Biomedical subjects

Shunji Sano

Publications and source records attributed to Shunji Sano.

At least 19 recordsLinked to original sources

PubMed2006

Beraprost sodium enhances neovascularization in ischemic myocardium by mobilizing bone marrow cells in rats.

Beraprost sodium, an orally active prostacyclin analogue, has vasoprotective effects such as vasodilation and antiplatelet activities. We investigated the therapeutic potential of beraprost for myocardial ischemia. Immediately after coronary ligation of Sprague-Dawley rats, beraprost (200 microg/kg/day) or saline was subcutaneously administered for 28 days. Four weeks after coronary ligation, administration of beraprost increased capillary density in ischemic myocardium, decreased infarct size, and improved cardiac function in rats with myocardial infarction. Beraprost markedly increased the number of CD34-positive cells and c-kit-positive cells in plasma. Also, four weeks after coronary ligation of chimeric rats with GFP-expressing bone marrow, bone marrow-derived cells were incorporated into the infarcted region and its border zone. Treatment with beraprost increased the number of GFP/von Willebrand factor-double-positive cells in the ischemic myocardium. These results suggest that beraprost has beneficial effects on ischemic myocardium partly by its ability to enhance neovascularization in ischemic myocardium by mobilizing bone marrow cells.

Animals↗

PubMed2006

High mechanical efficiency of left ventricular arrhythmic contractions during atrial fibrillation.

We analyzed the frequency distribution of the left ventricular (LV) mechanical efficiency of individual arrhythmic beats during electrically induced atrial fibrillation (AF) in normal canine hearts. This efficiency is the fraction of the external mechanical work (EW) in the total mechanical energy measured by the systolic pressure-volume area (PVA). The mean, median, and mode of this efficiency (EW/PVA) were as high as 78%, 80%, and 81%, respectively, on average in six hearts. These high efficiencies were comparable to that of the regular beats in these hearts. The frequency distribution of the EW/PVA during AF tended to skew to the higher side in all the hearts. Since the EW/PVA is directly related to both the ventriculo-arterial (or afterload) coupling ratio (E(a)/E(max); E(a) = effective arterial elastance, E(max) = end-systolic ventricular elastance) and the ejection fraction on a per-beat basis, we also analyzed their frequency distributions. We found them to skew enough to account for the rightward skewed frequency distribution of the EW/PVA during AF with the unexpectedly high mean EW/PVA. These results indicate that the LV arrhythmia during AF per se does not directly suppress the mean level of LV mechanical efficiency in normal canine hearts.

Animals↗

PubMed2006

Effect of sustained limb ischemia on norepinephrine release from skeletal muscle sympathetic nerve endings.

Acute ischemia has been reported to impair sympathetic outflow distal to the ischemic area in various organs, whereas relatively little is known about this phenomenon in skeletal muscle. We examined how acute ischemia affects norepinephrine (NE) release at skeletal muscle sympathetic nerve endings. We implanted a dialysis probe into the adductor muscle in anesthetized rabbits and measured dialysate NE levels as an index of skeletal muscle interstitial NE levels. Regional ischemia was introduced by microsphere injection and ligation of the common iliac artery. The time courses of dialysate NE levels were examined during prolonged ischemia. Ischemia induced a decrease in the dialysate NE level (from 19+/-4 to 2.0+/-0 pg/ml, mean+/-S.E.), and then a progressive increase in the dialysate NE level. The increment in the dialysate NE level was examined with local administration of desipramine (DMI, a membrane NE transport inhibitor), omega-conotoxin GVIA (CTX, an N-type Ca(2+) channel blocker), or TMB-8 (an intracellular Ca(2+) antagonist). At 4h ischemia, the increment in the dialysate NE level (vehicle group, 143+/-30 pg/ml) was suppressed by TMB-8 (25+/-5 pg/ml) but not by DMI (128+/-10 pg/ml) or CTX (122+/-18 pg/ml). At 6h ischemia, the increment in the dialysate NE level was not suppressed by the pretreatment. Ischemia induced biphasic responses in the skeletal muscle. Initial reduction of NE release may be mediated by an impairment of axonal conduction and/or NE release function, while in the later phase, the skeletal muscle ischemia-induced NE release was partly attributable to exocytosis via intracellular Ca(2+) overload rather than opening of calcium channels or carrier mediated outward transport of NE.

