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Culprit lesions of acute coronary syndrome can be detected by angioscopy as the disrupted yellow plaques. Angioscopy is a very sensitive diagnostic tool that can detect thrombus in human coronary arteries, and can identify the disrupted plaques as those with thrombus on them. Those culprit plaques may have a high risk of thrombotic occlusion; and stenting may be beneficial for those lesions. Therefore, identifying the real site of culprit lesions is important but difficult without angioscopy. Furthermore, it is important to clarify if stenting at the disrupted yellow plaques identified in the asymptomatic patients is beneficial or not. The detection of myocardial ischemia is an established indication for stenting, but the detection of thrombotic culprit lesion may be another indication.

Diabetes mellitus (DM) is an independent and distinct risk factor of ischemic heart disease. Therefore, early identification and management of coronary atherosclerosis for patients with DM is being desired. For the purpose of visualizing coronary atherosclerosis, various imaging modalities have been proposed especially to identify an unstable plaque that has a thin fibrous cap and a large lipid core. These modalities include intravascular ultrasound, coronary angioscopy, intracoronary thermography, optical coherence tomography, multi-slice CT, MRI, and so on. The development of these modalities are now pushing all cardiologists to get interested in a new field called as "plaque imaging".

Background: Endoscopic vessel harvesting is becoming common for the patients undergoing coronary artery bypass grafting. Insufflation of carbon dioxide (CO2) during the procedures has been reported elsewhere to affect arterial carbon dioxide tension, but the occurrence of hypercapnia is still controversial., Methods: We investigated the effects of CO2 insufflation during endoscopic harvesting of the saphenous vein (SV, n = 34), radial artery (RA, n = 14), or internal mammary artery (IMA, n = 7) for coronary artery bypass surgery. The conduit harvesting was performed using Vasoview Dissecting Cannula with insufflation of CO2 maintaining a cavity pressure of 8-10 mmHg., Results: After insufflation of CO2, significant elevation of partial pressure of CO2 in arterial blood (PaCO2) was found during harvesting of SV (35.4 +/- 3.8 to 49.2 +/- 7.5 mmHg, P < 0.01) and of IMA (38.0 +/- 2.3 to 44.2 +/- 3.2 mmHg, P < 0.05), but no significant elevation of PaCO2 occurred during RA harvesting using a tourniquet. The extent of PaCO2 elevation in SV harvesting showed negative correlation with patient's body weight, body mass index, and body surface area., Conclusions: Significant hypercarbia occurs during endoscopic harvesting of SV or IMA. It is recommended that PaCO2 should be carefully monitored during endoscopic conduit harvesting for coronary artery bypass surgery.

Coronary plaque rupture and the following formed thrombus have been revealed the cause of acute coronary syndrome. This evidence had been proposed by the pathologists 100 years ago; however, the intravascular imaging such as intravascular ultrasound (IVUS) or coronary angioscopy has revealed the clinical evidences in live human being. Thrombus and yellow plaque detected by coronary angioscopy as well as the ruptured fibrous cap detected by IVUS are the characteristics for the lesion of ACS, which does not show the significant stenosis. Thus, ACS lesion should be diagnosed by IVUS or coronary angioscopy.

We observed pulmonary artery thrombi and parietal lesions in patients with acute pulmonary thromboembolism (APTE), using intravascular ultrasound (IVUS) and angioscopy (AS). In APTE without underlying disease mainly non-echorich intraluminal mass was noted, with a pulsatile and thin intima. On AS red thrombi with white fibrin coating could be directly observed, and no parietal lesions were found. The findings of the pulmonary arterial intima and thrombus were different between APTE and chronic pulmonary thromboembolism (CPTE), and even among CPTE cases. IVUS and AS are useful in characterizing the thrombi and related pulmonary artery lesions in PTE.

Hyperlipidemia is one of the major coronary risk factors, which leading to the clinical worse outcome in patients with coronary artery disease, that is, acute coronary syndrome. Coronary plaque rupture followed by the formation of thrombus has been revealed to be a major cause of acute coronary syndrome. It would be important to detect the vulnerable plaque before its rupture, but there were no ways to detect by the conventional methods except coronary angioscopy. Yellow plaque and thrombus are mostly observed at the culprit lesion by the coronary angioscopy, which suggests that vulnerable plaque is dark yellow. Coronary angioscopy may diagnose the high-risk group among patients with hyperlipidemia.

