Cardiac Syndrome X Medication

Updated: Dec 18, 2014
  • Author: Subodh Raja Devabhaktuni, MD; Chief Editor: Richard A Lange, MD, MBA  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Beta-Blockers, Beta-1 Selective

Class Summary

Beta blockers seem to be most effective in reducing the frequency and severity of angina and in improving exercise tolerance. [41, 42, 43]

Atenolol and metoprolol, in low doses, selectively block beta1 -adrenergic receptors in the heart and vascular smooth muscle. Pharmacodynamic consequences of beta1 -receptor blockade include decreases in (1) resting and exercise heart rate, (2) cardiac output, and (3) systolic and diastolic blood pressure. Like all selective adrenergic antagonists, they lose their selectivity for the beta1 receptor at higher doses and can competitively block beta2 -adrenergic receptors in the bronchial and vascular smooth muscles, potentially causing bronchospasm.

Actions that generally make beta blockers useful include a negative chronotropic effect that decreases the heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the central nervous system (CNS), and suppression of renin release from the kidneys. Thus, beta blockers affect blood pressure via multiple mechanisms.

Metoprolol (Lopressor, Toprol-XL)

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During intravenous (IV) administration, carefully monitor blood pressure, heart rate, and the ECG. No dosage adjustment is required with renal failure.

Atenolol (Tenormin)

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types.

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Angiotensin-Converting Enzyme Inhibitors

Class Summary

The precise mechanism of action is not known. It is thought to be from increased bioavailability of nitric oxide [44] and improvement in endothelial function. [45]

Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and lower aldosterone secretion. They are effective and well-tolerated drugs with no adverse effects on plasma lipid levels or glucose tolerance.

Cough and angioedema are less common with newer members of this class than with captopril. Serum potassium and serum creatinine concentrations should be monitored for the development of hyperkalemia and azotemia.

Captopril

Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. It is rapidly absorbed, but bioavailability is significantly reduced with food intake. Captopril achieves a peak concentration in 1 hour and has a short half-life. The drug is cleared by the kidney; impaired renal function requires reduction of the dosage. Captopril is absorbed well orally.

Give captopril at least 1 hour before meals. If it is added to water, use it within 15 minutes. The dose can be low initially, then titrated upward as needed and as tolerated by the patient.

Enalapril (Vasotec)

Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Lisinopril (Prinivil, Zestril)

Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Benazepril (Lotensin)

Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Fosinopril

Fosinopril is a competitive ACE inhibitor. It prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Quinapril (Accupril)

Quinapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion.

Ramipril (Altace)

Ramipril inhibits partially inhibits both tissue and circulating ACE activity, therefore reducing the formation of angiotensin II in the tissue and plasma.

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Lipid-Lowering Agents, Statins

Class Summary

Statins improve the exercise tolerance in terms of duration, time to electrocardiographic changes on stress testing, and brachial artery flow–mediated dilation. [46] The exact mechanism of benefit by statins is unclear, and several hypotheses have been proposed. Statins, especially atorvastatin and simvastatin, modulate lysyl oxidase transcriptional activity, counteracting the down-regulation of lysyl oxidase caused by tumor necrosis factor-alpha (TNF-alpha) in porcine, bovine, and human aortic endothelial cells. Statins can normalize vascular lysyl oxidase expression altered by atherogenic risk factors through a RhoA/Rho kinase-dependent mechanism. [47]

Simvastatin (Zocor)

Simvastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. It may be administered 5-40 mg/day PO hs.

Pravastatin (Pravachol)

Pravastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. It may be administered 10-20 mg PO hs; may increase to 40 mg hs.

Atorvastatin (Lipitor)

Atorvastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. It may be administered 10 mg PO once daily; titrate to a maximum 80 mg/day, as necessary.

Rosuvastatin (Crestor)

Rosuvastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. It may be administered 5 mg PO once daily; titrate up to 40 mg PO once daily.

Pitavastatin (Livalo)

Pitavastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. It may be administered 2 mg PO once daily, not to exceed 4 mg/day.

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Tricyclic Antidepressants

Class Summary

Agents in this class have demonstrated effectiveness in the treatment of psychosomatic and chronic pain.

Imipramine (Tofranil-Tofranil PM)

Imipramine improved the symptoms of patients with chest pain and normal coronary angiograms, possibly through a visceral analgesic effect. [48] It may act by inhibiting reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.

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Estrogen Derivatives

Class Summary

Hormone therapy may be beneficial in postmenopausal women. Hormone therapy significantly reduced the frequency of anginal episodes. [49] Estrogen may act by improving endothelium-dependent coronary vasomotion. [50] However, these benefits must be weighed against the overall effect of hormone therapy on cardiovascular outcomes. The Women's Health Initiative trial showed that estrogen-progestin replacement had no cardioprotective effect and may have produced harm, increasing the risk of coronary disease, stroke, venous thromboembolism, and breast cancer. [51]

Conjugated estrogens (Premarin)

Multiple aspects of menopause respond to estrogen replacement therapy, including vasomotor symptoms. Decisions for hormone replacement therapy should be made on an individual basis in consultation with a gynecologist. Dosing may need to be titrated individually, with each patient monitored for risks and adverse effects. Premarin is available in tablet form for oral administration in strengths of 0.3 mg, 0.625 mg, 0.9 mg, 1.25 mg, and 2.5 mg.

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