Effects of timing and extent of smoking, type of cigarettes, and concomitant risk factors on the association between smoking and subclinical atherosclerosis

Background and Purpose \u2014 The purpose of this study was to evaluate the effects of timing and extent of smoking, type of cigarettes, and concomitant vascular risk factors (VRFs) on the association between smoking and carotid intima-media thickness (C-IMT) in a lipid clinic population. Methods \u2014 1804 patients (869 men, age 21 to 85 year) participated in the study. Smoking habits were recorded and C-IMTs were measured by B-mode ultrasound. The associations of C-IMT with smoking status (never, former, and current) and with the cigarettes\u2019 content of tar, nicotine, and carbon monoxide (alone or combined to define \u201clight\u201d or \u201cregular\u201d cigarettes) as well as the interactions between smoking status, gender, and VRFs were evaluated before and after adjustment for confounders. Results \u2014 C-IMT was highest in current smokers, lower in former, and lowest in never smokers. C-IMT of former and current smokers differed only after data adjustment for variables describing the extent and timing of smoking exposure. C-IMT was positively related to the number of pack-years (number of cigarettes smoked per day [cigarettes/d] multiplied by number of years smoked/20) in both former and current smokers. There were no differences in C-IMT between smokers of cigarettes with high or low nicotine, tar, or carbon monoxide content. Both diabetes and hypertension interacted positively with smoking in determining C-IMTs. Conclusions \u2014 In the present cross-sectional observational investigation, carried out in a cohort of patients attending a lipid clinic, consumption of light cigarettes does not reduce the atherogenic effect of smoking on C-IMT. The number of pack-years, cigarettes/d, and years of smoking are relevant covariates in evaluating the effects of smoking on vascular health. The presence of diabetes or hypertension strengthens the association between smoking and cardiovascular risk

Carotid intima-media thickness by B-mode ultrasound as surrogate of coronary atherosclerosis

Objective: In the present study, we have investigated whether a strong in-vivo correlation between carotid and coronary arteries can be obtained by using homogeneous variables such as carotid and coronary IMT, detected by external carotid ultrasound (ECU) and intravascular ultrasound (IVUS), respectively. Background: Although well supported by post-mortem studies, the reliability of carotid atherosclerosis as surrogate marker of coronary atherosclerosis has been put in doubt by in-vivo studies showing a poor correlation between carotid IMT detected by ECU, and coronary stenosis assessed by quantitative coronary angiography (QCA). Methods and Results: ECU, QCA and IVUS measurements were made in 48 patients. Carotid IMT was correlated with both angiographic and IVUS findings. A significant but weak correlation was observed between ECU and QCA variables (r\uf0bb0.35, p 1 mm was associated with an 18-fold increase of risk of having a positive IVUS test (OR = 17.99, 95% CI: 1.83-177.14, p=0.013). Conclusions: Carotid atherosclerosis correlates better with coronary atherosclerosis when both circulations are investigated by the same technique (ultrasound) using the same parameter (IMT). This supports the concept that carotid IMT is a good surrogate marker of coronary atherosclerosis

Parental earliness of CHD and parental history of smoking as determinants of carotid IMT in the progeny

Objective To assess whether earliness of CHD (< 60 year of age) is a determinant of carotid intima media thicknes (IMT) in the progeny; and whether the parental history of smoking may act as a confounder in the estimation of atherosclerosis heritability by carotid IMT measurements Method 116 offspring of patients with premature CHD (P-CHD) and 42 offspring of patients with not premature CHD (NP-CHD) were assessed clinically and with carotid B-mode ultrasound Results The age of CHD onset was 50\ub16y in parents with P-CHD and 64\ub13y in parents with NP-CHD. These groups had similar prevalence of hypertension, NIDDM and dyslipidemia. History of cigarette smoking was positive in 74% of parents with P-CHD and in 45% of parents with NP-CHD (p<0.001).The offspring were basically healthy young subjects (age 33\ub15.8; females 51%, never smokers 61%, normal weight 74%; normotensive 89%, LDL-C\uf0a3130 66%). As expected, IMT was significantly lower in females and directly related to age. Progeny of P-CHD and NP-CHD had similar BP, BMI, TC, LDL-C, HDL-C and TG but the former were younger (28.5\ub15.4 vs. 32.6\ub12.3 y, p <0.0001). After data adjustment for sex, age, and smoking habits, Max IMT in offspring of P-CHD subjects was significantly higher than in offspring of NP-CHD (0.94\ub10.02 vs. 0.86\ub10.03, p=0.048). No differences in IMT measures were found when the progeny of CHD patients with or without history of smoking were compared Conclusions parental earliness of CHD is a determinant of carotid Max IMT in the progeny whereas parental history of smoking is not. Funding Centro Cardiologico Monzino. Italian Ministry of Healt

Is the enlargement of brachial artery diameter a novel marker of atherosclerotic risk?

