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Post  counselor on Mon Oct 15, 2012 11:47 am


Is the main symptom of ischemic heart disease, syndrome related to a discrepancy between the metabolic demands of the heart and the possibility of oxygen by the coronary arteries.
May be due to atherosclerotic coronary artery disease, spasms of the coronary vessels, cardiac hypertrophy, etc..

Angina pectoris is manifested by pain substernal, sudden, severe and oppressive that radiates to the left shoulder and left arm.

Is triggered by physical exertion, excitement, exposure to cold, food intake.
It is usually due to reduction of the lumen of a coronary artery atherosclerosis.

ANGINA Variant (Prinzmetal's)
It occurs at rest and during sleep.
E 'caused by spasms of the coronary vessels.
May not be accompanied by coronary atherosclerosis.

Unstable angina
In most cases it is due to rupture of an atherosclerotic plaque resulting in intravascular thrombosis and reduced coronary reserve.


Nitrates are nitric acid polyesters:
Isosorbide dinitrate-

The nitrites are esters of 'nitrous acid:
amyl nitrite
So the term nitro is improper.

All these compounds lead to the liberation of nitrogen monoxide, which activates the guanylate cyclase.
The cyclic GMP produces smooth muscle relaxation to dephosphorylation of myosin light chain.

a) The relaxation affects various types of smooth muscle:
-Among the most sensitive blood vessels are the veins and medium-sized arteries such as coronary
-It is also noted relaxation of the bronchi
-Biliary tract
-Of the gastrointestinal tract
b) The venodilatazione reduces the ventricular end-diastolic pressure by reducing the cardiac output.
c) A low dose of the blood pressure is not substantially modified.
d) At higher doses, especially after sublingual administration, it is observed dilation of arterioles with reduction in peripheral resistance and blood pressure.
e) The expansion of district venous and arteriolar peripheral vessels decreases both the precarious afterload reducing the oxygen demand of the heart.

Nell'angina effort by reducing the amount of oxygen is the most important mechanism, the intracoronary infusion of nitroglycerin is not effective.
The coronary vasodilation may be the main mechanism in the case of angina vasospasm.

The biotransformation of nitrate compounds denitrati is operated by glutathione-organic nitrate reductase.
• For good oral absorption, but strong first pass metabolism which are necessary for high doses. The maximum effect after 60-90 min. Duration of action of 3-6 hours.
• For sublingual absorption prompt and immediate effect (1-2 minutes). It avoids the hepatic metabolism of the passage, however, short duration of action (about 1 hour).
• Intravenous immediate effect, but short.
• In ointment effect in 60 min and lasting for 4-8 hours. In systems with transdermal adhesive patch the maximum effect in 1-2 hours and lasts up to 24 hours.

Repeated exposure to doses of nitrates leads to reduced intensity of their effects.
Appears to be due or down-regulation of guanylate-cyclase or depletion of intracellular thiol groups, necessary for the biotransformation of nitrates.

The tolerance was observed especially for oral administration and transdermal, as well as in industries that produce nitroglycerin.
To reduce the incidence of tolerance, it is recommended that a pattern of discontinuous administration with therapeutic window of 10 hours.

Do not stop abruptly chronic intake of nitrates, are possible spasm of the coronary arteries

• Headache.
• Postural hypotension can cause dizziness and loss of consciousness.
• Tachycardia reflected
• Rashes.
• Do not associate with phosphodiesterase inhibitors (to treat erectile dysfunction)

• Typical angina and variant.
• Congestive heart failure acute.
• Treatment of post-myocardial infarction

All channel blockers Ca + + reduce coronary vascular resistance and increase coronary flow.
However, there are differences in the haemodynamic effects of dihydropyridines, on the one hand, and of the verapamil or diltiazem, on the other.

The dihydropyridines cause:
1) arteriolar vasodilation with afterload reduction.
2) Reduction in blood pressure.
3) Sympathetic Activation
4) Increase rate and cardiac output.

The verapamil / diltiazem cause:
1) arteriolar vasodilatation with reduction in afterload, less intense than with the dihydropyridines
2) Reduction in blood pressure.
3) Sympathetic Activation.
4), however, do not increase frequency and cardiac output for the direct cardiac effects.

USE AS antianginal
All channel blockers Ca + + are effective nell'angina variant, however, the dihydropyridines seem more effective than verapamil, probably for most effect coronarodilatatore.

Nell'angina also stress the calcium channel blockers may be useful, by a decrease in oxygen consumption
Verapamil may be used alone.
The dihydropyridines alone may instead aggravate the symptoms of angina for:
1) Increase in heart rate.
2) Decrease marked cardiac perfusion pressure.
For this are usually associated with -adrenergic blockers.

Oral absorption is good, but the bioavailability is reduced to a strong metabolism of the passage.
The bioavailability may be 20-50%, however, in liver disease may be much higher.
-Strong binding to plasma proteins and possibility of significant pharmacokinetic interactions.
-They are almost eliminated by metabolism completions.

Especially the dihydropyridines may cause excessive vasodilatation with:
• hypotension, headache,
• peripheral edema and pulmonary edema.
• The use of verapamil with -blockers or digitalis may result in the marked depression of AV conduction.

Antagonists -ADRENERGIC


Nell'angina effort by these compounds act are useful because they reduce the myocardial oxygen consumption for:
a) negative chronotropic effect.
b) negative inotropic effect.
c) Reduction of blood pressure.

