Medications to treat cardiovascular disease

Drugs that alter the function of the HEART or the BLOOD vessels. Plants provided the earliest forms of DRUG therapy for heart problems. Healers in ancient Egypt and Greece brewed teas of foxglove leaves, the source of digitalis, to slow a rapid heartbeat and strengthen a weakened heart. By the 17th century physicians were using a relatively standardized formulation of powdered foxglove to treat congestive HEART FAILURE. Foxglove leaves remain the source from which laboratories extract digitalis to manufacture digoxin and digitoxin, the digitalis-based medications that remain in use today. Quinidine, a medication to treat ARRHYTHMIA (irregular heartbeat), derives from the bark of the South American Cinchona ledgeriana tree (also the original source of the antimalarial drug quinine). Scientists isolated quinidine as an extract to treat ATRIAL FIBRILLATION in 1918. Rauwolfia serpentina was a staple in the PHARMACOPOEIA of healers in ancient India, who used its dried roots to lower BLOOD PRESSURE. The antihypertensive medication reserpine, which debuted in the 1950s, contains Rauwolfia alkaloid extracts. Today medications are the mainstay of treatment for most forms of CARDIOVASCULAR DISEASE (CVD), though most are synthetic formulations that come from the laboratory.

Cardiovascular disease often involves multiple, interrelated components. HYPERTENSION (high blood pressure) often arises from underlying ATHEROSCLEROSIS, the most common cardiovascular disease. CORONARY ARTERY DISEASE (CAD), a manifestation of atherosclerosis that affects the CORONARY ARTERIES supplying the heart, may generate arrhythmias and ANGINA PECTORIS. Heart failure typically features numerous symptoms arising from a constellation of cardiovascular dysfunctions. The recent direction of research has correspondingly produced medications that treat the constellation, not just a single symptom. A calcium channel blocker, a classification of medication that debuted in the 1990s, dilates peripheral arteries, and slows the HEART RATE; these actions lower blood pressure, regulate the heart’s rhythm, and strengthen the heart’s pumping action. Combining medications often produces more effective results. For example, the cardiologist may also prescribe a diuretic to extract additional fluid from the body, which lowers blood volume and thus blood pressure, which in turn relieves the heart’s workload to reduce heart failure. The combination of the diuretic and the calcium channel blocker may restore nearly normal cardiovascular function.

People respond differently to cardiovascular drugs, even when they have the same diagnoses. It may take a trial and error period to find the right medication or combination of medications for each individual. Cardiovascular medications may interact or interfere with each other, with medications for other health conditions, with herbal preparations, and with certain foods. For example, grapefruit (whole fruit or juice) interferes with the actions of calcium channel blockers, statin lipid-lowering medications, digoxin, potassium channel blockers, and warfarin. The herb GOLDENSEAL, taken to enhance immune function, elevates blood pressure and interacts with antihypertensive medications. Dark green leafy vegetables contain VITAMIN K, which increases clotting and interferes with anticoagulant medications.

Most medications to treat cardiovascular conditions have the potential for side effects, some of which may be life-threatening. Sodium channel and potassium channel blockers, digoxin, warfarin, and heparin all are NARROW THERAPEUTIC INDEX (NTI) drugs, for which the margin between helpful and harmful is exceedingly thin. These drugs have the potential to create life-threatening arrhythmias. Other cardiovascular medications may cause symptoms such as COUGH, HEADACHE, ERECTILE DYSFUNCTION, tiredness, CONSTIPATION, dizziness, flushing, and edema (swelling, particularly of the ankles and wrists). It is important for people to know what side effects are possible with they medications they are taking and to notify the doctor if any of them occur. Though some side effects are common to all of the drugs within a classification, sometimes switching to a different medication within the same classification eliminates the troublesome side effect.

ACE Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors block the action of angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that raises blood pressure. Blocking the conversion of its precursor, angiotensin I (angiotensinogen), prevents these events and lowers blood pressure. ACE inhibitors also have a mild to moderate diuretic effect, further lowering blood pressure by reducing blood volume.

Pregnant women should not take ACE inhibitors during the second and third trimesters of PREGNANCY, as these drugs may cause harm or death to the fetus.

