cardiology alternatives

Medical guidelines should insists on proof that time-honored medical practices and procedures that cost money and may harm or kill patients are actually effective. This Forum is about how to force organized veterinary medicine to issue Evidence Based Guidelines.

cardiology alternatives

Postby malernee » Wed Nov 23, 2005 6:39 pm ... /index.pdf
Integrating Complementary
Medicine Into Cardiovascular Medicine
A Report of the American College of Cardiology Foundation
Task Force on Clinical Expert Consensus Documents
(Writing Committee to Develop an Expert Consensus
Document on Complementary and Integrative Medicine)
*Former members of Task Force; †Former chair of Task Force
The recommendations set forth in this report are those of the Writing Committee
and do not necessarily reflect the official position of the American College of Cardiology Foundation.
When citing this document, the American College of Cardiology Foundation
would appreciate the following citation format: Vogel JHK, Bolling SF, Costello RB,
Guarneri EM, Krucoff MW, Longhurst JC, Olshansky B, Pelletier KR, Tracy CM,
Vogel RA. Integrating complementary medicine into cardiovascular medicine: a
report of the American College of Cardiology Foundation Task Force on Clinical
Expert Consensus Documents (Writing Committee to Develop an Expert Consensus
Document on Complementary and Integrative Medicine). J Am Coll Cardiol
2005;46:184 –221.
Copies: This document is available on the World Wide Web site of the American College
of Cardiology ( Reprints of this document may be purchased for $10 each by
calling 1-800-253-4636, ext. 694, or by writing to the American College of Cardiology,
Educational Services, 9111 Old Georgetown Road, Bethesda, MD 20814-1699.
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution
of this document are not permitted without the express permission of the
American College of Cardiology Foundation. Please direct requests to:
Journal of the American College of Cardiology Vol. 46, No. 1, 2005
© 2005 by the American College of Cardiology Foundation ISSN 0735-1097/05/$30.00
Published by Elsevier Inc. doi:10.1016/j.jacc.2005.05.031
I. Introduction .......................................................................185
Organization of Committee and Evidence Review ......185
Purpose of This CECD................................................186
II. Nutrition and Supplements ...............................................187
Nutrition ........................................................................187
Bioactive Components in Foods ...................................188
Vitamin and Mineral Supplements ...............................191
Herbal Preparations.......................................................194
Herb-Drug Interactions: What We Need to Know.....196
Related Alternative Therapy .........................................199
III. Mind/Body and Placebo....................................................200
The Mind/Body Relationship and its Correlation
to CVD..........................................................................200
Impact of Stress on CVD Risk Factors........................201
Depression and the Development of CVD ..................202
IV. Acupuncture.......................................................................203
V. Bioenergetics (Energy Medicine) ......................................205
Methods to Study Bioenergy ........................................205
Forms of Bioenergetics..................................................206
VI. Spirituality/Intentionality ..................................................207
Spirituality in Cardiovascular Applications...................207
Compendia ....................................................................208
Review Articles and Meta-Analyses..............................208
Specific Reports of Spirituality and
Cardiovascular Care.......................................................208
Key Issues in Spirituality Applied to
Cardiovascular Care.......................................................209
Delivery Roles, Accreditation, and Certification
Standards .......................................................................210
Summary and General Recommendations....................210
Staff ...........................................................................................210
Appendix I: Relationships With Industry ................................210
Appendix II: Glossary...............................................................210
The following additional appendices are located on www. only:
Appendix III: Internet Sources for Complementary Medicine
Appendix IV: Review of the Literature for Cardiovascular-Related
Integrative Medicine
Appendix V: Dietary Supplement Intake Form
Appendix VI: Books and Compendia on Spirituality in Cardiovascular
Appendix VII: Structured Reviews and Meta-Analyses of Spiritual
Descriptors and Therapies and Their Correlations With
(Noncardiology) Clinical Outcomes
This document was commissioned by the American College
of Cardiology Foundation (ACCF) Task Force on Clinical
Expert Consensus Documents (CECDs) to provide a perspective
on the current state of complementary, alternative,
and integrative medical therapies specifically as they relate
to cardiovascular diseases (CVDs). It is intended to inform
practitioners, payers, and other interested parties of many
evolving areas of clinical practice and/or technologies associated
with this topic that are widely available or new to the
practice community. Topics chosen for coverage by CECD
are so designated because the evidence base and experience
with technology or clinical practice are not considered
sufficiently well developed to be evaluated by the formal
American College of Cardiology/American Heart Association
(ACC/AHA) Practice Guidelines process. Often, the
topic is the subject of considerable ongoing investigation.
The Task Force on CECDs recognizes that considerable
debate exists regarding the clinical utility of alternative
medicine practices. By their nature, alternative medicine
practices differ widely in their scientific support. Despite
this varying evidence base, these practices are widely employed
by patients, including those with CVD. Many
practitioners are not familiar with many alternative medicine
techniques. Thus, the reader should view this CECD
as the best attempt of the ACCF to inform and guide
clinical practice in an area where rigorous evidence is not yet
available or the evidence to date is not widely accepted.
Where feasible, CECDs include indications or contraindications.
The ACC/AHA Practice Guidelines Committee
may subsequently address some topics covered by CECDs.
The Task Force on Clinical Expert Consensus Documents
makes every effort to avoid any actual or potential
conflicts of interest that might arise as a result of an outside
relationship or personal interest of a member of the writing
panel. Specifically, all members of the writing panel are
asked to provide disclosure statements of all such relationships
that might be perceived as real or potential conflicts of
interest. These statements are reviewed by the parent task
force and updated as changes occur. Please see Appendix I
for the relationship with industry information pertinent to
this document.
Robert A. Vogel, MD, FACC
Chair, ACCF Task Force on Clinical Expert
Consensus Documents
Organization of Committee and Evidence Review
The Writing Committee consisted of acknowledged experts
in the field of complementary, alternative, and integrative
medicine. Both the academic and private sectors were
represented. The document was reviewed by five official
reviewers nominated by the ACCF, representatives from
the American Association of Critical Care Nurses, AHA,
American Nurses Association, Preventive Cardiovascular
Nurses Association, and the Society of Thoracic Surgeons,
as well as 20 content reviewers nominated by the Writing
Committee. This document will be considered current until
the Task Force on CECDs revises or withdraws it from
JACC Vol. 46, No. 1, 2005 Vogel et al. 185
July 5, 2005:184–221 ACCF Complementary Medicine Expert Consensus Document
Alternative medical therapies encompass a broad spectrum
of practices and beliefs (1). From a historical standpoint,
they may be defined as, “ . . . practices that are not accepted
as correct, proper, or appropriate or are not in conformity
with the beliefs or standards of the dominant group of
medical practitioners in a society” (2). The Institute of
Medicine (IOM) has recently reviewed complementary and
alternative medical practices in the U.S. from a general
viewpoint (3). This document will focus on cardiac aspects
of complementary medicine. From a functional standpoint,
alternative (also known as “complementary” or “integrative”)
therapies may be defined as interventions neither taught
widely in medical schools nor generally available in hospitals
(4). Ernst et al. (5) contend that “complementary medical
techniques [complement] mainstream medicine by contributing
to a common whole, by satisfying a demand not met
by orthodoxy or by diversifying the conceptual frameworks
of medicine.” The terminology currently in use to describe
these practices remains controversial. Many commonly used
labels (e.g., “alternative,” “unconventional,” or “unproven”)
are judgmental and may inhibit the collaborative inquiry and
discourse necessary to distinguish useful from useless techniques
(6). Complementary and alternative medicine (CAM)
is the language currently used by the National Institutes of
Health (NIH) to describe this field of inquiry. The term
“integrative medicine” has been used with increased frequency.
