~Cardiovascular Disease Comprehensive 16 - Auxilliary Factors
AUXILIARY FACTORS THAT AFFECT CARDIOVASCULAR HEALTH
Anemia-- a predictor of death from acute heart attack
- Sodium Restriction
- What You Drink
- Autonomic Balancing
- Calcium Channel Blockers
Anemia reflects a reduction below normal in the number of red blood cells, hemoglobin level, or hematocrit (a measure of the packed cell volume of red cells in blood). Hematocrit has emerged as an extremely important assessment in targeting individuals at high risk of succumbing to a heart attack (Wu et al. 2001).
Note: A normal hematocrit is between 36-50%; below 36% indicates anemia.
A study reported in the New England Journal of Medicine evaluated 78,974 patients, ages 65 and older, who were hospitalized with acute myocardial infarction. Patients were categorized according to hematocrit upon admission. Researchers considered the prognostic value of hematocrit percentages as well as the impact of blood transfusions on 30-day mortality. Their findings follow:
Hematocrit Percentages as Predictor of Cardiac Survival
Reduction in Cardiac Mortality Following Transfusion
- Hematocrit 5.0%-24.0% = 78% chance of patient dying within 30 days
- Hematocrit 24.1%-27.0% = 52% chance of patient dying within 30 days
- Hematocrit 30.1%-33.0% = 31% chance of patient dying within 30 days
- Hematocrit >33.1% = No increased risk
Note: Transfusion benefits with increased severity of anemia.
It should be emphasized that transfusion therapy is only effective in reducing cardiac mortality among anemic patients; mortality actually increased when transfusions were given to nonanemic patients.
- Patients with hematocrit < 24% reduced mortality 64% with transfusion.
- Patients with hematocrit 24.1-27% reduced mortality 31%.
- Patients with hematocrit 27.1-30% reduced mortality 25%.
Does Sodium Restriction Lower Blood Pressure?
An evaluation of a hypertensive patient should include measuring plasma renin activity (PRA) to determine if renin is a factor in the pathogenesis of elevated blood pressure. In order to stimulate renin release, the individual is told to follow a diet very low in sodium for 3 days prior to the test. Normal values of adult plasma renin, measured in an upright position and sodium-depleted, are 2.9-10.8 ng/mL an hour.
Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney in response to many cardiovascular factors, such as a fall in blood pressure, reduced plasma volume, and/or sodium depletion. In an attempt to maintain homeostasis, renin is released, increasing the conversion of angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II, which in turn causes an increase in aldosterone secretion, a sequence that increases peripheral vascular resistance and blood pressure.
Patients with low renin levels respond best to sodium restriction and diuretic therapy. Those with high baseline renin levels will not respond to sodium restriction. According to Jeff Bland, Ph.D., most individuals who have essential hypertension are not salt sensitive. Putting those individuals on a rigorous salt-restricted diet has little impact on their hypertension. Conversely, if an individual is salt sensitive, sodium restriction will have a profound effect upon modulating blood pressure. This is an example of matching an appropriate dietary program with the right genotype (Bland 2000b).
Acknowledging that dietary salt appears to account for only a minor segment of increased blood pressure in hypertensive people, it has been proposed that a larger segment of essential hypertension is caused by enhanced renal sodium retention prompted by hyperinsulinemia. Insulin resistance may also play a role by altering internal sodium and potassium distribution in a direction associated with increased peripheral vascular resistance (Zavaroni et al. 1992; Lukaczer 2000). Researchers were able to demonstrate that blood pressure increased or decreased when lesser or greater amounts of insulin were administered to obese, hypertensive patients (Tedde et al. 1989; Randeree et al. 1992).
The most effective dietary treatment for hypertension appears to be weight loss and a dietary intervention to increase calcium, magnesium, and potassium intake. Results of the Dietary Approaches to Stop Hypertension (DASH) study showed that a diet rich in fruits, vegetables, and low-fat dairy products significantly lowered blood pressure. These foods are excellent sources of potassium, magnesium, and calcium, accounting for the success of the diet. In the study, blood pressure was reduced by 5.6 mmHg and 2.8 mmHg (systolic and diastolic pressures), making dietary intervention comparable to first generation antihypertensives. Weight loss and dietary manipulation appears to control hypertension in nearly one-half of individuals with high blood pressure (Bland 2000a).