Doctors prescribe ACE inhibitors as first-line treatment, usually in combination with diuretics, to treat hypertension and heart failure and to reduce the risk of subsequent heart attacks after an initial heart attack. Some ACE inhibitor products combine an ACE inhibitor with a diuretic.

benazepril (Lotensin) captopril (Capoten)
enalapril (Vasotec) fosinopril (Monopril)
lisinopril (Prinivil, Zestril) moexipril (Univasc)
perindopril (Aceon) quinapril (Accupril
ramipril (Aceon (Altace) trandolapril (Mavik)

Among the common side effects are HEADACHE, gastrointestinal upset, dizziness, SKIN RASH or skin sensitivity to sunlight, and fatigue. ACE inhibitors have a propensity to cause a dry, nonproductive cough; though annoying, the cough is benign and typically goes away within two months of stopping the medication.


Adenosine is an intravenously administered medication that momentarily interrupts the flow of the heart’s electrical pacing signals, creating an “electrical short” of sorts that very briefly stops the heart. It is a treatment for PAROXYSMAL ATRIAL TACHYCARDIA (PAT), also called paroxysmal supraventricular tachycardia (PSVT), that converts the heart to normal sinus rhythm. Sometimes cardiologists refer to this treatment as chemical or pharmaceutical CARDIOVERSION. Adenosine is available in the United States as the brand name product Adenocard. The effects of adenosine last only one to two minutes. Side effects may include headache, lightheadedness, NAUSEA, and shortness of breath (DYSPNEA). Adenosine also may trigger angina pectoris in people who have CAD.

Alpha Blockers

Alpha blockers, also called alpha adrenergic antagonist medications, block alpha receptors in the cells from binding with EPINEPHRINE (also called adrenaline). These drugs were among the first generation of antihypertensive medications, though beta blockers and other antihypertensives have generally replaced them. Alpha blockers relax smooth MUSCLE, including that in the walls of the arteries to produce arterial dilation. This reduces the resistance for the flow of blood, lowering blood pressure. The most common cardiovascular use of alpha blockers is to treat hypertension that arises from PHEOCHROMOCYTOMA. This endocrine tumor secretes the hormones epinephrine and NOREPINEPHRINE, causing extreme spikes in blood pressure.

Alpha blockers are not a first-line treatment approach for general hypertension because their effects are widely systemic and because their longterm use increases the risk for heart failure. Alpha blockers affect other sites of smooth muscle tissue throughout the body, such as in the gastrointestinal tract, acting to slow peristalsis, and in the genitourinary system, causing URINARY INCONTINENCE and ERECTILE DYSFUNCTION. Other side effects may include dizziness and SYNCOPE (fainting). Some alpha blockers also block beta receptors.

clonidine (Catapres) doxazosin (Cardura)
guanabenz (Wytensin) guanfacine (Tenex)
labetalol (Normodyne) methyldopa (Aldomet)
phenoxybenzamine (Dibenzyline) prazosin (Minipress)
terazosin (Hytrin)  

Angiotensin II Receptor Blockers (ARBs)

Angiotensin II receptor blockers, also called angiotensin II receptor antagonists or ARBs, prevent the enzyme angiotensin II from binding with cells the walls of the arteries. Angiotensin II is a powerful endogenous vasoconstrictor (substance the body makes to narrow the blood vessels) that raises blood pressure. Preventing its actions relaxes and dilates the arteries, reducing the resistance blood encounters flowing through them and lowering blood pressure.

Pregnant women should not take angiotensin II receptor blockers (ARBs) during the second and third trimesters of PREGNANCY, as these drugs may cause harm or death to the fetus.

ARBs may be the first-line choice to treat hypertension, depending on the person’s overall health profile and other medications. ARBs do not cause the cough and other side effects that can be troublesome with ACE inhibitors, though they do put more strain on the kidneys. The most common side effect with ARBs is headache, especially with losartan. Other side effects, though uncommon, may include anxiety, fatigue, and gastrointestinal upset.

candesartan (Atacand) eprosartan (Teveten)
irbesartan (Avapro) losartan (Cozaar)
olmesartan medoxomil (Benicar) tasosartan (Verdia)
telmisartan (Micardis) valsartan (Diovan)


People commonly refer to anticoagulant drugs as “blood thinners” though this is somewhat of a misnomer. The first stage of clotting, which anticoagulants delay, is a thickening of the blood as CLOTTING FACTORS begin causing cells to stick together. Anticoagulants prevent the body from processing vitamin K, which interferes with the blood’s ability to activate clotting factors. Heparin, low molecular weight heparin (LMWH), and fondaparinux are injectable anticoagulants that are relatively short-acting though have cumulative effects when administered for extended periods of time. Surgeons use anticoagulants to completely suppress the blood’s clotting ability during operations that require CARDIOPULMONARY BYPASS. Warfarin (Coumadin) is currently the only oral anticoagulant available, though research continues to search for alternatives. Anticoagulants are NTI drugs that require continual monitoring to maintain therapeutic levels.

