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atherosclerosis
a condition in which plaque builds up inside the arteries
the plaque consists of fatty deposits, cholesterol, calcium, and other substances found in the blood
as the plaque grows, it can harden and calcify, further narrowing the arteries and stiffening them
this reduces their flexibility and ability to respond to changes in blood pressure
over time, this plaque hardens and narrows the arteries, leading to reduced blood flow to vital organs and tissues
the plaque may rupture, triggering the formation of a blood clot at the site
this can partially or completely block blood flow, leading to serious conditions like heart attack or stroke
the reduced blood flow can also cause conditions such as angina (chest pain), peripheral artery disease (PAD), or chronic kidney disease, depending on which arteries are affected
types of cardiovascular disease (CVD)
atherosclerotic CVD (ASCVD)
non-atherosclerotic CVD
atherosclerotic CVD (ASCVD)
atherosclerosis that causes ASCVD medical conditions in the coronary arteries
eg. heart attack (MI)
or, atherosclerosis that causes ASCVD medical conditions in the brain, kidney, aorta, mesentary, or peripheral arteries
eg. ischemic stroke or CVA
non-atherosclerotic CVD (non-ASCVD)
non-athersclerotic factors cause non-ASCVD medical conditions in the heart or vasculature, such as
hemorrhagic stroke
heart failure
arrhythmias (eg. Afib)
venous thromboembolism (VTE)
deep vein thrombosis (DVT)
heart valve disorders
congenital heart diseases
basically conditions that have nothing to do with plaque build-up in the arteries
coronary vessel ASCVD
atherosclerosis that occurs in the primary blood vessels that supply oxygen and nutrients to the heart muscle (coronary arteries), including conditions such as:
ischemic heart disease (IHD)
aka coronary artery disease (CAD)
aka coronary heart disease (CHD)
chronic stable angina
myocardial infarction (MI)
acute coronary syndrome (ACS) / unstable angina
surgical revascularization of coronary artery
coronary artery bypass graft (CABG)
percutaneous coronary intervention (PCI)
coronary stent or angioplasty
non-coronary vessel ASCVD
ischemic stroke - cerebrovascular accident (CVA)
transient ischemic attack (TIA) - “mini stroke”
renal artery stenosis
can involve single or both kidneys
mesenteric artery disease
“bowel infarction”
abdominal aortic aneurysm (AAA)
“triple” A
peripheral vascular disease (PVD)
eg. peripheral artery disease (PAD)
“intermittent claudication”
surgical revascularization of non-coronary artery (eg. AAA repair)
guidelines for CVD
American College of Cardiology (ACC)
American Heart Association (AHA)
primary prevention of ASCVD
lifestyle and/or drug therapy used to reduce the risk of CVD development in adults
eg. clinician patient discussion on benefit vs. risk of treatment to optimize pt outcomes
basically, the pt has no existing clinical manifestations of ASCVD, but they may have high risk factors, so you’re aiming to reduce the risk of developing ASCVD in the first place
this includes interventions to reduce ASCVD risk, such as addressing risk factors
includes use of risk estimation tools to guide decisons on preventative care according to risk level, such as the pooled cohort equation (PCE)
pooled cohort equation (PCE)
used in AHA/ACC guidelines on management of HTN, cholesterol, and ASCVD primary prevention
you put in your demographics (age, race, sex, etc) and you get:
10 year risk score
30 year risk score
assess risk enhancing factors and coronary artery calcium (CAC) score along with the results
limitations to the pooled cohort equation (PCE)
validated in non-hispanic whites and african-american populations
however, it may underestimate ASCVD risk in higher risk populations
eg. south asian, american-indian or puerto-rican populations
it may also overestimate ASCVD risk in lower risk populations
eg. east asian or mexican populations
it will not calculate if the LDL is ≥ 190 mg/dL
