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Resistin is an adipocytokine that may link inflammation and atherosclerosis.We studied the associations of resistin levels with cardiovascular events and restenosis.We measured pre-procedural serum resistin levels in 140 patients with coronary artery disease undergoing elective percutaneous coronary intervention (PCI), of whom 97 had a stent. Restenosis was defined as50% stenosis at follow-up angiography. Patients were followed for 3 years for major adverse cardiovascular events (MACE).At 8±6 months after PCI, reangiography was performed in 94 (67%) patients, of whom 42 had restenosis. Between 42 patients with restenosis and 52 without restenosis, resistin (4.5±2.6 vs. 4.5±2.5 ng/mL) and Creactive protein (CRP) (median 0.70 vs. 0.70 mg/L) levels did not differ. During 3-year follow-up, MACE occurred in 24 patients (1 death, 21 unstable angina, 2 stroke). Compared with 116 patients without MACE, 24 with MACE had higher resistin (5.4±2.4 vs. 4.3±2.5 ng/mL) and CRP (1.30 vs. 0.60 mg/L) levels (p0.05). Patients with MACE more often had resistin4.0 ng/mL than without MACE (75% vs. 35%, p0.001). Resistin correlated with CRP levels (r= 0.31). To clarify the association between MACE and resistin, patients were divided into 2 groups by resistin levels. Kaplan-Meier analysis showed a lower event-free survival rate in patients with resistin4.0 ng/mL than without it (p0.001). On multivariate analysis, resistin, but not CRP, was an independent predictor of MACE. The hazard ratio for MACE was 3.6 (95%CI=1.4-9.2) for resistin4.0 ng/mL.Serum resistin levels were found to be associated with further cardiovascular events in patients undergoing PCI.

Background Magnetic resonance imaging was recently reported to detect atherosclerotic plaques in thoracic and abdominal aortas. Methods Using magnetic resonance imaging, we investigated associations of risk factors and plasma inflammatory markers with plaques in both thoracic and abdominal aortas in 102 patients undergoing coronary angiography. Associations between coronary artery disease (CAD) and aortic plaques were also evaluated. Results Plaques in thoracic and abdominal aortas were detected in 61% and 90% of patients, respectively. Age and systolic blood pressure correlated with plaque extents in both the aortas. Serum LDL cholesterol level correlated with plaque extent in the thoracic aorta ( r s = 0.42). The degree of smoking correlated with plaque extent in the abdominal aorta ( r s = 0.43). In multivariate analysis, age and systolic blood pressure were associated with plaques in both the aortas. The LDL cholesterol and smoking were characteristically associated with plaques in the thoracic and abdominal aortas, respectively. Regarding inflammatory markers, fibrinogen and C-reactive protein levels correlated with total plaque extent in the aortas ( r s = 0.50 and r s = 0.51). Compared with 24 patients without CAD, 78 with CAD more often had plaques in the thoracic (71% vs 29%) and abdominal (95% vs 75%) aortas. Although plaque extents in both the aortas correlated with the severity of CAD, only thoracic plaques were independently associated with CAD. Conclusions The thoracic and abdominal aortas may have different susceptibilities to risk factors. However, plasma inflammatory markers appear to reflect total extent of aortic atherosclerosis. Although aortic plaques are common in patients with CAD, only thoracic plaques are an independent factor for CAD.

Background: Vascular endothelial growth factor (VEGF) has been implicated in both angiogenesis and ischemia. However, the relationship between plasma VEGF level and coronary artery disease remains unknown. Hypothesis: Plasma VEGF level may be associated with severe coronary artery disease and other cardiovascular risk factors. Methods: We examined plasma VEGF concentration and coronary risk factors in 73 patients who underwent coronary angiography and 70 apparently healthy control subjects. According to the number of the three major coronary vessels with significant (≥ 75%) stenosis, we divided the patients into two groups: the mild stenosis group (0- and single-vessel disease, n = 36) and the severe stenosis group (double- and triple-vessel disease, n = 37). Results: The log VEGF value of the severe stenosis group was significantly higher than that of the mild stenosis (p < 0.05) and control groups (p < 0.05). Furthermore, there was a significant positive trend in the log VEGF value according to the number of vessels with significant stenosis (p = 0.016). However, there was no significant difference in log VEGF value between the mild stenosis and control groups. Soluble vascular cellular adhesion molecule, soluble intracellular adhesion molecule, and other coronary risk factors were found to be associated with the presence of vessel stenosis. Conclusion: Unlike established coronary risk factors, the plasma VEGF level may be associated with only severe coronary ischemia such as multiple coronary vessel disease.

