JRSM Cardiovascular Disease最新文献

Objective: Apelin is a novel adipocytokine with a significant role in ischemia/reperfusion injury that is synthesized and secreted in myocardial cells and coronary endothelium. There is debate on its value for the diagnosis and prognosis of myocardial infarction. We aimed to investigate plasma apelin level in patients with acute ST segment elevation (STEMI) and non-ST segment elevation (NSTEMI) myocardial infarction and its relationship with left ventricular function and prognostic parameters.

Methods: Forty-one patients with STEMI, 21 patients with NSTEMI and 10 patients as control group with normal coronary angiograms were included. Plasma apelin level at presentation was investigated regarding its relationship with other diagnostic and prognostic parameters.

Results: Apelin level was significantly higher in acute myocardial infarction (0.31 ± 0.56 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Likewise, it was found to be significantly higher in STEMI group (0.45 ± 0.73 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Although apelin was higher in NSTEMI group (0.13 ± 0.10 ng/mL) compared to control group (0.08 ± 0.05 ng/mL), this difference was not statistically significant (p > 0.05). No correlation was found between apelin and NT-proBNP, hsCRP, troponin, ejection fraction (EF) and Killip score (p > 0.05). A positive correlation was found between apelin and TIMI, GRACE and Gensini scores (p < 0.05). Only GRACE score was found to be correlated with apelin in MI groups.

Conclusion: Apelin level was found to be high in acute myocardial infarction. With its inotropic and vasodilator effects, apelin was thought to have a protective role against severe ischemia.

The coronary angiogram is an indicator of flow limiting coronary artery disease but coronary physiology at the time of angiography is vital in assessing the true functional significance of coronary artery disease. With advances in guidewire technology and the greater use of physiology within the catheter laboratory, there is now a slow evolution of physiological indices in being able to reliably assess the functional significance of individual lesions and also the adequacy of revascularization in a growing range of clinical scenarios. As co-registration of physiology with the angiogram and intravascular imaging will become easier, we will find ourselves increasingly in an era of 'Precision PCI'.

Objective: We evaluated the efficacy and safety of the bosentan as a sequential add-on therapy with sildenafil in pulmonary arterial hypertension with congenital heart disease (PAH-CHD) patients.

Material and method: Twenty patients who were receiving sildenafil were given generic bosentan for up to a year. Hemodynamic data was collected from cardiac catheterization at pretreatment and at three months. Comparisons were made between the total scores of the four, low-risk criteria adapted from the 2015 ESC/ERS pulmonary hypertension guidelines, which are: 1) WHO functional class of I or II, 2) 6MWD of more than 440 m, 3) right atrial pressure of less than 8 mm Hg, and 4) cardiac index ≥2.5 L/min/m², performed at the beginning of therapy, 3-months, 6-months, and 1 year.

Results: Patients' average age was 27 ± 11 years old (12-53). PVRi decreased from 16.7 ± 9.5 to 12.7 ± 10.3 Wood unit (WU) m2 (p = 0.025) and PVRi/SVRi decreased from 0.69 ± 0.33 to 0.49 ± 0.32 (p = 0.001). During the follow-up, the composite scoring of the low risk scores for 19 patients was increased significantly from 1.8 ± 1.0 at baseline to 2.3 ± 0.9 at 3 months, to 2.9 ± 0.8 at 6 months, and 3 ± 0.7 at 1 year (p = 0.001).

Conclusion: We demonstrated intermediate term benefits for generic bosentan as an add-on therapy to sildenafil in patients with PAH-CHD by improving PVRi, and PVRi/SVRi at three months. A significant improvement was also seen in the combined scores of the low-risk criteria from below 2 to 3 at one year (p = 0.001).Thai Clinical Trials Registry (TCTR): TCTR identification number is TCTR20200506006.