Several recently published studies and editorials
wrestle with the challenges of properly labeling and describing
this field of inquiry (7–12). Herbs, vitamins, and
non-herbal dietary products, as well as therapies conducted
around issues such as spirituality, bioenergetics (i.e., acupuncture
and energy fields), and mind/body, are all considered
to be forms of complementary, alternative, or integrative
Purpose of This CECD
The purpose of this CECD is to put the emerging area of
CAM treatment and investigation into focus in order to
enable the physician to provide better patient care in a
meaningful and safe manner. The document will be concerned
with the most recent advances and utilization of
CAMs and therapies in a traditional cardiovascular practice.
In 2000, nearly 50% of all Americans sought the help of
an alternative health care practitioner. This represents over
600 million visits (13). Nearly $30 billion was spent in the
year 2001 on CAM (13,14). Many CAM interventions,
including numerous herbal supplements, have been employed
in an attempt to treat CVD. Of prime importance is
putting CAM into perspective with its potential benefits
and knowledge of important interactions with traditional
cardiovascular medicines. In response to an enormous involvement
in CAM, medical facilities have developed specialized
CAM centers to investigate the potential benefits
and integrate those benefits into routine care and lifestyle
The most complete and comprehensive findings to date
on Americans’ use of CAM were released on May 27, 2004,
by the National Center for Complementary and Alternative
Medicine (NCCAM) and the National Center for Health
Statistics (NCHS, part of the Centers for Disease Control
and Prevention) (15). The new data came from a detailed
survey on CAM included for the first time in 2002 in the
National Health Interview Survey (NHIS). The NHIS, a
survey done annually by the NCHS, interviews people in
tens of thousands of American households about their
health- and illness-related experiences.
The findings are yielding (and will continue to yield,
through future analyses) a wealth of information on who
uses CAM, what they use, and why. In addition, researchers
can examine CAM use as it relates to many other factors
such as age, race/ethnicity, place of residence, income,
educational level, marital status, health problems, and the
practice of certain behaviors that impact health (such as
smoking cigarettes or drinking alcohol).
The survey showed that a large percentage of American
adults are using some form of CAM—36% (15). When
prayer specifically for health reasons is included in the
definition of CAM, that figure rises to 62%. Dr. Stephen E.
Straus, NCCAM Director, said, “The survey data will provide
new and more detailed information about CAM use and the
characteristics of people who use CAM. One benefit will be to
help us target NCCAM’s research, training, and outreach
efforts, especially as we plan NCCAM’s second five years, 2005
through 2009.”
There is little doubt that CAM represents a revolution
within our health care delivery system. Nevertheless, our
traditional views of the medical establishment do not fully
support CAM. There is a lack of significant instruction of
CAM in medical schools, there is a paucity of CAM in most
major hospitals, and there is little solid research published in
peer-reviewed journals. Compensation by insurance companies
for CAM is also an issue.
A recent report of the IOM entitled “Complementary
and Alternative Medicine in the U.S.” (3) described and
characterized CAM therapies used by the American public.
Additionally, the IOM sought to identify major scientific
policy and practice issues related to CAM research and to
the translation of validated therapies into conventional
practice. In short, the report recommended that the same
principles and standards of evidence of treatment effectiveness
apply to all treatments, whether currently labeled as
conventional medicine or CAM. Although randomized
controlled trials (RCTs) remain the “gold standard” of
evidence for treatment efficacy, the IOM noted that other
study designs can be used to provide information about the
effectiveness when RCTs cannot be done or may not be
generalizable to CAM practice. Other acceptable clinical
research designs included: preference RCTs (trials that
include both randomized and non-randomized treatment
186 Vogel et al. JACC Vol. 46, No. 1, 2005
ACCF Complementary Medicine Expert Consensus Document July 5, 2005:184–221
arms); observational and cohort studies; case-control studies;
studies of bundles (combinations) of therapies; studies
that specifically incorporate, measure, or account for placebo
or expectation effects; and attribute-treatment interaction
analyses. Prioritization criteria were also proposed to assist
researchers regarding which CAM therapies might warrant
further investigation.
Integrating CAM into medicine must be guided by
compassion, but enhanced by science, and made meaningful
through solid doctor-patient relationships. Most importantly,
CAM involves a commitment to the core mission of
caring for patients on a physical, mental, and spiritual level.
This document attempts to enable us to fulfill these objectives.
A glossary of terms is contained in Appendix II. For
additional information on CAM, please refer to www.acc.
org for Appendix III: Internet Sources for Complementary
Medicine Information and Appendix IV: Review of the
Literature for Cardiovascular-Related Integrative Medicine.
This section provides a discussion of general nutrition and
dietary supplements, including vitamins, minerals, and
herbs that are related to the prevention and reduction of risk
of CVD. Please see Appendix V at for a
sample dietary supplement intake form.
Diet is a major determinant of cardiovascular health. General
nutrition affects body weight, lipoproteins, blood pressure,
blood glucose, endothelial function, inflammation, and
coagulation. Dietary modification is an important component
of primary and secondary prevention of coronary heart
disease (CHD) and hypertension. The essentials of proper
nutrition include appropriate caloric intake and consumption
of the essential macronutrients (carbohydrate, proteins,
and fats) and micronutrients (vitamins, minerals). Specific
nutrients can either accelerate or retard the development of
Obesity. Obesity contributes to CHD, diabetes, and hypertension
(16). Obesity (body mass index [BMI] greater
than 30 kg/m2) increased 50% in this country from 1991 to
1998 (17). Almost one-third of Americans are now obese
and another one-third are overweight (BMI 25 to 30
kg/m2). The major cause of this recent increase in obesity is
a 150 to 200 kcal increase in our daily caloric intake, mainly
from snacks (18). A decrease in physical activity associated
with more television viewing has also contributed. A third
factor has been an increase in sugar consumption, which
now averages 150 lbs per person per year (19). The latter
factor has also contributed to an increased prevalence of type
2 diabetes.
Weight loss is often an important part of the management
of CHD, diabetes, and hypertension (20). Excess
weight increases low-density lipoprotein (LDL) cholesterol,
triglycerides, and markers of inflammation, such as
C-reactive protein; and decreases high-density lipoprotein
(HDL) cholesterol. Even modest weight reduction can
improve these atherogenic markers (20). Weight loss only
occurs when caloric intake is less than caloric expenditure.
The daily caloric requirement for sedentary and physically
active individuals, respectively, is about 12 and 15 kcal per lb
of ideal weight. A 3,500 kcal deficit results in approximately
1 lb of weight loss. On the average, a deficit or excess of 500
calories a day brings about weight loss or gain at the rate of
1 lb a week. Increasing physical activity also results in
weight loss. One mile walked or jogged is equivalent to
about 100 calories burned. The most successful weight loss
programs use calorie restriction, exercise, counseling, and
group support.