Background: Oxidized low-density lipoprotein (oxLDL) not only plays an important role in plaque formation, but also impairs the endothelium-dependent relaxation. Constrictive remodeling rather than intimal hyperplasia mainly contributes to restenosis after balloon angioplasty. Probucol (powerful antioxidant) reduced restenosis rate by improving constrictive remodeling. Thus, oxLDL may modulate coronary arterial remodeling. Hypothesis: The study was designed for using intravascular ultrasound to test the hypothesis that arterial constrictive remodeling (CR) was associated with oxLDL in patients with coronary artery disease. Methods: Intravascular ultrasound was performed in 36 patients with de novo atherosclerotic coronary. Remodeling was defined and evaluated as follows: remodeling index (RI) = lesion vessel area (VA)/(proximal reference VA + distal reference VA)/2. Constrictive remodeling (CR) was defined as remodeling index (RI) < 0.9. Neutral and expansive remodeling (NER) was defined as RI ≥0.9. The level of plasma ox-LDL was measured by sandwich ELISA using the monoclonal antibody (DLH3)-recognized oxidatively modified lipoproteins and the antihuman apoprotein B monoclonal antibody. Results: Neutral and expansive remodeling was found in 24 lesions, and CR in 12 lesions. Remodeling index was significantly lower in the CR group than in the NER group (0.8 ± 0.1 vs. 1.0 ± 0.1, p< 0.001). The level of oxLDL in the CR group was significantly higher than that in the NER group (24.0 ± 12.1 vs. 16.4 ± 6.2 U/ml, p < 0.05). The level of high-density lipoprotein-cholesterol (HDL-C) in the CR group was significantly lower than that in the NER group (40.5 ± 4.8 vs. 46.2 ± 10.6 mg/ml, p < 0.05). There was a statistically significant correlation between the value of HDL-C/ ox-LDL and the RI (r = -0.48, p< 0.005). Conclusions: Oxidized LDL and HDL-C were associated with arterial remodeling in de novo atherosclerotic lesions.

Vulnerable plaque generally contains a thin fibrous cap, lipid pools, and reduced internal plaque collagen. Arterial fluorescence analysis can differentiate atherosclerotic lesions from normal arteries; however, the contribution of the lipid core to atherosclerotic arterial fluorescence remains controversial. This study aimed to identify lipid core fluorophores and to differentiate the lipid core from normal artery and atheroma. The helium-cadmium laser–induced fluorescence spectra of cadaveric arteries and known chemical constituents were recorded. Lipid core fluorescence spectra exhibited marked red shifts and broadening compared with the fluorescence spectra of normal tissue and atheroma. Similar fluorescence spectra were obtained for lipid core and oxidized low density lipoprotein, for atheroma and collagen, and for normal artery and elastin. A classification based on collagen, elastin, and oxidized low density lipoprotein spectral decomposition could discriminate the lipid core (n=29), normal artery (n=74), atheroma (n=73), and preatheroma (n=10) with 86% accuracy. Fibrous cap thickness was correlated with the spectral collagen content index ( r =0.65, P

A 65-year-old man was admitted to the National Defense Medical College Hospital for acute anterolateral myocardial infarction and cardiogenic shock. Emergency coronary angiography demonstrated occlusion of the proximal left anterior descending artery. Primary percutaneous transluminal coronary angioplasty (PTCA) was successfully performed with the support of intra-aortic balloon pumping (IABP) and medical treatment to stabilize the patient's blood pressure. On the second hospital day, the patient suffered cardiac tamponade. Pericardiocentesis showed bloody fluid and revealed that an oozing-type of left ventricular rupture had occurred after the myocardial infarction. Cardiogenic shock persisted after successful removal of the pericardial effusion. Although the heparinization required during percutaneous cardiopulmonary support (PCPS) can increase pericardial effusion, PCPS was initiated to correct the systemic hypoperfusion; a surgical team was on standby in case massive pericardial effusion resulted, but fortunately that did not occur, and cardiac function recovered. The patient was weaned successfully from PCPS and IABP and has remained in a satisfactory condition for over 1 year. PCPS contributed to the patient's recovery from cardiac shock and may have decreased the effusion from the oozing-type rupture by reducing ventricular wall tension.

