Brain natriuretic peptide can be a useful biochemical marker for myocarditis in patients with Kawasaki disease

2002 ◽  
Vol 12 (2) ◽  
pp. 153-158 ◽  
Author(s):  
Takashi Kawamura ◽  
Masakuni Wago

So as to determine the value of brain natriuretic peptide in the plasma as a biochemical marker for myocarditis of Kawasaki disease, we studied 69 patients. The blood samples, electrocardiograms and cross-sectional echocardiograms were obtained before the commencement of treatment and in the convalescent phase. Results: The mean concentration of brain natriuretic peptide in the plasma was 73.2 ± 107.7 (mean ± SD) pg/ml in the acute phase, and 7.9 ± 7.5 pg/ml in the convalescent phase. We checked the electrocardiograms to find abnormal Q waves, elevation or depression of the ST segments, change in the pattern of the QRS complexes, and flattening or inversion of the T wave, all believed to be markers of myocarditis in Kawasaki disease. Those in whom the concentrations were greater than 50 pg/ml in the acute phase showed abnormal electrocardiograms more frequently than did those in whom the values were less than 50 pg/ml (21/29 vs 3/40, p < 0.0001 odds ratio 32.4). Amplitudes of the T wave in standard limb leads were measured both in the acute and convalescent phases, and the differences calculated. We regarded the sum total of these differences as representing “flattening T wave”, and we named this variable as the total suppressed T wave voltage. We examined the correlation between the variable and the levels of brain natriuretic peptide in the plasma during the acute phase, demonstrating a significant correlation (r = 0.500, p < 0.0001). We conclude, therefore, that the concentration of brain natriuretic peptide measured in the plasma can be a useful biochemical marker for the myocarditis of Kawasaki disease. When the titer is over 50 pg/ml, the patient probably has an abnormal electrocardiogram and is most likely to have myocarditis.

2016 ◽  
Vol 175 (12) ◽  
pp. 1997-2003 ◽  
Author(s):  
Hyuksool Kwon ◽  
Jin Hee Lee ◽  
Jae Yun Jung ◽  
Young Ho Kwak ◽  
Do Kyun Kim ◽  
...  

2016 ◽  
Vol 58 (11) ◽  
pp. 1105-1111 ◽  
Author(s):  
Daisuke Yanagisawa ◽  
Mamoru Ayusawa ◽  
Masataka Kato ◽  
Hirofumi Watanabe ◽  
Akiko Komori ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tomoya Tsuchihashi ◽  
Nobuyuki Kakimoto ◽  
Takashi Takeuchi ◽  
Tomohiro Suenaga ◽  
Takayuki Suzuki ◽  
...  

Abstract Background Coronary artery aneurysm (CAA) is an important complication of Kawasaki disease (KD) that is associated with arterial structure damage. However, few studies have examined structural changes in coronary arteries that are not associated with CAA. Methods We examined coronary arteries in KD patients with CAAs who underwent follow-up coronary angiography (CAG) and optical coherence tomography (OCT). Coronary arterial branches with no abnormal findings during the most recent CAG were classified into two groups. Arteries with an acute-phase CAA that later regressed were classified as group R; arteries with no abnormal findings on either acute or convalescent phase CAG were classified as group N. Coronary arterial wall structural changes were compared between groups using OCT. Results Fifty-seven coronary arterial branches in 23 patients were evaluated by OCT. Thirty-six branches showed no abnormality during the most recent CAG. Both groups R and N comprised 18 branches. Maximum intimal thicknesses in groups R and N were 475 and 355 µm, respectively (p = 0.007). The incidences of media disruption were 100% and 67%, respectively (p = 0.02). Calcification, macrophage accumulation, and thrombus were not found in either group. Conclusions Intimal thickening and disruption of the media occur in coronary arteries with acute phase CAAs that later regress in the convalescent phase, as well as in arteries with normal CAG findings in the acute and convalescent phases.


2001 ◽  
Vol 49 (10) ◽  
pp. 1293-1300 ◽  
Author(s):  
Gad M. Bialik ◽  
Zaid A. Abassi ◽  
Ilan Hammel ◽  
Joseph Winaver ◽  
Dina Lewinson

The natriuretic peptides are believed to play an important role in the pathophysiology of congestive heart failure (CHF). We utilized a quantitative cytomorphometric method, using double immunocytochemical labeling, to assess the characteristics of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in atrial granules in an experimental model of rats with CHF induced by aortocaval fistula. Rats with CHF were further divided into decompensated (sodium-retaining) and compensated (sodium-excreting) subgroups and compared with a sham-operated control group. A total of 947 granules in myocytes in the right atrium were analyzed, using electron microscopy and a computerized analysis system. Decompensated CHF was associated with alterations in the modal nature of granule content packing, as depicted by moving bin analysis, and in the granule density of both peptides. In control rats, the mean density of gold particles attached to both peptides was 347.0 ± 103.6 and 306.3 ± 89.9 gold particles/μm2 for ANP and BNP, respectively. Similar mean density was revealed in the compensated rats (390.6 ± 81.0 and 351.3 ± 62.1 gold particles/μm2 for ANP and BNP, respectively). However, in rats with decompensated CHF, a significant decrease in the mean density of gold particles was observed (141.6 ± 67.3 and 158.0 ± 71.2 gold particles/μm2 for ANP and BNP, respectively; p < 0.05 compared with compensated rats, for both ANP and BNP). The ANP:BNP ratio did not differ between groups. These findings indicate that the development of decompensated CHF in rats with aortocaval fistula is associated with a marked decrease in the density of both peptides in atrial granules, as well as in alterations in the quantal nature of granule formation. The data further suggest that both peptides, ANP and BNP, may be regulated in the atrium by a common secretory mechanism in CHF.


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