CTA-verified HRP was an independent predictor of ACS. However, the cumulative number of ACS patients with HRP(-) was similar to patients with HRP(+). Additionally, plaque progression detected by serial CTA was an independent predictor of ACS.
Statin treatment induces favorable plaque morphologic changes with an increase in fibrous cap thickness, and decreases in both percentage plaque and lipid volume indexes.
In contrast to the situation with RFC-ACS, distinct culprit lesion characteristics associated with non-rupture-related mechanisms are not identified by CT angiography. It will therefore not be possible to differentiate plaques likely to develop IFC-ACS from stable plaques.
Aims In the updated guidelines for cardiac sarcoidosis (CS) proposed by the Japanese Circulation Society (JCS), the definition of isolated CS (iCS) was established for the first time. This prompted us to examine the characteristics of patients with CS including iCS according to them by reviewing patients undergoing 18 F-fluoro-2-deoxyglucose positron-emission tomography/computerized tomography (FDG-PET/CT), compared with those with CS determined by the conventional international criteria. Methods and results From 2013 to 2019, 94 patients (61 ± 15 years, 50 female patients) with suspected CS underwent whole-body and cardiac FDG-PET/CT scanning. In contrast to 22 patients with CS based on the international criteria, 34 [27 with systemic sarcoidosis including cardiac involvement (sCS) and 7 with definitive iCS] were diagnosed with CS according to the new JCS guidelines (P = 0.012), and 60 were not (4 suspected iCS, 13 systematic sarcoidosis without cardiac involvement, and 43 no sarcoidosis). In addition to 26 of 34 patients with CS, corticosteroids were also started in 6 of 60 without CS according to clinical need. Conclusions Diagnostic yield with the new JCS guidelines was higher, with approximately 1.5-fold of the patients diagnosed with CS compared with the previous international criteria and definitive iCS accounting for approximately 20% of the whole CS cohort. In addition to 75% of the patients with sCS or definitive iCS in the updated guidelines, 10% in whom CS was not documented were also started on corticosteroids for clinical indications such as reduced cardiac function or arrhythmia.
BACKGROUND
Although early reperfusion is the most desirable intervention after ischemic myocardial insult, it may add to damage through oxidative stress.
OBJECTIVES
We investigated the cardioprotective effects of a single intravenous dose of heat shock protein (HSP72) coupled to a single-chain variable fragment (Fv) of monoclonal antibody 3E10 (3E10Fv) in a rabbit ischemia-reperfusion model. The Fv facilitates rapid transport of HSP72 into cells, even with intact membranes.
METHODS
A left coronary artery occlusion (40 min), reperfusion (3 h) model was employed in 31 rabbits. Of these, 12 rabbits received the fusion protein (Fv-HSP72) intravenously. The remaining 19 control rabbits received a molar equivalent of 3E10Fv alone (n = 6), HSP72 alone (n = 6), or phosphate buffered saline (n = 7). Serial echocardiographic examinations were performed to assess left ventricular (LV) function before and after reperfusion. Micro-single photon emission computed tomography imaging of 99mTc-labeled annexin-V was performed with micro-computed tomography to characterize apoptotic damage in vivo, followed by gamma counting of the excised myocardial specimens to quantify cell death. Histopathological characterization of the myocardial tissue, and sequential cardiac troponin I measurements were also undertaken.
RESULTS
Myocardial annexin-V uptake was 43% lower in the area at risk (p = 0.0003) in Fv-HSP72-treated rabbits compared to controls receiving HSP72 or 3E10Fv alone. During reperfusion, troponin I release was 42% lower and the echocardiographic LV ejection fraction 27% higher in the Fv-HSP72-treated group compared to controls. Histopathological analyses confirmed penetration of 3E10Fv-containing molecules into cardiomyocytes in vivo, and treatment with Fv-HSP72 showed fewer apoptotic nuclei compared to control rabbits.
CONCLUSIONS
A single-dose administration of Fv-HSP72 fusion protein at the time of reperfusion reduced myocardial apoptosis almost by half, and improved LV functional recovery following myocardial ischemia-reperfusion injury in rabbits. It might have a potential to serve as an adjunct to early reperfusion in the management of myocardial infarction.