Animals↗

PubMed2006

Monolayered mesenchymal stem cells repair scarred myocardium after myocardial infarction.

Mesenchymal stem cells are multipotent cells that can differentiate into cardiomyocytes and vascular endothelial cells. Here we show, using cell sheet technology, that monolayered mesenchymal stem cells have multipotent and self-propagating properties after transplantation into infarcted rat hearts. We cultured adipose tissue-derived mesenchymal stem cells characterized by flow cytometry using temperature-responsive culture dishes. Four weeks after coronary ligation, we transplanted the monolayered mesenchymal stem cells onto the scarred myocardium. After transplantation, the engrafted sheet gradually grew to form a thick stratum that included newly formed vessels, undifferentiated cells and few cardiomyocytes. The mesenchymal stem cell sheet also acted through paracrine pathways to trigger angiogenesis. Unlike a fibroblast cell sheet, the monolayered mesenchymal stem cells reversed wall thinning in the scar area and improved cardiac function in rats with myocardial infarction. Thus, transplantation of monolayered mesenchymal stem cells may be a new therapeutic strategy for cardiac tissue regeneration.

Animals↗

PubMed2006

Prediction of functional recovery of 60-minute warm ischemic hearts from asphyxiated canine non-heart-beating donors.

BACKGROUND: Cardiac function of non-heart-beating donors (NHBDs) is uncertain due to severe myocardial damage. We developed an isolated myocardial perfusion system to resuscitate NHBD hearts and attempted to predict functional recovery of 60-minute warm ischemic hearts by analyzing systolic and diastolic functions. METHODS: Hypoxic cardiac arrest was induced in 8 mongrel dogs without any pre-treatments. After 60-minute ischemia, intracoronary microthrombi were flushed out by retrograde blood cardiopledia with tissue-type plasminogen activator. Coronary arteries were initially perfused from the aortic root with tepid hyperkalemic blood (20 mmol/liter) at low pressure (20 mm Hg) for the first 60 minutes and then with normothermic blood for the next 60 minutes. After 120 minutes of reperfusion, pre-load was increased for ejection against an after-load of 80 mm Hg. Pressure-volume loops were recorded to obtain the end-systolic pressure-volume relationship (ESPVR) and end-diastolic pressure-volume relationship (EDPVR). Stroke volume at a given pre-load was calculated from averaged ESPVR, EDPVR and after-load identical to an averaged baseline value. The Frank-Starling relationship was obtained and cardiac status was classified according to Forrester's hemodynamic sub-set. RESULTS: End-systolic elastance decreased significantly to about 60% of baseline and the time constant of isovolumic relaxation was prolonged significantly by about 20%. Cardiac index was decreased to about 50% and cardiac status was classified in the Forrester III or IV sub-set. CONCLUSIONS: The extent of functional recovery of NHBD hearts is predictable by cardiac output. Although 120 minutes of recovery time may be short for 60-minute ischemic damage, this system may be feasible to predict post-transplant cardiac function before transplantation.

Animals↗

PubMed2006

Celsior preserved cardiac mechanoenergetics better than popular solutions in canine hearts.

BACKGROUND: Better protective effects of Celsior on cardiac function than the other conventional solutions have been reported in acute experiments and in clinical trials for at-risk patients. However, no study has yet precisely elucidated how these preservation solutions affect cardiac mechanoenergetics. Therefore, we evaluated the effects of St. Thomas' Hospital solution No. 2, University of Wisconsin solution, and Celsior on left ventricular contractility (Emax: end-systolic pressure-volume ratio) and oxygen consumption. METHODS: We used 32 canine excised cross-circulated hearts. Twenty-three hearts served as donor hearts after hypothermic ischemia with one of the three solutions, and the remaining 9 served as controls. After arrest with each solution, the hearts were preserved for 4 hours at 4 degrees C. Then, we measured left ventricular pressure, volume, and oxygen consumption to obtain Emax and the relation between ventricular pressure-volume area (a measure of total mechanical energy) and oxygen consumption. We also evaluated the oxygen cost of Emax by changing Emax with calcium administration. RESULTS: Celsior did not significantly affect E(max) (6.3 +/- 2.4 in control versus 5.3 +/- 1.3 mm Hg.mL(-1).100 g with Celsior) nor the oxygen cost of Emax (1.2 +/- 0.6 versus 1.6 +/- 0.5 mL O2.mL.mm Hg(-1).beat(-1).100 g(-2), respectively). In contrast, St. Thomas' Hospital and University of Wisconsin solutions significantly decreased Emax (4.5 +/- 1.1 and 3.5 +/- 0.9 mm Hg.mL(-1).100 g, respectively) and increased the oxygen cost of Emax (2.5 +/- 0.8 and 2.4 +/- 0.9 mL O2.mL.mm Hg(-1).beat(-1).100 g(-2), respectively) compared with control and Celsior-preserved hearts. The slope and intercept of the oxygen consumption versus pressure-volume area relation showed no significant difference among the four groups. CONCLUSIONS: Celsior showed better protective effects on cardiac mechanoenergetics than St. Thomas' Hospital and University of Wisconsin solutions in the acute phase of heart transplantation.