Can What You Drink Make a Difference?
Endorsing alcohol consumption is difficult considering the number of health risks imposed by drinking. But when considering the health of the heart and vascular system, statistics appear to flip in favor of moderate alcohol consumption. Studies involving atherosclerosis (disease authenticated by cardiac catheterization or autopsy) show less arterial closure among persons who consume moderate amounts of alcohol. A moderate drinker, in fact, decreases the possibility of heart disease by 30-50% (Gaziano 1993; Pearson 1996). This is true for both men and women, particularly imbibers middle-aged or older.
As encouraging as this information is, the line is extremely narrow in regard to the amount of alcohol one can consume and still reap benefits. For example, teetotalers or occasional drinkers lose the alcohol advantage because of inconsistent consumption. Conversely, persons consuming 3 or more drinks a day experience a rapid rise in total morbidity, that is, cardiomyopathy, hypertension, and hyperhomocysteinemia, as well as mortality. The bottom line indicates that nondrinkers, as well as individuals who aggressively imbibe, have a higher risk of succumbing from heart disease than an individual consuming 1-2 drinks a day (Rimm et al. 1996).
It is speculated that about 50% of the protective nature of alcohol is due to alcohol's ability to increase HDL cholesterol (Gordon et al. 1981). An additional edge comes by reducing blood glucose and insulin levels (Facchini et al. 1994). It appears that no advantage is gained from alcohol in regard to lowering either blood pressure or LDL cholesterol levels, but the blood clotting mechanism is altered by alcohol consumption (Renaud et al. 1992; Ridker et al. 1994). It is debatable how alcohol accomplishes this. Perhaps it is by influencing coagulation factors, such as PAI-1, t-PA, and the activity of platelets.
Reports appearing in The Lancet added to the benefits obtained from alcohol, citing the antioxidants found in red wine and dark beer (Maxwell et al. 1994). Antioxidants, regardless of their source, always play heroic roles in heart health. Interestingly, alcohol is still able to convey a cardiovascular advantage, even in light of a poor diet or cigarette smoking.
Is alcohol the utopia we are all searching for? Probably not, considering the dangers imposed by excessive consumption. Persons with a personal or family history of alcoholism and those with hypertriglyceridemia, pancreatitis, liver disease, certain blood disorders, or hypertension, as well as pregnant women, are not candidates for either beginning or continuing to drink alcohol. Those on diets should not forget that alcohol is a significant source of calories as well as carbohydrates. It is also important to recall that drug and alcohol interactions can be fatal. Yet, after acknowledging the negatives, if current consumers of alcohol all abstained from drinking, about 80,000 additional heart deaths would occur annually (Pearson et al. 1994). Although the research is compelling, alcohol should never be considered to be a treatment for either Syndrome X or heart disease.
The pleasure of a cup of green tea is well accepted, but it appears to accomplish far more than satisfy the palate. Published literature confirms the hypolipidemic nature of green tea, reporting decreases in triglycerides and LDL cholesterol, while increasing the beneficial HDL cholesterol. In addition, green tea suppressed the oxidation of LDL cholesterol, further deterring the atherosclerotic process (Chan et al. 1999).
Some researchers liken green tea to aspirin because of similar therapeutic qualities. Information published in Beyond Aspirin (Newmark et al. 2000), states that green tea contains salicylic acid, a naturally occurring COX-2 inhibitor. Green tea, like aspirin, inhibits thromboxane A2; the inhibition of thromboxane A2 lessens the risks of blood clot formation and the dangers imposed by arterial constriction.
Heart attacks and strokes are less likely to occur if neither fibrinogen levels nor the activity of platelet-activating factor (PAF) become excessive. Green tea lowers fibrinogen levels and is a PAF inhibitor. A 4-year study involving 5910 Japanese women (ages 40 and older) showed twice as many strokes among trial participants who used less green tea (less than 5 cups a day) than in those who used more (greater than or equal to 5 cups daily) (Sato et al. 1989).
