What is the role of BNP in heart failure? 

BASEL Study on the role of BNP estimation in heart failure has shown that BNP as a diagnostic test for heart failure can avoid several unnecessary admissions. BNP values less than 100 pg/ml have a 98% negative predictive value. BNP levels in highest quartile of VALHEFT trial were associated with highest mortality.

70% reduction in BNP at discharge has a good correlation with good 6 month prognosis. There is direct correlation between the reduction of pulmonary capillary wedge pressure and BNP levels as patient improves with treatment. In heart failure patients treated on an outpatient basis, 50% rise of BNP levels from the basal levels indicate need for in patient treatment. In paediatric patients in whom differentiation of heart failure from dyspnoea due to respiratory infection is difficult, BNP is very useful.

False positive BNP can occur in old age, renal failure, myocardial infarction and cor pulmonale. False negative BNP can occur in obesity, flash pulmonary edema (BNP elevation may be delayed) and mitral stenosis (heart failure without dilatation of left ventricle).

What is the result of neurohormonal activation in heart failure?

Epinephrine, angiotensin II, endothelin and TNF alpha are elevated in heart failure as a result of neurohormonal activation.

Which are the angiotensin II receptors?

They are AT 1, 2, 3 and 4. AT 1 is the most important and is involved in vasoconstriction, proliferation, matrix formation and aldosterone secretion.

What is the rationale for the use of angiotensin II receptor blockers (ARB) in heart failure?

ARBs produce more complete blockage of RAS (rennin angiotensin system) – only 30% of angiotensin II production is suppressed by ACE inhibitors. Angiotensin II can be produced by non ACE dependant pathways. Chymases and Cathepsin G can convert angiotensin I to II. There is an additional role for ARBs in patients with intolerance to ACE inhibitors, either due to cough or allergy.

What is aldosterone escape?

Aldosterone escapte ccurs in chronic treatment with aldosterone antagonists. One of the mechanisms is Potassium dependant aldoseterone secretion (unrelated to RAAS).