automatic high risk
intended for use at base-line, to decide on lipid-lowering therapy
lastly, it does not account for CKD or metabolic health
higher risk populations for ASCVD risk
south asian (eg. indian or pakistani)
american-indian
puerto-rican
lower risk populations for ASCVD risk
east asian (eg. korean or chinese)
mexican
primary prevention guideline for ASCVD
recommended interventions to lower risk of developing ASCVD
20-39 yrs old: assess traditional CV risk factors every 4-6 years
40-75 yrs old: routinely assess traditional CV risk factors AND routinely estimate 10-year ASCVD risk score
if estimated 10-year ASCVD is 5-19.9% (intermediate risk):
consider risk enhancing factors (REF)
may consider coronary artery calcium (CAC) score if risk-based decisions remain uncertain after discussing risk factors/REF
if 40-59 yrs old and estimated 10-year risk is < 7.5%:
may consider 30-year ASCVD risk score
10-year risk score (PCE)
“short-term” risk
decribes the risk for a patient of developing their first ASCVD event (heart attack or stroke) within 10 years
only applicable to patients without clinical manifestations of ASCVD (primary prevention)
only applicable to patients who are 40-79 years old
in primary prevention guidelines, it’s from ages 40-75 years old)
30-year risk score (PCE)
“long-term” or “lifetime” risk
only applicable to patients without clinical manifestations of ASCVD (primary prevention)
only applicable to patients who are 40-59 years old
mostly used for clinician-patient dicussion on the importance of lifestyle and/or drug therapy
compares risk with vs without optimal risk factor management
eg. 50% vs 35%
let’s say they get a lifetime 30% risk of developing ASCVD, but if they optimized their risk factors (like lowered their BP for example), their risk score would potentially only be 35%
10-year risk score is < 5% (PCE)
low risk for developing ASCVD in 10 years
10-year risk score is 5-7.4% (PCE)
borderline risk for developing ASCVD in 10 years
10-year risk score is 7.5-19.9% (PCE)
intermediate risk for developing ASCVD in 10 years
10-year risk score is > 20% (PCE)
high risk for developing ASCVD in 10 years
primary prevention algorithm for low risk patients
10-year ASCVD risk score is < 5%:
risk discussion: emphasize the importance of lifestyle modification to reduce risk factors
no drug therapy
primary prevention algorithm for borderline risk patients
10-year ASCVD score is 5 to <7.5%:
clinican-patient discussion considering risk-enhancing factors and net benefit of therapy
if uncertainty remains, consider CAC score and revise decision based on results
lifestyle modifications only or lifestyle AND drug therapy
primary prevention algorithm for intermediate risk patients
10-year ASCVD score is 7.5 to <20%:
clinican-patient discussion considering risk-enhancing factors and net benefit of therapy
if uncertainty remains, consider CAC score and revise decision based on results
lifestyle modifications only or lifestyle AND drug therapy
primary prevention algorithm for high risk patients
10-year ASCVD score is ≥ 20%:
patient should definitely start drug therapy (statins) to decrease risk AS WELL AS lifestyle modifications
lifestyle AND drug therapy initiation
calcium artery calcium (CAC) score
a tool used in assessing the risk of developing ASCVD
it quantifies the amount of calcium buildup in the coronary arteries using a CT scan, which helps to estimate the presence of atherosclerotic plaque in the arteries
calcium is a marker of plaque (atherosclerosis), so a higher CAC score suggests more plaque in the arteries
CT scan may be costly and not often covered by insurance though
especially useful in patients with a borderline/intermediate 10-year risk score to help determine what they want to do for therapy
for example, if someone has borderline cholesterol or hypertension, a score of 0 might suggest that aggressive treatment isn’t needed
