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Media Thickness (media + thickness)
Selected AbstractsHow to identify patients with vulnerable plaquesDIABETES OBESITY & METABOLISM, Issue 10 2008Salim S. Virani Multiple strategies are available for clinicians to identify patients at high risk for cardiovascular events. Two commonly discussed strategies are the identification of vulnerable plaques and the identification of vulnerable patients. The strategy of identifying vulnerable patients is less invasive, easy to implement and not restricted primarily to one vascular bed (e.g. coronary or cerebral). This review discusses the utility as well as the limitations of global risk assessment tools to identify such patients. The utility of biomarkers [C-reactive protein, lipoprotein-associated phospholipase A2 and lipoprotein(a)] and non-invasive measures of atherosclerosis burden (coronary artery calcium scores, carotid intima,media thickness and ankle,brachial index) in identifying patients at high risk for cardiovascular events are also discussed. [source] CETP inhibition in cardiovascular risk management: a critical appraisalEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2007R. P. F. Dullaart Abstract In view of the cardioprotective effect of high-density lipoproteins (HDL) and the limited effects of statin and fibrate therapy on HDL cholesterol, it is clinically relevant to test whether pharmacological treatment aimed at raising HDL lowers cardiovascular risk. Cholesteryl ester transfer protein (CETP) is a new therapeutic target, because the cholesteryl ester transfer process lowers HDL cholesterol and contributes to an atherogenic lipoprotein profile, particularly when plasma triglycerides are high. Clinical evidence suggests that coronary artery calcification as well as intima media thickness is positively related to plasma cholesteryl ester transfer, and that high plasma CETP concentration is associated with increased cardiovascular risk in hypertriglyceridaemia. However, CETP could also have anti-atherogenic potential, since it provides a potentially beneficial route for delivery of HDL-derived cholesteryl esters to the liver. In addition, CETP could also favourably stimulate peripheral cell cholesterol removal and enhance hepatic cholesterol uptake. Recent evidence suggests that a high CETP level may confer lower cardiovascular risk in the context of low triglycerides. At maximal doses, the CETP inhibitors JTT-705 and torcetrapib elicit a marked rise in HDL cholesterol of up to 34% and 91,106%, respectively. The effectiveness of these drugs on (intermediate) clinical outcome measures is currently being tested in large-scale phase III clinical trials, with torcetrapib being only evaluated in combination therapy with atorvastatin. When and how to use CETP inhibitors, e.g. in combination with a statin or a fibrate, is a major challenge. We propose that low HDL cholesterol in the context of high triglycerides, such as found in type 2 diabetes mellitus, could become an important indication area for this new class of drugs. [source] Variations in carotid arterial compliance during the menstrual cycle in young womenEXPERIMENTAL PHYSIOLOGY, Issue 2 2006Koichiro Hayashi The effect of menstrual cycle phase on arterial elasticity is controversial. In 10 healthy women (20.6 ± 1.5 years old, mean ±s.d.), we investigated the variations in central and peripheral arterial elasticity, blood pressure (carotid and brachial), carotid intima,media thickness (IMT), and serum oestradiol and progesterone concentrations at five points in the menstrual cycle (menstrual, M; follicular, F; ovulatory, O; early luteal, EL; and late luteal, LL). Carotid arterial compliance (simultaneous ultrasound and applanation tonometry) varied cyclically, with significant increases from the values seen in M (0.164 ± 0.036 mm2 mmHg,1) and F (0.171 ± 0.029 mm2 mmHg,1) to that seen in the O phase (0.184 ± 0.029 mm2 mmHg,1). Sharp declines were observed in the EL (0.150 ± 0.033 mm2 mmHg,1) and LL phases (0.147 ± 0.026 mm2 mmHg,1; F= 8.51, P < 0.05). Pulse wave velocity in the leg (i.e. peripheral arterial stiffness) did not exhibit any significant changes. Fluctuations in carotid arterial elasticity correlated with the balance between oestradiol and progesterone concentrations. No significant changes were found in carotid and brachial blood pressures, carotid artery lumen diameter, or IMT throughout the menstrual cycle. These data provide evidence that the elastic properties of central, but not peripheral, arteries fluctuate significantly with the phases