Prognostic value of tissue-tracking mitral annular displacement by speckle-tracking echocardiography in asymptomatic aortic stenosis patients with preserved left ventricular ejection fraction.

BACKGROUND: Tissue-tracking mitral annular displacement (TMAD) by speckle-tracking echocardiography provides rapid and simple assessment of left ventricular (LV) longitudinal deformation. The purpose of this study was to evaluate the value of TMAD for the assessment of LV longitudinal deformation in patients with severe AS and preserved LV ejection fraction (LVEF). METHODS: We studied 44 patients with severe AS preserved and LVEF in whom TMAD was assessed. Using TMAD analysis software, the base-to-apex displacement of automatically defined mid-point of mitral annular line in four-chamber view was quickly assessed, and the percentage of its displacement to LV length at end-diastole (%TMAD) was calculated. We investigated the association between %TMAD and the cardiac events including appearance of symptom (dyspnea on exertion and hospitalization due to heart failure), decreased LVEF (< 50%), and cardiac death. RESULTS: During follow-up, the cardiac events developed in 16 (36%) of 44 patients. %TMAD was significantly impaired in patients with the cardiac events compared with those without the cardiac events (9.6 ± 1.9 vs 12.1 ± 2.6, p = 0.002). The cardiac events were predicted by %TMAD (HR 0.68, 95% CI 0.54-0.85; p = 0.0012). CONCLUSIONS: The present study suggests that TMAD easily and rapidly estimated by speckle-tracking echocardiography may be used as a simple method to predict occurrence of the cardiac events in asymptomatic severe AS patients with preserved LVEF.

Assessment of decreased left ventricular longitudinal deformation in asymptomatic patients with organic mitral regurgitation and preserved ejection fraction using tissue-tracking mitral annular displacement by speckle-tracking echocardiography.

BACKGROUND: Application of speckle-tracking echocardiography (STE) provides rapid assessment of tissue-tracking mitral annular displacement (TMAD). We investigated the value of TMAD for the assessment of decreased LV longitudinal deformation in asymptomatic patients with severe or moderate-to-severe mitral regurgitation (MR) and preserved LV ejection fraction (LVEF). METHODS: We retrospectively studied 50 patients with severe or moderate-to-severe organic MR and preserved LVEF (>60%) in whom global longitudinal strain (GLS) was successfully measured by STE. TMAD was quickly assessed in the apical four-chamber view using STE. We calculated the percentage of TMAD to LV length from the midpoint of mitral annulus to the apex at end-diastolic (%TMAD). The study population was divided into two groups: decreased GLS patients (>-20%; Group A) and preserved GLS patients (≤-20%; Group B). We examined whether %TMAD could be used as a diagnostic factor of decreased GLS. RESULTS: %TMAD was significantly lower in Group A than Group B (12.5 ± 0.5 vs 16.8 ± 2.2, P < 0.0001). By univariate logistic regression analysis, %TMAD was a diagnostic factor of decreased GLS. By multiple regression analysis, %TMAD remained an independent diagnostic factor of decreased GLS (Odds ratio [OR] = 4.21, 95% confidence interval [CI] = 1.34-28.94, P < 0.0001). A cutoff value of %TMAD <14.6 had a sensitivity of 94% and specificity of 94% for the presence of decreased GLS. CONCLUSIONS: Tissue-tracking mitral annular displacement is useful in the assessment of decreased LV longitudinal deformation in asymptomatic patients with severe or moderate-to-severe MR and preserved LVEF.

In vivo optical coherence tomography imaging and histopathology of healed coronary plaques.