Animals↗

PubMed2006

Resuscitation of non-beating donor hearts using continuous myocardial perfusion: the importance of controlled initial reperfusion.

BACKGROUND: Warm ischemia is a major cause of cardiac allograft failure in transplants from non-heart-beating donors. To minimize myocardial ischemia, we used a continuous myocardial perfusion technique for resuscitation of donor hearts. The purpose of the present study was to investigate an optimal duration of controlled initial reperfusion. METHODS: Cardiac arrest was induced by asphyxia in 18 donor pigs. The hearts were harvested 30 minutes after global warm ischemia. Continuous myocardial reperfusion was immediately commenced from the aortic root with blood cardioplegic solution (20 degrees C, 40 mm Hg) and then with oxygenated blood (20 degrees to 37 degrees C, 40 to 60 mm Hg). Animals were divided into three groups according to the duration of the initial reperfusion: group I = 5 minutes, group II = 20 minutes, and group III = 60 minutes. Orthotopic transplantation was performed while keeping the heart beating by continuous myocardial perfusion. Cardiac function was evaluated before anoxia and after transplantation. Lactate extractions were determined during reperfusion. Myocardial edema was assessed by heart weight and posterior wall thickness of the left ventricle. RESULTS: Recovery rates of cardiac function in group II hearts after transplantation were better than in groups I and III (cardiac output, 61% +/- 9% versus 41% +/- 5% versus 44% +/- 4%, respectively; p < 0.05; left ventricular end-systolic pressure-volume ratio, 64% +/- 8% versus 36% +/- 9% versus 42% +/- 6%, respectively; p < 0.05). Lactate extractions in groups II and III returned to 0 within 20 minutes of reperfusion. Myocardial edema after transplantation in group II hearts was less than in groups I and III. CONCLUSIONS: The best recovery was observed in the non-beating donor hearts resuscitated by continuous myocardial perfusion when the initial controlled reperfusion with lukewarm blood cardioplegic solution at 40 mm Hg lasted for 20 minutes.

Animals↗

PubMed2006

Discrepancy between intraoperative transesophageal echocardiography and postoperative transthoracic echocardiography in assessing congenital valve surgery.

BACKGROUND: The purpose of this study was to investigate the discrepancy between intraoperative transesophageal and postoperative transthoracic echocardiography in assessing residual regurgitation in children undergoing valve repair. METHODS: Forty-two consecutive children (median age, 5.1 years) who underwent valve repair for valvar regurgitation from 2001 to 2004 were retrospectively analyzed. The patients were divided into two groups: atrioventricular valve group (n = 33) and aortic valve group (n = 9). Regurgitation grade, fractional shortening, and atrioventricular inflow velocity obtained by intraoperative transesophageal echocardiography were compared with those obtained by transthoracic echocardiography at discharge (median, 11 days) and at follow-up (median, 8 months). RESULTS: Intraoperative transesophageal echocardiography revealed specific residual lesions in 4 patients, leading to successful re-repair. Fractional shortening obtained by intraoperative transesophageal echocardiography was lower than that obtained by predischarge transthoracic echocardiography (p < 0.01). In the atrioventricular valve group, the regurgitation grade obtained by intraoperative transesophageal echocardiography was lower than that obtained by predischarge transthoracic echocardiography (0.7 +/- 0.8 versus 1.4 +/- 0.9; p < 0.01), and agreement between the two examinations was found in 12 patients (38%). Peak atrioventricular inflow velocity obtained by intraoperative transesophageal echocardiography was lower than that obtained by predischarge transthoracic echocardiography (p < 0.01). In the aortic valve group, there was no significant difference between the regurgitation grades in the two examinations (0.8 +/- 0.8 versus 1.1 +/- 0.9), and complete agreement in regurgitation grade was found in 5 (56%) of 9 patients. CONCLUSIONS: There were considerable discrepancies between the examinations in evaluation of residual atrioventricular valve regurgitation and potential atrioventricular valve stenosis: most of the residual regurgitations were underestimated by intraoperative transesophageal echocardiography. In contrast, reasonable agreement was found between the two examinations in evaluation of aortic valve regurgitation.

