Sonographic characteristics of carotid artery plaques: Implications for follow-up planning?

UNLABELLED: The aim of our study was to analyze the ultrasound characteristics of carotid plaques in an outpatient population and to determine their implications for planning the ultrasound follow-up. MATERIALS AND METHODS: We studied 747 consecutive outpatients (397 [53%] of whom were women) who underwent color Doppler sonography of the carotid arteries. Most of the patients presented multiple cardiovascular risk factors or were being followed-up for carotid artery stenosis. RESULTS: Stenosis ranging from 1% to 69% was observed at the level of the right internal carotid arteries (ICA) in 419 (56.1%) of the 747 patients and in the left ICA in 408 of 747 (54.5%). One hundred twenty-four (29.5%) of the 419 RICA plaques and 77 (18.8%) of the 408 LICA plaques were classified as type 1 or type 2 according to the modified Gray-Weale classification. CONCLUSIONS: Type 1 and type 2 plaques, which are referred to as "vulnerable plaques," were found in 160 (21.4%) of the 747 patients we examined. These patients should be subjected to closer ultrasound follow-up, even if they have only moderate carotid artery stenosis.

Management of pseudoaneurysm of the leg: is Color Doppler US enough?

The authors describe two clinical cases showing that Color Doppler Ultrasonography (US) examination is effective and sufficient in the presence of a clinical suspicion of pseudoaneurysm. In cases of iatrogenic damage and post-traumatic lesions, US provides an easy and accurate diagnosis depicting the location and the morphology of the false aneurysm. The patient can thus be referred to appropriate treatment without undergoing further diagnostic examinations. Moreover, regardless of the performed treatment, Color Doppler US is an efficient non-invasive diagnostic tool in the follow-up.

Color Duplex evaluation of the mesenteric artery().

Ischemic colitis is the most common form of intestinal ischemia. Diagnosis is made at clinical examination and endoscopy and completed by vascular imaging, but color Doppler US may become a first-line imaging technique for the evaluation of the mesenteric circulation.We present the case of an 80-year-old woman hospitalized for recurrent ischemic colitis of the sigmoid. At a previous hospitalization, color Doppler US examination showed medium to severe stenosis at the origin of the inferior mesenteric artery. However, CT angiography was negative and the condition was therefore misdiagnosed. Eight months later the patient was admitted again with abdominal pain and rectal hemorrhage. Rectosigmoidoscopy documented the presence of ischemia of the sigmoid mucosa. Angiography showed the presence of severe stenosis at the origin of the inferior mesenteric artery so revascularization was carried out by percutaneous transluminal angioplasty (PTA) during the same session. Follow-up showed normal patency of the inferior mesenteric artery after revascularization, and subsequent endoscopic evaluation documented gradual colonic mucosal ischemia resolution. Blood flow at the level of the inferior mesenteric artery was assessed using color Doppler US. The presented case confirms that color Doppler US is a valid first-line imaging technique in the assessment of ischemic intestinal lesions. It is reliable in the evaluation of the mesenteric arterial circulation, and it also allows assessment of blood flow alterations caused by stenosis and identification of localized hemodynamic stenosis which may be missed at CT-angiography or MR-angiography. Arteriography remains the examination of choice in case of discrepancy between first-and second-line imaging techniques and in all cases which offer the possibility of endovascular revascularization.

Idiopathic floating thrombus of the common carotid artery: Diagnosis and treatment options.

The authors report a case of ischemic stroke caused by a floating thrombus in the common carotid artery and review the diagnostic techniques used to identify the cause of ischemic strokes. They also examine the possible origins of idiopathic carotid thrombi and the current options for their management, with emphasis on the difficulties and risks associated with medical and surgical approaches.

Aldosterone synthase alleles and cardiovascular phenotype in young adults.