A 48-year-old man with a history of hypertension and diabetes mellitus was hospitalized with sudden onset of severe chest pain. He was in cardiogenic shock with a systolic pressure of 60 mm Hg. His electrocardiogram (ECG) showed ST-segment elevation in the precordial leads suggestive of acute anteroseptal myocardial infarction. The ST-segment returned to baseline after the systolic blood pressure rose to 100 mm Hg with the administration of sympathomimetic agents. Aortography and transesophageal echocardiography demonstrated type A aortic dissection and aortic regurgitation. Aortography and short-axis transesophageal echocardiography showed during diastole almost complete collapse of the true lumen of the ascending aorta caused by the intimal flap. The patient underwent surgical repair of the aortic dissection and implantation of Palmaz stents in the carotid arteries. Decreased blood pressure and the presence of aortic regurgitation accelerated the collapse of the true lumen during diastole in the ascending aorta, resulting in functional obstruction of the left main coronary artery, which may have been related to ST-segment changes in this case.

Background and hypothesis: Brachial artery flow-mediated dilation (FMD), a noninvasive, widely used clinical index of endothelial function and magnitude of FMD, has been reported to be closely related to many coronary risk factors and coronary atherosclerosis. However, there has been no study that examines the diurnal change of FMD. We designed this study to reveal the diurnal variation of FMD in healthy volunteers. Methods: We examined FMD in response to reactive hyperemia by high resolution ultrasound in 13 healthy young men (age 25–32) at four different times over the course of a day. Results: Mean measures of brachial artery FMD was 4.0% at 8:00, 5.3% at 12:00, 9.7% at 17:00, and 6.9% at 21:00 hours. Flow-mediated dilation at 8:00 and at 12:00 hours was significantly lower than that at 17:00 (p

Coronary artery fistulas are uncommon entities with communication between the coronary artery and cardiac structure. We encounter a 70-year-old, asymptomatic woman with a large right coronary artery to left ventricle fistula. Non-invasive echocardiogram was helpful in detecting an enlarged right coronary that drained from the aorta into the left ventricle. Clinical importance of coronary artery fistula is due to an increased risk of heart failure, myocardial ischemia, and rupture. Treatment of asymptomatic patients without significant shunting is controversial. We decided to follow-up on her medically without surgical closure of the fistula because her hemodynamics are stable. Echocardiogram is very useful to diagnose and evaluate these diseases. (J Echocardiogr 2007; 5: 58-60)

To clarify the pathogenesis of an impending infarction and to investigate the difference between the pathogenesis of an acute myocardial infarction and an impending infarction, we have performed percutaneous transluminal coronary angioscopy in 13 patients with an impending infarction and in 13 patients with an acute myocardial infarction. As a result, coronary thrombi were observed in 12 of the 13 patients with an impending infarction, and a similar frequency of thrombi was observed in the patients with an acute myocardial infarction. Further, grayish white thrombi were observed in 9 of 12 patients with an impending infarction, but no such thrombi were noted in those with an acute myocardial infarction. Reddish thrombi, however, were observed in all patients with acute myocardial infarction, whereas such thrombi were observed in only 3 of 12 patients with an impending infarction. Informatively, occlusive thrombi occurred more frequently in patients with an acute myocardial infarction than in those with an impending infarction. As a thrombus plays an important role in an impending infarction, we also evaluated the effect of anticoagulant and thrombolytic therapy for an impending infarction in 79 patients. The incidence of recurrent angina and a subsequent acute myocardial infarction were significantly higher in non-heparin-treated patients and in thrombolytic-treated patients than in heparin-treated patients. In conclusion, a thrombus plays an important role in the pathogenesis of an impending infarction and in an acute myocardial infarction, though the characteristics of the thrombus differ in each instance. This difference may account for the differing results of thrombolytic therapy. Heparin was found an effective treatment for myocardial ischemia in an impending infarction.