Introduction: A significant proportion of ischemic strokes are caused by emboli from unstable atherosclerotic carotid artery plaques. Inflammation is a key feature of plaque instability. Positron emission tomography/computed tomography (PET/CT) with 2-deoxy-2-(¹⁸F)-fluoro-D-glucose (¹⁸F-FDG) is a promising technique to quantify plaque inflammation, but a consensus on the methodology has not been established. High inter-reader agreement is essential if ¹⁸F-FDG PET/CT is to be used as a clinical tool for the assessment of unstable plaques and stroke risk.

Methods: We assessed the inter-reader variability of different methods for quantification of ¹⁸F-FDG uptake in 43 patients with carotid artery stenosis ≥70%. Two independent readers delineated the plaque and collected maximum standardized uptake value (SUV_max) from all axial PET slices containing the atherosclerotic plaque.

Results: Uptake values with and without background correction were calculated and intraclass correlation coefficients were highest for uncorrected uptake values (0.97-0.98) followed by those background corrected by subtraction (0.89-0.94) and lowest for those background corrected by division (0.74-0.79).

Conclusion: Quantification methods without background correction have the highest inter-reader agreement for ¹⁸F-FDG PET of carotid artery plaque inflammation. The use of the single highest uptake value (max SUV_max) from the plaque will facilitate the method's clinical utility in stroke prevention.

The floating venous thrombus in the common femoral vein has a high potential risk for pulmonary embolization. Clinical treatments, using anticoagulants or fibrinolytic, open thrombectomies, or thrombectomies by endovascular devices have all been used. Our case describe an obese patient affected by floating thrombus coming from GSV and diving in common femoral vein successful treated by combined both temporary vena cava insertion and open surgical thrombectomy.

The netrins form a family of laminin-related proteins which were first described as modulators of cell migration and axonal guidance during fetal development. Netrin-1 is the most extensively studied member of this family and, since its discovery, non-neural roles have been associated with it. Together with its receptors, DCC/neogenin and UNC5, netrin-1 has been shown to be involved in the regulation of angiogenesis, organogenesis, cancer and inflammation. An NF-κB-dependent truncated isoform of netrin-1 has also been shown to be produced in endothelial and some types of cancer cells, which both accumulates in and affects the function of the nucleus. In atherosclerosis, conflicting roles for netrin-1 have been reported on plaque progression via its receptor UNC5b. Whereas endothelial-derived netrin-1 inhibits chemotaxis of leukocytes and reduces the migration of monocytes to the atherosclerotic plaque, netrin-1 expressed by macrophages within the plaque plays a pro-atherogenic role, promoting cell survival, recruiting smooth muscle cells and inhibiting foam cell egress to the lymphatic system. In contrast, there is evidence that netrin-1 promotes macrophage differentiation to an alternative activated phenotype and induces expression of IL-4 and IL-13, while downregulate expression of IL-6 and COX-2. Further work is needed to elucidate the precise roles of the two isoforms of netrin-1 in different cell types in the context of atherosclerosis, and its potential as a putative novel therapeutic target in this disease.

Objective: Right heart catheterization (RHC) is associated with a higher procedural risk in older adults, but non-invasive estimation of pulmonary hypertension (PH) is a challenge. We aimed to elaborate a non-invasive prediction model to estimate PH.

Methods and design: We retrospectively analysed 134 older adults (70.0 years ±12.3; 44.9% males) who reported to our clinic with unclear dyspnea between 01/2015 and 01/2020 and had received RHC as a part of their diagnostic workup. Lung function testing, analysis of blood gas samples, 6 min walk distance and echocardiography were performed within 24 hours of RHC.

Main outcome measures: In a stepwise statistical approach by using an in/exclusion algorithm (using the AIC criterion) we analysed non-invasive parameters to test their value in predicting PH (defined as mean pulmonary artery pressure, PA_mean, >25mmHg). Discrimination capability of the final model was measured by the AUC (area under curve) from an ROC (receiver operating characteristics) analysis.

Results: We yielded a sensitivity of 87.2% and a specificity of 62.5% in a combinatorial logistical model with systolic pulmonary artery pressure (sPAP) and forced vital capacity (VC_max), the discrimination index was 86.7%. The odds ratios for an increase of 10 mmHg of sPAP were 2.99 (2.08-4.65) and 1.86 (1.11-3.21) for a 1 l decrease in VC_max. On their own, VC_max proved to be specific (83.3%), while sPAP was a sensitive (79.1%) predictor for PH.

