[Coronary artery bypass in octogenarians; how to reduce operative mortality and enhance long-term quality of life].

Octogenarians are at increased risk for perioperative morbidity and mortality after coronary artery bypass. This study is aimed to elucidate the suitable operative strategy and perioperative management. A retrospective analysis was conducted of 54 consecutive patients with 80-years of age or older, who underwent elective isolated coronary artery bypass between May 1999 and May 2008. Mean follow-up was 43.3 months and 96.3% complete. Operavive mortality was 3.7% and the incidence of stroke was 3.7%. The 7-year cardiac survival was 80.4% and the 7-year cardiac event free was 65.0%. The use of arterial graft to the right coronary artery was identified as independent predictor of late cardiac event. Neither total arterial revascularization nor bilateral internal thoracic artery grafting was a significant cardiac event factor. This retrospective study suggests a benefit of the less invasive strategy in terms of operative mortality and morbidity. Application of fast-track treatment in octogenarians appears to be an effective approach to reduce perioperative morbidity and enhance long-term quality of life.

[Successful treatment for prosthetic valve endocarditis with use of strip shaped pericardum].

We presented a case of endocarditis with methicillin-resistant Staphylococcus epidermidis that was successfully treated with linezolid. Endocarditis has been hard to cure completely with either antibiotics or surgery. In particular, it is harder to eradicate disease-causing bacteria when it is staphylococci or streptococci. In this case, an innovative operative technique and a new kind of antibiotics were involved after the failure with some sorts of antibiotics. We put a strip shaped pericardium around a newly implanted artificial ring to prevent its organism from touching it. This technique costs little and may be easy to handle, thus it may become a reliable technique for endocarditis.

Treatment of acute stanford type B aortic dissection with a novel cylindrical balloon catheter in dogs.

BACKGROUND: Despite recent progress in medical and surgical treatment, acute type B aortic dissection still carries a high mortality rate. We have developed a novel cylindrical balloon catheter for less invasive treatment to block the entry of the dissection and induce thrombotic occlusion of the false lumen. The balloon has the shape of a sheet when deflated but a double-cylinder shape when inflated. Therefore, aortic blood flow is maintained through the cylindrical lumen during balloon inflation. METHODS AND RESULTS: Six beagle dogs underwent a left thoracotomy at the 6th intercostal space. An acute dissection of 4-cm length was created surgically on the descending aorta. The balloon catheter was inserted through the distal descending aorta and advanced to the entry site. The balloon catheter was inflated for 6 hours. The blood flow in the descending aorta and the position of the balloon was monitored by color Doppler echovasculography. Four dogs were killed humanely on the following day and 2 dogs 10 days after the surgery. The descending aorta was examined macroscopically and microscopically in all dogs. In all dogs, the false lumen was occluded by thrombi. Although no dog had clinical evidence of distal thromboembolism, 2 of the 4 dogs that were killed on the second postoperative day had fresh mural thrombi in the true lumen. CONCLUSIONS: The false lumen of the acute type B aortic dissection was effectively occluded by the novel cylindrical balloon catheter in the canine experimental model. The thrombus formation in the true lumen is the problem to be solved.

Initial effects of the left ventricular repair by plication may not last long in a rat ischemic cardiomyopathy model.

BACKGROUND: Long term effects of left ventricle (LV) repair surgery (LVR) for ischemic cardiomyopathy are not well understood. METHODS AND RESULTS: Sixty-nine rats developed ischemic cardiomyopathy with large akinetic LV area 4 weeks after the left anterior descending artery was ligated. In a second surgery 4 weeks later, 33 rats underwent LVR by plication of the akinetic LV area (LVR group), and 36 underwent rethoracotomy alone (sham group). No medication was used in either group. All rats survived the second surgery. LV end-diastolic dimension as measured by echocardiography, LV fractional shortening, and the maximal end-systolic pressure-volume relationship (E(max)) as calculated from the data by catheter-tipped manometer and echocardiography improved in the LVR group after the second surgery, but LV end-diastolic dimension and E(max) gradually deteriorated as time passed. LV end-diastolic pressure improved 1 week after LVR but rose significantly 4 weeks after LVR. Brain natriuretic peptide mRNA was lower in the LVR group than in the sham group 1 week after LVR but not 4 weeks postoperatively. CONCLUSIONS: Initial improvement in LV function and neurohormonal status after LVR did not last for 4 weeks in this rat model when untreated medically. The mechanism of deterioration should be elucidated to improve long-term results of LVR.

