Nakabumi Kuroda

Intimal hyperplasia regression from 6 to 12 months after stenting

death in hibernating human myocardium. J Am Coll Cardiol 1996;27:1577–1585. 11. Shivalkar B, Maes A, Borgers M, Ausma J, Scheys I, Nuyts J, Mortelmans L, Flameng W. Only hibernating myocardium invariably shows early recovery after coronary revascularization. Circulation 1996;94:308–315. 12. Elsasser A, Schlepper M, Kl‘vekorn WP, Cai W, Zimmermann R, Muller KD, Strasser R, Kostin S, Gagel C, Munkel B, Schaper W, Schaper J. Hibernating myocardium: an incomplete adaptation to ischemia. Circulation 1997;96:2920– 2931. 13. Dakik HA, Howell JF, Lawrie GM, Espada R, Weilbaecher DG, He Z-X, Mahmarian JJ, Verani M. Assessment of myocardial viability with 99mTCsectamibi tomography before coronary bypass graft surgery: correlation with histopathology and postoperative improvement in cardiac function. Circulation 1997;96:2892–2898. 14. Maes A, Borgers M, Flameng W, Nuyts JL, Werf F, Ausma JJ, Serseant P, Mortelmans LA. Assessment of myocardial viability in chronic coronary artery disease using technetium-99 sestamibi SPECT; correlation with histologic and positron emission tomographic studies and functional follow-up. J Am Coll Cardiol 1997;29:62–68. 15. Schwarz ER, Schoendube FA, Kostin S, Schmiedtke N, Schulz G, Buell U, Messmer BJ, Morrison J, Hanrath P, Dahl J. Prolonged myocardial hibernation exacerbates cardiomyocyte degeneration and impairs recovery of function after revascularization. J Am Coll Cardiol 1998;31:1018–1026. 16. Nagueh SF, Mikati I, Weilbaecher D, Reardon MJ, Al-Zaghrini GJ, Cacela D, He Z-X, Letsou G, Noon G, Zoghbi WA. Relation of the contractile reserve of hibernating myocardium to myocardial structure in humans. Circulation 1999; 100:490–496. 17. Shirani J, Lee J, Quigg RJ, Pick R, Bacharach SL, Dilsizian V. Relation of thallium uptake to morphologic features of chronic ischemic heart disease: evidence for myocardial remodeling in non-infarct myocardium. J Am Coll Cardiol 2001;38:84–90. 18. Shirani J, Pick R, Roberts WC, Maron BJ. Morphology and significance of the left ventricular collagen network in young patients with hypertrophic cardiomyopathy and sudden cardiac death. J Am Coll Cardiol 2000;35:36–44. 19. Dilsizian V, Rocco TP, Freedman NM, Leon MB, Bonow RO. Enhanced detection of ischemic but viable myocardium by the reinjection of thallium after stress-redistribution imaging. N Engl J Med 1990;323:141–146. 20. Dilsizan V, Freedman NMT, Bacharach SL, Perrone-Filardi P, Bonow RO. Regional thallium uptake in irreversible defects; Magnitude of change in thallium activity after reinjection distinguishes viable from nonviable myocardium. Circulation 1992;85:627–634.

Damage to Polymer of a Sirolimus-Eluting Stent

A 75-year-old man with a history of bare-metal stent implantation in the right coronary artery was admitted for unstable angina. Coronary angiography revealed in-stent restenoses of 90% severity in the mid-right coronary artery and the right posterolateral coronary artery (Figure 1A). Attempts to pass a 33-mm sirolimus-eluting stent (Cypher, Cordis, a Johnson & Johnson Company, Miami Lakes, Fla) premounted on a 3.0-mm balloon catheter after predilatation with a 3.0-mm balloon catheter inflated at 16 atm …

Pioglitazone induces regression of coronary atherosclerotic plaques in patients with type 2 diabetes mellitus or impaired glucose tolerance: A randomized prospective study using intravascular ultrasound

