Redo aortic valve replacement due to early structural valve deterioration in a trifecta valve: A case report.

INTRODUCTION AND IMPORTANCE: While the number of SAVR cases has been increasing for patients below their sixties due to the improvement of bioprosthetic valves, some early structural valve deterioration (SVD) in Trifecta valves has been reported. CASE PRESENTATION: We present a case of a female who presented with sudden shortness of breath. Ultrasonography diagnosed SVD. We performed redo aortic valve replacement due to SVD in Trifecta valve. With our surgical technique we could remove the bioprosthetic valve easily. CLINICAL DISCUSSION: We could easily remove the mounted prosthetic valve along with the titanium band. These cases may emerge with acute heart failure due to sudden massive aortic regurgitation, not like the gradual progression of stenosis due to calcification. CONCLUSION: The postoperative course in Trifecta recipients must be followed carefully.

[Endoventricular Stepwise Plication for Left Ventricular Aneurysm].

A 69-year-old man was treated with oral anticoagulation for the left ventricular (LV) aneurysm. Echocardiography revealed dyskinetic apex with a mobile thrombus. The estimated LV end-diastolic and end-systolic volume index (LVEDVI, LVESVI) was 76 and 44 ml/m2, respectively. After the LV was opened at the apex parallel to the left anterior descending artery, removal of LV thrombus was performed. LV volume was 70 ml, and diameter of LV aneurysm was 3 cm. After setting a neo-apex, the boundary between the normal and aneurysmal scar tissue were doubly encircled by a pledgeted 2-0 polypropylene suture, and preserved the same diameter as the "aneurysmal neck" (3 cm) in order to secure the minimal residual LV volume. Similarly, second and third circular stitches were placed toward the neo-apex to make the ventricle into an elliptical shape. A postoperative echocardiography showed a well-reconstructed physiologic shape, LV volume( LVEDVI 62 ml/m2, LVESVI 27 ml/m2), and improved LV function.

Bioelectrical impedance analysis for perioperative water management in adult cardiovascular valve disease surgery.

PURPOSE: Bioelectrical impedance analysis (BIA) has been used recently to measure the body water of patients with acute heart failure. We used BIA in this study to better understand, and possibly identify a predictive marker for, perioperative water behavior in cardiac surgery patients. METHODS: We measured body water and studied its behavior in 44 patients undergoing surgery for cardiac valvular disease at our hospital. Measurements included the levels of extracellular water (ECW), intracellular water (ICW), and total body water, the edema index (EI), and the ratio of ECW to total body water. The first measured EI was defined as the "preoperative EI" and the maximum as the "peak EI". RESULTS: A negative correlation was found between the preoperative EI and the preoperative estimated glomerular filtration rate (eGFR) (R = 0.644, p < 0.001). Positive correlations were found between the peak EI and the ICU stay (R = 0.625, p < 0.001), the peak EI and the ventilation time (R = 0.366, p < 0.01), and the preoperative EI and the ICU stay (R = 0.464, p = 0.026). CONCLUSION: The EI is possibly a predictive marker for perioperative water management in cardiac surgery.

A case of biventricular thrombi in a patient with dilated cardiomyopathy: Utility of multimodality imaging for diagnosis and management of treatment strategy.

A 54-year-old man was transferred to our hospital due to congestive heart failure and left ventricular thrombi. Transthoracic echocardiography (TTE) showed mobile "ball-like" not only left ventricular but also right ventricular thrombi associated with severe impaired left and right ventricular function. Contrast-enhanced computed tomography (CT) and cardiac magnetic resonance imaging (MRI) also detected biventricular apical thrombi complicated with right renal infarction. Coronary angiography showed non-significant stenosis. Due to the mobility of thrombi and complication of systemic infarction, the surgical transatrial video-assisted removal of biventricular thrombi was performed and postoperative course has been uneventful over a period of 6 months. Endomyocardial biopsy performed during an operation showed no specific findings such as endomyocarditis, indicating the diagnosis of dilated cardiomyopathy (DCM). This is a rare case of DCM complicated with biventricular apical thrombi detected clearly by multimodality imaging such as TTE, contrast-enhanced CT and cardiac MRI, and surgical removal was performed successfully. .

Thoracic endovascular aortic repair for patent ductus arteriosus in an elderly patient with congestive heart failure.