Gelatin sheet incorporating basic fibroblast growth factor enhances healing of devascularized sternum in diabetic rats.

BACKGROUND: Poor healing of the sternum often limits the use of bilateral internal thoracic arteries (BITAs) after coronary bypass surgery in diabetic patients. We have reported that a gelatin sheet that incorporates basic fibroblast growth factor (bFGF) accelerates sternal healing after BITA removal in normal rats. This study evaluated the effects of the above method for sternal healing in diabetic animals. METHODS AND RESULTS: Diabetic Wistar rats with blood glucose levels >400 mg/dL and body-weight loss >20 g were established by a single intravenous injection of streptozotocin (55 mg/kg). After median sternotomy and BITA removal, 16 diabetic rats received either a gelatin sheet that incorporated bFGF (100 microg/sheet) on the posterior table of the sternum (FGF group, n=9) or no gelatin sheet (control, n=7). Peristernal blood flow, as measured by a noncontact laser Doppler 4 weeks after surgery in the FGF group, recovered to the preoperative level (106+/-10% versus 82+/-9%, P<0.01), and marked angiogenesis was also observed around the sternum in the FGF group (30.5+/-3.2 versus 15.8+/-2.7 vessels/unit area, P<0.01). Deep sternal wound complications developed in 5 control rats but only in 1 rat in the FGF group (P<0.05). In the FGF group, histological examination showed improved sternal healing (excellent in 6 rats and slow/poor healing in 3). Bone mineral content as assessed by dual-energy x-ray absorptometry was greater in the FGF group (75.9+/-18.1 versus 48.9+/-10.7 mg, P<0.05). Bone mineral density of the sternum was similar between the 2 groups. CONCLUSIONS: A gelatin sheet that incorporates bFGF may offset sternal ischemia and accelerate sternal bone regeneration and healing, even in diabetic patients.

Novel method to enhance sternal healing after harvesting bilateral internal thoracic arteries with use of basic fibroblast growth factor.

BACKGROUND: Poor healing of the sternum often limits the use of bilateral internal thoracic arteries (BITAs) in coronary bypass surgery, especially for diabetic patients. We have reported that basic fibroblast growth factor (bFGF) enhanced regeneration of the skull. This study was designed to evaluate the effects of topical use of bFGF on sternal healing after removing the BITAs. METHODS AND RESULTS: Forty-five Wistar rats were subjected to median sternotomy and were divided into 3 groups: 15 had the BITAs removed and had a bFGF sheet applied on the posterior table of the sternum (group A), 15 had just the BITAs removed (group B), and 15 had intact BITAs (group C). Five and 10 rats were euthanized 2 and 4 weeks after surgery, respectively, in all 3 groups. Peristernal blood flow, measured with use of a noncontact laser flowmeter, decreased after removal of the BITAs (P:<0.001). Four weeks after the surgery, PBF markedly increased only in group A (9.7+/-1.2, 6.5+/-0.6, and 8.2+/-0.5 mL x min(-1) x 100 g(-1) for groups A, B, and C, respectively; P:<0.01 by ANOVA). Four weeks after surgery, the following findings were obtained only in group A: (1) nearly completely healed sternum filled with regenerated bone tissue, (2) marked angiogenesis around the sternum, and (3) osteoblasts in an active form around the edge of the sternum. CONCLUSIONS: The results suggest that use of the bFGF sheet offset the sternal ischemia and accelerated sternal healing. This method may help to decrease sternal necrosis in high-risk patients or allow extended use of BITAs in coronary bypass surgery.

