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SUMMARYIntroduction: There is considerable interindividual variation in response to the antiplatelet agent clopidogrel. Hyporesponse predicts negative outcomes in patients presenting with a variety of ischemic cardiac conditions and following intracoronary stent placement. Many tests of clopidogrel activity are time consuming and complex. Short thromboelastography (s-TEG) allows rapid measurement of platelet clopidogrel response. Aims: We initiated this study to investigate the utility of s-TEG in assessing the response to clopidogrel in patients presenting with acute coronary syndromes (ACS) and to compare these results with established clopidogrel monitoring techniques. Methods: Patients admitted with unstable angina (UA) or Non ST elevation myocardial infarction (NSTEMI) undergoing coronary angiography were recruited. After routine loading with clopidogrel, all patients were tested with s-TEG and Accumetrics Verify-Now rapid platelet function analyzer (VN-RPFA). We used the modified TEG technique of measuring area under the curve at 15 min (AUC15), which allows a rapid estimation of antiplatelet response. Vasodilator-stimulated phosphoprotein phosphorylation (VASP) was also tested in a subgroup of patients. Clinical follow-up was obtained at 1 year. s-TEG results were correlated with VN-RPFA and VASP findings. Results: A total of 49 patients (33 male, mean age 63) were recruited and tested with s-TEG and VN-RPFA and a total of 39 patients were also assessed with VASP. s-TEG readings correlated well with VN-RPFA (r 2 = 0.54, P < 0.0001) and VASP (r 2 = 0.26, P = 0.001). Conclusion: s-TEG provides timely results which compare to current tests of clopidogrel activity. This technique can also be used to measure a variety of other clotting parameters and as such could develop into a valuable near patient test for the interventional cardiologist.
While the results in term infants are consistent with our belief that capillary rarefaction in essential hypertension is likely to be a primary vascular abnormality, the results in preterm infants may suggest that the intrauterine environment may exert some influences on the remodeling of the microcirculation which may delay the onset of capillary rarefaction in these infants.
Abstract-Low birth weight predicts adult essential hypertension and is linked to increased cardiovascular mortality in adult life. A reduction in capillary density (ie, rarefaction) is a hallmark of essential hypertension, and evidence suggests that rarefaction precedes the onset of the rise in blood pressure, because it is found in normotensive individuals at high risk of developing hypertension, suggesting that rarefaction is likely to be a primary structural abnormality. We hypothesized that low birth weight infants would have significant capillary rarefaction at birth. We studied 44 low birth weight infants born to normotensive mothers (33 were born preterm, birth weight: 1823Ϯ446 g; and 11 were born at term, birth weight: 2339Ϯ177 g) and compared them with 71 infants born at term with normal weight (birth weight: 3333Ϯ519 g). We used orthogonal polarized spectroscopy to measure basal (ie, functional) and maximal (ie, structural) skin capillary densities. Low birth weight infants, whether born preterm or at term, had significantly higher functional capillary density (mean difference of 10.5 capillaries per millimeter squared; 95% CI: 6.6 -14.4 capillaries per millimeter squared; PϽ0.0001) and higher structural capillary density (mean difference of 11.1 capillaries per millimeter squared; 95% CI: 7.6 -14.5 capillaries per millimeter squared; PϽ0.0001) when compared with normal weight term infants. We conclude that low birth weight infants born to normotensive mothers do not have capillary rarefaction at birth. These results contradict what might have been predicted from the concept of the intrauterine origins of adult disease and suggest that microcirculatory abnormalities observed in individuals of low birth weight occur in postnatal life rather than during their intrauterine existence. (Hypertension. 2011;58:847-851.)Key Words: capillary rarefaction Ⅲ microcirculation Ⅲ hypertension Ⅲ low birth weight M icrocirculatory abnormalities and impaired tissue perfusion have been implicated in the pathogenesis of essential hypertension, obesity, diabetes mellitus, and insulin resistance. 1 In essential hypertension in particular, a reduction in the spatial density of arterioles and capillaries (ie, rarefaction) appears to play a central role. 2 We have shown previously that much of the capillary rarefaction in essential hypertension is attributed to the structural (ie, anatomic) absence of capillaries. 3 We have also shown significant capillary rarefaction in patients with borderline intermittent essential hypertension and in normotensive offspring of hypertensive parents, suggesting a familial predisposition in which capillary rarefaction represents a primary vascular abnormality that antedates the onset of sustained elevation of blood pressure (BP). 4,5 There is now a strong body of evidence showing that low birth weight (LBW), that is, birth weight of Ͻ2.5 kg regardless of gestation or causation, 6 is associated with structural and functional vascular abnormalities, 7 the development of essential hypertension, 8...
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