Search

Aging represents an important risk factor in the development of cardiovascular disease (CVD). Nevertheless, the question arises: How immutable is age as a risk factor? Can we make a distinction between physiologic or successful arterial aging, which may be immutable, and accelerated, pathologic arterial aging—frequently referred to as early vascular aging (EVA)—which is not? Indeed, blood pressure (BP) components that change over time are useful metrics for assessing and comparing physiologic versus pathologic aging. Because EVA often starts in adolescence, while CVD events may not appear until middle-age or beyond, there is a potential opportunity to attenuate pathological aging with early and effective lifestyle and/or therapeutic intervention. EVA can occur prior to and in association with elevated in-office BP and commonly clusters with other CVD risk factors. Increased peripheral vascular resistance and arterial stiffness are two important hemodynamic abnormalities that accelerate pathologic aging. The proportion of increased resistance versus increased stiffness varies with age, sex, and a variety of covariates that include obesity, metabolic syndrome, diabetes, and prior CVD events. Pathologic aging occurs predominantly with increased vascular resistance in the early adult years (more often in men) and predominantly with increased stiffness in the later adult years (more often in women). Pathologic aging over many years predisposes to later CVD events, including coronary heart disease, heart failure, stroke, cogitative impairment, and chronic kidney disease. Early and aggressive treatment of persons at risk may provide greater protection against pathologic vascular aging of heart, kidneys, and brain, and hence delay or prevent later CVD events. The establishment of the optimal level of BP to initiate antihypertensive therapy and optimal target goal of therapy to minimize pathologic arterial aging, are questions that will require further investigations

Early Vascular Aging (EVA): New Directions in Cardiovascular Protection brings together the last decade of research related to the characterization of EVA, as well as the predictive power of pulse wave velocity (PWV). The book presents a novel approach to the problem of cardiovascular disease, showing it in relation to great vessels disease and revealing a comprehensive approach to the problem of increased rigidity of the great vessels, its causes, and further consequences. Information provided is accompanied by online access to a supplemental website with video clips of anatomic specimens, cardiac imaging, and surgical procedures

Risk stratification for primary prevention of cardiovascular disease is today performed using traditional risk factors such as age, gender, blood pressure, serum cholesterol, smoking habits, and plasma glucose. However, these factors perform poorly in the daily clinic where individual risk prediction is needed. It has been suggested to supplement traditional factors with markers of subclinical organ damage to identify subjects with increased susceptibility for the negative influence from the traditional risk factors. Although many new markers are independently associated with cardiovascular risk, their clinical impact on risk prediction is uncertain. In this chapter the evidence for incremental risk prediction for the most promising markers is reviewed, and it is demonstrated that many new markers provide only modest impact on risk prediction with greatest improvement in intermediate risk groups. However, several aspects are still uncertain and need to be examined in the setting of a randomized study. These include actual net benefit of the use of these new markers in risk stratification after taking into account cost, risk associated with the measurements, and the increased downstream medication and examinations, as well as actual changes in patient and physician behavior and clinical outcome.

OBJECTIVE: The N-terminal prohormone B-type natriuretic peptide (NT-proBNP) is a reliable marker of cardiac strain. In hypertensive heart disease, NT-proBNP levels increase and may lose its protective function. Simultaneously, the vasculature is also subject to hemodynamic stress, resulting in vascular matrix remodeling and stiffening which contribute to further cardiac alterations. Alkaline phosphatase (ALP) is a marker of osteoblast activity and is involved in vascular calcification. We explored the link between NT-proBNP and ALP in Black and Caucasian African men. DESIGN AND MAIN OUTCOME MEASURES: This study included 128 Black (mean age, 41.1 years) and 118 Caucasian (mean age, 36.4 years) men. Conventional measurements were acquired along with serum NT-proBNP and ALP. RESULTS: NT-proBNP correlated positively with ALP (r=0.29; p

