Cardiovascular pharmacology - PowerPoint Presentation

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Cardiovascular pharmacologyChest painAngina

Dr. Mohammed Al Manna

PhD pharmacology/ college of medicine

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Chest pain :

In emergency unit ; chest pain either life threatening or simple causes.

Danger chest pain may caused by:

1. Angina pectoris

2. Acute

coronary

artery syndrome

{

myocardial infarction

and

unstable angina

}.

3.Pulmonary embolism

4.Pneumothorax

5. Aortic dissection & aortic aneurism .

6.Pericarditis

7. Myocarditis

8. Endocarditis

9. Pulmonary hypertension

10.Atrial fibrillations

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Non cardiac chest pain ( not dangerous cases)

1.GERD

2.Peptic ulcer

3.Muscles spasm

4.Peumonia

5. Pleurisy /

Pleuritis

6

.Herpes zoster

7

.Gallbladder diseases

8

.

.Esophageal

rupture

9-Psychosomatic

10.Pancreatitis

11. asthma

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1. Angina pectoris

Index of suspicion :

Elderly

Smoker

Nervous patient

DM

HT

Hyperlipidemia

previous MI , CABG or PCI

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Risk factors of atherosclerosis

 

HTN, diabetes, smoking, obesity,

family history, and an unhealthy diet.

Plaque

is made up of fat, cholesterol,

 calcium, and other substances found in the bloodDental plaque is also known as bacterial plaque biofilm. Bacterial plaque is one of the major causes for dental decay , gum disease and dental calculus (consists primarily of calcium phosphate) plaque calculus .

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The pain is usually central (towards the center of the chest) and fanning outwards (diffuse).

.

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1) Chronic stable angina

:

Also called “

Atherosclerotic angina

or

angina of effort or classic angina ”This refers to the more common type {about 90% of angina cases} of angina.*It is characterized by fixed stenosis caused by sub-intimal deposition of plaque (cholesterol and calcium) leading to narrowing the lumen of coronary artery that prevent coronary dilatation during efforts leading to ischemia . Moreover this patient not respond to coronary vasodilator alone because this will dilates normal artery leading to coronary stealing effect.

So , the drug treatment is usually concern with decreasing cardiac work ( such as beta blocker)-

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When cardiac work increases (

eg

, in exercise), the obstruction of flow and inadequate oxygen delivery results in the accumulation of

acidic metabolites

that stimulate myocardial pain endings

Clinical features :-Discomfort is precipitated by activity-Minimal or no symptoms at rest-Rest usually leads to complete relief of the pain within 15 minutes following cessation of precipitating activities.- Rapidly relive with nitrate .

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Diagnosis

Angina pain

Site

(retrosternal i.e. in center ) that may radiated to neck or left inner arm

Character :

mostly sense of pressure or burning .Precipitating factor : effort , emotion , eatingAssociating : sweating and sensation of impending doom. Duration : 5-15min Note : Pain more than 15 min it is either not angina or the patient enter acute coronary syndrome

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Investigation

1) ECG:

it is positive only in acute attack ; in which

ST depression

and

T wave inversion in affected area.Usually patient with stable angina has normal ECG because it usually done during rest.So not depend on ECG alone in diagnosis.2)Treadmill ECG (stress ECG) can show ECG changes in stable angina

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Treatment of stable angina

1) Patient with acute attack

Nitrate

: nitroglycerin (short acting : angised sublingual )

Aspirin

300mg Role of O2 is doubtful But should be given if O2 saturation below 94%2) Patient in between attack Rx1) Beta blocker or cardiac ca channel blocker

2)Nitrate (intermediate or long acting)3) Antiplatelet : Aspirin or clopidogrel ( plavix ) or Brilinta . 4)Lipid lowering drugs statins ( atorvastatin) 5) Other adjuvant drugs { Trimetazidine , Ranolazine }

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2)Unstable angina

:

-

It is between stable angina

and

MI -also called "crescendo angina;" this is a form of acute coronary syndrome)In which the plaque will ruptured causing release of its content leading to partially obstruction of lumen that causing sudden chest pain It can lead to complete obstruction causing acute MI so it is called unstable.It has at least one of these three features:1) It occurs at rest (or with minimal exertion) usually not respond to nitroglycerin.2)usually lasting >15 min;3)It is severe and of new onset (i.e., within the prior 4–6 weeks); and/or It occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than before).

#Requires hospital admission and more aggressive therapy to prevent progression to MI and death .