Extremely low-carbohydrate or ketotic diets have become
popular for weight loss (21). Some randomized trials have
found that obese individuals lose more weight on lowcarbohydrate
diets than on low-fat diets, although the
difference is not uniformly significant (22,23). The mechanisms
by which extremely low-carbohydrate diets facilitate
weight loss include osmotic diuresis, glycogen and associated
water depletion, anorexia due to ketosis, and exclusion
of foods. Although LDL cholesterol decreases during the
weight loss phase of low-carbohydrate dieting, levels return
to baseline in the long term. Two benefits of extremely
low-carbohydrate diets are a decrease in triglycerides and an
increase in insulin sensitivity. The long-term cardiovascular
effects of low-carbohydrate/high-fat diets are unknown, but
epidemiologic data suggest that they would increase atherosclerosis
Extremely low-fat diets have been used to treat established
coronary artery disease (CAD) (25). One small study
has demonstrated modest CAD regression (26). Extremely
low-fat diets are difficult to apply widely. Low-fat diets are
consistent with the general epidemiologic finding that
atherosclerosis prevalence correlates with saturated fat intake,
and more specifically, with trans fat intake. However,
low-fat diets can increase small LDL particles. These diets
also do not recognize the cardiovascular benefits that can be
derived from omega-3 fatty acids. They also may increase
triglyceride levels and decrease insulin sensitivity.
Macronutrients. Fatty acids can be generally characterized
into saturated, trans, monounsaturated, and polyunsaturated
classes depending on the number and configuration of
double bonds. Saturated and trans fatty acids increase serum
LDL cholesterol and directly impair endothelial function
(27,28). Trans fatty acids also decrease HDL cholesterol
(29). Considerable data suggest an association between
dietary saturated and trans fats and CHD (24). Dietary
cholesterol is also associated with CHD, but elevations in
serum cholesterol are individually variable with dietary
intake. Monounsaturated fatty acids have neutral effects on
serum LDL and HDL cholesterol (30). Polyunsaturated
fatty acids reduce HDL cholesterol, but their use in randomized
trials is associated with decreased cardiovascular
events (27).
JACC Vol. 46, No. 1, 2005 Vogel et al. 187
July 5, 2005:184–221 ACCF Complementary Medicine Expert Consensus Document
Omega-3 fatty acids have three to six double bonds, the
first one occurring between the third and fourth carbon
from the methyl end. The omega-3 fatty acids have
triglyceride-reducing, membrane-stabilizing, antiplatelet,
and anti-inflammatory properties (31). Omega-3 fatty acids
include alpha-linolenic, eicosapentaenoic, and decosahexaenoic
acids. The former is contained in plant oils, whereas
the latter two are contained in fish oils. Prospective randomized
trials have demonstrated that consuming plant and
fish omega-3 fatty acids reduces cardiovascular events,
sudden death, and overall mortality (32).
Carbohydrates include monosaccharides, such as sugars,
oligosaccharides, and polysaccharides or starches. Complex
carbohydrates consist of starches and indigestible fiber.
Fiber adds bulk to food and slows carbohydrate digestion.
Soluble fiber in the form of psyllium, guar gum, and oat
bran reduces serum LDL cholesterol (33). The blood
glucose raising property of a food per 50 g of carbohydrate
and per portion is measured by its glycemic index and load,
respectively (34). High glycemic load foods such as cookies,
rice, and potatoes increase serum triglycerides, decrease
insulin sensitivity, and probably facilitate obesity.
Dietary recommendations. There are two types of dietary
guidelines. The first type recommends specific quantities of
macronutrients, such as less than 200 mg of cholesterol per
day and less than 7% of calories as saturated fat, as in the
AHA Step 2 diet (1). A second type recommends consumption
and exclusion of specific foods, often in combination.
An example is the recommendation to eat stanol/sterol ester
margarines, soy products, soluble fiber, and walnuts or
almonds to lower LDL cholesterol (33,35,36). The latter
specific food portfolio recommendation has been found to
lower LDL cholesterol more (29%) than an AHA Step 2
approach (8%) (37). In general, diets containing unsaturated
fats, whole grains, fruits, vegetables, fish, and moderate
alcohol are optimal for preventing heart disease (38,39). In
October 2000, the AHA revised its dietary guidelines for
Americans (1). The new guidelines retain the principles of
the Step 1 and Step 2 diet but place emphasis on foods and
an overall eating pattern (see the following text) rather than
on percentages of food components such as fat.
The National Cholesterol Education Program (NCEP)
has issued new practice guidelines on the prevention and
management of high cholesterol in adults (40). The Third
Adult Treatment Panel (ATPP III) of the NCEP further
modified its dietary recommendations to include a more
intense and effective eating plan than previously advocated.
The new Therapeutic Lifestyle Changes (TLC) treatment
plan complements that of the AHA guidelines and recommends
less than 7% of calories from saturated fat and less
than 200 mg of dietary cholesterol daily. Total allowed fat
ranges from 25% to 35% of total daily calories provided that
saturated fats and trans fatty acids are kept low. The ATP
III encourages the use of foods that contain plant stanols
and sterols or are rich in soluble fiber, to achieve greater
LDL cholesterol-lowering power.
Mediterranean diet. The prevalence of CVD is considerably
less in Mediterranean and Pacific Rim countries than in
the U.S. at equivalent cholesterol levels (41). Common to
such societies is a diet high in fruits, vegetables, beans,
whole-grain carbohydrates, nuts, fish, and monounsaturated
and polyunsaturated oils. Dairy products are consumed in
low-to-moderate amounts and little red meat is eaten.
Alcohol is consumed in moderation. The Lyon Diet Heart
Study (42,43) tested the effectiveness of a Mediterraneantype
diet, modified by substitution of an alpha-linolenic
acid-enriched canola oil margarine for olive oil, on cardiovascular
risk after a first myocardial infarction. After an
average follow-up of 46 months, subjects following the
modified Mediterranean-style diet had 72% fewer cardiovascular
events and 60% lower all-cause mortality. Findings
from the Lyon Diet Study have been reproduced recently
using an Indo-Mediterranean diet in subjects with CHD
(44). The intervention diet recommending increased consumption
of fruits, vegetables, nuts, whole grains, and
mustard and soybean oils reduced cardiovascular events by
45% and sudden cardiac death by 66%. Additionally, recommendations
to increase fruit, vegetables, and low-fat
dairy product consumption has been found to lower blood
pressure in the Dietary Approaches to Stop Hypertension
(DASH) study (45).
Summary of general nutritional recommendations.
• Achieve and maintain ideal body weight by limiting
foods high in calories and low in nutrient density,
including those high in sugar, such as soft drinks and
• Eat a variety of fruits, vegetables, legumes, nuts, soy
products, low-fat dairy products, and whole grain breads,
cereals, and pastas.
• Eat baked or broiled fish at least twice per week.
• Choose oils and margarines low in saturated and trans fat
and high in omega-3 fat, such as canola, soybean, walnut,
and flaxseed oils, including those fortified with stanols
and sterols.
• Avoid foods high in saturated and trans fats, such as red
meat, whole milk products, and pastries.
• If you drink alcohol, limit consumption to no more than
2 drinks per day for a man or 1 drink per day for a
• Eat less than 6 g of salt or less than 2,400 mg of sodium
per day.
