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Cardi Vascular Disease
Tuesday, August 18, 2009

Cardiovascular Disease

Introduction

Diseases of the heart and circulation are so common and the laity is so well acquainted with the major symptoms resulting from these disorders that patients, and occasionally physicians, erroneously attribute many noncardiac complaints to cardiovascular disease.(1) It should not be a surprise that this occurs since most patients are aware that cardiovascular disease remains the leading cause of death in the United States. More than 50 percent of patients with ischemic heart disease initially present with acute myocardial infarction, and 50 percent of patients who suffer acute myocardial infarction do not survive.(2)

There are four principle properties of the cardiovascular system that can be evaluated to provide diagnostic, prognostic, and therapeutic management information. These include (1) electrical conduction, (2) pump function, (3) myocardial perfusion, and (4) anatomy.(3)


Ischemia, or inadequate myocardial perfusion, is manifest most frequently as chest discomfort. A cardinal principle is that cardiac function that is adequate at rest may be inadequate during exertion. Thus, a history of chest pain or discomfort only during activity is characteristic of heart disease. Reduction in the pumping ability of the heart frequently manifests as weakness and fatigability, or as the disease process continues and becomes more severe, produces cyanosis, hypotension, syncope, and elevated intravascular pressure behind a failing ventricle. A failing ventricle will also produce the accumulation of fluid (edema) either in the systemic or pulmonary circulation, and may cause dyspnea, and orthopnea. Obstructions to blood flow, such as is found in valvular stenosis, can cause symptoms resembling congestive heart failure. Arrhythmias, or disorders of electrical conduction usually develop suddenly. The accompanying signs and symptoms—palpitations, dyspnea, angina, hypotension, and syncope may disappear as rapidly as they develop.

Patients with cardiovascular disease may also be completely asymptomatic. They may present, however, with elevated arterial pressure, a heart murmur, abnormal chest x-ray or abnormal ECG upon medical evaluation. In cardiovascular disease, the history taking, interview, and physical examination remain the most important elements of patient assessment.(4) While there are many technologically advanced tests available, they are only effective when used in conjunction with a complete history and physical examination. History taking enables the examiner to establish a relationship with the patient, develop an awareness of the patient’s perception of problems and quality of life, and an assessment of the problem’s acuity and severity.(5) Particular attention should be paid to the family history, as familial clustering is common in many forms of heart disease.

The New York Heart Association has outlined the elements of a complete cardiac diagnosis. They include consideration of:(6)

  1. The underlying etiology. Is the disease congenital, infectious, hypertensive, or ischemic in origin?
  2. The anatomic abnormalities. What chambers are involved? Which valves are affected? Is there pericardial involvement? Has there been a myocardial infarction?
  3. The physiologic disturbances. Is there an arrhythmia present? Is there evidence of congestive heart failure or myocardial ischemia?
  4. The extent of functional disability. How strenuous is the physical activity required to elicit symptoms? The latter should be evaluated in light of the intensity of therapy.

There are several risk factors for cardiovascular disease that are essentially immutable. These are older age, male gender, and a family history of CVD. Additionally, three major risk factors identified include cigarette smoking, dyslipidemia (high cholesterol), and hypertension.(7),(8) Other identified factors associated with increased risk for cardiovascular disease include physical inactivity, sleep problems,(9) diabetes mellitus,(10) obesity,(11) excessive intake of alcohol, thrombotic and fibrinolytic factors, elevated homocysteine levels, certain infections and inflammation, exogenously administered estrogens and androgens, certain psychosocial factors, increased fasting glucose.(12) and frequency of migraines.(13) The synergism of the presence of multiple risk factors must also be considered.

The American Heart Association/American College of Cardiology (AHA/ACC) have set up guidelines for preventing heart attack and death in patients with atherosclerotic cardiovascular disease.(14) Their recommendations regarding each of the following risk factors are listed at the end of the subheading.

Cigarette smoking is unlike the other CVD risk factors in that it can be completely eliminated. The benefits of smoking cessation are dramatic particularly in decreasing risk of coronary heart disease—the incidence of CHD falls to near non-smoking levels in 2 years. For patients who smoke, event rates are three to four times higher than in non-smokers, with a dose-response relationship.

AHA/ACC guideline recommendation: completely stop smoking

Dyslipidemia is probably a better term than hyperlipidemia because it includes all lipid and lipoprotein abnormalities, such as low levels of high-density lipoprotein (HDL)-cholesterol (hypoalphalipoproteinemia), which can be a potent risk factor. Early epidemiologic studies confirmed that elevated serum cholesterol level was an independent risk factor for CVD, with a strong dose-response relationship that is exponential at higher levels of cholesterol.(15) The best single lipid measure in predicting risk is the total cholesterol/HDL-cholesterol ratio. Total cholesterol includes LDL-cholesterol, VLDL-cholesterol (a triglyceride surrogate), and HDL-cholesterol, while the denominator is the protective HDL-cholesterol.(16) Results below 3 indicate the least risk, with values of 3-5 being considered within normal limits. Ratios above 5 represent elevated risk, and continued higher ratios indicate increased risk proportionally. Not only does this ratio hold true as an indicator of cardiovascular risk, it has also proven clinically to be a better indicator of treatment benefit than any other changes in lipid or lipoprotein parameters. Lp(a) is a lipoprotein identical to LDL except for the addition of a highly glycosylated protein, apolipoprotein (a). Lp(a) has been associated with elevated CHD risk in several studies, and the similarity of the amino acid sequence between Lp(a) and plasminogen is suggestive of a possible connection between atherogenesis and thrombosis. Treatment is somewhat problematic, with only niacin and estrogen showing some effect in lowering Lp(a).

