Effect of direct renin inhibitor, aliskiren, on peripheral blood monocyte subsets and myocardial salvage in patients with primary acute myocardial infarction.

BACKGROUND: It remains unclear whether angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs) have fully delivered the expected reduction in cardiovascular diseases. We investigated the effects of adding the direct renin inhibitor (DRI), aliskiren, to an ACEI or an ARB on monocyte subsets and myocardial salvage in patients with primary acute myocardial infarction (AMI). METHODS AND RESULTS: Twenty-one consecutive patients were treated with an ACEI or an ARB (non-DRI group), and another 21 consecutive patients received aliskiren combined with an ACEI or an ARB (DRI group). Two monocyte subsets (CD14(+)CD16(-) and CD14(+)CD16(+)) were measured by flow cytometry. The extent of myocardial salvage 7 days after AMI was evaluated by cardiac magnetic resonance imaging. Both plasma renin activity and aldosterone levels were significantly lower in the DRI group than in the non-DRI group. Peak levels of CD14(+)CD16(-) monocyte number and ratio were also significantly lower in the DRI group. The extent of myocardial salvage was significantly higher in the DRI group than in the non-DRI group (44.8 [41.2-53.1] vs. 36.0 [28.5-42.6], P=0.001). CONCLUSIONS: A DRI combined with an ACEI or an ARB can better improve the extent of myocardial salvage after AMI than an ACEI or an ARB alone in association with the decrease in circulating CD14(+)CD16(-) monocytes.

Comparison of contrast media and low-molecular-weight dextran for frequency-domain optical coherence tomography.

BACKGROUND: Although an intracoronary frequency-domain optical coherence tomography (FD-OCT) system overcomes several limitations of the time-domain OCT (TD-OCT) system, the former requires injection of contrast media for image acquisition. The increased total amount of contrast media for FD-OCT image acquisition may lead to the impairment of renal function. The safety and usefulness of the non-occlusion method with low-molecular-weight dextran L (LMD-L) via a guiding catheter for TD-OCT image acquisition have been reported previously. The aim of the present study was to compare the image quality and quantitative measurements between contrast media and LMD-L for FD-OCT image acquisition in coronary stented lesions. METHODS AND RESULTS: Twenty-two patients with 25 coronary stented lesions were enrolled in this study. FD-OCT was performed with the continuous-flushing method via a guiding catheter. Both contrast media and LMD-L were infused at a rate of 4 ml/s by an autoinjector. With regard to image quality, the prevalence of clear image segments was comparable between contrast media and LMD-L (97.9% vs. 96.5%, P=0.90). Furthermore, excellent correlations were observed between both flushing solutions in terms of minimum lumen area, mean lumen area, and mean stent area. The total volumes of contrast media and of LMD-L needed for OCT image acquisition were similar. CONCLUSIONS: FD-OCT image acquisition with LMD-L has the potential to reduce the total amount of contrast media without loss of image quality.

Assessment by optical coherence tomography of stent struts across side branch. -Comparison of bare-metal stents and drug-elution stents.-.

BACKGROUND: Late stent thrombosis (LST) after drug-eluting stent (DES) implantation is a major clinical problem that has not been fully explained. Incomplete neointimal coverage of stent struts is an important morphometric predictor of LST, which may be associated with impaired healing and the absence of full coverage of struts at branch-point ostia. Optical coherence tomography (OCT) was performed to compare 3 types of stents placed across side branches. METHODS AND RESULTS: At 9-month follow-up, the neointimal coverage of the struts of 58 stents across a side branch was measured by OCT (bare metal (BMS), n = 20; sirolimus-eluting (SES), n = 23; paclitaxel-eluting (PES), n = 15). According to the diameter ratio of side branch to main vessel, the side branches were classified as either large (ratio > 0.33) or small (ratio ≤ 0.33). BMS had the lowest frequency of uncovered struts (29.4%) and the greatest neointimal thickness on the struts (123 ± 33 µm). Neointimal thickness on the struts was less for SES than for PES (72 ± 16 vs. 91 ± 22 µm, P = 0.009), but there was no difference in the frequency of uncovered struts (66.1% vs. 58.6%, P=0.493). For large side branches, the frequency of uncovered struts was greater than in the small group for SES (87.5% vs. 40.7%, P = 0.0002) and PES (83.3% vs. 18.2%; P = 0.0013); there was no significant difference for BMS (43.8% vs. 16.7%, P = 0.138). CONCLUSIONS: Neointimal coverage on struts across a side branch was less frequently observed in DES than in BMS, particularly in large side branches.

