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Last updated 10:45 PM on 3/25/26
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26 Terms

1
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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

2
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what speeds up an earlier onset of myocardial infarction

higher cholesterol leads to the speed that plaque builds

3
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Modifiable risk factors

  • high BP

  • high LDL

  • diabetes

  • smoking

  • obesity

  • physical inactivity

4
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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

5
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emerging risk factors

  • homocysteine

    • diet deficiencies

  • elevated Lp(a) levels

  • clotting factors

  • hsCRP

  • pro-thrombotic factors

  • pro-inflammatory factors

6
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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

7
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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

8
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Myocardium supply can be affected by

  • atheroma

  • thrombosis

  • spasm

  • embolus

9
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Myocardium demand can be affected by

  • anemia

  • hypertension

  • high cardiac output

10
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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

11
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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

12
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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

13
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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

14
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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)

15
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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

16
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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)

17
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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

18
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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

19
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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

20
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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

21
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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

22
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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

23
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Coronary Death

  • reflects ultimate failure of coronary perfusion to support myocardial function & electrical stability

24
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Sustained ventricular tachycardia

if rhythm last more than 30s

25
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non-sustained ventricular tachycardia

if the fast rhythm self terminates within 30s

26
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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

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