Women who are pregnant or planning to become pregnant should not take warfarin, as it can cause birth defects (highest risk during first trimester).

Doctors prescribe anticoagulant medications to prevent blood clots from forming, typically to prevent DEEP VEIN THROMBOSIS (DVT) and PULMONARY EMBOLISM in PERIPHERAL VASCULAR DISEASE (PVD) with INTERMITTENT CLAUDICATION, and to prevent heart attack and stroke. Anticoagulants cannot dissolve clots that already exist (though thrombolytic agents can). The most significant side effect is excessive bleeding. Anticoagulants can interact with numerous medications. Foods high in vitamin K (such as dark green leafy vegetables) may increase the blood’s clotting capability.

heparin fondaparinux (Arixtra)
warfarin (Coumadin)  
ardeparin (Normiflo) dalteparin (Fragmin)
enoxaparin (Lovenox) nadroparin (Fraxiparine)
reviparin (Clivarine) tinzaparin (Innohep)

Antiplatelet Agents

Antiplatelet agents also interfere with the blood’s ability to clot by blocking platelets, the cells that initiate clotting, from aggregating or sticking together. PLATELET AGGREGATION sets in motion the sequence of chemical interactions that activate clotting factors; blocking PLATELET aggregation delays the start of the clotting process. Antiplatelet agents often are part of an ANTICOAGULATION THERAPY regimen, in combination with anticoagulant medications.

The most commonly used antiplatelet agent is low-dose aspirin, which health experts recommend for people who have increased risk for cardiovascular disease or who have already had heart attack or ischemic stroke. Like anticoagulants, antiplatelet agents require close monitoring to maintain therapeutic levels. Three antiplatelet agents are injectable only-abciximab (Rheopro), eptifibatide (Integrilin), and tirofiban (Aggrastat)-which doctors use during ANGIOPLASTY and sometimes other CARDIAC CATHETERIZATION procedures. The oral antiplatelet agent cilostazol (Pletal) also acts to dilate the blood vessels, so doctors often prescribe it to treat intermittent claudication.

Doctors typically prescribe antiplatelet agents to prevent clots from forming in people who havePVD, CAD, valvular heart disease, prosthetic heart valves, PACEMAKER or IMPLANTABLE CARDIOVERTER DEFIBRILLATOR (ICD), or who have had heart attack, stroke, or certain kinds of heart surgery. The most significant side effect of antiplatelet agents is excessive bleeding. Over-the-counter NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) such as ibuprofen, and the herbal product ginkgo biloba, also have mild antiplatelet activity; it is important to check with the doctor or pharmacist before taking them with prescribed antiplatelet agents.

abciximab (Rheopro) cilostazol (Pletal)
clopidogrel (Plavix) dipyridamole (Persantine)
eptifibatide (Integrilin) sulfinpyrazone (Anturane)
ticlopidine (Ticlid) tirofiban (Aggrastat)

Beta Blockers

Beta blockers, also called beta adrenergic antagonist medications or class II antiarrhythmics, block beta receptors in the cells from binding with epinephrine. Beta receptors are specific to the arteries and MYOCARDIUM, so the actions of beta blockers are selective and specific to these sites. In the heart, beta blockers slow the conduction of electrical impulses, which slows the heart rate and reduces the amount of blood the heart pumps (CARDIAC OUTPUT). These effects result in lowered blood pressure and also reduced cardiac workload, which relieves angina pectoris. In the arteries, beta blockers cause smooth muscle tissue to relax, which dilates the arteries to decrease the resistance blood encounters to lower blood pressure. Most beta blocker medications thus do not have the systemic or generalized effects of alpha blockers, though a few of the beta blockers (notably propanolol and sotalol) also have some alpha antagonist activity as well and may have mild systemic effects.