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Diagnosis and investigation

Same as of stable angina but …..

Routine blood test of cardiac enzymes such as

Troponin

to exclude MI (NSTEMI).

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Medical treatment of unstable angina

Rx

1. Dual Antiplatelet (aspirin and ticagrelor )

2. Nitrate

3. Beta blockers or

ca channel blockers4.Heparin 5. Lipid lowering agents (statin)6. ACE Inhibitors7. Anxiolytics (valium ).

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3)Prinzmetal’s angina

Is a

variant

and

uncommon

form of angina with normal coronary vessels or minimal atherosclerosisIt is occur usually occur at morning with rest probably due to spasm of coronary artery.More common in femaleEtiology :1)In this type of angina the patient has alpha-1 receptors more predominant than B2 receptors so this mediate vasospasm .2) , also the platelets release thromboxane A2 that mediate vasoconstriction.

3) Other mediators Q/ Why the alpha blockers not used clinically in treatment of variant angina?

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Treatment

-Generally responds to coronary vasodilators such as

nitrates

and vasodilators

calcium channel blockers (like ?……)

.if combination fails , CABG may be indicated -Use of B –blockers is contraindication.

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Therapeutic Strategies

1) Reducing oxygen requirement

Nitrates, calcium channel blockers, and the β- blockers.

2) Increasing oxygen delivery

.

Nitrates, calcium channel blockers and revascularization

.

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Classification of anti- anginal agents

1) Nitrates

a. Short acting :

Glyceryl

Trinitrate (GTN or Angised).b. Long acting : isosorbide mononitrate and isosorbide dinitrate2) Calcium channel blockers: -Phenyl alkylamine ( verapamil act only on heart)-Benzothiazipine(Diltiazim act on both heart and blood vessels )-Dihydropyridines (

Nifedipine , amlodipine , nimodipine)3) Beta – blockers ( metoprolol , atenolol , Bisoprolol)4) Potassium channel openers : Nicorandil 5) Others : Trimetazidine , Ranoline , Ivabradine

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1) Organic Nitrates :

prodrugs that release

nitric oxide

; mainly venodilators but also cause arteriolar dilation and as a result reduces both preload and afterload

.

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.

.

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Nitrates side effects

1.Headache :

The most common side effect of nitrates is headache due to

veno

-dilation; lack of headache often indicates degradation of agent with a loss of therapeutic effect.

2.Postural hypotension & syncope particularly with sublingual use. 3.Tachycardia induced by decreased PVR may itself induce anginal symptoms especially with unstable symptoms. 4. Methhaemoglobinemia .

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Drug interactions

#

Sildenafil &

Tadalafil

{ absolute contraindicated with nitrate } and other vasodilators potentiate the hypotensive action of nitrates that may resulted in MI and sudden death if taken through same day.

Tolerance

: lack of response due to high exposure to nitrate so , nitrate free intervals (required 10-12hrs typically at night ; however variant angina worsens early in the morning therefore it should be used in the late afternoon).

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inferior MI

that

may cause

right ventricular infarction in which the preload will decreased and severe hypotension and shock may occur if we give nitrate ; this condition diagnosed by reveres V4 lead position that showed ST elevation ; this condition is treated effectively by increase preload by normal saline infusion.

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2) Calcium Channel-Blocking Drugs

{

Diltiazem

and verapamil}.

Mechanism of Action

Calcium channel blockers block voltage-gated L-type calcium channels, the calcium channels most important in cardiac and smooth muscle.

By decreasing calcium influx during action potentials these agents reduce intracellular calcium concentration and muscle contractility. .

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3) Beta-Blocking Drugs (metoprolol, atenolol)

Because they reduce cardiac work (and oxygen demand), all blockers are effective in the

prophylaxis

of atherosclerotic angina attacks.

Effects and Clinical Use

Actions include (decreased heart rate, cardiac force, blood pressure) .

Beta blockers are used only for prophylactic therapy of angina; they are of no value in an acute attack. They are effective in preventing exercise-induced angina but are ineffective against the vasospastic form. ..

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The combination of blockers and nitrates is useful because the adverse undesirable compensatory effects evoked by the nitrates (tachycardia and increased cardiac force) are

prevented or reduced by beta- blockers .

#

Patient use beta-blockers should be gradually tapered off over to 5- 10 days to avoid rebound angina

.

.

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MI

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Potassium channel openers: nicorandil

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MI

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Dental considerations

Q/ What is the dental consideration in case of angina pectoris??

.

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End