Editorial
Arterial stiffness and cardiovascular disease. What does pulse wave velocity measurement contibute to clinical practice?
Rigidez arterial y enfermedad vascular. ¿Qué aporta la medida de la velocidad de la onda del pulso en la práctica clínica?
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"tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "160" "paginaFinal" => "162" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "P. Armario, M. Gómez-Choco" "autores" => array:2 [ 0 => array:4 [ "nombre" => "P." "apellidos" => "Armario" "email" => array:1 [ 0 => "parmario@ub.edu" ] "referencia" => array:3 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 2 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "M." "apellidos" => "Gómez-Choco" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Área de Atención Integrada de Riesgo Vascular, Hospital Moisès Broggi, Consorci Sanitari Integral, Sant Joan Despí, Barcelona, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Universitat de Barcelona, Barcelona, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Servicio de Neurología, Hospital Moisès Broggi, Consorci Sanitari Integral, Sant Joan Despí, Barcelona, Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Rigidez arterial y enfermedad vascular. ¿Qué aporta la medida de la velocidad de la onda del pulso en la práctica clínica?" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Arterial stiffness, central blood pressure, and vascular disease.</span> There is extensive evidence on the role that arterial stiffness in the large arteries plays in cardiovascular health. First, arterial stiffness translates into an increase in isolated systolic blood pressure, which represents an important burden in cardiovascular morbidity and mortality. Second, arterial stiffness reduces coronary perfusion pressure and produces an increase in left ventricular overload that can lead to dysfunction and heart failure, even in the absence of coronary disease. Third, it has an effect on pressure and pulsatile flow, which causes an increase in the penetration of pulsatile energy towards microcirculation in the target organs, especially in those which require a high flow and have low arteriolar resistance.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The brain, heart, and kidneys—the target organs of hypertension—are more exposed to aortic blood pressure given their anatomical location. Measuring aortic blood pressure, also called central blood pressure (CBP), yields lower values than brachial blood pressure (BBP). This is due to an amplification phenomenon that takes place as the pulse wave travels along the aorta and reaches the more distal, stiffer muscular arteries. This pulse wave is partially reflected in arterial bifurcations, causing a reduction in the amount of energy transmitted to distal vascular beds. The reflected wave is added to the pulse wave entering the proximal aorta. In a normal vascular bed, the reflected wave reaches the aorta at the end of diastole, contributing to diastolic blood pressure. On the other hand, in a stiffer vascular bed, the pulse wave progresses more quickly and the reflected wave contributes to the systolic part of the pulse wave, leading to an increase in systolic pressure in the proximal aorta.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In addition, stiffer arteries allow for a greater transmission of pulse pressure in microcirculation due to a lower mechanical impedance between the proximal elastic arteries and the more distal muscular arteries.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Arterial stiffness increases with aging due to a progressive replacement of elastic fibers with collagen fibers in the artery wall. It more frequently involves the central and elastic arteries than the more peripheral arteries. This process would be accelerated in the presence of other risk factors, especially if they are uncontrolled. The results of some studies suggest that target organ involvement could be caused by abnormalities in microcirculation due to excess transmission of the pulsatility of pressure secondary to an increase in arterial stiffness, beyond the effect of an elevation in peripheral blood pressure. Mitigation of arterial stiffness could thus reduce the total target organ lesion burden and in turn reduce cardiovascular events.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The inflammatory and endocrine mechanisms mediated by the renin-angiotensin-aldosterone system (RAAS) are involved in this process. Therefore, RAAS inhibitors can achieve a more significant reduction in CBP compared to ® blockers and diuretics, even after a similar reduction in BBP.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> The use of statins has also been shown to reduce arterial stiffness and central blood pressure through mechanisms that are not fully known.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Arterial stiffness and cerebrovascular disease.</span> The relationship between arterial stiffness and cardiac and renal disease is well known.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> However, its important relationship to cerebrovascular disease, especially cerebral small vessel disease (CSVD), is less known.<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8,9</span></a> CSVD is relatively frequent, especially in its silent form, and is related to future risk of stroke or cognitive impairment. It can manifest on a cranial MRI examination as dilated perivascular spaces, leukoaraiosis, lacunar strokes, or microbleeds.