301 ACUTE ACALCULOUS CHOLECYSTITIS AND CARDIOVASCULAR DISEASE, WHICH CAME FIRST?

Background The existence of a close association between disease of the biliary tract and heart's disease is known from the mists of time. Acute acalculous cholecystitis (AAC) can be defined as an acute necro-inflammatory disease of the gallbladder in the absence of cholelithiasis. AAC is a challenging diagnosis. The atypical clinical onset associated to a paucity and similarity of symptoms and to laboratory data mimicking cardiovascular disease (CVD) often results in under and misdiagnosed cases. Moreover, AAC has commonly a fulminant course compared to calculous cholecystitis and it is often associated with gangrene, perforation and empyema as well as considerable morbidity and mortality(up 50%). Early diagnosis is crucial to a prompt treatment in order to avoid complications and to increase survivability. Even today, although scientific evidence has shown a close association between AAC and CVD, due to the lack of RCT, there is still a lot of confusion regarding the relationship and consequently the clinical management AAC and CVD. In addition, emergency physicians are not always familiar with transient ECG changes with AAC. Aim the aim of this review was to provide evidence regarding epidemiology, pathophysiology, clinical presentation and treatment of the complex association between AAC and CVD. Methods we searched for publications addressing Acalculous cholecystitis and cardiovascular disease, consulting Medline and Scopus databases. Any retrospective or prospective study design or systematic review focusing on the aforementioned topic was accepted. This study was conducted in accordance with the PRISMA and AMSTAR Guidelines. Our search rendered 1422 hits (995 from Medline and 427 from Scopus). After removing the duplicates, there were 114 studies. After progressive screening, 268 full texts were assessed for eligibility and 135 studies were included in qualitative synthesis. Results According to the literature, 11 cases of AAC were reported after cardiopulmonary bypass surgery. Besides, in patients recovering from open-heart surgery with extracorporeal circulation, prolonged bypass time and depressed cardiac output were identified 22 cases of AAC. Similarly, in 6 of 7 patients following aortic reconstruction. Small vessel occlusion has shown to be the predominant phenomenon in AAC, concluding that the common cause was visceral hypoperfusion. Histological analysis of AAC resulted in leukocyte margination of blood vessels, suggesting involvement of ischaemia and reperfusion mediated injury. These types of histopathological alterations are typical of myocardium after reperfusion injury. Moreover, bile infiltration into the bladder mucosa demonstrated by many authors, validates the abnormal epithelial permeability in AAC. Data suggest that AAC is a manifestation of systemic critical illness. The most common ECG alterations noted in AAC are changes in T waves in significant leads, slurring and notching of the QRS complex and elevation or depression of the S-T segment, hypothesizing a vagally reflex mechanism, due to the distention of the common bile duct, with a reduced coronary blood flow. Finally it was reported a resolution of ECG changes due to AAC after cholecystectomy or antibiotic treatment within a few days. Conclusion AAC should be suspected after each general disease leading to hypoperfusion such as cardiovascular diseases and major heart or aortic surgery. ECG changes in absence of significant laboratory data for IMA could be related to a misdiagnosed AAC. Ultrasonography plays a key role in the early diagnosis and also in the follow up of AAC. Cholecystostomy and cholecystectomy represent the two prevailing treatment options for AAC.