The validity of coronary angioscope was discussed in several clinical settings in this article. First of all, although smooth coronary surface was observed by coronary angiography after the intervention of chronic total occlusion, protrusion or thrombus observed by angioscope occupied the arterial lumen and closed the vessel lumen. After implantation of the stent, lumen was widely opened. Serial angioscopic observation revealed that the neointima became thick and non-transparent until 6 months and then became thin and transparent by 3 years after stent implantation. These findings suggested the validity of angioscope in coronary intervention. Second, coronary angioscope revealed the morphologic and pathologic characteristics of culprit lesions in patients with acute coronary syndrome. The thrombus was observed on the yellow plaque in the culprit lesion. The thrombus formed directly over the plaque was mainly white and red thrombus might be formed after the blood flow was disturbed by the white thrombus formed by the platelet aggregation. These findings imply the importance of anti-platelet therapy after acute coronary syndromes. Finally, the angioscope can detect the minimal changes of the plaque formation, progression and rupture, that is, the entire process of the atherosclerosis. The early detection of yellow plaque might be able to intervent mechanically or pharmacologically to prevent its rupture.

Invasive cardiovascular examination by coronary angioscopy and by using a Doppler guide wire, a pressure guide wire and intravascular ultrasound has extensively developed. A Doppler guide wire is used for measurement of flow velocity and evaluation of coronary blood flow. Previous studies demonstrated by assessing maximum coronary vasodilatory capacity that endothelium-dependent or independent vasodilation was impaired in hypertension and hypercholesterolemia or in syndrome X. Elevation of coronary vascular resistance during coronary microvascular spasm has been verified by using a Doppler wire. A pressure guide wire provides coronary transstenotic pressure and is available in calculating myocardial fractional flow reserve(FFRmyo). FFRmyo is an important parameter to assess the coronary functional stenosis that is culprit for myocardial ischemia. It is calculated from the ratio of the mean transstenotic pressure to the mean pressure proximal to the stenosis during maximum coronary hyperemia. The value of FFRmyo considered as necessary for coronary intervention is below 0.75. Intravascular ultrasound(IVUS) is applied as both a diagnostic tool and for intervention purpose. It enabled tissue characterization of the vascular wall as well as measurements of vascular diameter, vascular lumen area and plaque area. It also aided in optimal devise selection, decision of interventional endpoint and assessment of restenosis. IVUS promoted deployment of high-pressure stents to obtain a large post-procedural lumen area as well as abolition of anticoagulation in case of optimal stent deployment. Coronary angioscopy has been developed to investigate the pathogenesis of acute coronary syndrome, where disrupted yellow plaque and overlying thrombus play important roles. Angioscopy has also evidenced regression of intimal hyperplasia after coronary stenting.

Pulmonary artery thrombi and parietal lesions were observed in 13 patients (mean age 58 +/- 18 years) with acute pulmonary thromboembolism (n = 4) and chronic pulmonary thromboembolism (n = 9) using intravascular ultrasound and angioscopy at the time of right heart catheterization. Patients with acute pulmonary thromboembolism without underlying disease mainly had non-echogenic intraluminal mass, and good pulsatile vessel without intimal thickening. Angioscopy directly showed red thrombi with white fibrin coating, and no parietal lesions. Patients with chronic pulmonary thromboembolism could be classified into 3 groups: 1) Poor extensibility of the vessel wall and intimal thickening with non-echogenic thrombi on intravascular ultrasound, and relatively fresh parietal thrombi consisting of a mixture of red blood cell and fibrin, and spider web-like fibrin net on angioscopy (6 patients). 2) Crescent parietal thrombi and wall irregularity on intravascular ultrasound, and probably organized thrombi with a mixture of red and white surface on angioscopy (one patient). 3) Marked and echogenic intimal thickening and poor extensibility on intravascular ultrasound, and intimal surface irregularities and yellowish changes on angioscopy (one patient). All patients suffering acute deterioration in the chronic phase belonged to groups 1) or 2). Intravascular ultrasound and angioscopy are useful for characterizing the thrombi and related pulmonary artery lesions in patients with pulmonary thromboembolism. The pulmonary artery intima and thrombus differ between acute and chronic pulmonary thromboembolism.

