Hawthorn improves cardiac function in patients with New York Heart Association stage II heart failure. Clinical trials support a minimum dose of 300 mg hawthorn extract to reduce debility from cardiac insufficiency. Various tolerance markers (standard bicycle ergometry, spiroergometry, radionucleotide ventriculography, and subjective complaints) support this conclusion. Further study is required to determine the effects of hawthorn on other cardiovascular conditions (hypertension, atherosclerosis, angina pectoris, and paroxysmal tachycardia) considered by herbalists to be indications for hawthorn therapy.

Hawthorn is a thorny, deciduous shrub up to five feet tall, found in deciduous forests of North America, Europe, North Africa, and western Asia. Flower clusters, which bloom in May, have five petals, five sepals, and numerous stamens. Leaves are variable, toothed or lobed, and alternate. Oval or round fruit (haws), which are red when ripe, contain five nutlets. Crude drug is prepared from leaves, white flowers, and berries.

• Flowers
• Leaves
• Fruit

Flavonoids (e.g., hyperoside, vitexin rhamnoside, rutin, vitexin, kaempferol, apigenin); oligomeric procyanidins (e.g., epicatechin, catechin)

Leaves and flowers in crude drug contain about 1% flavonoids (hyperoside as marker), 1% to 3% oligomeric procyanidins (epicatechin as marker); berries in crude drug contain about 0.1% hyperoside.

Aqueous, aqueous-alcohol, solid, glycerite, dried (powdered), and compounded extracts are available as liquid, tablet, or capsule, standardized to flavonoid/oligomeric procyanidin content

Traditional: cardiotonic, hypotensive, coronary vasodilator, mild diuretic, astringent

Conditions: coronary artery disease, congestive heart failure, essential hypertension, angina pectoris, postmyocardial infarction rehabilitation, cardiac weakness following infectious disease, antiarrythmias, possibly varicose veins, thrombosis

Clinical applications: for diminishing or deteriorating cardiac capacity due to stage II heart failure, according to New York Heart Association standards

Animal studies originated with a 1966 genetic experiment that focused on gypsy moths. The colony, about to die due to inbreeding and a diet of alder leaves, recovered completely when fed hawthorn leaves, and also became stronger and larger. Subsequent in vivo and in vitro animal experiments showed that hawthorn extracts increase coronary blood flow, cause vasodilation (and hypotension), reduce peripheral resistance, benefit peripheral blood flow (and circulation), and have positive inotropic effects (increasing rat myocyte efficiency more than isoprenaline). Hawthorn extracts also block beta-adrenoceptors, are antiarrhythmic, and, in rat hearts subject to ischemia and reperfusion, increase recovery rate, reduce lactate release, reduce ventricular fibrillation, and prolong survival.

In humans, hawthorn, a positive inotropic agent, increases the refractory period that cardiac glycosides shorten, reducing the probability of arrhythmia while stabilizing heart rhythm. Also a peripheral vasodilator, hawthorn reduces blood pressure and increases coronary flow. It has positive dromotropic effects and negative bathmotropic effects, and increases coronary and myocardial circulatory perfusion. Actions may be due to inhibition of cAMP (cyclic adenosine monophosphate) or TXA₂ (thromboxane₂) or to other undetermined actions.

To decrease NYHA stage II cardiac insufficiency:

• 160 to 900 mg standardized (4 to 20 mg flavonoids/30 to 160 mg oligomeric procyanidins) fluid crude extract daily for at least six weeks
• 120 to 240 mg extract, standardized to 1.8% vitexin rhamnoside/10% procyanidins three times daily for at least six weeks.

American Herbal Products Association (AHPA) safety rating: class 1 (safe with appropriate use)

Infrequent side effects: Two of 367 subjects in placebo-controlled trials reported nausea, headache, migraine, palpitations, and soft stools.

Toxicity: After IP dosing of 3 g per kg body weight (rats and mice), toxicity was indicated by sedation, difficulty breathing, and tremors, but not death. Oral doses—30, 90, or 300 mg per kg body weight administered to rats and dogs for 26 weeks and 300 to 600 mg per body weight administered for one month—were nonfatal and nontoxic.

Advise patients not to self-medicate. If symptoms do not improve after six weeks of treatment, reevaluate the condition. Encourage frequent follow-ups. Take appropriate precautions regarding potential heart failure, imminent surgery, and prescription change.

Patients should not use hawthorn during pregnancy.

Although hawthorn reportedly potentiates the activity of digoxin (Mashour et al. 1998; Miller 1998), case reports of clinically significant interactions have not been cited in the literature.

In rat mesenteric artery, hawthorn fruit alcoholic extract counteracted the effects of phenylephrine, a vasoconstrictive agent (Chen et al. 1993). The extract completely inhibited the contraction induced by phenylephrine at a concentration of 1 micromole. The clinical relevance of these experimental findings is unknown at this time.

In the United States, the FDA classifies hawthorn as a dietary supplement; in Canada, it has new-drug status and is not approved for self-treatment of cardiovascular disease. Hawthorn is not licensed through the General Sale List (GSL) in England, and while the Commission E in Germany approves the use of hawthorn leaf and flower for the treatment of NYHA stage II heart failure, it does not approve the use of hawthorn berry.

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