation with antioxidant vitamins is safe and seems to positively influence the clinical outcome of patients with acute myocardial infarction. A larger study is warranted to provide further evidence of this promising and inexpensive regimen. (Jaxa-Chamiec et al 2005)

Vitamin E – Levels of oxidative-stress markers are increased, and concentrations of antioxidants (e.g., vitamin E) are decreased in patients with vasospastic angina. (Kusuma et al 2011)

Withania somnifera (Ashwagandha) – Post-ischemic reperfusion injury resulted in significant cardiac necrosis, apoptosis, decline in antioxidant status and elevation in lipid peroxidation in the IR control group as compared to sham. Withania somnifera prior-treatment favorably restored the myocardial oxidant-antioxidant balance, exerted marked anti-apoptotic effects {upregulated Bcl-2 protein, decreased Bax protein, and attenuated TUNEL positivity}, and reduced myocardial damage as evidenced by histopathologic evaluation. The antioxidant and anti-apoptotic properties of Withania somnifera may contribute to the cardioprotective effects. (Mohanty et al 2008)

Ziziphus Total saponins of Semen Ziziphi spinosae are a kind of effective component extracted from Chinese medicine obtained from the seed of Ziziphus spinosa Hu. These agents have shown blood pressure lowering, anti-arrhythmic and anti-ischemic effects. (Yuan & Jing 2011)

Benefits of Diet and Exercise and Lifestyle Changes in Reducing the Risk of Heart Attack or Heart Disease
Numerous clinical triggers of myocardial infarctions have been identified, including blizzards, the Christmas and New Year’s holidays, experiencing an earthquake, the threat of violence, job strain, Mondays for the working population, sexual activity, overeating, smoking cigarettes, smoking marijuana, using cocaine, and particulate air pollution. Avoiding clinical triggers or participating in therapies that prevent clinical triggers from precipitating cardiac events could potentially postpone clinical events by several years and improve cardiovascular morbidity and mortality. (Schwarz et al 2010)

Both coronary heart disease and ischaemic stroke share links to many of the same predisposing, potentially modifiable risk factors (hypertension, abnormal blood lipids and lipoproteins, cigarette smoking, physical inactivity, obesity and diabetes mellitus). This highlights the prominent role lifestyle plays in the origin of cardiovascular disease. (Lennon & Blake 2009)

Exercise regimens – The American College of Cardiology/American Heart Association recommends at least 30 minutes of moderate (at 50–70% of maximal predicted heart rate) exercise on most days to reduce the risk of cardiovascular events. Several human studies clearly demonstrate that chronic aerobic exercise regimens improve cardiovascular function. This is true not only in healthy subjects without any underlying risk factors, but also in older people, and those with cardiovascular risk factors. Indeed, those with cardiovascular risk factor/disease will benefit more. There is a much higher consistency in the results of studies which assess participants with cardiovascular disease/risk factors compared to healthy subjects. Patients with hypertension, type 2 diabetes, metabolic syndrome, stable cardiovascular disease, myocardial infarction, and congestive heart failure, all benefit from exercise training compared to those who do not participate in any training. Importantly, an exercise regimen that improves endothelial function in diabetic patients fails to benefit healthy subjects. In healthy individuals, a longer and more intense exercise protocol is needed to induce measureable changes in cardiovascular parameters, while older and sicker subjects can benefit from less intense exercise regimens. (Golbidi & Laher 2012)

Regular exercise reduces CRP, IL-6, and TNF-αlevels and also increases anti-inflammatory substances such as IL-4 and IL-10. In healthy young adults, a 12-week high-intensity aerobic training program down regulates cytokine release from monocytes. In fact, even leisure time physical activity (e.g., walking, jogging, or running, etc.) reduces hs-CRP concentration in a graded manner. Subjects with higher baseline CRP levels (>3.0mg/L) will benefit more. (Golbidi & Laher 2012)

Exercise training improved autonomic function, assessed by heart rate recovery, resting heart rate and systolic blood pressure, in the absence of changes in diet or medication. (Ribeiro et al 2012)
Exercise training has beneficial effects on left ventricular remodeling in clinically stable post-MI (myocardial infarction) patients with greatest benefits occurring when training starts earlier following MI (from one week) and lasts longer than 3 months according to this meta-analysis. (Haykowsky et al 2011)

Increased fitness. After adjusting for weight change, fitness was independently associated (p < 0.05) with improvements in R(2 )for glucose (+0.7%), HbA1c (+1.1%), high-density lipoprotein (HDL) cholesterol (+0.4%), and triglycerides (+0.2%) in ILI and diastolic BP (+0.3%), glucose (+0.3%), HbA1c (+0.4%), and triglycerides (+0.1%) in DSE. Taken together, weight and fitness changes explained from 0.1-9.3% of the variability in cardiovascular risk factor changes. Conclusion: Increased fitness explained statistically significant but small improvements in several cardiovascular risk factors beyond weight loss. (Gibbs et al 2012)

