11) - ischemic heart disease - classification , etiology , pathogenesis , differentiate diagnosis of chest pain. Stable angina pectoris Flashcards

1
Q

what are the different types of angina?

A

atherosclerotic plaque stable angina

unstable angina - coronary arteri occlusion because of thrombi in the atherosclerotic plaque

spasm - prinzimental angina

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2
Q

what are the factors increasing the oxygen demands of the heart

A

preload

increased contractility and heart rate 
more muscle mass 
anemia 
thyrotoxicosis
atriovenous communications 

afterload

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3
Q

when is significant stenosis accepted ?

A

when the lumen of the coronary arteries is more than 50 percent

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4
Q

what is the classification of coronary artery disease

A

1) chronic form

A ) stable angina pectoris

B ) silent myocardial ischemia - can be detected by ECG

temp ST segment depression

===============

2) acute from

A ) acute coronary syndrome ^ without ST elevation (NSTEMI) -

a.1 ) normal troponin = unstable angina

AMI with st elevation- stemmi

B suddenc cardiac death

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5
Q

what is the aetiology of ischemic heart disease ?

A

male
old age
stress

usually resulting from artheroscleoritic plaques so anything which increases that

hypertension 
smoking 
hsCRP 
lipoprtein A 
homocystein
infection - chlamydia 
hyperlipidemia 
endothelia dysfunction 
diabetes mellitus
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6
Q

as long as the atherosclerotic plaque does not rupture it results in what form of ischemic heart disease ?

A

chronic form of ischemic heart disease
stable angina
and silent myocardial ischemia

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7
Q

when the artherosceortic plaque ruptures what does it lead to ?

A

acute coronary heart syndrome

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8
Q

why does sudden cardiac death occur

A

the plaque ruptures - giving thrombus formation - occluding blood vessel -consequently does not give enough blood supply demand even at a resting heart

NITROGLYCERIN does not help

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9
Q

what is the clinical presentation of stable angina ?

A

retrosternal location - radiating to jaw and shoulders , ulnar zones of the arms

stable - maximum 15 mins duration 
same intensity 
same irriadiation
gradual initiation - maximum and gradual passing away 
sublingual short acting NG relieves it

triggered by exercise

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10
Q

what are the ischemic diagnosis of the heart

A

ST segment depression
T wave flattening or inversion

However after the attack should be normal

echo during the ischemic bout
segmental kinetic disturbance
impaired left ventricle relaxation
HOWEVER OUTSIDE OF IT SHOULD BE NORMAL

treadmill stress test

dobutamine stress test on ECG

myocardial perfusion scintigraphy

invasive for detailed study of plaques (golden standard ) - selective coronary arteriography :
digital and intravasuclar ultrasound + fractional flow reserve + optical coherence tomography

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11
Q

which coronary artery has the highest rate of occlusion

A

left anterior descending artery

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12
Q

what is the pathogenesis with ischemic heart disease ?

A

1) endothelial dysfunction due to atherogenic factors
or sheer stress
ROS from smoking

2)lipoprotein entry and modification
LDL into the vessel intima
Oxidation – by local ROS derived from endothelial cells or macrophages
Glycation – in diabetic patients with sustained hyperglycemia
Modified LDL has antigenic and pro-inflammatory

3)Leukocyte recruitment

4) foam cell formation
Upon entering the intima, monocytes differentiate into phagocytic macrophages and upregulate their expression of scavenger receptors.

Scavenger receptors mediate the uptake of modified LDL into macrophages
develop into foam cells which produce additional cytokines

——-fatty streak ito fibrofatty lesion—–

5) plaque progression
Thickening of the intima due to migration of SMCs from the media to the intima, proliferation of SMCs and extracellular matrix production

Apoptosis of SMCs yields a relatively acellular fibrous capsule that surrounds a lipid-rich core

6) plaque disruption
SMCs synthesize constituents of the fibrous cap such as collagen and elastin

Foam cells synthesize proteolytic enzymes including collagen-degrading matrix metalloproteinases

Over time hemodynamic stresses and degradation of extracellular matrix increase the risk of fibrous cap rupture

plaques with thicker fibrous caps tend to cause more pronounced arterial narrowing, they have less propensity to rupture (stable plaques);

conversely, thinner less obstructive plaques tend to be more fragile and rupture (vulnerable plaques

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13
Q

what are the dd for angina ?

A

musculoskeletal pain
- myalgia
intercostal neuralgia

diseases of peripheral nervous system
- herpes zoster

pleural adhesions - plerodynia

reflux esophagitis

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14
Q

what are the life style changes that need to be implemented ?

A

mediterranean diet

weight loss by exercise

quit smoking

fish consumption at least once a week -omega-3- polyunsaturated fatty acids

control of concomitant diseases, especially diabetes and hypertension

presence of anemia and hypothyroidism corrected

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15
Q

what are the type of anti platelet drugs given ?

A

Аacetylsalicylic acid (ASA) – first choice

Clopidogrel – when prevention with ASA not possible – preventive dose 75 mg daily

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16
Q

Lipid-lowering drugs?

A

Statins

fibrates and nicotinic acid

17
Q

the duration statin needs to be taken ?

and exceptions for the duration ?

A

Duration – permanent!, because there are proves that cessation of statin therapy in patients with CHD is related to “rebound” phenomenon.

statin therapy stopped only if :
- allergy

  • 3x increase in transaminases
  • Careful in chronic liver diseases,
18
Q

what is the immediate management and first line treatment for stable angia

A

reduce the pre load

vertical position

vasodilators - short acting sublingual nitroglycerine

long acting - mono and denitrates
Isosorbide mononitrate

molsidomine - long standing releases NO

19
Q

Characteristics / side effects of nitrate treatment?

and what can be used instead

A

e headache which is due to the increased intracranial pressure during the first days of treatment and is not an indication to stop the treatment

Large doses of short-acting forms may cause a severe orthostatic reactions

tolerance develops, patients begin loose the effects of the long-acting nitrate therapy. providing a nitrate-free interval 10-12hrs, or declining nitrate levels at night

when tolerance is present give MOLSIDOMINE

20
Q

when are nitrates contraindicated ?

A

elevated intraocular pressure is present

21
Q

what is the algorithm for managmnet of chronic ischemic heart disease ?

A

short acting nitrates + asa + statins ( ezetemibe or other medications ) + ACE inhibitor

first line
1) heart rate above 60BPM

a) SBP is 120 or more
= BB / NON DHP CCB

b) SBP below 120
= ranolazine / ivabradine

2) heart rate below 60bpm

a) SBP above 120
DHP

b) SBP below 120
ranolazine
——
symptoms persist move to second line

1a) DHP / ranolazine / ivabradine

1b ) trimetazidne

========

third line treatment

1a) LA nitrates / nicorandil (K channel opener)

symptoms persist - coronary angiography

==============
long term

Antiplatelet agents

Lipid-lowering medications = statins fibratase nicotinic acid
adjuvant to statin therapy in patients with high risk which remain with low levels of HDL-C and high triglycerides

ACE-inhibitors

b-blockers