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About Coronary Heart Disease
Coronary heart disease (CHD) is a condition in which the arteries that supply the heart muscle with oxygen-rich blood become narrow or blocked. As a result, the heart does not receive enough oxygen to function properly. The arteries are blocked by fatty deposits called atherosclerotic plaques. Also known as coronary artery disease (CAD), it is the top cause of death in the United States.
Physical symptoms include chest pain and shortness of breath. There are a number of risk factors for this disease, some of which are based upon the patient's lifestyle. Treatment and management may require medicinal or surgical intervention. Physicians may choose to treat their patients with any of several coronary heart disease medications.
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Many patients will undergo aspirin therapy to combat the effects of CHD. Aspirin plays double duty in fighting the symptoms of heart disease. In the blood, fatty acid compounds called prostaglandins trigger a cascade of events that cause platelets—cell fragments present in the blood—to group together forming clots. Aspirin inhibits the production of prostaglandins, thus preventing the formation of blood clots within arteries and veins.
One of the other symptoms of CAD is pain in the chest called angina pectoris. Aspirin is an analgesic, which helps to relieve or reduce pain. Doctors usually prescribe a dose of 80 to 160 mg per day for patients with atherosclerosis or who have previously had a heart attack or stroke. Some risks are associated with aspirin therapy, so check with your doctor before taking any.
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Patients with high blood pressure (hypertension), abnormal heart rhythms (arrhythmias) or who have suffered from congestive heart failure may be prescribed beta blockers. Beta blockers inhibit the body's two main beta receptors that receive adrenaline and cause the heart to beat faster and harder. With the beta receptors “blocked”, the heart slows down, beats less intensely and requires less oxygen.
Beta receptors can be selective or nonselective; selective beta blockers inhibit beta 1 receptors more than beta 2. Beta 1 receptors are responsible for heart rate and the strength of each beat, while beta 2 receptors are responsible for the function of smooth muscle which you have no conscious control over, such as the muscle in the walls of arteries and veins.
Beta blockers have several side effects. If you experience any adverse side effects, especially if you are taking other medications, let your doctor know.
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Patients experiencing angina pectoris may be prescribed nitroglycerin as a method of preventing or relieving the pain. Its three most common forms are tablets, sprays and patches. Nitroglycerin works by dilating the blood vessels so that the heart does not need to pump as hard. In the body, nitroglycerin is converted to nitric acid, a natural vasodilator. The nitric acid relaxes the smooth muscle lining of the blood vessels allowing blood to flow more freely and easing the pain associated with lack of blood supply.
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Doctors have several choices to choose from in this category of medications. One of the major risk factors in CAD is high levels of low-density lipoproteins (LDLs) and triglycerides coupled with low levels of high-density lipoproteins (HDLs). Positive changes in a patient's blood lipid profile can slow the progression of disease, particularly if part of a healthy management program.
Cholesterol modifiers come in several forms, such as statins, niacin, fibrates and bile acid sequestrants. Statins are the first choice for cholesterol modification drugs because it has several other benefits, including inhibition of platelet clumping and helping the inner lining of blood vessels work more effectively. Niacin may be taken in order to raise HDL levels by decreasing the amount of LDLs being allowed to move into the blood stream from adipose tissues. Fibrates stimulate cells to take up and use fatty acids for energy. Bile acid sequestrants work to lower LDL levels in the blood by stimulating the liver to convert more cholesterol to bile acid; the bile acid is removed through the digestive tract in the patient's waste.
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Calcium Channel Blockers
Calcium channel blockers (CCBs) are a group of medications that inhibit calcium ions from entering “excitable” cells, specifically those of cardiac muscle and smooth muscle of the blood vessels. Calcium ions act as intracellular messengers. The heart's pacemaker, the sinoatrial (SA) node, and the relay between the chambers of the heart, the atrioventricular (AV) node require calcium ions to propagate an electrical signal to the heart muscle. However, the rest of the electrical conduction system requires sodium ions to move the electrical signal. CCBs slow the heart rate by acting on these two particular portions of the heart, but do not interfere with the normal contractile function.
If your doctor has prescribed CCBs and you feel that you are suffering adverse effects from the medications, do not stop taking them without consulting your physician. Abrupt cessation of the drug may cause a dangerous rise in blood pressure.
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ACE Inhibitors and ARBs
The renin-angiotensin system (RAS) causes arteries to constrict and blood pressure to rise, among a few other reactions. In this pathway, angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. ACE also degrades bradykinin, a protein which causes vessels to dilate. ACE inhibitors keep this pathway from being completed, allowing arteries to remain open and blood pressure down. These drugs have widespread use for patients with hypertension.
Similar types of drugs inhibit the sites where angiotensin binds to cells in order to reduce two hormones that increase blood pressure through different means, vasopressin and aldosterone, ultimately lowering blood pressure by causing arteries to dilate. These angiotensin receptor blockers (ARBs) or angiotensin II receptor antagonists were developed to overcome the limitations of ACE inhibitors. Also the adverse side effects of ACE inhibitors have shown significantly reduced frequency in patients prescribed ARBs.
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Used in conjunction with other medications, ranolazine, which is sold under the brand name Ranexa, relieves chronic angina and improves exercise tolerance in CAD patients by increasing blood flow to the heart muscle. Its improvements to blood flow take place in the late stages of the heart beat.
During each heart beat, sodium ions enter the cardiac muscle cells to allow the electrical signal, an action potential, to travel through the cell causing it to contract. At the end of the action potential, the channels that allow the sodium in are supposed to shut in order to reset for the next beat, but some of them stay open and more sodium gets in. What this does on a macroscopic scale, is cause the end of the heart beat, when the heart should begin relaxing, to continue contracting the muscle and squeezing the coronary arteries. The squeezing of the arteries limits blood flow and results in ischemia-induced angina pectoris. Ranolazine works to correct this “late sodium” that crosses the cell's membrane.
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Cleveland Clinic: CAD Treatment: Medical Management
University of Maryland Medical Center: Coronary Artery Disease-Medications
Mayo Clinic: Coronary Artery Disease: Treatments and Drugs
Cleveland Clinic: Aspirin Therapy in Heart Disease
Texas Heart Institute: Beta-Blockers
MedlinePlus Drug Information: Nitroglycerin
The Journal of Nutritional Biochemistry: Niacin and Cholesterol: Role in Cardiovascular Disease
Ganji, SH; Kamanna, VS; Kashyap, ML
Staels, Bart, PhD, et al.
Johns Hopkins Point of Care Information Technology Center: Diabetes Guide: Bile Acid Sequestrants
Journal of Clinical Hypertension: Pharmacology and Mechanism of Action of Calcium Channel Blockers
American Heart Association: Calcium Channel Blockers
Circulation: Angiotensin-Converting Enzyme Inhibitors
Brown, Nancy J., MD; Douglas E. Vaughn, MD
Baylor University Medical Center Proceedings: Angiotensin II Receptor Blockers
Barreras, Amy, PHARMD and Cheryle Gurk-Turner, RPH
European Heart Journal: The Mechanism of Ranolazine Action to Reduce Ischemia-Induced Diastolic Dysfunction
Belardinelli, Luiz; John C. Shryock; Heather Fraser