Endothelial function is thought to be an important factor in the pathogenesis of atherosclerosis, hypertension and heart failure. In the 1990s, high-frequency ultrasonographic imaging of the brachial artery to assess endothelium-dependent flow-mediated vasodilation (FMD) was developed. The technique provokes the release of nitric oxide, resulting in vasodilation that can be quantitated as an index of vasomotor function. The noninvasive nature of the technique allows repeated measurements over time to study the effectiveness of various interventions that may affect vascular health. However, despite its widespread use, there are technical and interpretive limitations of this technique. State-of-the-art information is presented and insights are provided into the strengths and limitations of high-resolution ultrasonography of the brachial artery to evaluate vasomotor function, with guidelines for its research application in the study of endothelial physiology.

TAPSE powerfully reflects RV function and prognosis in PAH.

Rationale: Transthoracic Doppler echocardiography is recommended for screening for the presence of pulmonary hypertension (PH). However, some recent studies have suggested that Doppler echocardiographic pulmonary artery pressure estimates may frequently be inaccurate. Objectives: Evaluate the accuracy of Doppler echocardiography for estimating pulmonary artery pressure and cardiac output. Methods: We conducted a prospective study on patients with various forms of PH who underwent comprehensive Doppler echocardiography within 1 hour of a clinically indicated right-heart catheterization to compare noninvasive hemodynamic estimates with invasively measured values. Measurements and Main Results: A total of 65 patients completed the study protocol. Using Bland-Altman analytic methods, the bias for the echocardiographic estimates of the pulmonary artery systolic pressure was 20.6 mm Hg with 95% limits of agreement ranging from 138.8 to 240.0 mm Hg. Doppler echocardiography was inaccurate (defined as being greater than 610 mm Hg of the invasive measurement) in 48% of cases. Overestimation and underestimation of pulmonary artery systolic pressure by Doppler echocardiography occurred with a similar frequency (16 vs. 15 instances, respectively). The magnitude of pressure underestimation was greater than overestimation (230 6 16 vs. 119 6 11 mm Hg; P 5 0.03); underestimates by Doppler also led more often to misclassification of the severity of the PH. For cardiac output measurement, the bias was 20.1 L/min with 95% limits of agreement ranging from 12.2 to 22.4 L/min. Conclusions: Doppler echocardiography may frequently be inaccurate in estimating pulmonary artery pressure and cardiac output in patients being evaluated for PH.Keywords: echocardiography; pulmonary hypertension; pulmonary systolic pressure; cardiac output; accuracy Pulmonary hypertension (PH), a syndrome characterized by increased pulmonary vascular resistance and remodeling, is associated with significant morbidity and mortality, which are directly related to cardiac function (1). Although the definitive diagnosis of PH is currently established through right-heart catheterization, accurate noninvasive assessment of pulmonary arterial pressure and cardiac output (CO) is desirable both for diagnostic purposes and to assess response to therapy.Transthoracic Doppler echocardiography (DE) is recommended as the initial noninvasive modality in the screening and evaluation of PH (2). Echocardiography can be used to evaluate right-sided chamber size and function and the presence of pericardial effusion, which are known to impact survival (3-5). Frequently, DE is used to estimate the right ventricular systolic pressure by estimating the pressure gradient between the right ventricle and the right atrium using the modified Bernoulli equation, 4v 2 , where v equals the velocity of the tricuspid regurgitant jet. An estimated right atrial pressure is added to this number to approximate the right ventricular systolic pressure, which equals the pulmonary artery systolic pres...

