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Samuel Trocio

Bio: Samuel Trocio is an academic researcher from Columbia University. The author has contributed to research in topics: Transcranial Doppler & Autoregulation. The author has an hindex of 2, co-authored 3 publications receiving 143 citations.

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Journal ArticleDOI
TL;DR: The objective of this study was to evaluate the inter‐reader reliability of sonographic measurements of common carotid artery (CCA) diameters and derived metrics of CD.
Abstract: Arterial distensibility is a measure of the arterial ability to expand and contract with cardiac pulsation and relaxation.1 A decrease of arterial distensibility (increased artery wall stiffness) seems to be a common pathologic mechanism for many factors that lead to the occurrence and progression of the vascular changes associated with cardiovascular disease (CVD).2,3 Functional impairment of the arterial wall may occur in an early stage of the atherosclerotic process before structural wall changes become detectible as well as before the occurrence of clinical symptoms of CVD.3 Early detection of this impairment can lead to more effective strategies for the prevention of CVD. This concept that early changes in functional properties of the arterial wall precede the clinical stage of atherosclerosis has been investigated in peripheral arteries (femoral and brachial) and in the aorta for many years. Recent development of high-resolution and high-definition sonography has focused new investigations on the carotid arteries. With these techniques, arterial wall and vessel diameters can be assessed in a dynamic fashion through-out the cardiac cycle as the artery expands and contracts with each cardiac pulsation and relaxation.2,3 Arterial distensibility is, however, only an estimate of the mean strain and modulus at best because the entire soft tissue surrounding the vessel is responding to the change in the volume of the vessel, and the standard boundary identification methods of the vessel wall may not be as reliable as speckle-tracking methods.4 Carotid distensibility (CD) has been introduced as a novel risk factor for CVD in cross-sectional study designs from population-based cohorts, including Atherosclerosis Risk in Communities (ARIC), Second Manifestations of Arterial Disease (SMART), the Rotterdam Study, the Baltimore Longitudinal Study of Aging (BLSA), and the Multiethnic Study of Atherosclerosis (MESA).5–9 Nevertheless, the value of CD in predicting future stroke is currently under debate.10,11 The discrepancy over CD and its relationship to atherosclerosis seems to arise from several plausible factors, such as small sample sizes, different clinical characteristics of the study populations, analyses of CD restricted to different vascular beds, and measurement variability. Additionally, there is a lack of information regarding the reliability of CD measures. Therefore, we sought to evaluate the inter-reader reproducibility of the common carotid artery (CCA) diameters and distensibility measurements in a sample of 118 stroke-free subjects derived from a multiethnic population of northern Manhattan.

119 citations

Journal ArticleDOI
01 Mar 1997-Stroke
TL;DR: Cardiac sources of embolism are a determinant of HITS in posterior cerebral circulation ischemia, suggesting that cardioembolic infarcts in that territory might be more common than suspected.
Abstract: Background and Purpose Microembolic high-intensity transient signals (HITS) on transcranial Doppler ultrasound (TCD) are associated with carotid stenosis, artificial heart valves, and other cardiac conditions. Only one case report describes stroke-related HITS in the posterior cerebral circulation. This study was designed to assess prospectively the prevalence of asymptomatic microemboli in vertebrobasilar ischemia and to determine whether potential cardioembolic sources, vertebral or basilar occlusive disease, and infarct subtypes predict the detection of HITS. Methods We investigated 52 consecutive patients with acute or recent vertebrobasilar ischemia within 48 hours after admission. TCD monitoring was performed according to established criteria for 20 minutes on each posterior cerebral artery. Fetal origin of the posterior cerebral artery was an exclusion criterion and ruled out by carotid compression. Results Microembolic signals were detected in 10 patients (19.2%). In a multivariate logistic regres...

31 citations

Journal ArticleDOI
TL;DR: By simultaneously assessing vasodilatory capacity (CVC) in anterior and posterior circulation, this work aimed to establish normative data for the vertebrobasilar system, to compare the two circulations, and to assess for differential contributions of age, gender or blood pressure.
Abstract: Loss of cerebral hemodynamic autoregulation plays an important pathophysiological role in brain injury such as stroke.1 It has been shown that the magnitude of vasodilation in the anterior circulation serves as an indirect measure of cerebral autoregulation and that degree of vasoreactivity loss correlates with subsequent risk of stroke in symptomatic and asymptomatic carotid occlusive disease. 2–6 Similar data for the posterior circulation have not been consistent. Some evidence suggests that vertebrobasilar circulation may harbor significantly different autoregulative characteristics which could explain its susceptibility to the posterior reversible leukoencephalopathies, hypertensive encephalopathy, immunosuppressive vasculopathy, and pre-/eclampsia. 7 Our goal was to better characterize the autoregulatory profile of the vertebrobasilar circulation in healthy controls. By simultaneously assessing vasodilatory capacity (CVC) in anterior and posterior circulation, we aimed to establish normative data for the vertebrobasilar system, to compare the two circulations, and to assess for differential contributions of age, gender or blood pressure.

