Takayoshi Adachi

Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study

OBJECTIVES To test our hypothesis that the development of vulnerable plaques is not limited to the culprit lesions, but is a pan-coronary process, we directly observed all three major coronary arteries by angioscopy and evaluated the prevalence of yellow plaques in patients with myocardial infarction (MI). BACKGROUND Although pathologic studies have suggested that the disruption of atheromatous plaque plays a major role in the development of acute MI, the prevalence of yellow plaques in the whole coronary arteries of patients with MI has not been clarified. METHODS Thirty-two patients undergoing follow-up catheterization one month after the onset of MI were prospectively and consecutively enrolled in this study. The prevalence of yellow plaques and thrombus in the major coronary arteries was successfully evaluated in 20 patients (58 coronary arteries, 21 culprit lesions) by coronary angioscopy. The diameter stenosis (DS) of the culprit lesions and the maximal diameter stenosis (maxDS) of nonculprit segments were angiographically measured for each coronary artery. RESULTS The DS of the culprit lesions and maxDS were 27 +/- 17% and 19 +/- 13%, respectively. Yellow plaques and thrombus were detected in 19 (90%) and 17 (81%) of 21 culprit lesions, respectively. Yellow plaques were equally prevalent in the infarct-related and non-infarct-related coronary arteries (3.7 +/- 1.6 vs. 3.4 +/- 1.8 plaques/artery). However, thrombus was only detected in the nonculprit segments of one (2%) coronary artery. CONCLUSIONS In patients with MI, all three major coronary arteries are widely diseased and have multiple yellow though nondisrupted plaques. Acute MI may represent the pan-coronary process of vulnerable plaque development.

Remodeling of In-Stent Neointima, Which Became Thinner and Transparent Over 3 Years Serial Angiographic and Angioscopic Follow-up

BACKGROUND Recently, it has been reported that the luminal diameter shows phasic changes after stenting: the progression of luminal narrowing followed by its regression. To elucidate the mechanisms involved in the phasic changes in luminal diameter after stenting, we examined the changes in neointimal thickness and the appearance of neointima by a series of angiographic and angioscopic observations for 3 years after stent implantation. METHODS AND RESULTS In 12 patients who received a Wiktor coronary stent, serial angiographic and angioscopic examinations were performed immediately, 2 to 4 weeks, 3 months, 6 months, and 3 years after the stenting without repetition of angioplasty. Neointimal thickness was determined by angiography as the difference between stent and luminal diameters. The angioscopic appearance of neointima over the stent was classified as transparent or nontransparent according to the visibility of the majority of the stent. Neointimal thickness increased significantly at 3 months (0.75+/-0.32 mm) without further changes at 6 months (0.74+/-0.32 mm). Thereafter, however, it decreased significantly over 3 years (0.51+/-0.26 mm). The angioscopic appearance was classified as transparent in 8 patients (100) immediately after stenting, 6 patients (100%) at 2 to 4 weeks, 2 patients (17%) at 3 months, 2 patients (20%) at 6 months, and 7 patients (58%) at 3 years. CONCLUSIONS The neointima became thick and nontransparent until 6 months and then became thin and transparent by 3 years. We conclude that neointimal remodeling exists after stenting and plays a major role in the alteration of coronary luminal diameter after stenting.

Collateral channels that develop after an acute myocardial infarction prevent subsequent left ventricular dilation

