the b - type natriuretic peptide ( bnp ) is synthesized predominantly by cardiac ventricular myocytes , the expression of which is regulated by changes in intracardiac pressure and/or stretch . cardiac bnp gene expression and plasma levels generally increase in patients with heart failure ( hf ) , myocardial infarction , hypertension , left ventricular ( lv ) hypertrophy , pulmonary hypertension , and renal failure.1 ) however , we have managed some patients with elevated concentrations of the bnp and no evidence of hf , hypertension , or renal dysfunction . thus , we report an interesting case of a young female patient with an elevated plasma level of the bnp . a 19-year - old female patient presented for evaluation on 7 april 2008 of non - specific chest pain of 1 month duration . the results of the complete blood count , blood chemistry , and urinalysis were within normal limits ; however , the bnp level was 3,354.84 pg / ml . the bnp level was rechecked the next day , and was still elevated ( 3,079.29 pg / ml ) . ten days later the bnp level was 2,982.31 pg / ml . on 30 june 2008 there were no abnormal findings on the chest x - ray , chest computed tomography , whole body scan , and coronary angiography with a spasm stress test . there were no regional wall motion abnormalities on the left ventriculogram and lv end - diastolic pressure was 10 mmhg . the laboratory findings , including a complete blood count , blood chemistries , a pregnancy test , the antinuclear antibody titer , a peripheral blood smear , and a urine test were all normal , except for a high plasma level of bnp ( 3,437.80 pg / ml ) . she was discharged on diltiazem and a diuretic and was symptom - free . during the follow - up , the bnp level was measured twice as an outpatient and was persistently elevated ( 2,904.1 pg / ml and 4,000 pg / ml ) ( fig . the bnp is synthesized and secreted primarily from lv cardiomyocytes in response to increasing wall stress , particularly during diastole.2 ) cleavage of the precursor peptide ( probnp ) produces bnp and the corresponding amino - terminal component ( nt - probnp ) , which are secreted in a 1 : 1 ratio and can be detected in the peripheral circulation.3 ) the plasma levels of these peptides correlate strongly with each other . the bnp is bioactive and has a shorter half - life as a result of clearance by neutral endopeptidase and natriuretic peptide c - type receptors . thus , levels are lower than for the more stable nt - probnp.4 ) the levels of both peptides increase with lv pressure or volume loading , and reflect the severity of lv dysfunction . in addition , the levels of both peptides correlate inversely with lv ejection fraction and positively with increasing lv mass and indices of lv filling pressure.5 ) there is wide inter - individual variation in bnp and nt - probnp levels . up to 80% of inter - individual variation in peptide levels is explained by lv and diastolic functions , right ventricular dysfunction , renal function , age , and mitral regurgitation.6 ) although baggish et al.7 ) previously reported the possible causes of nt - probnp elevation unrelated to hf , such as heart muscle disease , valvular heart disease , atrial arrhythmias , anemia , critical illnesses , ischemic stroke , and pulmonary heart disease syndromes , the patient presented herein had none of the these causes . hereditary factors may be responsible for a significant proportion of residual variation in bnp levels.8 ) in this interesting case , the patient has no remarkable findings to account for the high levels of the bnp . we therefore suggest that hereditary factors may be responsible for a significant proportion of residual variation in bnp levels and further studies are required to describe the basis and need for treatment ( if any ) of elevated bnp levels in such patients .
we report a case of a 19-year - old female with an elevated plasma b - type natriuretic peptide ( bnp ) level , but without evidence of heart failure ( hf ) . 
 she presented with non - specific chest pain and a high level of the b - type natriuretic peptide , despite having unremarkable findings on physical examination , laboratory analysis , electrocardiogram , echocardiogram , chest x - ray , chest computed tomography , whole body scan , and coronary angiography . 
 we attribute this finding to a genetic variation in the synthesis and cleavage of the natriuretic peptides .