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J Thorac Cardiovasc Surg 2009;138:172-178
© 2009 The American Association for Thoracic Surgery

Evolving Technology/Basic Science

Chronic septal infarction confers right ventricular protection during mechanical left ventricular unloading

James Mau, BSc, MB, BSa,*, Stuart Menzie, MB, BS, FRACSa, Yifei Huang, MD, PhDa, Michael Ward, MB, BS, PhD, FRACPb, Stephen Hunyor, MB, BS, MD, MTM, FRACP, FACCa,b

a Cardiac Technology Centre, Kolling Institute, St Leonards, Australia
b Department of Cardiology, University of Sydney at Royal North Shore Hospital, Sydney, Australia

Received for publication November 7, 2008; revisions received February 19, 2009; accepted for publication March 9, 2009.

* Address for reprints: James Mau, BSc, MB, BS, Cardiac Technology Centre, Kolling Bld, Royal North Shore Hospital, Pacific Hwy, St Leonards, Sydney, NSW, Australia 2065. (Email: jmau{at}med.usyd.edu.au).

Objective: Right ventricular failure manifests in 25% of left ventricular assist device recipients because of ventricular coupling mechanism disruption. Septal ischemia accentuates this process, but the effect of septal infarction has not been elucidated. Right ventricular response to incremental left ventricular unloading was studied in sheep with septal infarction.

Methods: Septal infarction was induced in 6 sheep using ethanol delivery into the main septal perforating artery. Six shams avoided ethanol. Load-independent and in-series right ventricular response to incremental (0%–100%) left ventricular unloading was measured 4 weeks later. Dimensions of whole heart, wall thickness, and chamber volumes were obtained using sonomicrometers. Selective perfusion with triphenyltetrazolium quantified septal damage.

Results: Right ventricular preload-recruitable-stroke-work, contractility, and ejection fraction were lower at 75% and 100% left ventricular unloading in sham compared with infarcted animals (75%: 26.3 ± 3.4, 0.70 ± 0.15, and 23.9 ± 4.6 vs 37 ± 2.6 erg*10^3, 0.99 ± 0.18 mm Hg/mL, and 35.5% ± 3.4%, all P < . 01, 100%: 24.8 ± 4.5, 0.67 ± 0.14, and 23.8 ± 5.8 vs 36.0 ± 4.6 erg*10^3, 0.90 ± 0.09 mm Hg/mL, and 32.7% ± 11.0%, all P < . 01). Central venous pressure was higher at 75% and 100% unloading in sham compared with infarcted animals (75%: 8.6 ± 1.0 vs 4.5 ± 1.0, 100%: 12.4 ± 0.8 vs 3.4 ± 1.0 mm Hg, all P < . 01). Right ventricular cardiac output was less in shams with 100% unloading (1.2 ± 0.2 L/min vs 2.1 ± 0.3 L/min, P < . 01). End-diastolic and end-systolic right ventricular short-axis dimension at 75% and 100% unloading was greater in sham compared with infarcted animals (75%: 34.4 ± 5.5 mm and 29.1 ± 5.5 mm vs 25.6 ± 4.7 mm and 20.5 ± 4.0 mm; 100%: 37.6 ± 6.6 mm and 29.9 ± 5.9 mm vs 25.5 ± 3.9 mm and 21.1 ± 3.8 mm, all P < .01). Prolonged diastolic relaxation (Tau) in infarcted animals was normalized with 75% and 100% unloading.

Conclusion: High-level (≥75%) left ventricular unloading causes right ventricular dilatation and compromised function. Chronic septal damage, however, confers protection by preserving right ventricular dimensions.

Abbreviations and Acronyms CO = cardiac output; CVP = central venous pressure; ED = end diastolic; EF = ejection fraction; ES = end systolic; LV = left ventricular; LVAD = left ventricular assist device; PRSW = preload recruitable stroke work; PTSMA = percutaneous transluminal septal myocardial ablation; RV = right ventricular






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