Association of Aging, Arterial Stiffness, and Cardiovascular Disease

Veerasamy, Murugapathy; Ford, Gary A.; Neely, Dermot; Bagnall, Alan; MacGowan, Guy; Das, Rajiv; Kunadian, Vijay

doi:10.1097/crd.0000000000000009

Cited by 45 publications

(30 citation statements)

References 90 publications

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“…4 Arterial stiffness has been identified as an independent risk factor for the development of CAD, both in the general population and in people with established CAD. 22 It has already been recognized that arterial stiffness, the main mechanism underlying pulse pressure widening, is an independent risk factor for cardiovascular disease. 23…”

Section: Discussionmentioning

confidence: 99%

Can we predict the presence of coronary lesions from blood pressure measurement? A new clinical method

et al. 2015

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The roles of arterial function and structure in cardiovascular physiology have expanded with the development of a variety of parameters that evaluate arterial stiffness. Markers of arterial stiffness have been correlated with cardiovascular outcomes. We aimed to find a simple, clinical, noninvasive method to predict atherosclerosis that leads to the development of coronary artery disease (CAD). We aimed to find a simple, clinical, noninvasive method to predict atherosclerosis that leads to the development of CAD. We included 100 cases that underwent coronary angiography in our center owing to different indications. The blood pressure in all cases was measured by two different observers. The oscillatory systolic blood pressure (OSBP) was defined as the point at which the mercury began to oscillate to a minimum level of 1 mm Hg. The auscultatory systolic blood pressure (AUSBP) was defined as the first Korotkoff sound. The difference between OSBP and AUSBP was calculated and called the oscillatory gap (OG). The correlation between the OG and the presence of coronary lesion in coronary angiography was statistically calculated. The study populations had a mean age of 57.3±9 years. The mean±s.d. OG was 14.44±10.44. There was a highly significantly positive correlation between the OG and the presence of coronary artery lesions (r=0.399 and P-value <0.000). There was also a significantly positive correlation between the presence of hypertension and the OG (r=0.376 and P-value <0.000). The difference between OSBP and AUSBP could be used as a simple method to detect atherosclerotic arterial changes. This method could indicate the degree of arterial stiffness. There was a significantly positive correlation between this new indicator of arterial stiffness and the presence of CAD. Any patient with a wide gap between OSBP and AUSBP should be treated early with antihypertensive drugs and statins before the development of CAD.

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Section: Discussionmentioning

confidence: 99%

Can we predict the presence of coronary lesions from blood pressure measurement? A new clinical method

et al. 2015

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“…68 In older patients, arterial stiffness assessed by increased PWV is associated with poor cardiovascular outcomes. 70 In the ICON1 study, carotid-femoral PWV is assessed by the Vicorder device (Skidmore Medical Limited, Bristol, UK). In addition, brachiofemoral PWV, pulse-wave analysis (includes pulse pressure, augmentation pressure and augmentation index) and ankle brachial pressure index are also assessed.…”

Section: Non-invasive Assessment Of Cardiovascular Status Arterial Stmentioning

confidence: 99%

Study to Improve Cardiovascular Outcomes in high-risk older patieNts (ICON1) with acute coronary syndrome: study design and protocol of a prospective observational study

et al. 2016

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Introduction The ICON1 study (a study to Improve Cardiovascular Outcomes in high-risk older patieNts with acute coronary syndrome) is a prospective observational study of older patients (≥75 years old) with non-ST-elevation acute coronary syndrome managed by contemporary treatment (pharmacological and invasive). The aim of the study was to determine the predictors of poor cardiovascular outcomes in this age group and to generate a risk prediction tool. Methods and analysis Participants are recruited from 2 tertiary hospitals in the UK. Baseline evaluation includes frailty, comorbidity, cognition and quality-of-life measures, inflammatory status assessed by a biomarker panel, including microRNAs, senescence assessed by telomere length and telomerase activity, cardiovascular status assessed by arterial stiffness, endothelial function, carotid intima media thickness and left ventricular systolic and diastolic function, and coronary plaque assessed by virtual histology intravascular ultrasound and optical coherence tomography. The patients are followed-up at 30 days and at 1 year for primary outcome measures of death, myocardial infarction, stroke, unplanned revascularisation, bleeding and rehospitalisation. Ethics and dissemination The study has been approved by the regional ethics committee (REC 12/NE/016). Findings of the study will be presented in scientific sessions and will be published in peer-reviewed journals. Trial registration number NCT01933581 : Pre-results.

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“…Advanced aging, an irreversible biological process, is a major independent risk factor for cardiovascular in particular heart diseases 1 2 3 . Aging has been shown to promote unfavorable cardiac structural and functional alterations, including increased left ventricular wall thickness and chamber size, alterations in diastolic filling pattern such as prolonged diastole, interstitial fibrosis and decreased myocardial contractile capacity, all of which contribute to the ever-rising cardiac morbidity and mortality in the elderly 1 2 3 4 . Ample of clinical and experimental studies have suggested dramatically declined cardiac performance with aging 1 5 6 7 .…”

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confidence: 99%

Macrophage Migration Inhibitory Factor (MIF) Deficiency Exacerbates Aging-Induced Cardiac Remodeling and Dysfunction Despite Improved Inflammation: Role of Autophagy Regulation

Pang

Chen

et al. 2016

Sci Rep

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Aging leads to unfavorable geometric and functional sequelae in the heart. The proinflammatory cytokine macrophage migration inhibitory factor (MIF) plays a role in the maintenance of cardiac homeostasis under stress conditions although its impact in cardiac aging remains elusive. This study was designed to evaluate the role of MIF in aging-induced cardiac anomalies and the underlying mechanism involved. Cardiac geometry, contractile and intracellular Ca2+ properties were examined in young (3–4 mo) or old (24 mo) wild type and MIF knockout (MIF−/−) mice. Our data revealed that MIF knockout exacerbated aging-induced unfavorable structural and functional changes in the heart. The detrimental effect of MIF knockout was associated with accentuated loss in cardiac autophagy with aging. Aging promoted cardiac inflammation, the effect was attenuated by MIF knockout. Intriguingly, aging-induced unfavorable responses were reversed by treatment with the autophagy inducer rapamycin, with improved myocardial ATP availability in aged WT and MIF−/− mice. Using an in vitro model of senescence, MIF knockdown exacerbated doxorubicin-induced premature senescence in H9C2 myoblasts, the effect was ablated by MIF replenishment. Our data indicated that MIF knockout exacerbates aging-induced cardiac remodeling and functional anomalies despite improved inflammation, probably through attenuating loss of autophagy and ATP availability in the heart.

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Association of Aging, Arterial Stiffness, and Cardiovascular Disease

Cited by 45 publications

References 90 publications

Can we predict the presence of coronary lesions from blood pressure measurement? A new clinical method

Can we predict the presence of coronary lesions from blood pressure measurement? A new clinical method

Study to Improve Cardiovascular Outcomes in high-risk older patieNts (ICON1) with acute coronary syndrome: study design and protocol of a prospective observational study

Macrophage Migration Inhibitory Factor (MIF) Deficiency Exacerbates Aging-Induced Cardiac Remodeling and Dysfunction Despite Improved Inflammation: Role of Autophagy Regulation

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