Pulse最新文献

{"title":"Dietary Sodium Intake and Serum Uric Acid: A Mini-Review.","authors":"Lei Lei,&nbsp;Ji-Guang Wang","doi":"10.1159/000490573","DOIUrl":"https://doi.org/10.1159/000490573","url":null,"abstract":"<p><p>The aim of the present review is to summarize recent studies on the relationship between dietary sodium intake and serum uric acid concentration. In short-term dietary sodium intervention studies, including a recent further analysis of a previously published trial, high dietary sodium intake (200 mmol/day), compared with a low sodium diet (20-60 mmol/day), resulted in a significant reduction in serum uric acid, being approximately 20-60 μmol/L. This finding, though consistent across short-term studies, is in contradiction to the long-term observational evidence on the relationship between dietary sodium intake and serum uric acid. Indeed, in a population-based prospective study, high dietary sodium intake was associated with a higher serum uric acid concentration. If serum uric acid would be followed up, several currently ongoing long-term randomized dietary sodium intervention studies may shed some light on how dietary sodium intake interacts with serum uric acid in the development of hypertension.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"6 1-2","pages":"124-129"},"PeriodicalIF":2.2,"publicationDate":"2018-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000490573","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36555485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between B-Type Natriuretic Peptide and N-Terminal pro-B-Type Natriuretic Peptide in a Large Japanese Population at Risk of Stage A Heart Failure.","authors":"Mizuri Taki,&nbsp;Satoshi Hoshide,&nbsp;Ken Kono,&nbsp;Kazuomi Kario","doi":"10.1159/000485660","DOIUrl":"https://doi.org/10.1159/000485660","url":null,"abstract":"<p><strong>Background: </strong>The measurements of B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are useful for ruling out heart failure and as prognostic markers in not only heart failure populations but also general populations. It is not clear whether these two biomarkers are elevated in parallel or associated with demographic characteristics in large populations at risk of stage A heart failure. Here we investigated the relationship between BNP and NT-proBNP and extended the evaluation of this association to known demographic disparities in stage A heart failure.</p><p><strong>Methods: </strong>Of 4,310 ambulatory patients, we analyzed the cases of the 3,643 (mean age 65 ± 11 years, 46$ male, and 79$ on antihypertensive medication) patients whose serum BNP and NT-proBNP levels were both measured and who had a history of and/or risk factors for cardiovascular disease from the Japan Morning Surge-Home Blood Pressure (J-HOP) Study dataset.</p><p><strong>Results: </strong>The median (25th-75th percentiles) BNP and NT-proBNP values were 18.7 (9.3-38.5) pg/mL and 50.3 (25.5-97.4) pg/mL. There was a significant association between log-transformed BNP and log-transformed NT-proBNP (<i>r</i> = 818, <i>p</i> < 0.001). A multiple linear regression analysis showed that log-transformed NT-proBNP was significantly associated with log-transformed BNP (beta coefficient = 0.774, <i>p</i> < 0.001). When stratified by demographic characteristics, these associations remained (all <i>p</i> < 0.001).</p><p><strong>Conclusion: </strong>In a large Japanese population at risk of stage A heart failure, there was a significant association between BNP and NT-proBNP after adjustment and stratification by demographics.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"6 1-2","pages":"1-8"},"PeriodicalIF":2.2,"publicationDate":"2018-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000485660","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36555562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum.","authors":"","doi":"10.1159/000471910","DOIUrl":"https://doi.org/10.1159/000471910","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1159/000448464.].</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"6"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000471910","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36099727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lower Heart Rate Variability Is Associated with Lower Pulse Pressure Amplification: Role of Obesity.","authors":"Nicola Di Daniele,&nbsp;Manfredi Tesauro,&nbsp;Alberto Mascali,&nbsp;Valentina Rovella,&nbsp;Angelo Scuteri","doi":"10.1159/000479701","DOIUrl":"https://doi.org/10.1159/000479701","url":null,"abstract":"<p><strong>Background: </strong>Heart rate variability (HRV), pulse pressure amplification, and obesity represent risk factors for cardiovascular events. The aims of the present study are (1) to explore the impact of HRV on pulse pressure amplification and (2) to investigate whether the association between HRV and pulse pressure amplification differs in obese and lean subjects.</p><p><strong>Methods: </strong>A total of 342 patients (age 61 ± 11 years) were enrolled. HRV was analyzed concerning both the frequency and time domain as well as concerning the HRV triangular index. Pulse pressure amplification was estimated as the ratio between brachial and carotid pulse pressure, the latter measured with SphygmoCor.</p><p><strong>Results: </strong>Time domain HRV indices were directly correlated with pulse pressure amplification (the lower the HRV indices, the lower the pulse pressure amplification). This association was stronger in obese than in lean subjects after controlling for age and sex.</p><p><strong>Conclusion: </strong>Larger controlled studies are needed to provide a more detailed insight into the relation between HRV and pulse pressure amplification and to determine which pathways are differentially activated in lean and obese subjects.