In order to develop a reliable laser-induced fluorescence (LIF) guided laser angioplasty system, real time, pulse-by-pulse fluorescence spectra were recorded and the same fiberoptic was used for both detection of the fluorescence and for atheromatous tissue ablation. A 308 nm XeCl excimer laser served as the laser source for both the induction of fluorescence and the ablation. The fluorescence signal was induced at high laser energies during ablation without any serious change in the fluorescence pattern. A new characteristic fluorescence peak at 540 nm for atheromatous tissue was observed after treatment with chlortetracycline hydrochloride (CTC). This allowed the development of an algorithm and a subsequent index to discriminate the atheromatous tissue from the normal tissue. During atheromatous tissue ablation, this index changed as normal tissue was approached, thereby avoiding vessel perforation. Our results suggest that monitoring of this index through the catheter delivering the laser energy enhances selective ablation while simultaneously reducing the risk of vessel perforation.

Osteopontin (OPN) mRNA is highly expressed in atherosclerotic plaques and plasma OPN levels are high in patients with coronary artery disease and in those with restenosis. OPN-overexpressing transgenic mice show markedly increased neointimal formation after arterial injury.The prognostic significance of the preprocedural plasma OPN level was investigated in 130 patients undergoing percutaneous coronary intervention (PCI). Patients were followed up for restenosis and major adverse cardiovascular events (MACE). At 7+/-3 months after PCI, angiography was performed again in 91 patients, of whom 40 had restenosis. Between patients with and without restenosis, OPN (492+/-200 vs 482+/-224 ng/ml) and C-reactive protein (CRP: 0.78 vs 0.70 mg/L) levels did not differ. During a 3-year follow-up, MACE occurred in 21 patients, who had higher OPN (586+/-230 vs 438+/-195 ng/ml) and CRP (1.30 vs 0.70 mg/L) levels than those without MACE (P0.005). Both OPN and CRP levels were independent predictors for MACE. Hazard ratios for MACE were 1.3 (95% confidence interval (CI) 1.1-1.5) for a 100 ng/ml increase in OPN and 3.6 (95%CI 1.4-9.3) for CRP1.0 mg/L.In patients undergoing PCI, the preprocedural OPN and CRP levels are independent predictors for further cardiovascular events, but not for restenosis.

Osteopontin (OPN) mRNA was shown to be highly expressed in atherosclerotic plaques. We reported plasma OPN levels to be high in patients (pts) with coronary artery disease. Moreover, OPN levels were recently shown to be high in acute coronary syndrome. Increased OPN mRNA expression was also shown in rat arteries after balloon injury. OPN transgenic mice showed markedly increased neointimal formation after arterial injury. OPN may play a role in the development of restenosis after percutaneous coronary intervention (PCI). Methods: We investigated the prognostic value of pre-procedural plasma OPN levels by ELISA on restenosis and clinical outcome in 130 pts undergoing PCI, of whom 89 (68%) had bare metal stent. Pts with AMI were excluded. Restenosis was defined as >50% diameter stenosis at follow-up angiography. Pts were followed up for 3 years for major adverse cardiovascular events (MACE) (death, MI, unstable angina, stroke). Results: At 7±3 months after PCI, re-angiography was performed in 91 (70%) pts, of whom 40 had restenosis. Between 40 pts with restenosis and 51 without it, plasma OPN (492±200 vs 482±224 ng/ml) and C-reactive protein (CRP) (median 0.78 vs 0.70 mg/l) levels did not differ. In multivariate analysis, reference diameter and smoking were independent predictors for angiographic restenosis, but OPN or CRP levels were not. During the 3-year follow-up, MACE occurred in 21 pts. Compared with 109 pts without MACE, 21 with it had higher OPN (586±230 vs 438±195 ng/ml, P500 ng/ml (62% vs 35%) and CRP >3.0 mg/l (33% vs 12%) than without it (P500 ng/ml than those without it (P500 ng/ml and 4.3 (1.3–14.0) for CRP >3.0 mg/l. Conclusion: Plasma levels of OPN as well as CRP were found to be independent predictors for cardiovascular events in pts undergoing PCI, but they were not predictors for restenosis.