on the other hand, a high CAC score would indicate a greater need for preventive therapies
in primary prevention, the goal is to avoid the first cardiovascular event (e.g., heart attack, stroke)
thus, the score is a way to personalize risk assessment, helping to identify patients who may benefit from early intervention with lifestyle changes, medications like statins, or more intensive monitoring
subclinical ASCVD
the patient falls into this classification if their CAC score is positive/high
don’t need to know the specifics of their CAC score, just know that these patients have a high CAC score
secondary prevention
lifestyle and/or drug therapy used to reduce progression of existing CVD in adults
eg. guideline directed medical therapy (GDMT) to optimize patient outcomes
if the patient has any of the clinical manifestations of ASCVD, both coronary and non-coronary ASCVD, they automatically fall into this classification
this is because once the pt has gotten atherosclerosis in one vessel, they’re likely to get it again in other vessels, so you want to prevent this progression
very specific guideline-directed medical therapies
evidence-based medicine
no risk estimation needed (since they already have ASCVD, making them high risk for more ASCVD)
secondary prevention guideline for ASCVD
recommend interventions to reduce ASCVD progression
routinely asses traditional CV risk factors
invalid to use any ASCVD risk score, CAC, or REF
follow guideline-directed medical therapy (GDMT) to optimize patient outcomes
traditional cardiovascular risk factors
age
≥ 55 years old for males
≥ 65 years old for females
hypercholesterolemia (dyslipidemia)
hypertension
diabetes mellitus
either type 1 or type 2
current tobacco use (within the last 30 days)
obesity
physical inactivity
risk enhancing factors (REF) for primary prevention of ASCVD
family history of premature ASCVD
first-degree relative (eg. parent, child, sibling) that developed CVD before age 55 in males, or before age 65 in females
higher risk race/ethinicity/ancestry
eg. south asian, puerto-rican, american-indian
primary hypercholesterolemia
high LCL → 160-189 mg/dL
elevated biomarker levels
C reactive protein, lipoprotein a, aproprotein B, low ankle brachial index (ABI), persistently elevated hypertriglyceridemia
non-fasting TG ≥ 175 OR fasting TG ≥ 150 on 2-3 occasions
metabolic syndrome (MetS)
chronic kidney disease (CKD)
eGFR of 15-19 with or without proteinuria
doesn’t count if they are treated with dialysis or kidney transplantation
chronic inflammatory conditions
premature menopause or pregnancy conditions
menopause under age 40 or conditions such as preeclampsia, gestational diabetes/ HTN, etc
diabetes specific risk enhancers
long- duration
having type 2 DM ≥ 10 years
type 1 DM ≥ 20 years
nephropathy (GFR <60 and proteinuria)
retinopathy (eye)
neuropathy (PAD)
systolic blood pressure (SBP)
the upper number on a blood pressure reading
diastolic blood pressure (DBP)
the lower number on a blood pressure reading
normal blood pressure
systolic blood pressure (upper number) is less than 120 mm Hg
AND…
diastolic blood pressure (lower number) is less than 80 mm Hg
eg. 110/74
elevated blood pressure
systolic blood pressure is 120-129 mmHg
AND…
diastolic blood pressure is less than 80 mmHg
eg. 120/68
high blood pressure (stage 1)
systolic blood pressure is 130-139 mmHg
OR…
diastolic blood pressure is 80-89 mmHg
eg. 135/67 or 120/87
high blood pressure (stage 2)
systolic blood pressure is greater than 140 mmHg
OR…
diastolic blood pressure is greater than 90 mmHg
eg. 133/95 or 154/60
hypertensive crisis
systolic blood pressure is greater than 180 mmHg
AND/OR…
diastolic blood pressure is greater than 120 mmHg
eg. 185/91 or 143/125 or 181/130
patient must consult with a doctor immediately
isolated systolic hypertension
the SBP is classified as stage 1 hypertension or higher (>130 mmHg), but the DBP is classified as normal (<80 mmHg)
however, the higher category always applies if the systolic and diastolic BPs fall into different categories