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"99-105"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000479701","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36099730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Various Indices of Arterial Stiffness: Are They Closely Related or Distinctly Different?","authors":"Hirofumi Tanaka","doi":"10.1159/000461594","DOIUrl":"https://doi.org/10.1159/000461594","url":null,"abstract":"<p><p>Arterial stiffness is an independent risk factor for cardiovascular disease. There are a number of techniques and devices that have been developed and utilized to capture the information pertaining to the elasticity of the blood vessel. Almost all the available indices of arterial stiffness are known to increase with advancing age and are elevated in the presence of hypertension and coronary heart disease. It is not known how closely these different measures of arterial stiffness are related to each other. Available evidence indicates that arterial stiffness indices that share a homogeneous methodology appear to demonstrate good correlations. However, there are no significant associations between some measures. These overall results may be surprising considering that all the indices are supposed to reflect the same property of the arterial wall (i.e., arterial elasticity). Interestingly, no or weak correlations between indices of vascular function are not confined only to arterial stiffness and can be extended to endothelial function and vascular reactivity measures.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"1-6"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000461594","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36099726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Options for Dealing with Pressure Dependence of Pulse Wave Velocity as a Measure of Arterial Stiffness: An Update of Cardio-Ankle Vascular Index (CAVI) and CAVI0.","authors":"Bart Spronck,&nbsp;Tammo Delhaas,&nbsp;Mark Butlin,&nbsp;Koen D Reesink,&nbsp;Alberto P Avolio","doi":"10.1159/000479322","DOIUrl":"https://doi.org/10.1159/000479322","url":null,"abstract":"<p><p>Pulse wave velocity (PWV), a marker of arterial stiffness, is known to change instantaneously with changes in blood pressure. In this mini-review, we discuss two main approaches for handling the blood pressure dependence of PWV: (1) converting PWV into a pressure-independent index, and (2) correcting PWV per se for the pressure dependence. Under option 1, we focus on cardio-ankle vascular index (CAVI). CAVI is essentially a form of stiffness index β - CAVI is estimated for a (heart-to-ankle) trajectory, whereas β is estimated for a single artery from pressure and diameter measurements. Stiffness index β, and therefore also CAVI, have been shown to theoretically exhibit a slight residual blood pressure dependence due to the use of diastolic blood pressure instead of a fixed reference blood pressure. Additionally, CAVI exhibits pressure dependence due to the use of an estimated derivative of the pressure-diameter relationship. In this mini-review, we will address CAVI's blood pressure dependence theoretically, but also statistically. Furthermore, we review corrected indices (CAVI₀ and β₀) that theoretically do not show a residual blood pressure dependence. Under option 2, three ways of correcting PWV are reviewed: (1) using an exponential relationship between pressure and cross-sectional area, (2) by statistical model adjustment, and (3) through reference values or rule of thumb. Method 2 requires a population to be studied to characterise the statistical model, and method 3 requires a representative reference study. Given these limitations, method 1 seems preferable for correcting PWV per se for its blood pressure dependence. In summary, several options are available to handle the blood pressure dependence of PWV. If a blood pressure-independent index is sought, CAVI₀ is theoretically preferable over CAVI. If correcting PWV per se is required, using an exponential pressure-area relationship provides the user with a method to correct PWV on an individual basis.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"106-114"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000479322","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36099732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Haemodynamic Indices of Central and Peripheral Pressure with Subclinical Target Organ Damage.","authors":"Junli Zuo,&nbsp;Shaoli Chu,&nbsp;Isabella Tan,&nbsp;Mark Butlin,&nbsp;Jiehui Zhao,&nbsp;Alberto Avolio","doi":"10.1159/000484441","DOIUrl":"https://doi.org/10.1159/000484441","url":null,"abstract":"<p><strong>Background: </strong>Central aortic pressure has often been shown to be more closely associated with markers of vascular function and incidence of cardiovascular events compared to peripheral pressure. However, the potential clinical use of central aortic or peripheral haemodynamic indices as markers of target organ damage (TOD) has not been fully established.</p><p><strong>Methods: </strong>We evaluated associations of TOD with central aortic and peripheral haemodynamic indices (central aortic [cPP] and peripheral pulse pressure [pPP], central aortic augmentation index, and central and peripheral waveform factor) in 770 hospital inpatients (age 60 ± 10 years, 473 males) with primary hypertension. TOD was quantified in terms of arterial stiffness as measured by carotid-femoral pulse wave velocity (cfPWV), carotid intima-media thickness (IMT), and urine albumin-to-creatinine ratio (ACR). Subclinical TOD was defined as carotid IMT >0.9 mm, urine ACR >3.5 mg/mmol in females and >2.5 mg/mmol in males and/or cfPWV >12 m/s.</p><p><strong>Results: </strong>Both cPP and pPP showed significant correlation with cfPWV (<i>r =</i> 0.41 vs. 0.40; <i>p</i> < 0.01), ACR (<i>r =</i> 0.24 vs. 0.27; <i>p</i> < 0.01) and carotid IMT (<i>r</i> = 0.14 vs. 0.15; <i>p</i> < 0.01). Each SD increase in pPP and cPP was associated with increased risk of cfPWV >12 m/s (odds ratio [OR] = 2.7 and 2.9 for pPP and cPP, respectively), ACR >2.5 mg/mmol (OR = 1.2 and 1.4, respectively), and carotid IMT >0.9 mm (OR = 1.46 and 1.53, respectively). Compared to pPP, cPP had higher predictive power for TOD for age ≥60 years (OR = 3.07, <i>p</i> < 0.001).