Objective— Coronary plaque instability causes myocardial infarction (MI). Angiographic lesions with such instability are complex lesions. Complex carotid plaques were reported to be prevalent in unstable angina. We investigated associations between coronary plaque instability, such as MI and angiographic complex coronary lesions, and aortic plaques. Methods and Results— Aortic MRI was performed in 146 patients undergoing coronary angiography, of whom 108 had coronary artery disease (CAD) and 44 also had MI. Prevalence of plaques in thoracic and abdominal aortas was higher in patients with than without CAD (73% and 94% versus 32% and 79%), but it was similar in CAD patients with and without MI. Notably, complex plaques in abdominal aorta were more prevalent in CAD patients with than without MI (36% versus 14%; P P Conclusion— Complex plaques in abdominal aorta were associated with MI and complex coronary lesions, suggesting a link between coronary and aortic plaque instability.

To the Editor: High levels of osteopontin (OPN) mRNA and proteins were reported in atherosclerotic plaques.1,2 Recently, we reported plasma OPN levels to be high in patients with coronary artery disease (CAD) and to correlate with the severity of CAD.3 However, no association between plasma OPN levels and restenosis after percutaneous coronary intervention (PCI) has yet been demonstrated. We measured plasma OPN levels in 90 patients with CAD undergoing elective coronary angiography for suspected restenosis. They had undergone PCI 0.6±0.4 years ago, of whom 52 (58%) had been treated with bare metal stents. OPN levels were also measured in 60 age- and gender-matched CAD patients with no history of PCI. Patients with acute coronary syndrome were excluded. Our study was approved by institutional ethics committee. After informed consent was obtained, fasting blood samples were taken. Plasma OPN levels were measured by ELISA (Human OPN …

We developed a hot balloon catheter for stenotic coronary diseases using Ar laser as a heat source. A circulation design of contrast medium in the balloon made it possible to attain rapid temperature elevation and temperature uniformity. The silica fiber power delivery of Ar laser offered flexibility and insulation for the balloon catheter. In vitro and acute in vivo experiment revealed the efficacy of this hot balloon.

Background — In-stent restenosis remains a pivotal problem after coronary and peripheral stenting. Sonodynamic therapy inhibits tumor growth by means of cytotoxicity after the activation of sonochemical sensitizers by ultrasound. PAD-S31 is known to be a water-soluble, chlorin-derivative sonochemical sensitizer. We assessed the efficacy of sonodynamic therapy using this sensitizer on neointimal hyperplasia in a rabbit stent model. Methods and Results — Stents were implanted in the iliac arteries of 16 rabbits. A total of 32 stented arteries were randomized to sonodynamic therapy, control, ultrasound exposure, and PAD-S31 groups. One hour after the intravenous administration of PAD-S31 (25 mg/kg body weight), ultrasound energy (1 MHz, 0.3 W/cm 2 ) was delivered transdermally to the sonodynamic therapy group. At 28 days, all stent sites were analyzed morphometrically. The size of the intimal cross-sectional area was smaller in the sonodynamic therapy group than in the control, ultrasound, and PAD-S31 groups (0.31±0.07 versus 1.38±0.47, 1.66±0.71, and 1.61±0.42 mm 2 , respectively; P 2 ; P Conclusions — Sonodynamic therapy with PAD-S31 is considered to be a feasible treatment modality for noninvasively inhibiting neointimal hyperplasia in a rabbit iliac stent model.

Thirty-one-year-old woman with Kawasaki disease wanted a child. She had a large coronary aneurysm on the left main coronary artery and complete obstruction of the right coronary artery, but there was no sign of ischemia. Heparin anticoagulant therapy was begun 8 weeks after the onset of pregnancy. The activated partial thromboplastin time (APTT) was successfully maintained at 1.5 to 2.0 times normal value during pregnancy and puerperium. There were no thromboembolic complications during pregnancy or after an uneventful cesarean delivery. The neonate was healthy.