Evaluation of the severity of coronary atherosclerosis by intracoronary imaging may be closely relevant with the prevention and treatment of acute coronary syndromes. Coronary angioscopy as one of the innovative methods of imaging and intravascular ultrasound makes the insight visualization of coronary vessel wall and histological recognition possible recently. Yellow plaques rich in lipid materials and covered by thin membrane are more often ruptured than white ones to cause acute coronary syndromes. In patients with unstable angina and acute myocardial infarction, the yellow plaques with intimal flaps and irregularities are frequently observed by angioscopy. Angioscopy is also the most powerful tool to detect intracoronary thrombus. In patients with acute myocardial infarction, thrombosis occludes vessel lumen totally, but it does not in the unstable angina cases. After thrombolytic therapy, the white thrombus is more often observed than the red one. Although angioscopy is superior to any other examination in diagnosing thrombosis, some complicated plaques are difficult to distinguish from thrombus. In addition to measurements of vascular dimension and plaque volume, histological diagnosis of plaque is being made by intravascular ultrasound. More precise evaluation of plaque histology may be a clue to predict the occurrence of acute coronary syndrome. Intravascular ultrasound is not so useful enough to diagnose thrombosis. In conclusion, the applications of intravascular imaging technologies, such as angioscopy and intravascular ultrasound, may play a critical role in the diagnosis and treatment of acute coronary syndromes.

The rupture of the unstable plaque and the thrombus formation caused the occlusion of the coronary artery and followed myocardial ischemia and/or myocardial necrosis, then resulted in clinical worse outcome. The reopen of the occluded artery is the most important things for the treatment of acute coronary syndrome, and there are usually two established ways to open the occluded artery. Thrombolysis and angioplasty are already established ways to reopen, however has some complications, that is, failure to reopen, reocclusion, and bleeding. Angioscopic observations reveal the mechanism underlying these complications and suggest that platelet rich white thrombus formation continues until a month after the onset and unstable yellow plaques exist until 18 months after the onset. The most problems for the treatment in today are the unaware of the mechanism of the occlusion. If the thrombus is the major mechanism for the occlusion, thrombolytic therapy must be chosen. If the plaque is the major occlusive mechanism, the angioplasty must be chosen. To reveal the mechanisms underlying the coronary artery occlusion, we will have to use the angioscope instead of coronary angiography. After we will be able to clarify the occlusive mechanism by angioscope, we will reduce the dosage of thrombolytic agents and resulted in the decrement of bleeding complications and reopen the coronary artery effectively without complications.

In recent years, laser angioplasty has been widely performed in the world. Since the 1980's we have investigated anigoplasy using Argon laser for patients with peripheral and coronary arterial diseases. This technique aims to open the obstructive arterial lumen. Based on the excellent results of experimental studies, this technique has been clinically applied. Laser angioplasty was carried out in 98 patients with stenotic or occlusive lesions of the peripheral arteries and 10 patients with anginal attack. Argon laser and an optical fiber delivery system with metal tip probe with thermal feedback control system were used for laser angioplasty. This procedure was performed under angioscopic and intravascular ultrasound imaging. Primary clinical success was achieved in 97 (82%) of all 119 lesions, that is, 53 (91%) of 58 in the stenotic lesions and 44 (72%) of 61 in the occlusive lesions. There were no complications required emergency operation. At 95 months of follow-up, the cumulative patency rate was 80% in 83 limbs with primary success. In the 43 stenoses and 40 occlusions, the cumulative patency rare were 87% and 71%, respectively. On the other hand, laser was simultaneously applied at the time of operation for 10 patients with anginal attack in addition to coronary artery bypass grafting. Thus, laser angioplasty was safe and effective to increase the initial success rate for the lesions that were difficult to treat by balloon anigoplasty. Angioscopy and intravascular ultrasound imaging were useful for the observation of the newly recanalized channel by lasing and selection of the recanalization technique, such as laser angioplasty, atherectomy and stent, according to the characterization of the lesions. These results suggested that laser angioplasty might be a useful treatment for patients with chronic peripheral arterial occlusion and improve the long-term patency rate by eliminating restenosis more than conventional balloon angioplasty.

Now, the standard operation for a case with AAE and AR is the composite graft replacement. In this case, an aortic valve sparing aortic root reconstruction, the so-called David's operation, and the intraoperative endoscopic study were performed. In the case of 68-year-old male with AAE and AR, the aortic valve was reimplanted in a tubular Dacron graft and coronary arteries were reconstructed with the Carrel patch technique. After the completion of the aortic root reconstruction, intraoperative endoscopic study revealed the disappearance of AR. Postoperative aortography revealed trivial AR and at present, seven months postoperatively, this patient have been uneventful. In this paper, we discuss the merits and demerits of the David's operation and the effectiveness of intraoperative endoscopic study for the aortic valve sparing operation.