There are two kinds of beta receptors, beta 1 and beta 2. Muscle cells in the myocardium and NERVE cells that regulate heart rate contain primarily beta 1 receptors. Peripheral arteries and arterioles contain primarily beta 2 receptors. Different beta blocker drugs target either beta 1 or beta 2 receptors. The smooth muscle cells in the airways also contain beta 2 receptors, so beta blockers that affect beta 2 receptors in the blood vessels also affect the airways. Medications to treat ASTHMA may interact with beta blockers taken to treat cardiovascular conditions. Beta blockers prescribed for other conditions such as asthma, BENIGN PROSTATIC HYPERTROPHY (BPH), migraine headaches, GLAUCOMA, and essential tremor may also affect cardiovascular function.

Do not suddenly stop taking a beta blocker, as doing so may cause intensified ANGINA PECTORIS and increased risk for HEART ATTACK.

Beta blockers are the “workhorse” drugs in cardiology, treating a broad spectrum of cardiovascular conditions. Doctors prescribe beta blockers to treat hypertension, heart failure (especially congestive heart failure), atrial fibrillation, mild to moderate ventricular tachycardia, CARDIOMYOPATHY, angina pectoris, and to improve survival following heart attack. The most common side effects are fatigue and sleepiness, which generally improve with taking the medication over time. Beta blockers may cause erectile dysfunction in men and diminished sexual response in women. CAFFEINE and antihistamines (such as in cold and allergy products) intensify, and ALCOHOL diminishes, the effects of beta blockers. Beta blockers may interfere with the actions of oral ANTIDIABETES MEDICATIONS.

acebutolol (Sectral) atenolol (Tenormin)
betaxolol (Kerlone) bisoprolol (Zebeta)
carteolol (Cartrol) esmolol (Brevibloc)
metoprolol (Lopressor, Toprol) nadolol (Corgard)
penbutolol (Levatol) pindolol (Visken)
propranolol (Inderal) timolol (Blocadren)

Calcium Channel Blockers

Calcium channel blockers, also called calcium channel antagonists, limit the amount of calcium that enters contractile cells. Two of the commonly prescribed calcium channel blockers act nearly exclusively on the heart (myocardial cells), diltiazem and verapamil. Cardiologists prescribe these drugs, also identified as class IV antiarrhythmics, to treat atrial fibrillation, PAT, hypertrophic cardiomyopathy, and angina pectoris. The other calcium channel blockers, sometimes called dihydropyridine calcium channel blockers, act primarily on the peripheral arteries, causing them to relax and dilate. This lowers resistance for blood flow and reduces blood pressure. Cardiologists prescribe these calcium channel blockers to treat hypertension, angina pectoris without arrhythmia, and RAYNAUD’S SYNDROME. Doctors use nimodipine following stroke to reduce the risk of arterial spasm and resulting HEMORRHAGE, as it affects primarily the arteries in the BRAIN.

Women who are pregnant or planning to become pregnant should not take calcium channel blockers, as these drugs can cause serious birth defects and STILLBIRTH.

amlodipine (Norvasc, Lotrel) diltiazem (Cardizem, Cartia, Dilacor, Diltia, Tiazac)
felodipine (plendil) nicardipine (Cardene)
isradipine (DynaCirx) nimodipine (Nimotop)
nifedipine (Adalat, Procardia) nisoldipine (Sular)
verapamil (Calan, Covera, Isoptin, Verelan)  

Side effects that may occur when taking calcium channel blockers include headache, gastrointestinal upset, fatigue, and peripheral edema. Most side effects retreat after a few weeks of taking the medication. Grapefruit and grapefruit juice interfere with most calcium channel blockers, preventing them from working properly.


People commonly refer to diuretic medications as “water pills” because they draw extra fluid from the body, increasing urination. The purpose is to reduce the volume of blood, which lowers blood pressure. Diuretics also help prevent edema (fluid accumulations in body tissues) such as may occur with heart failure. Doctors often prescribe diuretics in combination with other medications. There are four classifications of diuretic medications, defined by the drug’s mechanism of action: ALDOSTERONE blockers, loop diuretics, potassium-sparing diuretics, and thiazides.

