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Hepatic morphology in cardiac dysfunction: a clinicopathologic study of 1000 subjects at autopsy
Insights
Chronic passive congestion (CPC) stems from high venous pressure, while centrilobular necrosis (CLN) results from low arterial pressure. These cardiac dysfunction indicators are linked and can worsen each other.
Area of Science:
- Cardiovascular Pathology
- Organ System Interplay
Background:
- Chronic passive congestion (CPC) and centrilobular necrosis (CLN) are known pathological changes.
- Their precise relationship with various cardiac dysfunctions remains unclear.
Purpose of the Study:
- To investigate the link between cardiac dysfunction and distinct hepatic morphologic changes (CPC and CLN).
- To analyze clinical and pathological data to differentiate the causes and consequences of CPC and CLN.
Main Methods:
- Retrospective review of clinical data and organ morphology (hepatic, renal, adrenal) in 1000 autopsy subjects.
- Statistical analysis of 14 pathological and 18 clinical variables related to cardiac dysfunction.
Main Results:
- CPC correlated with right-sided congestive heart failure, cardiac weight, and chamber enlargement.
- CLN was associated with profound hypotension, renal failure, acute tubular necrosis, and adrenal necrosis, indicating shock.
- Both CPC and CLN were significantly correlated, with one potentiating the other.
Conclusions:
- Hepatic CPC originates from elevated systemic venous pressure.
- CLN arises from reduced systemic arterial pressure.
- The presence of CPC or CLN can influence the development of the other, highlighting their interconnectedness in cardiac dysfunction.
Abstract:
Chronic passive congestion (CPC) and centrilobular necrosis (CLN) are well recognized pathologic changes, but their exact relationship to different forms of cardiac dysfunction is uncertain. We reviewed clinical data and hepatic, renal, and adrenal morphology related to cardiac dysfunction in 1000 autopsy subjects at The Johns Hopkins Hospital whose hearts had been studied after postmortem arteriography and fixation in distention. Fourteen pathologic variables, including body and organ size, and microscopic changes graded on a semiquantitative scale, and 18 clinical variables including congestive heart failure, shock, and cardiovascular disease, were analyzed statistically. Distinct patterns of cardiac dysfunction emerged for the two spectra of hepatic morphologic change. Among patients with variable CPC, but slight or absent CLN, the amount of CPC was predicted in a multivariate analysis by severity of right-sided congestive heart failure. CPC severity correlated with cardiac weight and chamber enlargement (P less than 0.001). Among patients with variable CLN, but slight or absent CPC, CLN was predicted by profound hypotension and by renal failure. In addition, CLN, but not CPC, was significantly correlated with renal acute tubular necrosis (P less than 0.001) and adrenal cortical medullary junction necrosis (P less than 0.05), two lesions associated with shock. Among all 1000 patients CPC and CLN were highly significantly correlated (P less than 0.001). The results show that hepatic CPC arises from conditions producing elevated systemic venous pressure but that CLN arises from reduced systemic arterial pressure; and the presence of one potentiates the development of the other.