Differential incidence and morphology of provoked spasm between intracoronary acetylcholine and ergonovine testing: recommendation of supplementary use.

When cardiologists diagnose patients with coronary spastic angina, Japanese Circulation Society (JCS) guidelines recommend the intracoronary injection of acetylcholine (ACh) and ergonovine (ER) as class I. However, the pharmacological difference between ACh and ER is controversial in the clinic. We performed both ACh and ER tests in the same 528 patients during 26 years. We investigated the provoked spasm configuration, spasm site, and clinical characteristics of provoked spasm between ACh and ER, retrospectively. We defined positive spasm as ≥90% luminal narrowing. Provoked positive spasm was observed in 161 right coronary arteries (RCA) including 83 ACh just positive, 35 ER just positive, and 43 both positive. In contrast, positive spasm was documented in 172 left coronary arteries (LCA) including 94 ACh just positive, 28 ER just positive, and 50 both positive. ACh provoked spasm more distally and diffusely, while ER induced spasm more proximally and totally or focally in the RCA. In the LCA, ACh provoked spasm more proximally, whereas ER induced spasm more distally. ER testing after the negative ACh tests of RCA and LCA documented new positive spasms in 10.3% (35/340) and 7.4% (28/376), respectively. Coronary artery trees may each have a sensitive receptor on each segment. We recommend the supplementary use of ACh and ER to document coronary artery spasm in the cardiac catheterization laboratory.

Impact of septal curvature on regional strain in patients with hypertrophic cardiomyopathy.

BACKGROUND: The interventricular septum in hypertrophic cardiomyopathy (HC) has a unique shape, which is characterized by the convex curvature toward the left ventricle (LV). The aim of this study was to examine the relationship between curvature of the LV wall and regional myocardial strain. METHODS AND RESULTS: Fifty-six patients with HC (mean age, 55±12 years) and 20 age- and sex-matched control subjects (mean age, 56±8 years) were enrolled. The curvature index (1/radius) was measured by drawing along the endocardial surface from the apical 4-chamber and short axis views. Peak systolic strain was calculated in the septal and lateral walls using 2-D speckle tracking echocardiography. The septal curvature index and septal longitudinal strain were significantly lower in the HC group than in the control group. A multivariate model using the HC patient data showed that the septal curvature index and septal thickness were the independent determinants of septal longitudinal strain (septal curvature index: ß=-0.421, P<0.001; septal thickness: ß=0.401, P=0.002). In addition, global longitudinal strain and E/e' were worse in the lower septal curvature index group compared with the higher group. CONCLUSIONS: Septal longitudinal strain is associated with the degree of septal curvature. This indicates a possible link between LV wall configuration and regional myocardial function.

Myocardial fibrosis attenuates the effect of cibenzoline on left ventricular diastolic function in patients with hypertrophic cardiomyopathy.

The aim of this study was to investigate the relationship between late gadolinium enhancement (LGE) and the effect of cibenzoline (CBZ) on left ventricular (LV) diastolic function in hypertrophic cardiomyopathy (HCM) patients. Echocardiography before and after intravenous CBZ (1.4 mg/kg over 5 minutes) and magnetic resonance imaging (MRI) were performed in 22 consecutive patients with HCM [mean age: 65 ± 14 years, obstructive HCM: 14, nonobstructive HCM (HNCM): 8]. The extent of LGE (%LGE = LGE volume/total LV volume) was obtained by contrast-enhanced MRI using custom software. LGE was observed in 19 patients (mean %LGE = 5.1% ± 3.9%). The propagation velocity of LV early filling flow (Vp) increased significantly in patients with obstructive HCM (26 ± 7 to 36 ± 14 cm/s, P = 0.001) and nonobstructive HCM (25 ± 9 to 36 ± 16 cm/s, P = 0.007). A significant negative correlation was observed between the change in Vp and %LGE in patients with HCM (r = 20.542, P = 0.009). Less extensive myocardial fibrosis, as demonstrated by LGE on contrast-enhanced MRI, may predict the ability of CBZ to improve LV diastolic function in HCM.

Right ventricular septal pacing preserves global left ventricular longitudinal function in comparison with apical pacing: analysis of speckle tracking echocardiography.