Background This study compared NT-proBNP levels and the association with cardiovascular markers between Africans and Caucasians from South Africa. Methods This cross-sectional study involved 201 Africans and 255 Caucasians from the North West province, South Africa. Serum NT-proBNP concentrations, blood pressure, pulse wave velocity and arterial compliance were measured. Results NT-proBNP levels were significantly higher (P < 0.001) in Africans than Caucasians, also after adjusting for gender, body mass index (BMI) and pulse wave velocity (P = 0.008). This significant difference became borderline significant after adjusting for systolic blood pressure (SBP) (P = 0.060), and non-significant after adjusting for arterial compliance (P = 0.35). In single regression, a significant positive correlation of NT-proBNP with SBP (r = 0.26; P < 0.001) and pulse pressure (PP) (r = 0.28; P < 0.001) were shown for Africans only. After multiple adjustments, the associations of NT-proBNP with SBP and PP remained significant in Africans (SBP: β = 0.187, P < 0.01; PP: β = 0.234, P < 0.001), with no significant associations in Caucasians. Conclusions NT-proBNP levels were higher in Africans than Caucasians, independently of BMI and gender. This difference was partly driven by higher SBP and lower arterial compliance in Africans. NT-proBNP was persistently associated with SBP and PP in Africans, but not in Caucasians. These associations may suggest early vascular changes contributing to cardiac alterations in Africans. http://dx.doi.org/10.1016/j.hlc.2011.10.009

Aims: Markers of subclinical target organ damage (TOD) increase cardiovascular (CV) risk prediction beyond traditional risk factors. We wanted to establish thresholds for three markers of TOD based on absolute CV risk in different risk chart categories. Methods and results: In a cohort of 1968 healthy patients, we measured urine albumin creatine ratio (UACR), pulse wave velocity (PWV), left ventricular mass index (LVMI) and traditional risk factors. Patients were categorized according to Systemic Coronary Evaluation (SCORE), European Society of Hypertension/European Society of Cardiology (ESH/ESC) risk chart and Framingham risk score (FRS) and three corresponding endpoints were recorded: CV death (SCORE-endpoint), a composite of CV death and nonfatal myocardial infarction and stroke (ESH/ESC-endpoint), and a composite that also included hospital admissions for ischemic heart disease, heart failure, peripheral arterial disease and transient cerebral ischemic attack (FRS-endpoint). During a median follow of 12.8 years events totaled 81 SCORE-, 153 ESH/ESC-endpoints and 280 FRS-endpoints. Thresholds for UACR, PWV and LVMI are presented using 10-year risk threshold of more than 5% (SCORE-endpoint), more than 10%(ESH/ESC-endpoint) and more than 20%(FRS-endpoint), which indicated high risk and eligibility for primary prevention. As an example, the threshold was 0.83 mg/mmol, 13.7 m/s and 119 g/m2 for UACR, PWV and LVMI, respectively, for patients at moderate added risk according to ESH/ESC risk chart. Conclusion: Thresholds for UACR, PVW and LVMI based on absolute risk have primarily impact on risk stratification in patients with intermediate risk. The thresholds for PWV and LVMI in patients with moderate risk according to the ESH/ESC risk chart were similar to currently applied thresholds whereas the threshold for UACR was considerable lower than the threshold for microalbuminuria.

Objective and design: This cross-sectional study aimed to investigate associations between a marker of cardiac strain, the N-terminal prohormone B-type natriuretic peptide (NT-proBNP), and inflammation as reflected by either a conventional or novel inflammatory marker in a bi-ethnic South African cohort. Methods and subjects: We measured NT-proBNP, C-reactive protein (CRP) and plasma-soluble urokinase plasminogen activator receptor (suPAR) levels along with conventional biomarkers in black (n = 117) and white (n = 116) men. Results: NT-proBNP, CRP and suPAR levels were higher in black compared to white men. NT-proBNP was significantly associated with both CRP (r = 0.38; p = 0.001) and suPAR (r = 0.42; p,0.001) in black men only. After full adjustment in multiple regression analyses, the above associations of NT-proBNP with CRP (b = 0.199; p = 0.018) and suPAR (b = 0.257; p,0.01) were confirmed in black men. Conclusion: These results suggest that a low-grade inflammatory state as reflected by both a conventional and novel marker of inflammation may contribute to higher cardiovascular risk as reflected by the associations obtained with a marker of cardiac strain in black South African men South African National Research Foundation Grant (GUN 2073040), the Medical Research Council (South Africa) and the Africa Unit for Trans-disciplinary Health Research of the North-West University (Potchefstroom campus, South Africa) http://www.plosone.org http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058506 DOI: 10.1371/journal.pone.0058506