AHA/ACC guideline recommendation:

  • Primary Goal: LDL<100mg/dL
  • Secondary Goal: If triglycerides are greater than or equal to 200mg/dL then the non-HDL should be less than 130mg/dL

    Hypertension has long been associated with, and is considered the dominant risk factor for stroke, and a potent risk factor for all forms of atherosclerotic CVD. Treatment with antihypertensives has proven beneficial, although, optimal regimens for each patient should be chosen carefully. In most patients, blood pressure, and often other cardiovascular risk factors may be decreased by simple life style changes, including weight loss, exercise, reduction of sodium intake, reduction of alcohol intake, and altering diet to one rich in consumption of fruits and vegetables.

    AHA/ACC guideline recommendation:

  • <140/90 mmHg
  • If heart failure or renal insufficiency, <130/85 mmHg
  • If diabetes, <130/80 mmHg

    Physical inactivity has been elevated to one of the four major risk factors for CVD. Evidence has shown that patients who exercise, have improved blood pressure, HDL-cholesterol, and improvement in fibrinolysis and triglycerides. While it is wise to evaluate individuals at high risk for exercise induced cardiac ischemia before introduction of an exercise program, in the vast majority of patients the benefits far outweigh any risk.

    AHA/ACC guideline recommendation: Minimum goal if 30 minutes of activity 3 to 4 times per week, optimally daily.

    Diabetes mellitus is also a proven risk factor for CVD. Patients with type II diabetes are considered to have approximately twice the risk in men, and an almost fourfold increase in women. Type I diabetics have an even higher risk, particularly in patients with proteinuria. Type II diabetics typically present with a low HDL-cholesterol, high triglycerides, elevated blood pressure and/or other metabolic abnormalities in addition to insulin and glucose abnormalities. Evidence suggests correction of lipid abnormalities substantially improves CHD risks.

    AHA/ACC guideline recommendation: HbA1c <7%

    Obesity not only is known to aggravate other CVD risk factors, it has been shown to be an independent risk factor. Traditionally measured as body mass index (weight/height), measures of central obesity or abdominal fat, such as the waist/hip ratio may be a better predictor.

    AHA/ACC guideline recommendation: Body Mass Index (BMI) between 18.5 to 24.9 kg/m2

    Alcohol consumption at less than 1 drink up to 3 drinks per day is protective against CHD, thrombotic stroke and peripheral vascular disease. The effect seems to be mediated by increases in HDL-cholesterol, as well as having possible effects on coagulation and fibrinolysis. For non-atherosclerotic CVD, such as hemorrhagic stroke and cardiomyopathies, risk is increased by alcohol consumption. Maximum overall benefit for alcohol is reached at a single drink a day, and consumption of two or more drinks per day is associated with increases in morbidity and mortality from total cardiovascular causes, cirrhosis, accidents and violence, and certain cancers. Additionally, benefit is essentially limited to older persons at relatively high risk of CHD, whereas younger persons at lower risk have minimal benefit, and are much more likely to suffer alcohol-related harm.

    Increasing attention has been paid to thrombotic and fibrinolytic factors as opposed to atherogenesis. The most consistent and reproducible risk factor in this group is fibrinogen, which has proven in independent studies, to be associated with CHD, stroke, and PVD. Low dose aspirin therapy has been used to inhibit platelet aggregation, which reduces CVD risk, but should be assessed for increased risk of bleeding.

    Homocysteine has been considered in numerous studies to be a strong independent risk factor for CVD. Clinical trials are in progress to determine whether reduction in homocysteine reduces the associated CVD risk. Intervention could theoretically be quite easy, since folic acid supplementation alone, or in combination with other B vitamins is known to lower total plasma levels of homocysteine.

    Increasing attention has been given to an old theory concerning infectious agents and inflammation as risk factors for CVD. Particular attention is being paid to Chlamydia pneumoniae, which has been isolated from atherosclerotic plaques, and has been shown to be present in higher levels in patients with CVD. Additionally, after MI, levels of Chlamydia pneumoniae may predict further CVD events, and treatment with macrolide antibiotics may reduce recurrent CVD events. Additionally cytomegalovirus titers have been reported in some studies to be increased in CVD patients. One study measured IgG or IgA antibodies to herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, Hemophilus influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Helicobacter pylori in 572 patients, who were then followed for 3.2 years. Patients with advanced atherosclerosis and seropositive for 0 to 3 pathogens experienced a mortality rate of 7.0% compared to a mortality rate of 20.0% in those seropositive for 6 to 8 pathogens.(17) The link of infection to atherogenesis and thrombosis is unclear, but inflammation is likely involved. For example, inflammatory markers such as C-reactive protein may predict future fatal and non-fatal CHD events in men.

