It is evident that only an event-based longitudinal study can provide an indisputable answer to the question of the clinical relevance of additional ABPM indices. Our previous work on the reliability of PTIN shows its good repeatability. The PTIN generated by the Vasotens technology can be recommended as an indicator of end organ damage resulting from hypertension.
The other authors report no conflicts of interest in this work. J Hypertens. Posokhov IN. Pulse wave velocity hour monitoring with one-site measurements by oscillometry. Med Devices Auckl. Analysis of hour pulse wave velocity in patients with renal transplantation.
Long-term growth hormone (GH) replacement of adult GH deficiency (GHD) benefits the heart
Int J Nephrol Renovasc Dis. Expert consensus document on the measurement of aortic stiffness in daily practice using carotid-femoral pulse wave velocity. Dtsch Med Wochenschr. Comparison of blood pressure control and left ventricular hypertrophy in patients on continuous ambulatory peritoneal dialysis CAPD and automated peritoneal dialysis APD. Electrolyte Blood Press. Blood pressure load, vascular permeability and target organ damage in primary hypertension.
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Central aortic blood pressure, augmentation index, and reflected wave transit time: reproducibility and repeatability of data obtained by oscillometry. Vasc Health Risk Manag. Medical Devices: evidence and research. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol.
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J Am Soc Echocardiogr. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. Ambulatory blood pressure monitoring vs self-measurement of blood pressure at home: correlation with target organ damage. Home vs ambulatory and office blood pressure in predicting target organ damage in hypertension: a systematic review and meta-analysis. Associations between nondipping of nocturnal blood pressure decrease and cardiovascular target organ damage in strictly selected community-dwelling normotensives. Relation between abnormalities in circadian blood pressure rhythm and target organ damage in normotensives.
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In fact, residual extracellular matrix abnormalities such as myocardial fibrosis are likely responsible for persistent abnormalities in LV diastolic function and increased morbidity and mortality after aortic valve replacement.
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The development of novel therapies requires the identification of molecular mechanisms that cause the development of diastolic dysfunction in these patients. The current study identifies one mechanism as a potential target: the excessive accumulation of collagen type I in the nonmysial regions of the myocardial collagen network resulting in increased stiffness of the extracellular matrix. In addition, circulating or imaging biomarkers that reflect these changes in myocardial collagen tissue could be used to both improve diagnostic criteria and prognostic assessment in severe AS with PEF and symptoms of HF.
In this regard, the possibility exists that, as shown in patients with hypertensive heart disease and HF with PEF, 22 changes in serum levels of the tissue inhibitor of matrix metalloproteinases-1 may serve to detect the earliest development of collagen-mediated LV diastolic dysfunction in AS patients, as well as to monitor the efficacy of aortic valve replacement to repair myocardial remodeling in severe AS with PEF and symptoms of HF..
This study has some limitations. First, this was a study involving a relatively small number of patients. In particular, the assessment of collagen phenotypes was performed in a limited number of biopsy samples that were consecutively but not randomly selected. However, because of the nature of the goals under investigation, it was adequately powered. Second, in addition to changes in the ratio between collagen types, collagen quality can also be affected by posttranslational modifications of collagen molecules, particularly increased cross-linking.
Third, myocardial stiffness is also determined by the sarcomeric protein titin, which regulates cardiomyocyte passive tension. However, none of these conditions were present in our study population.. In conclusion, we report that nonmysial accumulation of collagen fibers, namely of type I, is associated with increased extracellular matrix stiffness and LV filling pressures in severe AS with PEF and symptoms of HF. Albeit descriptive in nature, these findings suggest that an increase in passive stiffness caused by phenotypic and biomechanical changes of the nonmysial collagen network may contribute to the development of diastolic dysfunction and dyspnea in severe AS with PEF..
None declared. In this context, it is unknown which characteristics of myocardial fibrosis have an impact on LV diastolic function.. The identification of these changes with appropriate biomarkers and their targeting with specific therapies are novel tools to face the medical challenge represented by HF in severe AS with PEF..
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Ravassa and R. Querejeta jointly supervised this work.. Home Articles in press Current Issue Archive. ISSN: Previous article Next article. Issue Pages October Download PDF. Corresponding author. This item has received. Article information. Show more Show less. Table 1. Table 2. Table 3. Introduction and objectives We investigated the anatomical localization, biomechanical properties, and molecular phenotype of myocardial collagen tissue in 40 patients with severe aortic stenosis with preserved ejection fraction and symptoms of heart failure.
Methods Two transmural biopsies were taken from the left ventricular free wall. Conclusions These findings suggest that, in patients with severe aortic stenosis with preserved ejection fraction and symptoms of heart failure, diastolic dysfunction is associated with increased nonmysial deposition of collagen, predominantly type I, resulting in increased extracellular matrix stiffness.
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