OBJECTIVES We sought to evaluate the effect of collateral channels that develop late after a first anterior myocardial infarction on left ventricular dilation and function. BACKGROUND Collateral channels in an infarct-related artery may develop long after occlusion of the artery. Well visualized collateral channels that appear immediately after a myocardial infarction reduce infarct size and preserve left ventricular function. However, the functional significance of collateral channels that develop late after myocardial infarction has not been evaluated in terms of left ventricular function. METHODS We studied 21 patients with a first anterior myocardial infarction and an infarct-related artery that remained totally occluded after reperfusion therapy and did not reopen within 1 month of infarction. No collateral channels were observed during the acute period. Patients were classified into two groups according to the extend of collateral formation 1 month after infarction: group C, patients with well developed collateral channels (n = 11), and group NC, patients with absent or poorly developed collateral channels (n = 10). Infarct size was determined by peak creatine kinase activity and thallium-201 single-photon emission computed tomography. Global and regional left ventricular function and left ventricular volumes were assessed by left ventriculography. These measurements were identical in both groups 1 month after infarction. Left ventricular function was reevaluated after 2.12 +/- 0.79 years (mean +/- SD). RESULTS There were no significant changes in global and regional left ventricular function between the two groups during the long-term follow-up period. However, the end-diastolic volume index of group NC increased from 71 +/- 14 to 85 +/- 19 ml/m2, whereas that of group C decreased from 64 +/- 18 to 59 +/- 12 ml/m2. This important change during the long-term follow-up period resulted in a significant difference (p = 0.0006) in the end-diastolic volume index between the groups 2 years after onset (p = 0.002), whereas 1 month after infarction the difference was not significant (p = 0.36). A similar pattern was observed for the end-systolic volume index (group C: 38 +/- 16 to 35 +/- 14 ml/m2; group NC: 45 +/- 12 to 58 +/- 18 ml/m2, p = 0.018). The power of the tests to detect the observed differences showing nonsignificant results ranged from 0.05 to 0.38, whereas the power of the tests indicating a significant difference in end-diastolic and end-systolic volume indexes was >0.88. CONCLUSIONS Collateral channels that develop after a myocardial infarction do not reduce the infarct size or prevent left ventricular dilation within 1 month of infarction. In contrast, such collateral channels prevent subsequent ventricular dilation and the deterioration of left ventricular function over 2 years. However, our results may have been biased because of the small number of patients.

Different Mechanisms of Ischemic Adaptation to Repeated Coronary Occlusion in Patients With and Without Recruitable Collateral Circulation

OBJECTIVES The aim of this study was to investigate the interaction between ischemic preconditioning (IP) and collateral recruitment (CR) during ischemic adaptation in patients. BACKGROUND The mechanism of ischemic adaptation still remains controversial in humans. METHODS The clinical, electrocardiographic, hemodynamic and echocardiographic responses to three 150-s occlusions of the left anterior descending coronary artery were assessed in relation to CR in 18 patients with effort angina undergoing elective percutaneous transluminal coronary angioplasty. RESULTS During the first occlusion, recruitable collateral circulation (RCC) to the occluded myocardium was detected by myocardial contrast echocardiography in 6 patients (Group C) and was not seen in 12 (Group N). In Group N, all patients manifested signs of severe ischemia during each inflation. However, their symptoms and ST segment shift significantly decreased from the first to the third occlusions, suggesting the occurrence of IP. The elevation of mean pulmonary artery pressure and deterioration of anterior wall motion were comparable between the first and the third occlusions in Group N. In contrast, myocardial ischemia was significantly less marked during occlusion in Group C than in Group N, and no preconditioning effect was observed. The extent of RCC did not differ between the first and the third occlusions in each group. CONCLUSIONS Both IP and CR may play independent roles in ischemic adaptation in humans. With RCC, myocardial ischemia was greatly reduced. Without RCC, preconditioning clinically and electrocardiographically lessened myocardial ischemia but failed to preserve left ventricular function.

Comparison of myocardial contrast echocardiography and coronary angiography for assessing the acute protective effects of collateral recruitment during occlusion of the left anterior descending coronary artery at the time of elective angioplasty

To assess the immediate change in collateral flow distribution within the occluded myocardium and the acute protective effects on myocardial ischemia after coronary occlusion, myocardial contrast echocardiography (MCE) was performed in 15 patients with normal left ventricular function undergoing elective coronary angioplasty of the left anterior descending artery, and the results were compared with those obtained from coronary angiography (CA). The sonicated or nonsonicated contrast material was injected into the right coronary artery before and during coronary occlusion and collaterals were graded on a 4-point scale (none = 0 to good = 3). Development of subjective anginal symptoms, ST-segment shift and wall motion abnormality during coronary occlusion were graded on a 4-point scale (none = 0 to severe = 3). Both MCE and CA detected a significant development in collateral flow during coronary occlusion. There was no significant correlation between MCE and CA collateral grades before or during coronary occlusion. The collateral flow assessed with MCE was inversely but significantly correlated with development of subjective anginal symptoms (r(s) = -0.70, p <0.01), ST-segment shift (r(s) = -0.78, p < 0.005) or wall motion abnormality (r(s) = -0.91, p < 0.001) during coronary occlusion. In contrast, the angiographic collateral flow was not correlated with development of anginal symptoms (r(s) = -0.46, p = 0.10), ST-segment shift (r(s) = -0.41, p = 0.14), or wall motion abnormality (r(s) = -0.26, p = 0.35). The present study suggested that the acute protective effects of coronary collaterals during coronary occlusion were closely associated with myocardial perfusion rather than the angiographic epicardial collateral vessel filling, and thus MCE was useful in assessing the acute protective effects of coronary collaterals during coronary occlusion.

