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whats a heart attack
occurs when arteries become blocked due to plaque buildup = ASCVD
atherosclerotic cardiovascular disease
high LDL is main driver of ASCVD → CAD, myocardial infarction (MI), angine & coronary artery stenosis
both genetic & lifestyle factors contribute to cholesterol levels
what speeds up an earlier onset of myocardial infarction
higher cholesterol leads to the speed that plaque builds
Modifiable risk factors
high BP
high LDL
diabetes
smoking
obesity
physical inactivity
Nonmodifiable risk factors
family history (FHX)
<55years father or M 1st relative experiencing HA
<65years mother or Fm1st relative experiencing HA
age
sex ( F or M)
Female post menopause
emerging risk factors
homocysteine
diet deficiencies
elevated Lp(a) levels
clotting factors
hsCRP
pro-thrombotic factors
pro-inflammatory factors
what is the underlying cause of most Heart Attacks
atherosclerosis
disease of the coronary arteries that takes several years to ‘usually’ develop
combination of genetic & lifestyle factors contribute to cholesterol levels
high cholesterol → higher speed plaque builds → early onset of MI
Ischemic Heart (IHD)
an imbalance bt the supply of oxygen and the demand of the myocardium resulting in myocardial ischemia
loss of ATP, ionic disturbances
Myocardium supply can be affected by
atheroma
thrombosis
spasm
embolus
Myocardium demand can be affected by
anemia
hypertension
high cardiac output
Common triggers of High Cardiac Output
anemia: less RBCs → demand faster pumping for O2 delivery
hyperthyroidism: XS thyroid hormones accelerate metabolism & HR
Obesity: higher tissue mass & vasodilation increase demand
sepsis/liver disease: vasodilation & inflammation reduce resistance
High Cardiac Output
reduced systemic vascular resistance or excess O2 consumption activates sympathetic responses, initially compensating but risking eventual systolic failure
often precedes heart failure from chronic overload
Myocardial Infarction (MI)
blood flow (O2) to an area if the myocardium is blocked off, causing tissue damage
myocardial cell death (necrosis)
usually plaque rupture with thrombus
major adverse CV event (MACE) leading to morbidity,, mortality, & LV remodeling
20-60% are silent, atypical, or unrecognized
Angina Pectoris
symptom not disease
stable - most common
triggered by an increase in myocardial demand
relieved by rest
unstable - more frequent
prolonged in duration & can occur at rest
variant - least common
random & transient episodes triggered bu vasospasm of the CA
more prevalent in women; occurs more often at night
Screening & diagnosis
electrocardiogram (ECG)
measures electrical impulse
stress test
measures blood supply to the heart
coronary angiography
shows specific sites of narrowing in the coronary artery
blood tests
can detect the chemical presence of dying heart cells (troponin, CK, or CK-MB)
Acute Coronary Syndrome (ACS)
ST waves shows heart’s contraction pattern when it pushes blood out the ventricles
changes in these waves correspond to type of damage
determine partial to complete blockage
unstable angine → No ST elevation MI → STEMI
Coronary revascularization
restoration of blood flow to ischemic myocardium in obstructive CAD
main modalities have shared goal of improving perfusion, symptoms & prognosis
percutaneous coronary intervention (PCI) (angioplasty ± stent)
coronary artery bypass grafting (CABG)
Percutaneous Coronary Intervention (PCI) / angioplasty
non surgical procedure, uses catheter to place a stent to open the blood vessel in the heart that has been narrowed by plaque build up
signs/symptoms occur around 75% of blockage
Percutaneous Coronary Intervention (PCI) / angioplasty Imaging
3D myocardial perfusion CV magnetic resonance permits whole heart coverage & can establish an estimation of myocardium at risk & ischemic burden
Type of plaque & the Burden (TCFA)
image of the artery & the percentages related with the type of plaque inside it
plaque
fibrous
fibro-fatty
lipid rich (necrotic)
calcified
Thin-Cap Fibroatheroma (TCFA)
lipid core >10%
calcium build up in lumen might not feel differently until demand is created which results in heart attack
chronic inflammation
proteolytic enzymes released from macrophages in lesions → unstable angina
establish paradigm of matrix degradation & the lesion instability of TCFA
Resolution
stable plaque is intact with thick fibrous cap; smooth muscle cells (SMC) in a matrix rich in collagen
Coronary Artery Bypass Grafting (CABG)
surgical “bypass graft” which enables oxygenated blood to reach the myocardium; bypasses the blocked portion of diseased artery
healthy blood vessel is removed from the leg, arm, or chest replaced the damaged one
mammary graft often used bc its endothelial layer has less openings, lower intercellular junction permeability, greater anti-thrombotic molecules, & higher endothelial NO production
Mechanism of death from coronary causes
fatal MI
pump failure with cardiogenic shock
lethal arrhythmias
mechanical complications of MI or progressive ischemic cardiomyopathy
during pullback from revascularization
Coronary Death
reflects ultimate failure of coronary perfusion to support myocardial function & electrical stability
Sustained ventricular tachycardia
if rhythm last more than 30s
non-sustained ventricular tachycardia
if the fast rhythm self terminates within 30s
Composite Endpoint
occurrence of any several prespecified events (MI, revascularization, coronary death) counting equally as “an event”
bundled outcomes - in cardiovascular clinical trials
boosts event #s for better statistical detection of treatment effects
rationale:
composite endpoints aggregate multiple events, raising total incidents from rare ones like death to 20%+ , enhancing the study trial power & feasibility with smaller samples/shorter durations