Mediterranean-style diet – Higher consumption of a Mediterranean-style diet was associated with decreased risk of vascular events. Results support the role of a diet rich in fruit, vegetables, whole grains, fish, and olive oil in the promotion of ideal cardiovascular health. (Gardener et al 2011)

Soy-based diet – In addition, the increase in lipid peroxidation seen in rats subjected to myocardial infarction was significantly mitigated when the isolated soy protein diet was given. These findings suggest a nutritional approach of using a soy-based diet for the prevention of oxidative-stress-related diseases such as heart failure. (Hagen et al 2012)
Isolated soy protein diet – The ISP (isolated soy protein) diet was able to improve ventricular systolic and diastolic function in the groups IS<25% and IS>25% (left ventricular end diastolic pressure was reduced by 44% and 24%, respectively) and to decrease myocardial oxidative stress. The overall results confirm the preventive role of soy-derived products in terms of post-MI myocardial dysfunction probably by an antioxidant action. (Hagen et al 2009)

Stopping smoking, modifying one’s diet and exercise – This study found that individuals who change their behavior (quit smoking and modify diet and exercise) after acute coronary syndrome (ACS) are at substantially lower risk of repeat cardiovascular events. These benefits are seen early (<6 months), and the benefits from each behavior modification are additive. These results indicate that adherence to behavioral recommendations in the immediate postevent care of patients with ACS should be given as high a priority by physicians and caregivers as other secondary preventive medications and invasive strategies and justify a significant investment in establishing programs that systematically enhance early lifestyle modification and secondary prevention. (Chow et al 2010)

Transcendental Meditation Randomized controlled trials, meta-analyses, and other controlled studies indicate this meditation technique reduces risk factors and can slow or reverse the progression of pathophysiological changes underlying cardiovascular disease. Studies with this technique have revealed reductions in blood pressure, carotid artery intima-media thickness, myocardial ischemia, left ventricular hypertrophy, mortality, and other relevant outcomes. The magnitudes of these effects compare favorably with those of conventional interventions for secondary prevention. (Walton et al 2002)

Reduce acute mental stress – Cardiovascular events can be triggered by acute mental stress caused by events such as an earthquake, a televised high-drama soccer game, job strain or the death of a loved one. Acute mental stress increases sympathetic output, impairs endothelial function and creates a hypercoagulable state. These changes have the potential to rupture vulnerable plaque and precipitate intraluminal thrombosis, resulting in myocardial infarction or sudden death. (Schwartz et al 2012)

Reduce chronic stress. Chronic stress has been shown to be associated with the development of cardiovascular disease and, in the case of particular types of stress such as job and marital strain, with recurrent adverse events afteracute myocardial infarction (AMI). (Arnold et al 2012)

Reduce financial stress. High financial stress is common and is an important risk factor for worse long-term outcomes post-acute myocardial infarction, independent of access and barriers to care. (Shah et al 2012)

Reduce hyperglycemia. Hyperglycemia on admission to the hospital is associated with increased mortality rates in patients with ST-elevation myocardial infarction (STEMI). (Eitel et al 2012)

Blood and Other Tests in Heart Attack and Heart Disease
Albumin-globulin ratio – is a significant independent predictor of long-term mortality after NSTEMI (non-ST-segment elevation myocardial infarction) in patients with normal serum albumin levels. Further studies are needed to explain the underlying mechanisms. (Azab et al 2012)

Apolipoprotein (Apo)B/ApoA1 – The overall population attributable risk (PAR) of the nine risk factors to acute myocardial infarction (AMI) was higher in the Middle East (ME) (97.5%) than worldwide (90.4%). Elevated apolipoprotein (Apo)B/ApoA1 had the strongest association with AMI, followed by smoking. ApoB/ApoA1 had greater association than the conventional low-density lipoprotein (LDL)/high-density lipoprotein (HDL) cholesterol ratio. Both diabetes and hypertension had greater association with AMI in women than men. Abdominal obesity and depression, but not conventional BMI, were significantly associated with AMI. (Gehani et al 2012)