First evaluation of real-time nitric oxide changes in the coronary circulation in patients with non-ischaemic dilated cardiomyopathy using a catheter-type sensor.

AIMS: No direct method has yet been developed to measure real-time plasma nitric oxide (NO) concentration in humans. In this study, we evaluated a new method for measuring plasma NO concentration in patients with dilated cardiomyopathy (DCM) and in normal controls using a catheter-type sensor. METHODS AND RESULTS: We simultaneously measured average peak velocity (APV) of the coronary artery flow and change in plasma NO concentration using the NO sensor placed in the great cardiac vein of 10 DCM patients and 10 control subjects. These evaluations were performed in response to sequential intracoronary infusions of acetylcholine (ACh, 10⁻8-10⁻6 M), N(G)-monomethyl-l-arginine (l-NMMA, 200 µmol) and co-infusion of ACh and l-NMMA. The change in plasma NO concentration in DCM patients was significantly impaired compared with the control group (P < 0.01). Pretreatment with l-NMMA completely suppressed the ACh-induced NO concentration, whereas APV in the left anterior descending coronary artery was partially suppressed in both groups. Plasma NO concentration reached its peak value later than the maximum APV following the injection of ACh (10⁻6 M) in both groups. CONCLUSION: The catheter-type NO sensor could be applied to clinically evaluate the endothelial function (i.e. reduced endothelium-derived NO bioavailability) in patients with cardiovascular diseases.

Advantage of next-generation frequency-domain optical coherence tomography compared with conventional time-domain system in the assessment of coronary lesion.

BACKGROUND: Intracoronary optical coherence tomography (OCT) is a high-resolution imaging modality used for evaluation of coronary lesion morphology. However, current time-domain OCT (TD-OCT) have a number of limitations with regard to both procedural usage and safety in the clinical setting. The next-generation frequency-domain OCT (FD-OCT), which has a much faster frame rate and pullback speed than TD-OCT, is expected to overcome these limitations. The aim of this study was to evaluate the feasibility and usability of next generation FD-OCT in the assessment of coronary lesions. METHODS: A comparison study was performed between FD-OCT and TD-OCT from the aspect of usability (set-up time), qualitatively (rate of clear image segment), and safety (adverse event) in 14 ischemic heart disease patients with 20 previously implanted coronary stents. RESULTS: The mean time of the OCT procedure in this study from setup to completion of image acquisition was 3.2 +/- 0.8 min for FD-OCT and 11.2 +/- 2.5 min for TD-OCT (P < 0.01). In qualitative image assessment, FD-OCT has the potential to yield a higher rate of clear image segments (CIS) than TD-OCT (99.4% vs. 80.8%, respectively; P < 0.01). In addition to these improved characteristics, there were no ischemic ECG changes or arrhythmia associated with FD-OCT. CONCLUSIONS: The next-generation intracoronary FD-OCT has better performance in the clinical setting and the potential to overcome several limitations of conventional TD-OCT systems.

Clinical characteristics of patients with kawasaki disease and levels of peripheral endothelial progenitor cells and blood monocyte subpopulations.

BACKGROUND: Coronary sequelae that persist after Kawasaki disease (KD) have been associated with coronary vascular events in adolescents and young adults. The aim of this study was to investigate the relationship between coronary sequelae late after KD and circulating endothelial progenitor cells (EPCs), as a marker of vascular repair, or monocyte subsets as a marker of inflammation. METHODS AND RESULTS: The 31 KD patients were divided into 3 groups according to the type of coronary artery lesion (CAL): group 1 consisted of 14 patients with persistent aneurysm; group 2 consisted of 9 patients with regressed aneurysms; group 3 included 8 KD patients with normal coronary arteries from disease onset. The control group (group 4) consisted of 10 healthy subjects. Flow cytometric analysis was used to quantify circulating EPCs defined as CD34(+)KDR(+) cells and 2 distinct monocyte subsets (CD14(+)CD16(+) and CD14(+)CD16(-)). The number of EPCs in group 1 and group 2 was significantly decreased compared with group 4. In contrast, neither the number of CD14(+)CD16(+) monocytes nor that of CD14(+)CD16(-) monocytes was significantly different among the 4 groups. Finally, there were not any significant relationship between the numbers of EPCs and the 2 monocyte subsets. CONCLUSIONS: There are lower numbers of EPCs in the chronic phase of KD, irrespective of both CAL formation and monocyte subsets.

