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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Cerebrovascular disease has emerged as one of the main causes of morbidity and mortality worldwide&#46; Having a stroke doubles the risk of developing dementia in the future&#44; and recurrent events raise the prevalence of dementia to 30&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">1</span></a> The relationship between hypertension and both brain structure and function is only partially known&#46; Current evidence suggests that several pathological factors can influence it&#46; Hypertension can produce vascular and functional changes in larger and small cerebral vessels in the brain&#46; Moreover&#44; cerebral small vessels and arterioles are more vulnerable to the mechanical stress associated with hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">2</span></a> In addition&#44; chronic hypertension induces a rightward shift in the autoregulatory curve&#44; and consequently&#44; can increase vulnerability to sudden changes in blood pressure&#44; resulting in ischemia or increased risk of brain hemorrhage&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">2&#44;3</span></a> On the other hand&#44; recent evidence suggests that acute and chronic hypertension could produce blood-brain barrier damage&#44; which is crucial for blood pressure regulation&#46; Brain sympathetic nervous system activation and brain&#8211;renin&#8211;angiotensin activation&#44; associated with endothelial injury&#44; oxidative stress and inflammation are involved in the breakdown of blood&#8211;brain barrier&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Cerebral small vessel disease &#40;CSVD&#41; refers to a syndrome of clinical and neuroimaging findings resulting from pathologies in the small perforating cerebral arterioles&#44; capillaries&#44; and venules&#44; manifested on magnetic resonance imaging &#40;MRI&#41; or pathology examination&#46; Clinically&#44; CVDS presents as ischemic and hemorrhagic stroke&#44; and it is responsible of 25&#37; of ischemic stroke &#40;lacunar strokes&#41;&#44; a higher percentage of hemorrhagic strokes and for up to 45&#37; of dementias either as vascular or mixed with Alzheimer disease&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">2&#8211;7</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Pathology studies describe abnormalities in arterioles&#44; such as arteriosclerosis&#44; lipohyalinosis&#44; or necrosis fibrinoide and the pathologic findings suggest that the pathogenesis of CSVD is more complex than only arteriolar occlusion that leads to infarcts&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">2</span></a> The characteristic findings of CSVD in RMI include lacunar infarcts&#44; white matter hyperintensities &#40;WMH&#41; cerebral microbleeds &#40;CMB&#41;&#44; enlarged perivascular spaces&#44; and brain atrophy&#46;<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">8&#44;9</span></a> Its prevalence is about 5&#37; in subjects over 50 and it is present in almost everyone by the age of 90&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">4</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">CSVD could be usually attributed to classical risk factors&#44; specifically to hypertension&#44; diabetes and smoking&#44; but of them&#44; hypertension represents a key factor in the development of CSVD&#46; Endothelial dysfunction is considered to appear at an early stage of CSVD&#44; before any radiologic signs evidence&#44; and although it can be measured by functional transcranial Doppler&#44; this technique has major limitations in terms of operator variability&#46;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">8</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Obstructive sleep apnoea &#40;OSA&#41; is a known risk factor of several cardiovascular diseases such as arrhythmia&#44; coronary head disease or stroke&#44; and is an independent cause of resistant hypertension&#46;<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">10&#44;11</span></a> In addition&#44; patients with refractory hypertension &#40;subjects that remain uncontrolled hypertension despite the administration of at least 5 antihypertensive drugs&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">12</span></a> have an even greater prevalence and severity of OSA than resistant hypertension patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">13&#44;14</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The relationship of OSA with CSVD is less well known&#44; and in the last few years several studies have started to explore the relationship of OSA and CSVD by neuroimaging findings&#46; In a systematic review and meta-analysis&#44; Chokesuwattanaskul et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">15</span></a> have shown an association between OSA and CSVD by MRI findings of WMH and covert lacunar infarction&#46; When compared to patients without OSA&#44; this study demonstrates that OSA is an independent risk factor of asymptomatic CSVD&#46; A more recent meta-analysis&#44; including thirty-two observational studies&#44;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">16</span></a> have reported that compared to patients without OSA&#44; the odds ratio of WMH were 3&#46;9 &#40;CI 95&#37; 2&#46;7&#8211;5&#46;5&#41; in subjects with moderate-severe OSA and 4&#46;3 &#40;CI 95&#37; 1&#46;9&#8211;9&#46;6&#41; in severe OSA&#46; In contrast&#44; OSA had no association with cerebral microbleeds and an undetermined association with both perivascular spaces and subcortical infarcts due to insufficient data&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">The possible mechanisms responsible for the present relationship of OSA with CSVD could include vascular endothelial