Apolipoprotein B-100 (apoB) – Although plasma LDL cholesterol is well established as a predictor of CAD, it may not be the best circulatory marker. Results from recent epidemiological studies and statin trials suggest that apolipoprotein B-100 (apoB), with or without apoA-I, is superior to LDL cholesterol in predicting coronary events. Measurements of apolipoproteins are internationally standardized, automated, cost-effective and more convenient and precise than those for LDL cholesterol. ApoB may also be preferable to the measurement of non-HDL cholesterol. Measurement of apolipoproteins (apoB and possibly apoA-I) should be routinely added to the routine lipid profile (cholesterol, triglycerides and high-density lipoprotein cholesterol) to assess the atherogenic potential of lipid disorders. This is particularly relevant to dyslipidaemias characterized by an elevation in plasma triglycerides. Apolipoproteins, especially apoB, could also replace the standard “lipid profile” as a target for therapy in at-risk patients. (Chan & Watts 2006)

ApoAI, apoB, and apoB/A – The present quantitative review suggests the existence of moderately strong associations between baseline levels of each of apoAI, apoB, and apoB/A and risk of coronary heart disease.(Thompson & Danesh 2006)

BNP and Nt-proBNP – After acute myocardial infarction (MI), B-type natriuretic peptide (BNP) and the N-Terminal fraction of its propeptide (Nt-proBNP) are major prognostic factors, independently of left ventricular ejection fraction (LVEF). Modulation of Nt-proBNP is multifactorial, depending on left ventricular dysfunction, remodeling, on left intraventricular pressure, and residual myocardial ischemia. Left ventricular remodeling is a complex process affected by many factors notably the autonomous nervous system (ANS) through sympathetic activation. (Lorgis et al 2012)

C-peptide – Patients with early diabetes type 2 and insulin resistance show increased levels of C-peptide in blood. Together with increased endothelial dysfunction, this leads to deposition of C-peptide in the intima of the vessel wall. According to the in vitro results, C-peptide may have chemotactic effect on the inflammatory cells involved in the onset of the atherosclerosis, like monocytes/macrophages and CD4+ lymphocytes. Further, C-peptide has an effect on the proliferation of smooth muscle cells in the media. These cells migrate into developing atheroma and together with inflammatory cell recruitment represent initial step in the developing of atherosclerosis. Based on the previous results, we demonstrated that C-peptide deposits in the vessel wall in ApoE-deficient mice and induces local inflammation that leads to increased lipid deposition in aortic arch and increased proliferation of smooth muscle cells, crucial processes in the onset of atherosclerosis. (Vasic & Walcher 2012)

C-reactive protein (CRP) – measured at admission of patients with non-ST-elevation acute coronary syndromesadds prognostic information to the TIMI-Risk Score. Additionally, the incorporation of this variable into the TIMI-Risk Score calculation is an effective manner to utilize CRP for risk stratification. (Correia et al 2007)

C-reactive protein and Fetuin-A — Fetuin-A is a ubiquitous anti-inflammatory glycoprotein that counteracts proinflammatory cytokine production. Previous studies have shown that low fetuin-A concentration is associated with cardiovascular death and may play an important role in the prognosis of patients with acute coronary syndromes (ACS). Multivariate analysis adjusted for GRACE risk score showed that low fetuin-A and high C-reactive protein (CRP) concentration remained associated with outcomes. In conclusion, fetuin-A combined with CRP level is associated with cardiovascular death in patients with ACS. (Lim et al 2012)

hs-C-reactive Protein (CRP) – Measurement of hs-CRP, an inflammatory biomarker, independently predicts future vascular events and improves global classification of risk of cardiovascular diseases. (Shen et al 2012)

hs-C-reactive Protein (CRP) – Over 20 large-scale prospective studies show that the inflammatory biomarker high-sensitivity C-reactive protein (hsCRP) is an independent predictor of future cardiovascular events that additionally predicts risk of incident hypertension and diabetes. In many studies, the relative impact of hsCRP is at least as large as that individually of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, blood pressure, or smoking, and knowledge of hsCRP correctly reclassifies a substantial proportion of “intermediate-risk” individuals into clinically relevant higher- or lower-risk categories. (Ridker PM 2007)

hs-CRP – High-sensitivity C-reactive protein (hs-CRP) is recognized as a reliable predictor of endothelial function and cardiovascular disease. (Sugiura et al 2011)

hs-CRP – One of the most appealing aspects of hs-CRP as a biomarker is that therapeutic approaches that lower hs-CRP also decrease cardiovascular events, and that the lower the hs-CRP on treatment, the lower the risk. (Davidson, M. 2011)

C-reactive protein – Our study demonstrated association between depression, anxiety and increased C-reactive protein level. Inflammation, the key regulator of CRP synthesis, plays a pivotal role in atherothrombotic cardiovascular disease. Our findings have important implications for explaining the pathophysiological mechanisms of cardiovascular disease.(Gegenava et al 2011)

