Biomedical subjects

Hiroshi Tsuneyoshi

Publications and source records attributed to Hiroshi Tsuneyoshi.

8 recordsLinked to original sources

PubMed2006

Multislice computed tomography accurately quantifies left atrial size and function after the MAZE procedure.

BACKGROUND: Although the MAZE procedure allows for the recovery of sinus rhythm and left atrial (LA) mechanical function in the great majority of patients with chronic atrial fibrillation (AF), the effects of MAZE on the precise LA geometry and wall motion remain to be elucidated. We hypothesized that LA size and mechanical function in patients with chronic AF and mitral valvular disease are well restored after MAZE. METHODS AND RESULTS: We studied 14 patients (MAZE group: mean+/-SD age, 63.9+/-8.6 years; 8 men and 6 women) who underwent MAZE for chronic AF and mitral valve surgery and 10 patients with sinus rhythm (coronary artery bypass graft [CABG] group: age, 70.0+/-7.9 years; 5 men and 5 women) who underwent CABG at Takeda Hospital between February 2002 and September 2005. MAZE was conducted by the endocardial application of radiofrequency ablation with a temperature-controlled multipolar radiofrequency catheter. LA volume and booster function were quantitatively evaluated by multislice computed tomography at 17.9+/-10.0 months (MAZE group) and 15.3+/-13.6 months (CABG group) postoperatively. All patients with MAZE were free of AF and other atrial arrhythmias during the follow-up period. In the CABG group, LA maximal and minimal volumes and ejection fraction were 109+/-12 mL, 82+/-11 mL, and 26+/-10%, respectively. In the MAZE group, LA maximal volume was 139+/-17 mL (P=0.187 versus CABG), and LA minimal volume was 121+/-16 mL (P=0.082 versus CABG), with an ejection fraction of 15+/-7% (P=0.004 versus CABG). In both groups, all parts of the LA wall contracted toward the geometric center of the LA. The extent of wall motion was significantly worse in the MAZE group compared with the CABG group. In both groups, LA booster function was inversely correlated with LA maximal volume. CONCLUSIONS: MAZE with radiofrequency ablation is safe and effective for the restoration of sinus rhythm in patients with chronic AF and mitral valve disease. However, chronic AF associated with mitral valve disease deteriorates LA mechanical function diffusely throughout the LA wall. Further studies with the use of multislice computed tomography are needed to sequentially evaluate LA function after MAZE in patients with and without mitral valve surgery.

Aged↗

PubMed2006

Chymase inhibition prevents cardiac fibrosis and dysfunction after myocardial infarction in rats.

Human chymase activates not only angiotensin II but also transforming growth factor-beta, a major stimulator of myocardial fibrosis, while rat chymase activates transforming growth factor-beta, but not angiotensin II. To clarify the role of chymase-dependent transforming growth factor-beta activation, we evaluated whether chymase inhibition prevents cardiac fibrosis and cardiac dysfunction after myocardial infarction in rats. Myocardial infarction was induced by ligation of the left anterior descending coronary artery. One day after the ligation, rats were randomized into 2 groups: 1) a chymase-treated group that received 10 mg/kg per day of the chymase inhibitor NK3201 orally for 4 weeks; and 2) a vehicle group of non-treated rats with myocardial infarction. We also included a control group who underwent sham-operation and no treatment. Four weeks after ligation, echocardiography revealed that chymase inhibitor treatment reduced the akinetic area and increased fractional area change but did not significantly change left ventricular end-diastolic area. Chymase inhibition significantly reduced left ventricular end-diastolic pressure, increased the maximal end-systolic pressure-volume relationship and decreased the time constant of left ventricular relaxation. Chymase activity in the non-infarcted myocardium was significantly increased in the vehicle group, but it was significantly reduced by chymase inhibitor treatment. The fibrotic area in the cardiac tissues and the mRNA levels of collagen I and collagen III were also significantly lower in the chymase inhibitor-treated group than in the vehicle group. Therefore, the pathway forming chymase-dependent transforming growth factor-beta may play an important role in myocardial fibrosis and cardiac dysfunction rather than left ventricular dilatation after myocardial infarction.

Acetamides↗

PubMed2005

Does the beta2-agonist clenbuterol help to maintain myocardial potential to recover during mechanical unloading?