Association between circulating monocyte subsets and in-stent restenosis after coronary stent implantation in patients with ST-elevation myocardial infarction.

BACKGROUND: Recent studies have shown that monocytes in human peripheral blood are heterogeneous. The clinical significance of 2 distinct monocyte subsets as a marker of late in-stent restenosis (ISR) following implantation of bare-metal stents (BMSs) in patients with acute myocardial infarction (AMI) was examined. METHODS AND RESULTS: Seventy-one consecutive patients with AMI who underwent BMS implantation were enrolled in the study. Peripheral blood was collected 12 days after AMI onset. Two distinct monocyte subsets (CD14(+)CD16(-)CCR2(+) and CD14(+)CD16(+)CX3CR1(+)) were measured by flow cytometry. All patients underwent angiography at a scheduled follow up after 9 months. CD14(+)CD16(+)CX3CR1(+) monocyte subset counts were significantly higher in patients with restenosis than in patients without restenosis, whereas neither the total monocytes nor the CD14(+)CD16(-)CCR2(+) subset counts differed significantly between the 2 groups of patients. There was also a significant positive correlation between the CD14(+)CD16(+)CX3CR1(+) monocyte counts and angiographic late lumen loss. In multivariate analysis, the CD14(+)CD16(+)CX3CR1(+) monocyte count was an independent predictor for in-stent late lumen loss. CONCLUSIONS: CD14(+)CD16(+)CX3CR1(+) monocytes might have a role in ISR following coronary BMS implantation in patients with AMI.

Upregulation of fractalkine and its receptor, CX3CR1, is associated with coronary plaque rupture in patients with unstable angina pectoris.

BACKGROUND: Recent studies suggest that fractalkine (FKN or CX3CL1) and its cognate receptor, CX3CR1, play a role in atherogenesis, so the relationship between coronary plaque rupture, as observed by preintervention optical coherence tomography, and plasma levels of FKN and CX3CR1 was investigated in this study. METHODS AND RESULTS: The study population consisted of 46 patients with unstable angina pectoris (UAP), 30 patients with stable angina pectoris, and 25 healthy controls. The UAP patients underwent a preintervention optical coherence tomography study, which revealed that the number of patients with and without plaque rupture at the culprit site was 27 (rupture group) and 19 (non-rupture group), respectively. Plasma levels of soluble FKN (sFKN) and CX3CR1 were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively. The plasma levels of sFKN were significantly increased in UAP patients with plaque rupture compared with patients in the other groups. Multiple logistic regression analysis showed that CD14(+)CD16(+)CX3CR1(+) monocytes and CD3(+)CX3CR1(+) lymphocytes were independent predictors of the presence of ruptured plaque. CONCLUSIONS: Increases in the FKN level and the number of CX3CR1-expressing mononuclear cells might contribute to coronary plaque rupture.

Post-reperfusion enhancement of CD14(+)CD16(-) monocytes and microvascular obstruction in ST-segment elevation acute myocardial infarction.

BACKGROUND: The presence of microvascular obstruction (MVO) after primary ST-segment elevation acute myocardial infarction (STEMI) is associated with a poor outcome. The aim of the paper was to examine the relationship between distinct monocyte subsets and gadolinium-enhanced cardiovascular magnetic resonance (CMR) characteristics of MVO after STEMI. METHODS AND RESULTS: Seventy-one patients with primary STEMI successfully treated with stenting were enrolled in the study. Two monocyte subsets (CD14(+)CD16(-) and CD14(+)CD16(+)) were measured on flow cytometry on admission and 2, 3, 4, 5, 8 days after the onset of STEMI. CMR was performed 7 days after revascularization to determine MVO on late gadolinium-enhanced imaging. The peak levels of CD14(+)CD16(-) monocytes, but not those of CD14(+)CD16(+) monocytes, were significantly higher in patients with MVO than in those without MVO. A multivariate logistic regression model showed that the post-perfusion peak levels of CD14(+)CD16(-) monocytes remained an independent factor for the presence of MVO (odds ratio=1.53; 95% confidence interval: 1.01-2.32; P=0.04). The absence of MVO was significantly associated with improvement in left ventricular ejection fraction. CONCLUSIONS: Post-reperfusion enhancement of CD14(+)CD16(-) monocytes was associated with MVO in patients with STEMI. The pathophysiologic and therapeutic implications of this association require further study.

