Associations between common carotid artery diameter, Framingham risk score and cardiovascular events.

BACKGROUND AND AIMS: Vascular biomarkers are associated with risk burden and are capable to predict the development of future cardiovascular (CV) events; yet, their additive predictive value over and above established risk algorithms seems to be only modest. The present study evaluated the cross-sectional associations between vascular biomarkers, 10-year Framingham risk (FR) and prevalent CV events in a population with a high prevalence of hypertension and diabetes. METHODS AND RESULTS: As many as 681 subjects (419 men, age = 60 ± 10 years, 282 diabetics, 335 hypertensives, mean FR score = 22.5 ± 16.5%) underwent an integrated vascular examination including: radiofrequency-based ultrasound of common carotid artery (cca) to measure intima-media thickness (IMT), inter-adventitial diameter (IAD) and local pulse wave velocity (PWV); applanation tonometry to assess carotid pulse pressure (PP) and augmentation index (AIx); carotid-femoral PWV (cfPWV) measurement. One hundred and thirty-five subjects (19.8%) had history of CV events, and CV events were independently associated with male sex, age, antihypertensive treatment, current smoking, HDL-cholesterol and ccaIAD. In logistic regression model, only ccaIAD was associated with prevalence of CV events after adjustment for FR score, with the OR of 1.71 [1.34-2.19] (P < 0.0001) that remained unchanged when ccaIMT was included into the model (OR = 1.76 [1.36-2.27]; P < 0.0001). The association between prevalent CV events and ccaIAD was significant (OR of 1.65 [1.24-2.20]; P = 0.0005) also in a subgroup of subjects being at a high 10-year risk of CV disease (N = 330). CONCLUSIONS: In a population with a high prevalence of diabetes and hypertension, ccaIAD was the only vascular measure associated with prevalent CV events, independently of FR score.

Hemodynamic overload and intra-abdominal adiposity in obese children: Relationships with cardiovascular structure and function.

BACKGROUND AND AIMS: Childhood obesity promotes adverse changes in cardiovascular structure and function. This study evaluated whether these changes are related to intra-abdominal adiposity and associated cardiometabolic risk or to body-size induced hemodynamic overload. METHODS AND RESULTS: 55 obese children/adolescents and 35 healthy-weight controls underwent carotid, cardiac and abdominal ultrasound to assess carotid artery intima-media thickness (IMT), diameter, distension and stiffness, left ventricular (LV) dimension, mass and function and extent of intra-abdominal adiposity. As compared to controls with healthy BMI, obese children had higher systolic blood pressure (BP), stroke volume and lower total peripheral resistance (P < 0.001-0.0001), higher plasma triglycerides, glycated hemoglobin, insulin and HOMA-IR index (P = 0.01-<0.0001), higher carotid IMT, diameter and distension (P < 0.005-0.0005), higher LV diameter, wall thickness and mass (P < 0.001-0.0001), and impaired LV diastolic function assessed by myocardial longitudinal performance (P < 0.005). In entire population, independent determinants of carotid diameter, LV diameter, wall thickness and mass were fat-free mass (or stroke volume, respectively) and BP. Carotid distension was determined by carotid diameter and BP, and carotid IMT by carotid diameter, BP, HDL-cholesterol and glycated hemoglobin. LV diastolic performance was inversely related to preperitoneal fat thickness and plasma insulin levels. CONCLUSIONS: Obese youths present signs of impaired lipid and glucose metabolism, hyperdynamic circulation and cardiovascular changes. Increase in LV dimensions and mass and in carotid diameter and distension seems to reflect adaptation to body-size induced increase in hemodynamic load, changes in LV diastolic performance a negative impact of intra-abdominal adiposity and associated metabolic risk, and increase in IMT both adaptive remodeling and metabolic risk.

Obesity and carotid artery remodeling.