BACKGROUND A large clinical trial clarified that pioglitazone reduces cardiovascular events in diabetic patients. However, effects of pioglitazone on structure of coronary atherosclerotic plaques have not been demonstrated. We examined whether pioglitazone reduces volumes of coronary atherosclerotic plaques using intravascular ultrasound (IVUS). METHODS Twenty-six consecutive patients with type 2 diabetes mellitus (DM) or impaired glucose tolerance (IGT) undergoing percutaneous coronary intervention (PCI) were enrolled. Echolucent plaques without significant stenosis were selected in IVUS video images at non-PCI-influenced coronary segments and volumetric analysis of the targeted plaques was performed. The patients were randomly assigned into 2 groups: pioglitazone group consisted of 13 patients taking pioglitazone 15 mg/day for initial 14 days after PCI and subsequent 30 mg/day during 6-month follow-up, and control group with 13 patients as control. The plaque volumes and some parameters such as plasma lipid profiles and high-sensitive C-reacting protein (hs-CRP) levels were compared between baseline and the follow-up in those groups. RESULTS In the pioglitazone group after 6 months, the plaque volume was significantly reduced (101.3+/-32.1 to 94.6+/-33.6 mm(3), -7.2%; p=0.0023), plasma triglyceride was significantly decreased (- 14.9%) and high density lipoprotein cholesterol was substantially increased (+20.0%) without any significant change in low density lipoprotein cholesterol (LDL-C). Also, hs-CRP level tended to be decreased. However, no significant change in plaque volumes and those parameters was observed in the control group. CONCLUSIONS Pioglitazone may induce regression of coronary atherosclerotic plaques without LDL-C reduction in patients with DM and IGT.

Effect of balloon inflation time on expansion of sirolimus-eluting stent

There is little information about the relationship between balloon inflation time and sirolimus-eluting stent (SES) expansion. In this randomized intravascular ultrasound (IVUS) study, 92 de novo lesions in native coronary arteries that underwent SES implantation were enrolled. Sirolimus-eluting stent was implanted using an inflation pressure of 14 atm. Stent balloon was gradually inflated until 14 atm in 10 s. In the short inflation group, it was deflated immediately after an image of the balloon inflated at 14 atm was taken. Stent balloon inflation lasted 60 s in the long inflation group. Intravascular ultrasound was then performed. The long balloon inflation resulted in a larger stent cross-sectional area (4.9 ± 1.6 mm2 vs 4.3 ± 1.4 mm2, P < 0.05) and expansion (71% ± 13% vs 60% ± 13%, P < 0.001) compared to the short balloon inflation, although stent expansion was relatively low in both groups. The relatively longer balloon inflation time using an inflation pressure of 14 atm results in better SES expansion. However, in the majority of lesions, adequate stent expansion is not achieved even using long balloon inflation, if it is inflated at 14 atm.

Difference in security of stent jail between Palmaz-Schatz, NIR, and Multi-Link stents: the effect of balloon inflation through stent struts.

After placing a stent in the main vessel of a bifurcation lesion, it is often necessary to perform further balloon inflation or stent placement through the stent struts in order to treat a lesion of the secondary vessel or side branch. This balloon inflation with dilatation through the cells of the stent in the main vessel results in stent strut disfigurement. This disfigurement causes various degrees of stenosis within the main vessel secondary to stent strut deformity. The degree of strut deformity, and therefore stenosis, may vary significantly depending on stent design and structure. A model of a bifurcation lesion with an angle of 45° was created from acrylic resin. The diameters of the main vessel and the secondary vessel were both 3.5 mm. Deployment of the Palmaz‐Schatz stent (PS, n = 5), NIR stent (n = 5), or Multi‐Link stent (n = 5) was performed in the main vessel with a 3.5‐mm balloon catheter inflated to 6 atm. A second 3.5‐mm balloon catheter was then inflated to 6 atm through the stent struts of the main vessel and into the ostium of the secondary vessel. The minimal lumen diameter (MLD) and cross‐sectional area (CSA) at the ostium of the side branch and the stenosis within the main vessel were then measured, taking into account the stent deformity that occurred. Kissing balloon dilatation with two 3.5‐mm balloon catheters was then performed and the stenosis secondary to stent deformity in the main vessel was remeasured. The MLD of the Multi‐Link stent at the side‐branch ostium was greater compared with those of the Palmaz‐Schatz stent or the NIR stent (2.4 ± 0.1, 1.6 ± 0.1, 1.7 ± 0.1 mm, P < 0.01) and CSA (4.9 ± 0.5, 2.7 ± 0.3, 2.5 ± 0.3 mm2, P < 0.01). Balloon inflation through the stent struts caused stent deformity that resulted in some degree of stenosis within the stent of the main vessel in all three stent types. Kissing balloon inflation reduced, but never eliminated, this stenosis. The percent stenosis in the main vessel secondary to stent deformity (PS 34% ± 9%, NIR 25% ± 8%, Multi‐Link 34% ± 7%, NS) and residual stenosis postkissing balloon inflation (PS 12% ± 1%, NIR 10% ± 3%, Multi‐Link 14% ± 3%, NS) were not significantly different among these three stents. At the side‐branch ostium, the MLD and CSA were significantly greater for the Multi‐Link stent compared with those of the Palmaz‐Schatz or NIR stent. Balloon inflation through the stent struts caused stent deformity that resulted in stenosis within the stent in the main vessel. Kissing balloon inflation reduced this stenosis, but some residual stenosis always remained. The stenoses within the main vessel did not differ among the three stent types. Cathet. Cardiovasc. Intervent. 48:230–234, 1999.

