Step-by-step typing for the accurate diagnosis of concurrent light chain and transthyretin cardiac amyloidosis.

While 99m Tc-pyrophosphate scintigraphy is clearly useful in diagnosing transthyretin amyloid cardiomyopathy (ATTR-CM), it is necessary to know the pitfalls of this test for proper use. We present a rare case of concurrent ATTR-CM and amyloid light chain (AL) cardiomyopathy. The patient showed congestive heart failure with left ventricular hypertrophy. 99m Tc-pyrophosphate scintigraphy revealed abnormal cardiac uptake of Grade 3, a typical feature for ATTR-CM. However, the patient showed renal impairment with proteinuria and the presence of monoclonal gammopathy, which rather suggested AL amyloidosis. Endomyocardial biopsy, immunohistochemistry, and proteomic analysis by laser microdissection with liquid chromatography-coupled tandem mass spectrometry were performed, which finally confirmed both ATTR-CM and AL cardiomyopathy. This case implicates the importance of combining examinations and precisely interpreting the results to diagnose cardiac amyloidosis accurately.

Difference in neointimal proliferation between ruptured and non-ruptured segments after bare metal stent implantation.

The difference in neointimal stent coverage (NSC) between ruptured segments and adjacent nonruptured segments in infarct-related lesions (IRL) of acute myocardial infarction after bare metal stent (BMS) implantation was evaluated using coronary angioscopy. Serial angioscopic observations were performed for 19 IRLs immediately after the implantation of a BMS and at 1-month and 6-month follow-up. Stented segments were divided into the ruptured segment and the nonruptured segment based on the presence of a thrombus. The grade of NSC was divided into 0 = complete exposure, 1 = partial coverage, or 2 = complete coverage. The grade of plaque color was classified semiquantitatively as 0 = white, 1 = light yellow, or 2 = intense yellow. The existence of a thrombus was also determined. The grade of NSC in the ruptured segment was lower than that of the nonruptured segment at each follow-up. The grade of plaque color at the 1-month follow-up was higher in the ruptured segment than in the nonruptured segment. At 6 months, the grade of plaque color was similar between the ruptured and nonruptured segments. In all cases, thrombi existed in the ruptured segments immediately after stenting. Although thrombi still remained frequently at 1-month, most had disappeared at the 6-month follow-up. Neointimal proliferation of the ruptured segment in IRL advanced slowly in comparison to the adjacent nonruptured segment. The presence of an atherosclerotic yellow plaque and a thrombus may affect the delayed neointimal coverage after BMS implantation.

Extended follow-up by serial angioscopic observation for bare-metal stents in native coronary arteries: from healing response to atherosclerotic transformation of neointima.

BACKGROUND: Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated. METHODS AND RESULTS: Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and >or=4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4+/-17.3% versus 3.6+/-4.2%, respectively; P=0.011). CONCLUSIONS: This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.

Angioscopic differences in neointimal coverage and in persistence of thrombus between sirolimus-eluting stents and bare metal stents after a 6-month implantation.

AIMS: The neointimal coverage and intracoronary thrombi within stented segments at 6 months after implantation between sirolimus-eluting stents (SESs) and bare metal stents (BMSs) were compared by direct visualization using angioscopy. METHODS AND RESULTS: Forty-six patients (36 stable angina and 10 acute coronary syndrome) were treated with 33 SESs and 33 BMSs. Immediately after and 6 months after stenting, each of the stented segments, edge body, and overlapping segment were observed by angioscopy and the grade of neointimal coverage over the stents was classified as 0: absent neointima, 1: visible struts through thin neointima, or 2: invisible struts. The existence of thrombi was also evaluated. The average grade of the neointimal coverage at 6 months follow-up was lower in the SES than that in the BMS (edge: 1.4+/-0.7 vs. 1.9+/-0.2, body: 1.0+/-0.5 vs. 1.8+/-0.5, overlapping segment: 0.6+/-0.7 vs. 1.8+/-0.5; P<0.0001, P<0.0001, P=0.0069, respectively). The frequency of persistence of thrombus was significantly higher in the SESs than that in the BMSs (86 vs. 29%, respectively; P=0.031). CONCLUSION: The present study suggested a delayed neointimal stent coverage and slower thrombus disappearance process in the SESs in comparison to the BMSs.