of the menstrual cycle. [source] Sonographic measurements of subcutaneous fat in obese individuals may correlate better with peripheral artery disease indicesJOURNAL OF CLINICAL ULTRASOUND, Issue 5 2009Serafim Tsitsilonis MD Purpose. The purpose of this study was to investigate the association of various methods for body fat assessment with indices of peripheral artery disease in the deep and superficial femoral arteries. Methods. The intima,media thickness (IMT), maximal IMT (max IMT), femoral wall thickness (FWT), maximal FWT (max FWT), cross-sectional intima media area (CIMA), and atherosclerotic burden score (ABS) were measured sonographically in 26 subjects. The minimum thickness of the abdominal subcutaneous fat layer (Smin) was measured sonographically close to the xyphoid process, and body fat percentage was calculated using various formulas. Results. Smin correlated significantly with body fat percentage calculated with all formulas and was the sole parameter that was associated significantly with all the femoral artery atherosclerotic indices IMT: r = 0.74, p < 0.001; max IMT: r = 0.53, p < 0.05; FWT: r = 0.78, p < 0.001; max FWT: r = 0.57, p < 0.005; ABS: r = 0.52, p < 0.05; CIMA: r = 0.86, p < 0.001; Smin was the major independent predictor of femoral IMT on a multiple stepwise regression analysis (, = 0.02; SE = 0.008, R2 = 0.35, p < 0.05). Conclusions. Smin correlates better than indirect indices and formulas of body fat estimation with markers of extracoronary atherosclerosis. Sonographic measurement of Smin may serve in the future as a useful tool in everyday clinical practice. © 2009 Wiley Periodicals, Inc. J Clin Ultrasound, 2009 [source] Intima,media thickness of the abdominal aorta of neonate with different gestational agesJOURNAL OF CLINICAL ULTRASOUND, Issue 9 2007Esad Koklu MD Abstract Purpose. To determine aortic intima,media thickness (aIMT) values in newborns with different gestational ages and to asses the effect of antenatal steroids on aIMT. Methods. Two hundred forty newborns from healthy mothers had their distal abdominal aIMT measured during abdominal sonographic examination. The neonates were divided into 4 groups (60 in each group) according to gestational age: group I (25,28 weeks), group II (29,32 weeks), group III (33,37 weeks), and group IV (38,42 weeks). Results. The interobserver and intersubject intraclass correlation coefficient was 0.93 and 0.94, respectively. Mean aIMT was 0.316 mm, 0.335 mm, 0.348 mm, and 0.385 mm, respectively, in group I, II, III, and IV, increasing significantly with gestational age at birth (p < 0.0001). There was no apparent effect of antenatal steroid use on aIMT. Multivariate regression models for mean aIMT demonstrated a significant association with aortic lumen diameter (p < 0.0001). Conclusion. Abdominal aIMT can be reproducibly measured in neonates and may be a useful tool for epidemiologic studies. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2007 [source] Carotid intima,media thickness in children and young adults with renal transplant: Internal carotid artery vs. common carotid arteryPEDIATRIC TRANSPLANTATION, Issue 8 2007Yelda Bilginer Abstract:, Cardiovascular diseases are the main causes of morbidity and mortality following renal transplantation. Atherosclerotic structural changes, which can be detected by high-resolution B-mode ultrasonography, begin before clinical findings. However, little is known about the extent of these abnormalities in children after renal transplantation. We aimed to determine early structural changes of large arteries in renal transplant recipients without cardiovascular disease and to evaluate the role of clinical and laboratory features on IMT of carotid arteries. IMT and hemoglobin, serum levels of creatinine, acute phase proteins, lipid profile, and homocysteine were examined in 24 asymptomatic renal transplant recipients (median age 16.5 yr; range 8,25), and 20 healthy controls (median age 16 yr; range 9,24). CCA and ICA were evaluated in patients and controls with a high-resolution B-mode ultrasonography in multiple projections to optimize detection of carotid IMT. Measurement of IMT of both CCA [0.36 mm (range 0.16,0.48) vs. 0.28 mm (range 0.21,0.35), p < 0.001] and ICA [0.27 mm (range 0.16,0.48) vs. 0.22 mm (range 0.1,0.26), p < 0.001] were significantly higher in renal recipients than in healthy controls. Among several parameters assessed, only significant correlations were found between duration of CRF, duration of dialysis prior to transplantation and ICA-IMT (p = 0.06 and p = 0.02, respectively) and