orthostasis (aka orthostatic hypotension or postural hypotension)
defined as a SBP that drops ≥ 20 mmHg and/or a DBP that drops ≥ 10 mmHg within 2-5 minutes of going from a sitting/laying down position to a standing position or vice/versa
can occur with OR without symptoms
symptoms could include significant dizziness or syncope (passing out)
risk factors for orthostasis
older age (>65 yrs), especially very old age (>80 yrs)
drug therapy side effects such as hypotension, excessive sweating, or more urination
when it occurs, its usually due to hypovolemia, which is defined as extracellular fluid loss often with inadequate fluid intake, which causes low intravascular volume and low tissue perfusion
make sure they are drinking enough fluid
bradycardia
resting HR is < 60 BPM
symptoms may include:
fatigue
dizziness
lightheadedness
syncope
tachycardia
resting HR is > 100 BPM
symptoms may include:
dizziness
lightheadedness
palpitations
angina (chest pain)
SOB
basic metabolic profile (BMP)
a common set of blood tests which evaluates certain assays such as:
sodium (Na+)
potassium (K+)
serum creatinine (SCr)
estimated glomerular filtration rate (eGFR)
blood urea nitrogen (BUN)
blood glucose (BG)
calcium (Ca++)
carbon dioxide
chloride (Cl-)
normal range for sodium in blood
135 - 145 mEq/L
hyponatremia
less than 135 mEq/L in blood
hypernatremia
more than 145 mEq/L in blood
normal range for potassium in blood
3.3 - 4.9 mEq/L
hypokalemia
less than 3.3 mEq/L in blood
hyperkalemia
more than 4.9 mEq/L in blood
normal range for serum creatinine (SCr)
0.6 - 1.1 mg/dL
should be interpreted with caution, and in combination with the eGFR
just because it may be within normal limits (WNL) doesn’t mean there is no kidney impairment
normal estimated glomerular filtration rate (eGFR)
≥ 60 mL/min
labs will use a standardized value
this standardizes the interpretation of kidney function without sole reliability on SCr
lab reports use standard calculation (MDRD equation) for estimating pt’s “renal function”
values may differ slightly from other estimates
eg. creatinine clearance (CrCl)
some FDA drugs that need renal dosing adjustments go based off of this value or CrCl, or sometimes even going based off of SCr
kidney function
can determine with the help of serum creatinine (SCr) levels and estimated glomerular filtration rate (eGFR)
CAUTION: just because SCr is within normal limits (WNL) doesn’t necessary mean normal kidney function → you must always interpret its results in conjunction with eGFR
pt’s age, gender, weight, and muscle mass may limit the predictability of SCr to detect “renal impairment”
chronic kidney disease (CKD)
typically involves an eGFR < 60 mL/min with abnormal SCr
can occur with OR without proteinuria (protein in urine)
proteinuria (aka microalbuminuria or macroalbuminuria)
defined as an albumin-creatinine ratio (ACR) ≥ 30 mg/g
normal range for albumin-creatinine ratio (ACR)
< 30 mg/g
indicates no proteinuria or insignificant proteinuria
comprehensive metabolic profile (CMP)
includes everything in the BMP assays plus:
albumin
total protein
alkaline phosphatase
bilirubin
aspartate transaminase (AST or SGOT)
alanine transaminase (ALT or SGPT)
normal range for AST in blood
11 - 47 IU/L
normal range for ALT in blood
7 - 53 IU/L
hepatic transanimases
AST and ALT
most common liver function tests (LFTs) referred to with pharmacotherapy warnings
some drugs, for example, need to be avoided if the ALT is greater than 3x the upper limit of normal (ULN)
abnormalities of these values are often based on degree of ALT or AST elevation relative to the upper limit of normal (ULN)
for example, “AST 2 x ULN” = AST 94 IU/L (since the AST ULN is 47 and you multiply that by 2)
eg. “ALT > 3 x ULN” = ALT is > 159 IU/L (since ALT ULN is 53 and you multiply that by 3)
cholesterol (lipid) profile
includes
HDL-C
triglycerides (TG)
total cholesterol (total-C or TC)
LDL-C
labs report a calculated LDL-C measurement