Inhibition of rho-associated kinase results in suppression of neointimal formation of balloon-injured arteries.

BACKGROUND: Rho-associated kinase (ROCK), an effector of small GTPase Rho, regulates vascular tone via a calcium sensitization mechanism and plays a key role in the pathogenesis of hypertension. However, its role in vascular growth remains unclear. METHODS AND RESULTS: Y-27632, a specific ROCK inhibitor, and the overexpression of dominant-negative ROCK suppressed the mitogen-induced DNA synthesis of cultured vascular smooth muscle cells (VSMCs), which indicates the essential role of ROCK in the control of VSMC proliferation in vitro. Y-27632 also suppressed the chemotaxis of VSMCs. Male Wistar rats were systemically given Y-27632 (35 to 70 mg. kg(-1). day(-1)) through an intraperitoneal infusion. The neointimal formation of balloon-injured carotid arteries was significantly suppressed in Y-27632-treated rats (intima/media ratio, 0.22+/-0.02) compared with vehicle-treated rats (intima/media ratio, 0.92+/-0.21) or hydralazine-treated rats with a similar blood pressure decrease (intima/media ratio, 1.03+/-0.15). The phosphorylation of myosin phosphatase and myosin light chain was elevated in injured arteries in a Y-27632-sensitive manner, indicating the augmentation of ROCK activity in neointimal formation. The downregulation of the cyclin-dependent kinase inhibitor p27(kip1) in injured vessels was reversed by Y-27632 treatment, reflecting the antiproliferative effect of ROCK inhibition in vivo. CONCLUSIONS: We conclude that ROCK plays a key role in the process of neointimal formation after balloon injury. Thus, the inhibition of ROCK may be a potential therapeutic strategy for treating vascular proliferative disorders and hypertension.

Accelerated reendothelialization with suppressed thrombogenic property and neointimal hyperplasia of rabbit jugular vein grafts by adenovirus-mediated gene transfer of C-type natriuretic peptide.

BACKGROUND: Vein graft disease limits the late results of coronary revascularization. C-type natriuretic peptide (CNP) inhibits the growth of vascular smooth muscle cells. Given the effects of CNP on cGMP cascade, we hypothesized that transfected CNP genes modulate endothelial repair and thrombogenicity in the vein graft. METHODS AND RESULTS: Autologous rabbit jugular vein grafts were incubated ex vivo in a solution of adenovirus vectors containing CNP gene (Ad.CNP) or Escherichia coli lac Z gene (Ad.LacZ) and then interposed in the carotid artery. Reendothelialization, mural thrombi formation, and intima/media ratio were evaluated on the 14th and 28th postoperative days. More reendothelialization was seen in Ad.CNP-infected grafts than in Ad.LacZ-infected grafts both at 14 days (0.81+/-0.05 versus 0.30+/-0.14, P<0.01) and at 28 days (0.96+/-0.01 versus 0.45+/-0.08, P<0.001). The mural thrombus area was smaller in Ad.CNP-infected grafts than in Ad.LacZ-infected grafts. Neointimal thickening was significantly suppressed in the Ad.CNP group. The in vitro wound assay with human coronary artery endothelial cells revealed significant potentiation of the wound repair process by CNP and atrial natriuretic peptide administration. CONCLUSIONS: Infected Ad.CNP accelerated reendothelialization and suppressed thrombosis and neointimal hyperplasia. The method may potentially prevent vein graft disease in patients undergoing coronary artery revascularization.

Pericardial fluid from patients with unstable angina induces vascular endothelial cell apoptosis.

