Mikitaka Murakami

Hepatocyte growth factor and vascular endothelial growth factor in ischaemic heart disease

Background Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are endothelial cellspecific growth factors, but the production of these growth factors in cardiomyocytes has also been demonstrated. However, there have been no reports focusing their attention on the changes in these growth factors after coronary intervention. We investigated the time‐course changes of the serum VEGF and HGF levels in angina pectoris (AP) and acute myocardial infarction (AMI). Methods The serum HGF and VEGF levels were measured in 60 patients with AP, in 62 patients with AMI (AP, before heparin administration, and at 24 and 48 hours, and one week after intervention; AMI, before heparin, and at 48 and 72 hours, and one, two, three and four weeks) and in 56 patients with neurocirculatory asthenia as controls. We defined the patients with remodelling who showed an increase in left ventricular end‐diastolic volume index (LVEDVI) in the sub‐acute phase of AMI. Results Hepatocyte growth factor levels in the AP and AMI were significantly higher than that in the control (p<0.0001). The AMI level was also significantly higher than AP (p<0.001). In the AMI and AP, HGF peaked at 48 hours. Vascular endothelial growth factor level in the AMI was significantly higher than that in the control and AP (p<0.0001). In the AMI, VEGF peaked at two weeks. There was a significant positive correlation between the peak VEGF and LVEDVI in the sub‐acute phase of AMI (p = 0.0089, r=0.436). Peak VEGF in the remodelling ( + ) group was significantly higher than that in the remodelling (−) group (p<0.001). In the AP, VEGF was unchanged. Conclusion While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub‐acute phase of myocardial infarction. Coron Artery Dis 14:301‐307

Comparison of the morphological changes of restenosis after the implantation of various types of stents in a swine model

BackgroundStent design causes the differences of restenosis rate, but the morphological differences after the various types of stent implantation have not been clarified. DesignSeven types of stents were implanted in pig coronary arteries to clarify how the mechanism of restenosis differs with coil stents and tube stents. MethodsThe left anterior descending coronary arteries (LADs) of pigs were injured using coronary angioplasty balloons (diameter: 3.0 mm; length: 20 mm; balloon/artery ratio: 1 : 2). Fourteen days after the injury, four types of coil stents (Cordis, Wiktor, GR-I, and GR-II) and three types of tube stents (Palmaz-Schatz, gfx, and Multilink) were implanted, and the LADs were extracted 28 days after the implantation. ResultsThe proliferated neointima was eccentric in the coil stents and concentric in the tube stents. Although there was no significant difference in the area of neointima, the area of the lumen was significantly larger in the tube stents than in the coil stents (P < 0.01) because of the larger area of stent. Cells positive for anti-proliferating cell nuclear antigen antibody were mainly observed around the stent struts, and most of these cells were also positive for either anti-macrophage or anti-smooth muscle actin antibodies. ConclusionsCompared to the coil stents, the tube stents induce less negative remodelling including stent recoil, resulting in a wider luminal area. In order to prevent restenosis, it is crucial to implant a stent that will cause less negative remodelling.

Plasma endothelin-1 and thrombomodulin levels in coronary sinus during right atrial pacing and percutaneous transluminal coronary angioplasty

Increases in the levels of plasma endothelins (ETs) have been reported after percutaneous transluminal coronary angioplasty (PTCA). To examine the mechanism of this increase, we measured plasma endothelin-1 (ET-1) and thrombomodulin (TM) levels in both the Valsalva sinus (VAL) and the great cardiac vein (GCV) together with oxygen saturation of the GCV (Sat.GCVO2) during right atrial pacing and PTCA. Thirty patients with stenoses in the left anterior descending coronary arteries were enrolled. A fiberoptic pulmonary artery catheter was placed in GCV for monitoring Sat.GCVO2, and blood sampling was repeated before and after each procedure. ET-1 did not increase during pacing, but after PTCA it significantly increased from basal levels to 24.4+/- 8.3 pg/ml in GCV (P<0.01) and 19.3 +/-7.4 in VAL (P<0.05). Basal TM levels in GCV and VAL were significantly higher in diabetic than in non-diabetic patients, but TM did not change during pacing and PTCA. Sat.GCVO2 significantly decreased from the basal level during pacing and PTCA. We speculate that direct endothelial cell damage is more responsible for the increase of ET-1 during PTCA than myocardial ischemia. Our data indicate that ET-1 may be a useful marker for acute endothelial damage, while TM reflects only chronic and general damage of endothelial cells.

Effect of angiotensin II receptor blockade, candesartan, on the ventricular remodeling after myocardial infarction: comparison with angiotensin converting enzyme inhibitor

Effect of Angiotensin II Receptor Blockade, Candesartan, on the Ventricular Remodeling after Myocardial Infarction: Comparison with Angiotensin Converting Enzyme Inhibitor Eiichi Geshi, Hiroshi Suzuki, Takatoshi Sato, Makoto Shoji, Yoshitaka Iso, Masayuki Shibata, Shinji Koba, Mikitaka Murakami, Kakashi Katagiri1—Third Department of Internal Medicine, ShowaUniversity School of Medicine, Tokyo, Japan

A case of ankylosing spondylitis complicated with mitral regurgitation

強直性脊椎炎に僧帽弁閉鎖不全症と多彩な不整脈を合併し,心筋生検で著明な心筋変性像を認めた1例を報告する.症例は58才,男性.リウマチ熱などの既往歴もない. 37才頃から腰痛出現し, 54才で強直性脊椎炎と診断. 5年前から労作時息切れと足背部の浮腫がみられ,今回心雑音と不整脈を指摘され入院.心尖部に全収縮期雑音,振戦と下腿浮腫を認め,腰背部痛と脊椎の運動制限がみられた.白血球数10400,血沈1時間値60mm, CRP 5 (+)であり,心電図上左室肥大像, I度房室ブロック,多彩な上室性および心室性の不整脈を認めた.心臓超音波検査で左室腔と左房の拡大を認めたが,弁尖の肥厚・変形等はなかつた.ヒス束心電図で房室結節の機能障害を認め,心臓カテーテル検査で肺動脈楔入圧16mmHg,左室拡張終期圧18mmHgと上昇していた.左室造影で僧帽弁逆流を認めたが,大動脈造影では異常を認めなつた.冠動脈造影では有意の狭窄性病変を認めず,心内膜心筋生検で著明な線維化と高度の心筋変性を認め,心筋炎後遺症が強く示唆された.強直性脊椎炎の心病変は大動脈弁閉鎖不全症や伝導障害が特異的であるとされている.僧帽弁閉鎖不全症のみの合併は極めてまれであり,本邦では最初の報告である.本例では左室の心筋炎が僧帽弁輪や刺激伝導系へ波及し,心病変を起こしたものと推察され,本疾患の心病変を考察する上に興味ある症例と思われた.