CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 189 Successful surgical treatment of left ventricular free wall rupture Hakan Kara Abstract Left ventricular free wall rupture (LVFWR) is a rare mechanical complication of acute myocardial infarction. The clinical course of LVFWR is very poor. Direct or patch closure of the rupture area and sutureless procedures constitute the treatment for LVFWR. We present the surgical treatment of a patient who developed LVFWR after high lateral myocardial infarction, and its successful outcome. Successful salvage of LVFWR remains relatively rare. Transthoracic echocardiography, myocardial contrast echocardiography and thoracic computed tomography are important diagnostic tools for LVFWR. These patients usually present with acute cardiac tamponade symptoms requiring immediate treatment. Keywords: left ventricular free wall rupture, myocardial infarction, cardiac tamponade Submitted 12/1/24; accepted 7/2/24 Published online 19/2/24 Cardiovasc J Afr 2024; 35: 185–192 www.cvja.co.za DOI: 10.5830/CVJA-2024-002 Left ventricular free wall rupture (LVFWR) is a mechanical complication of myocardial infarction with an exceedingly high mortality rate. The overall incidence of LVFWR ranges from 4–6% but it accounts for up to 26% of mortalities associated with myocardial infarction.1,2 Although its incidence has decreased in parallel with the development of reperfusion techniques in recent years, it remains a fatal complication. It usually occurs within a few days of a myocardial infarction. The most important diagnostic tool for LVFWR is echocardiography. Early cardiac surgery should be performed in these patients. Traditional techniques are linear closure of the ventricular wall defect and infarctectomy with subsequent closure of the created defect by a prosthetic patch or pericardium. Surgical techniques can sometimes be ineffective in cases of poor myocardial tissue quality. We present the surgical treatment of a patient who developed LVFWR after high lateral myocardial infarction, and its successful outcome. Case report A 51-year-old male patient presented to our emergency department with severe chest pain, dyspnoea, palpitations, significant chest discomfort and confusion. His medical history revealed that he had undergone right coronary artery stenting 10 years earlier, and he had systemic hypertension, alcohol dependence and excessive cigarette smoking. His physical examination revealed an undetectable systolic blood pressure, his heart rate was 130 bpm, and he had dyspnoea, tachycardia and severe jugular venous distension associated with cyanosis of the face and extremities. His electrocardiogram (ECG) showed an acute high lateral ST-segment elevation myocardial infarction (Fig. 1). Furthermore, his laboratory tests revealed the following: white blood cell count 16.31 cells/µl, haemoglobin 15.3 g/dl, haematocrit 45%, platelets 238.00 cells/µl, glucose 189 mg/dl (10.49 mmol/l), sodium 138 mEq/l, potassium 3.80 mEq/l, blood urea nitrogen 22 mg/dl, creatinine 1.22 mg/dl, aspartate aminotransferase 56 IU/l, alanine transaminase 46 IU/l, C-reactive protein 4.37 mg/ dl, lactate dehydrogenase 306 IU/l, total cholesterol 146 mg/ dl (3.78 mmol/l), low-density lipoprotein cholesterol 98 mg/dl (2.54 mmol/l) and triglycerides 109 mg/dl (1.23 mmol/l). Cardiac markers showed an elevated creatine kinase mass of 6.70 ng/ml and cardiac troponin level of 8.50 ng/ml. Coronary angiography was then performed, which revealed 40% stenosis in the left anterior descending coronary artery mid and proximal portion, 50% stenosis in the first diagonalis, 70% stenosis in the first marginal branch and 95% stenosis in the second marginal branch of the circumflex coronary artery (Fig. 2).The stent in the right coronary artery was open. Percutaneous coronary balloon angioplasty was performed in the second marginal branch of the circumflex coronary artery Department of Cardiovascular Surgery, Giresun Ada Hospital, Giresun, Turkey Hakan Kara, MD, hakankarakdc@hotmail.com Fig. 1. ECG showing high lateral ST-segment elevation myocardial infarction.
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