Effect of human peripheral monocyte subsets on coronary flow reserve in infarct-related artery in patients with primary anterior acute myocardial infarction.

1. In the present study, we investigated the relationships between relative levels of specific peripheral monocyte subsets and coronary flow velocity reserve (CFVR) during the subacute phase in patients with acute myocardial infarction (AMI). 2. The study was performed on 29 patients with primary anterior AMI who had been successfully treated using primary percutaneous coronary intervention. Two monocyte subsets (CD14(+)CD16(-) and CD14(+)CD16(+)) were measured by flow cytometry. Transthoracic Doppler echocardiography was used to measure CFVR on Days 4 and 7 after the onset of AMI onset. We defined DeltaCFVR as the difference in CFVR values between Days 4 and 7. The extent of myocardial salvage on Day 7 after AMI was evaluated by cardiovascular magnetic resonance (CMR) imaging as the difference between the area of myocardium at risk and the area of necrotic myocardium. 3. There was a significant negative correlation between DeltaCFVR and peak CD14(+)CD16(-) monocyte counts in AMI patients, whereas no significant association was found between CD14(+)CD16(+) monocyte counts and DeltaCFVR. There was a significant positive correlation between DeltaCFVR and the extent of myocardial salvage. 4. In conclusion, peak levels of CD14(+)CD16(-) monocytes following primary anterior AMI were closely related to the extent of microvascular injury.

Lipid-rich plaque and myocardial perfusion after successful stenting in patients with non-ST-segment elevation acute coronary syndrome: an optical coherence tomography study.

AIMS: Although some recent guidelines recommend an early invasive strategy for non-ST-segment elevation acute coronary syndrome (NSTEACS), several studies have failed to identify any benefit for very early intervention for NSTEACS. The no-reflow phenomenon may inhibit the expected benefit from very early recanalization for NSTEACS subjects. The aim of this study was to investigate whether optical coherence tomography (OCT) could predict no-reflow in patients with NSTEACS. METHODS AND RESULTS: This study comprised 83 consecutive patients with NSTEACS who underwent OCT and successful emergent primary stenting. On the basis of post-stent TIMI flow, patients were divided into two groups: no-reflow group (n = 14) and reflow group (n = 69). Thin-cap fibroatheroma (TCFA) was defined as a plaque presenting lipid content for >90 degrees , and with thinnest part of the fibrous cap measuring <70 microm. Thin-cap fibroatheroma were more frequently observed in the no-reflow group than in the reflow group (50% vs. 16%, P = 0.005). The frequency of the no-reflow phenomenon increases according to the size of the lipid arc in the culprit plaque. Final TIMI blush grade also deteriorated according to the increase in the lipid arc. A multivariable logistic regression model revealed that lipid arc alone was an independent predictor of no-reflow (odds ratio 1.018; CI 1.004-1.033; P = 0.01). CONCLUSION: Optical coherence tomography can predict no-reflow after percutaneous coronary intervention (PCI) in NSTEACS. The lipid contents of a culprit plaque may play a key role in damage to the microcirculation after PCI for NSTEACS. From our results, it is found that OCT is useful tool for stratifying risk for PCI for NSTEACS.

Morphology of exertion-triggered plaque rupture in patients with acute coronary syndrome: an optical coherence tomography study.