    Gonadal hormones, both endogenous and exogenously administered androgens and estrogens, are associated with CVD events in men and women. The most notable and clinically relevant data show a reduction in CVD events in post menopausal women using estrogen replacement therapy. Estrogen raises HDL-cholesterol, lowers LDL-cholesterol, and appears to have a direct benefit on arterial tone.

    Psychosocial factors such as anger, anxiety, hostility, depression,(18) type A behavior, and various measures of social support have been associated with occurrence or recurrence of CVD. Currently, inadequate data are available to prove whether or not psychosocial interventions can reduce CVD risk.

    • Statistics

    World Health Organization, 2007.

    • CVDs are the number one cause of death globally: more people die annually from CVDs than from any other cause.
    • An estimated 17.5 million people died from CVDs in 2005, representing 30% of all global deaths.
    • Over 80% of CVD deaths take place in low- and middle-income countries and occur almost equally in men and women.
    • By 2015, almost 20 million people will die from CVDs, mainly from heart disease and stroke. These are projected to remain the single leading causes of death.
    American Heart Association, 2006.
    • According to 2003 estimates, 71,300,000 Americans have one or more forms of cardiovascular disease (CVD).
    • Claimed 910,614 lives in 2003 (37.3 percent of all deaths or 1 of every 2.7 deaths).
    • Over 152,000 Americans killed by CVD are under age 65.
    • 2003 death rates from CVD were 359.1 for white males and 479.6 for black males; for white females 256.2 and for black females 354.8 (Death rates are per 100,000 population. The rates listed use the year 2000 standard U.S. population as the base for age adjustment).
    • From 1993 to 2003 death rates from CVD declined 22.1 percent.
    • Despite this decline in the death rate, in the same 10-year period the actual number of deaths declined only 4.6 percent.
    Signs and Symptoms
    The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.
    Patients with cardiovascular disease may be asymptomatic, with recognition of disease occurring only as a result of a physical examination. Such important signs as hypertension and dyslipidemias may only be found incidentally when the patient visits a doctor for other reasons. With other patients, the initial presenting symptom may actually be the occurrence of a myocardial infarction. Many patients do exhibit signs and symptoms, however, and some of the most recognizable include; chest pain and or heaviness, dyspnea with or without orthopnea, paroxysmal nocturnal dyspnea, cyanosis, easy fatigability or weakness, palpitations, cough, edema, and syncope.
    Primary symptoms
    • Chest pain
    • Dyspnea with or without orthopnea
    • Paroxysmal nocturnal dyspnea
    • Cyanosis
    • Fatigue
    • Palpitations
    • Cough
    • Edema
    • Syncope
    Treatment Options
    Conventional
    Treatment consists of a wide variety of interventions from life style changes to surgical revascularization.

    Generally, if a patient has no evidence of cardiovascular disease, but has one or more known risk factors for the development of ischemic heart disease, a plan for risk reduction should be developed and implemented. This may include dietary restrictions, smoking cessation, weight loss or other life-style modifications. The patient should be reevaluated at intervals to assess compliance, and see whether risk factors are actually being reduced.

    Asymptomatic, or mildly symptomatic patients with valvular heart disease should be evaluated at 6 to 12 month intervals. Early signs of deterioration can be detected in this manner, and invasive treatment such as cardiac catheterization or surgery may be performed, if necessary, prior to development of disabling symptoms or irreversible myocardial damage.

    It is important to establish criteria for deciding the form of treatment to be used in patients with ischemic heart disease. Surgery, including a coronary artery bypass graft (CABG), and angioplasty should be reserved for patients with ischemic heart disease in whom it has been demonstrated that these treatments are superior to medical treatments.

    Specific treatments employed for patients with symptoms of congestive heart failure, cardiac arrhythmias, etc. are widely varied, and should be reserved for a discussion of individual complaints.

    Nutritional Supplementation
    Astaxanthin

    Carotenoids are also reported beneficial in helping decrease cardiovascular diseases, particularly high cholesterol levels or hypercholesterolemia. Many studies have been performed on the various carotenoids in decreasing oxidation of LDL cholesterol (so called "bad" cholesterol) and thereby decreasing the incidence of arteriosclerosis.(19)  As the carotenoids are exclusively transported by lipoproteins, this suggests that they might protect these particles against  oxidation. The xanthophylls have been reported to be superior to other carotenoids in the process.(20)  One laboratory study of interest reported that astaxanthin actually increased HDL cholesterol levels, a positive effect for cardiovascular health.(21)

    Vitamin E
    Experimental and epidemiological evidence supports the hypothesis that oxidation of LDL cholesterol is a risk factor in the development of atherosclerosis. Vitamin E is a well researched substance with evidence suggesting it prevents the oxidative damage that leads to atherosclerosis. In one study, patients taking 1,600 mg/day of vitamin E recorded a 50% decrease in oxidative damage to LDL cholesterol.(22)

    In the Cambridge Heart Antioxidant Study (CHAOS), over 2000 patients with angiographically proven coronary atherosclerosis were followed for periods ranging from 3 to 910 days (median 510 days). In this double-blind, placebo-controlled trial, three groups of patients were randomly assigned to receive daily doses of 400 IU vitamin E, 800 IU of vitamin E, or a placebo. The patients taking the doses of vitamin E had a 47% reduction in subsequent heart attacks (both fatal and non-fatal) compared to the placebo controls. The overall reduction in non-fatal secondary heart attacks was 77%.(23)