BACKGROUND/OBJECTIVE: The present study tested the hypothesis that obesity-related changes in carotid intima-media thickness (IMT) might represent not only preclinical atherosclerosis but an adaptive remodeling meant to preserve circumferential wall stress (CWS) in altered hemodynamic conditions characterized by body size-dependent increase in stroke volume (SV) and blood pressure (BP). SUBJECTS/METHODS: Common carotid artery (CCA) luminal diameter (LD), IMT and CWS were measured in three different populations in order to study: (A) cross-sectional associations between SV, BP, anthropometric parameters and CCA LD (266 healthy subjects with wide range of body weight (24-159 kg)); (B) longitudinal associations between CCA LD and 3-year IMT progression rate (ΔIMT; 571 healthy non-obese subjects without increased cardiovascular (CV) risk); (C) the impact of obesity on CCA geometry and CWS (88 obese subjects without CV complications and 88 non-obese subjects matched for gender and age). RESULTS: CCA LD was independently associated with SV that was determined by body size. In the longitudinal study, baseline LD was an independent determinant of ΔIMT, and ΔIMT of subjects in the highest LD quartile was significantly higher (28±3 µm) as compared with those in the lower quartiles (8±3, 16±4 and 16±3 µm, P=0.001, P<0.05 and P=0.01, respectively). In addition, CCA CWS decreased during the observational period in the highest LD quartile (from 54.2±8.6 to 51.6±7.4 kPa, P<0.0001). As compared with gender- and age-matched lean individuals, obese subjects had highly increased CCA LD and BP (P<0.0001 for both), but only slightly higher CWS (P=0.05) due to a significant increase in IMT (P=0.005 after adjustment for confounders). CONCLUSIONS: Our findings suggest that in obese subjects, the CCA wall thickens to compensate the luminal enlargement caused by body size-induced increase in SV, and therefore, to normalize the wall stress. CCA diameter in obesity could represent an additional biomarker, depicting the impact of altered hemodynamics on arterial wall.

Gender-specific differences in carotid intima-media thickness and its progression over three years: a multicenter European study.

BACKGROUND AND AIMS: This multicentre European study evaluated, in a young-to-middle-aged healthy population without carotid atherosclerosis, the gender-related differences in carotid intima-media thickness (IMT) and its short-term (3-year) progression, and whether these differences are related to different vascular ageing rate, cardiovascular risk profile or different susceptibility to family predisposition to cardiovascular diseases (CVD). METHODS AND RESULTS: 366 men and 422 women (age between 30 and 60 years) underwent B-mode carotid ultrasound at baseline and after 3-year follow-up period. IMT in 3 carotid segments was higher in men than in women (p < 0.0001 for all segments). When evaluated according to age decade, differences between men and women disappeared in the 6th decade, as in this decade a 3-year IMT progression rate accelerated in women (p < 0.05 as compared to the 4th and 5th age decade). Age was a major determinant of baseline all-segment IMT in women; in men all-segment IMT was influenced by age and LDL-cholesterol. IMT progression did not correlate with established cardiovascular risk factors, their short-term changes or family predisposition to CVD. Yet, a 3-year IMT progression in common carotid artery (CCA) was higher in men (p = 0.01) and women (p < 0.01) in whom relative Framingham risk increased during the corresponding period. CONCLUSION: This study provides reference values on IMT and its short-term progression in healthy young-to-middle-aged population, and demonstrates gender-related differences in the susceptibility of carotid wall to ageing and LDL-cholesterol. Increase in Framingham risk accelerated a short-term CCA IMT progression rate in both genders, whereas family predisposition to CVD did not influence carotid IMT.

Fat distribution influences the cardio-metabolic profile in a clinically healthy European population.

BACKGROUND AND AIMS: Waist and hip circumferences are largely influenced by Fat Mass and several other determinants. To evaluate the specific effects of a preferential fat distribution, we corrected the waist and hip circumferences for all their determinants. We then examined the association between fat distribution and several cardio-metabolic parameters in a clinically healthy population. SUBJECTS AND METHODS: In a subgroup of 625 females (F) and 490 males (M) from the RISC (Relationship between Insulin Sensitivity and Cardiovascular Disease) study, we evaluated insulin sensitivity by hyperinsulinaemic euglycaemic clamp and intima-media thickness (IMT) of the common (CCA) and internal (ICA) carotid artery by ultrasound imaging. Waist and hip circumferences were adjusted for age, height, fat and fat-free mass; in males, waist was also adjusted by hip and vice versa. RESULTS: Both F and M with enlarged waist showed significantly increased plasma insulin, C-peptide, total cholesterol, non-high density lipoprotein-cholesterol, low density lipoprotein cholesterol and triglycerides, when compared with subjects with a smaller waist circumference. Males also showed lower glucose uptake and higher heart rate and ICA-IMT. A larger hip in both females and males was linked to a significantly greater inhibition of free fatty acids during the clamp test. CONCLUSION: Adjustment of waist circumference for its determinants permits the detection of early impairment of cardiovascular function and of glucose and lipid metabolism in a clinically healthy population, in particular in normal body weight subjects. Enlarged hip adjusted values are associated with greater insulin sensitivity.