C-reactive protein and interleukin-6 – Elevated levels of C-reactive protein and interleukin-6 are strong independent markers of increased mortality among patients with acute coronary syndrome. (Moe & Wong 2011)

D-dimer – Total of 74 non-ST elevation Acute Coronary Syndrome (NSTE-ACS) patients were enrolled (29 in unstable angina and 45 in non-ST elevation myocardial infarction). Mean age of these patients was 66 years. D-Dimer was significantly increased with the number of coronary arteries affected. In non-significant and single coronary artery disease (CAD) patients, median D-dimer was 406 mcg/L. In multivessel CAD, median D-dimer was 94 mcg/L. D-dimer levels had a trend to be increased with percentage of maximum stenosis of coronary artery lumen; atheromatosis (deposit or degenerative accumulation of lipid-containing plaques on the innermost layer of the wall of an artery). In mild and moderate atheromatosis (coronary artery stenosis < 70%), median D-dimer was 479 mcg/L while median D-dimer was 789 (131-7110) mcg/L in severe atheromatosis (coronary artery stenosis > 70%). Moreover plasma D-dimer levels correlated with complication of NSTE-ACS (congestive heart failure; arrhythmia; and death; and was increased in patients who underwent treatment with CABG more often than those who received PCI (percutaneous coronary intervention) and medication treatment alone. D-dimer also correlated with serum creatinine, creatinine clearance, troponin-T level and left ventricular ejection fraction . D-dimer is a useful coagulation marker use to evaluate extent of coronary affected and may predict in-hospital CV complication. (Charoensri & Pornratanarangsi 2011)

D-dimer, fibrinogen and D-dimer/fibrinogen ratio – was increased in cardioembolic stroke patients. (Alvarez-Perez et al 2011)

ECG Holter analysis is a validated non-invasive approach to evaluate the level of sympathetic and vagal tone. Loss of ANS balance frequently associated with coronary artery disease, is characterized by a fall in vagal modulation and a rise in sympathetic modulation. Heart Rate Variability (HRV) reflects cardiovascular response to the ANS. After MI, reduced HRV is an independent predictive factor of mortality and sudden cardiac death. Experimental studies in animals and humans strikingly showed that BNP infusion affects activity of the ANS through a decrease in sympathetic activity. (Lorgis et al 2012)

Fibrinogen – Fibrinogen elevation is associated with a worse prognosis in patients with acute coronary syndrome(ACS). (Ferraro et al 2012)

Glucose – In-hospital mortality and complications were significantly increased in diabetic acute myocardial infarction (AMI) patients and in non-diabetic AMI patients with stress hyperglycemia (transient elevation of blood glucose due to the stress of illness). Both a history of diabetes mellitus and stress hyperglycemia have strong influence on AMI prognosis. It seems to be more plausible to collaborate blood glucose level with history of diabetes in considering risk factors in AMI patients. (Peng et al 2011)

Glucose Acute myocardial infarction (AMI) patients with hyperglycaemia on admission, independent of a history of diabetes, represent a high-risk population for 180-day mortality. The worst outcome occurs in non-diabetic hyperglycaemic patients. Further studies are warranted to clarify the questions of hyperglycaemia treatment in AMI patients. (Ainla et al 2005)

Glucose – High blood glucose concentration may increase risk of death and poor outcome after acute myocardial infarction. Stress hyperglycaemia with myocardial infarction is associated with an increased risk of in-hospital mortality in patients with and without diabetes; the risk of congestive heart failure or cardiogenic shock is also increased in patients without diabetes. (Capes et al 2000)

HbA1c and glucose – In nondiabetic patients with ST-segment-elevation myocardial infarction, both elevated admission glucose and HbA(₁c) levels were associated with adverse outcome. Both of these parameters reflect different patient populations, and their association with outcome is probably due to different mechanisms. Measurement of both parameters enables identification of these high-risk groups for aggressive secondary risk prevention. (Timmer et al 2011)

Heme oxygenase-1 (HO-1, HSP 32) belongs to the family of heat shock proteins, which can be induced byischemia, local hypoxia, oxidative stress and other stressful stimuli. HO-1 has been shown to have cell-protective and anti-apoptotic properties. Hence, increased expression of HO-1 indicates perturbed cellular homeostasis. (Wohlschlaeger et al 2005)

Homocysteine – Total homocysteine (Hcy) elevations above 15 micromol/L are an independent risk factor forischemic stroke, whereas mild elevations of tHcy of 10 to 15 micromol/L are less predictive. The vascular effects of tHcy are greatest among whites and Hispanics, and less among blacks.(Sacco et al 2004)

