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Arteriograph

2014-05-29 18:33:26 | 高血圧



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Arteriograph

2014-05-29 18:32:20 | 高血圧



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Arteriograph

2014-05-29 18:31:09 | 高血圧



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Arteriograph

2014-05-29 18:30:00 | 高血圧



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Arteriograph

2014-05-29 18:28:41 | 高血圧



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Arteriograph

2014-05-29 18:24:13 | 高血圧



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Arterial Stiffness

2014-05-20 17:48:51 | 高血圧
Why you should buy an Arteriograph

Arteriograph- Comprehensive cardiovascular risk assessment in only 3 minutes! - A medical breakthrough in early diagnostics of atherosclerosis!
A big problem today is that many individuals with high risk of cardiovascular diseases otherwise have normal values; normal blood pressure, blood lipids and resting-EKG. The catastrophe strikes without any prior warning. The Arteriograph is an evidence based, fast, easy, noninvasive and user independent way of assessing cardiovascular risk. For the first time one have a good chance of finding high risk patient before it is too late.
1. Screening of early atherosclerosis among ”healthy” individuals. Only the Arteriograph is useful for this. The Arteriograph gives an overall picture of the risk of assessing cardiovascular disease.
2. Evaluating the effects of treatments (drugs, nutritional supplements and lifestyle changes etc) on the vascular functions among patients with established atherosclerosis (CAD, POST MI, STROKE, PAD)
3. Is it not enough to check the blood lipids and blood pressure to prevent atherosclerosis and thereby strokes? No, 40-60% of patients with stroke or heart attacks do not have any know abnormal values such as high amount of blood lipids or high blood pressure (Johns Hopkins White Papers, Coronary Heart Disease - 1998, etc). They also have normal blood glucose values, resting-EKG, are non-smokers and have a healthy diet. Up until now it has been impossible to find there individuals.
4. Todays metods of assessing cardiovascular risk (SCORE, Framingham) all have limits. They do not take into account important factors such as lack of physical activity, overweight, psychological factors or previous cardiovascular circumstances. (Simon, A. and Levenson, J.: May subclinical arterial disease helps to better detect and treat high-risk asymptomatic individuals? J Hypertension 2005, 23: 1939-1945)
5. In most cases, lowering the blood pressure is not enough to avoid early death. Individuals who can lower both their arterial stiffness and blood pressure have a much greater chance of a longer life.Circulation 2001;103:987
6. The Arteriograph is mobile and easy to use. The screening is fast, comfortable, harmless and user independent. It takes only a few minutes and can be described as a computerized blood pressure measurement.
7. Today´s other available methods are hard to use, expensive, and requires an adequate educated staff. In the future, the Arteriograph may replace the regular blood pressure measurement as it is just as easy but gives much more information.

The Arteriograph is intended for DAILY USE at your clinic to measure AIx, PWV and Central blood pressure etc.
Arteriograph- Comprehensive cardiovascular risk assessment in only 3 minutes!

- A medical breakthrough in early diagnostics of atherosclerosis!

A big problem today is that many individuals with high risk of cardiovascular diseases otherwise have normal values; normal blood pressure, blood lipids and resting-EKG. The catastrophe strikes without any prior warning.
The Arteriograph is an evidence based, fast, easy, noninvasive and user independent way of assessing cardiovascular risk. For the first time one have a good chance of finding high risk patients before it is too late .The Arteriograph is also used to evaluate the effect of different medications.

Free demonstration of the Arteriograph on Wednesdays at 5-7 pm at Söderkliniken, Götgatan 82. Please call in advance to let us know that you will be there.