BACKGROUND: Right ventricular (RV) pacing alters left ventricular (LV) mechanical activation, resulting in adverse impacts on LV function. This study was aimed to investigate the acute effect of RV apical (RVA) and septal pacing (RVS) on LV dyssynchrony and function using speckle tracking echocardiography. METHODS AND RESULTS: The 103 patients (749 years) with symptomatic bradyarrhythmia and preserved LV ejection fraction, and 50 age-matched control subjects were studied. All patients received a permanent pacemaker and were randomly assigned into 2 groups (RVA: n = 51, RVS: n = 52). After insertion, patients underwent an echocardiographic study during RV pacing. LV dyssynchrony and global strain parameters were analyzed using speckle tracking echocardiography. The QRS width and dyssynchrony indices by longitudinal and radial strain were significantly greater in RVA than in both the control and RVS. The LV longitudinal dyssynchrony index was significantly related to global longitudinal strain (GLS) among 103 patients receiving RV pacing (R² = 0.25, P < 0.0001). The GLS in RVA were the lowest among the 3 groups (GLS: CONTROL: -18.22.4%, RVA: -14.33.1%, P < 0.001 vs. control, RVS: -16.82.7%, P<0.01 vs. RVA). CONCLUSIONS: RVA created heterogeneous LV contraction, which resulted in deteriorated LV longitudinal contraction. RVS could be a better pacing alternative in terms of less LV dyssynchrony and better longitudinal function compared to RVA.

Eplerenone with valsartan effectively reduces atherosclerotic lesion by attenuation of oxidative stress and inflammation.

OBJECTIVE: Angiotensin II contributes to atherogenesis, mainly through oxidative stress and inflammation. Recent data suggest that aldosterone is implicated in some effects of angiotensin II. We hypothesized that aldosterone could directly contribute to oxidative stress and atherosclerotic lesion formation. METHODS AND RESULTS: Male apolipoprotein E-deficient mice 6 weeks of age were placed on a normal diet or 1.25% high-cholesterol diet. After 6 weeks of the high-cholesterol diet, a marked increase in atherosclerotic lesion formation was observed in the aorta, accompanied by significant elevation of plasma cholesterol level. Production of superoxide anion and expression of NAD(P)H oxidase subunit p47phox, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 in the aorta were increased with the high-cholesterol diet. Eplerenone (1.67 g/kg in high-cholesterol diet) did not affect blood pressure or plasma cholesterol but decreased the atherosclerotic area by nearly 70% (P<0.05), associated with attenuation of oxidative stress and inflammatory response. Valsartan (0.5 mg/kg per day) also decreased the atherosclerotic lesion, whereas coadministration of valsartan and eplerenone further decreased it. Moreover, aldosterone (0.1 micromol/L) enhanced NADPH oxidase activity in cultured vascular smooth muscle cells. CONCLUSIONS: These results suggest that aldosterone may play a critical role in atherogenesis subsequent to oxidative stress in part independent of angiotensin II-mediated signaling, and that eplerenone could prevent atherosclerosis by attenuating oxidative stress and inflammation.

Heterogeneous Intravascular Ultrasound Findings of Stent Thrombosis.

Objective The underlying mechanisms of stent thrombosis are not completely understood. Methods We experienced 12 definite stent thrombosis cases (1 early, 1 late, and 10 very late) at our hospital from July 2011 to April 2016 and evaluated the possible causes of stent thrombosis by intravascular ultrasound (IVUS). Results Five different potential morphological causes of stent thrombosis (neoatherosclerosis, stent malapposition, stent fracture, edge dissection, and stent underexpansion) were detected by IVUS in 10 cases (83.3%); in 1 of the remaining 2 cases, the discontinuation of antithrombotic drugs resulted in early stent thrombosis without abnormal IVUS findings. Of the 12 stent thrombosis cases, 4 occurred at a bare-metal stent (average time from stent implantation, 106 months); in all 12, significant neointimal hyperplasia was observed on IVUS, and 2 had plaque ruptures at an in-stent or proximal reference. Malapposed stent struts were observed in three very-late stent thromboses, and all of these underwent sirolimus-eluting stent implantation. Stent thrombosis due to mechanical (stent fracture) or procedure-related complications (edge dissection and stent underexpansion) was observed in three cases. Conclusion In patients with stent thrombosis, heterogeneous findings were observed in IVUS. This IVUS case series illustrates the possible mechanisms of stent thrombosis.

Amlodipine treatment reduces stroke size in apolipoprotein E-deficient mice.