OBJECTIVES: The purpose of this study was to investigate whether pericardial fluid from patients with unstable angina (UA) would modulate vascular endothelial cell survival. BACKGROUND: Apoptosis of vascular endothelial cells promotes the coagulation process, playing an important role in the formation of coronary arterial thrombi. However, little is known about the mechanisms of vascular endothelial cell death in acute coronary syndrome. We hypothesized that factors inducing apoptosis are produced by the ischemic heart and accumulated in high concentrations in pericardial fluid. METHOD: Pericardial fluid was obtained during coronary artery bypass surgery from patients with UA (group A, n = 8) and those with stable angina (group B, n = 23). A survival assay of F2 cells from a mouse vascular endothelial cell line was performed in the presence of 10% pericardial fluid from each patient. RESULTS: Pericardial fluid levels of vascular endothelial growth factor were significantly higher in group A than in group B, indicating that group A had more ischemic insults than group B. Pericardial fluid from group A, but not from group B, markedly induced F2 cell death (cell survival relative to fetal bovine serum; group A: 33 +/- 26% vs. group B: 91 +/- 22%, p < 0.01). Cell death was associated with internucleosomal DNA fragmentation, a hallmark of apoptosis. Fractionation of pericardial fluid using a Centricon C-100 demonstrated that apoptosis-inducible activities exist in the Centricon C-100 retentates but not in the filtrates. CONCLUSIONS: Factors that induce vascular endothelial cell apoptosis are secreted into the pericardial space from the hearts of patients with UA. These factors are large complexes or unknown new proteins larger than 100 kDa.

Expression of SR-PSOX, a novel cell-surface scavenger receptor for phosphatidylserine and oxidized LDL in human atherosclerotic lesions.

Receptor-mediated endocytosis of oxidized low density lipoprotein (Ox-LDL) by macrophages and the subsequent foam cell transformation in the arterial intima are key events in early atherogenesis. Recently, we have identified a novel macrophage cell-surface receptor for Ox-LDL by expression cloning from a cDNA library of phorbol 12-myristate 13-acetate-stimulated THP-1 cells, designated as the scavenger receptor for phosphatidylserine and oxidized lipoprotein (SR-PSOX). Here, we examined SR-PSOX expression in human atherosclerotic lesions. Total cellular RNA and fresh frozen sections were prepared from human carotid endarterectomy specimens (from 21 patients) and directional coronary atherectomy specimens (from 11 patients). Fragments of human aortas of 2 patients without visible atherosclerotic lesions served as negative controls. Quantitative reverse transcription-polymerase chain reaction demonstrated that SR-PSOX mRNA expression was prominent in atherosclerotic lesions but undetectable in normal aortas. Immunohistochemistry showed that SR-PSOX was predominantly expressed by lipid-laden macrophages in the intima of atherosclerotic plaques in carotid endarterectomy and directional coronary atherectomy specimens, although its expression was not detectable in normal arterial wall. Double-labeled immunohistochemistry confirmed that SR-PSOX is expressed by intimal macrophages. Taken together, SR-PSOX may be involved in Ox-LDL uptake and subsequent foam cell transformation in macrophages in vivo and thus may play important roles in human atherosclerotic lesion formation.

C-type natriuretic peptide induces redifferentiation of vascular smooth muscle cells with accelerated reendothelialization.

We recently reported that C-type natriuretic peptide (CNP) occurs in vascular endothelial cells and acts as a vascular-type natriuretic peptide. In the present study, we stimulated the cGMP cascade in proliferating smooth muscle cells (SMCs), in which particulate guanylate cyclase-B, the specific receptor for CNP, is predominantly expressed, by use of an adenovirus encoding rat CNP cDNA (Ad.CNP). In the Ad.CNP-treated cultured SMCs, CNP caused the growth inhibition of SMCs at G(1) phase with an early increase of p21(CIP1/WAF1) expression and subsequent upregulation of p16(INK4a). The expression of smooth muscle myosin heavy chain-2, which is the molecular marker of highly differentiated SMCs, was reinduced in the Ad.CNP-treated SMCs. The Ad.CNP-treated SMCs also reexpressed particulate guanylate cyclase-A, which shows high affinity to atrial and brain natriuretic peptide and is exclusively expressed in well-differentiated SMCs. CNP, which was overexpressed in rabbit femoral arteries in vivo at the time of balloon injury, significantly suppressed neointimal formation. Furthermore, an enhancement of the expression of smooth muscle myosin heavy chain-2 occurred in the residual neointima. In addition, early regeneration of endothelial cells was observed in the Ad.CNP-infected group. Thus, stimulation of cGMP cascade in proliferating dedifferentiated SMCs can induce growth inhibition and redifferentiation of SMCs with accelerated reendothelialization.