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Arterial Stiffness

2014-05-20 17:47:39 | 高血圧
1. Hypertension. 2010; 55: 124-130 Blood Vessels
Noninvasive Assessment of Arterial Stiffness Should Discriminate Between Systolic and Diastolic Pressure Ranges
1. Evelien Hermeling,
2. Arnold P.G. Hoeks,
3. Mark H.M. Winkens,
4. Johannes L. Waltenberger,
5. Robert S. Reneman,
6. Abraham A. Kroon,
7. Koen D. Reesink
+ Author Affiliations
1. From the Departments of Biomedical Engineering/Biophysics (E.H., A.P.G.H., K.D.R.), Cardiology (M.H.M.W., J.L.W.), Physiology (R.S.R.), and Internal Medicine (A.A.K.), Cardiovascular Research Institute Maastricht/Maastricht University Medical Centre, Maastricht, The Netherlands.
1. Correspondence to Koen D. Reesink, Department of Biomedical Engineering/Biophysics, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands. E-mail k.reesink@bf.unimaas.nl

Next Section
Abstract
Arterial stiffening plays an important role in the development of hypertension and cardiovascular diseases. The intrinsically nonlinear (ie, pressure-dependent) elastic behavior of arteries may have serious consequences for the accuracy and interpretation of arterial stiffness measurements and, ultimately, for individual patient management. We determined aortic pressure and common carotid artery diameter waveforms in 21 patients undergoing cardiac catheterization. The individual pressure-area curves were described using a dual exponential analytic model facilitating noise-free calculation of incremental pulse wave velocity. In addition, compliance coefficients were calculated separately in the diastolic and systolic pressure ranges, only using diastolic, dicrotic notch, and systolic data points, which can be determined noninvasively. Pulse wave velocity at systolic pressure exhibited a much stronger positive correlation with pulse pressure (P<0.001) and age (P=0.012) than pulse wave velocity at diastolic pressure. Patients with an elevated systolic blood pressure (>140 mm Hg) had a 2.5-times lower compliance coefficient in the systolic pressure range than patients with systolic blood pressures <140 mm Hg (P=0.002). Most importantly, some individuals, with comparable age or pulse pressure, had similar diastolic but discriminately different systolic pulse wave velocities and compliance coefficients. We conclude that noninvasive assessment of arterial stiffness could and should discriminate between systolic and diastolic pressure ranges to more precisely characterize arterial function in individual patients.
Key Words:
arterial structure and compliance
pulse wave velocity
blood pressure measurement
systolic hypertension
carotid arteries
Previous SectionNext Section
Introduction
Decreased elasticity of the arterial wall plays an important role in the development of hypertension and related cardiovascular complications, such as heart failure, stroke, and renal failure.1–4 Therefore, noninvasive assessment of arterial stiffness has recently entered the European Society of Hypertension/European Society of Cardiology guidelines for the management of hypertension.5 Basic studies have shown that the elastic behavior of the arterial system is nonlinear, that is, arterial stiffness is pressure dependent.6–11 This intrinsic property of the arterial system may have serious consequences for the quantitative assessment of arterial stiffness, and changes therein, in response to age,12,13 physiological stress,7 and possibly antihypertensive treatment.14,15
Currently, arterial stiffness is assessed noninvasively either at the diastolic pressure level (aortic or carotid-femoral pulse wave velocity [PWV]) or estimated as an average over the diastolic-systolic pressure range. In the latter case, distensibility and compliance coefficients are calculated as, respectively, the relative and absolute changes in the cross-sectional area normalized to pulse pressure from diastolic minimum to systolic peak,16 tacitly assuming a linear pressure-area relationship. In ex vivo human cranial and femoral arteries, Hayashi et al8 found that the relationship between transmural pressure and vessel radius can be described by a single exponential relation. Meta-analysis of studies on the relationship between pressure and cross-sectional vessel area by Powalowski and Pensko17 confirmed this finding. However, Wolinsky and Glagov11 (in rabbit aorta, ex vivo) and Armentano et al6 (in dog aorta, in vivo) observed a more marked change in elasticity as a function of distending pressure, which is related to the ultrastructural interaction of elastin and collagen fiber networks in the tunica media. Viscous behavior of the arterial wall, associated with smooth muscle cell function, is observed ex vivo, especially with prolonged dynamic distension of the vessel, but appears insignificant in vivo if the waveforms are properly acquired and processed.18,19 To the best of our knowledge, the degree of nonlinearity of arterial stiffness in individual cardiovascular patients has not been studied in detail yet. Invasive measurement of pressure-area curves in vivo permits such a comprehensive description of arterial stiffness as a function of pressure.10,19,20 However, the challenge is to derive the pressure-dependent relationship for data obtained noninvasively.
The aim of the present study was to quantify the degree of nonlinearity of the arterial pressure-area relationship to evaluate its consequences for the (noninvasive) assessment of arterial elastic properties. We obtained carotid artery diameter and proximal aortic pressure recordings in patients undergoing cardiac catheterization. We used a dual exponential analytic model to derive incremental PWV for each individual, using all of the data points in the pressure-area range. To explore clinical applicability, we also calculated compliance and distensibility coefficients for the diastolic and systolic pressure ranges separately, on the basis of only diastolic, dicrotic notch, and systolic data points, which can be measured noninvasively with certain confidence. We discuss our findings with regard to the associations with pulse pressure, systolic blood pressure (SBP), and age within our study population and the potential for the application of noninvasive methods in clinical practice.
Previous SectionNext Section
Materials and Methods
Study Population
Patients referred for a diagnostic coronary angiographic procedure were recruited in the outpatient clinic.21 Included patients were either suspected of coronary artery disease (anginal complaints) or had had previous percutaneous transluminal coronary angioplasty or coronary artery bypass grafting. All 21 of the patients gave written informed consent before enrollment. The study was approved by the joint medical ethical committee of Maastricht University and Maastricht University Medical Centre.
Protocol
Patients were prepared for the invasive diagnostic procedure following a standard protocol: overnight fast, refrainment from smoking, and prophylactic anticoagulation (Clopidogrel). Diabetes medication (Metformin), if any, was discontinued on the day of the examination; other medications were taken as usual. Age, weight, and height of the patients were copied from their clinical files. During antiseptic preparations and application of ECG electrodes, patients were in the supine position on the catheterization table, allowing localization of the left common carotid artery by means of a 7.5-MHz linear array/high frame-rate ultrasound system (PICUS, Esaote Europe). All of the ultrasound recordings (see below) were obtained with the patients in this position. If the common carotid artery was located too deep for high frame-rate image acquisition (because of dermal fat), the patient was excluded from the study. After percutaneous access was established by the intervention cardiologist, an angiographic guiding catheter (6F or 7F Wiseguide, Boston Scientific) was advanced over a guide wire and placed with the tip in the ostium of the targeted coronary artery. After initial coronary angiograms were obtained, the catheter was flushed with saline to wash out radiopaque contrast fluid, and the connection to the contrast pump was blocked to achieve the highest possible bandwidth for, and minimal ringing in, the aortic pressure signal. Bench testing of the fluid-filled system showed a flat frequency response from 0 to 25 Hz. At least 3 and maximally 5 repeated echo recordings of the left common carotid artery were obtained simultaneously with a continuous registration of aortic root pressure. The recording session took <4 minutes. After the last ultrasound recording, the angiographic procedure was continued.