In addition to a disruption of yellow plaque, vasospasm may also play a role in thrombotic occlusions of coronary arteries in small cases of infarction. Macroscopic vascular injury and thrombus seemed to be unnecessary for vasospasm culminating in myocardial infarction.

Objectives.The purpose of this study was to determine the prevalence of intracoronary thrombus and associated anatomic abnormalities in patients with postinfarction angina using coronary angioscopy and angiography.Background.Postinfarction angina, previously studied by angiographic methods only, identifies patients at high risk for sudden death, recurrent angina and refractory angina. The recent development of coronary angioscopy, which permits direct observation of a thrombus or atheroma and is especially used for the detection of intraluminal changes, encourages a reexamination of the pathogenesis of postinfarction angina.Methods.Fifty-one consecutive patients with a diagnosis of acute myocardial infarction underwent cardiac catheterization. Coronary angiography followed immediately by coronary angioscopy was performed in 17 patients with and 34 without postin farction angina during the same period of time (10.2 ± 3.7 or 15.7 ± 5.5 days [mean ± SD]) after the onset of acute myocardial infarction.Results.The frequency of thrombus, as observed by angioscopy, was significantly higher in patients with than without postinfarction angina (17 of 17 vs. 5 of 34, respectively, p < 0.01). There were no significant differences between groups with respect to degree of stenosis in the infarct-related artery, number of vessels with significant stenosis, presence of collateral flow, type of therapy and risk factors.Conclusions.Infarct-related artery thrombus is universally present in postinfarction angina and may be the primary pathogenic factor. Angioscopy is much more sensitive than coronary angiography for the detection of coronary thrombus.

Present study tested the hypothesis that the great decline of left ventricular volume (LVV) during Head-up tilt (HUT) triggers ventricular mechanoreceptor activation and subsequently increases parasympathetic activation associated with hypotension-bradycardia. We measured temporal changes of frequency domain heart rate variability indices (HRV) and LVV using M mode echocardiogarphy during HUT (80° up to 40 min) in 15 patients (pts, 50 ± 23 years) with syncope of undetermined etiology. HRV consisted of low (L, 0.04 Hzl, high (H, 0.15–0.40 Hz) and total (T, 0.01–1.00 Hz) components. For LVV analysis, EDV. ESV and EF were calculated using Teichholtz formula. HRV and LW indices were measured in consecutive 2 min segments throughout the study. Results Eight pts had positive tests (syncope was induced by HUT; Group 1, G1) and 7 pts in negative tests (Group 2, G2). Data were shown below [SSP, systolic blood pressure; mean in HR and SBP; Suo supine; Δ and Δ%, differenct es between values at 2 min of HUT and maximally changed values (Mx) during HUT; L/H, ratio of Land H components]. HR (bpm) SBP(mmHg) ΔH ΔLJH Δ%EDV Δ%ESV Δ%EF Gl (Su/Mx) 77/64 # 117/79 # 2.8 0.058 -53+ -49 * +23 G2(Su/Mx) 6S/75 # 132/124 -11.6 0.063 -19 -20 +22 * p l 0.05 vs G2 # P l 0.05 vs Su Before syncope, LVVs in G1 gradually and more profoundly declined than those in G2. The values of H significantly increased from supine to 2 min prior to syncope in G1. Also, the values of H at 2 min prior to syncope in G1 was significantly higher than those at Mx in G2 (14 ± 7 vs. 7 ± 4 ms, p l 0.05). Conclusions Simultaneous measurements of LW and HRV during HUT are useful for evaluating pathophysiology of neurally mediated syncope. Preceding decrease of LVV can trigger exaggerated parasympathetic activity in patients with vasovagal syncope.

