Horse chestnut

Latin name: Aesculus hippocastanum L. [Hippocastanaceae]
Plant part: Seed



Native to the Near East, the horse chestnut tree was brought to
northern Europe in the sixteenth century. As early as the 1800s, horse
chestnut seed extracts were used therapeutically in France. Although
preparations of other parts of the tree have been used medicinally,
only the efficacy of the dried seeds has been proven. Powdered dried
seeds contain 3 to 5 percent saponins, and powdered hydroalcoholic
extracts of the seeds contain 16 to 20 percent triterpene glycosides (a
class of saponins), calculated as aescin (escin). Aescin, itself a mixture
of several glycosides derived from two triterpenoid aglycones, is
believed to be the main active constituent of horse chestnut seed extract
(Schulz, Hänsel, and Tyler, 2001).

Horse chestnut has been used traditionally as an herbal remedy for
chronic venous insufficiency, and numerous clinical trials support
that use. Chronic venous insufficiency (CVI) is characterized by
chronic inadequate drainage of venous blood and venous hypertension,
which results in leg edema, dermatosclerosis (hardening of the
skin), and feelings of pain, fatigue, and tenseness in the lower extremities.
As a result, patients often require hospitalization and surgery,
for instance, for symptomatic varicose veins. Pharmacological therapies
and/or leg compression with specialized stockings or surgery are
the treatment options (Pittler and Ernst, 2002).

CVI is divided into three stages according to the degree of severity.
The symptoms of Grade I, according toWidmer and Marshall, are dilation
of the veins of the feet and a tendency for edema. Grade II is defined
by additional symptoms, including pigmentation of the skin,
hypertrophy of the skin corneal layer, and hardening of the skin.
Grade III is characterized by leg ulcers, either healed (IIIa) or unhealed
(IIIb). In the early stages of CVI (Grade I), the veins have not
suffered any permanent damage, and pharmacological therapy may
reduce the leakage of fluid from the veins. At the later stages of CVI
(Grades II and III), the disease process involves the larger veins, and
ultimately the damage to the veins is irreversible (Ottillinger and
Greeske, 2001). Studies reviewed here included patients with CVI
Grades I or II. One study, on a generic product, included patients with
CVI Grade II according to Hach. Although we found no information
on this scale the description of symptoms were similar to Grade II according
toWidmer and Marshall. They were obstructive edema, possible
tropic skin changes, and venous capacity and/or venous return
outside normal limits (Diehm et al, 1992).

 Chronic Venous Insufficiency

Venaforce was reported to statistically reduce ankle edema, but not
subjective symptoms of heaviness, pain, burning, itching, or pins and
needles in the legs. This placebo-controlled study included 52 subjects
with CVI Grades I or II. Treatment consisted of six tablets, containing
120 mg aescin, per day for six weeks (Shah, Bommer, and
Degenring, 1997).


 Chronic Venous Insufficiency

A well-conducted, placebo-controlled trial with 39 patients with
CVI (Stage II according to Hach) reported a statistical reduction in
mean leg volume after six weeks of treatment, both before and after
edema provocation, compared to placebo. Treatment was an unbranded
extract delivering 150 mg aescin per day (Diehm et al., 1992).


 Hematoma

Escin gel containing 2 percent aescin was compared to placebo in
an experimentally induced hematoma model. Hematomas are swellings
filled with blood that can form as the result of physical trauma to
the body, causing damage to blood vessels beneath the skin. In this
study, hematomas were induced in 70 healthy volunteers by subcutaneous
injection of 2 ml of the subjects’ own blood. Treatment with
10 g of gel or placebo followed within five minutes. Sensitivity measurements
were taken from one to nine hours after treatment. As a result,
the Escin gel statistically reduced pain at all time points compared
to placebo (Calabrese and Preston, 1993). Our reviewer, Dr.
Mary Hardy, criticized the model because the subcutaneous injection
of blood does not produce all of the parameters as a bruise or
hematoma acquired through trauma. Thus, she rated the possible benefit
as undetermined.

Hawthorn

Other common names: English hawthorn; May tree; white
thorn
Latin name: Crataegus laevigata (Poir.) DC. and C. monogyna
Jacq. as well as other species [Rosaceae]
Latin synonyms: Crataegus oxyacantha L. = C. laevigata
Plant parts: Leaf, flower


Hawthorn, a tall shrub that grows throughout Europe, was first
documented as having medical use in the first century A.D., but the
plant’s use as a heart medicine can only be traced back to the 1600s.
The two primary species are Crataegus laevigata (Poir.) DC. and C.
monogyna Jacq. However, other species have been used medicinally,
and to make matters more complex, the two primary species are
known to hybridize (Upton, Graff, Williamson, et al., 1999). Therapeutic
efficacy has been documented most reliably for the leaves and
flowers. The dried, berrylike fruits have also been used, either alone
or in combination with the leaves and flowers. The main constituents
of hawthorn are identified as procyanidins, flavonoids, triterpenoids,
catechins, aromatic carboxylic acids, and amino and purine derivatives.
For quality control purposes, the flavonoid content and/or the
oligomeric procyanidin content are determined. The leaves and flowers
contain approximately 1 percent flavonoids and 1 to 3 percent
oligomeric procyanidins (Schulz, Hänsel, and Tyler, 2001).

Hawthorn has been studied for its clinical use in the treatment of
early stage heart failure, which is also called cardiac insufficiency.
Heart failure is defined as the inadequate supply of oxygen and nutrients
to the body as the result of heart disease. Animal studies indicate
that hawthorn preparations increase the contraction of the heart muscle,
increase the integrity of the blood vessel wall, and improve the
flow of blood to the heart without changing heart rate or aggregation
of red blood cells (Loew, 1997).

The New York Heart Association (NYHA) has classified heart
failure in four stages. Patients with Class I heart failure have cardiac
disease but are able to conduct ordinary physical activity without limitation.
Class II is defined as a slight limitation of ordinary physical
activity due to fatigue, palpitation, dyspnea, or anginal pain. Class III
is defined as marked limitation of physical activity even on light exertion.
Patients with Class IV heart failure are unable to carry on any
physical activity without discomfort—they may experience symptoms
of congestive heart failure even at rest (Cochran Foundation,
1997). Many of the clinical studies using hawthorn have been conducted
on patients with Class II disease.


The American Herbal Pharmacopoeia (AHP) lists hawthorn leaf
and flowers for the treatment of Class I and II cardiac insufficiency,
hypertonic heart with and without signs of coronary insufficiencies,
myocardial insufficiencies, arrhythmia, cerebral insufficiency, mild
hypertension, and patients with a history of myocardial infarction. It
is also distinguished as having the ability to potentiate the effects of
cardiac glycosides. The actions listed by the AHP include: increases
coronary and myocardial perfusion, lowers peripheral resistance, and
has economizing action with respect to oxygen and energy consumption;
it is positively inotropic, positively dromotropic, negatively
chronotropic, and negatively bathmotropic; and hawthorn is considered
to be an antiarrhythmic, an antioxidant, a diuretic, a hypocholesterolemic,
a hypotensive, and a sedative (Upton, Graff, Williamson,
et al., 1999). The AHP has also published a monograph on hawthorn
berry with similar indications (Upton, Graff, Bencie, et al., 1999).