    A World Health Organization-sponsored study reported the fact that a low blood level of vitamin E is an important risk factor in deaths from ischemic heart disease — possibly more important than elevated cholesterol, high blood pressure or smoking.(24) Ischemic heart disease is a localized anemia due to a mechanical obstruction of the blood supply, which is usually due to arterial narrowing from atherosclerosis. In another study, 156 men aged 40-59 years with previous coronary artery bypass graft surgery reported that individuals taking 100 IU of vitamin E or more daily had a substantial reduction in the progression of atherosclerosis.(25)

    Vitamin C
    Vitamin C also plays an important role in the prevention of cardiovascular disease. In a study that was conducted at UCLA, it was reported that men who took 800 mg of vitamin C daily had a 42% reduction in mortality from cardiovascular disease, compared to men who only consumed the FDA's Recommended Dietary Allowance (RDA) of 60 mg of vitamin C daily. This study also reported that men consuming the larger amounts of vitamin C lived an average of 6 years longer than the men who only consumed the RDA of 60 mg of vitamin C daily.(26)

    In another study, 316 women and 511 men (aged 19-95 years) were administered vitamin C well above RDA. The results were improved lipid profiles corresponding to possible reduced risk of cardiovascular disease.(27)

    L-Carnitine
    Carnitine is an important nutrient for cardiovascular health. Carnitine’s primary function is to facilitate the transport of fatty acids across cellular membranes into the mitochondria where they are utilized in the production of energy. This is extremely important for the heart, which is the most energy-demanding muscle in the body. Studies report that carnitine can be therapeutically useful in the treatment of various forms of cardiovascular disease such as angina,(28),(29) acute myocardial infarction,(30) congestive heart failure,(31) peripheral vascular disease,(32) arrhythmias(33) and abnormal blood lipids.(34)
    Coenzyme Q10 (CO-Q10)
    Coenzyme Q10 is a nutrient recently being recognized as playing a role in cardiovascular health. It functions as an antioxidant and is also a cofactor in several enzymatic steps in the generation of energy in the mitochondria of all cells. The heart is the most active muscle in the human body, a decline in energy due to a deficiency of CoQ10 can first affect heart function.

    In one double-blind study, patients with severe congestive heart failure who were given 150 mg/day of CoQ10 had a 38% decrease in hospitalizations due to worsening of heart failure compared to the control group. At the same time, episodes of pulmonary edema decreased by 60% and angina episodes decreased by 53%.(35) In another study it was shown that the symptoms of cardiovascular disease got progressively worse as CoQ10 levels declined. Treatment with 100 mg of coenzyme Q10 daily resulted in both subjective and objective improvement in 69% of patients with cardiomyopathy and 43% of patients with ischemic heart disease.(36)

    Two other studies reveal how effective coenzyme Q10 is in treating various forms of cardiovascular disease. In one study, 109 patients that had been diagnosed by a cardiologist with symptomatic essential hypertension began treatment with high-dose coenzyme Q10 (average dose 225 mg/day) in addition to their existing antihypertensive drug regimen. In 80% of these patients, the diagnosis of essential hypertension was established for greater than one year, with an average of 9.2 years. A definite and gradual improvement in function status was observed with the concomitant need to gradually decrease antihypertensive drug therapy within the first one to six months. Ultimately, 51% of the patients come completely off from one to three antihypertensive drugs at an average of 4.4 months after starting therapy with coenzyme Q10.(37)

    In the second study, 424 patients began adding coenzyme Q10 to their existing medical regimens. These patients were divided into the following six different diagnostic categories: ischemic cardiomyopathy, dilated cardiomyopathy, primary diastolic dysfunction, hypertension, mitral valve prolapse, and valvular heart disease. The dosages ranged from 75 to 600 mg/day (average 242 mg/day). Before treatment with coenzyme Q10 began, most patients were taking from one to five cardiac medications. During this study, overall medication requirements dropped considerably and 43% of the patients were able to completely stop from one to three cardiovascular medications.(38)

    The authors of another study noted that coenzyme Q10 is transported throughout the body packaged into the LDL and VLDL fractions of cholesterol. They emphasized that the transport of CoQ10 by LDL-cholesterol means that CoQ10 is acting as an antioxidant to prevent the oxidation of LDL-cholesterol and the subsequent development of atherosclerosis.(39)

    Numerous categories of prescription drugs can inhibit the body’s ability to synthesize coenzyme Q10. Drugs that can deplete coenzyme Q10 include sulfonylureas, biguanides, beta-blockers, hydralazine-containing vasodilators, thiazide diuretics, centrally-acting antihypertensives (clonidine and methyldopa), the "statin" cholesterol-lowering drugs, tricyclic antidepressants, and phenothiazines.(40),(41),(42),(43),(44),(45)

    Magnesium
    Magnesium is a key mineral for cardiovascular health. It performs functions similar to numerous cardiovascular drugs. It inhibits platelet aggregation (like aspirin), thins the blood (like warfarin), blocks calcium uptake (like nifedipine), and relaxes blood vessels (like ACE inhibitors such as enaparil). Magnesium also increases oxygenation of the heart muscle by improving cardiac contractibility.(46)