Adolescent↗

PubMed2006

A cell-permeable NFAT inhibitor peptide prevents pressure-overload cardiac hypertrophy.

The activation of the calcineurin-nuclear factor of activated T cells cascade during the development of pressure-overload cardiac hypertrophy has been previously reported in a number of studies. In addition, numerous pharmacological studies involving calcineurin inhibitors such as FK506 and cyclosporine A have now demonstrated that these agents can prevent such hypertrophic responses in the heart. However, little is known regarding the roles of the calcineurin downstream effector--nuclear factor of activated T cells. Our present study has further examined the roles of nuclear factor of activated T cells in pressure-overload cardiac hypertrophy by employing a recently developed cell-permeable nuclear factor of activated T cells inhibitor peptide. Rat hearts were subjected to pressure overload attributable by 4 weeks of aortic banding, and then treated with this cell-permeable nuclear factor of activated T cells inhibitor peptide and a control peptide. Treatment with the inhibitor was found to significantly decrease the heart weight/body weight ratio, the size of cardiac myocytes, and the serum brain natriuretic peptide and atrial natriuretic peptide levels. These results suggest that nuclear factor of activated T cells functions in a key role in the development of cardiac hypertrophy during pressure overload. Inhibition of nuclear factor of activated T cells by a specific inhibitor peptide is a suitable method for characterization of the molecular mechanisms underlying cardiac hypertrophy as well as in the search for new promising therapies for disease.

Animals↗

PubMed2006

Mitral-aortic intervalvular pseudoaneurysm with ventricular septal defect.

A 35-year-old woman was found on echocardiography to have a pseudoaneurysm of the mitral-aortic intervalvular fibrosa, residual ventricular septal defect, and aortic regurgitation. She had undergone surgical closure of a ventricular septal defect at age 7 and was found to have residual shunt several years later. She had been followed nonsurgically and had symptoms of cardiac failure during her 2 pregnancies. The pseudoaneurysm and the septal defect were successfully repaired.

Aneurysm, False↗

PubMed2006

Late outcome after repair of aortico-left ventricular tunnel: 10-year follow-up.

Despite successful surgical repair, patients with congenital aortico-left ventricular tunnel (ALVT) are at risk of developing aortic incompetence in the late postoperative period. Two cases of ALVT were followed for 10 years with special reference to aortic incompetence and geometry of the aortic root. The patients underwent repair of ALVT, one at 4 years of age and the other at 4 months of age. The first patient had a slit-like tunnel (type I) and the aortic orifice was closed with a pericardial patch. The second patient had a large tunnel with an extracardiac aneurysm (type II) and was closed with a pericardial patch at the aortic orifice and a Dacron patch at the left ventricular orifice, thereby completely obliterating the tunnel. The last echocardiographic evaluation showed no residual flow in the tunnel and no aortic incompetence in case 1, but there was mild aortic valvular regurgitation with deformity of the right sinus in case 2. Careful long-term follow-up is necessary because patients with ALVT have some inherent structural abnormalities from the left ventricular outflow tract to the aortic root.

Aortic Aneurysm↗

PubMed2006

Intraatrial extension of thyroid cancer: a case report.

A 61-year-old man, who was diagnosed with superior vena cava syndrome by papillary thyroid carcinoma, was referred to our hospital. A bulky thyroid tumor with tracheal invasion extended from the left neck to the right atrium without distant metastases. The risk of sudden death due to airway occlusion, tumor embolism or obstruction of the tricuspid valve led us to elect surgery. Extended resection of thyroid cancer was performed with cardiopulmonary bypass. Peritoneal dissemination was found via laparotomy. A histological diagnosis of anaplastic carcinoma arising from transformation of papillary carcinoma was made. After the operation, bilateral ureteral occlusion by peritoneal dissemination and multiple lung metastases were detected. The patient died with acute renal failure on postoperative day 12. Intraatrial extension of thyroid cancer is rare, and only 12 cases have been reported in the literature. We present a case of thyroid cancer with intraatrial extension.