BACKGROUND: Plaque rupture and secondary thrombus formation play key roles in the onset of acute coronary syndrome (ACS). One pathological study suggested that the morphologies of plaque rupture differed between rest-onset and exertion-triggered rupture in men who experienced sudden death. The aim of the present study was to use optical coherence tomography to investigate the relationship in patients with ACS between the morphology of a ruptured plaque and the patient's activity at the onset of ACS. METHODS AND RESULTS: The study population was drawn from 43 consecutive ACS patients (with or without ST-segment elevation) who underwent optical coherence tomography and presented with a ruptured plaque at the culprit site. Patients were divided into a rest group and an exertion group on the basis of their activities at the onset of ACS. The thickness of the broken fibrous cap correlated positively with activity at the onset of ACS. The culprit plaque ruptured at the shoulder more frequently in the exertion group than in the rest group (rest 57% versus exertion 93%, P=0.014). The thickness of the broken fibrous cap in the exertion group was significantly higher than in the rest-onset group (rest onset: 50 microm [interquartile median 15 microm]; exertion: 90 microm [interquartile median 65 microm], P<0.01). CONCLUSIONS: The morphologies of exertion-triggered and rest-onset ruptured plaques differ in ACS patients. Our data suggest that a thin-cap fibroatheroma is a lesion predisposed to rupture both at rest and during the patient's day-to day activity, and some plaque rupture may occur in thick fibrous caps depending on exertion levels.

Effects of telmisartan, a unique angiotensin receptor blocker with selective peroxisome proliferator-activated receptor-gamma-modulating activity, on nitric oxide bioavailability and atherosclerotic change.

OBJECTIVE: Telmisartan is a unique angiotensin II (Ang II) receptor blocker (ARB) with selective peroxisome proliferator-activated receptor-gamma (PPAR gamma). We therefore investigated the effects of telmisartan on endothelial function and atherosclerotic change in genetically hyperlipidemic rabbits, compared with candesartan, an ARB without PPAR gamma activity. METHODS: A total of 30 Watanabe heritable hyperlipidemic (WHHL) rabbits equally derived (n = 6 each) were treated with (1) vehicle (control), (2) GW9662, a PPAR gamma antagonist (0.5 mg/kg per day), (3) telmisartan (5 mg/kg per day), (4) telmisartan + GW9662, (5) candesartan (5 mg/kg per day) for 8 weeks. After treatment, acetylcholine (ACh)-induced nitric oxide production was measured as a surrogate for endothelium protective function, and vascular nitrotyrosine (a product of superoxide and nitric oxide) was measured for assessing dysfunctional endothelial nitric oxide synthase activity. Plaque area was quantified by histology. RESULTS: Telmisartan increased ACh-induced nitric oxide by 5.5 nmol/l, significantly more than control. Interestingly, cotreatment with GW9662 significantly attenuated telmisartan-induced ACh-induced nitric oxide almost to the levels observed with candesartan. Vascular nitrotyrosine concentration was 1.4 pmol/mg protein in the control group and significantly higher than that in the telmisartan or candesartan group. The lowest nitrotyrosine concentration was observed in the telmisartan group, which was significantly lower than that in the candesartan or telmisartan + GW9662 group. Histology of the thoracic aorta revealed that the plaque area was more significantly decreased in the telmisartan group than in the candesartan or telmisartan + GW9662 group. CONCLUSION: In addition to a class effect of ARBs, telmisartan may have additional effects on nitric oxide bioavailability and atherosclerotic change through its PPAR gamma-mediated effects in genetically hyperlipidemic rabbits.

Combined effects of an 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor and angiotensin II receptor antagonist on nitric oxide bioavailability and atherosclerotic change in myocardial infarction-prone Watanabe heritable hyperlipidemic rabbits.