We have evaluated the feasibility of percutaneous transluminal coronary angioscopy for detecting intraluminal pathological changes as a diagnostic tool, and investigated the pathogenesis of two acute coronary disorders, acute myocardial infarction and unstable angina. Twelve patients with an acute coronary disorder and 20 patients who underwent percutaneous transluminal coronary angioplasty were selected for this comparison between the diagnostic accuracy of angioscopy and arteriography. One hundred and thirty patients were investigated by angioscopy as follows in order to investigate the pathogenesis of their acute coronary disorders: 22 within 8 h of onset acute myocardial infarction; 28 from one day to 2 months since onset recent myocardial infarction; 37 with an old myocardial infarction; 26 with unstable angina; and 23 with stable angina. Our results have indicated thrombi were detected more frequently by angioscopy than by arteriography (p less than 0.01). Also, thrombi, intimal irregularities, and xanthomatous atheromas were observed more frequently in patients with acute myocardial infarction, recent myocardial infarction, and unstable angina. It is concluded that coronary angioscopy is a much more sensitive method for detecting intraluminal changes, and that a thrombus overlying a rupture in the lining of plaque plays a major role in an acute coronary disorders, and that the fragile, lipid-rich gruel atheroma may precede its rupture.

The goal ofihis sludy was o develop a reliable laser inducedfluorescence specira analysis system using the 308nm Excimer Laser as an ablaiion andfluorescence inducing source. During our analysis we also aflempled lo determine whether exogenous chloroeiracycline hydrocloride (CTC) increased the discrimination capacity of the LIFS system. We then assessed the ability of CTC to improve the detection of the boundary between atheroma and normal media.

We developed a new percutaneous transluminal coronary angioscopic catheter for visualization of coronary artery.This angioscopic catheter has an inflatable balloon at the distal tip and one - directional angulation mechanism.We performed percutaneous transluminal coronary angioscopy during cardiac catheterization cosecutively in 155 patients. With this angioscope , we could get good'-'fair visualization in 81%(131 of 162 lesions)without major complications.We could investigate the endothelial macropathology of ischemic heart disease such as unstable angina and acute myocardial infarction.

Human atherosclerotic arterial samples were ablated via a fiber with a XeCl excimer laser. The resulting tissue fluorescence was recorded for each ablating pulse. The pulse-to-pulse evolution of the fluorescence intensity at 430 nm was obtained and compared to the histological findings. The characteristic transition observed in such curves exhibited good correlation with the transition from the atheromatous layer to the normal media, as determined by the histological examination. The establishment of such a relation led to the development of a simple computer algorithm able to detect plaque to normal media transitions. The limitations of this approach are discussed.

A study was made of a laser angioplasty system using a CO laser, 5 mu m in wavelength. To achieve therapeutic irradiation in a water solution, the authors developed a contact CO laser irradiation method which uses an optical fiber to carry the laser beam to the lesion. The authors have also developed a thin coronary angioscope catheter for diagnosis and targeting of this therapy. >

We successfully demonstrated usefulness of CO laser angioplasty. We investigated in vivo CO laser angioplasty using contact irradiation under visualization by a thin endoscope in atheromatous rabbit aorta, which was temporary filled by saline during the irradiation. 4W, 4s contact irradiation via 400μm As-S glass fiber to atheromatous aorta wall made a fine ablation hole with the minimum heat injuries to remained vascular tissue. A small amount of char was found on ZnSe contact tip after approximately 20 irradiations. But no damage was occurred in the tip. We think the visualization in the arterial lumen by the thin endoscope may be useful for pre-diagnosis and targeting of laser therapy.

Excimer laser ablation (308nm) of canine aortic samples was performed via an UV grade fused silica fiber. The influence of the repetition rate (2-20 Hz) and of the applied pressure (1-6 Atm) on the ablation rate was studied. Operative fluences between 30mJ/mm to 40mJ/mm were used. Results show a linear dependence of the ablation rate on the repetition rate for all fluences. The linearity was also preserved at various applied pressures and at low repetition rates for the same range of fluences. A saturation effect was observed at increased values of repetition rate. No dependence of the ablation rate on the repetition rate was observed when the experiment was performed using direct irradiation with a mask instead of a fiberoptic. 1. INTRODUCTION In recent years, the interaction of the Excimer laser light with tissue has triggered numerous studies due to the emerging cardiovascular and ophthalmic applications. The dependence of the ablation rate on the wavelength, fluence, and pulse width has been presented in a number of publications. Yet, little attention has been paid to the influence3of the laser repetition rate on the ablation rate of tissue. Clinical applications such as excimer laser angioplasty necessitate the use of fiber optic delivery systems. Thus, the additional mechanical effects of the applied pressure on the tissue, via the fiber optic, need to be considered.This work investigates the effect of the laser repetition rate and the applied pressure on the ablation rate.