Significance of plaque disruption sites in acute coronary syndrome.

Coronary plaque disruption and subsequent thrombosis occur in both unstable angina (UA) and acute myocardial infarction (AMI). However, it is unclear why UA and AMI have different clinical courses. The purpose of this angiographic study was to examine whether the longitudinal plaque disruption site is a factor that can be used to distinguish these two conditions. Seventy-two patients with AMI or UA in whom ischemia- or infarct-related arteries and plaque disruption sites could be determined were enrolled. The plaque disruption sites were classified as upstream type or downstream type. The upstream type and downstream type were defined as plaque rupture site located proximal and distal, respectively, to the maximum stenosis on angiography. The frequency of the upstream type was significantly higher in patients with AMI (60.0%) than in patients with UA (18.5%). On the other hand, the frequency of the downstream type was higher in patients with UA (81.5%) in patients with AMI (40.0%; p<0.01). The longitudinal plaque disruption site may thus be a factor that can be used to distinguish these two diseases.

Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions.

OBJECTIVES: Changes of ruptured plaques in nonculprit lesions were evaluated using coronary angioscopy. BACKGROUND: The concept of multiple coronary plaque ruptures has been established. However, no detailed follow-up studies of ruptured plaques in nonculprit lesions have yet been reported. METHODS: Forty-eight thrombi in 50 ruptured coronary plaques in nonculprit lesions in 30 patients were identified by angioscopy. The percent diameter stenosis (%DS) at the target plaques on quantitative coronary angiographic analysis and the serum C-reactive protein (CRP) level were measured. RESULTS: The mean angioscopic follow-up period was 13 +/- 9 months. Thirty-five superimposed thrombi still remained at follow-up, and the predominant thrombus color changed from red (56%) at baseline to pinkish-white (83%) at follow-up. The healing rate increased according to the angioscopic follow-up period (23% at 12 months, p = 0.044). The %DS at the healed plaque increased from baseline to follow-up (12.3 +/- 5.8% vs. 22.7 +/- 11.6%, respectively; p = 0.0004). The serum CRP level in patients with healed plaques (n = 10) was lower than that in those without healed plaques (n = 19; 0.07 +/- 0.03 mg/dl vs. 0.15 +/- 0.11 mg/dl, respectively; p = 0.007). CONCLUSIONS: The present study demonstrated that: 1) ruptured plaques in nonculprit lesions tend to heal slowly with a progression of angiographic stenosis; and 2) the serum CRP level might reflect the disease activity of the plaque ruptures.

Effects of green tea intake on the development of coronary artery disease.

BACKGROUND: Green tea, a popular beverage in Japan, contains many polyphenolic antioxidants, which might prevent atherosclerosis. This study was designed to determine whether the consumption of green tea is proportionately associated with a decreased incidence of coronary artery disease (CAD) and the cardiovascular and cerebrovascular prognosis. METHODS AND RESULTS: The study group comprised 203 patients who underwent coronary angiography (109 patients with significant coronary stenosis and 94 patients without). Predictors for CAD were analyzed and the patients' cardiovascular and cerebrovascular events were followed. Green tea consumption was significantly higher in patients without CAD than in those with CAD (5.9+/-0.5 vs 3.5+/-0.3 cups/day; p<0.001). An inverse relationship between the intake of green tea and the incidence of CAD was observed (p<0.001). The green tea intake per day was an independent predictor for CAD based on a multivariate logistic regression analysis (odds ratio: 0.84 and 95% confidence interval: 0.76-0.91). In contrast, the green tea intake was not a predictor of cardiovascular and cerebrovascular events based on the Cox proportional hazard model. CONCLUSIONS: Green tea consumption was associated with a lower incidence of CAD in the present study population in Japan. Therefore, the more green tea patients consume, the less likely they are to have CAD.