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Arterial Stiffness

2014-05-20 17:46:46 | 高血圧
The Scientific World Journal
Volume 2013 (2013), Article ID 792693, 6 pages
http://dx.doi.org/10.1155/2013/792693
Clinical Study
Evaluation of Arterial Stiffness for Predicting Future Cardiovascular Events in Patients with ST Segment Elevation and Non-ST Segment Elevation Myocardial Infarction
Oguz Akkus,1 Durmus Yildiray Sahin,2 Abdi Bozkurt,3 Kamil Nas,4 Kazım Serhan Ozcan,1 Miklós Illyés,5 Ferenc Molnár,6 Serafettin Demir,7 Mücahit Tüfenk,3 and Esmeray Acarturk3
1Sanliurfa Siverek State Hospital, 63600 Sanliurfa, Turkey
2Department of Cardiology, Adana Numune Training and Research Hospital, Adana, Turkey
3Department of Cardiology, Faculty of Medicine, Cukurova University, Adana, Turkey
4Department of Radiology, Szent János Hospital, Budapest, Hungary
5Heart Institute, Faculty of Medicine, University of Pécs, Pécs, Hungary
6Department of Hydrodynamic Systems, Budapest University of Technology and Economics, Budapest, Hungary
7Department of Cardiology, Adana State Hospital, Adana, Turkey
Received 18 August 2013; Accepted 15 September 2013
Academic Editors: H. Kitabata and E. Skalidis
Copyright © 2013 Oguz Akkus et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background. Arterial stiffness parameters in patients who experienced MACE after acute MI have not been studied sufficiently. We investigated arterial stiffness parameters in patients with ST segment elevation (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI). Methods. Ninety-four patients with acute MI (45 STEMI and 49 NSTEMI) were included in the study. Arterial stiffness was assessed noninvasively by using TensioMed Arteriograph. Results. Arterial stiffness parameters were found to be higher in NSTEMI group but did not achieve statistical significance apart from pulse pressure . There was no significant difference at MACE rates between two groups. Pulse pressure and heart rate were also significantly higher in MACE observed group. Aortic pulse wave velocity (PWV), aortic augmentation index (AI), systolic area index (SAI), heart rate, and pulse pressure were higher; ejection fraction, the return time (RT), diastolic reflex area (DRA), and diastolic area index (DAI) were significantly lower in patients with major cardiovascular events. However, PWV, heart rate, and ejection fraction were independent indicators at development of MACE. Conclusions. Parameters of arterial stiffness and MACE rates were similar in patients with STEMI and NSTEMI in one year followup. The independent prognostic indicator aortic PWV may be an easy and reliable method for determining the risk of future events in patients hospitalized with acute MI.
1. Introduction
Acute myocardial infarction (AMI) continues a worldwide cause of mortality [1]. In-hospital and 6-month-mortality are approximately 5–7% versus 12-13%, respectively [2, 3]. Estimated risk of mortality for AMI is based on the clinical status of the patients [4]. Recent studies showed that conventional risk factors are inadequate for predicting cardiovascular (CV) mortality and morbidity. A novel risk factor called arterial stiffness, which is a defined reduction of the compliance of arterial wall, and relationship between coronary heart disease (CHD) have been demonstrated. Arterial stiffness results in faster reflection of the forward pulse wave from bifurcation points in peripheral vessels. As a result of new waveform, systolic blood pressure (SBP) increases, diastolic blood pressure (DBP) decreases, cardiac workload increases, and coronary perfusion falls down. It plays a major role in the determination of cardiovascular outcomes, and it is not inferior to the traditional risk factors to assess the future risk [5, 6]. Elevated arterial stiffness is associated with increased major adverse cardiovascular events (MACE) such as unstable angina, AMI, coronary revascularization, heart failure, stroke, and death [7]. Arterial stiffness parameters including mean arterial pressure (MAP), pulse pressure (PP), PWV (m/s), and augmentation index (AI) are directly proportional to the risk of MACE [8–10].