• Be physically active. Get 30 min of exercise daily.
Bioactive Components in Foods
Food components recommended for lowering the risk of
CVD include plant sterols, soluble fiber, omega-3 fatty
acids, nuts, and soy. Additional foods, such as garlic and
teas, and moderate alcohol use will be discussed.
Omega-3 fatty acids. Individual fatty acids have remarkably
diverse effects on coronary risk factors and vascular
biology (41–45). Omega-3 and -6 fatty acids are essential
188 Vogel et al. JACC Vol. 46, No. 1, 2005
ACCF Complementary Medicine Expert Consensus Document July 5, 2005:184–221
nutrients. Dietary fatty acids affect eicosanoid products (e.g.,
thromboxanes, leukotrienes, prostaglandins) responsible for
vasoregulation, inflammation, and coagulation. Omega-3
fatty acids may also affect CHD outcomes by decreasing
triglyceride levels, ventricular arrhythmias, decreasing fibrinogen
levels and platelet counts, modestly reducing blood
pressures, and decreasing cell proliferation. Improvements
in arterial compliance and endothelial function have also
been documented with fish oil, a major supply of dietary
omega-3 fatty acids. There are changes in autonomic tone
(as observed by improvement in heart rate variability measures)
and in mood (depression) (46).
Epidemiologic studies (47–51) have generally shown an
inverse correlation between consumption of fish or other
sources of dietary omega-3 fatty acids and cardiovascular
events. Conversely, other epidemiologic studies (52–55)
have failed to document the benefits of fish consumption.
Good plant sources of the 18 carbon omega-3 fatty acid,
alpha-linolenic acid, include flaxseed, canola, pumpkin seed,
walnut, and soybean oil.
Omega-3 fatty acids have been tested in several secondary
prevention trials. Four prospective, controlled intervention
trials with either oily fish (56) or omega-3 fatty acid capsules
(42,57,58) have demonstrated reduced cardiovascular
events. However, in the DART trial, fish consumption
reduced overall mortality early after myocardial infarction
(MI) (56), but was associated with higher risk over the
subsequent three years of the study (53). The GISSIPrevenzione
study is the largest of the controlled trials
investigating omega-3 fatty acid supplements (1 g per day)
and CHD risk. In this trial, total mortality was reduced by
20% and sudden death by 45% in an intention-to-treat
analysis. Mortality was reduced through a decreased incidence
in sudden death.
Studies published to date are mixed regarding a role for
dietary omega-3 fatty acids in the prevention of restenosis
after percutaneous coronary angioplasty (59–62). They have
not been found to reduce coronary atherosclerosis progression
to a significant extent (58,63). One study demonstrated
that occlusion of aortocoronary venous bypass grafts was
reduced after one year by daily ingestion of 4 g of fish-oil
concentrate (64).
Stanol/sterol esters. Plant sterols or phytosterols have
been known to have a cholesterol-lowering effect since the
1950s. The esterification of plant stanols renders them
soluble in dietary fat, an effective vehicle for delivering plant
stanols and sterols to the site of cholesterol absorption in the
small intestine. Commercially available margarines that provide
3.4 to 5.1 g a day of plant stanol esters can significantly
reduce serum total and LDL cholesterol levels without
affecting HDL cholesterol or triglycerides (65–67). A decrease
in LDL cholesterol levels of 9% to 20% can be
achieved with consumption of approximately 2 g per day of
plant sterol esters (36). In a randomized, eight-week
placebo-controlled trial in 167 subjects, using plant stanol
esters incorporated into an oil-based margarine, there was a
significant reduction in serum total (12%) and LDL (17%)
cholesterol levels in individuals taking a stable dose of a
statin drug (68). No trials have studied the effects of
stanol/sterol esters on cardiovascular risk. Stanol and sterol
esters should be avoided by the rare individual with familiar
Garlic (Allium sativum). Garlic is an herb that has been
used for thousands of years as a food and spice. Garlic
potentially affects plasma lipids, fibrinolytic activity, platelet
aggregation, blood pressure, and blood glucose (69). Various
formulations/preparations of garlic and different study designs
have led to contradictory results. The Agency for
Healthcare Research and Quality (AHRQ) (70) noted on
review of 36 randomized trials modest, short-term effects of
garlic supplementation on lipid and antithrombotic factors.
Various garlic preparations led to small but significant
reductions in total cholesterol at one month and at three
months (range of average pooled reductions 11.6 to 24.3
mg/dl). Eight six-month controlled trials showed no significant
reductions. Effects on clinical outcomes are not established,
and effects on glucose and blood pressure are none to
minimal. A similar meta-analysis conducted by Stevinson et
al. (71) that included 13 randomized, placebo-controlled
trials concluded that the use of garlic for hypercholesterolemia
was of questionable value. Superko and Krauss (72)
demonstrated in a randomized, placebo controlled trial in
hypercholesterolemic subjects that garlic has no effect on
major plasma lipoproteins and that it does not impact HDL
subclasses, Lp(a), apolipoprotein B, postprandial triglycerides,
or LDL subclass distribution.
Soy. Soy-based foods have cholesterol-lowering, estrogenic,
and antioxidant properties. The mechanism underlying
the cholesterol-lowering effect of soy is likely multifactorial.
Soy-based foods reduce lipid oxidation, promote
increased vascular reactivity, and improve arterial compliance
(73). Favorable effects of soy phytoestrogens on lipid
profiles, vascular reactivity, thrombosis, and cellular proliferation
have been reported (74). Dietary intake of foods
containing phytoestrogens is associated with a favorable
cardiovascular risk profile as was demonstrated in 939
postmenopausal women participating in the Framingham
Off-Spring Study (75). The consumption of soy protein can
improve lipid profiles in hypercholesterolemic individuals
above a background NCEP Step I diet. Soy decreases LDL
cholesterol more in hypercholesterolemic individuals. Soy
supplementation may also increase the levels of HDL
cholesterol regardless of whether an individual is hypercholesterolemic
or not. A meta-analysis of 38 trials of soy
protein demonstrated reductions in total cholesterol of
9.3%, LDL cholesterol of 12.9%, and triglyceride levels of
10.5%, accompanied by an increase of 2.5% in HDL
cholesterol (76). However, more recent studies in postmenopausal
women fail to show improvements in plasma
lipids (77). A recent placebo-controlled study in 108 men
and 105 postmenopausal women randomized to either soy
protein isolate or casein placebo for three months demon-
JACC Vol. 46, No. 1, 2005 Vogel et al. 189
July 5, 2005:184–221 ACCF Complementary Medicine Expert Consensus Document
strated an increase in levels of Lp(a) on soy supplementation
with no improvement in indices of arterial function (78).
Extracts of soy isoflavones given to human subjects do not
result in cardiovascular benefits except for improvements in
systemic arterial compliance (79).
The clinical benefit of isoflavones is unclear. In light of
the recent findings about estrogen from the Women’s
Health Initiative, the U.S. Preventive Services Task Force
has stated that the evidence is inconclusive to determine
whether phytoestrogens, such as soy isoflavones, are effective
for reducing the risk of CVD (80).