OBJECTIVE: Chronic mechanical unloading induces left ventricular (LV) atrophy, which may impair functional recovery during support with an LV-assist device. Clenbuterol, a beta2-adrenergic receptor (AR) agonist, is known to induce myocardial hypertrophy and might prevent LV atrophy during LV unloading. Furthermore, beta2-AR stimulation is reported to improve Ca2+ handling and contribute to antiapoptosis. However, there is little information on the effects of clenbuterol during LV unloading. METHODS AND RESULTS: We investigated LV atrophy and function after LV unloading produced by heterotopic heart transplantation in isogenic rats. After transplantation, rats were randomized to 1 of 2 groups (n=10 each). The clenbuterol group received 2 mg.kg(-1).d(-1) of the drug for 2 weeks; the control group received normal saline. The weight of unloaded control hearts was 48% less than that of host hearts after 2 weeks of unloading. Clenbuterol significantly increased the weight of the host hearts but did not prevent unloading-induced LV atrophy. Papillary muscles were isolated and stimulated, and there was no difference in developed tension between the 2 groups. However, the inotropic response to the beta-AR agonist isoproterenol significantly improved in the clenbuterol group. The mRNA expression of myocardial sarco(endo)plasmic reticulum Ca2+-ATPase 2a (SERCA2a) and fetal gene shift (myosin heavy chain [MHC] mRNA isozyme) was also significantly improved by clenbuterol treatment. There was no difference in beta1-AR mRNA expression between the 2 groups. In contrast, beta2-AR mRNA was significantly decreased in the clenbuterol-treated, unloaded heart. This indicates that clenbuterol may downregulate beta2-ARs. In the evaluation of apoptosis, mRNA expression of caspase-3, which is the central pathway for apoptosis, tended to be better in the clenbuterol group. CONCLUSIONS: During complete LV unloading, clenbuterol did not prevent myocardial atrophy but improved gene expression (SERCA2a, beta-MHC) and beta-adrenergic responsiveness and potentially prevented myocardial apoptosis. However, chronic administration of clenbuterol may be associated with downregulation of beta2-ARs.

Adrenergic beta-Agonists↗

PubMed2005

Update on mitral valve surgery.

Recently, the outcome for patients with mitral valve disease has significantly improved. This may be due to concomitant advances in many fields. In particular, the development of surgical techniques has contributed to this improvement, and many surgical techniques and topics are introduced in this article. After the evaluation of results in mitral valve surgery and exploration of the relationship between the mitral valve and the mitral subvalvular apparatus, it is currently accepted that mitral valve repair is superior to replacement and that replacement with preservation of the mitral subvalvular apparatus is preferable to replacement alone. Another current topic is mitral repair in dilated cardiomyopathy. Mitral regurgitation is a known complication of end-stage cardiomyopathy and is associated with a poor prognosis because of progressive mitral annular dilatation. Recently, to solve this problem, undersized mitral annuloplasty or cardiomyoplasty has been advocated. In the future, mitral valve surgery may be performed off-pump or by a percutaneous approach. Several groups are investigating the use of new devices and new techniques that avoid cardiopulmonary bypass in experimental studies. In this article, we review current topics and discuss our experiences in mitral valve surgery.

Heart Valve Diseases↗

PubMed2004

Atrial natriuretic peptide helps prevent late remodeling after left ventricular aneurysm repair.

BACKGROUND: Left ventricular aneurysm repair (LVR) reduces LV wall stress and improves LV function. However, as we reported previously, the initial improvement of LVR was short-term because of LV remodeling but could be maintained longer with postoperative use of an angiotensin-converting enzyme (ACE) inhibitor. Atrial natriuretic peptide (ANP) has been used to treat patients with heart failure by natriuretic and vasodilatory actions. Recent reports have suggested that ANP inhibits the rennin-angiotensin system. In this study, the effects of ANP after LVR were evaluated. METHODS AND RESULTS: Rats that had an LV aneurysm 4 weeks after left anterior descending artery ligation underwent LVR by plicating the LV aneurysm and were randomized into 2 groups: LVR+A group was intravenously administrated with 10 microg/h of carperitide, recombinant alpha-hANP, by osmotic-pump for 4 weeks, and the LVR group was given normal saline. Echocardiography revealed better LV remodeling and function in LVR+A group than in LVR group. Four weeks after LVR, left ventricular end diastolic pressure (LVEDP) and Tau were significantly lower in LVR+A group (LVEDP: 10+/-4 in LVR+A group versus 18+/-6 mm Hg in LVR group, Tau: 13+/-2 versus 17+/-2ms). End-systolic elastance (Ees) was higher in LVR+A group (Ees: 0.34+/-0.2 versus 0.19+/-0.11 mm Hg/microL). The levels of myocardial ACE activity in LVR+A group was significantly lower than in LVR group. The mRNA expressions of brain natriuretic peptide and transforming growth factor beta1 inducing fibrosis significantly decreased in LV myocardium in LVR+A group. Histologically, myocardial fibrosis was significantly reduced in LVR+A group. CONCLUSIONS: Intravenous administration of ANP had beneficial effects on LV remodeling, function, and fibrosis after LVR. ANP could be a useful intravenous infusion drug for postoperative management after LV repair surgery.

Animals↗

PubMed2002

Angiotensin-converting enzyme inhibitor helps prevent late remodeling after left ventricular aneurysm repair in rats.