Homocysteine – is a highly reactive amino acid and is known to produce endothelial cell injury in both experimental animal and cell culture studies. The pathophysiological consequences of such endothelial injury may include impaired release of nitric oxide, associated with significant alterations in vascular function. Homocysteine-related endothelial dysfunction may be involved in the initiation and progression of atherogenesis and/or thrombosis. (Shen et al 2010)

Homocysteine – Increased homocysteine levels predispose to atherosclerosis. A study done on 6405 subjects found that homocysteine levels and the presence of hyper-homocysteinemia decreased with increasing number of quartile of vitamins B6 and B12 in both genders and folate in men. (Waskiewicz et al 2010)

Homocysteine – Elevated plasma homocysteine levels have been associated with higher risks of cardiovascular disease. (Clarke et al 2010)

High-sensitivity cardiac troponin T (hs-cTnT) – is a useful prognostic biomarker in patients with chest discomfort suspected for coronary artery disease. In addition, hs-cTnT was an independent predictor for cardiac events when corrected for cardiovascular risk profiling, calcium score and CT-angiography results. (Mingels et al 2012)

MPV/platelet ratio – Our novel finding is that the MPV/platelet ratio is superior to the MPV alone in predicting long-term mortality after NSTEMI (non-ST segment elevation myocardial infarction). We suggest that using this ratio will magnify any existing relationship between platelet indices and mortality post-NSTMI. Further studies are needed to confirm our finding. (Azab et al 2011)

Neutrophil/lymphocyte ratio (NLR) – is an independent predictor of short-term and long-term mortalities in patients with NSTEMI (non-ST segment elevation myocardial infarction) with an average NLR >4.7. We strongly suggest the use of NLR rather than other leukocyte parameters (e.g., total white blood cell count) in risk stratification of the NSTEMI population. (Azab et al 2010)

Red blood cell distribution width (RDW) – is an independent predictor of all-cause long-term mortality in NSTEMI (non-ST segment elevation myocardial infarction) patients. Further studies are needed to clarify the mechanisms of this association between RDW and adverse outcomes in patients with coronary artery disease. (Azab et al 2011)

Cholesterol, Statins and Heart Disease
Statins work by inhibiting HMG-CoA Reductase which plays a key role in producing cholesterol. Hence it lowers cholesterol.

The absolute risk for incident diabetes
was about 31 and 34 events per 1000 person years for atorvastatin and rosuvastatin, respectively. There was a slightly lower absolute risk with simvastatin (26 outcomes per 1000 person years) compared with pravastatin (23 outcomes per 1000 person years). Our findings were consistent regardless of whether statins were used for primary or secondary prevention of cardiovascular disease. (Carter et al 2013)

If our findings are generalizable, clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial. (Petursson et al 2012)
In view of the mounting evidence of a higher risk of diabetes with statins, specifically from the randomized trials — the FDA recently announced a label change to some statin therapies. Based on current evidence from the literature, a note of ‘an effect of statins on incident diabetes and increases in HbA1c and/or fasting plasma glucose’ has been added to the safety labelling of all drugs in the statin class. (Sattar & Taskinen 2012)

Dr. Shirya Rashid — senior author of the study and assistant professor in the department of medicine at McMaster University — notes that a staggering 40 per cent of people taking statins are resistant to their impact on lowering blood LDL. (From research presented October 28, 2012 at the Canadian Cardiovascular Congress, reported inScience Daily, Oct. 28, 2012)
Statin medication use in postmenopausal women is associated with an increased risk for diabetes mellitus (DM). This may be a medication class effect. Further study by statin type and dose may reveal varying risk levels for new-onset DM in this population. (Culver et al 2012)

Although reductions in all-cause mortality, composite endpoints and revascularisations were found with no excess of adverse events, there was evidence of selective reporting of outcomes, failure to report adverse events and inclusion of people with cardiovascular disease. Only limited evidence showed that primary prevention with statins may be cost effective and improve patient quality of life. Caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk. (Taylor et al 2011 Cochrane Database Syst. Rev.)

