Carotid Lumen Diameter Is Associated With All-Cause Mortality in the General Population.

Background Common carotid intima-media thickness (cIMT) is a biomarker for subclinical atherosclerosis and is associated with all-cause as well as cardiovascular mortality. Higher cIMT is accompanied by a compensatory increase in lumen diameter (LD) of the common carotid arteries. Whether cIMT or LD carry more information with regard to mortality is unclear. Methods and Results A total of 2751 subjects (median age 53 years; 52% female) were included. During a median follow-up of 14.9 years (range: 12.8-16.5) a total of 506 subjects died. At baseline, cIMT and LD were assessed by carotid ultrasound scans. Multivariable Cox regression models were used to relate cIMT, LD, LD adjusted for cIMT (LD+cIMT), and LD/cIMT ratio with all-cause, cardiovascular, and noncardiovascular mortality. All models were ranked using Akaike's information criterion. Harrel's c statistic was used to compare the models' predictive power for mortality. A 1-mm increase in LD was related to a higher risk for all-cause mortality (hazard ratio [HR], 1.29; 95% CI, 1.14-1.45, P<0.01). This association remained significant when cIMT was added to the model (HR, 1.26; 95% CI, 1.11-1.42; P<0.01). A 1-mm higher cIMT was also related with greater mortality risk (HR, 1.73; 95% CI, 1.09-2.75). The LD/cIMT ratio was not associated with all-cause mortality. LD had the lowest Akaike's information criterion regarding all-cause mortality and improved all-cause mortality prediction compared with the null model (P=0.01). CIMT weakened all-cause mortality prediction compared with the LD model. Conclusions LD provided more information for all-cause mortality compared with cIMT in a large population-based sample.

A Vascular Aging Index as Independent Predictor of Cardiovascular Events and Total Mortality in an Elderly Urban Population.

The morphology and function of the arteries can be directly measured using different established methods. This prospective cohort study aimed to translate 2 of these, aortic pulse wave velocity (aPWV) and carotid intima-media thickness (cIMT), into a combined Vascular Aging Index (VAI) and then evaluate the predictive power of aPWV, cIMT, and VAI. Patients (n = 2718) were included from the cardiovascular arm of the Malmö Diet and Cancer Study (median age 71.9 years, 62.2% females). Total follow-up time was 16 448 person-years and a composite cardiovascular disease (CVD) end point was used. Cox regressions yielded adjusted hazard ratios (95% confidence interval) per 1 standard deviation increment of loge aPWV, loge cIMT, and loge VAI of 1.25 (1.08-1.45, P = .003), 1.27 (1.13-1.44, P < .001), and 1.45 (1.26-1.68, P < .001), respectively. The C-statistics increased from 0.714 to 0.734 when adding aPWV and cIMT to a model of conventional risk factors. Net Reclassification Index also showed a significant (P < .001) improvement for the classification of event-free patients and no change for patients with events. A VAI based on aPWV and cIMT had a good predictive performance. Used together, aPWV and cIMT incrementally and significantly improve the prediction of CVD events by correctly down-adjusting the predicted risk for noncases.

Carotid Artery Plaques, Carotid Intima-Media Thickness, and Risk of Cardiovascular Events and All-Cause Death in Older Adults: A 5-Year Prospective, Community-Based Study.

We assessed the effect of asymptomatic carotid atherosclerosis (CAS) on the development of cardiovascular diseases (CVDs) in a community-based population aged ≥55 years in China. A total of 1376 residents underwent CAS assessment by ultrasonography in July 2009. New CVD events, including stroke and coronary heart events, were collected at the follow-up survey at the end of 2014. After adjusting for baseline demographic characteristics and traditional CVD risk factors, the risk of CVD in patients with minimal CAS (mean common carotid artery intima-media thickness [CCA-IMT] ≥1 mm and no plaques), nonstenotic plaques (carotid stenosis <50%), and stenotic plaques (carotid stenosis ≥50%) was 0.8 (hazard ratio [HR]: 0.75, 95% confidence interval [CI]: 0.33-1.69), 2.0 (HR: 2.01, 95% CI: 1.24-3.25), and 3.1 (HR: 3.05, 95% CI: 1.62-5.74) times greater, respectively, than that of patients without CAS (CCA-IMT <1 mm and no plaques). Our findings provide direct evidence of the independent predictive value of the severity of asymptomatic CAS for the development of CVD in older Chinese adults.

Ventricular-Arterial Coupling in Breast Cancer Patients After Treatment With Anthracycline-Containing Adjuvant Chemotherapy.

