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Antianginal drugs, Ranolazine, Pathophysiology of angina, MOA of nitrates,…
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Ranolazine
Ranolazine was initially assigned to this group. However now it is believed that it acts by blocking a late sodium current that facilitates the calcium entry via NCX.
Ranolazine is the first new antianginal drug to be approved by FDA in many years, and it is approved as first line agent for chronic angina. It has no effect on heart rate and blood pressure.
And it has been shown in clinical trials to prolong exercise duration and time to angina both as monotherapy and when administered with conventional antianginal therapy.
It is safe to use with erectile dysfunction drugs like sildenafil as compared to nitrates.
Ranolazine can cause QT prolongation.
It also decreases occurrence of atrial fibrillation and results in small decrease in HbA1C.
Contraindicated in significant liver and kidney disease.
Not to be used for treatment of acute anginal episodes.
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MOA of nitrates
Nitrates act by releasing NO, which increase cGMP and results in venodilation.
At high doses arteriolar dilation can also occur.
The enzyme responsible for releasing NO from the nitrates is present mainly in the veins(therefore it has selective venodilator action).
Venodilation results in peripheral pooling of the blood and consequently decrease in preload and end diastolic pressure.
This is the main action of nitrates responsible for relief in classical angina.
Nitrates also cause favourable redistribution of blood flow to the ischemic area(total coronary flow is not increased)
by dilation of large epicardial coronary arteries.
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Sublingual nitrates
Nitroglycerine and isosorbide dinitrate sublingually can be used for aborting the acute attack of angina.
Nitroglycerine by oral or transdermal route and other nitrates by oral routes are used for prophylaxis of anginal attacks.
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Beta blockers
Major beneficial effect of beta blockers in angina pectoris is by reducing cardiac work.
These drugs donot dilate coronary vessels, rather vasoconstriction due to blockade of B2 mediated vasodilation.
These drugs are contraindicated in variant angina.
Abrupt withdrawl of B blockers may precipitate acute angina and MI(dose should be gradually tapered).
B blockers can be combined with nitrates and DHPs to counteract tachycardia.
B blocker are the only anti-anginal drugs that decrease mortality in patients with CAD(Post-MI).
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Two major strategies
Two major strategies for the treatment and prevention of angina are to decrease the oxygen requirement
or to increase the blood supply to the ischemic region.
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Nitrates
Nitrates: glyceryl trinitrate(nitroglycerine), ISDN, ISMN, erythrityl trinitrate, pentaerythritol tetranitrate and amyl nitrite are important compounds in this category.
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Molsidomine
Molsidomine is an emerging agent in this category to which tolerance doesn’t develop.
Phosphodiesterase inhibitors like sildenafil should never be prescribed with nitrates.
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Ivabradine
Ivabradine is a newer drug for angina.
It is known as bradycardiac agent as it decreases heart rate without affecting the conduction or contractility.
It acts by blocking a hyperpolarization activated sodium channel(known to carry funny current If).
Apart from bradycardia, visual disturbances is the most important adverse effect of ivabradine.
Fasudil
Fasudil is a selective RhoA/rho kinase(ROCK) inhibitor.
ROCK is an enzyme that plays important role in vasoconstriction and cardiac remodelling.
By inhibiting this enzyme, fasudil acts as a vasodilator and thus can be used in angina and cerebral vasospasm.
Because small vessels in the ischemic area are already maximal dilated(ischemia is a powerful vasodilator), blood flow to this area is selectively increased on dilation of large vessels and collaterals.
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