Background. During the atherogenic process, the arterial diameter measured in plaques free areas tends to enlarge. This enlargement does not reflect the process defined "vascular remodeling", which occurs primarily as a local response to the rheological changes induced by the presence of atherosclerotic plaques, but rather it occurs as simple compensatory response of arteries to the presence of atherosclerosis risk factors. Several studies suggested this arterial enlargement as a further surrogate marker of atherosclerosis. In a recent study (1), we have shown that the addition of the inter-adventitia common carotid artery diameter (ICCAD) measured in plaque-free areas to algorithms for the assessment of global cardiovascular risk improves the patient's risk stratification. However, carotid arteries are rarely free of atherosclerotic lesions, especially in adult or elderly subjects, and even if the measures are taken in plaque free areas, it cannot be excluded the presence of plaques in the surroundings which might alter the vessel rheology, thus being the indirect responsible of the enlargement observed. Some studies have recently evaluated the diameter of other arterial districts known to be less prone to the development of atherosclerosis lesions. Most of these studies, focused on the brachial artery diameter (BAD), indicate that the arterial enlargement is a generalized phenomenon, and suggest that, as carotid diameter, also the enlargement of this arterial district may be useful to further improve the prediction of vascular events. All these studies, however, have been carried out in relatively small samples. In addition, limited information is available regarding the determinants of the enlargements evaluated simultaneously in different vascular districts. Aim of the Study. To validate, in a large sample, the role of BAD as an independent marker of atherosclerosis and to investigate whether the addition of BAD measurements to ICCAD measurements may actually offer additional information for the definition of patients' cardiovascular risk profile. Methods. 4641 patients (44.6% women and 55.4% men; age (mean\ub1SD) 58\ub113 and 55\ub113, respectively) have their BAD, ICCAD and carotid Intima media thickness (C-IMT) measured by B-Mode ultrasound. Measurements have been taken during the first visit at the Centro Dislipidemie E. Grossi Paoletti, (Ospedale Ca' Granda di Niguarda) or at the Centro Cardiologico Monzino, IRCCS. Both BAD and ICCAD were measured in plaque free areas. A total of 4271 subjects were asymptomatic, whereas 335 (64 women and 27I men) experienced a myocardial infarction and 35 (11 women and 24 men) a stroke. Results. BAD was associated with the prevalence of vascular events in both women and men. After adjustment for age, traditional risk factors, C-IMT and ICCAD, this associations persisted in women (O.R and CI: 2.2 [1.1-4.4]; p<0.05) but not in men (O.R and CI: 1.1 [0.8-1.7]; p=NS). When the analysis was performed considering myocardial infarction and stroke separately, it becomes clear that the observed significant association was mainly due to association with myocardial infarction (O.R and CI: 2.6 [1.2-5.6]; p<0.05). BAD was closely associated with ICCAD (Beta of about 0.30\ub10.03; P<0.0001, in both sexes). Despite this, determinants of the enlargement of the two vascular districts were very different. (For example, the relationship between BAD and the Framingham risk score was two times lower than that observed with ICCAD). Conclusions. The BAD is an independent marker of myocardial infarction, which, at least in women, may provide information which is complementary to that coming from vascular risk factors and ICCAD. Reference: 1. Baldassarre. J Am Coll Cardiol. 2012:60:1489-99

Analysis of data from the ERA-EDTA Registry indicates that conventional treatments for chronic kidney disease do not reduce the need for renal replacement therapy in autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is a major cause of end-stage kidney failure, but is often identified early and therefore amenable to timely treatment. Interventions known to postpone the need for renal replacement therapy (RRT) in non-ADPKD patients have also been tested in ADPKD patients, but with inconclusive results. To help resolve this we determined changes in RRT incidence rates as an indicator for increasing effective renoprotection over time in ADPKD. We analyzed data from the European Renal Association-European Dialyses and Transplant Association Registry on 315,444 patients starting RRT in 12 European countries between 1991 and 2010, grouped into four 5-year periods. Of them, 20,596 were due to ADPKD. Between the first and last period the mean age at onset of RRT increased from 56.6 to 58.0 years. The age- and gender-adjusted incidence rate of RRT for ADPKD increased slightly over the four periods from 7.6 to 8.3 per million population. No change over time was found in the incidence of RRT for ADPKD up to age 50, whereas in recent time periods the incidence in patients above the age of 70 clearly increased. Among countries there was a significant positive association between RRT take-on rates for non-ADPKD kidney disease and ADPKD. Thus, the increased age at onset of RRT is most likely due to an increased access for elderly ADPKD patients or lower competing risk prior to the start of RRT rather than the consequence of effective emerging renoprotective treatments for ADPKD