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Though a high frequency of postoperative complications after an original Bentall procedure has been reported, several procedures that reduce the incidence of complications have been developed. Complications relating to anastomoses of the interposed graft are infrequent but life-threatening. This report describes a case of a 61-year-old man who presented with heart failure secondary to bilateral detachment of coronary ostial anastomoses and graft stenosis 21 years after undergoing a modified Bentall procedure. These complications were successfully repaired by reconstructing the conduit and coronary arteries.

We describe a rare case of surgical repair of a coronary artery aneurysm with arteriosclerotic changes accompanied by coronary arteriovenous fistula (CAVF) after 26 years of conservative therapy. A 71-year-old woman, diagnosed with CAVF 26 years previously, was admitted to our hospital for general fatigue and dyspnea on exertion. Physical examinations revealed that the CAVF originated from the distal portion of the left circumflex artery (LCX), draining into the coronary sinus (CS); it affected the coronary artery aneurysm with arteriosclerotic changes and was calcified from the left coronary main trunk to the distal portion of the LCX. Treatment without resection of the calcified coronary aneurysm was suggested because of fear of excessive bleeding. The CAVF was closed directly from inside the dilated coronary sinus under cardiopulmonary bypass. The dilated ostium of the left coronary artery was closed using a Xenomedica patch. Coronary artery bypass grafting was performed in the left anterior descending artery (LAD) and posterolateral branch (PL) of the LCX using saphenous vein grafts. Postoperatively, the coronary aneurysm was spontaneously thrombosed for low blood flow. The bleeding might have been uncontrolled if the arteriosclerotic and calcified coronary aneurysm had been incised. Therefore, we successfully thrombosed the calcified coronary aneurysm without resection, after reducing the systemic blood flow to the coronary aneurysm and sustaining the coronary blood flow, performed with CABG.

Ischemic cardiomyopathy complicated by severe mitral regurgitation (MR) has a poor prognosis. In such cases, whether mitral valve repair for MR improves the prognosis of survival remains unclear. In this study, 50 patients diagnosed with ischemic cardiomyopathy at our hospital between August 1991 and August 1996 were studied to examine the long-term prognosis and factors determining the prognosis. Among 17 patients with the complication of severe MR, 11 underwent mitral valve repair (repair group) and 6 did not (nonrepair group). Among the 33 patients without MR, 15 underwent revascularization (revascularization group) and 18 received medical treatment alone (medical group). Patients with MR showed significantly poorer baseline activities of daily living (ADL) [New York Heart Association (NYHA) class III or above: MR(+) vs MR(-) = 14 vs 8; P = 0.0001] and survival rate [MR(+) vs MR(-); log rank = 3.8, P = 0.05]. In contrast, patients in whom mitral valve repair was actively performed to resolve MR had favorable outcomes for both ADL (NYHA class improved from 3.9 +/- 0.3 to 2.7 +/- 1.0; P = 0.0004) and survival rate (MV repair vs nonrepair: long rank = 10.1, P = 0.0015). In addition, among patients without MR, the revascularization group showed more favorable results in terms of ADL (NYHA class improved from 3.5 +/- 0.7 to 2.5 +/- 0.8; P = 0.0059) and survival rate (revascularization vs medical: log rank = 3.7, P = 0.05), irrespective of improvement of left ventricular function. When the factors determining the prognosis for ischemic cardiomyopathy were examined by multivariate analysis, whether or not revascularization was conducted, the presence or absence of mitral regurgitation, and if present, whether or not mitral valve repair was performed were identified as independent factors determining the prognosis (revascularization: hazard ratio = 0.121, P = 0.012; absence of MR: hazard ratio = 0.104, P = 0.050; mitral valve repair: hazard ratio = 0.018, P = 0.005). These results showed that revascularization should be conducted as actively as possible in patients with ischemic cardiomyopathy; in addition, for those patients with mitral regurgitation, mitral valve repair should be conducted actively to relieve it.