[Mechanical complications of myocardial infarction in elderly patients].

As mechanical complications after myocardial infarction in the elderly, we described the therapeutic strategies for postinfarction ventricular septal perforation (PVSP), ischemic cardiomyopathy (ICM), and ischemic mitral regurgitation (IMR). To improve operative results for PVSP in the elderly, it is important to maintain hemodynamics by cardiac support device such as intraaortic balloon pumping, and to perform prompt surgical intervention before cardiogenic shock and multiple organ failure. Infarct exclusion technique is a standard surgery for PVSP. Both ICM and IMR are common disease caused by severe cardiac ischemia and mitral valve (MV) function is related to left ventricular (LV) geometry. We consider total MV-LV geometrical repair by LV restoration surgery, MV repair, and coronary revascularization is essential to improve morphological abnormality in LV and MV even in the elderly. To maximize LV function, septal anterior ventricular exclusion (SAVE) technique for antero-septal myocardial ischemia, apex-sparing Batista operation for lateral ischemia, and undersized mitral annuluoplasty to improve LV sphericity are procedures of choice. However, it is still difficult to save elderly patients with very low cardiac function. Novel treatments such as regenerative medicine by angiogenic cytokines and/or cell transplantation, and advanced medical treatments are waited for this high-risk group.

[Modified technique creating fenestration in the extracardiac Fontan completion; kissing anastomosis].

Acute or subacute occlusion of a fenestration between the Fontan chamber and the atrium causes low cardiac output status, sustained pleural effusion, and protein losing enteropathy in critical cases. To achieve reliable and long patency of the fenestration in extracardiac Fontan operations, we modified our technique for creating a fenestration, namely "kissing" anastomosis, in which the atrial incision is directly sutured to the surface of the extracardiac conduit leaving a few millimeters outside from the edge of the punched-out hole (fenestration). We applied this modification in 2 cases. The diameter of the hole is 4 mm (case 1) and 3 mm (case 2). The patients were anticoagulated by warfarin potassium after the surgery. The fenestrations were patent at 3- (case 1) and 1-month (case 2) after the surgery. Peripheral oxygen saturations at discharge were 86 (case 1) and 88% (case 2). There was no death or major complication. The described procedure is an effective alternative to maintain patency and function of the fenestration in extracardiac Fontan operations.

[Prophylactic treatment of oral sildenafil citrate for pulmonary hypertension in an infant treated with inhaled nitric oxide after open-heart surgery].

A 3-month-old boy with coarctation of the aorta (CoA), ventricular septal defect (VSD), atrial septal defect, and severe pulmonary hypertension (PH) underwent one-stage repair consisting of patch closure of VSD and coarctation repair. Inhalation of nitric oxide (iNO) was commenced to treat residual severe PH on the day of the operation. Oral sildenafil citrate was commenced on the day 1 and iNO was gradually weaned off on the day 3. There was no "rebound", severe increase in pulmonary artery pressure, which commonly occurs after discontinuation of iNO. Then the patient was extubated without any difficulties or recurrent PH. The oral sildenafil citrate therapy was ceased on the day 8. Prophylactic use of oral sildenafil citrate for PH might be an useful alternative to shorten the duration of iNO therapy and intensive care unit (ICU) stay in the selected patients after congenital open heart surgery.