Carcinoma↗

PubMed2006

Repair of a dysplastic tricuspid valve using artificial chordae: case report.

Atrioventricular valve repair with artificial chordal replacement has been widely used for congenital and acquired mitral valve abnormalities, but not for tricuspid valve abnormalities. A case is presented of dysplastic tricuspid valve that was successfully repaired using artificial chordae. A 2-year-old female presented with poor weight gain. Echocardiography revealed severe tricuspid regurgitation due to dysplastic tricuspid valve, poor coaptation by prolapse of the anterior leaflet, and tethering of the septal leaflet by short chordae. The prolapsed anterior leaflet was repaired with three pairs of 6-0 expanded polytetrafluoroethylene sutures. The short chordae of the septal leaflet were detached, and the septal and posterior leaflets were sutured together. Trivial tricuspid regurgitation was noted postoperatively. There was no tricuspid regurgitation during the follow up period of three years. The present case provides further evidence that artificial chordal replacement is a useful technique even for small children with congenitally abnormal tricuspid valves.

Child, Preschool↗

PubMed2006

Protein-losing enteropathy seven years after total right ventricular exclusion procedure for arrhythmogenic right ventricular dysplasia.

A 27-year-old man who was diagnosed with arrhythmogenic right ventricular dysplasia (ARVD) underwent the total right ventricular (RV) exclusion procedure: the RV free wall was resected and an extracardiac total cavopulmonary connection (TCPC) was created using a 24-mm-diameter polytetrafluoroethylene (PTFE) graft. After an uneventful period of 7 years, he began to develop protein-losing enteropathy (PLE), which was resistant to medical therapy, moderate mitral regurgitation (MR) and right femoral arteriovenous fistula due to heart catheterization. Therefore, fenestration of TCPC, mitral annuloplasty and ligation of arteriovenous fistula were performed. After the operation, symptoms and levels of total protein and albumin were immediately improved and normalized.

Adult↗

PubMed2005

Contribution of catechol O-methyltransferase to the removal of accumulated interstitial catecholamines evoked by myocardial ischemia.

Catechol O-methyltransferase (COMT) plays an important role for clearance of high catecholamine levels. Although myocardial ischemia evokes similar excessive catecholamine accumulation, it is uncertain whether COMT activity is involved in the removal of accumulated catecholamines evoked by myocardial ischemia. We examined how COMT activity affects myocardial catecholamine levels during myocardial ischemia and reperfusion. We implanted a dialysis probe into the left ventricular myocardial free wall and measured dialysate catecholamines levels in anesthetized rabbits. Dialysate catecholamine levels served as an index of myocardial interstitial catecholamine levels. We introduced myocardial ischemia by 60 min occlusion of the main coronary artery. The ischemia-induced dialysate catecholamines levels were compared with and without the pretreatment with entacapone (COMT inhibitor, 10 mg/kg, i.p.). Acute myocardial ischemia progressively increased dialysate catecholamine levels. Acute myocardial ischemia increased dialysate norepinephrine (NE) levels (20,453+/-7186 pg/ml), epinephrine (EPI) levels (1724+/-706 pg/ml), and dopamine (DA) levels (1807+/-800 pg/ml) at the last 15 min of coronary occlusion. Inhibition of COMT activity by entacapone augmented the ischemia-induced NE levels (54,306+/-6618 pg/ml), EPI levels (2681+/-567 pg/ml), and DA (3551+/-710 pg/ml) levels at the last 15 min of coronary occlusion. Myocardial ischemia evoked NE, EPI, and DA accumulation in the myocardial interstitial space. The inhibition of COMT activity augmented these increments in NE, EPI, and DA. These data suggest that cardiac COMT activity influences on the removal of accumulated catecholamine during myocardial ischemia.

Animals↗

PubMed2005

Variable Unstressed Volume Keeps Normal Distributions of Canine Left Ventricular Contractility and Total Mechanical Energy under Atrial Fibrillation.