In elderly patients, open surgery for patent ductus arteriosus (PDA) is more difficult than that in children and often requires a cardiopulmonary bypass. We report the case of a 67-year-old patient with a PDA that was successfully treated with thoracic endovascular aortic repair (TEVAR). The patient was diagnosed with congestive heart failure (ejection fraction, 36 %) and PDA (9.7 mm in diameter). TEVAR was successfully performed to exclude the PDA. After TEVAR, the patient's heart failure was well controlled by diuretics. TEVAR may be a good alternative to open surgery.

Successful bicuspid aortic valve repair using external aortic annuloplasty.

A 33-year-old man presented with severe aortic insufficiency due to a prolapsed bicuspid aortic valve. The ventriculoaortic junction was dilated to 29 mm without root dilatation, and external ring annuloplasty was performed using a Gelweave (Terumo, Tokyo, Japan) graft to reduce the size to 22 mm. The leaflets were repaired by dividing and suturing a raphe between the right and left cusps. This combination provided adequate coaptation depth (8 mm) and showed excellent results, with trivial aortic insufficiency. This approach is suitable for repair of a bicuspid aortic valve with a dilated ventriculoaortic junction without root dilatation.

Off-pump suture repair of left ventricular rupture utilizing TachoComb® sheet: a case report and literature review.

A 70-year-old woman was admitted to our institution with acute myocardial infarction. Coronary angiography demonstrated total occlusion of the left anterior descending artery, which was successfully revascularized. Four days later, the patient suddenly went into shock. The subsequent emergency operation revealed a blowout rupture of the left ventricular free wall. Several TachoComb® (CSL Behring, Tokyo, Japan) sheets were applied to control bleeding and avoid the need for a cardiopulmonary bypass. Horizontal mattress sutures were used in combination with a pair of Teflon felt strips for reinforcement. The combination of TachoComb® sheets and sutures is a novel hybrid method and an effective life-saving procedure for the treatment of left ventricular blowout ruptures. This approach avoids the need for a cardiopulmonary bypass. Sutureless repairs with TachoComb® sheet achieve rapid hemostasis without the need for cardiopulmonary bypass. This stabilizes patient hemodynamics immediately and preserves the fragile myocardium. This allows emergency room physicians to open the chest and apply the TachoComb® sheet to stabilize the patient before the cardiac surgeons arrive at the operating room. This technique will be very useful in emergency situations.

Reconstruction of the intraparenchymal pulmonary artery aneurysm.

Pulmonary artery aneurysms are rare and often arise in the left main trunk. Because they are uncommon, standardized treatment and clinical management are not clearly established. We present the case of a pulmonary artery aneurysm arising intraparenchymally and its surgical reconstruction using autologous pericardium. In terms of preserving pulmonary function, this procedure is effective compared with surgical procedures such as removal of part of the lungs.

Reoperation for mid-term failure of a freestyle bioprosthesis using a full root technique --a surgical case--.

The aortic root of a 30-year-old man was replaced with a Freestyle stentless aortic bioprosthesis for aortic regurgitation associated with annuloaortic ectasia. His clinical course was uneventful, and he was discharged without complications. Three years and six months after surgery, he presented with a high fever. Four years after surgery, transthoracic echocardiography revealed severe aortic regurgitation. We performed exploratory surgery and discovered a torn left coronary cusp of the Freestyle bioprosthesis. Organized vegetation was adherent to the left coronary cusp leaflet. The non-coronary cusp and the right coronary cusp were normal. The diagnosis was aortic regurgitation due to valve failure related to infective endocarditis. Consequently, we reconstructed the aortic root with a composite graft (26-mm Valsalva graft and a 21-mm ON-X mechanical valve).

Cardiac epinephrine synthesis and ischemia-induced myocardial epinephrine release.