Aldosterone blockers

Aldosterone blockers act by restricting adrenal gland production of the HORMONE aldosterone, which increases the amount ofsodium the KIDNEYS withdraw from the blood. They affect the RENIN-angiotensin-aldosterone (RAA) hormonal system, one of the body’s primary blood pressure regulatory systems. Though aldosterone blockers prevent the kidneys from reabsorbing sodium, they decrease the loss of potassium so they are also designated as “potassium-sparing.” However, new understanding emerged in the early 2000s about other effects aldosterone has on the heart, particularly following heart attack and in heart failure and with respect to the RAA hormonal system, that have caused doctors to view aldosterone blockers as a separate category of diuretic.

The two aldosterone blockers available in the United States are eplerenone (Inspra) and spironolactone (Aldactone).

Loop diuretics

Loop diuretics act on a site within the glomerular structure of the kidney called the loop of Henle, which regulates sodium reabsorption. Loop diuretics cause the kidneys to pass more sodium, and consequentially more water, into the urine, and are the most potent of the diuretic drugs. As the loop of Henle also plays a role in potassium regulation, loop diuretics also decrease potassium reabsorption and can result in potassium depletion. Doctors may also prescribe potassium supplementation to offset this effect. The most common side effect of loop diuretics is headache. Loop diuretics also can damage the structures of the inner EAR, resulting in temporary or permanent HEARING LOSS.

bumetanide (Bumex) ethacrynic acid (Edecrin)
furosemide (Lasix, Myrosemide) torsemide (Demadex)

Potassium-sparing diuretics

These drugs prevent the kidneys from withholding sodium, the electrolyte most responsible for fluid retention, though allow the kidneys to pull potassium from the blood. They are the least potent of the diuretic drugs, acting on other sites in the glomeruli that regulate specifically sodium reabsorption. The two potassium-sparing diuretics available in the United States are amiloride (Midamor) and triamterene (Dyrenium). The aldosterone blockers eplerenone and spironolactone are also potassium sparing.

Thiazide diuretics

The thiazide diuretics are the first line of therapy for hypertension and heart failure, often in combination with other cardiovascular medications. Their actions are more moderate than those of the loop diuretics, creating less of a risk for potassium depletion though such risk still exists. There are numerous thiazide diuretics, only some of which doctors prescribe for cardiovascular conditions. Because thiazides are so commonly used with other medications, there are also numerous formulations that incorporate a thiazide with another cardiovascular drug.

chlorothiazide (Diuril, Diurigen)
chlorthalidone (Hygroton, Thalitone)
hydrochlorothiazide (Ezide, Esidrix, HCTZ, Hydro-Chlor, Hydro-D, HydroDIURIL, Microzide, Oretic)
hydroflumethiazide (Diucardin, Saluron)
methyclothiazide (Aquatensen, Enduron)
metolazone (Diulo, Mykrox, Zaroxolyn)
polythiazide (Renese)
quinethazone (Hydromox)
trichlormethiazide (Metahydrin, Naqua, Trichlorex)


Inotropic drugs draw more calcium into myocardial cells, intensifying their contractility (the force with which they contract) and increasing the heart’s effectiveness while decreasing the effort required. Inotropic drugs administered intravenously during cardiovascular emergency include dopamine, dobutamine, and milrinone; these drugs give the heart a “jolt” to help it pull out of CARDIAC ARREST. Digoxin (short-acting) and digitoxin (long-acting), forms of digitalis, are the inotropic medications for chronic or extended oral therapy. Though once the cornerstone of therapy for heart failure (notably congestive heart failure), digoxin has a very narrow therapeutic index, making toxicity a worrisome concern. Digoxin interacts with numerous other medications including those that more effectively treat heart failure, and the heart becomes dependent on it.

Digoxin also acts to slow the number of electrical impulses that cross the ATRIOVENTRICULAR (AV) NODE, slowing and regulating the contractions of the myocardial cells. Cardiologists may prescribe digoxin to treat atrial fibrillation. The most common brand name digoxin product in the United States is Lanoxin.


Lipid-lowering medications reduce blood levels of cholesterol and triglycerides, lowering the risk for atherosclerosis and its related conditions CAD and PVD. There are four classifications of lipid-lowering medications, each with a different mechanism of action: BILE acid sequestrants, fibrates, statins, and selective cholesterol absorption inhibitors. As well, niacin acts to block cholesterol and lipoprotein synthesis in the LIVER.