dysfunction&#44; hypoxia&#44; hypoperfusion&#44; reperfusion&#44; oxidative stress&#44; neuroinflammation and hypercoagulability state&#46; In addition&#44; OSA is associated with sympathetic activation&#44; which is detectable even in early stages of its evolution and in the absence of comorbidities or other cardiometabolic diseases&#46; This activation is directly proportional to the frequency of apnoeas and hypopneas during sleep&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">17</span></a> In chronic untreated OSA&#44; sympathetic activation during wakefulness could be attributed to long-term structural or functional neural adaptations to hypoxia and oxygen free radical generation due to recurring apnoeas and hypopneas during sleep&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">18</span></a> In <a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#44; we show the possible mechanisms involved in the relation between OSA&#44; hypertension and cerebral small vessel disease&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">On the other hand&#44; OSA has been associated with resistant or refractory hypertension&#44; and has shown a high prevalence of uncontrolled nocturnal hypertension&#44; possibly one of the causes of the worse functional prognosis of cerebrovascular disease in these patients&#46; It is very well known that abnormal dipping patterns may affect vascular health independent of BP level&#44; and several studies have shown that higher night-time BP levels and a riser pattern are independently associated with the total cardiovascular event rate&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">19</span></a> Elevated night-time BP and reverse-dipping compared with normal dipping BP pattern have been associated with subclinical cerebrovascular disease&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">20&#44;21</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Hypertension is the most important modifiable risk factor to prevent stroke&#44; and it is strongly associated with the development of CSVD&#46; Therefore&#44; the primary prevention of stroke and its recurrences is a priority strategy for the prevention of dementia&#46; Despite the deleterious effects of hypertension&#44; BP control remains suboptimal&#58; less than 50&#37; of adults achieve adequate BP control&#46; These data have worsened in recent years&#44; probably due to low adherence and early discontinuation of antihypertensive treatment&#46; In addition&#44; it is known that OSA is associated with resistant and uncontrolled nocturnal hypertension&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Primary and secondary prevention of stroke and CSVD is a priority for the prevention of dementia&#46; Mild cognitive impairment &#40;MCI&#41; is often considered as an intermediate phase between normal cognition and dementia&#44; common in patients with hypertension&#46; MCI has an overall prevalence of 11&#46;8&#8211;30&#37; and it increases the likelihood of progression to dementia or death compared with having no cognitive impairment&#46; Suvila et al&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">22</span></a> also observed that early- but not late-onset hypertension is related to midlife cognitive function&#46; In addition&#44; among patients with OSA and resistant hypertension&#44; CPAP treatment for 12 weeks compared with control&#44; resulted in a reduction in 24<span class="elsevierStyleHsp" style=""></span>h BP and an improvement in nocturnal BP or circadian BP pattern&#46;<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">23</span></a> On the other hand&#44; recent meta-analysis has shown that adherence to CPAP was associated with a reduced or major cardiovascular events recurrence risk&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">24</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">In conclusion&#44; OSA is highly prevalent in hypertension patients&#44; especially in resistant or refractory hypertension&#46; Although OSA increases the risk of all-cause and cardiovascular mortality&#44; this condition is often underrecognized and undertreated in cardiovascular practice&#46; We believe that early improvement in hypertension control among middle-aged hypertensive individuals&#44; coupled with ensuring adequate adherence to antihypertensive treatment and CPAP therapy in patients with hypertension and OSA&#44; are essential components for preventing cardiovascular events and the onset of early cerebrovascular disease and cognitive decline&#46;</p><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Acknowledge</span><p id="par0065" class="elsevierStylePara elsevierViewall">The authors would like to express their gratitude to Mariana Ubeda-Romero Araujo for reviewing the manuscript&#46;</p></span><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interests</span><p id="par0060" class="elsevierStylePara elsevierViewall">The authors state that they have no conflict of interests&#46;</p></span></span>"
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Vol. 60. Issue 2.
Pages 77-79 (February 2024)
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Vol. 60. Issue 2.
Pages 77-79 (February 2024)
Editorial
Early Detection and Treatment of Hypertension and Obstructive Sleep Apnoea: Can We Prevent the Progression of Small Vessel Cerebrovascular Disease?
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Pedro Armarioa,b,c,
Corresponding author
parmario@csi.cat

Corresponding author.
, Carla Avellaneda-Gómeza,c,d, Manuel Gómez-Chocoa,c,d
a Cardiovascular Risk Area, Complex Hospitalari Universitari Moisès Broggi, Spain
b Universitat de Barcelona, Spain
c Bellvitge Biomedical Research Institute (IDIBELL), Spain
d Neurology Department, Complex Hospitalari Universitari Moisès Broggi, Spain
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