Soluble fiber. Soluble or viscous fibers, such as oat bran,
psyllium, guar, and pectin, are thought to reduce heart disease
by lowering total and LDL cholesterol levels without affecting
serum triglycerides. Conversely, insoluble wheat fiber and
cellulose have no cholesterol-lowering effects unless used in the
diet to replace foods supplying saturated fats or cholesterol
(81). Increasing dietary fiber has been recommended as a safe
and practical approach to cholesterol reduction. Large epidemiologic
studies (82–84) have demonstrated a reduced risk for
MIs and death from CHD in both men and women who
consume higher amounts of dietary fiber. These studies provide
strong support linking dietary fiber intake to protection
from CHD. These data are supported by numerous ecological,
cohort, case-comparison, population-based, and, most recently,
clinical trials demonstrating an inverse relationship
between dietary fiber consumption and atherosclerotic CVD
The hypocholesterolemic effects of psyllium (86), guar
gum (87), and oat bran (88) are documented by metaanalyses
(89). A meta-analysis of 67 controlled trials studying
the cholesterol lowering effect of four types of soluble
fiber (oat, psyllium, pectin, and guar gum) reported small but
significant reductions in total cholesterol (1.7 mg/dl per g
soluble fiber) and LDL (cholesterol (1.9 mg/dl per g soluble
fiber) (81). Hypercholesterolemic subjects with initially
higher cholesterol levels experienced the most significant
reductions. Triglycerides and HDL cholesterol were not
significantly influenced by soluble fiber. The magnitude of
lipid lowering was found to be similar for oat, psyllium, or
pectin-based fibers.
Because of the favorable effect of soluble fiber on LDL
cholesterol levels, the ATP III panel recommends that the
diet be enriched by foods that provide a total of at least 5 to
10 g of soluble fiber daily (90). Dietary fiber also reduces
blood pressure, obesity, insulin resistance, and clotting
factors—all independent risk factors for CHD (85).
Nuts. The few studies that have looked at the consumption
of whole nuts in relation to CHD have reported a consistent
and substantial protective effect. Three of the largest nutritional
epidemiologic prospective studies evaluating multiple
population groups, ages, races, and gender have found a
consistent inverse relationship between nut consumption
and coronary risk (91–93).
The improvement in serum lipids associated with the
consumption of nuts does not explain the magnitude of the
CHD risk reduction of approximately 40% to 50% found in
the epidemiologic studies. Nuts, especially walnuts and
almonds, are high in arginine, magnesium, folate, plant
sterols, and soluble fiber. Some nuts contain high levels of
omega-3 essential fatty acids (e.g., walnuts), and they are an
excellent source of vitamin E. In a prospective study of
86,016 women between the ages of 34 to 59 years, without
previously diagnosed CHD, eating 5 oz of nuts per week
was associated with a relative risk (RR) of 0.66 (95%
confidence interval [CI] 0.47 to 0.93, p for trend  0.005)
of coronary events adjusted for risk factors and independent
of fiber, fruit, and vegetable supplements (92). Recent
prospective data from the Physicians’ Health Study demonstrated
consumption of nuts two or more times a week
significantly reduced the risk of sudden cardiac death (RR)
of 0.53 (95% CI 0.30 to 092, p for trend  0.01) and a RR
of 0.70 (95% CI 0.50 to 0.98, p for trend  0.06) for total
CHD deaths compared with men who rarely or never
consumed nuts (93). The association between nut consumption
and sudden cardiac death became stronger after adjustment
for lifestyle, cardiac risk factors, and diet. Like some
nuts, canola oil and flaxseed oil are the richest known source
of alpha-linolenic acid, an omega-3 fatty acid.
Tea. Tea drinking appears to be protective against CHD in
a number of epidemiologic studies (94–97). In the older
cohort of the Rotterdam Study, an inverse association was
demonstrated between tea drinking and advanced aortic
atherosclerosis (98). Data from a more recent follow-up of
the Rotterdam Study highlighted a strong inverse relation
between tea intake (greater than 375 ml/day) and MI with
the relation being stronger in women than in men. The
inverse association with tea drinking was stronger for fatal
events than for nonfatal events. For flavonoid (quercetin 
kaempferol  myricetin) intake, a strong association with
MI was observed only in women (99). Results are inconclusive
for clinical and case control studies. However, a
recent prospective cohort study of 1,900 patients hospitalized
with an acute MI followed for 3.8 years found a
significantly reduced hazard ratio for subsequent total and
cardiovascular mortality of 0.56 (95% CI 0.37 to 0.84) for
heavy tea drinkers (more than 14 cups/week) compared to
non-tea drinkers (100). A recent clinical study has shown
that consumption of black tea improves brachial artery
flow-mediated dilation in patients with CAD (101). Despite
the favorable epidemiology and mechanistic investigations,
no studies have prospectively documented a reduction
in cardiovascular risk with tea drinking.
Alcohol. Epidemiologic studies have shown that the incidence
of MI, angina pectoris, and coronary-related deaths
are inversely related to moderate alcohol intake, as defined
by 1 to 3 drinks daily. Although many mechanisms for this
effect have been suggested, the best documented effect is an
increase in HDL cholesterol by alcohol (102). Recent
studies have shown that moderate drinkers are less likely to
suffer ischemic stroke (103,104), peripheral vascular disease
(105), and death following an acute MI (106). Cooper et al.
190 Vogel et al. JACC Vol. 46, No. 1, 2005
ACCF Complementary Medicine Expert Consensus Document July 5, 2005:184–221
(107) found that light-to-moderate drinkers with left ventricular
systolic dysfunction had fewer adverse outcomes. In
the Framingham Heart Study, Walsh et al. (108) found that
the incidence of congestive heart failure was lower in
subjects who consumed moderate amounts of alcohol.
Abramson et al. (109) were able to demonstrate that
subjects who consumed moderate levels of alcohol had a
significantly lower risk of developing heart failure.
Moderate consumption of alcohol-containing beverages
does not appear to result in significant morbidity; however,
heavy alcohol consumption can result in cardiomyopathy,
hypertension, hemorrhagic stroke, cardiac arrhythmia, and
sudden death. Alcohol ingestion poses such a number of
health hazards with irresponsible consumption that the
AHA recommends that physicians and patients discuss the
adverse and potentially beneficial aspects of moderate drinking
Overview of dietary supplements. The Dietary Supplement
Health and Education Act (DSHEA) of 1994 defined
dietary supplements as a product (other than tobacco)
intended to supplement the diet for such ingredients as
vitamins, minerals, herbs, or other botanicals, amino acids,
and substances such as enzymes, organ tissues, glandulars,
and metabolites. Whatever their form, the DSHEA places
dietary supplements in a special category under the general
umbrella of “foods,” not drugs, and requires that every
supplement be labeled a dietary supplement. The establishment
of dietary supplements as foods limited the Food and
Drug Administration (FDA)’s premarketing regulatory authority
and placed the FDA in a reactive, postmarketing
role. Thus, for the FDA to remove a supplement from the
market it most prove that the supplement presents a
significant or unreasonable risk of injury or illness when
used as recommended on the label. Recently, the IOM has
urged that the U.S. Congress and federal agencies, in
conjunction with industry, research scientists, consumers,
and other stakeholders, amend DSHEA and the current
regulatory practices for dietary supplements in an effort to
improve product consistency and reliability (IOM, 2005).