Angiographic and clinical outcome of a new self‐expanding intracoronary stent (RADIUS): Results from multicenter experience in Japan

The RADIUS coronary stent featuring a multisegmented slotted tube design and self‐expanding nitinol delivery system has a high radial force and flexibility, uniform expansion, and contours to the shape of the vessel. Successful stent deployment was achieved in 104 stable angina patients (106 lesions; 44% LAD, 19% circumflex, and 37% RCA). Mean minimal lumen diameter (MLD) increased from 0.77 ± 0.46 mm to 2.88 ± 0.61 mm and mean percent diameter stenosis (% DS) decreased from 73 ± 14% to 6 ± 13% immediately after the procedure. At 6‐month follow‐up, two patients (2%) underwent urgent target revascularization, and cerebral bleeding occurred in one patient (1%). Angiographic follow‐up was performed in 94 lesions (89%) and mean MLD and mean % DS were 2.08 ± 0.92 mm and 30% ± 24%, respectively. Stent restenosis (>50% diameter stenosis at follow‐up) was observed in 16 (17%) of all lesions. The high success rate for stent deployment, low incidence of major adverse cardiac event, and lower restenosis rate after stent implantation indicate that the RADIUS stent is useful for coronary intervention. Cathet. Cardiovasc. Intervent. 49:401–407, 2000.

Is the Presence of Hyperlipidemia Associated with Impairment of Endothelium-Dependent Neointimal Relaxation After Percutaneous Transluminal Coronary Angioplasty?

SummaryTo determine whether hyperlipidemia affects the endothelium-dependent vasomotor response along the dilated vessel after percutaneous transluminal coronary angioplasty (PTCA), we evaluated 32 patients with one-vessel disease, 3–6 months after successful PTCA without restenosis. Fourteen patients had mild stenotic lesions not subjected to PTCA (non-PTCA sites) in addition to the PTCA sites. Vessel diameter changes at 32 PTCA and 36 non-PTCA sites were assessed by quantitative angiography, before and after intracoronary injection of acetylcholine (20µg to the right and 50µg to the left coronary artery) and of nitroglycerin (0.1–0.3mg). The acetylcholine response ranged from 46% (dilation) to −100% (constriction). All coronary arteries were dilated in response to nitroglycerin, which suggested preservation of the function of vascular smooth muscle, and the presence of an abnormality in endothelial function in those patients with a constrictor response to acetylcholine. There was a negative correlation between the acetylcholine response and the serum total cholesterol level at PTCA sites (r = −0.37;P = 0.038) and at non-PTCA sites (r = −0.46;P = 0.005). These findings indicate that hyperlipidemia is associated with a loss of endothelium-dependent vasodilation, not only at non-PTCA but also at PTCA sites, at which restoration of endothelial function might have occurred. They also suggest that hyperlipidemia may be related to the functional state of the regenerated endothelium at sites where PTCA had been previously performed.

Comparison of time of reperfusion during anterior wall acute myocardial infarction to left ventricular volume one month and 20 months later.

