Repair of a Large Posterior Left Ventricular PSA Involving the Mitral Apparatus

A sixty-two-year-old former smoker with chronic obstructive pulmonary disease presented to the authors’ institution with multiple recent embolic strokes and worsening heart failure symptoms. Careful diagnostic evaluation revealed a large postmyocardial infarction left ventricular (LV) pseudoaneurysm (PSA). Multimodality imaging was used to further characterize the PSA, demonstrating a large outpouching of the posterior LV wall (8 x 5 centimeters) with mural thrombus and calcifications. LV function was estimated to be reduced with LV ejection fraction less than 35 percent. There were no significant valve lesions. A coronary angiogram demonstrated a chronic total occlusion of the right coronary artery with left-to-right collaterals. Given the presence of ongoing embolic events and persistent heart failure symptoms, the patient was brought to the operating room for repair.Following median sternotomy, cardiopulmonary bypass was initiated via aortic and bicaval cannulation. Care was taken not to manipulate the heart prior to aortic cross clamping to avoid dislodging any LV thrombus. The aorta was clamped and the heart arrested with antegrade and retrograde cardioplegia. A vent was then placed across the atrial septum. Adhesions between the inferoposterior LV wall and the diaphragmatic surface were taken down and the heart retracted to expose the PSA. A longitudinal incision was then made over the PSA parallel to the posterior descending artery. A large amount of LV thrombus was extracted with copious irrigation. A triangular Dacron patch was fashioned and anchored to the fibrous scarred myocardium at the edges of the PSA with the mitral annulus at the base of the triangle patch. Care was taken not to disrupt the geometry of the subvalvular apparatus of the mitral valve to avoid mitral valve dysfunction after repair. The PSA sac was then closed over the patch with two Teflon felt strips. The patient was easily weaned off cardiopulmonary bypass. Post-repair intraoperative transesophageal echocardiography demonstrated reduction of the LV cavity, no new mitral regurgitation, and a modest improvement in LV function.The patient’s postoperative course was notable for complete heart block requiring a pacemaker. She was discharged home 16 days following surgery. At the most recent follow up, her heart failure symptoms were much improved with ongoing titration of guideline-directed medical therapy. Follow up imaging showed an intact repair with reduction in LV dimension. The patient has not experienced any more embolic events.LV PSAs represent a rare but serious mechanical complication of acute myocardial infarction. The mechanism is thought to be secondary to acute myocardial infarction leading to free wall rupture contained by pericardium. In the acute setting, patients are at high risk for rupture. For large, chronic PSAs, patients are at risk for heart failure and LV thrombus formation with embolization. Repair of posterior LV PSAs requires recognition of the relation between the mitral valve apparatus and the edge of the PSA to avoid disruption of the subvalvular apparatus geometry and postoperative mitral regurgitation. Surgical repair with patch closure as described in this report is a reproducible and effective technique. Reference(s)1. Torchio F, Garatti A, Ronco D, Matteucci M, Massimi G, Lorusso R. Left ventricular PSA: the niche of post-infarction mechanical complications. Ann Cardiothorac Surg. 2022;11(3):290-298. doi:10.21037/acs-2022-ami-252. Narin C, Ege E, Ozkara A, et al. Surgical treatment of postinfarction PSAs of the left ventricle. J Card Surg. 2008;23(4):294-298. doi:10.1111/j.1540-8191.2007.00544.x</p

Increased CD177 expression in PMN derived from WF.

<p>Cells from WF and PB were immunostained with CD177 followed by flow cytometry or cytospin analysis. Representative <b>A</b>, scatter plot and <b>B</b>, histogram and <b>C</b>, quantification from flow cytometry analysis showing cells with low (lo) or high (hi) expression of CD177. <b>D</b>, Representative images of cytospun cells derived from WF or PB. The cells were immunostained with CD177 (green) and DAPI (nucleus, red). Scale bar = 10 µm.</p

Increased endogenous opioid peptide levels in wound fluid at late inflammatory phase.

<p>Wound fluid (WF) was obtained from sternal wounds. Opioid peptide β-endorphin (END) and met-enkephalin (ENK) levels in WF was determined using ELISA at the indicated time points after surgery. The peptide levels were normalized to total albumin level in the fluid. Data are mean±SD (n = 5).* <i>p</i><0.05 compared to 24 h post-surgery.</p

Sternal wound environment induces opioid peptide expression in PMN: presence of opioid inducing IL-4 and IL-10 in sternal wound environment.

