Successful Repair of a Forme Fruste Bicuspid Aortic Valve by the Raphe Suspension Technique.

A 52-year-old man underwent surgery due to shortness of breath caused by severe aortic regurgitation with right coronary cusp prolapse. Operative findings revealed 3 symmetric cusps with small raphe between the right and noncoronary cusps situated lower than the others, indicating a forme fruste bicuspid aortic valve (BAV). The BAV was successfully repaired by tricuspidization, including raphe suspension, right coronary cusp plication, and double annuloplasty. The postoperative course was uneventful, and echocardiography at 3 months showed mild aortic regurgitation with adequate left ventricular reverse remodeling. Here we present the technical details of the raphe suspension procedure for forme fruste BAV.

Aortic root destruction after aortic valvuloplasty for bicuspid aortic valve.

Ultrasound cardiography showed severe aortic regurgitation (AR) due to bicuspid aortic valve with dilatation of the aortic annulus and sinotubular junction in a 27-year-old man hospitalized with loss of consciousness. He underwent aortic valvuloplasty combined with external suture annuloplasty using an expanded polytetrafluoroethylene (ePTFE) suture. Intraoperative findings revealed thickening and adhesion of the aortic root despite the first surgery. He developed recurrent AR 7 months later and underwent redo surgery. An ePTFE suture was found inside the aorta. Aortic root replacement with a mechanical composite graft was performed, as reconstruction appeared difficult because the aortic annulus was damaged and there were multiple holes on all cusps. Here, we report a rare case of aortic root destruction after external suture annuloplasty.

The Composition and Structure of Biofilms Developed by Propionibacterium acnes Isolated from Cardiac Pacemaker Devices.

The present study aimed to understand the biofilm formation mechanism of Propionibacterium acnes by analyzing the components and structure of the biofilms. P. acnes strains were isolated from the surface of explanted cardiac pacemaker devices that exhibited no clinical signs of infection. Culture tests using a simple stamp culture method (pressing pacemakers against the surface of agar plates) revealed frequent P. acnes colonization on the surface of cardiac pacemaker devices. P. acnes was isolated from 7/31 devices, and the isolates were categorized by multilocus sequence typing into five different sequence types (STs): ST4 (JK18.2), ST53 (JK17.1), ST69 (JK12.2 and JK13.1), ST124 (JK5.3), ST125 (JK6.2), and unknown ST (JK19.3). An in vitro biofilm formation assay using microtiter plates demonstrated that 5/7 isolates formed biofilms. Inhibitory effects of DNase I and proteinase K on biofilm formation varied among isolates. In contrast, dispersin B showed no inhibitory activity against all isolates. Three-dimensional live/dead imaging of P. acnes biofilms with different biochemical properties using confocal laser microscopy demonstrated different distributions and proportions of living and dead cells. Additionally, it was suggested that extracellular DNA (eDNA) plays a role in the formation of biofilms containing living cells. Ultrastructural analysis of P. acnes biofilms using a transmission electron microscope and atmospheric scanning electron microscope revealed leakage of cytoplasmic components along with cell lysis and fibrous structures of eDNA connecting cells. In conclusion, the biochemical properties and structures of the biofilms differed among P. acnes isolates. These findings may provide clues for establishing countermeasures against biofilm-associated infection by P. acnes.

Spontaneous closure of a large left ventricular pseudoaneurysm after mitral valve replacement.

Left ventricular pseudoaneurysm is a rare, but potentially fatal, condition that generally occurs as a complication of myocardial infarction, infective endocarditis, or cardiac surgery. Surgical repair is the treatment of first choice because of the marked risk of rupture, but deteriorated hemodynamics and complicated procedures to treat the pseudoaneurysm may lead to a high mortality rate. We report a 62-year-old woman with a large left ventricular pseudoaneurysm after mitral valve replacement for rheumatic mitral valve stenosis. Surgical repair was not performed due to the patient's refusal, but her pseudoaneurysm resolved spontaneously by 2 years after mitral valve replacement. Spontaneous obliteration of a large left ventricular pseudoaneurysm is very rare in a patient on warfarin therapy. This case suggests that a left ventricular pseudoaneurysm with a narrow neck may resolve spontaneously in rare settings.

Reversal of oxidant-mediated biochemical injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in the infantile piglet heart by terminal warm-blood cardioplegia supplemented with phosphodiesterase III inhibitor.

PURPOSE: The benefit of terminal blood cardioplegia (TWBCP) is insufficient after prolonged ischemia associated with inevitable oxidant-mediated injury by this modality alone. We tested the effects of TWBCP supplemented with high-dose olprinone, which is a phosphodiesterase III inhibitor, a clinically available compound with the potential to reduce oxidant stress and calcium overload. We evaluated the effects with respect to avoiding oxidant-mediated myocardial reperfusion injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in a infantile piglet cardiopulmonary bypass (CPB) model. METHODS: Fifteen piglets were subjected to 90 min of cardioplegic arrest on CPB, followed by 30 min of reperfusion. In group I, uncontrolled reperfusion was applied without receiving TWBCP; in group II, TWBCP was given; in group III, TWBCP was supplemented with olprinone (3 µg/ml). Myocardial performance was evaluated before and after CPB by a left ventricular (LV) function curve and pressure-volume loop analyses. Biochemical injury was determined by measurements of troponin-T and lipid peroxide (LPO) in coronary sinus blood. RESULTS: Group III showed significant LV performance recovery (group I, 26.5% ± 5.1%; group II, 42.9% ± 10.8%; group III, 81.9% ± 24.5%, P < 0.01 vs. groups I and II), associated with significant reduction of troponin-T and LPO at the reperfusion phase. No piglets in group III needed electrical cardioversion. CONCLUSION: We concluded that TWBCP with olprinone reduces myocardial reperfusion injury by reducing oxidant-mediated lipid peroxidation, and it accelerates prompt and persistent LV functional recovery with suppression of reperfusion arrhythmia.