We investigated the effects of co-administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor and angiotensin II type 1 receptor blocker (ARB) on nitric oxide (NO) bioavailability in genetically hyperlipidemic rabbits with our newly developed NO sensor. A total of 36 myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits equally derived (n=6 per group) were treated with 1) vehicle (control), 2) hydralazine (15 mg/kg/d), 3) the HMG-CoA reductase inhibitor pitavastatin (P: 0.5 mg/kg/d), 4) the ARB valsartan (V: 5 mg/kg/d), and 5) pitavastatin+valsartan (P+V) together without or 6) with N(G)-nitro-L-arginine methyl ester (L-NAME) for 8 weeks. After treatment, acetylcholine (ACh)-induced NO production was measured as a surrogate for endothelium protective function, and vascular peroxynitrite (a product of superoxide and NO) was measured for assessing dysfunctional endothelial NO synthase activity. Plaque area was quantified by histology as well as optical coherence tomography (OCT). Intra-aortic infusion of ACh produced an increase in plasma NO concentration, which was significantly greater with all drug treatments than with the control. P+V increased ACh-induced NO by 4.1 nmol/L significantly more than either P or V singly. The vascular peroxynitrite concentration was 1.6 pmol/mg protein in the control group and significantly less than those in the P- and V-monotherapy-groups. The lowest peroxynitrite concentration was observed in the P+V group (0.4 pmol/mg protein), which was significantly lower than those in the P- and the V-monotherapy-groups. OCT and histology of the thoracic aorta revealed that the plaque area decreased significantly more with the combination than with the monotherapy. In conclusion, the combined treatment with an HMG-CoA reductase inhibitor and an ARB may have additive protective effects on endothelial function as well as atherosclerotic change.

Incremental value of coronary flow velocity reserve, measured by transthoracic echocardiography, compared with computed tomography angiography alone, for detecting flow-limiting coronary stenoses.

BACKGROUND: Computed tomographic (CT) angiography provides high sensitivity for the detection of coronary stenosis, while its specificity is relatively low. The aim of this study was to determine the incremental value of coronary flow velocity reserve (CFVR) by transthoracic echocardiography when used with CT angiography for detecting stenosis of the major coronary arteries compared with invasive quantitative coronary angiography. METHODS: Sixty patients who underwent CFVR measurement before coronary angiography were retrospectively selected, and the cutoff value of CFVR to predict diameter stenosis > 70% was determined using receiver operating characteristic curve analysis. Second, CFVR measurement and CT angiography were prospectively performed in 50 patients who were scheduled to undergo coronary angiography. CT angiography using a 64-detector row scanner and CFVR measurement in the proximal to middle portions of the three major coronary arteries by transthoracic echocardiography were performed on the same day, <48 hours before invasive angiography. RESULTS: The cutoff values of CFVR were determined to be 2.0 for the left anterior descending coronary artery and 2.1 for the circumflex and right coronary arteries. Using these determined cutoff values, the sensitivity, specificity, and positive and negative predictive value of CFVR to identify diameter stenosis ≥ 70% stenosis on invasive quantitative coronary angiography were determined to be 84%, 87%, 66%, and 95%, respectively, and those of CT angiography were 91%, 80%, 58%, and 97%, respectively, in the prospective study with 50 patients. The combination of ≥70% stenosis on CT angiography and impaired CFVR was 94% specific for ≥70% stenosis, while the presence of <70% stenosis on CT angiography and preserved CFVR was 100% specific for the exclusion of ≥70% stenosis on invasive quantitative coronary angiography. CONCLUSIONS: When the results of CT angiography and CFVR are concordant, the combination is highly accurate in the detection and exclusion of coronary stenosis. CFVR measurement in addition to CT angiography could be helpful in identifying false-positive CT angiographic results.

Optical coherence tomography: from research to practice.

Optical coherence tomography (OCT) is a high-resolution imaging technique with great versatility of applications. In cardiology, OCT has remained hitherto as a research tool for characterization of vulnerable plaques and evaluation of neointimal healing after stenting. However, OCT is now successfully applied in different clinical scenarios, and the introduction of frequency domain analysis simplified its application to the point it can be considered a potential alternative to intravascular ultrasound for clinical decision-making in some cases. This article reviews the use of OCT for assessment of lesion severity, characterization of acute coronary syndromes, guidance of intracoronary stenting, and evaluation of long-term results.

Head to head comparison between the conventional balloon occlusion method and the non-occlusion method for optical coherence tomography.

