ASCVD (Duval) Flashcards
What are the 3 patterns of vascular disease manifested by the thickening and inelasticity of the arteries?
1) Atherosclerosis
2) Monckeberg’s medial calcific sclerosis
3) Arteriosclerosis
What is medial calcific sclerosis and who does it affect?
The calcification of the muscle wall (media) of the arteries that may ossify. There is NO narrowing of the vessel lumen. Affects patients older than 50 years
What is arteriosclerosis?
The thickening and narrowing of the vascular walls and arterioles. It’s associated with HTN and DM.
What are the 2 variants of arteriolosclerosis?
1) Hyaline
2) Hyperplastic
What is atherosclerosis?
The build up of intimal fibro-fatty plaques that narrow the vascular lumen and weaken the atrial walls (media).
What are the major targets of atherosclerosis and what could they cause?
1) The aorta (AAA, PVD, intestinal ischemia
2) Coronary arteries (IHD and MI)
3) Cerebral arteries (stroke)
What is and what happens in the 3 phases of atherosclerosis?
Preclinical phase - when a normal artery becomes gets fibro-fatty plaques and endothelial dysfunction occurs
Clinical horizon - when the plaques get advanced and vulnerable. You see cell death, thrombus formation, calcification
Clinical phase - WHere you would see critical stenosis, aneurysm or plaque rupture
What has a significant reduction in IHD and stroke in the last 50 years been due to?
1) Life style changes
2) Improved IHD therapy
3) the prevention of reoccurrences
What is CRP, what does it correlate with and what reduces it
C-reactive Protein - a systemic marker of inflammation synthesized by the liver. It correlates with the risk of IHD, stroke, PVD and SCD. Its levels are reduced by smoking cessation, weight loss, exercise and statins
T/F Risk factors are additive?
False: Two risk factors correspond to 4x risk of MI
3 risk factors correspond to a 7x risk.
Outside of the normal, what are some other risk factors of atherosclerosis?
Type A personality, estrogen deficiency, chlamydia pneumonia, hyperhomocysteinemia and Lipoprotein (Lp(a))
What is hyperhomocystinemia?
An inborn error of metabolism resulting in high levels of circulating homocysteine. It can be caused by low folate and vitamin B intake. It correlates with CAD, PVD, stroke and venous thrombosis.
What is Lipoprotein Lp (a)
An altered form of LDL. There is a correlation btwn that and coronary and cerebral vascular disease
What is the 5 steps to the response to injury hypothesis?
1) Chronic endothelial injury
2) Endothelial dysfunction and monocyte adhesion/emigration
3) Smooth muscle cell emigration & macrophage activation
4) Macrophages and smooth muscle cells engulf lipids.
5) Proliferation of Smooth muscle cells , extra cellular matrix and extracellular lipid
What are the 2 most important contributors to endothelial injury?
1) Hemodynamics
2) Hypercholesterolemia
What is hemodynamics?
Shear stress and turbulent flow to arteries where plaques occur at branch points and the posterior abdominal aorta
What are macrophages role in atherosclerosis?
The engulf lipoproteins to become foam cells. Also they rercruit WBC, oxidize LDL and elaborate growth factors.
Atherosclerosis starts off as a ______ _________?
Fatty streak
Where are fatty streaks more commonly found?
The long axis of the aorta. The aortic valve ring, posterior thoracic aorta, coronary arteries and abdominal aorta
Where are fatty streaks most found
Abdominal aorta (most), coronary arteries 2nd, popliteal arteries 3rd, and thoracic artery 4th.
Name the 6 types of atherosclerosis lesions classified by the AHA
Type 1 - Fatty dot (precursor) Type 2 - Fatty streak Type 3 - Intermediate lesion Type 4 - Atheroma Type 5 - Fibroatheroma Type 6 - Complicated plaque
What are 4 causes of an aneurysm?
1) congenial defect
2) local infection
3) trauma
4) systemic disease (AS syphilis)
What is the most common aortic aneurysm?
Atherosclerotic aneurysms
Where are most Atherosclerotic aneurysms found?
In the infrarenal aorta
what is the most common cause of Ischemic Heart disease?
Atherosclerosis
What are the 4 syndromes associated with Ischemic Heart disease?
1) Angina pectoris
2) MI
3) Sudden cardiac death
4) Chronic IHD
Who is more at risk for Ischemic Heart disease?
Men over women until 9th decade
Males over 60 and females over 70.
Those with HTN, DM, smoking, elevated LDL or genetic issues
What is critical stenosis defined as
75 percent narrowing.
What are some other causes of IHD?
Reduced blood supply issues - Emboli from vegetations, vasculitis and systemic HTN Increased demand (LVH) - Systemic HTN, valvulopathy
What is angina pectoris?
Intermittent chest pain d/t reversible myocardial ischemia
What are the 3 variants of Angina Pectoris?