<p><b>A,</b> HL-60 cells were differentiated to PMN and then treated with varying dilutions (0–25%, v/v, 24 h) of wound fluid (WF) derived from sternal wounds. WF was sterile filtered and added directly to the PMN culture medium. POMC mRNA levels in WF treated PMN was measured using qPCR. Data are mean ± SD (n = 3).*, p<0.05 compared to 0% treated cells. <b>B</b>, HL-60 cells were differentiated to PMN and then were treated with 100 ng/ml of IL-10 or IL-4 for 48 h. The expression of POMC transcripts were measured using qPCR. Data are mean ± SD (n = 3). * p<0.05 compared to control. Both IL-4 and IL-10 that are abundantly present in WF significantly induced POMC mRNA expression. <b>C</b>, Levels of IL-4 and IL-10 in wound fluid (WF) and plasma were determined using ELISA at the indicated time points after surgery. The cytokine levels were normalized to the total albumin level in the fluid or plasma. Data are mean ± SD (n = 5). * <i>p</i><0.01 compared to plasma.</p

Cells from WF show activated PMN phenotype: increased CD66b and decreased CD43 expression.

<p>The WF and PB cells were subjected to flow cytometry analysis following immunostaining with CD66b or CD43. <b>A&C,</b> representative flowcytometry histograms of CD66b and CD43; <b>B&D,</b> quantification of CD66b and CD43 flow cytometry analysis. Data presented as mean±SD, n = 4. *<i>p</i><0.05 compared to PB.</p

Increased endogenous opioid peptide expression in wound-site PMN.

<p>WF derived cells were isolated from sternal wounds. <b>A</b>, mRNA expression of pro-opiomelanocortin (POMC) or preproenkephalin (PENK), the precursors of END and ENK, respectively, were determined in WF and peripheral blood (PB) PMN using quantitative PCR (qPCR). Data are mean±SD (n = 3).* <i>p</i><0.05 compared to PB; <b>B</b>, <b><i>Left</i></b>: Representative images of cytospun cells derived from WF or PB. Cells were immunostained with anti-β-Endorphin (β-END; red) and DAPI (nucleus, blue). Scale bar = 20 µm. <b><i>Right:</i></b> zoomed images of white box shown in corresponding left panels. Scale bar = 5 µm. <b>C</b>, Intracellular opioid peptide β-endorphin (END) and met-enkephalin (ENK) levels in WF derived PMN determined using ELISA at the indicated time points after surgery. The peptide levels were normalized to total cellar protein levels. Data are mean±SD (n = 3).* <i>p</i><0.05 compared to 24 h post-surgery.</p

Fluid and cell collection from sternal wound environment.

<p><b>A</b>, image of the sternal wound before closure where the Blake drain is yet to be placed; <b>B</b>, after closure of the sternum, the surgeon placed a Blake drain over the sternum, and then closed the wound in layers. The Blake drain was connected to a heparinized J-VAC bulb suction reservoir for wound fluid collection.</p

MRSA Strain USA300 biofilm exhibits enhanced tolerance to tobramycin when grown as a biofilm on surgical wires.

<p>USA300 was used to inoculate in vitro wells containing sections of wire. Planktonic bacteria and wire-associated biofilms were challenged with 10 ug/ml of tobramycin for 2 hours. Bacteria tolerant to antibiotic challenge were enumerated using viability plating and compared to untreated parallel controls. Percent survivability of triplicate cultures is represented. nd, not detected, ns, not significant. Data are mean±SD (n = 3), *p<0.05 compared to untreated planktonic (Mann Whitney test).</p

Presence of staphylococci within the infected debrided wound tissues.

<p>Representative confocal microscopy images of debrided tissue using immunofluorescence staining (debrided tissues was counterstained red with Phalloidin). Note large aggregates of staphylococci (intense green granular stain) colonizing the debrided tissues of infected sternal wound (lower panels), while tissues taken from a non-infected sternal wound during resternotomy (upper panels) show no colonization with staphylococci. Scale bar = 50 µm, 400x magnification. (SWI: sternal wound infection). Right panel is the zoom of the dashed boxed area in the left panel (scale bar = 20 µm).</p

Demographic characteristics of patients (n = 9) and SWI status.

<p>M, male, F, female; AKI, acute kidney disease; BMI, body mass index, CAD, coronary artery disease; CGH, coronary heart disease; DM, diabetes mellitus; END, endocarditis; GERD, gastro esophageal reflux disease; HTN, hypertension; HTN- P, Pulmonary hypertension; HLD, hyperlipidemia; RD, renal dysfunction; COPD, chronic obstructive pulmonary disease; PVD, peripheral vascular disease; OSA, obstructive sleep apnea; RHD, rheumatic heart disease; CABG, coronary artery bypass graft; MVR, mitral valve replacement; LVAD, left ventricular assisted device; PM, pace maker; RV, right ventricle; N, negative; MSSA, Methicillin-sensitive <i>Staphylococcus aureus</i>; MRSA, Methicillin-resistant <i>Staphylococcus aureus;</i> SVT, supraventricular tachycardia.</p