this is because a direct LDL-C is a more costly and specific study
fasting lipid profile (FLP)
the gold standard for cholesterol/lipid profile, especially when screening or managing dyslipidemia
you want the patient to have not eaten/drank for at least 8-12 hours before
if screening a patient for dyslipidemia, it’s reasonable to use a non-fasting profile in pts who are low risk since you wouldn’t expect high TGs anyway
when a pt is not fasting, the lipid profile can demonstrate higher triglycerides
formula for LDL-C on a FLP
[TC] - [HDL-C] - [TG/5]
cannot calculate when TG ≥ 400 mg/dL
this is because triglycerides are the fatty portion of cholesterol, and too much will ruin the sample, making it an inaccurate read
thus, cannot accurately calculate
formula for percent LDL lowering
[change in value (baseline value – current value) ÷ baseline value] * 100
baseline value = value before treatment
current value = value after treatment/currently
dyslipidemia
consists of abnormally high levels of LDL-C and/or triglycerides
LDL-C levels are the primary focus in its management
the goal is to reduce the pt’s levels to target level
range for elevated LDL-C
70-159 mg/dL
may or may not treat with drug therapy comparative to the patient’s baseline risk for ASCVD
range for high LDL-C
160-189 mg/dL
targets for drug therapy in most cases
unless the pt has the contraindications, will almost always start with statin therapy
range for very high LDL-C
≥ 190 mg/dL
targets for drug therapy in most cases
unless the pt has contraindications, will almost always start with statin therapy
hyperlipidemia/hypercholesterolemia
increases risk of ASCVD in a log-linear manner
basically, the higher the LDL, the higher the ASCVD risk
range for borderline high triglycerides
150-199 mg/dL
range for high triglycerides
200-499 mg/dL
range for very high (severe) triglyceridemia
≥ 500 mg/dL
increases risk for ASCVD if persistently elevated
also increases risk for pancreatitis
an acute condition leading to abdominal pain due to inflammation of the pancreas
range for moderate hypertriglyceridemia
150-499 mg/dL
may increase ASCVD risk, especially if it is persistently elevated
range for persistently elevated TGs (fasting)
TG ≥ 150 on 2-3 occasions
range for persistently elevated TGs (NON-fasting)
TG ≥ 175 on 2-3 occasions
hypertriglyceridemia (HTG)
often goes along with other conditions
for example, uncontrolled diabetes can increased TG levels
dietary choices can also increase TGs
non-pharmacologic approaches to CVD
diet
emphasizing intake of fruits, vegetables, and whole grains
include low fat dairy options, poultry, fish, legumes, non-tropical vegetable oils
limited intake of sweets and red meats
reduced intake/calories from saturated fat and limit trans fat
3-12g of soluble fiber per day
exercise, primarily 150-300 minutes per week of moderate intensity or 75-150 minutes/week of vigorous intensity, especially involving all muscle groups at least twice weekly
limiting sedentary time
and lifestyle changes, such as weight loss/maintenance, and smoking cessation (if applicable)
goals of treatment for dyslipidemia
it’s NOT necessarily to get “good” LDL-C/TG numbers, but to decrease the risk of future hospitalizations due to CVD, or progression of disease
dietary supplemetation for CVD prevention/treatment
the benefits are not fully clear, but the risks are (risk>benefit), which poses safety issues
eg. not FDA-regulated, which raises concerns for purity or dosage of the product
there are also efficacy issues
often involves conflicting, weakly powered, small, short-term studies, and any efficacy data often focused on therapeutic target (eg. LCL-C) without any outcome data
CVA
cerebrovascular accident
basically the medical term for a stroke
3 types of cerebrovascular accidents
ischemic stroke
hemorrhagic stroke
transient ischemic attack (TIA)
major ASCVD events
myocardial infarction (MI)
ischemic cerebrovascular accidents (CVA)