Arterial wave intensity and ventricular-arterial coupling by vascular ultrasound: rationale and methods for the automated analysis of forwards and backwards running waves.

Wave intensity (WI) in the circulation is estimated noninvasively as the product of instantaneous changes in pressure and velocity. We recorded diameter as a surrogate for pressure, and velocity in the right common carotid artery using an Aloka SSD-5500 ultrasound scanner. We developed automated software, applying the water hammer equation to obtain local wave speed from the slope of a pressure/velocity loop during early systole to separate net WI into individual forwards and backwards-running waves. A quality index was developed to test for noisy data. The timing, duration, peak amplitude and net energy of separated WI components were measured in healthy subjects with a wide age range. Age and arterial stiffness were independent predictors of local wave speed, whereas backwards-travelling waves correlated more strongly with ventricular systolic function than with age-related changes in arterial stiffness. Separated WI offers detailed insight into ventricular-arterial interactions that may be useful for assessing the relative contributions of ventricular and vascular function to wave travel.

Glucose turnover and intima media thickness of internal carotid artery in type 2 diabetes offspring.

BACKGROUND: First-degree offspring (OFF) of type 2 diabetic (T2DM) patients bear a approximately 40% lifetime risk of developing T2DM. They are insulin resistant and carry a risk of premature atherosclerosis, the extent of which can be estimated by intima media thickness (IMT) of the carotid artery (CA). Thus, this study examines parameters of glucose and lipid metabolism, insulin sensitivity, beta cell function (BCF) and IMT with their interrelationships in middle-aged OFF. MATERIALS AND METHODS: T2DM-OFF (n = 18, 14f/4m, 45.6 +/- 2.1 years, BMI: 26 +/- 1 kg m(-2)) were compared with 18 matching humans without a family history of diabetes (CON; 14f/4m, 44.5 +/- 2.1 years, BMI: 24 +/- 1 kg m(-2); each P > 0.30), all with normal glucose tolerance as tested by three-hour (75 g) oral glucose tolerance tests (OGTT). Two-hour hyperinsulinaemic (40 mU min(-1).m(-2))isoglycaemic clamp tests were performed with simultaneous measurement of endogenous glucose (D-[6,6-(2)H(2)]glucose) production (EGP). IMT [internal (ICA), common CA, and bulb] were measured sonographically. BCF was assessed by Adaptation Index (AI). RESULTS: Before and during OGTT, both groups were similar in plasma glucose, insulin, C-peptide and free fatty acids (FFA), whereas OFF showed ~30% lower (P < 0.03) fasting plasma triglycerides before OGTT. During hyperinsulinaemic clamps, insulin sensitivity was approximately 38% lower (P < 0.03) in OFF who showed higher plasma FFA (44 +/- 9 micromol L(-1)) than CON (26 +/- 3 micromol L(-1), P < 0.05) after 90 min. EGP was similar in both groups. OFF had 38% (P < 0.007) reduced AI. ICA-IMT was approximately 18% higher in OFF (P < 0.002), but did not correlate with insulin sensitivity. CONCLUSION: The data obtained show middle-aged T2DM-OFF with normal glucose tolerance displaying reduced total insulin sensitivity and impaired beta cell function, which relates to impaired insulin-dependent suppression of plasma FFA and increased ICA-IMT.

In vivo noninvasive identification of cell composition of intimal lesions: a combined approach with ultrasonography and immunocytochemistry.