Elevated troponin T levels and lesion characteristics in non-ST-elevation acute coronary syndromes.

BACKGROUND: Elevated troponin T levels in non-ST-elevation acute coronary syndromes (NSTE-ACS) have been shown to predict an adverse outcome. Furthermore, it has been reported that troponin T could help improve the effectiveness of such new antithrombotic drugs as platelet GPIIb/IIIa antagonists and low-molecular-weight heparins. We hypothesized that such elevated troponin T levels in NSTE-ACS indicate the presence of thrombus at culprit lesions, and this hypothesis was verified through the use of coronary angioscopy. METHODS AND RESULTS: We studied 57 consecutive patients with NSTE-ACS who underwent preinterventional angioscopy. Before catheterization, we obtained blood samples to determine troponin positivity, and the patients were then classified as either troponin-positive or troponin-negative groups (diagnostic threshold, 0.1 ng/mL). Using angioscopy at the culprit lesions, we examined the presence of coronary thrombus, yellow plaque, and complex plaque. Moreover, we compared the preinterventional angiographic parameters (thrombus and complexity of the culprit lesion, and TIMI flow) between the two groups. Twenty-two patients were troponin-positive and 35 patients were troponin-negative. Univariate analyses indicated that the TIMI flow and the incidence of coronary thrombus detected with angioscopy correlate with the elevated troponin T levels. A multivariate logistic regression analysis showed the presence of coronary thrombus detected with angioscopy to be the only independent factor associated with elevated troponin T levels in patients with NSTE-ACS (odds ratio, 22.1; 95% CI, 2.59 to 188.42; P=0.0046). CONCLUSIONS: Using angioscopy, the elevated troponin T levels in NSTE-ACS were confirmed to be strongly associated with the presence of coronary thrombus.

Effects of statins on circulating oxidized low-density lipoprotein in patients with hypercholesterolemia.

UNLABELLED: Recently, it has been reported that circulating oxidized low-density lipoprotein (Ox-LDL) might be a pivotal indicator for coronary artery disease and the severity of acute coronary syndromes. The purpose of this study was to investigate the effects of statins on Ox-LDL in patients with hypercholesterolemia. Sixteen patients with hypercholesterolemia were randomly assigned to 2 groups, one received 10 mg of pravastatin (n = 8) and the other received 20 mg of fluvastatin (n = 8). The plasma level of Ox-LDL was measured using a newly developed sandwich enzyme-linked immunosorbent assay (ELISA) method. There were no differences between the two groups in Ox-LDL, total cholesterol (TC), or LDL cholesterol (LDL-C) at the baseline. The reduction in Ox-LDL in the fluvastatin group was significantly higher than that in the pravastatin group (47.5% versus 25.2%, P = 0.033). The reductions in TC and LDL-C did not differ between the two groups. CONCLUSION: The present study has shown for the first time that the level of circulating Ox-LDL was significantly decreased by treatment with statins. In addition, the lowering effect of statins on the circulating Ox-LDL was independent of their lipid-lowering effect. Fluvastatin was more effective than pravastatin with regard to decreasing the circulating Ox-LDL.

Morphologic changes in infarct-related plaque after coronary stent placement: a serial angioscopy study.