BACKGROUND: Anthracycline-containing chemotherapy (Anth-C) is associated with long-term cardiovascular mortality. Although cardiovascular risk assessment has traditionally focused on the heart, evidence has demonstrated that vascular dysfunction also occurs during and up to 1 year following Anth-C. Whether vascular dysfunction persists long-term or negatively influences cardiac function remains unknown. Hence, the present study evaluated ventricular-arterial coupling, in concert with measures of vascular structure and function, in the years following Anth-C. METHODS: Arterial elastance (Ea), end-systolic elastance (Ees), and ventricular-arterial coupling (Ea/Ees) were measured during rest and exercise using echocardiography. Resting vascular function (flow-mediated dilation) and structure (carotid intima-media thickness, arterial stiffness) were also measured. RESULTS: Thirty breast cancer survivors (6.5 ± 3.6 years after Anth-C) with normal left ventricular ejection fraction (LVEF) (60% ± 6%) and 30 matched controls were studied. At rest, no differences were found in Ea, Ees, Ea/Ees, or LVEF between groups. The normal exercise-induced increase in Ees was attenuated in survivors at 50% and 75% of maximal workload (p < .01). Ea/Ees was also higher at all workloads in the survivors compared with the controls (p < .01). No differences in vascular structure and function were observed between the two groups (p > .05). CONCLUSION: In the years after Anth-C, ventricular-arterial coupling was significantly attenuated during exercise, primarily owing to decreased LV contractility (indicated by a reduced Ees). This subclinical dysfunction appears to be isolated to the heart, as no differences in Ea were observed. The previously reported adverse effects of Anth-C on the vasculature appear to not persist in the years after treatment, as vascular structure and function were comparable to controls. IMPLICATIONS FOR PRACTICE: Anthracycline-induced cardiotoxicity results in significantly impaired ventricular-arterial coupling in the years following chemotherapy, owing specifically to decreased left ventricular contractility. This subclinical dysfunction was identified only under exercise stress. A comprehensive evaluation of vascular structure and function yielded no differences between those treated with anthracyclines and controls. Combined with a stress stimulus, ventricular-arterial coupling might hold significant value beyond characterization of integrative cardiovascular function, in particular as a part of a risk-stratification strategy after anthracycline-containing chemotherapy. Although vascular function and structure were not different in this cohort, this does not undermine the importance of identifying vascular (dys)function in this population, because increases in net arterial load during exercise might amplify the effect of reductions in contractility on cardiovascular function after anthracycline-containing chemotherapy.

Carotid plaque calcification predicts future cardiovascular events in type 2 diabetes.

OBJECTIVE: The presence of carotid plaques is associated with future cardiovascular events, with local plaque composition being an independent outcome predictor. We examined the association between ultrasonographically determined carotid plaque calcification and incident major adverse cardiovascular events (MACE) and death in type 2 diabetes (T2D). RESEARCH DESIGN AND METHODS: We enrolled 581 patients with T2D who underwent routine carotid ultrasonography. Plaques were classified as echolucent (lipid rich), heterogenous, and echogenic (calcific). We collected demographic, anthropometric, and clinical data at baseline and followed the patients for up to 9 years. RESULTS: Plaques were detected in 81.8% of the patients (echolucent in 16.4%, heterogenous in 43.2%, and echogenic in 22.2%). During follow-up (4.3 ± 0.1 years), 58 deaths (27 cardiovascular) and 236 fatal and nonfatal MACE occurred. In univariate analyses, presence versus absence of any carotid plaque was associated with incident MACE, and the hazard ratio (95% CI) progressively increased from echolucent (1.97 [0.93-3.44]), to heterogeneous (3.10 [2.09-4.23]), to echogenic (3.71 [2.09-5.59]) plaques. Compared with echolucent plaques, echogenic plaques were associated with incident MACE independently from confounders. This association was attenuated after adjusting for the degree of stenosis, but in patients with stenosis ≤30%, echogenic plaque type still predicted total and atherosclerotic MACE, even after further adjusting for mean intima-media thickness. CONCLUSIONS: In T2D, carotid plaque calcification predicts MACE, especially in patients with a low degree of stenosis. The biology of atherosclerotic calcification in diabetes needs to be further elucidated to understand the basis of this association.

Gastrectomy for early gastric cancer is associated with decreased cardiovascular mortality in association with postsurgical metabolic changes.

BACKGROUND: Bariatric surgery effectively induces weight loss and resolves cardiovascular comorbidities in obese patients. We investigated cardiovascular and all-cause mortality in patients who underwent gastrectomies for early gastric cancer (EGC) and analyzed the changes in metabolic parameters after surgery. METHODS: A total of 2,477 patients who underwent gastrectomies for EGC between 1995 and 2004 were enrolled in the study and followed for mortality through 2007. Standardized mortality ratios (SMRs) were calculated using sex- and age-matched mortality in the general Korean population in 2005. Effects of gastrectomy on changes in body weight and metabolic parameters were investigated in 51 of the patients before and after surgery. RESULTS: During the 15,096.4 person-years of follow-up, 244 deaths were recorded. The all-cause mortality was not significantly different from that of the general population (SMR [95 % confidence interval (CI)] = 1.01 [0.89 - 1.14]); however, cardiovascular mortality was significantly lower (SMR = 0.35 [0.22 - 0.53]). In the 51 patients included in the second part of the study, significant reductions in body weight and visceral fat areas occurred after surgery, regardless of whether the patients were previously obese. Triglycerides, LDL-cholesterol, and plasminogen activator inhibitor-1 levels were significantly decreased, whereas HDL-cholesterol and adiponectin levels were increased. Carotid intima-media thickness also was significantly decreased in previously obese and nonobese patients. CONCLUSIONS: Patients with EGC who undergo gastrectomy have a lower cardiovascular mortality but similar all-cause mortality as that of the general population. In these patients, a significant reduction in body weight and visceral fat after surgery may improve impaired lipid metabolism and prevent atherosclerotic changes.

[Increased cardiovascular risk and premature atherosclerosis in rheumatoid arthritis]. / Augmentation du risque cardiovasculaire et accélération de l'athérosclérose au cours de la polyarthrite rhumatoïde.

UNLABELLED: Patients with rheumatoid arthritis (RA) are at increased risk of mortality compared with the general population. Evidence suggests that this increased mortality can largely be attributed to increased cardiovascular (CV) death. In a prospective study, 34 patients with RA were compared with age- and sex-matched controls. RESULTS: We found a lower C-HDL, apolipoprotein A1 and B in patients with RA. However, CT/C-HDL and C-LDL/C-HDL were significantly higher than control patients. The intima-media thickness was significantly higher in patients with RA (0.759 mm vs 0.558 mm; P<0.001). CONCLUSION: Increased attention to cardiovascular risk in RA will be necessary to reduce the excess CV mortality and morbidity in RA patients. It appears that the excess risk that is observed in the RA population can be explained, in part, by promotion of CV disease through increased systemic inflammation associated with RA.