BACKGROUND: This study investigated the effects of amlodipine, an L-type calcium channel blocker, on stroke size after focal brain ischemia in apolipoprotein E-deficient (ApoE KO) mice. METHODS: Mice were subjected to middle cerebral artery (MCA) occlusion after being given a high-cholesterol (HCD) or normal diet for 10 weeks with or without amlodipine at a nonhypotensive dose of 3 mg/kg/day. Ischemic brain area was measured by 2,3,5-triphenyltetrazolium chloride staining. Cerebral blood flow was analyzed by laser-Doppler flowmetry. Superoxide anion production in the brain was detected by dihydroethidium staining. RESULTS: The ApoE KO mice given HCD for 10 weeks showed a larger ischemic lesion size than mice with a normal diet. Amlodipine treatment in parallel with HCD feeding reduced the ischemic lesion size in ApoE KO mice. Interestingly, amlodipine treatment for only the last 2 weeks was also effective in reducing the ischemic lesion size in HCD-fed ApoE KO mice. The neurologic deficit after MCA occlusion was also improved by amlodipine treatment for either 10 weeks or 2 weeks. The decrease in surface cerebral blood flow after MCA occlusion was significantly attenuated in the peripheral region of the MCA territory in amlodipine-treated mice. Amlodipine treatment in HCD-fed ApoE KO mice also reduced superoxide production in the ischemic area of the brain. CONCLUSIONS: These results suggest that amlodipine treatment reduces stroke size and neurologic deficit after focal brain ischemia, possibly through an increase in cerebral blood flow and inhibition of superoxide production.

Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions.

We examined whether amlodipine, an L-type calcium channel blocker (CCB), has an inhibitory effect on oxidative stress and inflammatory response, and thereby atherosclerosis, in apolipoprotein E-deficient (ApoEKO) mice. Adult male ApoEKO mice (6 weeks of age) were fed a high-cholesterol diet (HCD) for 8 or 10 weeks with or without oral administration of amlodipine (3 mg/kg/day) for 10 weeks or for only the last 2 weeks of the HCD. After HCD feeding, atherosclerotic lesion formation, in situ superoxide production and nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity were evaluated in the proximal aorta. The expressions of NADPH oxidase subunits (p47(phox) and rac-1), monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) were determined with immunohistochemistry and quantitative real-time reverse-transcription polymerase chain reaction. After 8 to 10 weeks of HCD administration to ApoEKO mice, marked atherosclerotic lesion formation was observed in the proximal aorta. In the atherosclerotic lesion, superoxide production, the expression of NADPH oxidase subunits, and NADPH oxidase activity were enhanced, and the expressions of MCP-1, ICAM-1, and VCAM-1 were increased. These changes were suppressed in mice that were treated with amlodipine for 10 weeks concomitant with HCD administration, with no significant change in blood pressure and plasma cholesterol level. We also observed that treatment with amlodipine for only the last 2 weeks regressed the atherosclerotic lesions with a decrease in oxidative stress and vascular inflammation. Inhibition of the atherosclerotic lesion area and lipid area in the proximal aorta by amlodipine was correlated with its inhibitory actions on oxidative stress, inflammation and the production of adhesive molecules. These results suggest that amlodipine not only inhibits atherosclerotic lesion formation, but also regresses atherosclerosis, and that these effects are at least partly due to inhibition of oxidative stress and inflammatory response.

Effect of combination of calcium antagonist, azelnidipine, and AT1 receptor blocker, olmesartan, on atherosclerosis in apolipoprotein E-deficient mice.

OBJECTIVE: Angiotensin II type 1 receptor blockers (ARB) are widely recognized to have a vasculoprotective effect. Accumulating data have revealed that calcium antagonists also retard atherosclerosis. We examined the possibility that combination therapy of ARB and calcium antagonists could more effectively prevent atherosclerosis than monotherapy. METHODS AND RESULTS: We observed a marked increase in the atherosclerotic area, associated with the exaggerated expression of nicotinamide adenine dinucleotide (phosphate), reduced form [NAD(P)H] oxidase subunits (p22 and p47) and superoxide anion production, in the aorta of apolipoprotein E-deficient mice maintained on a 1.25% high-cholesterol diet for 10 weeks. A calcium antagonist, azelnidipine, at a dose of 1 mg/kg a day or an ARB, olmesartan, at a dose of 3 mg/kg a day, significantly inhibited these parameters, with no change in systolic blood pressure and the blood cholesterol level. Moreover, the co-administration of lower doses of azelnidipine (0.1 mg/kg a day) and olmesartan (1 mg/kg a day) significantly inhibited the atherosclerotic area and oxidative stress, whereas azelnidipine or olmesartan alone at these doses did not affect these parameters. Furthermore, we observed similar inhibitory effects of azelnidipine or olmesartan on angiotensin II-induced NADPH oxidase activity and Akt activity in cultured vascular smooth muscle cells. CONCLUSION: These results suggest that the co-administration of calcium antagonists and ARB synergistically blunts oxidative stress at least partly through the inhibition of Akt activity and enhances the beneficial effects of these drugs on atherosclerosis compared with monotherapy.