PWV is a susceptible diagnostic element, and it is also involved in risk stratification for subclinical organ damages [11]. Few studies regarding arterial stiffness demonstrated that PWV exhibits a close effect with coronary heart disease [5, 12, 13]. Whether arterial stiffness parameters are related to MACE after acute MI has not been studied sufficiently. The aim of our study was to compare arterial stiffness parameters in patients with ST segment elevation (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI) and to validate its prognostic value.
2. Patients
Ninety-four patients with acute MI (72 men and 22 women, mean age 60,41 ± 11,17) were included in the study. There were 45 STEMI and 49 NSTEMI. Data of patients were analyzed within 24 hours after hospitalization. All patients received eligible treatment according to ESC guidelines. The choice of preparations was entrusted to the investigator. Hemodynamically compromised patients (Killip classifications II, III, and IV), patients with chronic atrial fibrillation and/or flutter, chronic renal failure, mild-severe valvular heart diseases and other chronic diseases were excluded. Our local ethics committee approved the study, and written informed consent was obtained from all participants. Patients were followed up for 12 months.
3. Diagnosis of Acute Myocardial Infarction
Diagnosis of AMI was based on symptoms, elevated cardiac markers, and electrocardiogram (ECG) changes. Patients with typical chest pain plus ECG changes indicative of an AMI (pathologic Q waves, at least 1 mm ST segment elevation in any 2 or more contiguous limb leads or new left bundle branch block, or new persistent ST segment and T wave changes diagnostic of a non-Q wave myocardial infarction) or a plasma level of cardiac troponin-T level above normal.
4. Laboratory Findings
Troponin T, creatine kinase-MB fraction (CK-MB), serum urea, creatinine, eGFR, and other hematological parameters were checked at the admission.
Risk factors, such as hypertension, hyperlipidemia, diabetes mellitus, cigarette smoking, and family history, were recorded. Hypertension was considered as SBP and DBP greater than 140 mmHg and 90 mmHg, respectively, using an antihypertensive medication. Diabetes mellitus, hyperlipidemia, and hypertriglyceridemia were defined as using antidiabetic drugs or fasting blood glucose over 126 mg/dL, as plasma low-density lipoprotein cholesterol (LDL-C) >130 mg/dL, using lipid-lowering drugs at the time of investigation, and as TG level >150 mg/dL, respectively, according to the Third Report of the National Cholesterol Education Program guidelines. First-degree relatives who are exposed to coronary artery disease (CAD) before the age for male is <55 and female <65 were considered as family history.
5. Pulse Waveform Analysis
Assessment of arterial stiffness was performed noninvasively with the commercially available TensioMed Arteriograph. We collected the oscillometric pulse waves from the patients. We measured the distance between the jugulum-symphysis (which is equal to the distance between the aortic root and the aortic bifurcation), and PWV was calculated. Pulse waves were recorded at suprasystolic pressure. The oscillation signs were identified from the cuff inflated at least >35 mmHg above the systolic blood pressure. In this state there was a complete brachial artery occlusion, and it functions as a membrane before the cuff. Pulse waves hit the membrane, and oscillometric waves were measured by the device and we could see the waveforms on the monitor. The AI was defined as the ratio of the difference between the second (P2 appearing because of the reflection of the first pulse wave) and first systolic peaks (P1 induced by the heart systole) to pulse pressure (PP), and it was expressed as a percentage of the ratio (AI = [P2 − P1]/PP × 100). SBP, DBP, PP, and heart rate and other hemodynamic parameters as return time (RT in sec.), diastolic reflection area (DRA), systolic area index (SAI %), and diastolic area index (DAI %) were measured noninvasively. DRA reflects the quality of the coronary arterial diastolic filling (SAI and DAI are the areas of systolic and diastolic portions under the pulse wave curve of a complete cardiac cycle, resp.). Hence, the bigger the DAI and DRA are, the better the coronary perfusion is. Furthermore, RT is the PWV time from the aortic root until the bifurcation and return, so this value is smaller as the aortic wall is stiffer.