    Adequate magnesium is associated with reduced incidence of angina, cardiac spasms, and arrhythmias, as well as having relaxing and antispasmodic effects of the blood vessels. On the other hand, magnesium deficiency is associated with increased incidence of atherosclerosis, hypertension, strokes, and heart attacks.(47) It is now recognized that many heart attacks happen to individuals with relatively healthy hearts. It is a magnesium deficiency that causes a cardiac spasm, which results in death.(48)

    Omega-3 Fatty Acids
    The authors of a paper in the June 2000 issue of the Mayo Clinic Proceedings provide a nice summary of the history of omega-3 fatty acids as they have gradually been recognized to play a key role in the prevention and treatment of cardiovascular-related diseases. Their review states the following. "During the past 25 years, the cardiovascular effects of marine omega-3 (omega-3) fatty acids have been the subject of increasing investigation. In the late 1970s, epidemiological studies revealed that Greenland Inuits had substantially reduced rates of acute myocardial infarction compared with Western control subjects. These observations generated more than 4,500 studies to explore this and other effects of omega-3 fatty acids on human metabolism and health. From epidemiology to cell culture and animal studies to randomized controlled trials, the cardioprotective effects of omega-3 fatty acids are becoming recognized. These fatty acids, when incorporated into the diet at levels of about 1 g/d, seem to be able to stabilize myocardial membranes electrically, resulting in reduced susceptibility to ventricular dysrhythmias, thereby reducing the risk of sudden death. The recent GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico)-Prevention study of 11,324 patients showed a 45% decrease in risk of sudden cardiac death and a 20% reduction in all-cause mortality in the group taking 850 mg/d of omega-3 fatty acids. These fatty acids have potent anti-inflammatory effects and may also be antiatherogenic. Higher doses of omega-3 fatty acids can lower elevated serum triglyceride levels; 3 to 5 g/ d can reduce triglyceride levels by 30% to 50%, minimizing the risk of both coronary heart disease and acute pancreatitis."(49) Results of a study involving 17 healthy men consuming 2 high-fat meals supplemented with omega-3 fatty acids (EPA) were improved elasticity of blood vessels which may reduce the risk of cardiovascular disease.(50)
    Potassium
    People consuming diets containing foods that are high in potassium may have a lower incidence of hypertension.(51) Epidemiological evidence reveals that increasing potassium intake can lower blood pressure in individuals who have essential hypertension and increasing dietary potassium can also result in a reduction of antihypertensive medications.(52)

    Diets high in potassium have also been reported to protect against death from strokes. In a 12-year study, individuals who died from strokes were found to have significantly lower potassium intake than survivors of strokes and individuals who died from other causes.(53)

    Selenium
    Low plasma selenium (less than 45 micrograms/L) has been considered a significant risk factor for cardiovascular disease.(54) Selenium's protective mechanisms include selenium's role in the enzyme glutathione peroxidase, which helps remove hydrogen peroxide and lipid peroxides. Lipid peroxidation may damage cell membranes and it may also activate the liberation of arachidonic acid from phospholipids, which may ultimately increase the risk to thrombogenesis, platelet aggregation and vasoconstriction. Selenium is antagonistic to cadmium, mercury, and lead which have been related to hypertension and it is also antagonistic to other cardiotoxic elements. Selenium has a cardioprotective effect against drugs and other xenobiotics that are cardiotoxic (e.g. Adriamycin). Selenium has a known antiviral capability, which may protect the heart from agents such as the coxsackie B4 viruses.(55)
    B Complex Vitamin
    Over the past several years, elevated homocysteine has become recognized as one of the primary risk factors to cardiovascular disease. Homocysteine is a toxic intermediate metabolite of the amino acid methionine that is capable of causing damage to arteries leading to atherosclerosis. In one metabolic pathway, vitamin B6 is necessary to convert homocysteine to cystathionine. In another metabolic pathway, folic acid and vitamin B12 are required to remethylate homocysteine back to methionine. A deficiency of any one of these three B-vitamins can lead to elevated homocysteine.(56)

    Several studies have documented the fact that supplementation with folic acid, vitamin B6, and vitamin B12 can effectively lower homocysteine levels.(57),(58),(59),(60) There are wide variations in the dosages of these B-vitamins used in different studies. The use of B-vitamins and folic acid for this purpose may be cost effective for the primary and secondary prevention of coronary heart disease.(61) It is now recognized that even moderate elevations of homocysteine represent a strong independent risk to cardiovascular disease.

    In a prospective, double-blind, randomized trial, 205 patients who had undergone a successful coronary angioplasty were given a combination of folic acid, vitamin B12 and pyridoxine or placebo for six months. Treatment significantly lowered plasma homocysteine levels and at follow-up, the minimal luminal diameter was significantly larger in the treatment group, the degree of stenosis was less severe, the rate of restenosis was significantly lower and the need for revascularization of the target lesion was less in patients assigned to folate treatment.(62)

    A randomized, double-blind placebo-controlled trial involving 553 patients was designed to evaluate the effect of homocysteine-lowering therapy on clinical outcome after percutaneous coronary intervention. After successful angioplasty of at least 1 significant coronary stenosis, patients were enrolled and randomized to either a combination of folic acid, vitamin B12 and vitamin B6 or a placebo for 6 months. After 1 year, the endpoints (death, nonfatal myocardial infarction, or revascularization) were lower in patients receiving the homocysteine lowering therapy.(63)

    It should be emphasized that the B-vitamin requirements necessary to maintain acceptable levels of homocysteine vary widely. There are numerous examples of people who had been taking vitamins B6, B12, and folic acid at substantially greater than RDA levels, who when tested, still had elevated homocysteine. The only way to ensure appropriate doses of these B-vitamins to maintain low homocysteine levels is by lab assessment.