OBJECTIVE: Phenylethanolamine-N-methyltransferase (PNMT), the enzyme that synthesizes epinephrine (EPI) from norepinephrine (NE) in the adrenal gland, is present in extra-adrenal tissues including heart. Ischemia evokes an excessive NE accumulation in the myocardial interstitial spaces. Therefore, cardiac PNMT activity with high NE levels may contribute to cardiac EPI synthesis and release evoked by ischemia. METHODS: We measured dialysate EPI levels in the left ventricle of anesthetized rabbits using a cardiac microdialysis technique. The dialysate EPI level served as an index of the myocardial interstitial EPI level. Locally administered NE-induced dialysate EPI responses were measured. The left circumflex coronary artery was occluded for 60 min and the dialysate EPI and NE levels in the ischemic region were measured. Coronary occlusion-induced EPI responses were compared with and without administration of a PNMT inhibitor (SKF29661) in the presence and absence of desipramine (catecholamine transport blocker). RESULTS: Local administration of NE (250, 2500 ng/ml) increased the EPI levels to 734+/-125 and 2088+/-367 pg/ml respectively. These increases in dialysate EPI were suppressed by the PNMT inhibitor. Acute myocardial ischemia significantly increased the EPI levels to 3607+/-1069 pg/ml in the ischemic region, and these were suppressed by the PNMT inhibitor (1417+/-581 pg/ml). The pretreatment with desipramine suppressed ischemia-induced EPI release, which did not differ with (725+/-155 pg/ml) and without administration of a PNMT inhibitor (743+/-172 pg/ml). CONCLUSION: The cardiac PNMT in the left ventricle is capable of synthesizing EPI with markedly elevated NE levels in the myocardial interstitial space.

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.

In situ measurements of crossbridge dynamics and lattice spacing in rat hearts by x-ray diffraction: sensitivity to regional ischemia.

BACKGROUND: Synchrotron radiation has been used to analyze crossbridge dynamics in isolated papillary muscle and excised perfused hearts with the use of x-ray diffraction techniques. We showed that these techniques can detect regional changes in rat left ventricle contractility and myosin lattice spacing in in situ ejecting hearts in real time. Furthermore, we examined the sensitivity of these indexes to regional ischemia. METHODS AND RESULTS: The left ventricular free wall of spontaneously beating rat hearts (heart rate, 290 to 404 bpm) was directly exposed to brief high-flux, low-emittance x-ray beams provided at SPring-8. Myosin mass transfer to actin filaments was determined as the decrease in reflection intensity ratio (intensity of 1,0 plane over the 1,1 plane) between end-diastole and end-systole. The distance between 1,0 reflections was converted to a lattice spacing between myosin filaments. We found that mass transfer (mean, 1.71+/-0.09 SEM, n=13 hearts) preceded significant increases in lattice spacing (2 to 5 nm) during systole in nonischemic pericardium. Left coronary occlusion eliminated increases in lattice spacing and severely reduced mass transfer (P<0.01) in the ischemic region. CONCLUSIONS: Our results suggest that x-ray diffraction techniques permit real-time in situ analysis of regional crossbridge dynamics at molecular and fiber levels that might also facilitate investigations of ventricular output regulation by the Frank-Starling mechanism.

Adrenomedullin gene transfer induces therapeutic angiogenesis in a rabbit model of chronic hind limb ischemia: benefits of a novel nonviral vector, gelatin.

BACKGROUND: Earlier studies have shown that adrenomedullin (AM), a potent vasodilator peptide, has a variety of cardiovascular effects. However, whether AM has angiogenic potential remains unknown. This study investigated whether AM gene transfer induces therapeutic angiogenesis in chronic hind limb ischemia. METHODS AND RESULTS: Ischemia was induced in the hind limb of 21 Japanese White rabbits. Positively charged biodegradable gelatin was used to produce ionically linked DNA-gelatin complexes that could delay DNA degradation. Human AM DNA (naked AM group), AM DNA-gelatin complex (AM-gelatin group), or gelatin alone (control group) was injected into the ischemic thigh muscles. Four weeks after gene transfer, significant improvements in collateral formation and hind limb perfusion were observed in the naked AM group and AM-gelatin group compared with the control group (calf blood pressure ratio: 0.60+/-0.02, 0.72+/-0.03, 0.42+/-0.06, respectively). Interestingly, hind limb perfusion and capillary density of ischemic muscles were highest in the AM-gelatin group, which revealed the highest content of AM in the muscles among the three groups. As a result, necrosis of lower hind limb and thigh muscles was minimal in the AM-gelatin group. CONCLUSIONS: AM gene transfer induced therapeutic angiogenesis in a rabbit model of chronic hind limb ischemia. Furthermore, the use of biodegradable gelatin as a nonviral vector augmented AM expression and thereby enhanced the therapeutic effects of AM gene transfer. Thus, gelatin-mediated AM gene transfer may be a new therapeutic strategy for the treatment of peripheral vascular diseases.