PURPOSE: We investigated whether differences in cellular composition of the shoulder region of carotid plaque, a cell-rich, debris-free area, can be revealed with computer-driven analysis of ultrasound scans. METHODS: In 26 patients referred for carotid endarterectomy, the shoulder region of plaque eligible for surgical removal was identified with ultrasound scanning. Digital images were obtained and evaluated with a specially developed computer-driven system (Medical Image Processing [MIP]). The gray level distribution of the region of interest (ROI), along with some statistical parameters exploring the spatial distribution of pixels, such as entropy and second angular moment, were analyzed. In the specimen retrieved at surgery, the area corresponding to the ROI was selected. Cryosections were tested at immunocytochemistry with monoclonal antibodies specific to smooth muscle cells (SMCs), macrophages), and lymphocytes. Computerized image analysis was performed to quantify each cellular component of the lesion. RESULTS: Mean gray levels were related positively to the content of SMCs (r = 0.576, P =.002) and negatively to the content of macrophages (r = -0.555, P =.003). Lymphocytes did not show any correlation. Prevalence of SMCs, expressed as the ratio SMC/(SMC + macrophages), was related positively with entropy (r = 0.517, P =.007) and negatively with the second angular moment (r = -0.422, P =.032). The quartiles of gray level were useful for detecting significant differences in terms of cellular composition. CONCLUSIONS: Some cellular features of the shoulder region of plaque are associated with specific videodensitometric patterns evaluated with MIP. This approach enables in vivo noninvasive prediction and monitoring of cell composition of the shoulder region, and could be extended to study of the thickened intima.

Quantification of extracranial carotid artery stenosis by ultrafast three-dimensional ultrasound.

This study was designed to evaluate the possible contribution of 3-dimensional (3D) ultrasound (US) for noninvasive detection of extracranial carotid artery stenosis. Sixty-nine stenotic lesions of extracranial carotid artery were studied by (1) B-mode (Bm) US, (2) Doppler spectral analysis, and (3) a prototype of 3D vascular system. When indicated (46 stenotic lesions), biplane carotid angiography (CA) was performed. The degree of luminal narrowing measured as percent area reduction in the 3D data set correlated well with the degree of stenosis estimated by CA (r = 0.79, P <.01, mean difference 7.8% +/- 15.5%); however, for stenosis between 40% and 70%, 3D US tended to give higher values. Compared with CA, the sensitivity, specificity, diagnostic accuracy, and positive predictive value of 3D US for significant (> or =70%) stenosis were 96.0%, 77.7%, 88.3%, and 85.7%, respectively. Thus, 3D US showed good sensitivity and diagnostic accuracy for detection of significant stenosis of extracranial carotid artery. For stenosis between 40% and 70%, 3D US indicated a higher degree than CA; this finding suggests that CA may underestimate the severity of stenosis due to known discrepancies between linear measurement and true anatomic situation.

[Echocardiography in the non-invasive evaluation of coronary reserve and myocardial perfusion in arterial hypertension]. / L'ecocardiografia nella valutazione non invasiva della riserva coronarica e della perfusione miocardica nell'ipertensione arteriosa.

Systemic hypertension is associated with structural and functional alterations of the coronary circulation, which increase the susceptibility of the hypertensive heart to myocardial ischemia. The spectrum of modifications in the coronary macro and microcirculation of the hypertensive heart is relatively wide, and their assessment requires advanced and possibly non-invasive diagnostic approaches. This paper describes the possibility and the additive value of myocardial contrast echocardiography and of coronary velocimetry by Doppler echocardiography for the assessment of coronary function in hypertensive subjects.

Right ventricular infarction: the role of echocardiography.

Echocardiographic evaluation of patients with right ventricular (RV) ischemia and infarction has a clear clinical relevance, because the presence of RV infarction is associated with a highly increased early in-hospital mortality, which can be dramatically reduced by successful early reperfusion. However, infarcted RV did recover its function regardless of the infarcted artery patency. This observation suggests that RV myocardium almost always remains viable. This article illustrates the clinical value of echocardiography, including the transthoracic and transesophageal approaches, Doppler, and three-dimensional ultrasound, for the assessment of RV dimensions, shape, and global and regional function, and the estimation of right atrial involvement that in cases of ischemia may further modulate RV performance. In addition, the use of stress echocardiography to detect RV ischemia and evaluate the viability of infarcted RV myocardium is discussed.

Coronary vasodilator capacity and epicardial vessel remodeling in physiological and hypertensive hypertrophy.