The thrombotest (TT) technique has been widely used in Japan for monitoring oral anticoagulant therapy (OAT). The therapeutic range was originally recommended to be 10%-25%. However, the International Committee for Standardization in Hematology/International Committee on Thrombosis and Hemostasis (ICSH/ICTH) recommended using the international normalized ratio of prothrombin time (PT-INR) for monitoring OAT. It is necessarv to use a universal standard measure for monitoring OAT in accordance with the ICSH/ISTH recommendation. We simultaneously measured TT and PT in blood samples from 1,157 patients on long-term warfarin therapy, and studied the correlation between TT and PT-INR. An excellent linear correlation was obtained between TT-INR and PT-INR with the regression equation PT-INR = 1.0420 TT-INR - 0.0987 (r = 0.905, P < 0.001). We also examined the correlation between the incidence of thromboembolism in 170 patients receiving warfarin therapy after prosthetic valve replacement; 50.5% received concomitant antiplatelet therapy. Thromboembolism occurred in 9 of 170 patients during a mean follow-up period of 2.44 years. The average TT values in patients with and without thromboembolism were 26.4% (PT-INR: 1.53) and 21.1% (1.73), respectively (P < 0.01). The incidence of thromboembolism did not differ significantly between patients on warfarin alone (average TT: 22.2%) and those on warfarin and antiplatelet agent (average TT: 20.9%). Our results suggest that the incidence of thromboembolism is low in Japan despite a less intensive regimen having been adopted.

A theoretical equation was derived based on the time-varying elastance model to predict theoretically the relationship between the delay in the onset of left ventricular outflow obstruction and the reduction in peak left ventricular pressure (LVP) caused by treatment in hypertrophic obstructive cardiomyopathy (HOCM). ECG, LVP, and other hemodynamic parameters were measured during catheterization at a constant heart rate with atrial pacing in 16 patients with HOCM before and after intravenous administration of disopyramide (1 mg/kg). After disopyramide administration, the duration between the R wave of the ECG and the onset of obstruction (T1) was prolonged significantly (from 117 +/- 30 to 155 +/- 32 ms, P < 0.0001), and peak LVP was reduced significantly (from 222 +/- 42 to 177 +/- 39 mmHg, P < 0.0001). The relation between the prolongation of T1 and the percent reduction in peak LVP was predicted well by the theoretical equation (coefficient of determination R2 = 0.926). Our model simplifies the therapeutic strategy for reducing the left ventricular outflow pressure gradient in patients with HOCM, which is to delay the time of onset of obstruction by some methods.

The inducibility of reentry was compared for four QT patterns in a heart conduction simulation model. Local (L) and gradual (G) QT prolongation models are more susceptible to reentry induction than the no (N) QT prolongation model (reentry induced episodes for N, L, and G numbered 90, 120, and 122, respectively). This increased vulnerability was diminished when the QT interval was prolonged at all simulation sites (reentry induced episodes for the diffuse QT prolongation model, D model, numbered 82). Decreased QT dispersion might be important for the prevention of reentry induction regardless of whether the QT interval is increased.

The cyclic AMP (cAMP)-dependent chloride channel in the heart has been identified in various species as the cystic fibrosis transmembrane conductance regulator (CFTR). Although functional expression of the channel in the human atrium has been reported, we could not induce any cAMP-dependent chloride conductance in the atrial cells even with maximal cAMP stimulation, whereas the conductance could be induced in rabbit ventricular cells. To clarify the discrepancy between the results, we examined the level of CFTR mRNA expression in both conductance-positive (human colonic epithelium and rabbit ventricle) and -negative (human atrium) tissues. Total RNA samples prepared from these tissues were subjected to the reverse transcription-polymerase chain reaction (RT-PCR). While CFTR transcripts were amplified from the conductance-positive samples, no amplified products could be detected from the conductance-negative sample. A nested PCR performed on the RT-PCR products of the conductance-negative sample resulted in successful amplification of the transcripts, indicating that the level of the CFTR mRNA expression in human atrium is extremely low compared with that in colonic epithelium and rabbit ventricle. The same molecular results were observed in human ventricular tissues. A nucleotide sequencing of the amplified transcripts showed that exon 5 of the CFTR gene was not alternatively spliced in human atrium and ventricle, and both the exon 5 spliced and unspliced isoforms were expressed in rabbit ventricle, unlike the findings of previous reports. Our data suggest that the amount of CFTR expressed in human myocardium might be physiologically insufficient to activate detectable cAMP-dependent chloride conductance.