The C(-344)T promoter polymorphism of the human aldosterone synthase (CYP11B2) gene has been associated with hypertension and cardiac hypertrophy, but there were contrasting data. We analysed the genotype/phenotype associations between this polymorphism and cardiovascular variables in a young adult population, where interactions among genes, gene-environment, and acquired ageing-related organ damage are reduced. Anthropometric measurements, blood pressure, heart rate, left ventricular variables (by echocardiography), and carotid artery wall intimal-media thickness (by high-resolution sonography and digitalized morphometry) were taken in 420 white Caucasian students (mean age 23.5 years, s.d. 2.5 years). CYP11B2 alleles were detected by genomic polymerase chain reaction followed by digestion. Taking into account the three possible models of inheritance, we found no differences in the considered variables, except for an independent effect of the C(-344) allele on SBP in males (TT 125.6 (1.6), TC 128.4 (1.2) and CC 130.5 (2.2), mmHg, media (ES), P=0.03), and on interventricular septum thickness in diastole in females (CC 6.98 (0.12) vs TT 6.87 (0.09) and TC 6.87 (0.07), mmHg, P<0.01), in the codominant model. In conclusion, the CYP11B2 C(-344)T polymorphism appears to have a slight role in the cardiovascular phenotype of young healthy adults, even if these genotype/phenotype relationships might change with ageing.

Cardiovascular phenotype of young adults and angiotensinogen alleles.

OBJECTIVES AND DESIGN: Angiotensinogen (AGT) gene variants influence angiotensinogen plasma levels in children and young adults. The angiotensinogen promoter (-6)A variant facilitates gene transcription in human tissues and it has been associated with high blood pressure in older adults. A young adult population can be used as a model to study genotype/phenotype associations between AGT (-6) variants and cardiovascular variables. METHODS AND RESULTS: Anthropometric measurements, blood pressure and heart rate were taken in 422 white Caucasian students (mean age 23.5 years, SD 2.5 years). Family history for hypertension, physical activity and smoking history were evaluated. Left ventricular variables were measured by echocardiography. Carotid artery wall intimal-media thickness (IMT) was measured by high resolution sonography and digitalized morphometry. The AGT G(-6)A alleles were evaluated by mutagenically separated polymerase chain reaction controlled by direct sequencing. No significant associations were found between angiotensinogen genotype and blood pressure, cardiac variables [except for deceleration time in females which increased with the number of (-6)A alleles] and IMT. Allele frequencies were similar between the first and third tertile of blood pressure and left ventricular mass, and were also similar between negative or positive family history for hypertension (the last group having significantly higher systolic blood pressure in males, P = 0.04 and diastolic blood pressure in females, P < 0.01). Moreover, no relevant interaction on the cardiovascular variables was found between AGT genotype and body mass index. CONCLUSIONS: The angiotensinogen G(-6)A variants do not affect cardiovascular parameters in young adults, but an effect of this polymorphism on cardiovascular phenotype (and hypertension) in older adults cannot be excluded. Additional factors, associated with ageing, should be present to unleash the supposed unfavourable potential of the (-6)A angiotensinogen variant.

Baseline reproducibility of B-mode ultrasonic measurement of carotid artery intima-media thickness: the European Lacidipine Study on Atherosclerosis (ELSA).

BACKGROUND AND OBJECTIVE: The European Lacidipine Study of Atherosclerosis (ELSA) is a prospective, randomized, double-blind, multi-national interventional trial to determine the effect of four-year treatment using the calcium antagonist lacidipine versus the beta-blocker atenolol on the progression of carotid atherosclerosis in 2259 asymptomatic hypertensive patients. B-mode ultrasound is used to measure the primary and secondary endpoints including the mean maximum intima-media thickness (IMT) of the carotid bifurcations and the common carotid arteries (CBM(max)), the mean maximum IMT of 12 standard carotid sites (M(max)) and the overall maximum IMT (T(max)). This paper reports the cross-sectional reproducibility of ultrasound measurements at baseline. METHOD: To evaluate measurement reliability, each patient is scanned twice at baseline and again at four annual visits, with 80% of the replicate scans performed by the same sonographer and 20% by a different sonographer; 50% of the replicate scans are read by the same reader and the other 50% by different readers. RESULTS: The overall coefficient of reliability (R) was 0.859 for CBM(max), 0.872 for M(max) and 0.794 for T(max). The reliability for CBM(max) was stable during the 1 3/4-year baseline period (R = 0.848 to 0.953) and was uniform among the 23 field centres (R = 0.798 to 0.926). Intra- and inter-reader reliability were 0.915 and 0.872 respectively, and intra-sonographer reliability was 0.866. CONCLUSION: The results demonstrate that by implementing standardized protocols and strict quality control procedures, highly reliable ultrasonic measurements of carotid artery IMT can be achieved in large multi-national trials.