Just prior to the release of the IOM report on Complementary
and Alternative Medicine in the U.S., the FDA
announced three major regulatory initiatives designed to
further implement DSHEA (
lrd/fr04119a.html, docket no. 2004N-0458). These initiatives
serve to inform the dietary supplement industry on a
regulatory strategy involving the monitoring and evaluation
of product and ingredient safety, assurance of product
quality via good manufacturing practice (CGMP regulations),
and monitoring and evaluation of product labeling.
At the same time these new initiatives will give consumers
a higher level of assurance about the safety of dietary
supplement products and the reliability of their labeling.
Vitamin and Mineral Supplements
Antioxidant vitamins. Antioxidant therapies are potentially
useful in preventing both atherosclerosis and its
complications by retarding LDL oxidation and by inhibiting
the proliferation of smooth muscle cells, platelet adhesion
and aggregations, the expression and function of adhesion
molecules, and the synthesis of leukotrienes (110). Antioxidants
may improve endothelial function, reduce ischemia,
and stabilize atherosclerotic plaques to prevent plaque
rupture (110).
VITAMIN E. Primary Prevention Trials. A potential benefit
of vitamin E in CHD is suggested by two large prospective
epidemiologic trials, which found lower event rates in
subjects who took at least 100 units of vitamin E per day
(111,112). However, 50 mg of vitamin E in the Alpha-
Tocopherol, Beta-Carotene (ATBC) cancer prevention trial
of male smokers did not decrease nonfatal MIs, and
increased hemorrhagic stroke (113,114). Vitamin E use was
not associated with decreased stroke in the Health Professionals
Follow-Up Study (115), the Nurses Health Study
(112), and the Iowa Women’s Health Study (116). Most
recently, the Collaborative Group of the Primary Prevention
Project (PPP) found no decrease in cardiovascular events in
4,495 subjects with one or more risk factors after 3.6 years
of synthetic vitamin E (300 units) therapy compared to
none (117). These data have been confirmed by a recent
pooled analysis of nine cohort studies (Pooling Project of
Cohort Studies on Diet and Coronary Disease) in 293,172
subjects free of CHD. A lower CHD risk at higher intake
of dietary vitamin E was present when adjusted for age and
energy intake. However, supplemental vitamin E intake was
found not to be significantly related to a reduced risk of
CHD (118).
Secondary Prevention Trials. Only one of several controlled
trials of vitamin E has shown a reduction in some
aspect of cardiovascular risk. In the Cambridge Heart
Antioxidant Study (CHAOS) (119) vitamin E reduced the
risk of nonfatal MI, but not of fatal MI. The Heart
Outcomes Prevention Evaluation (HOPE) study found no
effect of vitamin E for several of primary and secondary
CVD end points, including disease progression monitored
by carotid ultrasound (120). The GISSI-Prevenzione trial
(42) failed to show benefit from vitamin E supplementation
on CHD or stroke in almost 8,000 patients. The Vitamin E
Atherosclerosis Prevention Study (VEAPS) provided additional
evidence that vitamin E supplementation (400 units)
did not reduce the progression of atherosclerosis as evaluated
by change in intimal medial thickness (121). A metaanalysis
of seven randomized trials of vitamin E (50 units to
800 units) in 81,788 patients confirmed that vitamin E did
not reduce mortality, decrease cardiovascular death, or
cerebrovascular accident (122). A more recent and larger
(135,967 participants in 19 clinical trials) meta-analysis that
considered the dose dependent effects of vitamin E supplementation
noted that at high dosage (400 units/day or
more) a pooled risk difference of 34 per 10,000 persons
(95% CI 5 to 63 per 10,000 persons, p  0.022). However,
it is unclear whether the investigators isolated the effects of
JACC Vol. 46, No. 1, 2005 Vogel et al. 191
July 5, 2005:184–221 ACCF Complementary Medicine Expert Consensus Document
vitamin E from those of other supplements. Most of the
evidence for an elevated mortality risk came from two trials
that administered vitamin E together with beta-carotene. It
is uncertain whether an increased risk for death from
high-dose vitamin E based on this most recent analysis of
RCTs exists (123).
VITAMIN C. Primary Prevention. When examined individually,
most observational and prospective cohort studies do
not demonstrate a relationship between vitamin C intake
and CVD (124,125) and there have been no RCTs specifically
examining the effects of vitamin C supplementation
on cardiovascular end points (115,126). In the Iowa Women’s
Health Study, women in the top quintile of vitamin C
intake versus the lowest quintile had a nonsignificant
increased risk for CHD mortality and a borderline significant
trend toward increased stroke (127). Long-term use of
vitamin C in a large prospective investigation was not
associated with a reduced risk of stroke, as well (115).
However, a more recent analysis from the Nurses’ Health
Study indicates that women in the highest quintile of intake
for vitamin C (greater than 360 mg per day from diet and
supplements) compared with the lowest quintile (less than
or equal to 93 mg per day), had a 27% lower risk for CHD,
and women taking supplemental vitamin C had a 28% lower
risk of nonfatal MI and fatal CHD compared with women
who took no vitamin C (128). In the recent pooled analysis
from the Pooling Project of Cohort Studies on Diet and
Coronary Disease (118), those subjects with higher supplemental
vitamin C intake (greater than 700 mg/day) had a
25% reduced risk of CHD. Nevertheless, the current consensus
does not find a value for supplemental vitamin C in
preventing heart disease (129).
BETA-CAROTENE. Trials of beta-carotene have demonstrated
no cardiovascular benefit, and one demonstrated an
adverse clinical outcome. An increased incidence of lung
cancer and CVD mortality were observed in the ATBC
cancer prevention study (130). Beta-carotene supplementation
was also associated with a slight increase in the
frequency of angina pectoris (131). A meta-analysis of eight
trials evaluating beta-carotene in 138,113 patients revealed a
small but significant increase in all-cause mortality and
cardiovascular death (128). Thus, beta-carotene supplementation
is discouraged (1).
Combination Vitamin Trials. The Heart Protection Study
(HPS) randomized 20,536 subjects at high risk for CHD to
40 mg simvastatin daily or placebo and vitamin E (600 mg),
vitamin C (250 mg), and beta-carotene (20 mg) or placebo.
After 5.5 years of study, no benefit from combination
vitamin therapy was evident (132). A small RCT, the HDL
Cholesterol Atherosclerosis Treatment Study (HATS),
found that vitamin C (1 g), vitamin E (800 units), betacarotene
(50 mg), and selenium (100 mcg) reduced the
benefit of simvastatin plus niacin therapy on CAD progression
and cardiovascular events (133) suggesting a potential
drug/supplement interaction affecting the efficacy of statin
therapies. Lack of benefit for combination vitamin E (400
units) and vitamin C (500 mg) was also documented in 423
postmenopausal women with CAD participating in the
Women’s Angiographic Vitamin and Estrogen (WAVE)
trial (134).
In contrast to the aforementioned negative trials, the
Antioxidant Supplementation in Atherosclerosis Prevention
(ASAP) study of 440 hypercholesterolemic patients randomized
to vitamins E and C, reported that combination
therapy decreased the rate of atherosclerosis progression
(especially in men) over a six-year period as measured by
carotid artery intima-media thickness. This study selected
subjects with high oxidative stress and maximized absorption
of the antioxidants by giving them with meals (135).