Bile acid sequestrants

The bile acid sequestrants were the first cholesterol-lowering medications to become available. They work by binding with bile in the gastrointestinal tract, preventing the body from reabsorbing cholesterol the bile contains. Bile acid sequestrants can reduce low-density lipoprotein cholesterol (LDL-C) by about 20 percent and total cholesterol by 5 to 10 percent. These medications come as powders to mix with juices or foods such as applesauce, and commonly cause gastrointestinal distress. Bile acid sequestrants interact with numerous medications, including beta blockers, diuretics, and the anticoagulant warfarin.

cholestyramine (Questran, Prevalite) colesevelam (WelChol)
colestipol (Colestid)  


The fibrates work by blocking the liver’s production of LDL and VLDL (very lowdensity lipoprotein), the carriers for triglycerides. However, fibrates do not lower LDL-C or VLDL-C in the blood. Rather, they primarily reduce triglycerides though also raise high-density lipoprotein cholesterol (HDL-C), the “good” cholesterol. The most common side effect of fibrates is gastrointestinal distress, which usually disappears after taking the medication for a few weeks.

clofibrate (Atromid-S) fenofibrate (Tricor)
gemfibrozil (Lopid)  


Statins-or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors-are the most commonly prescribed lipid-lowering medications. They work by blocking the action of HMGCoA reductase, an enzyme necessary for the liver to synthesize cholesterol. Statins can lower blood LDL cholesterol by as much as 35 percent in just three to six weeks, making them very effective at quickly lowering the risk for atherosclerosis-related cardiovascular events. Statins reduce the risk for the progression of CAD, which could improve heart function after heart attack and are part of the standard medication regimen after heart attack and HEART TRANSPLANTATION. Common side effects of statins include gastrointestinal distress, fatigue, headache, and sleep disturbances.

atorvastatin (Lipitor) fluvastatin (Lescol)
lovastatin (Mevacor) pravastatin (Pravachol)
simvastatin (Zocor)  

Selective cholesterol absorption inhibitors

The selective cholesterol absorption inhibitors block the gastrointestinal tract from absorbing dietary cholesterol, limiting the cholesterol that enters the bloodstream. Ezetimibe (Zetia) is currently the only drug in this classification that is available in the United States. Doctors often prescribe ezetimibe in combination with statin medications for the most effective lipid-lowering effect.

Potassium Channel Blockers

Potassium channel blockers, also called potassium channel antagonists or class III antiarrhythmics, limit the amount of potassium, a key electrolyte (chemical that can carry an electrical impulse), that can enter myocardial cells. This limitation restricts the flow and pattern of electrical impulses through the heart in very specific ways. Cardiologists prescribe potassium channel blockers to treat atrial fibrillation that does not respond to other medications and to treat atrial tachycardia. These drugs interact with numerous medications, including those prescribed to treat cardiovascular conditions (notably digoxin and warfarin) and to treat other health conditions such as DIABETES. Amiodarone increases sensitivity to ultraviolet light, which can result in severe SUNBURN even through clothing. Potassium channel blockers have numerous serious side effects including life-threatening or fatal arrhythmias and TORSADE DE POINTES, a highly unstable form of ventricular tachycardia.

amiodarone (Cordarone) dofetilide (Tikosyn)
ibutilide (Corvert)  

Sodium Channel Blockers

Sodium channel blockers, also called sodium channel antagonists or class I antiarrhythmics, limit the amount of sodium that enters myocardial cells. This limitation restricts the flow and pattern of electrical impulses through the heart in very specific ways that differ from the actions of potassium channel blockers. Because sodium is critical for myocardial contraction, restricting it requires a delicate therapeutic balance. Cardiologists reserve sodium channel blockers to treat potentially lifethreatening ventricular tachycardia that does not respond to other treatment. The risks and complications of these medications are numerous and serious; they can cause fatal arrhythmias.

disopyramide (Norpace) flecainide (Tambocor)
mexiletine (Mexitil) moricizine (Ethmozine)
procainamide (Pronestyl) propafenone (Rythmol)
quinidine (Cardioquin, Quinidex)  

Thrombolytic Agents

Thrombolytic agents, commonly called “clot busters,” dissolve blood clots that have already formed. Given early enough, they can prevent the clot from forming, essentially halting heart attack or stroke before the event can cause any damage. However, doctors must administer them within three to four hours of clot formation. After four hours the clot has hardened and thrombolytic agents cannot dissolve them.