</p><p id="par0025" class="elsevierStylePara elsevierViewall">The classical concept indicates that the vascular damage of CSVD is caused by lipohyalinosis and/or fibrinoid necrosis in the walls of small-caliber vessels. However, in recent years, it has been suggested that endothelial dysfunction and an increase in vascular permeability may play an important role in the physiopathology of CSVD. Through the use of MRI tests with contrast, Wardlaw et al.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> demonstrated that patients who had had a lacunar stroke presented with diffuse dysfunction of the hematoencephalic barrier that was not observed in patients who had had cortical strokes. Although some studies have shown an association between arterial stiffness, cerebrovascular abnormalities, and cognitive impairment,<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> the results of other studies are not unanimous.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Measurement of central hemodynamics.</span> CBP was initially evaluated with invasive methods, that is, catheterization and the recording of blood pressure in the ascending aorta. However nowadays, several noninvasive methods have been developed that use recording of pulse wave pressure in peripheral arteries. Those that are more widely available are based on applanation tonometry of the radial artery or oscillometry of the brachial artery. Devices based on oscillometry offer the advantage of obtaining multiple blood pressure measurements over 24 hours in addition to showing simultaneous brachial and central blood pressure values. Measuring CBP based on brachial oscillometry using a Mobil-O-Graph device has been compared to invasive and noninvasive methods and is considered relevant for studying CBP.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The most frequent evaluation of central hemodynamics includes the determination of central systolic blood pressure, central diastolic blood pressure, carotid-femoral pulse wave velocity (PWV), and the augmentation index.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Although there are no cut-off points that are as clearly established as those for BBP, CBP reference values according to age and sex have been suggested based on a population of more than 80,000 subjects.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Other authors have suggested that a value equal to or greater than 130 mmHg for central systolic blood pressure and 90 mmHg for central diastolic blood pressure is predictive of an increase in vascular mortality.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Pulse wave velocity.</span> PWV is the velocity at which a pulse wave travels along a specified artery segment and is considered the gold standard for the noninvasive study of arterial stiffness. The more rigid the artery, the greater the PWV value. At present, based on extensive experience of its use in large populations, the reference method is measurement of carotid-femoral PWV through applanation tonometry or Doppler, given the advantage of the superficial location of both arteries.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> European guidelines from the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH)<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> consider that a value greater than 10 m/s is a conservative estimate of aortic function abnormality. Various studies have shown that a PWV value >10 m/s provides additional information beyond what can be derived from classic risk factors, including the SCORE risk table or Framingham risk score.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Nevertheless, the use of this technique cannot be systematically applied in clinical practice due to the high cost and lack of widespread availability of these techniques. An alternative method is brachial-ankle pulse wave velocity (baPWV) measurement or the cardio-ankle vascular index (CAVI). These techniques are widely used in Japan and other Asian countries, but due to technical and financial limitations along with other factors, they are less frequently used in other areas<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> and the normal values in this territory are different from the aforementioned values for carotid-femoral PWV.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">20,21</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The work published in this issue by Sánchez-Bacaoica et al.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> shows data of interest from a study carried out on 113 subjects through the use of a device of their own making (ABIPWV), validated with a reference machine (VASERA). It calculates PWV independently in the arm and legs, allowing for studying new indexes that they share between them. The authors observed that measurement of baPWV with the ABIPWV machine is safe and has a clinical utility similar to that of the VASERA, with a correlation coefficient of 0.93. If the cost of this new machine is affordable and lower than that of currently available techniques, it could be used more widely and contribute to an improvement in vascular risk stratification in many patients.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Armario P, Gómez-Choco M. Rigidez arterial y enfermedad vascular. ¿Qué aporta la medida de la velocidad de la onda del pulso en la práctica clínica? 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