Heart Disease Flashcards
(34 cards)
Acute Coronary Syndrome
Onset of chest pain w/o exertion b/c of clotting and plaque rupture
Stable Angina
Chest pain during exertion
Coronary Artery Stenosis
NO PLAQUE RUPTURE
ACS Diagnosing
STEMI - after using ECG - can determine if ST elevation
- no need for blood test
Unstable Angina - don’t get tissue death - should be - no blood test
NSTEMI - have a lab test
1st biomarker and best one now
AST -non specific though: muscle, heart and liver
Troponin
1979 MI Defition
2 of 3 Crit:
Symptoms need to be suggestive (but this is subjective)
-STI change
-Unequivocal serial enzyme changes-but enzyme levels may be still normal
2018 MI Definition
Objective Evidence - from imaging or ECG + injury to heart + symptoms + troponin rise or fall
Now need biochemical evidence of damage to heart
MI types
Type I - thrombosis and plaque rupture -NSTEMI
T2 - injury to heart but no evidence of clot - supply - called supply-demand
T3-troponin measurements but pass away early
T4- PCI - complications
T5 - MI after cardiac surgery
Cardiac Troponin
11 mg/tissue
cTnTIC complex
T and I specific to cardiac
-Can get some segregation from CTnTIC into CTNI-C and CTnT
Impact of WHO diff definitions
Negative for both def- almost 100% survival rate
Positive for both - almost 75% survival rate
Positive for both =almost 50% survival rate
More sensitive troponin testing
Decreased amount of time needed to detect MI
High-sensitivity cardiac troponin testing
Perhaps after one hour
High Sensitivity Assays Lab Measurements
3 diff concentrations of QC at least one per day
High Sensitivity Assays Use
Could measure once
Quicker results
Might even be able to get risk stratification
Clinical Utility of High Sensitivity Assay
5 ng - 99% NPV
Heart Failure
Fatigue, shortness of breath, exercise intolerance + fluid retention
Chronic
- unable to supply oxygen-enriched blood to tissues to meet metabolic demands
- impairment of filling due to disorders of myocardium, endocardium, pericardium etc
Risk Factor for HF and Types
Heart Disease = due to tissue death, Type 1 MI, hypertension, diabetes + metabolic syndrome
HFref
Left Ventricular Ejection Fraction lower than 40%
Scan and see less
Has been treated more b/c has been around more
HFpef
Preserved EF
What does less blood flow lead to in heart failure
RAA activation
- Vasoconstriction
- Na and H20 Retention
- Hypertension
In response, heart stretching leads to vasodilation and naturesis
- due to BNP/ANP release
- ANP released from atrium but B from ventricle
What does shape change of heart result in for heart failure
You get cardiac enlargement and remodelling
Spherical shape is dilated and not energetically efficient
BNP releaase
Also releases BNP and NT-proBNP
- NT-pro is inactive -longer half life
- Gets released in 1:1 ratio
- Marker for BNP production
- Higher classes = more BNP release
BNP production
Pre-proBNP processed to pro
- Pro cleaved by furin or corin to from NT-pro and BNP
- Active BNP will bind to 2 main NP receptors
- Results natiuresis and vasodilation
BNP and proteases
Proteases can cleave BNP like NEP
Patients with NEP inhibitors do better and increase NP levels
proBNP can be glycosylated so proBNP also elevated in heart disease patients
HFpef vs HFref BNP levels
lower BNP/NP relative to those w/ HFref