We evaluated the effects of disopyramide in terms of the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy (HOCM). The myocardial oxygen supply was evaluated by measuring coronary flow velocity and the myocardial oxygen demand was assessed by the pressure-volume area (PVA). The time velocity integral of coronary flow did not change significantly (20 +/- 6 to 21 +/- 8 cm), but the peak left ventricular pressure and left ventricular external work decreased significantly (206 +/- 44 to 157 +/- 37 mmHg, P < 0.001; 1.09 +/- 0.33 to 0.80 +/- 0.23 J/beat, P < 0.001) after disopyramide administration. From theoretical analysis using these data, we concluded that disopyramide improves the myocardial oxygen supply-demand balance in patients with HOCM.

Angiogenesis plays an important role in various diseases and conditions such as malignant tumor, wound healing, and atherosclerosis. Since cell-to-cell adhesion may play a key role in angiogenesis, we investigated the effect of the cadherin-catenin-cytoskeleton complex on angiogenesis in human umbilical vein endothelial cells (HUVECs). Immunofluorescence staining revealed that alpha-catenin, beta-catenin, and plakoglobin were concentrated at cell-cell contacts in HUVECs. Antisense oligonucleotide (AS-oligo), complementary to the region of human plakoglobin was dissolved in saline and applied to the media at 1 mM every 12 h for 4 days, and sense oligonucleotide (S-oligo) was used as control. HUVEC migration from an injury line was enhanced by AS-oligo. Interestingly, HUVECs migrated in line with S-oligo, and in a scattered fashion with AS-oligo. Tube formation on Matrigel occurred earlier with AS-oligo than with S-oligo. These findings indicate that plakoglobin inhibited HUVEC migration and tube formation (angiogenesis) by regulating cell-cell adhesion.

From 1993 to 1997, nine Japanese heart transplant candidates were accepted by the University of California at Los Angeles (UCLA) Medical Center, because no donor heart was available in Japan from a brain-dead patient. In all nine heart transplant patients described in this investigation, the preoperative diagnosis was dilated cardiomyopathy. One patient underwent implantation with a Novacor left ventricular assist device (Baxter Japan, Tokyo, Japan) as a bridge to heart transplant. All patients survived surgery and for a long-term period. The actuarial 1-year and 3-year survival curves of these patients were both 100%. The postoperative functional status was New York Heart Association Class 1 in all patients (100%). Immunosuppressive triple drug therapy (azathioprine, steroids, and cyclosporine) was given in seven patients; in two patients, cyclosporine was withdrawn and replaced by FK506 due to refractory rejection. The incidence of acute rejection per patient of more than grade 3 according to the International Society for Heart and Lung Transplantation was 6% within 3 months and 4.5% in 3-6 months; there was no rejection episode more than 6 months after transplantation. Post-transplant coronary artery disease was seen in two patients. However, no disease progression was seen after diltiazem therapy. These results may encourage heart transplantation in Japan.

The calcium concentration in papillary muscles was measured by X-ray microanalysis in order to clarify the role played by mitochondria in intracellular calcium regulation during ischemia and reperfusion. Rat hearts perfused by the Langendorff method were rapidly frozen prior to and during ischemia, as well as following reperfusion. Sections prepared by cryoultramicrotomy were freeze-dried, carbon-coated, and analyzed in an electron microscope. A new freeze-drying procedure was developed, in which the ultrastructure was well-preserved, with sarcomeres, triads, and mitochondria easily recognized. Calcium accumulation into the mitochondria occurred during 30-min ischemia (29.7 +/- 17.0 mmol/kg dry weight) and increased further after 15-min reperfusion (157.1 +/- 104.5), the calcium concentration decreased after 60-min reperfusion (58.1 +/- 29.0). However, the calcium concentration in the cytosol did not change significantly. It is thought that mitochondrial calcium accumulation is reversible, to a certain degree, and that the mitochondria play a part in intracellular calcium regulation in pathological states.