</p><p><strong>Conclusions: </strong>Although both pPP and cPP show an association with TOD in a hypertensive population, cPP provides additional information beyond pPP associated with TOD in a hypertensive cohort. Central aortic haemodynamic indices as potential biomarkers of subclinical TOD need to be validated by further prospective studies.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"133-143"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000484441","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36098878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Vascular Calcification in Heart Failure and Cognitive Decline.","authors":"Hao-Min Cheng,&nbsp;Jiun-Jr Wang,&nbsp;Chen-Huan Chen","doi":"10.1159/000484941","DOIUrl":"https://doi.org/10.1159/000484941","url":null,"abstract":"<p><p>Vascular calcification is heterogeneous and triggered by multiple mechanisms. It has been implicated in the development of heart failure with preserved ejection fraction (HFpEF) and cognitive function impairment. Understanding the pathophysiology of vascular calcification may help us improve the management of HFpEF, atherosclerosis, accelerated arterial stiffness, hypertension, and cognitive dysfunction. Currently, there are no effective strategies for treating accelerated arterial stiffness. This may indicate that once arterial stiffness or vascular calcification has developed, it may be less likely to stop the ongoing pathophysiology. Therefore, earlier intervention targeting the probable pathways of vascular calcification may benefit the patients with vascular calcification and related pathological conditions. In this review, we briefly discuss the proposed pathophysiological roles of vascular calcification in the development of heart failure and cognitive decline, the animal models used to study the link between vascular calcification and cardiovascular diseases, and the possible corresponding management strategies.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"144-153"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000484941","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36098879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular Aging and Cognitive Dysfunction: Silent Midlife Crisis in the Brain.","authors":"Chen-Hua Lin,&nbsp;Hao-Min Cheng,&nbsp;Shao-Yuan Chuang,&nbsp;Chen-Huan Chen","doi":"10.1159/000481734","DOIUrl":"https://doi.org/10.1159/000481734","url":null,"abstract":"<p><strong>Background: </strong>Vascular aging may cause cerebral microvascular damage and cognitive dysfunction. There is incremental evidence that consistently implicates arterial stiffness being involved in the manifestation of cognitive impairment in the elderly. However, few investigations have examined the relationship between arterial stiffness and cognitive impairment in midlife.</p><p><strong>Summary: </strong>Past studies inconsistently showed improved cognitive outcomes after antihypertensive therapy in elderly populations. Nevertheless, recent findings revealed that blood-pressure-lowering treatment in young adults might eliminate or halt the progression of the detrimental effects related to arterial stiffness, indicating that younger adults may have more favorable outcomes in cognition than their older counterparts if early intervention is conducted at the subclinical stage. Stiffening of the aorta may lead to an excessive flow pulsatility in the brain that may cause microvascular structural brain damage and worse cognitive performance. Recent investigations have suggested that arterial stiffness is likely to trigger initial silent brain damage, possibly preceding midlife, while the manifestation of cognitive decline and deterioration can be foreseen in the subsequent life span.</p><p><strong>Key message: </strong>Despite the recent novel findings, definite conclusions on causality between vascular aging and cognitive dysfunction cannot be drawn at present. Further well-powered longitudinal studies with superior neuroimaging indicator, vascular mechanical biomarkers, and sensitive cognitive assessment tools that examine a broad range of age populations may help extend our understanding of the association between vascular aging and cognitive dysfunction throughout the life span.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"127-132"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000481734","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36098877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced Aortic Pressure Wave Reflection in Patients with Aortic Coarctation after Aortic Arch Repair.","authors":"Tomoaki Murakami","doi":"10.1159/000478530","DOIUrl":"https://doi.org/10.1159/000478530","url":null,"abstract":"<p><strong>Background: </strong>In patients with aortic coarctation after successful aortic arch repair, it is well known that early-onset cardiovascular diseases can develop.</p><p><strong>Summary: </strong>We studied the pressure waveform in patients after aortic arch repair focusing on a pressure wave reflection. In patients after aortic arch repair, the repaired portion generates a new reflected pressure wave. As a result, the newly generated pressure wave causes aortic pressure augmentation, loss of pressure amplification, and left ventricular hypertrophy with fibrosis. Balloon dilatation of the aortic arch may also generate a new pressure wave reflection.</p><p><strong>Key messages: </strong>In patients with aortic coarctation after aortic arch repair, the reconstructed site generates a new pressure wave reflection. This could be one of the causes of their future cardiovascular diseases.</p>","PeriodicalId":29774,"journal":{"name":"Pulse","volume":"5 1-4","pages":"82-87"},"PeriodicalIF":2.2,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000478530","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36099728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}