BACKGROUND AND AIMS: The aim of this study was to assess agreement between optical coherence tomography (OCT) and histopathology for healed coronary plaques (HCPs) in human coronary arteries ex vivo, and to evaluate the prevalence and characteristics of HCPs in vivo. METHODS: Ex vivo OCT images were co-registered with histopathology in 144 cross-sections with ≥50% stenosis. Of these, 30 randomly selected pairs were employed to define morphological features of OCT for HCPs (OCT-derived HCPs); the remaining 114 pairs were used to evaluate the accuracy of OCT in detecting histologically-defined HCPs. In a clinical study, 60 target lesions from 60 patients with stable ischemic heart disease were divided into 2 groups according to the presence or absence of OCT-derived HCPs. Plaque characteristics were compared between the two groups. RESULTS: In the autopsy study, an OCT-derived HCP was defined as a plaque with heterogeneous signal-rich layers of different optical signal density. The sensitivity, specificity, positive predictive value, and negative predictive value of OCT-derived HCP to detect histologically-defined HCPs were 81%, 98%, 93%, and 93%, respectively. In the clinical study, 46 (77%) had OCT-derived HCPs. Both microvessels and macrophages were more frequently identified in OCT-derived HCPs compared to their counterparts (43% vs. 0%; p<0.01, 70% vs. 21%; p<0.01, respectively). CONCLUSIONS: An ex vivo OCT image has a good agreement with histology for HCPs detection. HCPs were frequently identified by OCT in target lesions in stable ischemic heart disease patients. OCT may be a useful intracoronary imaging for HCPs detection in vivo.

Prognosis of spontaneous coronary artery dissection treated by percutaneous coronary intervention with optical coherence tomography.

BACKGROUND: Although about half of patients with spontaneous coronary artery dissection (SCAD) face ongoing necrosis, conservative therapy is recommended due to a high complication rate in angiography-guided percutaneous coronary intervention (PCI). The aim of this study was to investigate clinical outcomes of SCAD treated by optical coherence tomography (OCT)-guided PCI. METHODS: This study consisted of consecutive 306 patients with acute coronary syndrome (ACS) who underwent OCT-guided PCI. Based on the culprit lesion morphology by OCT, patients were assigned to four groups: a SCAD group, a plaque rupture (PR) group, a calcified nodule (CN) group, and an undetermined etiology (UE) group. Successful PCI was defined as thrombolysis in myocardial infarction flow grade 3 in final angiography without any complications. Primary endpoint was defined as occurrence rate of major adverse cardiac events (MACE) including cardiac death, myocardial infarction, and unstable angina pectoris. RESULTS: OCT revealed 12 SCADs, 149 PRs, 16 CNs, and 129 UEs, respectively. No significant difference was observed in the success rate of PCI (SCAD 91.7%, PR 85.2%, CN 81.2%, UE 86.8%, p=0.88), while wire repositioning was needed in 2 SCAD cases (p<0.01). The mean follow-up periods were 17.1±13.3 months. No significant difference was observed in MACE among the groups (p=0.56). CONCLUSIONS: The clinical outcomes of OCT-guided PCI for SCAD were favorable, as well as those for other ACS etiologies. OCT-guided PCI could become a therapeutic option for SCAD compromised with ongoing necrosis.

Optimal threshold of postintervention minimum stent area to predict in-stent restenosis in small coronary arteries: An optical coherence tomography analysis.

OBJECTIVES: The aim of this study was to determine the best threshold of postintervention minimum stent area (MSA) assessed by optical coherence tomography (OCT) to predict long-term in-stent restenosis (ISR) for 2.5 mm-diameter everolimus-eluting stents (EES). BACKGROUND: Percutaneous coronary intervention (PCI) for small coronary arteries remains challenging. Stent underexpansion is a strong predictor of late ISR. METHODS: We performed a retrospective analysis of 69 lesions in 69 patients undergoing PCI with 2.5 mm-diameter stents using OCT for the assessment of postintervention MSA and subsequent 9-month angiographic follow-up. RESULTS: The rates of angiographic ISR and target lesion revascularization were 7.2% and 1.4%. The postintervention OCT-MSA of EES < 3.5 mm(2) for predicting ISR yielded a sensitivity of 80%, specificity of 71%, positive predictive value of 18%, and negative predictive value of 98%. There was a marginally significant trend between increasing MSA quartiles and decreasing ISR rate (P for trend = 0.07). CONCLUSIONS: Postintervention OCT-MSA of 3.5 mm(2) best predicted 9-month ISR following PCI with 2.5-mm-diameter EES. Further large, prospective, observational studies are warranted that validate this result. © 2015 Wiley Periodicals, Inc.

Circulating CD14++CD16+ Monocyte Subsets as a Surrogate Marker of the Therapeutic Effect of Corticosteroid Therapy in Patients With Cardiac Sarcoidosis.