[Successful implantation of a metal coronary angioplasty stent for bronchomalacia of the right tracheal bronchus associated with right isomerism complex in an early infant].

One-month-old boy had severe emphysema of the right upper lobe due to the stenotic tracheal bronchus compressed between the distorted right patent ductus arteriosus (PDA) and the right aortic arch associated with right isomerism complex. He underwent a left modified Blalock-Taussig shunt and a division of the PDA on cardiopulmonary bypass. Extracorporeal lung support (ECLS) was introduced because of severe hypoxemia caused by remaining bronchomalacia of the tracheal bronchus. On postoperative day 3, a metal coronary angioplasty stent was implanted at the stenotic lesion under fluoroscopic and bronchoscopic guidance. He was successfully weaned from ECLS and then respirator after the implantation. This simple stenting procedure might be an effective alternate in the treatment of bronchomalacia or bronchial stenosis in early infancy.

[Successful resection of left ventricular myxoma in a toddler; report of a case].

A 4-year-old girl was found to have large left ventricular myxoma without any tumor-related symptoms. She underwent an urgent surgery and the myxoma was successfully removed through a left ventriculectomy. Great care was taken to prevent tumor-embolization during surgery, and to resect the endocardium attaching directly to the tumor. Future surveillance of this case warrants our operative technique described in this report.

VCAM-1 expression precedes macrophage infiltration into subendothelium of vein grafts interposed into carotid arteries in hypercholesterolemic rabbits--a potential role in vein graft atherosclerosis.

Intimal hyperplasia and atherosclerosis are major causes of late vein graft failure after coronary artery bypass surgery. Hypercholesterolemia appears to be a key risk factor for atherosclerosis in vein grafts as well as in native arteries. We used a rabbit model of interposition jugular vein graft to the carotid artery and compared intimal thickening, macrophage accumulation, and VCAM-1 expression between hypercholesterolemic (H group) and normocholesterolemic (N group) rabbits. Fifty-nine rabbits were divided into H and N groups. Intimal thickening in vein grafts was approximately three times more prominent in the H group than in the N group. Macrophage accumulation progressively increased with time in H group vein grafts, although it was negligible in the N group. In the H group, moreover, macrophages were initially more abundant in deep intima, and subsequently accumulated in subendothelium of the grafted vein. VCAM-1 expression in luminal endothelial cells of the grafted veins was time-dependently increased after the vein graft surgery in both the H and N groups, and was more prominent in the H group. Comparison of the time-courses between macrophage accumulation and VCAM-1 expression revealed that VCAM-1 expression in luminal endothelium preceded subendothelial accumulation of macrophages. VCAM-1 expression and macrophage accumulation may be key factors which regulate progression of vein graft atherosclerosis.

Simultaneous assessment of myocardial free fatty acid utilization and left ventricular function using 123I-BMIPP-gated SPECT.