Occurrence of Multiple Fibrofatty Replacements Exclusively in the Left Ventricle of a Patient With Monomorphic Sustained Ventricular Tachycardia

A 34-year-old man presented with cardiovascular syncope with sustained ventricular tachycardia (VT). ECG showed VT with morphologically right bundle-branch block with a-superior-axis. Cardioversion and endotracheal intubation were performed. After resolution of VT, a 12-lead ECG showed sinus rhythm, normal axis deviation, and isolated premature ventricular contraction of right bundle-branch block morphology with a-superior-axis. The transthoracic echocardiogram showed regional abnormality of contraction in the posterior area of the left ventricle with no abnormality of the right ventricle. Obstructive coronary heart disease was excluded by angiography …

Ubiquitous atherosclerosis in coronary arteries without angiographically significant stenosis

Previous intravascular ultrasound (IVUS) studies have shown coronary artery atherosclerosis even in angiographically normal reference segment. However, IVUS has not been performed in all of the three major coronary arteries. A total of 50 patients with single-vessel disease underwent IVUS evaluation in the proximal two-thirds of the three major coronary arteries. Lumen and external elastic membrane cross-sectional areas were measured at 1-mm intervals. To compensate the difference in pullback length among coronary arteries, normalized total plaque and media volume (TPV) was calculated as TPV/number of slices in pullback × median number of slices in study population. Percent plaque and media volume (PPV) was calculated as TPV/Σ external elastic membrane cross-sectional area × 100. A cross section was defined as atherosclerotic if maximum intimal thickness exceeded 0.5 mm at any point in the vessel circumference. There was no significant difference in normalized TPV, PPV, and the incidence of abnormal intimal thickness between coronary arteries with and without significant stenosis. Frequency distribution of plaque burden was similar. Atherosclerosis is ubiquitous even in coronary arteries without angiographically significant stenosis. The extent of atherosclerosis is similar between coronary arteries with and without significant stenosis.

Antiplatelet effect of 50-mg maintenance dose of clopidogrel compared to 200 mg ticlopidine: a preliminary study

In the United States and Europe, patients with coronary stents are maintained on 75 mg clopidogrel. Because the maintenance dose of ticlopidine in patients with coronary stents is 100 mg twice daily in Japan and 250 mg twice daily in the United States and Europe, in Japanese patients a lower dose of clopidogrel may achieve an antiplatelet effect comparable to 200 mg ticlopidine. Platelet aggregation was evaluated in 104 consecutive patients on 50 mg clopidogrel plus aspirin (n = 54) and 200 mg ticlopidine plus aspirin (n = 50). Platelets were stimulated with adenosine diphosphate (5 and 20 μmol/l) and aggregation was assessed by optical aggregometry. There was no significant difference in platelet aggregation induced with 5 (37% ± 11% vs 38% ± 15%, not significant) and 20 μmol/l adenosine diphosphate (48% ± 13% vs 51% ± 12%, not significant) between 50 mg clopidogrel and 200 mg ticlopidine. In Japanese patients, there is the possibility that a maintenance dose of 50 mg clopidogrel on platelet inhibition is comparable to 200 mg ticlopidine.

Multivessel Coronary Artery Spasm Refractory to Intensive Medical Treatment

This case report describes multivessel coronary artery spasm refractory to oral nifedipine, intravenous isosorbide dinitrate, diltiazem and nicorandil, and intracoronary nitroglycerin. Intracoronary administration of nicorandil only transiently relieved coronary artery spasm. Prednisolone was effective in preventing coronary artery spasm.

Effect of 450-mg loading dose of clopidogrel on platelet function in Japanese patients undergoing coronary stent placement

Usefulness of higher (>300 mg) loading doses of clopidogrel has been demonstrated in studies from the United States and Europe. The present study evaluated platelet aggregation after the administration of a 450-mg loading dose of clopidogrel in Japanese patients undergoing coronary stenting. Platelet aggregation was serially measured at baseline, and 2, 4, 6, and 8 h after 450-mg clopidogrel loading in 25 patients undergoing coronary stenting. Platelets were stimulated with 5 and 20 μmol/l adenosine diphosphate (ADP) and aggregation was assessed by optical aggregometry. Platelet aggregation (5 μmol/l ADP 42.8% ± 13.5% and 20 μmol/l ADP 51.2% ± 11.6%) was significantly suppressed ≤4 h after 450-mg clopidogrel loading. There were no adverse events except one minor nasal bleed. The present study shows that platelet inhibition is achieved ≤4 h after the administration of a 450-mg clopidogrel loading dose in Japanese patients.