BACKGROUND: We reported in a previous study that the initial effects of left ventricular (LV) repair (LVR) for LV aneurysm were not long lasting. Angiotensin-converting enzyme inhibitor (ACE-I) is known to attenuate remodeling after myocardial infarction, and could be effective after LVR. METHODS AND RESULTS: Left ventricular aneurysms were developed in rats after left anterior descending artery ligation. Rats were divided into 3 groups: sham operation with ACE-I (lisinopril 10 mg/kg/d) (n=10; group A), LVR (by plicating the LV aneurysm) with placebo (n=8; group R), and LVR with ACE-I (n=10; group RA). LV function was evaluated by echocardiography and catheterization. Oxidative stress in the myocardium was estimated by immunohistochemistry for 8-hydroxy-2'-deoxyguanosine. One week after LVR, LV end-diastolic area was smaller and fractional area change was better in the 2 LVR groups. Four weeks after LVR, LV end-diastolic area, and fractional area change deteriorated in group R but not so much in group RA; E-max was higher in group RA (0.79+/-0.20 mm Hg/mL) than in groups A (0.25+/-0.03 mm Hg/mL; P<0.01) and group R (0.27+/-0.03 mm Hg/mL; P<0.01). Oxidative stress was much lower in the 2 ACE-I groups. CONCLUSIONS: LVR improved LV size and systolic function only in the early phase. Adjuvant use of ACE-I was useful for preventing redilation and maintaining LV systolic function, was associated with suppressed oxidative stress, and may make LVR a more effective surgical procedure for LV aneurysm.

8-Hydroxy-2'-Deoxyguanosine↗

PubMedDate not supplied

Effects of two inhibitors of renin-angiotensin system on attenuation of postoperative remodeling after left ventricular aneurysm repair in rats.

We reported that the initial beneficial effects of left ventricular repair (LVR) surgery for LV aneurysm after myocardial infarction (MI) did not persist because of postoperative LV remodeling in a rat model. The renin-angiotensin system (RAS) plays an important role in postinfarction LV remodeling. Inhibition of RAS may be useful to preserve LV function by preventing remodeling. We studied the effects of two inhibitors of RAS in an attempt to improve the operative results of LVR. LV aneurysms were created in rats after ligating the left anterior descending artery. These rats underwent LVR by plicating the LV aneurysm and were treated by three methods: no treatment, treatment with angiotensin-converting enzyme inhibitor (ACE-I) (lisinopril 10 mg/kg per day), and treatment with angiotensin II receptor blocker (ARB) (candesartan 5 mg/kg per day). One week after LVR, echocardiography revealed smaller LV size and better LV motion than before surgery. Four weeks after LVR, LV size returned to the preoperative value in the untreated group, but not as much in the treated groups. Cardiac catheterization revealed lower LV end-diastolic pressure and higher E-max in the treated groups. There was no difference between ACE-I and ARB groups except for systolic blood pressure. LVR decreased LV size and improved systolic function only in the early phase. Adjuvant therapy of ACE-I or ARB-attenuated LV remodeling and maintained LV function at the same level after LVR. This probably indicates that tissue RAS is associated with postoperative remodeling. Concomitant use of RAS inhibitors may make LVR a longer-lasting procedure for LV aneurysm.

Angiotensin Receptor Antagonists↗

PubMedDate not supplied

Heterotopic transplantation of the failing rat heart as a model of left ventricular mechanical unloading toward recovery.

The left ventricular assist device (LVAD) is usually used in patients with end-stage heart failure as a bridge to transplantation. Recently, some studies have reported functional recovery with the use of an LVAD, although the mechanisms responsible for recovery are not fully understood. We investigated the functional recovery of the infarcted, failing rat heart in response to mechanical unloading after heterotopic transplantation. Heart failure was induced in Lewis rats by ligating the left anterior descending artery. After 4 weeks, the infarcted hearts were harvested and heterotopically transplanted. The transplanted infarcted heart was removed after 2 weeks of unloading and examined for hypertrophy and fibrosis, as well as for mRNA levels encoding for brain natriuretic peptide, sarco(endo)plasmic reticulum Ca(2+)-ATPase2a (SERCA2a), and beta1- and beta2-adrenergic receptors. Normal and infarcted rats without transplantation served as control animals. The infarcted heart was hypertrophied as evidenced by an increase in heart weight and myocyte diameter. After unloading the infarcted heart for 2 weeks, there was a decrease in heart weight and myocyte diameter. However, the percentage of myocardial fibrosis increased after unloading. The mRNA expression of brain natriuretic peptide and the beta2-adrenergic receptor significantly improved after mechanical unloading. The levels of SERCA2a mRNA tended to increase after unloading. In conclusion, unloading the failing, infarcted heart can help normalize left ventricular hypertrophy and cardiac gene expression. This unloading model appears to partially mimic the conditions of hemodynamic support with an LVAD in heart failure patients and potentially offers insights into the mechanisms of functional recovery.

Animals↗