Even when low density lipoprotein cholesterol (LDL-C) targets are attained, over half of patients continue to have disease progression and clinical events. This residual risk is of great concern, and multiple sources of remaining risk exist. Though clinical evidence is incomplete, altering or raising the blood high density lipoprotein cholesterol (HDL-C) level continues to be pursued. One study by Brugts et al 2009 found the relative risk reduction from statin use for primary prevention was comparable to that for secondary prevention. (Kones R 2011)
Statin use seems to be associated with an increased risk of developing rheumatoid arthritis. (de John et al 2011)

Even brief exposure to atorvastatin causes a marked decrease in blood CoQ(10) concentration. Widespread inhibition of CoQ(10) synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria (the presence of myoglobin in the urine, usually associated with rhabdomyolysis or muscle destruction). (Rundek et al 2004)
Individuals prescribed statins that have a greater impact on CoQ10, such as atorvastatin, may benefit from higher CoQ10 dosage levels. (Stargrove et al 2008) It appears that levels of coenzyme Q10 are decreased during therapy with HMG-CoA reductase inhibitors, gemfibrozil, Adriamycin, and certain beta blockers. (Sarter B 2002)
Some of the side effects of Atorlip (a statin) include nasopharyngitis, arthralgia, diarrhea, pain in the extremity, UTIs., muscle spasms, tremor, vertigo, memory loss, decline in cognitive function and raised liver enzymes. (from Drugs.com)
Herbal Remedies Supply a Novel Prospect for the Treatment of Atherosclerosis: A Review of Current Mechanism Studies – Increasing lines of evidence have questioned the statins-dominated treatment for atherosclerosis, including their dangerous side-effects such as the breakdown of muscle when taken in larger doses. Given the complicated nature of atherosclerosis and the holistic, combinational approach of herbal remedies, we propose that mixed herbal preparations with multiple active ingredients may be preferable for the prevention and treatment of atherosclerosis. (Zeng et al 2011)