Relationship between augmentation index and left ventricular diastolic function in healthy women and men.

BACKGROUND: The aim of this study was to investigate the effect of sex on the correlation between arterial stiffness and left ventricular (LV) diastolic function in a healthy population without significant atherosclerosis. METHODS: Subjects (n = 446) who had simultaneous echocardiography and arterial stiffness recordings were enrolled. From these subjects, 95 men and 72 age-matched women without atherosclerotic risk factors (hypertension, dyslipidemia, and diabetes mellitus) were included in the analysis. We measured brachial-ankle pulse wave velocity (baPWV) and carotid augmentation index (AIx) as arterial stiffness parameters. RESULTS: Peak early diastolic mitral annular velocity (e') was significantly correlated with baPWV (men: r = -0.428, P < 0.001; women: r = -0.515, P < 0.001) and carotid AIx (men: r = -0.295, P = 0.004; women: r = -0.558, P < 0.001). The ratio of early diastolic mitral flow velocity to e' (E/e') was significantly correlated with both arterial stiffness parameters in women but not men. Multivariable regression analysis revealed carotid AIx (ß = -0.257; P = 0.02) was a significant independent predictor of e' in women but not men. CONCLUSIONS: These results suggest that the correlation between AIx and LV diastolic function is stronger in women than men in a healthy population.

Role of transthoracic Doppler echocardiography in patients with a proximal left coronary artery lesion that cannot be diagnosed by computed tomography angiography.

The diagnosis of lesions with severe calcium or in-stent stenosis using coronary computed tomography angiography (CCTA) is still difficult. The aim of the present study was to evaluate the accuracy of transthoracic Doppler echocardiography (TTDE) in patients with suspected angina pectoris, who had a proximal left coronary artery (LCA) site that could not be evaluated by CCTA. Fifty-eight patients were evaluated. The proximal LCA was defined as the left main coronary artery and proximal left anterior descending coronary artery. All patients underwent TTDE and had coronary angiography performed as a reference method. We measured the proximal left coronary flow velocity (CFV) by both color and pulse Doppler methods. Proximal coronary flow was detected in 45 (78%) of 58 patients. CFVs measured by both methods were significantly greater in the group with severe stenosis (percent diameter stenosis >70%) than in the groups with moderate stenosis (percent diameter stenosis 40% to 70%) or without stenosis (color Doppler: 148 ± 42 cm/s, 89 ± 40 cm/s, and 41 ± 22 cm/s, respectively, p <0.05; pulse Doppler: 143 ± 61 cm/s, 82 ± 33 cm/s, and 39 ± 17 cm/s, respectively, p <0.05). Receiver operating characteristic curve analysis showed that the optimal CFV cut-off values obtained by color and pulse Doppler to diagnose severe stenosis were 92 cm/s (sensitivity, 100%; specificity, 90%) and 81 cm/s (sensitivity, 100%; specificity, 85%), respectively. In conclusion, TTDE could diagnose proximal LCA stenosis with good accuracy in patients who could not be evaluated by CCTA.

Carotid arterial circumferential strain by two-dimensional speckle tracking: a novel parameter of arterial elasticity.

Recently, the development of two-dimensional speckle-tracking (2DST) technology has allowed the direct measurement of the elastic parameters of the carotid arterial wall. The aims of this study were to determine the feasibility of measuring peak circumferential strain (CS) of the carotid arterial wall using 2DST and to compare this value with conventional arterial stiffness parameters in subjects with and without hypertension. The study included 90 healthy subjects and 40 age-and sex-matched patients with hypertension. The short-axis view of the right common carotid artery was recorded. The CS in the posterior region of the carotid artery was calculated by 2DST using special software and corrected by the following equation: ɛ(circ)=ln (systolic blood pressure/diastolic blood pressure)/CS. We simultaneously measured the stiffness index ß (ß) at the same location and the brachial-ankle pulse wave velocity (baPWV). Sixty randomly selected healthy subjects were used to assess the inter/intra-observer variability of ɛ(circ) and ß. In healthy subjects, ɛ(circ) was significantly correlated with ß, age and baPWV. These correlations were slightly better than the corresponding correlations of ß with age and baPWV. The hypertensive patients had a significantly larger ɛ(circ) than the healthy subjects (0.112 ± 0.074 vs. 0.066 ± 0.029/%, P<0.001). The inter/intra-observer variability for ɛ(circ) was significantly lower than that for ß. Our data suggest that the measurement of carotid ɛ(circ) using 2DST is feasible and has better reproducibility than conventional carotid arterial stiffness.