1 citations


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Journal ArticleDOI
TL;DR: The underlying causes of age-related vessel stiffening are discussed, focusing on age- related crosslinking of the ECM proteins as well as through increased matrix deposition, and very recent work that demonstrates endothelial cells are mechano-sensitive to arterial stiffening, where changes in stiffness can directly impact EC health is discussed.
Abstract: Arterial stiffening occurs with age and is closely associated with the progression of cardiovascular disease. Stiffening is most often studied at the level of the whole vessel because increased stiffness of the large arteries can impose increased strain on the heart leading to heart failure. Interestingly, however, recent evidence suggests that the impact of increased vessel stiffening extends beyond the tissue scale and can also have deleterious microscale effects on cellular function. Altered extracellular matrix (ECM) architecture has been recognized as a key component of the pre-atherogenic state. Here, the underlying causes of age-related vessel stiffening are discussed, focusing on age-related crosslinking of the ECM proteins as well as through increased matrix deposition. Methods to measure vessel stiffening at both the macro- and microscale are described, spanning from the pulse wave velocity measurements performed clinically to microscale measurements performed largely in research laboratories. Additionally, recent work investigating how arterial stiffness and the changes in the ECM associated with stiffening contributed to endothelial dysfunction will be reviewed. We will highlight how changes in ECM protein composition contribute to atherosclerosis in the vessel wall. Lastly, we will discuss very recent work that demonstrates endothelial cells (ECs) are mechano-sensitive to arterial stiffening, where changes in stiffness can directly impact EC health. Overall, recent studies suggest that stiffening is an important clinical target not only because of potential deleterious effects on the heart but also because it promotes cellular level dysfunction in the vessel wall, contributing to a pathological atherosclerotic state.

270 citations

Journal ArticleDOI
TL;DR: It is suggested that the components of MS interact to synergistically impact vascular thickness and stiffness and that the excess cardiovascular risk associated with MS is partly mediated through the amplified alterations in these vascular properties.

137 citations

Journal ArticleDOI
TL;DR: Measurements of carotid stiffness are associated with extent of PTH elevation, suggesting that those with more severe PHPT may have impaired vascular compliance and that PTH, rather than calcium, is the mediator.
Abstract: Context: Data on the presence, extent, and reversibility of cardiovascular disease in primary hyperparathyroidism (PHPT) are conflicting. Objective: This study evaluated carotid structure and function in PHPT patients compared with population-based controls. Design: This is a case-control study. Setting: The study was conducted in a university hospital metabolic bone disease unit. Participants: Forty-nine men and women with PHPT and 991 controls without PHPT were studied. Outcome Measures: We measured carotid intima-media thickness (IMT), carotid plaque presence and thickness, and carotid stiffness, strain, and distensibility. Results: IMT, carotid plaque thickness, carotid stiffness, and distensibility were abnormal in PHPT patients, and IMT was higher in patients than controls (0.959 vs. 0.907 mm, P < 0.0001). In PHPT, PTH levels, but not calcium concentration, predicted carotid stiffness (P = 0.04), strain (P = 0.06), and distensibility (P = 0.07). Patients with increased carotid stiffness had significantly higher PTH levels than did those with normal stiffness (141 ± 48 vs. 94.9 ± 44 pg/ml, P = 0.002), and odds of abnormal stiffness increased 1.91 (confidence interval = 1.09–3.35; P = 0.024) for every 10 pg/ml increase in PTH, adjusted for age, creatinine, and albumin-corrected calcium. Conclusions: Mild PHPT is associated with subclinical carotid vascular manifestations. IMT, a predictor of cardiovascular outcomes, is increased. Measures of carotid stiffness are associated with extent of PTH elevation, suggesting that those with more severe PHPT may have impaired vascular compliance and that PTH, rather than calcium, is the mediator.

129 citations

Journal ArticleDOI
01 Oct 1999-Stroke
TL;DR: Endovascular treatment using balloon angioplasty with intravascular stent placement for symptomatic stenotic lesions resulting in VBI that is unresponsive to medical therapy appears to be of benefit in this high-risk subset of patients with poor collateral flow.
Abstract: Background and Purpose—Vertebrobasilar territory ischemia (VBI) leads to disabling neurological symptoms and poses a risk for stroke by an embolic or flow-related mechanism. We present our clinical experience in the endovascular treatment of patients with symptomatic VBI from severe atherosclerosis or dissection of the vertebral and subclavian arteries that was unresponsive to medical therapy. Methods—Twenty-one patients (9 female, 12 male) with a mean age of 65.7 years (range 47 to 81 years) underwent treatment with percutaneous endovascular balloon angioplasty and stent placement. Sixteen patients (76.2%) had evidence of contralateral involvement, and 9 (42.8%) demonstrated severe anterior-circulation atherosclerosis. Nine patients had a previous infarct in the occipital lobe, cerebellum, or pons before treatment. Follow-up was available for all patients. Results—Balloon angioplasty with intravascular stent placement was performed in 13 vertebral artery lesions (10 at the origin, 3 in the cervical segme...

122 citations

Journal ArticleDOI
TL;DR: Current depressive or anxiety disorders were associated with a higher central augmentation index, a manifestation of early wave reflection because of arterial stiffness, which may enhance the development and progression of atherosclerosis and other cardiovascular conditions.

89 citations