We have reported that the contractility index (E(max)) and the total mechanical energy (PVA) of arrhythmic beats of the left ventricle (LV) distribute normally in canine hearts under electrically induced atrial fibrillation (AF). Here, E(max) is the ventricular elastance as the slope of the end-systolic (ES) pressure-volume (P-V) relation (ESPVR), and PVA is the systolic P-V area as the sum of the external mechanical work within the P-V loop and the elastic potential energy under the ESPVR. To obtain E(max) and PVA, we had to assume the systolic unstressed volume (V(o)) as the V-axis intercept of the ESPVR to be constant despite the varying E(max), since there was no method to obtain V(o) directly in each arrhythmic beat. However, we know that in regular stable beats V(o) decreases by approximately 7 ml/100 g LV with approximately 100 times the increases in E(max) from ~0.2 mmHg/(ml/100 g LV) of almost arresting weak beats to approximately 20 mmHg/(ml/100 g LV) of strong beats with a highly enhanced contractility. In the present study, we investigated whether E(max) and PVA under AF could still distribute normally, despite such E(max)-dependent V(o) changes. The present analyses showed that the E(max) changes were only approximately 3 times at most from the weakest to the strongest arrhythmic beat under AF. These changes were not large enough to affect V(o) enough to distort the frequency distributions of E(max) and PVA from normality. We conclude that one could practically ignore the slight E(max) and PVA changes with the Emax-dependent V(o) changes under AF.

Animals↗

PubMed2005

Predictability of O2 consumption from contractility and mechanical energy of absolute arrhythmic beats in canine heart.

Left ventricular (LV) O2 consumption (V(O2)) per minute is measurable for both regular and arrhythmic beats. LV V(O2) per beat can then be obtained as V(O2) per minute minute divided by heart rate per minute minute for regular beats, but not for arrhythmic beats. We have established that V(O2) of a regular stable beat is predictable by V(O2) = a PVA + b E(max) + c, where PVA is the systolic pressure-volume area as a measure of the total mechanical energy of an individual contraction and E(max) is the end-systolic maximum elastance as an index of ventricular contractility of the contraction. Furthermore, a is the O2 cost of PVA, b is the O2 cost of E(max), and c is the basal metabolic V(O2) per beat. We considered it theoretically reasonable to expect that the same formula could also predict LV V(O2) of individual arrhythmic beats from their respective PVA and E(max) with the same a, b, and c. We therefore applied this formula to the PVA - Emax data of individual arrhythmic beats under electrically induced atrial fibrillation (AF) in six canine in situ hearts. We found that the predicted V(O2) of individual arrhythmic beats highly correlated linearly with either their V(O2) (r = 0.96 +/- 0.01) or E(max) (0.97 +/- 0.03) while both also highly correlated linearly with each other (0.88 +/- 0.04). This suggests that the above formula may be used to predict LV Vo2 of absolute arrhythmic beats from their Emax and PVA under AF.

Animals↗

PubMed2005

Mid-term results of open aortic valvotomy for infants with critical aortic stenosis: seven-year experience including delayed Ross strategy.

OBJECTIVES: The purpose of this study is to provide short- and mid-term results of open aortic valvotomy (OAV) for patients with critical aortic stenosis (AS). METHODS: Between December 1993 and June 1996, 6 patients with critical AS underwent an OAV in our unit. Their ages and body weights at operation ranged from 1 to 65 days (median age, 9 days) and from 2.4 to 5.7 kg (median weight, 3.3 kg), respectively. Peak pressure gradient and diameter of the aortic valve ranged from 25 to 111 mmHg (mean value, 79 mmHg) and from 4.6 to 7.5 mm (mean diameter, 6.1 mm), respectively. OAV comprised the valvular commissurotomy and excision of the myxomatous nodules with cardiopulmonary bypass. RESULTS: No early or late death occurred. Mean peak pressure gradient across the aortic valve was reduced to 33 mmHg (from 15 to 44 mmHg) with no aortic insufficiency in 2 patients and trivial insufficiency in 4. During the follow-up period of 6 to 9 years, 3 out of 6 patients required no reintervention. The other 3 patients required repeated valvotomy for recurrent stenosis within 0.2 to 1.3 years after the operation. Of these, 2 patients required the Ross procedure at 7 years of age or older, and another at 6 years of age awaits the Ross procedure. CONCLUSION: OAV for critical AS was effective without causing mortality or significant aortic insufficiency. Our current strategy comprising the initial OAV and "delayed Ross procedure" for recurrent stenosis with or without insufficiency is a promising therapeutic option for infants with critical AS.

Aortic Valve↗