We isolated and purified 35 kDa protein from the myocardium of the beagle dog and identified it to be annexin V from partial amino acid sequence determination. It was confirmed that anticanine cardiac annexin V rabbit polyclonal antibody, which was produced using the 35 kDa protein, cross-reacts with annexin V of the myocardium, lung, liver, kidney, and brain of the rat. The localization of cardiac annexin V and the effect of ischemia for 30-180 min in the rat were immunohistochemically studied with the use of the Langendorff perfusion heart. In the normal myocardium, annexin V, accompanied by cross-striation, was observed throughout the cell. In ischemia of 30 min, extracellular leakage of annexin V was observed with uneven staining in the cytoplasm. When the ischemic time exceeded 60 min, annexin V was observed in the cell membrane with a decrease of annexin V in the cytoplasm. Also, extracellular leakage of annexin V was observed prominently. In ischemia for 180 min, almost all the annexin V in the cytoplasm disappeared. These results suggest that the level of ischemia can be estimated from the changes in localization of annexin V.

The aim of this study was to evaluate the contractions of postmortem human saphenous veins under pulsatile flow conditions as a simulation of coronary-aortic bypass graft (CABG) surgery. Twenty-five cylindrical specimens of veins, obtained from 20 cadavers several hours after death, were mounted in a pulsatile flow system with a pulse rate of 80/min and a mean flow rate of 7 ml/min at various perfusion pressures. Prostaglandin F2 alpha(PGF2 alpha) was then applied to the outer physiological salt solution at a concentration of 3 X 10(-6) mol. Of the 25 veins, 18 (72%) contracted and seven did not. Contractions were observed at a mean perfusion pressure of less than 60 mmHg but not at higher pressures. Three contraction patterns were observed: One caused pressure gradients between the proximal and distal sites of the vein and showed periodic contractions (P); one showed only tonic contractions (T); the other showed pulse pressure increase without developing the pressure gradients (PP). The incidences of P, T, and PP in the 18 instances of contraction were 50%, 33%, and 17%, respectively. Repeated applications of PGF2 alpha to the same vein with the same and/or increased perfusion pressure caused changes of pattern in the direction of P to T, to PP, and to no response, whereas decreasing perfusion pressure caused the patterns to change in the reverse direction. The pressure gradients that developed in veins showing P and T patterns correlated well with the mean perfusion pressure (r = 0.68, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

To observe cytoplasmic microfilaments in the endothelial cells of flow-loaded arteries, an arteriovenous shunt was constructed between the common carotid artery and the external jugular vein in 26 dogs. After measuring the flow rates of the arteries, the endothelial layer was examined ultrastructurally with a transmission electron microscope at three different times: 1 week (acute experiments), 2-4 weeks (subacute experiments), and 4-7 months (chronic experiments). Six-to seven-nanometer microfilaments were found forming bundles, which usually ran longitudinally along the long axis of the vessel. In the acute experiments, the bundles increased in the endothelial cells of the flow-loaded arteries. They showed incomplete striation and were mostly located close to the basal cell membrane. In the subacute experiments, they showed an increase with the development of cross-striation. The half-desmosomal structure of the basal cell membrane had developed a close connection to the bundles. In the chronic experiments, the bundles were especially conspicuous around the intercellular junction. Tennanometer microfilaments increased in the endothelial cells of the flow-loaded artery in the subacute and chronic experiments. We consider that the bundles of 6- to 7-nm microfilaments might be structures developed to combat wall shear stress corresponding to actin filament stress fibers.