    Soy Isoflavones
    Soy isoflavones have demonstrated a beneficial role in atherosclerosis and platelet aggregation. Specifically, genistein reportedly inhibits platelet aggregation and smooth muscle cell proliferation. Smooth muscle cells are one of the primary cell types comprising plaques.(64),(65) It has been proposed that isoflavones play a beneficial role in the prevention of atherosclerosis via several mechanisms.

    A study involving monkeys evaluated the impact of a soy-based diet on several variables that can impact the severity of cardiovascular disease. One group of monkeys was fed a casein-lactalbumin diet, a second group received soy protein diet as alcohol extracted isoflavones and the third group received an isoflavone intact soy protein diet. Significant improvements were noted for several cholesterol markers in the soy-based diets over the casein diet. Beneficial effects on plasma lipid concentrations are likely one possible mechanism for atherosclerosis prevention. Though not significant, lower rates of atherosclerosis were noted in the soy protein based diets, with the intact isoflavone diet being the least.(66) Antioxidant properties and effects on arterial compliance may also have a positive impact on the prevention of atherosclerosis.(67)

    Results of a randomized, double-blind, placebo-controlled, parallel-group dietary intervention study involving 61 men at high risk for cardiovascular disease were that intake of 20 grams (with 80 mg of isoflavones) of soy protein for five weeks could help reduce total cholesterol and blood pressure which might be effective in reducing cardiovascular disease.(68) Studies have found that supplementation with soy isoflavones exerted favorable effects of a reduction in LDL and an increase in HDL levels.(69),(70),(71)

    Beta-1,3 Glucan
    Beta-glucans appear to be the major cholesterol lowering agents in oat bran fiber. This dietary fiber, 0.75 g/serving and four servings a day, has been approved by The US Food and Drug Administration (FDA) to reduce cardiovascular disease risk. A randomized crossover study fed a high-fiber (beta-glucan or psyllium) and a control low-fat, low-cholesterol diet for 1 month each to 68 hyperlipidemic adults. Based on various reductions in cholesterol measures and ratios, a risk reduction of 4.2 +/- 1.4% (P = 0.003), as calculated by the Framingham cardiovascular disease risk equation, was noted for cardiovascular disease.(72)
    Lycopene
    One study matched a control group of 483 healthy middle-aged to elderly women to an equivalent group that had CVD. Blood levels of lycopene, other carotenoids, and retinol were measured in both groups. The results of this study were adjusted for smoking, cholesterol, and age. The results found that those who had the highest blood levels of lycopene had a 50% reduced risk of CVD when compared to those who had the lowest levels. These results were not seen in the other carotenoids measured. The authors concluded that the results of this study warrant further investigations into the mechanisms of lycopene.(73)
    Herbal Supplementation
    Coleus
    Coleus is reported to have two significant mechanisms of action. First, it is claimed to activate the enzyme, adenylate cyclase.(74) This action would have the effect of increasing cyclic adenosine monophosphate (c-AMP) within the cells. Coleus reportedly creates c-AMP activation independent of receptor site specificity.(75) The stimulation of c-AMP has an impact on body chemistry in several ways. It stimulates thyroid function, increases insulin secretion, inhibits mast cell release of histamine and increases the burning of fats as fuels.(76) Coleus is claimed to inhibit platelet activating factor (PAF) by possibly directly binding to PAF receptor sites.(77),(78) PAF is a key factor in allergic and inflammatory pathways. By inhibiting it, neutrophil activation may be inhibited, vascular permeability reduced, smooth muscle contraction decreased and coronary blood flow increased.(79)
    Hawthorn
    Hawthorn is used as a vasodilator and circulatory stimulant.(80) It has been used extensively by doctors in Europe in its standardized form in various cardiovascular and peripheral circulatory conditions. Its combination of effects on the heart leads to its use as a tonic, especially for the elderly where mitral stenosis and minor heart failure may be present. Studies have reported a reduction in blood pressure due to arteriosclerosis and chronic nephritis with the use of hawthorn.(81) It is also used for peripheral vascular diseases, such as Raynaud’s disease. Hawthorn is used in Europe by physicians to help maintain digoxin levels while decreasing the need for the pharmaceutical medication. Hawthorn is reported to have the ability to regulate both low and high blood pressure. Its bioflavonoids reportedly dilate both peripheral and coronary blood vessels.(82) This leads to its use in decreasing angina attacks. The proanthocyanidin (PCO) content is claimed to support the spasmolytic effects.(83) The PCO content also is thought to be responsible for the coronary circulatory effects, increasing the amplitude of the heartbeat.(84) Hawthorn’s glycoside component reportedly increases the vagal tone of the heartbeat.(85) It is also thought that hawthorn inhibits angiotensin-converting enzyme.(86) It has a slight diuretic effect which may help lower high blood pressure. Laboratory studies have reported that proanthocyanidins may actually aid in reversing atherosclerotic plaque.(87)
    Garlic
    Garlic has been reported to lower total cholesterol, LDL cholesterol and triglycerides, and increase HDL cholesterol.(88),(89),(90) Garlic may be of benefit in the prevention of heart disease and atherosclerosis.(91),(92) Garlic may inhibit platelet aggregation and influence blood viscosity through its fibrinolytic activity.(93),(94),(95) This leads to the use of garlic in the prevention of strokes, heart attacks and various thrombus events.(96),(97),(98) Also, the antioxidant effect in aged garlic has been reported to be beneficial in preventing stroke and arteriosclerosis.(99)

