DEVTOME.COM HOSTING COSTS HAVE BEGUN TO EXCEED 115$ MONTHLY. THE ADMINISTRATION IS NO LONGER ABLE TO HANDLE THE COST WITHOUT ASSISTANCE DUE TO THE RISING COST. THIS HAS BEEN OCCURRING FOR ALMOST A YEAR, BUT WE HAVE BEEN HANDLING IT FROM OUR OWN POCKETS. HOWEVER, WITH LITERALLY NO DONATIONS FOR THE PAST 2+ YEARS IT HAS DEPLETED THE BUDGET IN SHORT ORDER WITH THE INCREASE IN ACTIVITY ON THE SITE IN THE PAST 6 MONTHS. OUR CPU USAGE HAS BECOME TOO HIGH TO REMAIN ON A REASONABLE COSTING PLAN THAT WE COULD MAINTAIN. IF YOU WOULD LIKE TO SUPPORT THE DEVTOME PROJECT AND KEEP THE SITE UP/ALIVE PLEASE DONATE (EVEN IF ITS A SATOSHI) TO OUR DEVCOIN 1M4PCuMXvpWX6LHPkBEf3LJ2z1boZv4EQa OR OUR BTC WALLET 16eqEcqfw4zHUh2znvMcmRzGVwCn7CJLxR TO ALLOW US TO AFFORD THE HOSTING.

THE DEVCOIN AND DEVTOME PROJECTS ARE BOTH VERY IMPORTANT TO THE COMMUNITY. PLEASE CONTRIBUTE TO ITS FURTHER SUCCESS FOR ANOTHER 5 OR MORE YEARS!

Angina Treatment

Three classes of antiischemic drugs are used in the management of chronic stable angina. These are nitrates, beta blockers and calcium channel blockers (1).

Nitrates

Nitrates decrease the myocardial oxygen demand through systemic vasodilation (1). The specific mechanism of action includes a conversion to nitric oxide, which activates guanlyate cyclase to cyclic guanosine 3’,5’-monophosphate (1). The protein kinase dependent phosphorylations in the smooth muscle cells will cause a release of calcium ions, which causes smooth muscle relaxation and vasodilation (1,2). Afterload reduction will be reduced and there will be a decrease in left ventricular systolic wall stress (1,2). The onset of action for sublingual nitrates is 1-3 min and the duration of effect is 30 min (1,2). The transdermal patch formulation of nitrates take 40-60 minutes to work and the duration of onset is 18-24 hours (1,2). The effects of nitrates is improve exercise tolerance, increasing the time to onset of angina and increasing the time to onset of ST-segment depression during exercise testing (1,2). Extensive first pass metabolism will occur after oral administration (1,2). The metabolism of nitroglycerin is through the liver to the less active dintiro and inactive mononitro metabolites(1,2).

Adverse effects include headache, dizziness, flushing, vomiting, nausea, weakness, palpitations, tachycardia and postural hypotension (3). These effects are dose related and can be minimized by a slow upward titration of the dose (3). Contact dermatitis can occur in up to 40% of patients that use the transdermal patches (3).

Contraindications include severe anemia, severe hypotension or uncompensated hypovolemia; increased intracranial pressure or use of sildenafil within previous 24 hours or use of vardenafil or tadalafil within previous 48 hours (1,2). Nitrates can produce additive vasodilation and severe postural hypotension when used with alcohol or hypotensive drugs (3). Use in patients with sildenafil, vardenafil or tadalfil may cause profound hypotension that may result in death (1,2).

Beta Blockers

Beta blockers are used to improve exercise capacity, reduce exercise induced ST depression, decreasing the frequency of angina episodes and decreasing sublingual nitroglycerin use (4). The mechanism of action is through the reduction of the myocardial oxygen demand by reducing the heart rate, myocardial contractility and intramyocardial wall tension (via blood pressure reduction) (1,2). The adverse effects of beta blockers include fatigue, depression, insomnia, bradycardia, hypotension, bronchoconstriction, impaired glucose metabolism and altered serum lipids (1,2). Contraindications include bradycardia, 2nd or 3rd degree AV block, LV dysfunction with unstable fluid status, unstable diabetes and frequent hypoglycemia, reactive airway disease and severe peripheral vascular disease (1,2). If taken together with oral hypoglycemics, nonselective beta blockers like propranolol can prolong hypoglycemic episodes (1,2). Cimetidine can increase propranolol effects (1,2). Barbiturates and rifampin can increase the metabolism of hepatically eliminated beta blockers such as propranolol (4). Metabolism: Propranolol is rapidly and completely absorbed after oral administration, however a large hepatic first pass effect will occur (1). This elimination is saturable with oral dose however (1). Metabolism is through CYP2D6 and CYP1A2 to 4-hydroxypropranol (active) and inactive compounds (1).

Calcium Channel Blockers

There are two types of calcium channel blockers: non-dihydropyridine and dihydropyridine (1,2). Non-dihydropyridine agents include verapamil and diltiazem which have negative dromotropic and inotropic effects (1,2). Dihydropyridine agents include amlodipine and felodipine which have vasodilation properties (1,2). The MOA of CCBs include reduction of myocardial oxygen demand by decreasing the blood pressure and decreasing the intramyocardial wall tension (1). The oxygen supply is increased by increasing myocardial blood flow through the dilation of coronary and systemic arteries (3).

Adverse effects include hypotension, worsening heart failure, and constipation (1,2). Reflex tachycardia, headache and peripheral edema do occur, but they are more common in DHP CCB (1,2). DHP CCB can increase pedal edema, whereas non-DHP CCB are contraindicated in HF (1,2). The metabolism of CCB is through CYP 450 metabolism with amlodipine being the exception (1,2). Thus drugs such as cimetidine and propranol can increase CCBs levels like diltazem. Bartbiturates can increase nifedipine metabolism (1,2).

Risk factor management is an important part of non pharmacological measures in controlling angina (3). It is important to treat systemic infections, correct hyperthyroidism as concomitant systemic illnesses like these may exacerbate angina (3). Risk reduction and lifestyle changes such as smoking cessation, management of hypertension, controlling of diabetes, weight loss, regular exercise, limitation of alcohol intake and stress reduction reduce the development of angina (3). If the symptoms are refractory to pharmacological therapy or if are unstable, percutaneous coronary intervention may be needed (3).

References

  1. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 7th ed. Toronto: McGraw-Hill; 2007. p. 249
  2. Chisholm-Burns MA, Wells BG, Schwinghammer TL, Malone PM, Kolesar JM, Rotschafer JC, Dipiro JT. Pharmacotherapy: Principles and Practice. McGraw-Hill: 2008. p. 64.
  3. Fraker TD Jr, Fihn SD, 2002 Chronic Stable Angina Writing Committee, et al. 2007 chronic angina focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 guidelines for the management of patients with chronic stable angina. J Am Coll Cardiol. 2007; 50:2264.
  4. Hodgson J, Quan Kara, Mueller DK, Saver DF, Murray JL. Stable Angina. MD Consult [online]. Maryland Heights MO: Elsevier Inc. 2011 [cited 2012 Mar 3]. Available from: www.mdconsult.com

Disclaimer

This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers


QR Code
QR Code stable_angina_treatment (generated for current page)
 

Advertise with Anonymous Ads