Cardiac Biomarkers

Question 1

What are natriuretic peptides?

Answer 1

Hormones produced by myocardial tissue

1. Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), etc

All are synthesizes as pre-prohormones, then are released, and cleaved into NT-proBNP and the biologically active BNP

ProANP and proBNP are produced by the myocardium

ANP - produced by atria

BNP - produced in the all myocardium, predominantly in ventricles

Stretch or stress or hypoxia causes the myocardium (primarily the ventricles) to release more. ProANP and proBNP
Release can also be induced by endothelin 1, Angiotensin II, IL1B and adrenergic agonists

Question 2

What is the function of active ANP and BNP?

Answer 2

Vasodilation and dieresis

They bind natriuretic receptors in vascular and renal tissue, then inhibit aldosterone release from the zona glomerulosa, inhibit angiotensin II mediated sodium and H2O resorption in the proximal tubule, and decrease renin secretion from the macula dense

BNP may also decrease cardiac sympathetic NS activity

They are essentially designed to counteract RAAS activation
BNP also has anti fibrotic and anti proliferation effects on the myocardium and endothelium

Question 3

Elevated NT-proBNP indicates what?

Answer 3

An indication for further cardiac disease workup - it is not definitive for cardiac disease - interpret results in the context of exam, history, and workup findings
Echo is still gold standard

Question 4

Why are troponin T and I useful biomarkers for cardiac disease rather than troponin C?

Answer 4

Troponin T and I have specific isoforms for skeletal and cardiac muscle

Troponin C is the same between skeletal and cardiac muscle

Troponin T has 50% homologous between cardiac and skeletal muscle, which can impact its diagnostic utility with injured skeletal muscle

Troponin I - <50% homologous with skeletal muscle, more specific for cardiac, increased diagnostic specificity for cardiomyocyte injury

Question 5

After cardiac muscle damage, when would you expect circulating troponin levels to peak?

Answer 5

Levels rise within 2-3 hours of cardiomyocyte injury and peak at 18-24 hrs

Question 6

Which dog breeds have inherently higher cTnI concentrations in comparison to other breeds?

Answer 6

Boxers and GReyhounds

Question 7

What is the equation for cardiac output?

Answer 7

HR x stroke volume

Question 8

Describe RAAS activation

Answer 8

Decreased cardiac output —-> decreased renal blood flow and associated decreased delivery of NaCl to renal juxtaglomerular apparatus —> fall in Na deliver to juxtaglomerular apparatus causes renin release

Renin causes inactive circulating antiogensinogen to be converted to angiotensin I

AT1 is converted to ATII by angiotensin converting enzyme, which occurs predominantly in the lung, but also in many other organs
Other enzymes, including Chumash, can also convert ATI to ATII