BACKGROUND: We aimed to evaluate whether specific monocyte subsets could serve as surrogate markers of disease activity in cardiac sarcoidosis (CS) evaluated by 18F-fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET). METHODS AND RESULTS: We studied 28 patients with CS (8 men; mean age: 61±9 years) diagnosed according to consensus criteria. We divided the patients into 2 groups: known CS receiving corticosteroid therapy (Rx(+); n=13) and new-onset CS (Rx(-); n=15), and analyzed 3 distinct monocyte subsets (CD14+CD16-, CD14++CD16+, and CD14+ -CD16+). Monocyte subsets were also analyzed in 10 Rx(-) patients before and 12 weeks after starting corticosteroid therapy. Inflammatory activity was quantified by 18F-FDG PET using the coefficient of variation (COV) of the standardized uptake value (SUV). The proportion of CD14++CD16+ monocytes in Rx(+) patients (10.8 [0.2-23.5] %) was significantly lower than in Rx(-) patients (23.0 [11.5-38.4] %, P=0.001). After corticosteroid therapy, the COV of the SUV was significantly improved from 0.32 [0.14-0.62] to 0.17 [0.04-0.43] (P=0.017). The proportion of CD14++16+ monocytes showed a significant decrease from 22.2 [8.8-38.4] % to 8.4 [1.8-16.8] % (P=0.001). The decrease in the proportion of CD14++16+ monocytes significantly correlated with the decrease in the COV of the SUV (r=0.495, P=0.027). CONCLUSIONS: CD14++16+ monocytes are a possible surrogate marker of the therapeutic effect of corticosteroid therapy in CS.

Long-term outcome after deferral of revascularization in patients with intermediate coronary stenosis and gray-zone fractional flow reserve.

BACKGROUND: A strategy of deferred percutaneous coronary intervention for coronary stenosis with fractional flow reserve (FFR) 0.75-0.80, termed the gray zone, remains a matter of debate. The aim of this study was to assess the safety of deferring revascularization for patients with FFR 0.75-0.80 compared with those with FFR >0.80. METHODS AND RESULTS: We assessed 3-year clinical outcome in 150 patients with angiographically intermediate stenosis who had revascularization deferred on the basis of FFR ≥ 0.75 (FFR 0.75-0.80, n=56; FFR >0.80, n=94). Target vessel failure (TVF), defined as a composite of cardiac death, target vessel-related myocardial infarction (MI), and ischemia-driven target vessel revascularization (TVR) was evaluated during follow-up. Cardiac death was observed in 1 patient with FFR 0.75-0.80. There was no target vessel-related MI in either group. The incidence of ischemia-driven TVR was higher in patients with FFR 0.75-0.80 than in those with FFR >0.80 (14% vs. 3%, P=0.020). TVF-free survival was significantly worse for the patients with FFR 0.75-0.80 than those with FFR >0.80 (hazard ratio, 5.2; 95% confidence intervals: 1.4-19.5; P=0.015). CONCLUSIONS: Patients with FFR 0.75-0.80 were at higher risk of TVF mainly due to TVR than those with FFR >0.80.

Feasibility of optical coronary tomography in quantitative measurement of coronary arteries with lipid-rich plaque.

BACKGROUND: The aim of the present study was to evaluate the feasibility of optical coherence tomography (OCT) for measurement of vessel area in coronary arteries with lipid-rich plaque as compared with intravascular ultrasound (IVUS). METHODS AND RESULTS: We investigated 80 coronary artery segments with lipid-rich plaque on OCT and non-attenuated plaque on IVUS. According to the lipid arc on OCT, the plaques were classified into 4 groups: group 1, lipid arc ≤90°; group 2, 90°270°. Vessel circular arcs that could not be identified due to OCT signal attenuation were interpolated using an approximating algorithm. OCT-measured vessel area was well-correlated with IVUS-measured vessel area (R=0.834, P<0.001). On Bland-Altman plot, there was a good agreement between OCT-measured vessel area and IVUS-measured vessel area, although mean difference and limits of agreement increased with increase of lipid arc (mean difference in groups 1-4: -0.21, -0.31, -1.02, and -2.13 mm(2); lower limit: -1.49, -3.22, -5.24, and -9.25 mm(2); and upper limit: 1.07, 2.60, 3.20, and 4.99 mm(2)). Intra-observer (R=0.97-0.99, P<0.001) and inter-observer (R=0.97-0.99, P<0.001) reproducibility for OCT measurement of vessel area was excellent. CONCLUSIONS: Like IVUS, OCT can be used to measure vessel area in coronary arteries with lipid-rich plaque.