    A recent study reported no effect of garlic oil on serum lipids.(100) However, the product used was garlic oil, which is processed and heated garlic. The impact of processing is an important fact to keep in mind when recommending garlic supplements. Changes can occur in the active constituents when exposed cooking or other processing which can render the garlic product virtually ineffective. Cooking is known to denature proteins and therefore may inactivate the enzyme (allinase) that is necessary in converting alliin into allicin, the major bio-active constituent in garlic.

    Also, research has reported that allinase may be irreversibly inhibited by stomach acid and may fail to form adequate amounts of allicin or other thiosulfinates below pH 3.6.(101),(102) Recommending a quality garlic supplement is essential, and enteric coating may be advantageous. Of further note, as reported in a few laboratory studies, is the potential for large amounts of allicin to damage liver tissue if absorbed due to its oxidation potential.(103),(104) However, there are positive studies while using high quality garlic preparations standardized to allicin potential without adverse effects.

    Cordyceps
    Cordyceps has traditionally been used for its improvement in respiration and in individuals with decreased lung function, such as asthma and bronchitis, by increasing oxygenation (improving VO2 max by 9-15%).(105) Cordyceps has been reported to have anticancer effects by decreasing proliferation and differentiation of cancerous cells and has immunomodulatory effects.(106),(107),(108) Cordyceps has been used for decreasing the renal toxicity of aminoglycosides and cyclosporine(109),(110) and in individuals with chronic renal failure.(111) Kidney protection is claimed to be due to: protecting tubular cell sodium pump activity; attenuating tubular cell lysosome overfunction stimulated by phagocytosis of aminoglycoside; and decreasing tubular cell lipoperoxidation in response to toxic injury.(112) Cordyceps was also reported to protect stem cells and red blood cells during chemotherapy and radiation.(113)

    Cordyceps has been reported to increase sexual vitality in both men and women and decrease male impotence. This may be due to an increase in sex hormones, or by directly acting on the sexual center of the brain and sex organs in parallel with the hypothalamo-pituitary-adrenocortical axis.(114) It may also reverse drug-induced impotence.(115)

    Kava
    Decreasing and managing stress may also play a key role in improving cardiovascular health. The herb kava has been used for centuries by South Pacific natives. The root is used in the preparation of a recreational beverage known by a variety of local names (kava, yaqona, awa) and occupies a prominent position in the social, ceremonial, and daily life of Pacific island peoples as coffee or tea does in the Western cultures. In European phytomedicine, kava has long been used as a safe, effective treatment for mild anxiety states, nervous tension, muscular tension, and mild insomnia.(116),(117) Studies have reported that kava preparations compare favorably to benzodiazepines in controlling symptoms of anxiety and minor depression, while increasing vigilance, sociability, memory, and reaction time.(118),(119) Reports are conflicting as to whether kava’s anti-anxiety actions are GABA mediated.(120),(121) Kavalactones appear to act on the limbic system, in particular the amygdala complex - the primitive part of the brain that is the center of the emotional being and basic survival functions.(122) It is thought that kava may promote relaxation, sleep, and rest by altering the way in which the limbic system modulates emotional processes. Tolerance does not seem to develop with kava use.(123),(124)
    Psyllium Seed
    One of psyllium’s findings is in its potential for management of cholesterol levels.(125),(126) Psyllium, 1.78 g/serving given four servings a day as a dietary fiber, has been approved by The US Food and Drug Administration (FDA) to reduce cardiovascular disease risk.(127) There have been several clinical trials reporting the effectiveness of psyllium in hypercholesterolemia.(128),(129),(130),(131) Fiber in the diet, especially soluble fiber, can reportedly reduce absorption of blood cholesterol and fecal bile acids that can lower cholesterol levels, decreasing the risk for heart disease and stroke. A randomized crossover study fed a high-fiber (beta-glucan or psyllium) and a control low-fat, low-cholesterol diet for 1 month each to 68 hyperlipidemic adults. Based on various reductions in cholesterol measures and ratios, a risk reduction of 4.2 +/- 1.4% (P = 0.003), as calculated by the Framingham cardiovascular disease risk equation, was noted for cardiovascular disease.(132)
    Acupuncture & Acupressure
    Li Xue Ling, et al. treated 40 cases of coronary disease with acupuncture therapy. The plasma levels of vitamin B2 in patients were significantly decreased and the therapeutic results were satisfactory. The total effectiveness rates were 85.0% for angina pectoris and 67.5% for improving ECG. (133)

