Arterial stiffness and 5-year mortality in patients with peripheral arterial disease

Scandale, Giovanni; Dimitrov, Gabriel; Recchia, Martino; Carzaniga, Gianni; Perilli, Edoardo; Carotta, Maria; Catalano, M.

doi:10.1038/s41371-019-0254-3

Cited by 19 publications

(19 citation statements)

References 35 publications

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“…NT-proBNP concentrations (expressed as decimal logarithms) were also significant predictors of cIMT and P2/P1 in multivariate analysis. While cIMT is a well-established marker of cardiovascular disease, P2/P1 and its derivative—the augmentation index shows a weaker correlation with hard-end points than the gold standard of arterial stiffness—aortic pulse wave velocity [ 36 , 37 ]. Little is known about pathophysiological relations between intimal and medial thickening and the heart.…”

Section: Discussionmentioning

confidence: 99%

NT-proBNP as a Potential Marker of Cardiovascular Damage in Children with Chronic Kidney Disease

Skrzypczyk

Okarska‐Napierała

Pietrzak

et al. 2021

JCM

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Assessing cardiovascular disease (CVD) in children with chronic kidney disease (CKD) is difficult. Great expectations have been associated with biomarkers, including the N-terminal pro-brain natriuretic peptide (NT-proBNP). This study aimed to determine the correlation between NT-proBNP and cardiovascular complications in children with CKD. Serum NT-proBNP, arterial stiffness, common carotid artery intima-media thickness (cIMT), echocardiographic (ECHO) parameters (including tissue Doppler imaging), and biochemical and clinical data were analyzed in 38 pediatric patients with CKD (21 boys, 12.2 ± 4.2 years). Mean NT-proBNP in CKD patients was 1068.1 ± 4630 pg/mL. NT-proBNP above the norm (125 pg/mL) was found in 16 (42.1%) subjects. NT-proBNP correlated with glomerular filtration rate (GFR) (r = −0.423, p = 0.008), and was significantly higher in CKD G5 (glomerular filtration rate grade) patients compared to CKD G2, G3, and G4 children (p = 0.010, p = 0.004, and p = 0.018, respectively). Moreover, NT-proBNP correlated positively with augmentation index (AP/PP: r = 0.451, p = 0.018, P2/P: r = 0.460, p = 0.016), cIMT (r = 0.504, p = 0.020), and E/E’ in ECHO (r = 0.400, p = 0.032). In multivariate analysis, logNT-proBNP was the only significant predictor of cIMT Z-score (beta = 0.402, 95CI (0.082–0.721), p = 0.014) and P2/P1 (beta = 0.130, 95CI (0.082–0.721), p = 0.014). Conclusions: NT-proBNP may serve as a possible marker of thickening of the carotid artery wall in pediatric patients with CKD. The final role of NT-proBNP as a biomarker of arterial damage, left ventricular hypertrophy, or cardiac diastolic dysfunction in CKD children needs confirmation in prospective studies.

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Section: Discussionmentioning

confidence: 99%

NT-proBNP as a Potential Marker of Cardiovascular Damage in Children with Chronic Kidney Disease

Skrzypczyk

Okarska‐Napierała

Pietrzak

et al. 2021

JCM

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“…Although some studies have shown that the development of arterial stiffness may be prior to hypertension (Celik et al, 2017; Kaess et al, 2012), which causes left ventricular remodeling (Ohyama et al, 2016; Zieman et al, 2005), it is well established that hypertension, associated or not with aging, leads to an increased arterial stiffness (Morgan et al, 2014; Rode et al, 2020), assessed by pulse wave velocity (PWV). In fact, arterial stiffness has been recognized as an independent predictor of all‐cause mortality in population with several diseases including hypertension (DuPont et al, 2019; Scandale et al, 2020), and understanding the mechanisms involved in vascular stiffness is an emerging target to treat hypertension.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of dexamethasone on arterial stiffness, myocardial remodeling and blood pressure between normotensive and spontaneously hypertensive rats

Tardelli

Duchatsch

Herrera

et al. 2021

J of Applied Toxicology

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Dexamethasone (DEX)‐induced hypertension is observed in normotensive rats, but little is known about the effects of DEX on spontaneously hypertensive animals (SHR). This study aimed to evaluate the effects of DEX on hemodynamics, cardiac hypertrophy and arterial stiffness in normotensive and hypertensive rats. Wistar rats and SHR were treated with DEX (50 μg/kg s.c., 14 d) or saline. Pulse wave velocity (PWV), echocardiographic parameters, blood pressure (BP), autonomic modulation and histological analyses of heart and thoracic aorta were performed. SHR had higher BP compared with Wistar, associated with autonomic unbalance to the heart. Echocardiographic changes in SHR (vs. Wistar) were suggestive of cardiac remodeling: higher relative wall thickness (RWT, +28%) and left ventricle mass index (LVMI, +26%) and lower left ventricle systolic diameter (LVSD, −19%) and LV diastolic diameter (LVDD, −10%), with slightly systolic dysfunction and preserved diastolic dysfunction. Also, SHR had lower myocardial capillary density and similar collagen deposition area. PWV was higher in SHR due to higher aortic collagen deposition. DEX‐treated Wistar rats presented higher BP (~23%) and autonomic unbalance. DEX did not change cardiac structure in Wistar, but PWV (+21%) and aortic collagen deposition area (+21%) were higher compared with control. On the other side, DEX did not change BP or autonomic balance to the heart in SHR, but reduced RWT and LV collagen deposition area (−12% vs. SHRCT). In conclusion, the results suggest a differential effect of dexamethasone on arterial stiffness, myocardial remodeling and blood pressure between normotensive and spontaneously hypertensive rats.

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“…Being a systemic atherosclerotic disease, it is frequently associated with an unacceptably high incidence of cardiovascular events, including new onset angina, coronary artery bypass grafting, nonfatal or fatal myocardial infarction, and congestive heart failure 137 . PAD also associated with an increase in overall all-cause and cardiac mortality 138 . The relationship between PAD and depression appears be bi-directional 139,140 .…”

Section: Depression and Peripheral Artery Diseasementioning

confidence: 93%

Depression and Cardiovascular Diseases

Agarwal¹

2021

ijmsci

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Cardiovascular diseases (CVD) are the leading cause of global morbidity and mortality. Besides imparting enormous human suffering and enhancing premature mortality, they also inflict huge direct and indirect financial costs on the worldwide society. With the easier availability of affordable therapeutics globally, and the relatively paucity of newer innovations, modifiable risk factors are gaining greater importance in the management of this cardiovascular epidemic. Depression is a modifiable risk factor. It is consistently and strongly associated with a higher risk of CVD incidence and mortality. CVD on the other hand, often induces the development of depression. This paper reviews the effects of depression on cardiovascular diseases.

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Arterial stiffness and 5-year mortality in patients with peripheral arterial disease

Cited by 19 publications

References 35 publications

NT-proBNP as a Potential Marker of Cardiovascular Damage in Children with Chronic Kidney Disease

NT-proBNP as a Potential Marker of Cardiovascular Damage in Children with Chronic Kidney Disease

Differential effects of dexamethasone on arterial stiffness, myocardial remodeling and blood pressure between normotensive and spontaneously hypertensive rats

Depression and Cardiovascular Diseases

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