We studied 95 patients with a first anterior wall acute myocardial infarction who received successful reperfusion within 72 hours after the onset. The patients were divided into 4 groups based on the time required to achieve reperfusion; <3 hours (n = 23), 3 to 6 hours (n = 42), 6 to 24 hours (n = 17), and >24 to 72 hours (n = 13). The infarct size, as evaluated by thallium-201 single-photon emission computed tomography, at 1 month after the infarct was significantly larger (p <0.05) in >24 to 72 hours (1,593 +/- 652 U) than that in <3 hours (749 +/- 650 U), but was not significantly different from that at 3 to 6 hours (1,353 +/- 770 U) or 6 to 24 hours (1,371 +/- 561 U). The end-diastolic volume index at 1 month did not differ among the 4 groups. However, the end-diastolic volume index during the follow-up period (20 +/- 8 months) in >24 to 72 hours (93 +/- 23 ml/m(2)) was significantly larger than that in the other 3 groups (<3 hours [65 +/- 21 ml/m(2)], 3 to 6 hours [65 +/- 22 ml/m(2)], and 6 to 24 hours [70 +/- 25 ml/m(2)]). Similar findings were observed in end-systolic volume index. In conclusion, although infarct size reduction was not observed by late reperfusion, left ventricular volumes at 1 month were comparable among patients with successful reperfusion within 3 and up to >24 hours. Left ventricular volumes 2 years after acute myocardial infarction were significantly larger in patients who did not under reperfusion for >24 hours.

Ultrasonic Integrated Backscatter Discloses Intramyocardial Hemorrhage in Patients with Acute Myocardial Infarction

Background: It has been reported that intramyocardial hemorrhage (IH) can be detected by magnetic resonance imaging (MRI) and IH correlates with the poor prognosis of acute myocardial infarction (AMI). We examined whether integrated backscatter (IBS) can disclose IH in patients with AMI. We recorded IBS images in 34 patients with AMI who underwent coronary angioplasty within 12 hours of symptom onset. Methods: We measured calibrated IBS (C‐IB) and cyclic variation (CV) in the center of the risk area on the third day after reperfusion. C‐IB was calculated as: average IBS value of risk area − average IBS value of intraventricular blood. MRI was performed within 3 days after reperfusion. Regional wall motion score index (RWMSI) was calculated as follows: sum of scores (0∼4) in risk area/number of segments of risk area. We evaluated left ventricular function using RWMSI shortly and one month after reperfusion. Results: RWMSI in the IH group (12 cases) was significantly higher than in the non‐IH group (2.3±0.5 vs. 1.8±0.6: P<0.01) one month later, while RWMSI in both groups was almost the same shortly after reperfusion. The IH group showed a significantly higher value of C‐IB than the non‐IH group (18.6±2.0 vs. 16.0±1.4: P<0.01), while there were no significant differences in CV values between two groups. Using 17 as a cutoff value of C‐IB, C‐IB can detect IH with 92% sensitivity and 91% specificity. Using both CV and C‐IB, however, IH can be detected more specifically. Conclusion: Ultrasonic IBS, especially C‐IB, discloses intramyocardial hemorrhage in patients with reperfused AMI.

Effect of successful angioplasty following thrombolysis on infarct size and left ventricular function.

The role of the angioplasty following thrombolysis in acute myocardial infarction has been discussed in several studies, however the effect of successful angioplasty on infarct size and left ventricular function has not been properly evaluated. Successful reperfusion was achieved in 79 out of 104 patients with primary anterior acute myocardial infarction. These patients were classified as follows, according to the type of intervention during the acute phase: 50 patients in which thrombolysis was successful (the thrombolysis group); 12 patients who underwent successful immediate angioplasty following successful thrombolysis (the immediate angioplasty group); and 17 patients in which rescue angioplasty was successful (the rescue angioplasty group). The 25 patients whose infarct-related vessels were not reperfused after intervention were classified as the non-reperfused group. Infarct size, evaluated as defect volume by T1-201 SPECT, 1 month after the onset, was 840 +/- 154 units (mean +/- S.D.) in the immediate angioplasty group and was similar to that in the thrombolysis group (948 +/- 88 units), but significantly smaller than in the non-reperfused group (1759 +/- 108 units). There were no significant differences in left ventricular function in the immediate angioplasty group and the thrombolysis group. Successful rescue angioplasty did not have any beneficial effect on left ventricular functions or infarct size, when compared with the failed thrombolytic group (1105 +/- 169 units vs. 1617 +/- 169 units). End-diastolic volume (52 +/- 3 ml/m2) in the successful rescue angioplasty group, however, was significantly smaller than in the failed thrombolysis group (67 +/- 3 ml/m2).(ABSTRACT TRUNCATED AT 250 WORDS)