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LAD����P4�����1!P �Fig. 3A�� QzOY 3.5�15 mm Lynx PTCA HIJ� �Cardio-Vascular Dynamics pI� qrsT� �� 20�(50RWX�P� ��P4+Q/0 LCX �11fAA bcS��?`� ���'T Ud�?`P�Fig. 3B�C�� provisional T stenting ��� NIR�� �I�<\�V�HIJ�zO�WXZ�{P�� 3.0�20 mm Hayate PTCA HIJ�Y<�1!lYP� 2.0�20 mm VIVA PTCA HIJ��<��zONOPQ� 3.0�20 mm Hayate PTCAHIJ���Z56�zONO��HIJ�[\�!�P �Fig. 3D�� [\�P PTCAHIJ�YNIR���[]NOl�^������1!P� ����_Y�`��F0V�������WX�EF �Fig. 3E�, NIR �� �I<��a��P���bc�!���"� 3.0�15 mmMulti-Link ���P4�����1!P �Fig.3F�� ��d���� e�"�zOF/G�'T�f��P����?�� ����g��P �Fig. 4��� Q56�' M7��f��hi PCPS "�G� IABP ��_b�����1!P�

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Topaz �5��/��� 24545 � ���d�U39 0.07� �j� LMT bc�K�?`��P�LMT �k���� PTCA Y� 1982� Von Es-sen R�6��/0 CABGl�# S���$%*m�k��X �P� ���HIJ� � PTCA ¡n� ¢L� CABG �£om¤:Y¥¦�N���P7�� � pq��� 1� ��rT§�¨�HIJ�zO# ©'��'X�'�ª«1!ls¡¬ zO��­�­®aZ����� 2� PTCA# S�s}nI�f�0¯�a��� 3�$% �;%�t°����_��$%± ²³��&a��� 4� Hn´~"µ�/0�'T �uN��a"a unprotected LMT PTCA�Fa�v�¶*`w 36��Ua���·¸���8�� � Q����_ ¹x� S�s}nI�yz���� 1!�������º��N�P�� �� LMT�KY¥¦�N���P� Macaya�9�Y CABG¥¦�� PTCA �GH�P LMT *m�Fa�� HIJ�zOQ S�s}nI�k��������56�e�"�¶����`���P� 2001� ULTIMA �unprotected left main trunk inter-

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vention multicenter� registry �46�� CABG���������� �� �������� 13.7�� 1 ����� 24.2� ����� ��� � 1���� 3.4� ������ !"#$%&'()*+�,-./"0� ���10��12� LMT34�056789:;� <=>34�?@��"� DeLezo 211��� <=>34�?@� PTCA �ABCDEFG9H"9IJ:;K"� Lefe◊vre 212��<=>34L 6 MN�<N:�O���P�Q type 2 9RS./"� <=>34� !")*+TUV�� 1� WX�YZ�

)*+[\:]�^�"_`�)*+L[\!"type A TU� 2� WX�^�"_`�)*+[\:� 5K YZabLcKdeH2)*+Lfg!" type B TU �provisional T stenting�� 3� Yhi� 2O�)*+LjZ�[\!" type CTU�4� <=>kl� 2O�)*+L[\:mn�0deH2fg)*+[\Lco type D TU��"13��pqr��� Lefe◊vre <N type 2� LMT 34�

:; provisional T stenting Lsc:�� provi-sional T stenting �<=>34� :;� W0tu

Figure 1. Right coronary arteriogram.

Right coronary artery in �A� LAO and �B� AP cranial view, showingtotal occlusion sending large collaterals to left coronary artery

�arrow�.LAO: left anterior oblique, AP: anteroposterior.

Figure 2. Left coronary angiogram.

Left coronary artery in �A� RAO caudal showing 99� ostial stenosisof the LAD �arrow� and the ostium of the obtuse marginal artery ofthe LCX, and �B� LAO cranial view showing moderate stenosis ofthe distal part of the LMT �arrow�.RAO: right anterior oblique, LAO: left anterior oblique, LAD: left

anterior descending coronary artery, LCX: left circumflex coronary

artery, LMT: left main trunk

LMT 34� !"&'()*+[\v 391

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Figure 3. Percutaneous transluminal coronary angioplasty �PTCA�.A: The lesion was stenting with a 3.0�16 mm NIR stent from LMT to LAD. B andC: After stenting, there was aggravation of the LCX ostial stenosis. D: An

additional balloon dilatation using a 3.0�20 mm Hayate PTCA balloon was

performed through the metallic structure of the NIR stent struts. E: After balloon

dilatation, there was still aggravation. F: A 3.0�15 mmMulti-Link stent was implant-ed across the metallic structure of the NIR stent.

LAD: left anterior descending coronary artery, LCX: left circumflex coronary

artery, LMT: left main trunk

Figure 4. Left coronary angiogram after procedure.

Left coronary artery in �A� RAO caudal, and �B� LAO caudal view,showing successful stenting with no residual stenosis. RAO: right

anterior oblique, LAO: left anterior oblique,

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¢­�, Express stent �Boston©ª� «¬¢­�14���� LMT��/ ����������������� ®¯-�'���°��.� ±²����*HIP³������®z LMT *´µ[\�P� AMI ��' provi-

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Figure 5. NIR stent.

A, Expanded NIR stent transforms into a diamond-like mesh of

cellular design. B, The stent cellular design was made from U joint

to obtain flexibility and thicker C joint to obtain rigid sca#olding of

the vessel wall.

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Abstract

Provisional T Stenting for the Left Main Coronary

Trunk Lesion in a Patient with

Cardiogenic Shock

Tomoyuki Kunishima, Toshio Sasaki, Hideshi Aoyagi, Ken Kongoji,

Katsuhiko Tsuchiya, Masahiro Yamauchi, Hidetaka Tochiki,

Nobuyuki Hashimoto and Fumihiko Miyake

A 67-year-old man was referred to our hospital with angina pectoris. While in hospital, he suddenly

developed severe chest pain and shock. Cardiopulmonary resuscitation and circulatory support were started

immediately. Emergency coronary angiography showed chronic ostial occlusion of right coronary artery,

99� ostial stenosis of the left anterior descending coronary artery �LAD�, and moderate stenosis of the distalpart of the of left main trunk �LMT� and the ostium of the obtuse marginal artery. We decided that the targetcoronary arteries were the LAD and LMT. We chose percutaneous transluminal coronary angioplasty

�PTCA� rather than coronary bypass surgery because he had a history of cerebral infarction . The distalLMT and ostial LAD stenosis were dilated with a 3.0�16 mm NIR stent �7-cell�. After stent implantation,there was aggravation of the left circumflex ostial stenosis. But performance of additional balloon dilatation

through the metallic structure of the NIR stent was di$cult due to balloon rupture. A cellular design of the

NIR stent was made from U joint to obtain flexibility and thicker C joint to obtain rigid sca#olding of the

vessel wall. We thought that this structure caused balloon rupture and di$cult to provisional T stenting with

a Multi-Link stent �3.0�15 mm�. After the procedure, stabilization of homodynamic was obtained and thepatient was weaned form circulatory support. PCI had been increasingly applied to LMT lesions with

variable long-term success. In this case, the 7-cell NIR stent proved di$cult to perform provisional T

stenting. Provisional T stenting for LMT stenosis may be a better strategy compared with systematic T

stenting, but we must be careful about the stent configuration.

Division of Cardiology, Department of Internal Medicine,

St.Marianna University School of Medicine, Kawasaki, Japan.

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