A cup of green tea appears to be beneficial to hypertensives through various mechanisms. The loss of arterial elasticity (arteriosclerosis) is one cause of high blood pressure. Youthful arteries expand and contract in compliance with the heartbeat to move blood to peripheral sites. Damaged vessels are unable to participate in this ritual. Green tea (by inhibiting thromboxane) reduces arterial constriction and consequently blood pressure is reduced. Also many antihypertensive drugs are ACE inhibitors, meaning angiotensin pathways are disrupted. Without interruption of this feedback loop, blood vessels vasoconstrict, water is retained, and blood pressure increases. Green tea breaks this sequence, acting as a natural (although mild) ACE inhibitor (Duke Database 1992; Faloon 2000).
The 1st International Symposium on Green Tea (September 22, 1989) reported that green tea reduces blood glucose levels. During the ensuing years, the Life Extension Foundation has frequently informed members that green tea reduces the expected glucose and insulin rise after a carbohydrate load. It should also be noted that green tea contains chemicals regarded as beta-adrenergic receptor blockers, anti-inflammatories, diuretics, and calcium antagonists, proving beneficial in arrhythmias and hypertension (Duke Database 1992).
Green tea, an antioxidant, helps remove excess iron from the liver (Carper 2001). Individuals with hemochromatosis should drink several cups or use two to four 300-mg capsules a day. (Each capsule should provide 95% active polyphenols.) Note: Research suggests that decaffeinated green tea has a different therapeutic disposition than that containing caffeine and may be more effective in reducing iron overload. Caffeine drinks are not appropriate for sympathetic dominant individuals and those taking beta-adrenergic drugs.
As similar as green tea and aspirin are in their defensive mechanisms, it would not be wise for an individual, relying on aspirin as a cardioprotective, to depend only on green tea to the exclusion of aspirin.
Nuts: A Heart Food
According to a report published in the American Journal of Clinical Nutrition, one of the most unexpected and novel findings in nutritional epidemiology in the past 5 years has been that nut consumption protects against ischemic heart disease (IHD) (Sabate 1999). Phytonutrients in nuts, such as luteolin (a flavonoid), tocotrienols, fiber, fatty acids, amino acids, and vitamins and minerals, appear to work synergistically to provide heart protection, lower blood pressure, reduce the risk of stroke, and increase longevity. The protective effect of nuts applies to men and women (both black and Caucasian), all age groups, smokers, and sedentary individuals.
Of the tree nuts, walnuts are unique because they are a rich source of linolenic acid. Almonds are a good source of vitamin E and calcium; peanuts provide folate (important in controlling homocysteine) and resveratrol (inhibits blood clots and the inflammatory process). Nuts are also good sources of arginine and fiber (Kris-Etherton 1999).
The Adventist's Health Study reported that individuals who ate nuts 1-4 times a week reduced their risk of acute myocardial infarction 22% (Fraser et al. 1992). Eating nuts more than 5 times a week resulted in a 51% lower cardiac risk compared to individuals who consumed nuts less than 1 time a week. Persons consuming nuts more than 5 times a week reduced their lifetime IHD risk 12%, and men who developed the disease did so 5.6 years later than men who consumed nuts infrequently.
In 1993, the New England Journal of Medicine published results of a walnut study conducted at Loma Linda University. All trial participants conformed to the National Cholesterol Education Program Step 1 Diet, except that 20% of the calories of one diet were derived from walnuts, offset by lesser amounts of fatty foods. Both diets contained identical foods and macronutrients, except for the addition of walnuts in the test diet.
At the conclusion of the study, participants eating the walnut diet had total cholesterol levels 22.4 mg/dL (12.4%) lower and LDL cholesterol levels 18.2 mg/dL (16.3%) lower than those consuming the control diet. Blood pressure was unaffected on either diet. Researchers noted that subjects on the walnut diet, despite increased energy intake, did not gain weight (Sabate et al. 1993). Comment: Nuts, in general, are healthy foods, but select those not roasted at high temperatures in oils of uncertain quality.