The aim of this study was to compare resting coronary flow velocity, determinants of myocardial oxygen demand, and coronary vasodilator capacity in subjects with physiological, exercise-induced, and hypertensive left ventricular hypertrophy. Sixteen healthy sedentary men, 16 endurance athletes, and 16 hypertensive subjects (mean+/-SEM for left ventricular mass index: 94.9+/-5.5, 184.6+/-8.4, 154.4+/-9.5 g/m(2), respectively) were studied by transesophageal and transthoracic Doppler echocardiography. Coronary flow velocity in left anterior descending artery and cross-sectional area of left main artery were assessed at rest and during dipyridamole-induced vasodilation. Myocardial oxygen demand was estimated through rate-pressure product, left ventricular wall stress, and inotropic function. Coronary flow reserve and minimum coronary resistance were comparable to those of sedentary men in athletes (mean+/-SEM: 3. 23+/-0.16 versus 3.60+/-0.18 and 0.96+/-0.06 versus 1.04+/-0.04 mm Hg. s. cm(-1)), while in hypertensive subjects they were decreased and increased, respectively (mean+/-SEM: 2.31+/-0.08 and 1.21+/-0.10 mm Hg. s. cm(-1); P:<0.05 for both). Resting flow velocity was directly related to rate-pressure product in sedentary men and athletes and also to wall stress in athletes, while these correlations were absent in hypertensives. Dilation of left main artery after dipyridamole was significantly higher in athletes than in sedentary men and hypertensive subjects (mean+/-SEM for area change: 32.9+/-3.7% versus 12.8+/-2.5% and 6.4+/-3.3%; P:<0.05 and 0.01). These data indicate that vasodilator capacity of coronary microcirculation is not impaired in athletes with physiological hypertrophy, in contrast to hypertensive patients. The relationship between resting flow velocity and determinants of oxygen demand is preserved in physiological hypertrophy but missing in hypertensive hypertrophy. Furthermore, the vasodilator capacity of coronary macrocirculation is also enhanced in exercise-trained subjects.

Early impairment of coronary flow reserve and increase in minimum coronary resistance in borderline hypertensive patients.

OBJECTIVE: To evaluate relations between coronary flow velocity and myocardial oxygen demand at rest, as well as coronary vasodilator capacity and flow reserve, in asymptomatic subjects with borderline hypertension as compared to normotensive controls and patients with sustained high blood pressure (HBP) and without left ventricular hypertrophy (LVH). SUBJECTS AND METHODS: Forty-two asymptomatic males were studied: 13 healthy normotensive volunteers; 12 subjects with borderline HBP and 17 asymptomatic subjects with sustained systemic hypertension. Coronary flow velocity in left anterior descending artery and coronary flow reserve were assessed by transesophageal echo-doppler at baseline and during intravenous adenosine infusion. Left ventricular mass, peak systolic wall stress (PSWS; Pa), and midwall fractional shortening (MFS; %) were obtained from M-mode images of the left ventricle in transthoracic long-axis view and in transesophageal transgastric view. RESULTS: Coronary flow velocity at baseline was not significantly different in the three groups, despite significantly higher rate-pressure product (RPP) in the hypertensive groups as compared with controls. Only in control subjects, was resting coronary flow velocity significantly correlated with RPP (y = 4279 + 200x, r = + 0.58, P < 0.05) and PSWS (y = 17.2 + 5.1 x, r = + 0.62, P < 0.05). Coronary reserve was 3.5 +/- 0.65 in controls and significantly lower (P < 0.05) in borderline hypertensive (2.87 +/- 0.46) and in sustained hypertensive subjects (2.66 +/- 0.56). Minimum coronary resistance was significantly increased in both hypertensive groups (1.30 +/- 0.29 and 1.39 +/- 0.48 mmHg/s per cm) as compared to normotensive controls (0.93 +/- 0.20 mmHg/s per cm, P < 0.01). CONCLUSIONS: In asymptomatic subjects with borderline hypertension and without LVH, a significant reduction in coronary flow reserve is already detectable and appears almost entirely related to an impaired coronary vasodilator capacity rather than to an increased myocardial oxygen demand.

Noninvasive detection of vascular dysfunction in alcoholic patients.