Association between P-selectin glycoprotein ligand-1 and pathogenesis in acute coronary syndrome assessed by optical coherence tomography.

OBJECTIVE: Although monocytes appear to be actively involved in the onset of acute coronary syndrome (ACS), they are heterogenous in human peripheral blood. How up-regulation of monocyte subsets leads to coronary plaque rupture followed by thrombus formation remains unclear. Recent studies have shown that P-selectin glycoprotein ligand-1 (PSGL-1) is involved in monocyte activation in patients with thrombus formation. We therefore investigated the relationship between the expression of PSGL-1 on monocyte subsets and thrombus formation using frequency-domain optical coherence tomography (FD-OCT) in patients with ACS. METHODS: We enrolled a total of 100 individuals in this study: patients with acute myocardial infarction (AMI, n=25), unstable angina pectoris (UAP, n=20), or stable angina pectoris (n=35) who underwent coronary angiography, and control subjects (n=20). Three monocyte subsets (CD14++CD16-, CD14++CD16+, and CD14+CD16+) and the expression of PSGL-1 were measured by flow cytometry. In patients with AMI and UAP, FD-OCT was performed before percutaneous coronary intervention. RESULTS: Circulating peripheral CD14++CD16+ monocytes expressed PSGL-1 more frequently than CD14++CD16- and CD14+CD16+ monocytes in patients with ACS. The expression of PSGL-1 on circulating peripheral CD14++CD16+ monocytes was significantly elevated in patients with AMI compared with the other 3 groups. Moreover, the expression levels of PSGL-1 on CD14++CD16+ monocytes were significantly higher in patients with plaque rupture or intracoronary thrombus assessed by FD-OCT. CONCLUSION: Up-regulation of PSGL-1 on CD14++CD16+ monocytes may be a crucial role in plaque rupture and thrombus formation.

Effect of direct renin inhibitor on left ventricular remodeling in patients with primary acute myocardial infarction.

Some patients with acute myocardial infarction (AMI) have a poor prognosis due to left ventricular remodeling (LVR), resulting in the recurrence of congestive heart failure even when therapy with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs) has been initiated. We investigated the effect of early administration of the direct renin inhibitor (DRI) aliskiren in combination with an ACEI or an ARB on LVR using cardiac magnetic resonance (CMR) imaging in patients with AMI.Twenty-one consecutive patients were treated with an ACEI or an ARB (non-DRI group), and another 21 consecutive patients received aliskiren 150 mg/day combined with an ACEI or an ARB (DRI group). CMR imaging was performed 7 days after AMI and 10 months later.CMR imaging revealed no significant changes in LV end-systolic volume, LV end-diastolic volume, or LV ejection fraction between the patients with and without DRI aliskiren. In the DRI group, plasma renin activity was significantly lower in both the acute and chronic phases; however, aldosterone levels were significantly lower in the acute but not the chronic phase.A low dose of aliskiren may be insufficient to maintain suppression of aldosterone under current standard therapies with an ACEI or an ARB and ß-blocker in patients with primary AMI, and results in no attenuation of LVR.

Acute-phase glucose fluctuation is negatively correlated with myocardial salvage after acute myocardial infarction.

BACKGROUND: It remains unclear whether glycemic fluctuation immediately after acute myocardial infarction (AMI) can affect myocardial damage. This study investigated the impact of glucose fluctuation on myocardial salvage following successful recanalization of primary AMI. METHODS AND RESULTS: A total of 36 consecutive patients with AMI were studied. Glycemic variability, as indicated by the mean amplitude of glycemic excursion (MAGE), was measured on a continuous glucose monitoring system. Three subsets (CD14(+)CD16(-), CD14(++)CD16(+) and CD14(+-)CD16(+)) were measured on flow cytometry 1, 2, 3, 4 and 5 days after AMI onset. A 2-h oral glucose test was performed in 23 patients who had no previous diagnosis of diabetes and/or glycated hemoglobin <6.5%, after the onset of AMI at 2 weeks. Plasma active glucagon-like peptide (GLP)-1 level was measured in each sample. The extent of myocardial salvage 7 days after AMI was evaluated on cardiovascular magnetic resonance imaging. MAGE and the peak CD14(+)CD16(-) monocyte level were significantly negatively correlated with myocardial salvage index (MSI). MAGE was significantly correlated with peak CD14(+)CD16(-) monocyte level. Of interest, plasma GLP-1 level was significantly positively correlated with MSI and significantly negatively correlated with MAGE. CONCLUSIONS: Glucose fluctuations during the acute phase of AMI affect MSI, indicating that manipulation of glucose variability from peak to nadir might be a potential therapeutic target for salvaging ischemic damage.