The Journal of the American Medical Association recently expanded the potential benefits of higher nut and peanut butter consumption, showing a significantly reduced risk for Type II diabetes among women who regularly include nuts in their diet (Jiang et al. 2002).
Autonomic Balancing: Right Messages, Good Results
The autonomic nervous system, consisting of the parasympathetic (PNS) and the sympathetic divisions (SNS), play major roles in heart function. For example, when the PNS is active, heartbeat, blood pressure, and respiration rate tend to be decreased, as well as the activity of the adrenal glands. Conversely, when the SNS is dominant, the brain alerts the adrenal glands (small organs located on top of the kidneys) to supply adrenaline, the stress hormone. Adrenaline rushes through the bloodstream to all tissues, organs, and glands, heightening their responsiveness. Subsequently, blood pressure, heart rate, blood glucose levels, respiration, and perspiration increase. It is referred to as the "fight or flight" division because a general state of excitement and preparedness is evidenced.
If the individual is healthy, an adrenaline surge is inconsequential. But, if the heart is diseased or damaged, the sympathetic stimuli can be dangerous, even deadly. Type A individuals often live with chronic stimulation of the SNS, a burdening handicap to long-term survival. Note: Interesting data released from the Stanford University School of Medicine showed that insulin-resistant individuals, with compensatory hyperinsulinemia, have a higher nocturnal heart rate, a finding consistent with the possibility that increased heart rates are secondary to insulin-induced sympathetic activity (Facchini et al. 1996b).
Although each of us is born with a propensity toward a sympathetic, parasympathetic, or balanced response from the autonomic nervous system (ANS), Dr. Nicholas Gonzalez (an authority on autonomic balancing) is finding that chemical pollutants and life-style abuses can shift balance and disrupt the natural tendency of the individual. If either division becomes abrasively dominant, the risks imposed upon the heart can be meaningful. For example, if the PNS becomes overly dominant, the risks are as genuine as if the SNS were overexpressed. A heart receiving its instructions from the PNS may become a bit passive, and cardiac output lethargic. Unable to cope with a one-sided response from the ANS, the heart can make fatal errors.
The SNS and PNS are a two-neuron system, meaning that two sets of nerves interconnect in the ganglion. Minerals play an extremely important role in the message sent to organs and glands from the ANS. For example, Dr. Gonzalez explains that magnesium blocks transmission between the two nerves and the ganglion and is regarded as the very best turn-off for sympathetic arousal. On the other hand, calcium arouses activity in the SNS. Potassium, although not a sympathetic toner, acts directly upon the PNS, encouraging increased responsiveness. Exercise quiets the SNS, burning off sympathetic hormones and making stronger parasympathetic expression.
The pH of a parasympathetic dominant tends to be alkaline; the pH of a sympathetic dominant migrates toward acidity. This principle may best explain the benefit some cardiac patients gain when eating a predominantly fruit and vegetable diet, with protein sources limited to smaller amounts of fish and chicken. The alkalinity of a plant-based diet makes the response from the PNS stronger and the activity in the SNS more subdued. Conversely, red meat turns on the SNS and is beneficial to an individual with an overactive parasympathetic response. In fact, Dr. Gonzalez feels a cholesterol level between 210-220 mg/dL is fitting for a parasympathetic because the cholesterol then assumes the nature of a powerful antioxidant.
A cardiac patient should seek counsel with a physician who can determine metabolic type. A physician who can make this determination will also make cohesive choices regarding supplements, diet, and exercise, eliminating conflicting messages being delivered to the heart. Note: Tapes of Dr. Gonzalez's lectures, addressing the ANS in-depth, may be purchased from Conference Recording Service Inc., (800) 647-1110 or at www.conferencerecording.com. Although the lectures focus on treating cancer, the tapes are extremely interesting and informative.
Since overexpression of the adrenergic system (increasing sympathetic activity) can provoke an irregular heartbeat, scientists have searched for drugs that could block its activity. Propranolol became the granddaddy of the family of beta-blockers and is one of the most prescribed drugs in America for arrhythmias, hypertension, and angina pectoris.