    Li Bao Liang, et al. treated 34 cases of angina pectoris with acupuncture therapy, and the following back-shu points were selected: Xin Shu (BL 15), Gan Shu (BL 18), and Shen Shu (BL 23). All points were punctured with the twirling vertical lifting-thrusting, and uniform reinforcing-reducing methods. The needles were retained for 25 minutes. One session was conducted each day. 12 days constituted one treatment course. A control group of 28 cases were treated only with a Guan Xin Dan Shen Pianin tablet, which contained Dan Shen (Salvia), San Qi (Notoginseng), and Jiang Xiang (Dalbergia Wood). The results of the treatment after 24 days were evaluated. The clinical effectiveness rate was 91.18% in the acupuncture group, and 82.14% in the control group (P>0.05). ECG improvement rates were 79.41% and 46.43%, respectively (P<0.05). In comparison between two groups, the clinical effectiveness rate in the acupuncture group was higher than that of the control group, but without statistical significance. However, regarding the ECG improvement rate, the treatment group was much higher than the control group, and difference was statistically significant.(134)

    Yu Li, et al. used acupuncture therapy in the treatment of 98 cases of coronary heart disease. The needle was inserted into point Nei Guan (PC6) until the needling sensation was felt, and then it was retained for 15 minutes. All the patients received acupuncture therapy once a day and ten days established one treatment course. During this treatment period, no drugs were administered. When comparing the results of ECG examination before and after the treatment at the end of three courses of acupuncture therapy, there were significant statistical differences as to the descending of S-T segment and the decrease of heart rate (P<0.01).(135)

    Acupoint Plastering Therapy
    Dai Ju Yun, et al. used acupoint adhesion therapy for the treatment of angina pectoris in 95 cases, using Dan Qi Yi Xin adhesive plaster, which contained extracts of Dan Shen (Radix Salviae miltiorrhizae), Huang Qi (Radix Astragali seu Hedysari) etc. The plasters were adhered to the following points: Tan Zhong (CV17), Shen Que (CV18), Xin Shu (BL15 left side), and Zhi Yang (GV9). All the patients received treatment once a day. Four weeks constituted one treatment course. Two control groups were treated with acupoint adhesion with nitroglycerin in one group of 20 cases, and oral administration of Dan Shen tablets in another group of 30 cases, respectively. The results were that the effectiveness rate for relieving chest pain in the treatment group was 91.1%, and those of the two control groups were 95% and 80%, while the ECG effectiveness rate of the treatment group was 68.6%, and for two control groups were 64.7% and 62.5%.(136)

    Gao She Guang, et al. treated angina pectoris with She Xiang Tong Bi plaster stuck at points of Tan Zhong (CV17) and Nei Guan (PC6) on both sides. The plasters were changed every three days. 15 days constituted one treatment course. The results showed that in this series of 130 cases, 111 cases were clinically resolved, 17 cases had improved, and 2 cases did not respond to the treatment. The total effectiveness rate was 98.5%.(137)

    Clinical Lab Assessments
    Some of the following laboratory testing can provide information necessary for diagnosis and treatment. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.
    Thyroid Profile
    Hypothyroidism is considered a risk factor for CVD. Assessment of thyroid hormone production, peripheral hormone conversion, cellular sensitivity response, thyroid hormone antibody activity, and hormone feedback response mechanisms can provide critical information for intervention with a goal of optimal function.
    C-reactive protein (CRP Thyroid Profile)
    An abnormal serum glycoprotein produced by the liver during acute inflammation, CRP has been used to monitor rheumatoid arthritis and rheumatic fever, to differentiate between Crohn’s disease and ulcerative colitis, and to detect or monitor inflammatory processes. Elevated levels of CRP have been shown to be present in those individuals who have mild or subclinical cardiovascular disease and significant elevations suggest risk of acute cardiovascular event. It disappears rapidly when inflammation subsides, thus it is a reliable measure of current inflammatory process. Recent advances in technology, not yet in common use, provide a very high sensitivity in the measure of this important marker of cardiovascular health.
    Lipid Profile

    Triglycerides:     Triglycerides carry fatty acids that provide primary long-term energy storage. A chronically elevated triglyceride level is associated with degenerative disease conditions and anaerobic metabolism demonstrating difficulty utilizing triglyceride fatty acids. The risk of cardiovascular disease is twice as high among adults with a triglyceride level ¡Ý 100 mg/dl.(138)
    Magnesium Level
    There is considerable attention in the scientific community to the significance of magnesium in cardiovascular function.(139),(140),(141)
    Homocysteine
    Data from a study on healthy U.S. physicians with no prior history of heart disease demonstrated that highly elevated homocysteine levels are associated with a more than three-fold increase in the risk of heart attack over a five-year period.(142) The study included nearly 15,000 male physicians.(143) The Framingham Heart Study and other studies have confirmed that elevated homocysteine is an independent risk factor for heart disease.

    A naturally synthesized by-product of methionine metabolism, homocysteine does not have a non-toxic level. Most laboratories report the reference range of homocysteine as 5-15 ìm/l even though epidemiological data suggests substantially increased cardiovascular risk at levels above 6.3 ìm/l.(144) One study found each 3-unit increase in homocysteine equals a 35% increase in risk of myocardial infarction.(145)

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