Detection of 3-methoxy-4-hydroxyphenylglycol in rabbit skeletal muscle microdialysate.

A high-performance liquid chromatography with electrochemical detection (HPLC-ED) method is described for determination of 3-methoxy-4-hydroxyphenylglycol (MHPG) in microdialysate from the skeletal muscle interstitial space. Using a microdialysis technique, we sampled 30 microl dialysate from the skeletal muscle interstitial space and injected dialysate directly into HPLC-ED system. The control MHPG concentration of dialysate was 213+/-18 pg/ml. The MHPG concentrations were reduced by entacapone (catechol-O-methyltransferase inhibitor, COMT), augmented by local infusion of dihydroxyphenylglycol. This system offers a new possibility for simple, rapid monitoring of MHPG as an index of COMT activity in skeletal muscle.

In vivo monitoring of norepinephrine and its metabolites in skeletal muscle.

Although skeletal muscle sympathetic nerve activity plays an important role in the regulation of vascular tone and glucose metabolism, relatively little is known about regional norepinephrine (NE) kinetics in the skeletal muscle. With use of the dialysis technique, we implanted dialysis probes in the adductor muscle of anesthetized rabbits and examined whether dialysate NE and its metabolites were influenced by local administration of pharmacological agents through the dialysis probes. Dialysate dihydroxyphenylglycol (DHPG) and 3-methoxy-4-hydroxyphenylglycol (MHPG) were measured as two major metabolites of NE. The skeletal muscle dialysate NE, DHPG and MHPG were 11.7+/-1.2, 38.1+/-3.2, and 266.1+/-28.7 pg/ml, respectively. Basal dialysate NE levels were suppressed by tetrodotoxin (Na(+) channel blocker, 10 microM) (5.1+/-0.6 pg/ml), and augmented by desipramine (NE uptake blocker, 100 microM) (25.8+/-3.2 pg/ml). Basal dialysate DHPG levels were suppressed by pargyline (monoamine oxidase blocker, 1mM) (24.3+/-4.6 pg/ml) and augmented by reserpine (vesicle NE transport blocker, 10 microM) (75.8+/-2.7 pg/ml). Basal dialysate MHPG levels were not affected by pargyline, reserpine, or desipramine. Addition of tyramine (sympathomimetic amine, 600 microM), KCl (100 mM), and ouabain (Na(+)-K(+) ATPase blocker, 100 microM) caused brisk increases in dialysate NE levels (200.9+/-14.2, 90.6+/-25.7, 285.3+/-46.8 pg/ml, respectively). Furthermore, increases in basal dialysate NE levels were correlated with locally administered desipramine (10, 100 microM). Thus, dialysate NE and its metabolite were affected by local administration of pharmacological agents that modified sympathetic nerve endings function in the skeletal muscle. Skeletal muscle microdialysis with local administration of a pharmacological agent provides information about NE release, uptake, vesicle uptake and degradation at skeletal muscle sympathetic nerve endings.

Acute limb ischemia does not facilitate but inhibits norepinephrine release from muscle sympathetic nerve endings in anesthetized rabbit.

Although myocardial ischemia is associated with regional cardiac sympathetic nerve deterioration, it remains unknown whether acute hindlimb ischemia impairs muscle sympathetic nerve function. In the study presented here we implanted dialysis probes in the adductor muscle of anesthetized rabbits and measured dialysate norepinephrine levels as an index of muscle sympathetic nerve activity. Acute hindlimb ischemia was induced by injection of microspheres and occlusion of the common iliac artery. Dialysate norepinephrine levels decreased from 19.3 +/- 3.5 pg/ml at control to 9.4 +/- 3.7 pg/ml at 30 min of ischemia and further to 1.7 +/- 0.2 pg/ml at 75 min of ischemia. During acute hindlimb ischemia, baroreflex (bilateral carotid occlusion) and high potassium level-induced norepinephrine response was inhibited, but tyramine-induced norepinephrine response was preserved. In conclusion, acute hindlimb ischemia caused decreases in dialysate norepinephrine levels. This reduction may be mediated by an impairment of axonal conduction and/or of norepinephrine releasing function at skeletal muscle sympathetic nerve endings.