Introduction Fatal arrhythmias such as ventricular fibrillation (VF) are a major cause of sudden cardiac death (SCD), with >100,000 deaths per year in the UK. Autonomic dysfunction is a hallmark of cardiac diseases like chronic heart failure (HF) post-myocardial infarction (MI). There is an increased risk of arrhythmogenesis with autonomic dysfunction; however, the exact mechanisms are still unknown. The main treatment for an acute MI typically involves blood clot dissolving drugs such as tissue plasminogen activators or percutaneous coronary intervention. These focus on removing the blockage and restoring blood flow to the affected area. Following MI treatment there is an increased risk of fatal arrhythmia development such as VF. However, the underlying mechanisms which lead to this remain unknown. Methods New Zealand White Male Rabbits (2.2–2.5 kg) underwent coronary artery ligation surgery. During surgery the coronary artery was either permanently occluded or occluded temporarily for either 40 or 80 minutes. Following a 4- or 8-week remodelling period, histology was conducted. Histology has been conducted on cardiac tissue to investigate scar size and structural remodelling. Histological staining was conducted using 2.5% Evans blue to demark healthy tissue, Triphenyl tetrazolium chloride to denote at risk tissue (border region) leaving the infarct region unstained. The heart is then frozen with special care taken to ensure no morphological changes. The heart is then imaged, weighed and the left ventricle dissected into 8 sections with a maximum thickness of 5 mm. Infarct and border region was analysed using Image J. Results Histology shows infarcted tissue is concentrated at the apex of the heart. Scar formation appears more heterogenous and patchy in hearts that have undergone 40-minute ligation compared to 80-minutes. There is a significant increase in infarct percentage when comparing individual slices from the apex and mid-apical region between permanent and temporary occlusion following 4 weeks remodelling (Slice 4 40-minute -3.9%, 80 minute – 6.1% and permanent – 13.6%). There is an increase in border region when analysing individual slices from the apex region (Slice 1 40-minute -11%, 80 minute - 3.4% and permanent – 1.5%) when comparing temporary occlusion to permanent occlusion. There is more sporadic and heterogenous development of border region post occlusion in temporary occlusion compared to permanent occlusion. There is a significant increase in border region in the mid-section of the heart when comparing 40 minutes (6.7%) to 80-minute (1%) temporary occlusion following 8 weeks remodelling. Conclusion This study has found that the infarct region is patchier, and the border region is increased following temporary occlusion. The increase in border region could potentially increase arrhythmogenic risk due to an increased risk of electrical heterogeneity.
Roper-Jones et al. (Wed,) studied this question.