心タンポナーデにおける弛緩期の左室循環動態を実験的,臨床的に検討した.弛緩期の指標として等容性弛緩期左室圧下降脚時定数(Tbf),漸近線(Pbf), Pbf=0時の時定数(Tln),等容性弛緩期時間(IRT)を測定し,心タンポナーデの重症度は1回心拍出量(SV)または1回心拍出係数(SI)で表わした.実験的に心タンポナーデでは奇脈,左室収縮期圧の低下, SVの減少, Pbfの上昇, Tbf, TlnおよびIRTの延長を認めた.臨床的にはSIの減少とともにTbf, Tln, IRTは延長し, Pbfは上昇した. IRTを心拍数で補正するとその変化は著明になった.以上の結果から,左室弛緩期指標は心タンポナーデの重症度を推定するのに有用と思われた.

The primary goal of this study was to devise an Optical Fiber based monitoring scheme of the arterial wall ablation by the use of laser induced fluorescence. Preliminary results indicate that the time evolution of the fluorescent light follows complex exponential decays. A comparison of the time characteristics of the decays with the findings of other investigators suggests that these decays may be related to the ablation of the successive arterial wall main layers.

A life-threatening cardiac asystole can be a malignant manifestation of vasovagal syncope induced by head-up tilt (HUT) testing. To investigate the mechanism of HUT-induced life-threatening cardiac asystole (T-LTAS), we measured a temporal change of frequency domain heart rate variability indices (HRV) in 25 patients (pts) with syncope of undetermined etiology. Three pts (37 ± 13 years, 2 male) had T-LTAS episode; asystole ≥ 10 seconds and cardiopulmonary resuscitation was necessary (Group 1, G1). Ten pts (48 ± 31 years, 6 male) had positive test (syncope was induced by HUT) but no asystole (Group 2, G2). and 12 pts (55 ± 20 years, 5 male) in negative test (Group 3, G3). After 10 min in supine (Su), HUT (80°) was performed up to 40 min. Power spectra of low (L, 0.04 Hzl, high (H, 0.15–0.40 Hz) and total (T, 0.01–1.00 Hz) frequency were measured in consecutive 2 min segments throughout the study. Maximally changed values (Mx) in HR, systolic blood pressure (BPs) and HRV during HUT were compared among 3 groups. Results Mx were obtained at 2 min or 4 min before the moment of T-LTAS or syncope in G1 and G2, respectively. HR (bpm) BP5 (mmHg) H(ms) L (ms) T (ms) G1 (Su/Mx) 60 ± 8/64 ± 13 105 ± 3/87 ± 13 15 ± 11/21 ± 6 # 20 ± 11/58 ± 41 # 30 ± 1/73 ± 29 # G2 (Su/Mx) 9/88 ± 21 * 126 ± 23/79 ± 13 * 11 ± 11/6 ± 4 * 14 ± 11/13 ± 9 28 ± 17/28 ± 1 G3 (Su/Mx) 71 ± 13/90 ± 20 * 138 ± 15/115 ± 15 * 15 ± 12/6 ± 4 * 16 ± 10/14 ± 13 36 ± 18/26 ± 16 mean ± SD * p l 0.05. vs Su # P l 0.05 vs G2, G3 H in G2 and G3 was decreased by HUT, whereas HUT did not decrease H in G1. H, L and T in G1 during HUT were significantly higher than those in G2 and G3, respectively. Findings were consistent with exaggerated sympathetic and failed withdrawal of parasympathetic activity during HUT in patients with T-LTAS. Conclusions Unusual autonomic responses to orthostatic stress can cause prolonged asystole, and this autonomic nerve dysfunction may lead to sudden cardiac death associated with cardiovascular collapse.