Ischemic postconditioning promotes left ventricular functional recovery after cardioplegic arrest in an in vivo piglet model of global ischemia reperfusion injury on cardiopulmonary bypass.

OBJECTIVE: An in vivo study of piglets on cardiopulmonary bypass was performed to determine whether postconditioning has a cardioprotective effect after cardioplegic arrest in large animals. METHODS: Eighteen piglets were subjected to 90 minutes of cardioplegic arrest followed by 30 minutes of reperfusion. In 6 animals (control), there was no intervention at reperfusion. In 6 other animals, 6 cycles of unclamping and reclamping for 10 seconds each were done before reperfusion (postconditioning 10), whereas 3 cycles of unclamping and reclamping for 30 seconds each were performed in another 6 piglets (postconditioning 30). RESULTS: Recovery of left ventricular contractility and diastolic function (percent of preischemic value) was significantly better in both postconditioning groups (contractility: 89.2% and 118.2; diastolic function: 142.3% and 120.4; in the postconditioning 10 and 30 groups, respectively) compared with the control (contractility: 46.1%; diastolic function: 218.5%). Recovery of global cardiac function (ventricular function curve analysis) was improved only in the postconditioning 30 group. Troponin-T release during reperfusion was significantly reduced in the postconditioning 10 group compared with all groups (plasma troponin-T was 0.58 ng/mL in postconditioning 10, 1.85 in postconditioning 30, and 2.54 in control). The myocardial lipid peroxide was significantly higher in the control group than in both postconditioning groups after reperfusion (199% vs 112% and 131%). CONCLUSIONS: Both postconditioning algorisms promoted functional recovery after cardioplegic arrest in a large animal model along with the limitation of lipid peroxidation with or without the reduction of troponin-T release.

Prevention of ischemia/reperfusion-induced pulmonary dysfunction after cardiopulmonary bypass with terminal leukocyte-depleted lung reperfusion.

OBJECTIVE: Pulmonary ischemia and reperfusion during routine open heart surgery with cardiopulmonary bypass can lead to pulmonary dysfunction and vasoconstriction, resulting in a high morbidity and mortality. We investigated whether ischemia/reperfusion-induced pulmonary dysfunction after full-flow cardiopulmonary bypass could be prevented by the infusion of leukocyte-depleted hypoxemic blood during the early phase of reperfusion (terminal leukocyte-depleted lung reperfusion) and whether the benefits of this method were nullified by using hyperoxemic blood for reperfusion. METHODS: Twenty-one neonatal piglets underwent 180 minutes of full-flow cardiopulmonary bypass with pulmonary artery occlusion, followed by reperfusion. The piglets were divided into 3 groups of 7 animals. In group I, uncontrolled reperfusion was achieved by unclamping the pulmonary artery. In contrast, pulmonary reperfusion was done with leukocyte-depleted hyperoxemic blood in group II or with leukocyte-depleted hypoxemic blood in group III for 15 minutes at a flow rate of 10 mL/min/kg before pulmonary artery unclamping. Then the animals were monitored for 120 minutes to evaluate post-cardiopulmonary bypass pulmonary function. RESULTS: Group I developed pulmonary dysfunction that was characterized by an increased alveolar-arterial oxygen difference (204 + or - 57.7 mm Hg), pulmonary vasoconstriction, and decreased static lung compliance. Terminal leukocyte-depleted lung reperfusion attenuated post-cardiopulmonary bypass pulmonary dysfunction and vasoconstriction when hypoxemic blood was used for reperfusion (alveolar-arterial oxygen difference, 162 + or - 61.0 mm Hg). In contrast, no benefit of terminal leukocyte-depleted lung reperfusion was detected after reperfusion with hyperoxemic blood (alveolar-arterial oxygen difference, 207 + or - 60.8 mm Hg). CONCLUSION: Reperfusion with leukocyte-depleted hypoxemic blood has a protective effect against ischemia/reperfusion-induced pulmonary dysfunction by reducing endothelial damage, cytokine release, and leukocyte activation.

Myocardial cyclic AMP augmentation with high-dose PDEIII inhibitor in terminal warm blood cardioplegia.

PURPOSE: Phosphodiesterase (PDE) III inhibitors have been reported in various cellular protective activities via the cyclic adenosine monophosphate (cAMP) pathway. We investigated the effects of amrinone on ischemia/reperfusion injury and intracellular calcium (Ca2+) handling if utilized as a component of terminal warm blood cardioplegia (TWBCP). METHODS: Anesthetized pig hearts were subjected to 90-min global ischemia with single-dose crystalloid cardioplegia, followed by 30-min reperfusion under cardiopulmonary bypass. The animals were divided into three groups according to the contents of TWBCP (n = 5 each): Control, no TWBCP; TWBCP, no additive; Amrinone, TWBCP with amrinone. The time course of cardiac function and biochemical samples were measured. Further, coronary perfusion and ventricular arrhythmia were evaluated during reperfusion. RESULTS: Cardiac function improved with amrinone. Specifically, the amrinone group showed an increase of myocardial cAMP (p <0.05) and a suppression of creatine kinase, troponin-T, and lipid peroxide after reperfusion (p <0.05); many cases also showed much improvement of coronary perfusion and spontaneous resuscitation after global ischemia. CONCLUSION: Ischemia and/or reperfusion deplete myocardial cAMP, leading to impaired Ca2+ handling and further to cardiac dysfunction. High-dose PDEIII inhibitor in TWBCP may replenish myocardial cAMP and promote rapid and sustained cardiac functional recovery with various cellular protective effects after open-heart surgery.