A 45-year-old man was admitted with the diagnosis of acute inferior myocardial infarction. After successful thrombolytic therapy, coronary angiography showed TIMI grade 3 flow with the filling defect and haziness on the infarct-related coronary segment. Repeat coronary angiography and coronary angioscopy were performed on the 28th hospital day. Coronary angiography showed 50% stenosis of the luminal diameter of the right coronary artery. Coronary angioscopy showed a white plaque with ruptured cap which occupied one third of the circumferential coronary artery. The torn ends of the cap were longitudinal, and projected into the lumen during the cardiac cycle. Plaque rupture and thrombus formation are important in the pathogenesis of acute coronary syndromes, although the mechanism of plaque rupture is still controversial. The present angioscopic findings seem to support the concept that circumferential tension or mechanical stretch from part of the coronary artery causes the longitudinal fissure at the weakened site of the plaque cap.

An urgent pulmonary embolectomy on a patient under intraoperative angioscopy for the treatment of massive pulmonary embolism was performed and successfully saved the patient. The case was a 19-year-old man who had been bedridden over along period of time. He developed pulmonary embolism immediately after the initiation of walking rehabilitation. Although anticoagulation therapy was immediately carried out, hemodynamics deteriorated, and as a result, it became necessary to treat this patient with the urgent surgical procedure. Under extracorporeal circulation with the clamping of the aorta, the pulmonary artery was opened. Following embolectomy for the left pulmonary artery, the right pulmonary artery, where the presence of clots had not been confirmed with the naked eye, was inspected using an flexible fiberoptic choledochoscope 4.9 mm in diameter. Consequently, amount of clots were removed using forceps or an aspirating tube. The patient recovered from hypoxemia after surgery. The use of intraoperative angioscopy in the pulmonary artery proved to be very useful to examine the presence of emboli up to tertiary branches of pulmonary artery.

The anti-thrombogenicity of argatroban and clopidogrel and the influence of these two agents on coagulation and fibrinolysis were investigated. After the infrarenal abdominal aorta of 21 dogs was replaced with a knitted Dacron prosthesis of 5 mm in internal diameter, the inner capsule of the graft was evaluated by angioscopy and angiography immediately and 1 week, 2 weeks and 1 month after surgery. The graft patency rate in group I (untreated group, n = 8), group II (argatroban group, postoperative infusion of 1 microgram/kg/min for 2 weeks, n = 7) and group III (clopidogrel group, postoperative oral administration of 12.5 mg/kg/day for 1 month, n = 6) was respectively 75%, 86% and 100% after 1 week; 75%, 86% and 100% after 2 weeks; and 50%, 71% and 100% after 1 month. The mean maximum stenosis measured by angioscopy was 31% in group I, 5% in group II and 4% in group III after 1 week; 52%, 23% and 13% after 2 weeks; and 61%, 40% and 9% after 1 month. An increase in thrombin antithrombin III complex (TAT) due to thrombus was observed in group I, but this was prevented in the treated groups. These results suggest that argatroban and clopidogrel are useful anti-thrombogenic agents for obtaining a thin inner capsule after graft implantation, especially in small caliber grafts.

During the progression of early atherosclerotic lesions, atherosclerotic plaque rupture, with intraluminal thrombosis superimposed, which is one of the principle mechanisms of evolving atherosclerosis, may lead to thrombotic occlusion and ischemic coronary syndrome. Pathologic studies suggest that plaque rupture and overlying thrombi, which are dynamic and repetitive may frequently occur. In most cases, healed ruptures and incorporation of thrombi produce plaque progression without manifestation of clinical symptoms. However, acute mural occlusive thrombi, overlying plaque ruptures, cause unstable angina and acute myocardial infarction. The different pathogenesis between unstable angina and acute myocardial infarction might depend on the composition and stability of the thrombus resulting from the degree of vessel injury and blood flow. Soft lipid-rich plaques appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages in the plaque may also facilitate plaque rupture by releasing proteases.

Angioscopic observation of the peripheral pulmonary arteries was performed in 14 patients with chronic lung diseases (male 9/female 5, age 70.8 +/- 8.3 years, pulmonary tuberculosis sequelae 6, chronic bronchitis 4, chronic pulmonary emphysema 3, pneumoconiosis 1). The blood flow was stopped by the inflated balloon of a 7F guiding catheter, and then the peripheral pulmonary arteries (inner diameter 1.0-4.5 mm) were observed with a fiberoptic catheter (outer diameter 0.7 mm). In 10 out of 14 patients abnormal findings were obtained, which included redness, erosion, ulceration of the vascular wall, thrombus, fibrous tissue, and occlusion of the lumen. The incidence of abnormal findings tended to be higher in chronic bronchitis and pulmonary tuberculosis sequelae than in chronic pulmonary emphysema. These results suggest that 1) various changes including "vasculitis" and thrombus exist in the peripheral pulmonary arteries of chronic lung diseases, and 2) that angioscopy may provide the detailed information about both the vascular wall and the lumen which cannot be obtained by pulmonary angiography.