Angiotensin converting enzyme gene polymorphism and carotid atherosclerosis in a low-risk population.

OBJECTIVES: Angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism has been shown to be an independent risk factor for myocardial infarction and other cardiovascular diseases. The aim of the study was to investigate the relationship between ACE genotype and carotid atherosclerosis evaluated by ultrasonography. PATIENTS AND METHODS: ACE I/D polymorphism was determined in 240 low-risk patients (mean age 53.6 +/- 7 years) in relation to traditional risk factors and the degree of carotid atherosclerosis. Intimal-medial thickness was measured at the level of the common carotid artery, bifurcation and internal carotid on both sides. Patients were defined as normal (n = 47, intimal-medial thickness <1.0 mm), thickened (n = 56, intimal-medial thickness > or = 1.0 and < or = 1.3 mm in the thickest wall) or with an atherosclerotic plaque (n = 137, intimal-medial thickness >1.3 mm for at least one level of examination). Age, sex, body mass index, blood pressure levels and prevalence of other risk factors were similar in the three groups. I/D polymorphism was determined by polymerase chain reaction using specific primers and genomic DNA from leukocytes as template. Plasma ACE levels, plasma renin activity and plasma aldosterone were evaluated in all patients by standard procedures. RESULTS: No significant differences were found in humoral parameters, ACE, genotype distribution and the corresponding allele frequency among the three groups of patients. Only ACE plasma levels were significantly higher in the DD and ID genotypes compared with the II genotype (DD 14.27 +/- 5.05 IU/ml, ID 12.70 +/- 4.31 IU/ml; II 8.04 +/- 3.45 IU/ml). The mean intimal-medial thickness was similar in all three genotypes. CONCLUSION: Although ACE genotype has been shown to be related to coronary atherosclerosis, the present data do not indicate that the DD genotype is associated with carotid atherosclerosis. However, further studies of larger populations are needed to clarify whether genetic ACE polymorphism is associated with carotid atherosclerosis.

Urinary kallikrein excretion and blood pressure response to angiotensin converting enzyme inhibitors and calcium antagonists in hypertensive patients.

OBJECTIVE: To investigate whether the hypotensive effects of angiotensin converting enzyme (ACE) inhibitors in comparison with those of calcium antagonist might be predicted by urinary kallikrein activity, a marker of the activity of the renal kallikrein-kinin system. DESIGN: Seventy-five essential hypertensive patients were randomly assigned to treatment with ACE inhibitors (enalapril or lisinopril 20 mg once a day) or with calcium antagonists (nifedipine 20 mg twice a day or lacidipine 4 mg once a day). Fifty-four had normal (NK) and 21 low (LK) kallikrein activity. Blood pressure was measured after 2 weeks, and 3 and 6 months. Patients whose diagnostic blood pressure, 2 weeks after the first dose, decreased by at least 15 mmHg or was < or = 90 mmHg were defined as responders. The others were defined as non-responders. In non-responders a second drug was added and the patients were not considered for further analysis. METHODS: Urinary kallikrein activity was determined by a spectrophotometric assay using a synthetic chromogenic substrate. RESULTS: After 2 weeks therapy with ACE inhibitors 88% of NK patients were responders, whereas in the LK subgroup 40% were responders, a significant difference between subgroups. For the patients treated with calcium antagonists, conversely, 59% of NK patients were responders in comparison with 82% of the LK subgroup, a significant difference between drug groups. After 3 and 6 months of treatment blood pressure was significantly lower in NK patients treated with ACE inhibitors and in LK patients treated with calcium antagonists. In the NK group on ACE inhibitors the mean arterial pressure after the first dose was significantly related to that observed after 6 months (n = 0.71, P < 0.01). CONCLUSIONS: Our data indicate that urinary kallikrein activity may represent an index to predict the chronic antihypertensive effect not only of ACE inhibition but also of calcium antagonism, and support the concept that the renal kallikrein-kinin system might play some contributory role in modulating the hypotensive action of ACE inhibitors.