OBJECTIVES: The aim of this study was to investigate the morphologic changes in infarct-related lesions after stenting in acute or recent myocardial infarction (MI) with coronary angioscopy. BACKGROUND: There is no information on the serial morphologic changes, which occur after stenting, and the time course of neointimal coverage of stents for disrupted unstable plaques. METHODS: Forty-three patients with MI within seven days of onset were examined. Angioscopy was serially performed for the infarct-related lesions at baseline (n = 43), after balloon angioplasty (n = 35), and after stenting following balloon angioplasty (n = 39) and at one (n = 36) and six months (n = 30) after stenting. RESULTS: At baseline, most of the lesions had complex morphology, yellow plaque color, and protruding thrombus (96%, 96%, and 74%, respectively). Although balloon angioplasty reduced the protruding thrombus, it remained in 37%, and an intimal flap was observed in 89% of the lesions. After stenting, the protruding thrombus and intimal flap disappeared, with an increased luminal size obtained in all lesions. At one-month follow-up, an irregular and yellow surface, along with a lining thrombus, was still observed, with partial neointimal stent coverage in most of the lesions. At six-month follow-up, the neointima was found to have sufficiently formed over the stent. The plaque shape and color were almost all classified as smooth (97%) and white (93%). CONCLUSIONS: These results suggest that a stent not only compressed and covered a disrupted plaque with a protruding thrombus and intimal flap, leading to a wide vessel lumen, but also helped to seal the unstable plaque through neointimal proliferation.

Prognostic significance of elevated creatine kinase MB after coronary bypass surgery and after an acute coronary syndrome: results from the GUARDIAN trial.

OBJECTIVE: To determine if the correlation between magnitude of creatine kinase-myocardial band release after coronary artery bypass surgery and 6-month mortality is comparable to that of patients admitted with an acute coronary syndrome. METHODS: The GUARDIAN trial tested the efficacy of cariporide, an Na+/H+ exchange inhibitor, on reduction of myocardial ischemia or death in high-risk patients. We compared 6-month survival in a cohort of 2332 GUARDIAN patients scheduled for coronary artery bypass surgery at entry with 4233 acute coronary syndrome patients stratified by level of creatine kinase-myocardial band release. Cumulative 6-month survival by creatine kinase-myocardial band categories was performed using life table analysis, adjusting for variables known to impact prognosis using Cox regression. RESULTS: The 6-month mortality rates for coronary artery bypass surgery patients with peak creatine kinase-myocardial band ratios of <1, > or =1 and <5, > or =5 and <10, and > or =10 upper limits of normal (ULN) were 5.8, 2.8, 5.9, and 12.0%, respectively (P <.0001). The 6-month mortality rates for acute coronary syndrome patients with peak creatine kinase-myocardial band ratios of <1, > or =1 and <5, > or =5 and <10, and > or =10 ULN were 6.3, 9.8, 10.0, and 12.3%, respectively (P <.0001). Patients with coronary artery bypass surgery or acute coronary syndrome had similar adjusted 6-month survival estimates at normal creatine kinase-myocardial band levels and when the creatine kinase-myocardial band level was > or =10 ULN. Patients with coronary artery bypass surgery had significantly better survival at intermediate enzyme levels (> or =1 and <10 ULN; P <.001). CONCLUSIONS: Modest elevations of creatine kinase-myocardial band release (> or =1 and <10 ULN) after coronary artery bypass surgery are not associated with adverse 6-month survival, in contrast to that seen in acute coronary syndrome patients. Routine creatine kinase-myocardial band sampling should be considered in all higher-risk patients undergoing coronary artery bypass surgery procedures to identify the sizable cohort of patients with creatine kinase-myocardial band release > or =10 ULN; these patients may benefit from postoperative angiotensin-converting enzyme inhibitor and beta-blocker therapy. Newer cardioprotective agents that reduce the number of patients with marked creatine kinase-myocardial band release are currently being tested in large randomized controlled clinical trials.

Visualized plaque debris as a cause of distal embolization after percutaneous coronary intervention in patient with unstable angina.

Procedural complications of percutaneous transluminal coronary angioplasty for unstable angina are higher than for stable angina. We report a case in which coronary angioscopy proved the dislodgment of a large plaque fragment after Cutting Balloon angioplasty and confirmed our suspicion that plaque fragmentation can cause distal embolization.