Nell'angina variant vasospasm -adrenergic antagonists are not helpful, may aggravate rather to increased  1-adrenergic receptor activation in the coronary arteries ( receptor blockade divert catecholamine receptor blocking ).

Can also be useful in unstable angina infarction because they reduce the workload of the heart and sympathetic hypertonus.
The use of -blockers in unstable angina reduces the risk of progression to myocardial infarction.
To use this you prefer -blockers without intrinsic sympathomimetic activity.

1) Nitrate + -adrenergic antagonists.
E 'useful nell'angina stress. The -blockers can block the tachycardia.
Nitrates can then reduce the increase in coronary resistance.

2) blockers of channels of Ca + + and -adrenergic antagonists. Is generally associated dihydropyridine and a -blocker nell'angina stress.
3) channel blockers Ca + + + nitrates.
E 'indicated in patients with exertional angina and heart failure.
The 'effect of the two drugs is additive because especially nitrates reduce preload and Ca channel blockers afterload.
4) -blockers + nitrates + channel blockers calcium. It is used when treatment with two drugs is not effective. We use only the dihydropyridine channel blockers such as Ca + +.


It inhibits the enzyme 3-keto-acyl-thiolase coenzimaA (3KAT). The inhibition of this enzyme deflects the metabolism of the cardiac cell from the oxidation of fatty acids (at increased oxygen consumption) to glucose (with marked saving of oxygen).
This helps to maintain the cardiac function in ischemic conditions


Syndromes are characterized by cardiac ischemia due to the formation of intravascular thrombi, typically for erosion, cracking and rupture of atherosclerotic plaques past.

The thrombus represents a hemostatic plug which is formed inside the vessels, in the absence of bleeding.
The most common causes of blood clots are 3 (Virchow's triad):
• injury of the vessel wall (atherosclerotic plaque rupture)
• altered blood flow (in the left heart during atrial fibrillation or for stasis in the leg veins)
• abnormal coagulability 'blood (contraception, pregnancy, etc.)

We distinguish thrombi in:

Arterial thrombus
E 'consists of white thrombus with platelets and leukocytes and little fibrin.

Venous thrombus
Thrombus red with small white head with red tail bulky. Small amount of platelets and large component of fibrin.

A portion of the clot can break off and form a blood clot. Thrombotic and thromboembolic diseases are due to:
•-myocardial infarction,
•-cerebral infarction,
•-deep vein thrombosis,
•-pulmonary embolism.

Among those with acute ischemic heart disease distinguish:
• Patients with chest pain and persistent ST-segment elevation dell'elettrocardiagramma. It occurs in the case of total occlusion of a vessel
• Patients with chest pain without persistent ST-segment elevation. Manifests itself in unstable angina and in some cases of myocardial

In the first case the main pharmacological approach involves the use of fibrinolytics

Appartengonoa this class of drugs
Streptokinase, Anistreplasi, urokinase, alteplase

Promote the conversion of plasminogen to plasmin, this breaks down fibrin in soluble fractions causing lysis of the thrombus

Risk of bleeding (especially intracranial)
Anaphylaxis with streptokinase and anistreplasi, which are antigenic

Are used in patients with myocardial infarction with chest pain for less than 12 hours
The best results are obtained with fibrinolytic therapy within 6 hours of onset of symptoms
There were no significant differences in the effect of various drugs
The use of fibrinolytics is to be associated with aspirin and heparin.
Use the fibrinolytic is not recommended in patients without ST-segment elevation.

In the second case serve drugs to inhibit the formation and propagation of the thrombus and to reduce cardiac ischemia.


Acetylsalicylic acid
Platelets are primarily responsible for thrombus formation after plaque rupture.
Aspirin inhibits platelet aggregation by reducing thromboxane A2 (see chapter on NSAIDs)
Doses of 160-325 mg / day produced a significant reduction in mortality and progression to heart failure
All studies agree on therapeutic effect of aspirin in acute coronary syndromes.

Ticlopidine and clopidogrel
Act by blocking the receptor for ADP on the platelet membrane.
The effect of ticlopidine is manifested after 48 hours; the effect of clopidogrel is more rapid.
Aspirin is best effect is ready.
Often these drugs are used in combination with aspirin in acute coronary syndromes without ST-segment elevation.
Clopidogrel is better tolerated than the ticlopidine, which can cause neutropenia, thrombocytopenia and allergic reactions.

Inhibitors of platelet receptor GPIIb / IIIa
Belong to this class of drugs:
abciximab (monoclonal antibody)

Receptor blocking platelet integrin GPIIb / IIIa is the last mechanism in the process of platelet aggregation, making it possible to build bridges between platelet fibrinogen

These drugs are in fact competitive antagonists of fibrinogen.
It is recommended for use in patients with unstable angina to prevent myocardial infarction.


It works by enhancing the effect of antithrombin

In unstable angina is used to reduce the progression of thrombus and occlusion of the coronary artery.

In case of heart attack is used after fibrinolytic and aspirin

The low molecular weight heparins have the following advantages, compared to unfractionated heparin:
• less binding to plasma proteins
• longer half-life
• lower incidence of thrombocytopenia.

It 'a direct thrombin inhibitor
It 'been approved for use in acute coronary syndromes in people who have heparin-induced thrombocytopenia.

Inhibit reactivation of vitamin K epoxide and therefore inhibit -carboxylation of clotting factors.
Their use is limited to thromboembolic prophylaxis in patients with atrial fibrillation.

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