Thrombolytic agents are substances, either natural extracts or recombinant forms, that convert plasminogen in the blood to plasmin, an enzyme that dissolves fibrin. Fibrin is the substance in the blood that forms the webbing of the clot structure to snare platelets and other substances in the blood that become the clot. Early in the COAGULATION process fibrin is a semisolid, stringlike substance similar to the strands of a spiderweb. As the coagulation process continues, however, the fibrin strands and the cellular matter they have captured harden into the solid structure of a blood clot. Once the fibrin hardens, plasmin has no effect on it.

The most frequently used thrombolytic agents are tissue plasminogen activators (tPAs). One of the original thrombolytic agents, streptokinase, derives from the streptococcus bacterium and causes the body to develop antibodies against it. Because of this, doctors cannot administer streptokinase if the person has received streptokinase within 12 months. However, it takes about five days for the body to produce antibodies, allowing multiple administrations within five days of the initial dose. The tPAs do not seem to have this limitation, although it is possible for the body to develop antibodies against them as well.

Doctors administer thrombolytic agents intravenously to treat heart attack, stroke, deep vein thrombosis, and pulmonary embolism. The effect is rapid and short acting. Excessive and severe bleeding is a significant risk, particularly when stroke is hemorrhagic rather than ischemic. Doctors make every effort to determine the nature of a stroke before administering thrombolytic agents, though sometimes bleeding occurs even with ischemic stroke. As well, these agents may disturb the integrity of clots that have formed within the previous 10 days, such as from surgery.

alteplase (Activase) anistreplase (Eminase)
reteplase (Retavase) streptokinase (Streptase, Kabinase)
tenecteplase (TNKase) urokinase (Abbokinase)


Vasoconstrictors cause the blood vessels to constrict, or tighten, to raise blood pressure. Doctors administer vasoconstrictors to treat cardiovascular SHOCK and HYPOTENSION. Many bronchodilating medications prescribed to treat asthma also have peripheral vasoconstriction action, and may raise blood pressure at the same time they open the airways. One of the most commonly used vasoconstrictors is pseudoephedrine, found in cold, flu, and some allergy medications. Caffeine and NICOTINE are also vasoconstrictors. Though doctors do not prescribe these products for cardiovascular use, they have the effect of raising blood pressure as well as increasing heart rate. The most commonly used vasoconstrictor for cardiovascular purposes is midodrine (ProAmatine).


Many medications to treat hypertension are vasodilators, drugs that cause the blood vessels to relax so more blood can flow through them with less resistance. These medications may lower blood pressure or relieve angina pectoris. Among the general vasodilators cardiologists might prescribe to treat hypertension are hydralazine and minoxidil. Both drugs regulate the calcium that enters the smooth muscle cells of the ARTERY walls, slowing their contractility and causing the arteries to relax (dilate). Minoxidil is an NTI drug that requires close monitoring because, although it is a potent peripheral vasodilator, it also increases heart rate and has other cardiovascular actions that require additional medications to moderate.

Nitrate vasodilators are especially effective at relaxing the coronary arteries to relieve angina pectoris, which is one of the leading reasons doctors prescribe them. Nitrates also dilate the peripheral veins, which decreases the heart’s workload. Nitrates come in sublingual tablets placed under the tongue at the onset of anginal symptoms, regular and long-acting oral medications, transdermal (skin) patches, and topical ointments. Because the body acquires a tolerance to nitrates, dosing schedules are particularly important. Other commonly prescribed medications that have vasodilating actions include certain of the beta blockers, calcium channel blockers, ACE inhibitors, and ARBs.

hydralazine (Apresoline) mecamylamine (Inversine)
minoxidil (Loniten)  
isosorbide dinitrate (Isordil, Sorbitrate)  
isosorbide mononitrate (Imdur, ISMO, Monoket)  
nitroglycerin (Nitro-Dur, Nitrolingual, Nitrostat)  


Open discussion on the topic Medications to treat cardiovascular disease

only title   fulltext  

The cardiovascular system

Top articles on health