BACKGROUND: Optical coherence tomography (OCT) has been introduced as a high-resolution imaging modality for the coronary arteries. The current OCT system, however, has a serious limitation in that the image acquisition method requires a soft balloon occlusion to avoid signal scattering from red blood cells. PURPOSE: The purpose of this study was to compare OCT images from the conventional balloon occlusion method and a non-occlusion image acquisition method, the continuous-flushing method, in the clinical setting. METHODS: OCT was performed with the conventional balloon occlusion method and the continuous-flushing method sequentially in 23 patients with stable angina. The image quality and quantitative measurements of OCT images were directly compared between the two methods. RESULTS: There were no adverse events related to the OCT procedure in any patients. There were no changes in systolic blood pressure and heart rate during the OCT procedure. ST-segment elevation (>2 mm) was recorded in 22 of 23 (96%) patients with the balloon occlusion method, but it was only observed in 1 of 23 (4%) patients with the continuous-flushing method (p<0.01). There were no differences in the visible length (the balloon occlusion method 28.6±2.3 mm vs. the continuous-flushing method 29.2±1.6 mm, p=0.49), image quality, or quantitative measurements between the two methods. CONCLUSIONS: OCT imaging with the continuous-flushing method could be performed safely and obtained similar quality images compared with the balloon occlusion method. OCT can be used to observe the proximal site of coronary arteries with this new technique.

Electrocardiographic strain and endomyocardial radial strain in hypertensive patients.

BACKGROUND: Electrocardiographic strain pattern (ECGS) is a well-recognized marker of the presence and severity of anatomic left ventricular hypertrophy (LVH) and also has been associated with adverse prognosis in hypertensive patients. Left ventricular (LV) endomyocardial radial strain (Endo-RS) is predominant in systolic LV wall thickening compared with epimyocardial radial strain (Epi-RS) in a normal heart. However, it remains unclear whether the ratio of Endo-RS to Epi-RS alters in hypertensive patients, especially in those with ECGS. METHODS: Endo-RS and Epi-RS in 9 non-hypertensive subjects (Group A), 26 hypertensive subjects without ECGS (Group B), and 16 hypertensive subjects with ECGS (Group C) were assessed by a tissue tracking system. RESULTS: Relative wall thickness, LV mass index, and voltage of SV1+RV5 were significantly greater in Group C than in both Groups A and B. Although no significant difference was seen in Epi-RS among the 3 groups, Endo-RS and the ratio of Endo-RS to Epi-RS (Endo/Epi-RS) in Group C were significantly lower than those in the other two groups. Multiple logistic regression analysis revealed that the only factor which significantly correlated with Endo/Epi-RS in the first tertile (<1.6) was the presence of ECGS (OR=9.28, p=0.01). CONCLUSIONS: The appearance of ECGS significantly correlated with not only the development of LV hypertrophy but also with the attenuation of Endo-RS.

Difference of culprit lesion morphologies between ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome: an optical coherence tomography study.

OBJECTIVES: The aim of this study was to investigate the difference of culprit lesion morphologies assessed by optical coherence tomography (OCT) between ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation acute coronary syndrome (NSTEACS). BACKGROUND: Autopsy studies have reported that rupture of a thin-cap fibroatheroma and subsequent thrombus formation is the most important mechanism leading to acute coronary syndrome (ACS). Optical coherence tomography is a high-resolution imaging modality that is capable of investigating detailed coronary plaque morphology in vivo. METHODS: We examined the culprit lesion morphologies by OCT in 89 consecutive patients with acute coronary syndrome (STEMI = 40; NSTEACS = 49). RESULTS: The incidence of plaque rupture, thin-cap fibroatheroma, and red thrombus was significantly higher in STEMI compared with NSTEACS (70% vs. 47%, p = 0.033, 78% vs. 49%, p = 0.008, and 78% vs. 27%, p < 0.001, respectively). Although the lumen area at the site of plaque rupture was similar in the both groups (2.44 ± 1.34 mm(2) vs. 2.96 ± 1.91 mm(2), p = 0.250), the area of ruptured cavity was significantly larger in STEMI compared with NSTEACS (2.52 ± 1.36 mm(2) vs. 1.67 ± 1.37 mm(2), p = 0.034). Furthermore, the ruptured plaque of which aperture was open-wide against the direction of coronary flow was more often seen in STEMI compared with NSTEACS (46% vs. 17%, p = 0.036). CONCLUSIONS: The present OCT study demonstrated the differences of the culprit lesion morphologies between STEMI and NSTEACS. The morphological feature of plaque rupture and the intracoronary thrombus could relate to the clinical presentation in patients with acute coronary disease.