UNLABELLED: This study was designed to evaluate the methodological feasibility of 123I-labeled beta-methyl-p-iodophenyl-pentadecanoic acid (BMIPP)-gated SPECT to assess regional and global left ventricular (LV) function in comparison with 99mTc-sestamibi (methoxyisobutyl isonitrile [MIBI])-gated SPECT and first-pass radionuclide angiography (FPRNA). METHODS: Forty-four patients with stable coronary artery disease underwent rest BMIPP-gated SPECT (111 MBq, 60 s/step) and rest MIBI-gated SPECT (600 MBq, 40 s/step) within a week. From both gated SPECT studies, regional defect scores (DS), wall motion scores (WMS) and wall-thickening scores (WTS) were evaluated visually using 4-point scales for nine segments, and LV ejection fraction (EF) (%) was automatically calculated using Quantitative Gated SPECT (QGS) software. FPRNA was also performed on injection of MIBI. RESULTS: Exact agreement between the two gated SPECT studies was 84.1% (kappa = 0.706, r = 0.907, P < 0.0001) in WMS and 87.1% (kappa = 0.662, r = 0.884, P < 0.0001) in WTS. LVEF obtained from BMIPP-gated SPECT linearly correlated with those from MIBI-gated SPECT (y = -0.27 + 0.944x, r = 0.948, SEE = 5.00, P < 0.0001) and FPRNA (y = -7.32 + 1.042x, r = 0.919, SEE = 6.19, P < 0.0001). Even in 21 patients with mismatch segments (BMIPP DS > MIBI DS), agreement was considered to be acceptable in WMS (81.5%, kappa = 0.707, r = 0.853, P < 0.0001) and in WTS (76.7%, kappa = 0.526, r = 0.754, P < 0.0001), and correlation in LVEF remained good between BMIPP-gated SPECT and MIBI-gated SPECT (y = -1.24 + 0.955x, r = 0.938, SEE = 6.25, P < 0.0001) or FPRNA (y = -6.03 + 1.024x, r = 0.913, SEE = 7.38, P < 0.0001). CONCLUSION: BMIPP-gated SPECT can evaluate regional and global LV function with the QGS software. Therefore, BMIPP-gated SPECT offers the opportunity for simultaneous assessment of myocardial free fatty acid utilization and LV function.

Usefulness of electromagnetic flowmetry in intraoperative evaluation of aortic regurgitation associated with ventricular septal defect.

In 38 patients with aortic regurgitation (AR) associated with ventricular septal defect (VSD), indications for aortic valvuloplasty (AVP) or aortic valve replacement (AVR) were investigated by assessing AR ratio, which was measured by electromagnetic flowmetry of the ascending aorta during the operation. Residual AR was evaluated by auscultation postoperatively. Patients were assigned to group A if they underwent VSD closure alone and to group B if they underwent AVP in addition to VSD closure; patients who had no postoperative AR were assigned to group I and those with persistence of AR to group II. Thus, the patients were separated into 4 subgroups; A-I (9 patients), A-II (5 patients), B-I (20 patients) and B-II (4 patients). In subgroup A-I, mean AR ratio decreased from 9% to 7% postoperatively, in A-II from 19% to 16% (p less than 0.1), in B-I from 36% to 9% (p less than 0.01) and in B-II from 44% to 20% (p less than 0.05). An AR ratio of more than 25% should be regarded as an absolute indication for AVP or AVR. If the AR ratio is between 20 and 25%, the indication of AVP is determined by inspection of the aortic valve. A good correlation was found between AR ratio and the AR rate determined by the aortic angiographic findings (Sellers classification): grade I AR corresponded to an AR ratio of 5 to 15%, grade II to 20 to 35%, grade III to 25 to 50% and grade IV to 45% or higher (r = 0.87, p less than 0.01).

Surgical treatment of postinfarction false aneurysm of the left ventricle.

Twelve patients underwent surgery for repair of false aneurysms of the left ventricle. The mean interval between the myocardial infarction and the diagnosis was 19 months (range 2 to 80 months). Congestive heart failure was the most common clinical presentation. Most patients had three-vessel coronary artery disease. The false aneurysm was posterior in 10 patients and anterior in two. Three patients with posterior aneurysm had severe mitral regurgitation. Repair was accomplished by resection of the false aneurysm and primary closure of the defect in four patients and by closure with a patch in eight. Nine patients also had coronary artery bypass. Mitral valve replacement was performed in three patients who had severe mitral regurgitation before the operation and in one patient who had severe mitral regurgitation after repair of the false aneurysm and could not be weaned from cardiopulmonary bypass. There were three operative deaths and one additional death after 2 months. All deaths occurred in patients who had mitral valve replacement. Eight patients survived the operation and remained well after a mean follow-up period of 62 months. Patients with false aneurysms of the left ventricle do well after surgical repair, except when concomitant mitral valve replacement is necessary.