Natural Compounds Which Can Be Used to Reduce the Dependency on Statins
  1. Omega-3 polyunsaturated fatty acids – are found in fish oil and they have been shown to mitigate the risk of cardiovascular disease. They reduce fatal and nonfatal myocardial infarction, stroke, coronary artery disease, sudden cardiac death, and all-cause mortality. They also have beneficial effects in mortality reduction after a myocardial infarction. Omega-3 fatty acids have also been shown to have beneficial effects on arrhythmias, inflammation, and heart failure. They may also decrease platelet aggregation and induce vasodilation. Omega-3 fatty acids also reduce atherosclerotic plaque formation and stabilize plaques preventing plaque rupture leading to acute coronary syndrome. Moreover, omega-3 fatty acids may have antioxidant properties that improve endothelial function and may contribute to its antiatherosclerotic benefits. (Kar S 2011)
  2. DHA & EPA – The most compelling evidence for the cardiovascular benefit provided by omega-3 fatty acids comes from 3 large controlled trials of 32,000 participants randomized to receive omega-3 fatty acid supplements containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or to act as controls.These trials showed reductions in cardiovascular events of 19% to 45%. These findings suggest that intake of omega-3 fatty acids, whether from dietary sources or fish oil supplements, should be increased, especially in those with or at risk for coronary artery disease. Patients should consume both DHA and EPA. (Lee et al 2008)
  3. Red yeast rice extract – The tested red yeast rice product demonstrated a significant cholesterol lowering effect compared to placebo, and was well tolerated in this Caucasian population. (Bogsrud et al 2010)
  4. Guggulsterone – A recent study demonstrates that guggulsterone upregulates the bile salt export pump (BSEP), an efflux transporter responsible for removal of cholesterol metabolites, bile acids from the liver. Such upregulation of BSEP expression by guggulsterone favors cholesterol metabolism into bile acids, and thus represents another possible mechanism for its hypolipidemic activity. (Deng R 2007)
  5. Red yeast rice extract – The treatment with a dietary supplement containing red yeast rice extract and policosanols has been for the first time successfully employed in hypercholesterolemic children. Results indicate this strategy as an effective, safe and well tolerated in a short-term trial. (Guardamagna et al 2011)
  6. Niacin – The use of FDA-approved niacin (nicotinic acid or vitamin B3) formulations at therapeutic doses, alone or in combination with statins or other lipid therapies, is safe, improves multiple lipid parameters, and reduces atherosclerosis progression. Niacin is unique as the most potent available lipid therapy to increase high-density lipoprotein (HDL) cholesterol. (Villines et al 2011)
  7. Artichoke leaf extract – Our results indicate that artichoke leaf extract may be useful for the prevention of hypercholesterolemia-induced pro-oxidant state in LDL+VLDL fraction and the reduction of increased serum cholesterol and triglyceride levels. (Kusku-Kiraz et al 2010)
  8. Curcumin – Long-term curcumin treatment lowers plasma and hepatic cholesterol and suppresses early atherosclerotic lesions comparable to the protective effects of lovastatin. The anti-atherogenic effect of curcumin is mediated via multiple mechanisms including altered lipid, cholesterol and immune gene expression. (Shin et al 2011)
  9. Olive leaf extract – In vitro, oleuropein and its major metabolite, hydroxytyrosol (which are polyphenols contained in olive leaf extract), exhibited a range of pharmacological properties beneficial for the cardiovascular system. These actions included enhanced nitric oxide production by mouse macrophages, antiinflammatory effects, protection against oxidative myocardial injury induced by ischemia and reperfusion , decreased blood pressure, inhibition of platelet aggregation and eicosanoid production, and scavenging of free radicals in addition to inhibition of 5- and 12-lipoxygenases . Oleuropein reduced infarct size, plasma lipid concentrations, and plasma markers of oxidative stress in cholesterol-fed rabbits. In vivo, olive leaf extract lowered blood cholesterol and lipid concentrations in cholesterol-fed rats and lowered blood pressure in nitro-L-arginine methyl ester-induced hypertensive rats as well as in normotensive rats. (Poudyal et al 2010)
Natural Compounds Which Can Help to Lower Blood Pressure
  1. Hawthorn (Crataegus oxyacantha) – Crataegus exerts mild blood pressure-lowering activity, which appears to be a result of a number of diverse pharmacological effects. It dilates coronary vessels, inhibits ACE, acts as an inotropic agent, and possesses mild diuretic activity. (Rewerski & Lewak 1967) (Uchida et al 1987) (Pepping et al 1995) (Weihmayr & Ernst 1996) This study showed no herb–drug interactions arising from hawthorn administration. Taken concomitantly with prescribed medications, the herb demonstrated a hypotensive effect for patients with type 2 diabetes. (Walker et al 2006)
  2. Olive leaf extract – In vitro, oleuropein and its major metabolite, hydroxytyrosol (which are polyphenols contained in olive leaf extract), exhibited a range of pharmacological properties beneficial for the cardiovascular system. These actions included enhanced nitric oxide production by mouse macrophages, antiinflammatory effects, protection against oxidative myocardial injury induced by ischemia and reperfusion, decreased blood pressure, inhibition of platelet aggregation and eicosanoid production, and scavenging of free radicals in addition to inhibition of 5- and 12-lipoxygenases . Oleuropein reduced infarct size, plasma lipid concentrations, and plasma markers of oxidative stress in cholesterol-fed rabbits. In vivo, olive leaf extract (OLE) lowered blood cholesterol and lipid concentrations in cholesterol-fed rats andlowered blood pressure in nitro-L-arginine methyl ester-induced hypertensive rats as well as in normotensive rats. (Poudyal et al 2010)
  3. Reserpine (which is in rauwolfia serpentina root) is effective in reducing systolic blood pressure roughly to the same degree as other first-line antihypertensive drugs. (Shamon & Perez 2009)
  4. Ginger (Zingiber officinale Roscoe), a well-known spice plant, has been used traditionally in a wide variety of ailments including hypertension. We report here the cardiovascular effects of ginger under controlled experimental conditions.These data indicate that the blood pressure-lowering effect of ginger is mediated through blockade of voltage-dependent calcium channels. (Ghayur & Gilani 2005)
