Various
heart diseases present with
sudden death; however, it is difficult to interpret the severity of or difference in respective preexisting and terminal cardiac dysfunction based on conventional morphology. The present study investigated the cardiac pathophysiology employing quantitative
mRNA measurement of atrial and brain
natriuretic peptides (
ANP and BNP) in the myocardium as markers of cardiac strain, using autopsy materials consisting of acute
ischemic heart disease (AIHD, n=40) with/without the pathology of apparent myocardial
necrosis (n=19/21), recurrent
myocardial infarction (RMI, n=19), chronic congestive
heart disease (CHD, n=11) and right ventricular
cardiomyopathy (RVC, n=5), as well as
hemopericardium (HP, n=11) due to
myocardial infarction (n=5) and
aortic rupture (n=6), and acute
pulmonary thromboembolism (PTE, n=5).
Cardiac death groups showed higher
ANP and/or BNP
mRNA expressions in the left ventricle than acute fatal
bleeding (sharp instrumental injury; n=15) and/or mechanical asphyxiation (strangulation; n=10). AIHD and RMI cases had similar
ANP and BNP
mRNA expressions in bilateral ventricular walls, but their bilateral atrial levels were lower in RMI. RVC showed higher
mRNA expressions of posterior left ventricular BNP, and right ventricular and bilateral atrial
ANP and BNP. HP cases had lower BNP
mRNA expression in the right ventricular wall, but PTE showed lower
ANP and BNP
mRNA expressions in the left ventricular wall; however, these
mRNA expressions at other sites were similar to those of AIHD. CHD presented findings similar to those of AIHD, but the pericardial BNP level was significantly increased. These observations indicate characteristic molecular
biological responses of myocardial
natriuretic peptides in individual
heart diseases and suggest the possible application of molecular pathology to demonstrate cardiac dysfunction even after death.