PP-321 Right Ventricle Myocarditis due to Acute Cholecystitis

Abstract

Inflammatory changes at the neighbouring tissues of heart can mimic cardiac pathologies. Acute cholecystitis, acute pancreatitisand pneumonia can make some electrocardiography (ECG) changes and most of the time the clinical course goes benign. Here, we present a case diagnosed with right ventricular myocarditis and right heart failure due to acute cholecystitis.Case ReportA 61 year old, male patient with a history of hypertension and coronary artery disease was preparing for elective cholecystectomy after a cholecystitis episode at general surgery clinic. He was consulted to cardiology for sudden onset, severe upper abdominal pain with ECG changes. ECG showed marked ST segment elevation in V 1-2 leads and right precordial leads (Figure 1). The patient underwent an urgent coronary angiography which revealed there was no obstructive coronary lesion. The echocardiography showed dilated right ventricle, moderate tricusbid regurgitation, mild pericardial effusion and normal left ventricular functions. Partial oxygen and carbondioxide pressures were normal at arterial blood gas, D-dimer level was at upper limit of normal values. Thorax CT angiography was performed to exclude pulmonary embolism and no thrombus formation detected. Cardiac markers (CKMB and troponin) were risen significantly and decreased at follow up that was supporting myocardial injury. At clinical follow up, symptomatic right heart failure developed (three positive pretibial oedema, hepatic congestion and jugular venous distension) and the patient treated for symptomatic right heart failure. At first month follow up, control echocardiography revealed impressive recovery of right ventricle functions and the patient had no symptom or complaint about right heart failure.Discussion Inflammatory changes at the neighbouring tissues of heart can mimic cardiac pathologies. Acute cholecystitis, acute pancreatitisand pneumonia can make some electrocardiography (ECG) changes and most of the time the clinical course goes benign. Here, we present a case diagnosed with right ventricular myocarditis and right heart failure due to acute cholecystitis. Case ReportA 61 year old, male patient with a history of hypertension and coronary artery disease was preparing for elective cholecystectomy after a cholecystitis episode at general surgery clinic. He was consulted to cardiology for sudden onset, severe upper abdominal pain with ECG changes. ECG showed marked ST segment elevation in V 1-2 leads and right precordial leads (Figure 1). The patient underwent an urgent coronary angiography which revealed there was no obstructive coronary lesion. The echocardiography showed dilated right ventricle, moderate tricusbid regurgitation, mild pericardial effusion and normal left ventricular functions. Partial oxygen and carbondioxide pressures were normal at arterial blood gas, D-dimer level was at upper limit of normal values. Thorax CT angiography was performed to exclude pulmonary embolism and no thrombus formation detected. Cardiac markers (CKMB and troponin) were risen significantly and decreased at follow up that was supporting myocardial injury. At clinical follow up, symptomatic right heart failure developed (three positive pretibial oedema, hepatic congestion and jugular venous distension) and the patient treated for symptomatic right heart failure. At first month follow up, control echocardiography revealed impressive recovery of right ventricle functions and the patient had no symptom or complaint about right heart failure. A 61 year old, male patient with a history of hypertension and coronary artery disease was preparing for elective cholecystectomy after a cholecystitis episode at general surgery clinic. He was consulted to cardiology for sudden onset, severe upper abdominal pain with ECG changes. ECG showed marked ST segment elevation in V 1-2 leads and right precordial leads (Figure 1). The patient underwent an urgent coronary angiography which revealed there was no obstructive coronary lesion. The echocardiography showed dilated right ventricle, moderate tricusbid regurgitation, mild pericardial effusion and normal left ventricular functions. Partial oxygen and carbondioxide pressures were normal at arterial blood gas, D-dimer level was at upper limit of normal values. Thorax CT angiography was performed to exclude pulmonary embolism and no thrombus formation detected. Cardiac markers (CKMB and troponin) were risen significantly and decreased at follow up that was supporting myocardial injury. At clinical follow up, symptomatic right heart failure developed (three positive pretibial oedema, hepatic congestion and jugular venous distension) and the patient treated for symptomatic right heart failure. At first month follow up, control echocardiography revealed impressive recovery of right ventricle functions and the patient had no symptom or complaint about right heart failure. Discussion