Acute effects of adaptive servo ventilation on hemodynamics, coronary flow, and flow reserve in a patient with idiopathic dilated cardiomyopathy.

Adaptive servo ventilation (ASV) is reported to be effective for the treatment of heart failure. We treated a patient with idiopathic dilated cardiomyopathy using ASV and assessed the effects on hemodynamics, coronary flow, and flow reserve before and after ASV therapy. This case suggests that ASV might decrease myocardial oxygen demand, which was represented by the decreased resting coronary flow velocity (the improvement of coronary flow velocity reserve) on ASV.

Direct measurement of radial strain in the inner-half layer of the left ventricular wall in hypertensive patients.

BACKGROUND: Two-dimensional speckle tracking echocardiography (2D-STE) is a novel technology that directly measures regional left ventricular (LV) wall contraction. This study aimed to directly measure inner-layer thickening (radial strain) of the LV using 2D-STE, and to examine the relationship between radial strain and the degree of hypertrophy. METHODS: The study enrolled 63 untreated hypertensive patients with normal geometry (N group, n=32) or concentric hypertrophy (CH group, n=31), classified according to LV mass index (LVMI) and relative wall thickness (RWT). Thirty normotensive subjects (C group, n=30) served as controls. Radial strain (ɛ) in the inner half (ɛi) and all layers of the LV wall (ɛa) were calculated from the LV short-axis view by 2D-STE. RESULTS: LV ejection fraction did not differ significantly among the groups. However, ɛi and ɛa were significantly lower in the CH group compared with the C and N groups (p<0.01). A ratio of ɛi to ɛa was significantly lower in the CH group compared with the C and N groups (p<0.01). A multivariate regression model that included midwall fractional shortening, E/e', LVMI, RWT, and LV ejection fraction showed that LVMI (p=0.002) and RWT (p=0.014) were independent predictors (R(2)=0.59) of ɛi. CONCLUSION: Radial strain in the inner half layer of the LV wall decreases in parallel with the degrees of LV concentricity and hypertrophy in hypertensive patients. Radial strain in the inner half layer may identify subtle systolic dysfunction even in hypertensive patients with preserved LV chamber function.

Clinical significance of global two-dimensional strain as a surrogate parameter of myocardial fibrosis and cardiac events in patients with hypertrophic cardiomyopathy.

AIMS: Late gadolinium enhancement (LGE) on contrast-enhanced magnetic resonance imaging (MRI) in hypertrophic cardiomyopathy (HCM) has been reported to be associated with myocardial fibrosis and cardiac events. In patients with HCM, two-dimensional (2D) strain can identify subclinical global systolic dysfunction despite normal left ventricular (LV) chamber function. Therefore, this study tested the hypothesis that global 2D strain could detect subtle myocardial fibrosis and serve as a novel prognostic parameter in HCM patients. METHODS AND RESULTS: Echocardiography and MRI were performed in 48 consecutive patients with HCM and normal chamber function. We measured global longitudinal strain (GLS) in apical two-chamber, four-chamber, and long-axis views using speckle-tracking analysis. The extent of LGE (%LGE = LGE volume/total LV volume) and LV mass index were calculated by MRI using Simpson's rule and custom software. All patients were followed up for major cardiac events. Global longitudinal strain in patients with LGE was significantly lower than that without LGE (-11.8 ± 2.8 vs. -15.0 ± 1.7%, P < 0.001). Multivariate analysis showed that GLS was an independent predictor of %LGE (standard coefficient = 0.627, P < 0.001). During a mean follow-up period of 42 ± 12 months, five patients had cardiac events. When the patients were stratified based on the median level of GLS (-12.9%), all events were observed in the worse GLS group (P = 0.018). CONCLUSION: These results suggest that global 2D strain might provide useful information on myocardial fibrosis and cardiac events in HCM patients with normal chamber function.

Impact of type 2 diabetes on serial changes in tissue characteristics of coronary plaques: an integrated backscatter intravascular ultrasound analysis.