  5. Omega-3 polyunsaturated fatty acids – are found in fish oil and they have been shown to mitigate the risk of cardiovascular disease. They reduce fatal and nonfatal myocardial infarction, stroke, coronary artery disease, sudden cardiac death, and all-cause mortality. They also have beneficial effects in mortality reduction after a myocardial infarction. Omega-3 fatty acids have also been shown to have beneficial effects on arrhythmias, inflammation, and heart failure. They may also decrease platelet aggregation and induce vasodilation. Omega-3 fatty acids also reduce atherosclerotic plaque formation and stabilize plaques preventing plaque rupture leading to acute coronary syndrome. Moreover, omega-3 fatty acids may have antioxidant properties that improve endothelial function and may contribute to its antiatherosclerotic benefits. (Kar S 2011)
  6. DHA & EPA – The most compelling evidence for the cardiovascular benefit provided by omega-3 fatty acids comes from 3 large controlled trials of 32,000 participants randomized to receive omega-3 fatty acid supplements containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or to act as controls.These trials showed reductions in cardiovascular events of 19% to 45%. These findings suggest that intake of omega-3 fatty acids, whether from dietary sources or fish oil supplements, should be increased, especially in those with or at risk for coronary artery disease. Patients should consume both DHA and EPA. (Lee et al 2008)
More Natural Compounds That Can Help to Lower Blood Pressure
  1. Andrographis – lowers blood pressure. It is a vasodilator. (Yoopan et al 2007)
  2. Antioxidants – vitamin C (500 mg) vitamin E (200 iu), co-enzyme Q10 (60 mg) and selenium (100 mcg)caused significant increases in large arterial elasticity index (LAEI) as well as small arterial elasticity index (SAEI). A significant decline in HbA1C and a significant increase in HDL-cholesterol were also observed. This beneficial vascular effect was associated with an improvement in glucose and lipid metabolism as well as decrease in blood pressure. (Shargorodsky et al 2010) A significant body of epidemiological and clinical trial data suggest that diets known to contain significant concentrations of naturally occurring antioxidants appear to reduce blood pressure and may reduce cardiovascular risk. Data suggest, regardless of etiology, excessive ROS is a common factor in the pathogenesis and morbidity of hypertension.(Kizhakekuttu & Widlansky 2010)
  3. Beetroot juice – lowers blood pressure. Only 250 ml is necessary to have this effect. (Kapil et al 2010)
  4. Capsaicin (in chili peppers) – can improve blood vessel function and lower blood pressure. (Yang et al 2010)
  5. Coenzyme Q10 – lowers blood pressure. (Burke et al 2001) (Singh et al 1999) A number of trials provide clinical evidence that some patients with high blood pressure may benefit from coenzyme Q10 supplementation. (Wyman 2010) Early data from non-controlled studies in human hypertension demonstrate reductions in blood pressure with CoQ supplementation. Further, small randomized studies using a CoQ dose of 100–120mg daily have demonstrated significant reductions in blood pressure with minimal side effects in patient with Stage II hypertension. Interestingly, a new, mitochondrial-targeted formulation of CoQ has demonstrated anti-hypertensive efficacy in a rat model. (Kizhakekuttu & Widlansky 2010)
  6. Egg white peptides – exhibited antihypertensive activity in vivo. (Garcia-Redondo et al 2010)
  7. Garlic – has been shown to reduce systolic blood pressure by 5.5% in animal studies. (Tapsell et al 2006) These findings point out the beneficial effects of garlic supplementation in reducing blood pressure and counteracting oxidative stress in humans, and thereby, offering cardioprotection in essential hypertensives. (Dhawan & Jain 2005) The effect of garlic on blood pressure cannot be ascertained. Previous meta-analyses have been based on trials with inadequate study designs, methodological deficiencies and with too little information about blood pressure measurement. In our view, use of garlic cannot be recommended as antihypertensive advice for hypertensive patients in daily practice. (Simons et al 2009)
  8. Magnesium – intake of 500 mg/d to 1000 mg/d may reduce blood pressure (BP) as much as 5.6/2.8 mm Hg. However, clinical studies have a wide range of BP reduction, with some showing no change in BP. The combination of increased intake of magnesium and potassium coupled with reduced sodium intake is more effective in reducing BP than single mineral intake and is often as effective as one antihypertensive drug in treating hypertension. Reducing intracellular sodium and calcium while increasing intracellular magnesium and potassium improves BP response. Oral magnesium acts as a natural calcium channel blocker, increases nitric oxide, improves endothelial dysfunction, and induces direct and indirect vasodilation. (Houston 2011) Our meta-analysis detected dose-dependent BP reductions from magnesium supplementation. (Jee et al 2002)
  9. Resveratrol – improved hypertension, dyslipidemia, hyperinsulinemia in vivo. (Rivera et al 2009)
  10. Royal Jelly peptides – were effective in lowering blood pressure in vivo. (Tokunaga et al 2004)
  11. Salmon – Salmon consumption three times per week can decrease diastolic blood pressure (DBP) similar to fish oil and significantly more than lean fish during an 8-wk energy restriction in young overweight individuals. A lower DHA content in erythrocyte membrane at baseline, which might indentify infrequent fish eaters, is associated with a greater DBP reduction in the course of an 8-wk dietary intervention providing fatty seafood. (Ramel et al 2010)
  12. Watermelon – can be an effective natural weapon against pre-hypertension. When 6 gms of the amino acidL-citrulline/L-arginine from watermelon extract was administered daily for 6 weeks there was improved arterial function and consequently lowered aortic blood pressure in all nine of the pre-hypertensive subjects. (Figueroa et al 2010)
Avoid High Salt and High Fructose Intake
High salt intake is linked to hypertension whereas a restriction of dietary salt lowers blood pressure (BP). Substituting potassium and/or magnesium salts for sodium chloride (NaCl) may enhance the feasibility of salt restriction and lower blood pressure beyond the sodium reduction alone. The substitution of Smart Salt [50% sodium chloride and rich in potassium chloride (25%), magnesium ammonium potassium chloride, hydrate (25%)] for Regular salt in subjects with high normal or mildly elevated BP resulted in a significant reduction in their daily sodium intake as well as a reduction in SBP (systolic blood pressure). (Sarkkinen et al 2011)
It has been shown that a high fructose (sugar) diet may contribute to high blood pressure. (Jalal et al 2010)

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