Beta-blockers bind to specific receptors on nerve endings in an effort to control blood pressure, anxiety, and arrhythmias occurring before or after a heart attack. The binding process blocks the effects of impulses transmitted by the adrenergic postganglionic fibers of the SNS. As beta-blockers compete with epinephrine (also known as adrenaline) for receptor sites, the excitory nature of epinephrine is curtailed. Beta-adrenergic receptors are located mainly in the heart, lungs, kidneys, and blood vessels (PDR 1999).
Conventional cardiologists conducting propranolol studies reported satisfaction with beta-blockers, citing fewer second heart attacks among users and a 26% reduction in heart mortality. Many patients were less pleased with beta-blockers, describing clinical depression, erectile dysfunction, and fatigue as compromising factors. Also, beta-blockers have been associated with an increased risk of developing diabetes by impairing insulin sensitivity. Newer beta-blocking drugs such as Toprol are now considered superior to Propranolol.
Calcium Channel Blockers
The heart is controlled by tiny electrical impulses that regulate the heart, not unlike a pacemaker. Calcium plays a key role in regulating the heart's response to these electrical signals. It flows between the heart cells and surrounding fluid through a sort of chemical turnstile, or calcium channel. The more calcium that gets through the turnstile before the electrical signal is received, the more strongly the heart contracts, an effort that increases the heart's workload. Calcium channel blockers do not totally block movement through the turnstile, but they significantly slows it down. For some, this process lessens the labor required of a damaged heart, signaling it to slow down and take it easy. Because calcium channel blockers dilate the arteries and reduce resistance to blood flow, they are also widely used to control hypertension. The FDA first approved calcium channel blockers in 1982 for the purpose of treating arrhythmias.
While most of the literature (cautiously) supports calcium channel blockers, a few clinicians adamantly oppose their usage. According to Gabe Mirkin, M.D., calcium channel blockers are classified as short-, intermediate-, and long-acting. Older studies showed that short- and intermediate-acting calcium channel blockers might increase the risk of heart attacks; a more recent study showed that longer-acting calcium channel blockers might as well (Estacio et al. 1998). Patients were followed for 67 months, at which time the Drug and Safety Monitoring Committee detected a significant difference in the rate of heart attacks among patients treated with nisoldipine (a long-acting calcium channel blocker) compared with those treated with enalapril (an ACE inhibitor). The termination of nisoldipine treatment was recommended, and patients receiving nisoldipine were switched to enalapril.
Professor Bruce Psaty (University of Washington) reported that the risk of a heart attack increased up to 60% among 2655 hypertensive patients taking calcium channel blockers (Psaty et al. 1995). In addition, The Lancet reported that calcium channel blockers, often hailed as an ace in cardiac pharmacology, appear to increase the risk of developing cancer (Pahor et al. 1996). Among 5000 men and women enrolled in a verapamil, diltiazem, and nifedipine study, the risk of cancer increased by about 72% (Atkins 1996c).
Other side effects associated with both calcium channel blockers and beta-blockers are congestive heart failure (CHF), lightheadedness, fatigue, low blood pressure, shortness of breath, and bradycardia (heartbeat less than 60 beats a minute). Although not enough studies exist to prove that calcium channel blockers cause heart attacks or increase the risk of cancer, the research is strong enough for doctors to use calcium channel blockers with the utmost caution (Mirkin 2002b).
Dispersed throughout the Therapeutic section are a few of the herbs (containing one or more chemicals) considered beta-adrenergic receptor blockers or calcium antagonists. The literature also supports magnesium as a SNS inhibitor as well as a calcium antagonist (Whitaker 1995b; Duke 2000; Gonzalez 2000). Researchers state that carnitine may provide independent benefit in ischemia when used as monotherapy or additional benefit when used in combination with conventional beta-blockers or calcium antagonists (Jackson 2001). Never should drug therapy be stopped and a nutraceutical started without counsel with a qualified physician.
Calcium blocking activity: Angelica, garlic, ginger, ginkgo biloba, grape seed, green tea (Camellia sinensis), hawthorn, magnesium, and olive leaf
Beta-blocking activity: Grape seed, green tea, hawthorn, and magnesium
Continued . . .
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