Relationship between plasma atrial natriuretic factor and urinary kallikrein excretion in essential hypertensives.

In order to seek possible relationships between renal kallikrein and atrial natriuretic factor (ANF), we measured urinary kallikrein (UK) and ANF in 84 normal subjects (NS) and in 104 uncomplicated essential hypertensives (HP). Atrial natriuretic factor was significantly higher in HP than in NS (38.5 +/- 1.3 vs 29.0 +/- 1.3 pg/mL, P less than .01), whereas UK was significantly lower in HP than in NS (11.1 +/- 0.9 v 15.3 +/- 0.6 nkatal/24 h, P less than .01). Calculating the 95% of the percentile distribution of the single values of UK in the group of NS we were able to show that 24 out of 104 HP had a UK which fell below the lowest limit (4.5 nkat/24 h) of the normal range. We therefore divided our HP into two subgroups: patients with normal kallikrein excretion (NK) (n = 80; mean UK 13.8 +/- 0.8 nkat/24 h) and patients with low kallikrein excretion (LK) (n = 24; mean UK 2.3 +/- 0.3 nkat/24 h). Normal kallikrein patients had a mean plasma ANF value of 31.9 +/- 1.2 pg/mL which was almost superimposable to that found in NS; on the contrary, the mean plasma level of ANF in LK patients (50.7 +/- 2.2 pg/mL) was significantly higher than that measured in NK patients and in NS (P less than .01 v NK patients and NS, respectively). Since a low urinary kallikrein excretion may represent a marker of an impaired production of renal kallikrein, the high levels of ANF found in the LK subgroup could be the result of a compensatory response of the atrium attempting to maintain sodium and volume homeostasis.

Relationship between urinary kallikrein excretion and plasma atrial natriuretic factor in essential hypertensives.

Relationships between renal kallikrein and plasma atrial natriuretic factor were investigated by measuring urinary kallikrein excretion (by spectrophotometric assay) and plasma atrial natriuretic factor (by radio-immunoassay after extraction from plasma) in 84 normal subjects and in 104 essential hypertensives with a normal renal function. The atrial natriuretic factor was significantly higher in the essential hypertensives than in the normal subjects (38.5 +/- 1.3 versus 29.0 +/- 1.3 pg/ml, P less than 0.01), whereas urinary kallikrein excretion was significantly lower in the hypertensives than in the normal subjects (11.1 +/- 0.9 versus 15.3 +/- 0.6 nkat/24 h, P less than 0.01). Taking the 95% confidence limits of urinary kallikrein excretion in the normal subjects (from 4.5 to 29.9 nkat/24 h), we divided our essential hypertensives into two subgroups, patients with a normal kallikrein excretion (n = 80; mean urinary kallikrein excretion 13.8 +/- 0.8 nkat/24 h) and patients with a low kallikrein excretion (n = 24; mean urinary kallikrein excretion 2.3 +/- 0.3 nkat/24 h) The patients with a normal kallikrein excretion had a mean plasma atrial natriuretic factor value of 31.9 +/- 1.2 pg/ml, which was similar to that found in normal subjects. In contrast, the mean plasma level of atrial natriuretic factor in the patients with a low kallikrein excretion (50.7 +/- 2.2 pg/ml) was significantly higher than that measured in the patients with a normal kallikrein excretion and in the normal subjects (P less than 0.01 versus patients with normal kallikrein excretion and normal subjects, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)