1) Stable angina
2) Prinzmetal’s or variant angina
3) Unstable angina
What is stable angina
Episodic chest pain associated with exertion or stress. The pain is described as crushing, squeezing and may radiate to left arm. A fixed lesion greater than 75% vessel lumen
What relieved stable angina
NTG it reduces preload and augments coronary blood flow
What is Prinzmetal’s or variant angina? What relieves it?
Where chest pain occurs at rest or while sleeping. There is a vasospasm near the plaque. It responds to vasodilators
What is Unstable Angina
Aka crescendo and perinfarction angina. It angina with increasing frequency, longer duration and more intense pain. Due to acute plaque changes like thrombosis, embolization and vasospasm
What is Myocardial infarction?
Local ischemia leading to corresponding myocardial necrosis and death of heart muscle
T/F Myocardial infarction is irreversible
True
What is the most common cause of MI
Coronary artery thrombosis (preexisting plaque disrupted)
How long after an MI does necrosis begin?
20-30 minutes and max size after 3-6 hours
What is the importance of the MI timeline
Its the window for thrombolytic therapy
What are the most common places infarcts occur (thrombi form)?
Left anterior descending artery - Anterior/apical (apex) infarcts
Right coronary artery - posterior/basal infarcts
Left circumflex artery - lateral infarct
What areas gets the larger infarcts
The ones with the more proximal occlusion
What happens in the first 24 hours of an MI?
0 to 12 hours - Gross -nothing, Microscopic wavy fibers and edema
12 to 18 hours - Gross nothing, Micro: coagulation necrosis CBN,
18 to 24 hours - Gross slight, Micro: neutrophils and necrosis
What happens in the first 10 days of an MI?
3 days - Gross- pallor, Microscopic - peak neutrophils
4-7 days - Gross - Central pallor and hyperemic border, Microscopic- macrophages with early granulation tissue (scaring)
10 days - Gross - yellow soft sunken, Microscopic prominent granular tissue
What happens from 10 days to 8 weeks for an MI?
4 weeks - maturing fibrosis
8 weeks - gross - firm and gray, microscopic - dense scar tissue
What is contraction band necrosis?
Coarse transverse bands of myocytes d/t hyper contraction of reperfused dying calls triggered by influx of calcium
What are some complications of MI?
1) Papillary muscle dysfunction
2) Rupture
3) Mural thrombi
4) Acute pericarditis
5) Ventricular aneurysm
When would papillary muscle dysfunction occur and what could it cause?
Occur about 3 days after MI.
Can result in severe Mitral regurg and LV failure
What are the two types of myocardial ruptures
External - in first 2 weeks (peak 4-7 days) of MI d/t poorly developed granulation tissue fibrosis
Internal (septal) - acute L to R shunt and CHF
What is a mural thrombi
A thrombi formed on an endocardial surface overlying an infarct that may cause stroke.
How common is acute pericarditis to a person with an MI and how long would it take?
About 15% of MI patients
It would occur 2 to 4 days after transmural infarct
What is a ventricular aneurysm?
When a fibrous myocardium bulges during systole. Usually anteroapical
What is the outcome of a ventricular aneurysm?
1) arrhythmia
2) papillary muscle dysfuction
3) CHF
4) embolization
T/F the pain from an MI can be relieved by nitroglycerine
False
What is the percent of MIs that are silent?
20-30 percent (in diabetic, HTN and elderly)
What is the percent of patients with MIs who make it alive to the hospital?
About 75%
Of the 75% that make it to the hospital alive having an MI what is their fate?
10-20% no complications 75-95% get arrhythmias 60% get LVF with pulmonary edema 10% get cardiogenic shock 4-8% get rupture 15-49% get a thromboembolism
What are the EKG abnormalities in a patient with MI
Q waves, ST changes and T wave inversions
What would you see in Creatine Kinase labs in a patient with MI
Total CK - rise 2-4 hours, peake 24 hours, decline 72 hrs.
CK-MB - rise 2-4 hours, peak 18 hours, decline 48 hrs.
How long after a clean CK test is an MI ruled out
2 days
T/F troponin I is more cardiospecific than CK-MB
True
What Troponin readings would you see in a patient with MI?
Rise 2-4 hours, persists 4-7 days
Other than an MI what other heart issue could be seen in elevated troponins?
Unstable angina progressing to an AMI
What is chronic ischemic heart disease
AKA ischemic cardiomyopathy. It’s progressive CHF d/t long term ischemic myocardial injury. Angina and infarcts are common
What gross morphology might you see in a patient with chronic ischemic heart disease?
Moderate to severe CAD, cardiomegaly, multiple foci of fibrosis, cardiac hypertrophy, a thick opaque endocardium and adherent thrombi
What microscopic features might you see in a patient with chronic ischemic heart disease?
Extensive fibrosis, atrophic and hypertrophic fibers, subendocardial vacuolation
What are the s/s of chronic ischemic heart disease
Severe progressive HF
possible angina or infarcts
Arrhythmias
What is the most common mechanism of sudden cardiac death
Lethal ventricular arrhythmia (Vfib) d/t IHD
What are 3 syndromes due in part to acute plaque changes?
1) Unstable Angina
2) Acute MI
3) Sudden cardiac death