In summary, aside from the recent pooled analysis of
vitamin C cohort studies, the consensus of antioxidant
vitamin study results do not support a cardiovascular benefit
related to the use of vitamins E and C and beta-carotene
FOLIC ACID, VITAMIN B6, AND VITAMIN B12. Elevated homocysteine
levels are associated with increased risk of coronary
artery and vascular disease. The mechanisms by which
elevated homocysteine impairs vascular function are not
completely understood, but may involve the stimulation of
vascular smooth muscle cell growth and collagen synthesis,
oxidative-endothelial injury and dysfunction, lipid peroxidation
and platelet activation, and hypercoagulability (136).
Intakes of folate, vitamins B6, and B12 are inversely related
to homocysteine levels as all three vitamins are directly
involved in the metabolism of homocysteine. Beginning in
1996 and mandatory in 1998, the FDA issued a regulation
requiring all enriched grain products be fortified with folic
acid (140 mcg/100 g serving portion), primarily for the
reduction of congenital neural tube defects. The fortification
of enriched grain product with folic acid has been associated
with an improvement in the folate status of middle-aged
and older adults (137). In the Framingham Offspring Study
cohort, mean homocysteine levels decreased from 10.1 to
9.4 mol/l with the introduction of fortified products (138).
Initial retrospective case-control studies (139–141) and
prospective studies (142–147) suggested an inverse relationship
between homocysteine and CVD. A recent metaanalysis,
combining 30 prospective and retrospective studies,
concluded that elevated homocysteine is less strongly related
to ischemic heart disease and stroke risk in healthy populations
than has been suggested (148). A meta-analysis of 14
prospective cohort studies, using the inclusion criterion of
time to first cardiac or cerebrovascular event, found that
elevated homocysteine levels moderately increased the risk
of a first cardiovascular event, regardless of age and duration
of follow-up (149).
In secondary prevention studies, two nonrandomized
trials in patients with vascular disease found an inverse
relationship between the intake of folic acid and vitamin B6
and vascular events (150). One study conducted in open-
192 Vogel et al. JACC Vol. 46, No. 1, 2005
ACCF Complementary Medicine Expert Consensus Document July 5, 2005:184–221
label fashion in 593 patients with coronary artery disease on
statin therapy showed no benefit of folic acid in reducing
cardiovascular events despite an 18% lowering in homocysteine
levels (151–153).
Most recently, a trial of folic acid (1 mg), vitamin B12
(400 units), and pyridoxine (B6) (10 mg) found a significantly
reduced homocysteine levels, rate of restenosis, and
need for revascularization in a group of 553 CAD patients
at one year of follow-up (151,152). A similar RCT of 626
patients treated with B-vitamin therapy following coronary
stenting procedures, however, found increased rates of
restenosis, particularly in patients receiving bare-metal
stents and major adverse cardiac events in the vitamin
treated group after one year of follow-up. The rate of
restenosis in the homocysteine-lowering group was 35%
compared with 27% in the group receiving placebo (154).
Although striking differences exist between the study populations,
it raises the potential of possible harm from use of
high-dose B-vitamins. Strong evidence for a benefit for B
vitamins in CVD is pending; there remain a number of
ongoing trials, including WACS, SEARCH, PACIFIC,
NORVIT, and CHAOS-2 (155).
Minerals. MAGNESIUM. Magnesium metabolism is involved
in insulin sensitivity and blood pressure regulation,
and magnesium deficiency is common in both diabetes and
hypertension. The links among magnesium, diabetes, and
hypertension suggest the possibility that magnesium can
affect CVD (156,157). Magnesium depletion is associated
with electrocardiographic changes, arrhythmias, and increased
sensitivity to cardiac glycosides (158). Epidemiologic
studies have suggested that ingesting hard water that
contains magnesium, consuming a diet higher in magnesium,
or using magnesium supplements decreases CVD
(159). The Honolulu Heart Program found a 1.7- to
2.1-fold excess risk of CHD among those subjects in the
lowest versus highest quintile of magnesium intake after 15
years of follow-up (160). Similarly, epidemiologic evidence
suggests that magnesium may play a role in regulating blood
pressure (161–165). A recent meta-analysis of 20 randomized
studies including both normotensive and hypertensive
subjects detected a dose-dependent blood pressure reduction
with magnesium supplementation (166). The DASH
intervention study demonstrated that a diet of fruits and
vegetables, which increased magnesium intake from an
average of 176 to 423 mg per day, significantly lowered
blood pressure in adults who were not classified as hypertensive
(167). However, studies in hypertensive patients
have led to conflicting results. Ascherio et al. (168) found an
inverse correlation between the intake of magnesium and
the risk of stroke.
Magnesium intake has been found to be inversely associated
with carotid artery thickness in women but not in
men (163). Oral magnesium therapy (365 mg twice daily for
6 months) in 187 patients with CAD demonstrated a 14%
improvement in exercise duration combined with a decrease
in exercise-induced chest pain compared to no change in the
placebo group (169). In patients with congestive heart
failure (CHF), a population at high risk for magnesium
deficiency, oral magnesium replacement decreases the frequency
of ventricular arrhythmias (170).
Dietary intakes of magnesium are suboptimal in the U.S.
as evidenced by recent NHANES survey intake data (171).
Diets rich in magnesium and magnesium supplementation
may be helpful in preventing CVD, especially hypertension.
Other bioactive supplements. COENZYME Q10. Coenzyme
Q10 (CoQ10) is involved in oxidative phosphorylation and
the generation of adenosine triphosphate (ATP). The
CoQ10 acts as a free radical scavenger and membrane
stabilizer. There have been over 40 controlled trials of the
clinical effect of CoQ10 on CVD, a majority of which show
benefit in subjective (quality of life, decrease in hospitalizations)
and objective (increased left ventricular ejection fraction,
stroke index) parameters. A recent review (172) and
meta-analysis (173) have shown benefit of CoQ10 as
adjunctive treatment in patients with CHF. The largest trial
to date was a one-year, placebo-controlled study of CoQ10
in 651 New York Heart Association (NYHA) functional
class III or IV CHF patients (174). These investigators
found a significant decrease (38% to 61%) in the number of
hospitalizations, incidences of pulmonary edema, and episodes
of cardiac asthma. No differences in death rates were
documented. However, two of the most recent placebocontrolled
trials found that the addition of 100 to 200
mg/day of oral CoQ10 to conventional medical therapy did
not result in significant improvement in left ventricular
ejection fraction, peak oxygen consumption, exercise performance,
or quality of life in patients with advanced heart
failure (175,176).