SummaryRecently two-dimensional (2D) speckle tracking echocardiography (STE) derived from right ventricular (RV) free wall has been shown to be a very useful tool for the estimation of RV performance. The purpose of this study was to examine whether RV basal free wall strain can detect increased mean pulmonary arterial pressure (mPAP) in patients with chronic thromboembolic pulmonary hypertension (CTEPH). We investigated a total of 126 patients with CTEPH (mean age, 56 ± 12 years). They underwent echocardiography and right heart catheter examination. 2D STE-derived longitudinal strain was measured by placing 2 regions of interests (ROIs) on the RV basal free wall in RV-focused apical 4-chamber view. Peak strain (RV-PS) was acquired between the 2 ROIs. Conventional echocardiographic RV parameters (RV fractional area change, RV myocardial performance index, tricuspid annular plane systolic excursion, tricuspid annular peak systolic velocity, and tricuspid regurgitant pressure gradient) were evaluated as well. Right heart catheterization was performed on the day following of echocardiographic evaluation. Among RV echo parameters, RV-PS showed the best correlation with mPAP (r = 0.75, P < 0.0001). Receiver operating characteristic analysis revealed that a cut-off value of RV-PS -20.8% could detect mPAP ≧ 25 mmHg (sensitivity 78%, specificity 93%, area under the curve 0.90, P < 0.001). RV basal free wall strain was a useful tool for the non-invasive detection of increased mPAP in patients with CTEPH. (Int Heart J 2015; 56: 100-104) Key words: Peak longitudinal strain, Right ventricular function, Mean pulmonary arterial pressure C hronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening condition characterized by pulmonary thromboemboli that obstruct or obliterate the pulmonary vascular bed, followed by increased pulmonary vascular resistance (PVR) and progressive pulmonary hypertension (PH).Most standard techniques for assessing pulmonary hemodynamics, such as mean pulmonary arterial pressure (mPAP) or PVR, are invasive and impractical for serial assessment. Therefore, a non-invasive method to measure pulmonary hemodynamics accurately is clearly more useful. Echocardiography is a key tool for estimating pulmonary artery pressure in patients with PH. It is valuable in diagnosing, assessing a prognosis, and monitoring the efficacy of treatment.1) However, conventional echocardiographic methods are often challenging to assess right-sided hemodynamics or right ventricular (RV) function because of the complexity of RV anatomy. The recently developed technique, two-dimensional (2D) RV speckle tracking echocardiography (STE), has been introduced for the evaluation of RV function.2,3) The purpose of this study was to examine the utility of 2D RV basal strain in comparison with other RV echocardiographic parameters as well as invasive estimation of pulmonary hemodynamics in patients with CTEPH.
Background:A modestly elevated circulating D-dimer level may be relevant to coronary artery disease (CAD), but its prognostic value, both independently and in combination with estimated glomerular filtration rate (eGFR), for long-term death has not been fully evaluated in stable CAD patients.
Methods and Results:Baseline plasma D-dimer levels and eGFR were measured in 1,341 outpatients (mean age: 65 years) with prior myocardial infarction (MI), coronary revascularization, and/or angiographic evidence of a significant stenosis (>50%) for at least one of the major coronary arteries. Among these patients, 43% had prior MI, 47% had prior coronary revascularization, 41% had multivessel CAD, 14% had paroxysmal or persistent atrial fibrillation, 32% had diabetes, and 32% had chronic kidney disease (eGFR <60 mL/min/1.73 m 2 ). D-dimer levels weakly correlated with eGFR (r=−0.25; P<0.0001). During a mean follow-up period of 73 months, there were 124 deaths, including 61 cardiovascular deaths. Multivariate Cox regression analysis identified D-dimer levels (P=0.001) and eGFR (P=0.006) as independent predictors of all-cause death. Adding both D-dimer and eGFR to a baseline model with established risk factors improved the net reclassification (P<0.005) and integrated discrimination improvement (P<0.05) greater than that of any single biomarker or baseline model alone.
Conclusions:The combinatorial value of assessing D-dimer levels and eGFR may provide useful insight regarding stable CAD patients' long-term risk stratification.
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