Vasodilation is impaired in various conditions, such as hypercholesterolemia and tobacco use. We evaluated brachial artery flow-mediated vasodilation (FMD) after blood pressure (BP) cuff occlusion using high-resolution B-mode ultrasound in 20 alcoholics, without any coexisting conditions such as smoking, hypertension, or cholesterolemia, after a 3-month period of abstinence. They were compared with a control group of 20 alcohol-free healthy subjects. We measured the diameter of the brachial artery under baseline conditions, during reactive hyperemia (with increased flow causing endothelium-dependent dilatation), and after administration of sublingual glyceryl trinitrate (GTN), an endothelium-independent dilator. We performed an echocardiographic study (Esaote Au3) according to guidelines of the American Society of Echocardiography to assess left ventricular mass (LVM), wall thickness, systolic stress, and diastolic function changes. FMD (% diameter change) was significantly less in the alcoholic patients than in the controls (6.03+/-3.67 v 13.7+/-4.65; P < .05), whereas no difference was noted after GTN administration (13.7+/-7.97 v 16.0+/-5.12, P = NS). Echocardiographic study showed no differences between the study group for LVM, wall thickness, and systolic stress; diastolic function expressed as E/A ratio inversion was significantly impaired. These data demonstrate an impairment of endothelial-dependent vasodilatation in chronic alcohol abusers, which may contribute to the excess prevalence of cardiovascular diseases in these individuals.

Alpha-adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction.

BACKGROUND: AMI reperfusion by thrombolysis does not improve TIMI flow and LV function. The role of infarct-related artery (IRA) stenosis and superimposed changes in coronary vasomotor tone in maintaining LV dysfunction must be elucidated. METHODS AND RESULTS: Forty patients underwent diagnostic angiography 24 hours after thrombolysis. Seventy-two hours after thrombolysis, the culprit lesion was dilated with coronary stenting. During angioplasty, LV function was monitored by transesophageal echocardiography. Percent regional systolic thickening was quantitatively assessed before PTCA, soon after stenting, 15 minutes after stenting, and after phentolamine 12 microg/kg IC (n=10), the alpha1-blocker urapidil 600 microg/kg IV (n=10), or saline (n=10). Ten patients pretreated with beta-blockers received urapidil 10 mg IC. Coronary stenting significantly improved thickening in IRA-dependent and in non-IRA-dependent myocardium (from 27+/-15% to 38+/-16% and from 40+/-15% to 45+/-15%, respectively). Simultaneously, TIMI frame count decreased from 39+/-11 and 40+/-11 in the IRA and non-IRA, respectively, to 23+/-10 and 25+/-7 (P<0.05). Fifteen minutes after stenting, thickening worsened in both IRA- and non-IRA-dependent myocardium (to 19+/-14% and 28+/-14%, P<0.05), and TIMI frame count returned, in both the IRA and non-IRA, to the values obtained before stenting. Phentolamine and urapidil increased thickening to 36+/-17% and 41+/-14% in IRA and to 48+/-11% and 49+/-17% in non-IRA myocardium respectively, and TIMI frame count decreased to 16+/-6 and to 17+/-5, respectively. Changes were attenuated with beta-blocker pretreatment. CONCLUSIONS: Our finding that alpha-adrenergic blockade attenuates vasoconstriction and postischemic LV dysfunction supports the hypothesis of an important role of neural mechanisms in this phenomenon.

Three-dimensional ultrasound study of carotid arteries before and after endarterectomy; analysis of stenotic lesions and surgical impact on the vessel.

BACKGROUND AND PURPOSE: It has been proved that symptomatic patients with severe carotid stenosis benefit from endarterectomy. Currently used methods for quantitation of the severity of carotid stenosis have limitations, and the impact of endarterectomy on the operated region of carotid artery remains unknown. The purpose of this study was to examine the accuracy of a 3-D ultrasound system for quantitation of stenotic lesions and to evaluate changes in regional vessel volume and cross-sectional area after carotid endarterectomy. METHODS: We studied 14 patients with both carotid angiography and 3-D ultrasound. Of 13 patients who underwent surgery, 12 were reexamined with 3-D ultrasound after surgery. The length and volume of 20 randomly selected plaques were measured from 3-D data sets. The severity of stenosis was quantified by 3-D ultrasound using both a diameter method and an area method on cross-sectional views at the most stenotic site; the results were then compared with those from carotid angiography. The segmental vessel volume and average cross-sectional area of the operated artery both before and after endarterectomy were measured from 3-D ultrasound data. RESULTS: Good correlation was obtained between 3-D ultrasound and carotid angiography in quantitative analysis of carotid stenosis (SEE=12.4%, r=0.76, and mean difference=7.0+/-12.3% with the diameter method; SEE=10.5%, r=0.82, and mean difference=1.8+/-10.5% with the area method by 3-D ultrasound). 3-D ultrasound had excellent reproducibility and small intraobserver and interobserver variability in plaque length and volume measurements. No significant changes in segmental vessel volume and average cross-sectional area of the operated artery were observed after surgery in patients with suture closure. However, a significant increase in segmental vessel volume was obtained in patients with polyfluorethylene patches applied to the surgical opening of the artery. CONCLUSIONS: 3-D ultrasound can be used for both qualitative and quantitative analysis of plaques in the carotid artery and to detect and quantify significant carotid stenosis. Its volumetric potential has important clinical implications in serial follow-up studies for observing the progression or regression of stenotic lesions and for evaluating the outcome of interventional procedures such as endarterectomy or stent placement.