Scanning electron microscopic analysis of polymer damage in drug-eluting stents during multiple stenting.

Polymer damage of drug-eluting stents (DES) during percutaneous coronary intervention procedure could be associated with stent restenosis. We assessed the damage to the drug-containing polymer of DES during multiple stenting in a phantom model by using scanning-electron microscopy (SEM). Unexpanded sirolimus-eluting stent (SES; n = 15) was delivered through the formerly expanded SES (n = 15) in a bended polytetrafluoroethylene plastic tube. The stent was subcategorized into 4 segments (S), including distal (S1), mid distal (S2), mid proximal (S3) and proximal segments (S4), for qualitative SEM assessment. Polymer damage, such as detachments, missing or tears, was observed not only in the outer surface of the unexpanded stents (100%) but also in the inner surface of the formerly expanded stents (100%). There was a significant difference in the frequency of polymer damage among the 4 segments in the unexpanded stents (S1 vs. S2 vs. S3 vs. S4: 86.7 vs. 80.0 vs. 53.3 vs. 40.0%, p = 0.022) and the formerly expanded stents (S1 vs. S2 vs. S3 vs. S4: 80.0 vs. 73.3 vs. 73.3 vs. 40.0%, p = 0.041). The damage was distributed more frequently in distal part than proximal part of either unexpanded stents (S1 vs. S4, p = 0.0079) and the formerly expanded stents (S1 vs. S4, p = 0.0079). Delivery of DES through a formerly expanded DES could cause damage to drug-containing polymer of the stents.

Impact of stress hyperglycemia on myocardial salvage following successfully recanalized primary acute myocardial infarction.

BACKGROUND: Elevated blood glucose on admission may worsen outcome after acute myocardial infarction (AMI). No relationship has been identified between admission blood glucose level and myocardial salvage in patients with AMI. METHODS AND RESULTS: This study assessed 150 consecutive patients with a first AMI who underwent percutaneous coronary intervention within 24 h from onset of symptoms. Plasma blood glucose was measured on admission. Stress hyperglycemia was defined as blood glucose ≥10 mmol/L (180 mg/dl). The extent of myocardial salvage 7 days after AMI was evaluated on cardiovascular magnetic resonance imaging (CMRI) as the difference between areas of myocardium at risk (T2-weighted hyperintense lesion) and areas of late gadolinium enhancement. The association between stress hyperglycemia and myocardial salvage index (MSI) was investigated in patients with and without diabetes. Among non-diabetic patients, MSI was lower in those with stress hyperglycemia than in those without. No significant difference in MSI was noted between diabetes patients with or without stress hyperglycemia. On multivariate analysis, stress hyperglycemia in patients without diabetes was an independent predictor of MSI. CONCLUSIONS: Stress hyperglycemia affects MSI, indicating that the manipulation of glucose levels could be a potential therapeutic target for salvaging ischemic damage.

Left ventricular apical aneurysm due to unrecognized sarcoidosis.

A 47-year-old woman was hospitalized for syncope. An electrocardiogram showed complete right bundle branch block and T-wave inversion in leads III, aVF, and V2-4. Cardiac catheterization was performed since the echocardiogram demonstrated the existence of a left ventricular apical aneurysm and apical thrombus. Coronary angiography revealed normal coronary arteries. An endomyocardial biopsied specimen from the right ventricular apical wall demonstrated typical noncaseating granulomas with giant cells. There was no evidence suggesting the involvement of other systemic organs. The patient was diagnosed as having cardiac sarcoidosis. Cardiac sarcoidosis should be considered within a spectrum of diseases that cause left ventricular apical aneurysm.