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Arterial Stiffness

2014-05-20 17:46:20 | 高血圧
Can arterial stiffness parameters be measured in the sitting position?
Jens Nürnberger,Rene Michalski,Tobias R Türk,Anabelle Opazo Saez,Oliver Witzke,Andreas Kribben
DOI: 10.1038/hr.2010.196
Despite the introduction of arterial stiffness measurements in the European recommendation, pulse wave velocity (PWV) and augmentation index (AI) are still not used routinely in clinical practice. It would be of advantage if such measurements were done in the sitting position as is done for blood pressure. The aim of this study was to evaluate whether there is a difference in stiffness parameters in sitting vs. supine position. Arterial stiffness was measured in 24 healthy volunteers and 20 patients with cardiovascular disease using three different devices: SphygmoCor (Atcor Medical, Sydney, Australia), Arteriograph (TensioMed, Budapest, Hungary) and Vascular Explorer (Enverdis, Jena, Germany). Three measurements were performed in supine position followed by three measurements in sitting position. Methods were compared using correlation and Bland-Altman analysis. There was a significant correlation between PWV in supine and sitting position (Arteriograph: P<0.0001, r=0.93; Vascular Explorer; P<0.0001, r=0.87). There were significant correlations between AI sitting and AI supine using Arteriograph (P<0.0001, r=0.97), Vascular Explorer (P<0.0001, r=0.98) and SphygmoCor (P<0.0001, r=0.96). When analyzed by Bland-Altman, PWV and AI measurements in supine vs. sitting showed good agreement. There was no significant difference in PWV obtained with the three different devices (Arteriograph 7.5±1.6 m s(-1), Vascular Explorer 7.3±0.9 m s(-1), SphygmoCor 7.0±1.8 m s(-1)). AI was significantly higher using the Arteriograph (17.6±15.0%) than Vascular Explorer and SphygmoCor (10.2±15.1% and 10.3±18.1%, respectively


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