between mean past serum calcium,phosphorus ion product and CCA-IMT (p = 0.002). In conclusion, our observations indicate that vascular changes begin early in the course of CRF and are directly related to time on CRF and dialysis. These changes can be detected by measuring CCA/ICA-IMT ultrasonographically. We suggest that early renal transplantation can potentially avoid long-term cardiovascular events in children with end stage kidney disease. [source] Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitisCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009J. W. Cohen Tervaert Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible. [source] INVOLVEMENT OF PROLYLCARBOXYPEPTIDASE IN THE EFFECT OF RUTAECARPINE ON THE REGRESSION OF MESENTERIC ARTERY HYPERTROPHY IN RENOVASCULAR HYPERTENSIVE RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2009Xu-Ping Qin SUMMARY 1Previous studies indicate that rutaecarpine blocks increases in blood pressure and inhibits vascular hypertrophy in experimentally hypertensive rats. The aim of the present study was to determine whether the effects of rutaecarpine are related to activation of prolylcarboxypeptidase (PRCP). 2Renovascular hypertensive rats (Goldblatt two-kidney, one-clip (2K1C)) were developed using male Sprague-Dawley rats. Chronic treatment with rutaecarpine (10 or 40 mg/kg per day) or losartan (20 mg/kg per day) for 4 weeks to the hypertensive rats caused a sustained dose-dependent attenuation of increases in blood pressure, increased lumen diameter and decreased media thickness, which was accompanied by a similar reduction in the media cross-sectional area : lumen area ratio in mesenteric arteries compared with untreated hypertensive rats. 3Angiotensin (Ang) II expression was significantly increased in mesenteric arteries of hypertensive rats compared with sham-operated rats. No significant differences in plasma AngII levels were observed between untreated hypertensive and sham-operated rats. Hypertensive rats treated with high-dose rutaecarpine had significantly decreased Ang II levels in both the plasma and mesenteric arteries. 4Expression of PRCP protein or kallikrein mRNA was significantly inhibited in the right kidneys and mesenteric arteries of hypertensive rats. However, expression of PRCP protein and kallikrein mRNA was significantly increased after treatment with rutaecarpine or losartan (20 mg/kg per day). 5The data suggest that the repression of increases in systolic blood pressure and reversal of mesenteric artery remodelling by rutaecarpine may be related to increased expression of PRCP in the circulation and small arteries in 2K1C hypertensive rats. [source] Enalapril Prevents Aortic Hyperreactivity And Remodelling In One-Kidney, One-Clip Hypertensive Rats Without Reducing Arterial PressureCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2000Valdeci Cunha SUMMARY 1. The present study was designed to evaluate the blood pressure-independent effects of angiotensin-converting enzyme (ACE) inhibition on cardiovascular structure and function in one-kidney, one-clip (1K1C) hypertensive rats. 2. The study was conducted in four groups of rats: (i) uninephrectomized normotensive rats (1K); (ii) 1K1C hypertensive rats; (iii) 1K rats treated with enalapril; and (iv) 1K1C rats treated with enalapril. Enalapril treatment (20 mg/kg per day, p.o.) was started after surgery to induce hypertension or nephrectomy and continued for 5 weeks. 3. The increase in blood pressure of 1K1C rats was associated with activation of cardiac and aortic, but not plasma, ACE activity and with hypertrophy of both heart and aorta. No difference in cardiac output and in vitro systolic function was observed among the groups. Hypertrophied aorta isolated from 1K1C rats displayed increased sensitivity to phenylephrine (PE) and unaltered responses to both acetylcholine (ACh) and sodium nitroprusside compared with the 1K group. 4. Enalapril treatment effectively inhibited plasma and tissue ACE activity in 1K1C and 1K rats. Enalapril did not prevent the development of hypertension and cardiac hypertrophy nor did it change haemodynamic parameters in 1K1C rats. However, enalapril prevented the increase in aortic media thickness and cross-sectional area and restored the hypersensitivity to PE in aortic rings of 1K1C rats. The endothelium-dependent response to ACh was enhanced by enalapril in the aorta of 1K but not 1K1C rats. 5. These results suggest a role for activated local angiotensin II generation in aortic but not cardiac hypertrophy secondary to 1K1C hypertension. [source] | ||||||||||