A mortality benefit for CoQ10 has not been established
in contrast to angiotensin-converting enzyme inhibitors,
beta-blockers, and aldosterone antagonists. Case reports
associate CoQ10 therapy with decreased internation normalized
ratio (INR) in patients taking warfarin (177);
however, CoQ10 had no effect on the INR in patients on
warfarin in a randomized, double-blind, placebo-controlled,
crossover trial (178). Caution is advised if patients are taking
CoQ10 and warfarin. The HMG-CoA reductase inhibitors
may inhibit the natural synthesis of CoQ10, and reduced
levels of CoQ10 have been documented in small controlled
clinical trials in patients on statin therapies (179). Reduced
levels of CoQ10 may place the patient at increased risk for
myopathy (180–183); however, studies of CoQ10 for decreasing
myalgias and myositis are not definitive. One
unique formulation of CoQ10 has received FDA Orphan
Drug status for treating mitochondrial disorders. The value
of CoQ10 in CVD and with statin use has not been clearly
L-CARNITINE. In 1986, the FDA-approved L-carnitine for
use in primary carnitine deficiency, which manifests as a
disruption in the transport of free fatty acids across the
mitochondrial membrane for energy production. In myo-
JACC Vol. 46, No. 1, 2005 Vogel et al. 193
July 5, 2005:184–221 ACCF Complementary Medicine Expert Consensus Document
pathic carnitine deficiency, muscle weakness is paramount
(184). Convincing evidence is lacking for the use of carnitine
in patients without carnitine deficiency undergoing
cardiac surgery, in patients with angina pectoris, acute
myocardial infarction, shock, and peripheral vascular disease
(185). Urinary carnitine excretion is known to be increased
in patients with heart failure (186). Several clinical RCTs
have evaluated the addition of L-carnitine to standard
medial therapy for heart failure with mixed results (187–
189). Significant improvements in maximum exercise times
and ejection fractions were reported by Mancini et al. (190)
in 60 patients with NYHA functional class II or III CHF
who were randomized either to propionyl-L-carnitine (50
mg t.i.d.) or placebo for 180 days. Two other small trials
reported similar results, and one trial showed improvement
at a higher dose. In a double-blind randomized trial in 155
patients with claudication, a significant improvement in
exercise treadmill performance (54% increased walking
time) and functional status was achieved with oral
propionyl-L-carnitine 2 g/day for 6 months (191). Differences
in effect may be due to the dose and formulation of
carnitine. In contrast, the investigators of the Study on
Propionyl-L-Carnitine in Chronic Heart Failure did not
show improved exercise tolerance on L-carnitine supplementation
At present, it is unclear whether L-carnitine provides any
benefit beyond well-established therapies. A more definitive
answer will come from the Carnitine Ecocardiografia Digitalizzata
Infarto Miocardico (CEDIM-2) trial, which will
assess the efficacy of L-carnitine in approximately 4,000
patients with acute MI over six months (192). Supplements
containing D- or DL-carnitine, often present in over the
counter preparations and dietary supplements, should not be
substituted for L-carnitine. Carnitine frequently causes
nausea, pyrosis, dyspepsia, and diarrhea. Concomitant use
of carnitine with warfarin may potentiate warfarin’s anticoagulant
L-ARGININE. L-arginine is the precursor of nitric oxide
(NO) and has been shown to improve coronary and brachial
artery endothelial function and reduce monocyte/
endothelial cell adhesion (193–195). In patients with recurrent
chest pain, improvements in coronary blood flow in
response to acetylcholine have also been documented. In
hypercholesterolemic subjects, dietary supplementation with
L-arginine over two weeks has been shown to normalize the
adhesiveness of mononuclear cells (196) and reduce platelet
aggregability (197). However, in a study in 30 patients with
CAD, supplemental L-arginine did not affect measures of
NO bioactivity and NO-regulated markers of inflammation
There are a few documented reports of adverse effects
from oral use of L-arginine. Several patients with hepatic
impairment and a recent history of spironolactone use were
reported to develop severe hyperkalemia upon initiation or
arginine hydrochloride for management of metabolic alkalosis
(199). Oral L-arginine appears to have potential
benefit in CHD, but hard evidence for its value is currently
not available.
Herbal Preparations
In the U.S. today, herbs may be marketed as dietary
supplements providing their intended use is not to diagnose,
treat, cure, or prevent disease. A number of approved drug
substances have their origin in plants, such as digoxin,
atropine, reserpine, and amiodarone. However, only a few
herbal products available in the U.S. have been tested for
cardiovascular purposes: hawthorn (heart failure and coronary
insufficiency), garlic (atherosclerosis), ginkgo (arterial
occlusive disease), and horse chestnut (chronic venous
insufficiency) (200). Few U.S. products benefit from rigorous
characterization and standardization necessary for clinical
Hawthorn (Crataegus). Hawthorn has positive inotropic
effects and is a peripheral vasodilator. It increases myocardial
perfusion and stroke volume and reduces afterload.
Antiarrhythmic effects have been reported in an ischemiareperfusion
model. Orally, hawthorn leaf extract has been
used for CHF, cor pulmonale, ischemic heart disease,
arrhythmias, blood pressure reduction, atherosclerosis, and
cerebral insufficiency (200). Preparations made from flowers
with leaves are sold as a prescription medication in parts of
Europe and Asia. For example, in Germany, hawthorn can
be prescribed for “mild cardiac insufficiency.”
Several double-blind clinical studies of patients diagnosed
with heart failure have shown objective improvement in
cardiac performance using bicycle ergometry (201,202) or
spiroergometry. In one study, hawthorn was found to be as
effective as captopril in improving exercise tolerance. Based
on ergometric performance parameters, the minimum effective
daily dose of hawthorn extract is 300 mg. In most
trials, the maximum benefit was seen after 6 to 8 weeks of
therapy. Weikl et al. (203) demonstrated an improvement in
exercise performance in 136 stage II CHF subjects receiving
160 mg hawthorn special extract WS 1442 (leaves and
flowers). The efficacy and safety of hawthorn extract WS
1442 (900 and 1,800 mg) were evaluated in a 16-week
randomized, controlled trial in 209 patients with NYHA
functional class III heart failure. The investigators found a
dose-dependent effect of WS 1442 on enhanci
Site Admin
Posts: 462
Joined: Wed Aug 13, 2003 5:56 pm

Cardiovascular Medicine alternatives review

Postby guest » Thu Nov 24, 2005 5:58 am

Consensus Document on "Integrating Complementary Medicine into
Cardiovascular Medicine." ... ... /index.pdf

Some of us reviewed parts of this document a few months ago. It is standard
altmed pap, of limited descriptive power because of "evidence-based" limits
(to clinical trials), biased, and typically naive. Most objections have to do
with the rather subtle problems of language, selection of references, and the
more obvious bias of the committee makeup.

t least three of the authors are frank altmed practitioners/advocates
(Krucoff/spirituality-Duke, Pelletier/altmed everything-UCSF-Stanford;
Longhurst/acupuncture-UCIrvine.) Several others have published in altmed and have grants
(Guarnieri?) Note that no one from the skeptical community was on the
committees. They know who the skeptics are. In this respect, the committee
resembles the Inst. of Medicine committee and White House Commission.

In addition to Tom Wleeler's findings, the language used is from the
postmodern "non-judgmental" assumption. Methods such as applied kinesiology need
more than "lack of evidence" for efficacy. Its practitioners know full well what
science thinks of it and published trial show it to be ineffective. Why do
they not say so?

References include one TT trial by Daniel Wirth, now serving 5 years in
Federal pen. for fraud, and who wrote the infamous, fraudulent Cha/Wirth prayer
study on distant effects on IVF; Eisenberg's discredited surveys. I did not
review every reference, but found none from quackwatch or reference to
commentary by skeptics.

Although the recommendations of most methods were duly cautious, the report
understates the evidence against the methods, omits comment on their
plausibility - near zero in most cases - and submits to the false criterion of use of
nonjudgmental words and language - admitted in the first pages.


Return to evidence based vet guidelines

Who is online

Users browsing this forum: No registered users and 1 guest