Chronic pancreatitis and the heart disease: Still terra incognita?
It has been suggested that chronic pancreatitis (CP) may be an independent risk factor for development of cardiovascular disease (CVD). At the same time, it seems that congestive heart failure (CHF) and CP share the responsibility for the development of important clinical conditions such as sarcopen...
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Published in: | World journal of gastroenterology : WJG Vol. 25; no. 44; pp. 6561 - 6570 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Baishideng Publishing Group Inc
28-11-2019
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Subjects: | |
Online Access: | Get full text |
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Summary: | It has been suggested that chronic pancreatitis (CP) may be an independent risk factor for development of cardiovascular disease (CVD). At the same time, it seems that congestive heart failure (CHF) and CP share the responsibility for the development of important clinical conditions such as sarcopenia, cachexia and malnutrition due to development of cardiac cachexia and pancreatic exocrine insufficiency (PEI), respectively.
To explore the evidence regarding the association of CP and heart disease, more specifically CVD and CHF.
A systematic search of MEDLINE, Web of Science and Google Scholar was performed by two independent investigators to identify eligible studies where the connection between CP and CVD was investigated. The search was limited to articles in the English language. The last search was run on the 1st of May 2019. The primary outcomes were: (1) Incidence of cardiovascular event [acute coronary syndrome (ACS), chronic coronary disease, peripheral arterial lesions] in patients with established CP; and (2) Incidence of PEI in patients with CHF.
Out of 1166 studies, only 8 were eligible for this review. Studies regarding PEI and CHF showed an important incidence of PEI as well as associated malabsorption of nutritional markers (vitamin D, selenium, phosphorus, zinc, folic acid, and prealbumin) in patients with CHF. However, after substitution of pancreatic enzymes, it seems that, at least, loss of appetite was attenuated. On the other side, studies investigating cardiovascular events in patients with CP showed that, in CP cohort, there was a 2.5-fold higher incidence of ACS. In another study, patients with alcohol-induced CP with concomitant type 3c diabetes had statistically significant higher incidence of carotid atherosclerotic plaques in comparison to patients with diabetes mellitus of other etiologies. Earlier studies demonstrated a marked correlation between the clinical symptoms in CP and chronic coronary insufficiency. Also, statistically significant higher incidence of arterial lesions was found in patients with CP compared to the control group with the same risk factors for atherosclerosis (hypertension, smoking, dyslipidemia). Moreover, one recent study showed that PEI is significantly associated with the risk of cardiovascular events in patients with CP.
Current evidence implicates a possible association between PEI and malnutrition in patients with CHF. Chronic pancreatic tissue hypoxic injury driven by prolonged splanchnic hypoperfusion is likely to contribute to malnutrition and cachexia in patients with CHF. On the other hand, CP and PEI seem to be an independent risk factor associated with an increased risk of cardiovascular events. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Undefined-1 ObjectType-Feature-3 content type line 23 Author contributions: Nikolic S and Vujasinovic M contributed to the conception and design of the study, literature review and selection of the eligible studies, analysis and interpretation of data and drafting of the manuscript; Dugic A contributed to literature review, selection of the eligible studies, analysis of data, and critical revision and editing; Steiner C , Tsolakis AV, Haugen Löfman IM, contributed to critical revision and editing; Löhr JM contributed to literature review and analysis, drafting of the manuscript and critical revision and editing. Corresponding author: Miroslav Vujasinovic, MD, PhD, Doctor, Department for Digestive Diseases, Karolinska University Hospital, Hälsovägen 11, Stockholm 14186, Sweden. miroslav.vujasinovic@sll.se Telephone:+46-72-4694938 |
ISSN: | 1007-9327 2219-2840 2219-2840 |
DOI: | 10.3748/wjg.v25.i44.6561 |