11) - ischemic heart disease - classification , etiology , pathogenesis , differentiate diagnosis of chest pain. Stable angina pectoris Flashcards
what are the different types of angina?
atherosclerotic plaque stable angina
unstable angina - coronary arteri occlusion because of thrombi in the atherosclerotic plaque
spasm - prinzimental angina
what are the factors increasing the oxygen demands of the heart
preload
increased contractility and heart rate more muscle mass anemia thyrotoxicosis atriovenous communications
afterload
when is significant stenosis accepted ?
when the lumen of the coronary arteries is more than 50 percent
what is the classification of coronary artery disease
1) chronic form
A ) stable angina pectoris
B ) silent myocardial ischemia - can be detected by ECG
temp ST segment depression
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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
what is the aetiology of ischemic heart disease ?
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
as long as the atherosclerotic plaque does not rupture it results in what form of ischemic heart disease ?
chronic form of ischemic heart disease
stable angina
and silent myocardial ischemia
when the artherosceortic plaque ruptures what does it lead to ?
acute coronary heart syndrome
why does sudden cardiac death occur
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
what is the clinical presentation of stable angina ?
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
what are the ischemic diagnosis of the heart
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
which coronary artery has the highest rate of occlusion
left anterior descending artery
what is the pathogenesis with ischemic heart disease ?
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
what are the dd for angina ?
musculoskeletal pain
- myalgia
intercostal neuralgia
diseases of peripheral nervous system
- herpes zoster
pleural adhesions - plerodynia
reflux esophagitis
what are the life style changes that need to be implemented ?
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
what are the type of anti platelet drugs given ?
Аacetylsalicylic acid (ASA) – first choice
Clopidogrel – when prevention with ASA not possible – preventive dose 75 mg daily
Lipid-lowering drugs?
Statins
fibrates and nicotinic acid
the duration statin needs to be taken ?
and exceptions for the duration ?
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,
what is the immediate management and first line treatment for stable angia
reduce the pre load
vertical position
vasodilators - short acting sublingual nitroglycerine
long acting - mono and denitrates
Isosorbide mononitrate
molsidomine - long standing releases NO
Characteristics / side effects of nitrate treatment?
and what can be used instead
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
when are nitrates contraindicated ?
elevated intraocular pressure is present
what is the algorithm for managmnet of chronic ischemic heart disease ?
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
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third line treatment
1a) LA nitrates / nicorandil (K channel opener)
symptoms persist - coronary angiography
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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