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Flow-mediated brachial artery vasoactivity has been recently proposed as a noninvasive means for assessing endothelial function. To better characterize this technique, we measured brachial artery diameter and flow using 7.5-MHz ultrasound following 1, 3, and 5 min of upper arm blood pressure cuff occlusion in 19 normal volunteers and 13 patients with coronary artery disease (CAD). Although similar flow increases were observed with each protocol, statistically significant vasodilatation (12.6 +/- 5.7%) was observed in the normals only after 5 min of occlusion. With the use of this protocol, postocclusion blood flow increased 528 +/- 271 and 481 +/- 247% in the normals and CAD patients, respectively (P = NS). More vasodilatation was observed in the normals compared with the CAD patients (11.3 +/- 5.4 vs. 1.6 +/- 5.2%, P < 0.001). Interestingly, vasodilatation persisted for 20 min despite return of blood flow to baseline in 2 min. With the use of lower arm occlusion, arterial diameter was found to decrease 4.4 +/- 3.9% in response to a 85 +/- 7% decrease in flow. We conclude that 1) longer brachial artery occlusion results in more vasodilatation despite similar hyperemic responses, 2) vasodilatation persists substantially beyond hyperemia, and 3) CAD patients have impaired flow-mediated vasodilatation using this noninvasive technique.

In terms of their postprandial effect on endothelial function, the beneficial components of the Mediterranean and Lyon Diet Heart Study diets appear to be antioxidant-rich foods, including vegetables, fruits, and their derivatives such as vinegar, and omega-3-rich fish and canola oils.

Alagebrium enhances peripheral artery endothelial function and improves overall impedance matching. Improved endothelial function correlates better with reduced vascular fibrosis and inflammation markers than with vessel distensibility. AGE-crosslink breakers may reduce cardiovascular risk in older adults by reduced central arterial stiffness and vascular remodeling.

Abstract-To investigate the cellular mechanisms for altered Ca 2ϩ homeostasis and contractility in cardiac hypertrophy, we measured whole-cell L-type Ca 2ϩ currents (I Ca,L ), whole-cell Ca 2ϩ transients ([Ca 2ϩ ] i ), and Ca 2ϩ sparks in ventricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age-and sex-matched Wistar-Kyoto and Sprague-Dawley control rats. By echocardiography, SHR hearts had cardiac hypertrophy and enhanced contractility (increased fractional shortening) and no signs of heart failure. C ardiac hypertrophy is associated with marked changes in myocardial contractility. Peak active tension increases, 1-4 and the rates of both contraction and relaxation are slowed. 3,[5][6][7][8] These contractile abnormalities are associated with alterations in the whole-cell calcium transient ([Ca 2ϩ ] i ). In the hypertrophied myocardium, the amplitude of [Ca 2ϩ ] i increases, 9 whereas in failing myocardium, the amplitude of [Ca 2ϩ ] i decreases. 10 -13 In most animal models of hypertrophy 8,10,11,[13][14][15] and in failing human hearts, 12,16 the duration of the whole-cell [Ca 2ϩ ] i is also prolonged. However, the precise cellular mechanisms that are responsible for changes in contractility and alterations in [Ca 2ϩ ] i are largely unknown. Identification of the cellular mechanisms that underlie altered excitation-contraction coupling in cardiac hypertrophy and heart failure is complicated by several issues, including differences in experimental animal models and disease progression. In addition, it has only recently proved possible using confocal microscopy to measure local nonpropagating elevations of Ca 2ϩ (Ca 2ϩ sparks) at the level of individual sarcomeres. [17][18][19][20][21][22] The ability to measure Ca 2ϩ sparks provides an opportunity to evaluate directly the role of sarcoplasmic reticulum (SR) Ca 2ϩ release in muscle cells from animal models associated with cardiac hypertrophy.In this study, we used laser scanning confocal microscopy and Ca 2ϩ -sensitive fluorescent indicators to detect Ca 2ϩ sparks evoked by electrical field stimulation in ventricular cells from normal rats and from spontaneously hypertensive rats (SHRs) with cardiac hypertrophy. By quantitative analysis of the kinetic characteristics of Ca 2ϩ sparks, we identify enhanced SR Ca 2ϩ release from hypertrophied SHR cells. In