Ultrafast three-dimensional ultrasound: application to carotid artery imaging.

BACKGROUND AND PURPOSE: Three-dimensional (3-D) vascular ultrasound can be expected to improve qualitative evaluation of vessel pathology and to provide quantitative data on vascular morphology and function. The objective of this study was to develop an ultrafast 3-D vascular system and to validate its performance for quantitation of atherosclerosis and assessment of regional arterial distensibility. METHODS: The quantitative analysis of focal atherosclerotic lesions was validated in vitro on 27 phantoms of fibroadipous plaques of known volume (range, 100 to 600 mm3). In vivo reproducibility of plaque volume measurement was tested in 33 patients who had a total of 47 predominantly fibroadipous carotid plaques. Distensibility assessment was validated indirectly through the evaluation of age-related changes in distensibility of common carotid artery in healthy and hypertensive subjects (25 men in each group). RESULTS: The volume of plaque phantoms measured from the 3-D data set showed a very close correlation with the true volume (r=0.99; y=0.96x+12.38; P<0.01), with the mean difference between the 2 measurements being -3.12+/-15.1 mm3. High reproducibility was found for measurement of carotid plaque volume in vivo: the mean difference between measurements from 2 observers for the same data set was 0.60+/-11.2 mm3. Indexes of arterial distensibility decreased with age in healthy population, whereas this relationship was lost in hypertensive subjects. CONCLUSIONS: Ultrafast 3-D ultrasound imaging of carotid artery demonstrates good accuracy and reproducibility for atherosclerotic plaque volume measurements. The system also allows the study of age-related degenerative vascular changes.

Postischemic left ventricular dysfunction is abolished by alpha-adrenergic blocking agents.

OBJECTIVES: We sought to evaluate the efficacy of alpha-adrenergic blocking agents in counteracting left ventricular (LV) dysfunction occurring after transient ischemia in humans. BACKGROUND: The mechanisms underlying postischemic LV dysfunction are largely unknown. METHODS: Percutaneous transluminal coronary angioplasty (PTCA) provides a clinical model of ischemia and reperfusion. In 50 patients undergoing coronary stenting for 77+/-5% stenosis, LV function was monitored by transesophageal echocardiography during and 30-min after PTCA. Fifteen minutes after stenting, 15 patients received 12 microg/kg body weight of the alpha-blocker phentolamine intracoronarily, 15 patients received 600 microg/kg of the alpha1-blocker urapidil intravenously, 10 patients received the combination of phentolamine and 1.2 mg of propranolol intracoronarily, and 10 patients received saline. RESULTS: Fifteen minutes after successful coronary dilation, significant contractile dysfunction occurred in previously ischemic and nonischemic myocardium. LV dysfunction was accompanied by an increase in coronary resistance and diffuse vasoconstriction. Alpha-blockers counteracted LV dysfunction and coronary resistance and the increase in vasoconstriction. Phentolamine and urapidil increased global LV shortening from 34+/-9% to 45+/-8% and to 49+/-8%, respectively (p < 0.05). After the administration of propranolol combined with phentolamine, LV dysfunction remained unchanged (34+/-6%), as in control subjects. CONCLUSIONS: LV dysfunction occurs after PTCA, as described in animal models after ischemia. Alpha-blockers abolished LV, macrocirculatory and microcirculatory dysfunction, whereas the alpha-blocker effect was prevented by combining alpha- and beta-blockers. The evidence of diffuse rather than regional dysfunction, together with the opposite effects of alpha- and beta-blockade, supports the hypothesis of neural mechanisms eliciting postischemic LV dysfunction.