Conclusions: We provide a combinatorial model to predict PH from sPAP and VC_max in older adults, which may help to avoid invasive procedures.

Introduction: In this study, we aimed to investigate the relationship between coronary slow flow (CSF) and carotid-femoral pulse wave velocity (CFPWV).

Methods: 78 (27 women, mean age 43.95 ± 7.28) patients with CSF, and 70 (22 women, mean age 44.34 ± 7.08) healthy individuals were included in the study. Arterial stiffness measurement was performed to both groups via CFPWV, which is considered the gold standard. Aortic elastic properties (ASI-β and aortic distensibility) were evaluated in both groups.

Results: The CSF group had significantly higher CFPWV and aortic distensibility values and significantly lower ASI-β values compared to the control group. There was a positive correlation between TIMI frame count (TFC) obtained in all coronary arteries and CFPWV and aortic distensibility, and a negative correlation between TFC and ASI-β. It was determined that CFPWV predicted CSF with 97% specificity and 98% sensitivity at a 7.68 cut-off value (ROC area = 994, p < 0.001). ASI-β was determined to predict CSF with 64% specificity and 47% sensitivity at a 2.98 cut-off value (ROC area = 047, p < 0.001). Aortic distensibility was determined to predict CSF with 76% specificity and 79% sensitivity at a 3.94 cut-off value (ROC area = 706, p < 0.001).

Conclusion: Arterial stiffness increases in CSF patients, suggesting that CSF is a systemic pathology rather than a local disease and that a systemic cause such as atherosclerosis plays a role in etiology.

Introduction: Fractional flow reserve (FFR) improves assessment of the physiological significance of coronary lesions compared with conventional angiography. However, it is an invasive investigation. We tested the performance of a virtual FFR (1D-vFFR) using routine angiographic images and a rapidly performed reduced order computational model.

Methods: Quantitative coronary angiography (QCA) was performed in 102 with coronary lesions assessed by invasive FFR. A 1D-vFFR for each lesion was created using reduced order (one-dimensional) computational flow modelling derived from conventional angiographic images and patient specific estimates of coronary flow. The diagnostic accuracy of 1D-vFFR and QCA derived stenosis was compared against the gold standard of invasive FFR using area under the receiver operator characteristic curve (AUC).

Results: QCA revealed the mean coronary stenosis diameter was 44% ± 12% and lesion length 13 ± 7 mm. Following angiography calculation of the 1DvFFR took less than one minute. Coronary stenosis (QCA) had a significant but weak correlation with FFR (r = -0.2, p = 0.04) and poor diagnostic performance to identify lesions with FFR <0.80 (AUC 0.39, p = 0.09), (sensitivity - 58% and specificity - 26% at a QCA stenosis of 50%). In contrast, 1D-vFFR had a better correlation with FFR (r = 0.32, p = 0.01) and significantly better diagnostic performance (AUC 0.67, p = 0.007), (sensitivity - 92% and specificity - 29% at a 1D-vFFR of 0.7).

Conclusions: 1D-vFFR improves the determination of functionally significant coronary lesions compared with conventional angiography without requiring a pressure-wire or hyperaemia induction. It is fast enough to influence immediate clinical decision-making but requires further clinical evaluation.

The peripheral venous system serves as a volume reservoir due to its high compliance and can yield information on intravascular volume status. Peripheral venous waveforms can be captured by direct transduction through a peripheral catheter, non-invasive piezoelectric transduction, or gleaned from other waveforms such as the plethysmograph. Older analysis techniques relied upon pressure waveforms such as peripheral venous pressure and central venous pressure as a means of evaluating fluid responsiveness. Newer peripheral venous waveform analysis techniques exist in both the time and frequency domains, and have been applied to various clinical scenarios including hypovolemia (i.e. hemorrhage, dehydration) and volume overload.