AIMS: Several studies have demonstrated that type 2 diabetes mellitus (T2DM) is associated with accelerated atherosclerosis, which results in an increased risk of coronary vascular events. However, serial changes in plaque characteristics have not been reported in vivo. We evaluated the progression of coronary atherosclerosis in patients with T2DM using an integrated backscatter intravascular ultrasound (IB-IVUS) examination. METHODS AND RESULTS: Forty-two T2DM and 48 non-diabetic patients who underwent percutaneous coronary intervention were enrolled in the study. Non-culprit 20-mm length coronary lesions with mild-to-moderate stenosis were measured using a 40-MHz (motorized pullback of 0.5 mm/s) IVUS catheter. IVUS examinations were performed on one target lesion in each patient. Six months later, a follow-up IVUS examination was repeated in the same coronary segment imaged at the baseline examination. T2DM patients demonstrated a greater total plaque volume (TPV; 139 ± 53 vs. 114 ± 45 mm(3), P = 0.02) and total lipid volume (TLV; 67 ± 26 vs. 55 ± 30 mm(3), P = 0.039) at the baseline examination. The progression of TPV (8.6 ± 15.4 vs. -2.2 ± 16.0%, P < 0.01) and TLV (10.8 ± 28.8 vs. -2.5 ± 20.0%, P < 0.05) from the baseline was observed in T2DM patients, but not in non-diabetic patients. The increase in TLV was blunted in T2DM patients who achieved HbA1c levels of <6.5%. CONCLUSION: Accelerated plaque progression with an increase in the lipid-rich component of non-culprit plaques was observed in T2DM, despite the use of standard medical treatment. Better glycaemic control ameliorated the worsening of plaque characteristics in T2DM.

Usefulness of the MOSAIC (measurement of stenosis by aliasing coronary flow) method using transthoracic color Doppler echocardiography in unstable angina patients.

BACKGROUND: The aim of this study was to investigate the significance of the MOSAIC (measurement of stenosis by aliasing coronary flow) method for the detection of proximal left coronary stenosis in patients with unstable angina (UA) using transthoracic Doppler echocardiography (TTDE). METHODS: Patients (n=107) with UA were evaluated. Proximal left coronary flow was sought in the short axis (SAX) at the aortic root level using color Doppler guidance. When detected coronary flow showed color aliasing, the color velocity range was gradually increased until color aliasing nearly disappeared. Then, the color baseline was shifted until the color flow showed "isovelocity". RESULTS: Proximal coronary flow was detected in 86 (80.4%) of 107 patients. In these 86 patients, an optimal cutoff value of isovelocity ≥ 47.5 cm/s predicted significant coronary stenosis (percent diameter stenosis ≥ 70%) of the proximal left anterior descending (AHA segment 6) or left main coronary artery with a sensitivity of 88%, specificity of 97%, positive predictive value of 98%, and negative predictive value of 86%. In all 107 patients, the same cutoff value predicted significant coronary stenosis with a sensitivity of 78%, specificity of 98%, positive predictive value of 98%, and negative predictive value of 81%. CONCLUSIONS: The MOSAIC method may play a complementary role in expeditious risk stratification and decision making in patients with UA.

The differences in left ventricular torsional behavior between patients with hypertrophic cardiomyopathy and hypertensive heart disease.

BACKGROUND: The aim of this study was to investigate the differences in left ventricular (LV) twisting behavior between patients with hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD). METHODS: Forty-four patients with HCM (mean age, 63±15 years), 35 patients with HHD (mean age, 63±13 years) and 20 age and sex-matched control subjects were evaluated. After a standard echocardiographic examination, LV twist and twisting velocity profiles from apical and basal short-axis images were analyzed using two-dimensional speckle tracking imaging. RESULTS: LV diastolic and systolic dimensions, and ejection fraction were not significantly different among the groups. LV mass index and early diastolic mitral annular velocity were not significantly different between the HCM and HHD groups. The peak torsion in the HCM and HHD groups was significantly greater than that in the control group. The peak untwisting velocity in the HCM group was comparable with that in the control group. However, when the peak untwisting velocity was corrected by peak torsion, this ratio was significantly decreased in the HCM group compared with the values in the HHD and control groups. The time to peak untwisting velocity in the HCM group was significantly longer than the values in the HHD and control groups. CONCLUSIONS: These results suggest that enhanced peak torsion in HCM may improve untwisting behavior, but this mechanism fails to fully compensate for impaired untwisting behavior compared with HHD.