Aortic stiffness is independently associated with interstitial myocardial fibrosis by native T1 and accelerated in the presence of chronic kidney disease

Abstract

Background Patients with chronic kidney disease (CKD) have considerable cardiovascular morbidity and mortality. Aortic stiffness is an independent predictor of cardiovascular risk and related to left ventricular remodeling and heart failure. Myocardial fibrosis is the pathophysiological hallmark of the failing heart. Methods and results An observational study of consecutive CKD patients ( n = 276) undergoing comprehensive clinical cardiovascular magnetic resonance imaging. The relationship between aortic stiffness, myocardial fibrosis, left ventricular remodeling and the severity of chronic kidney disease was examined. Compared to age-gender matched controls with no known kidney disease ( n = 242), CKD patients had considerably higher myocardial native T1 and central aortic PWV ( p ≪ 0.001), as well as abnormal diastolic relaxation by E/e′ (mean) by echocardiography ( p ≪ 0.01). A third of all patients had LGE, with similar proportions for the presence and the (ischaemic and non-ischaemic) pattern between the groups. PWV was strongly associated with and age, NT-proBNP and native T1 in both groups, but not with LGE presence or type; the associations were amplified in severe CKD stages. In multivariate analyses, PWV was independently associated with native T1 in both groups ( p ≪ 0.01) with near two-fold increase in adjusted R 2 in the presence of CKD (native T1 (10 ms) R 2 , B(95%CI) CKD vs. non-CKD 0.28, 0.2(0.15–0.25) vs. 0.18, 0.1(0.06–0.15), p ≪ 0.01). Conclusions Aortic stiffness and interstitial myocardial fibrosis are interrelated; this association is accelerated in the presence of CKD, but independent of LGE. Our findings reiterate the significant contribution of CKD-related factors to the pathophysiology of cardiovascular remodeling.

Cardiac biomarkers in chronic kidney disease are independently associated with myocardial edema and diffuse fibrosis by cardiovascular magnetic resonance

“…An independent cohort of controls with eGFR ≥ 60 ml/min/1.73 m 2 (including CKD stages 1 and 2 [ 16 , 17 ]), matched for age, gender and traditional CVD risk factor profile, was sourced from the ongoing International T1 Outcome Study using propensity score matching (PSM, n = 242, recruited between 03/16 to 03/19 (NCT03749343), ongoing recruitment since March 2016). The details of both registries, inclusion/exclusion criteria, imaging protocols and sequence parameters were reported previously [ 14 , 15 , 18 ], and are included in Additional file 3 . A further group of healthy controls (n = 38) with similar age and sex distribution was gathered from an ongoing multicenter study including healthy individuals without CVD risk factors or any regular medication (NCT04444128).…”

Cardiac Remodeling in Chronic Kidney Disease

“…Factors related to hemodynamic alterations in CKD patients like senescence, ischemia, catecholamines, angiotensin II and aldosterone further promote the development of cardiac fibrosis [21]. Arterial stiffening is accelerated in the presence of CKD and is caused by a loss of elastic fibers and vascular calcification [24]. Increased vascular stiffness leads to increased cardiac afterload, which promotes cardiac hypertrophy and fibrosis [21,25].…”

Impact of aortic stiffness by velocity-encoded magnetic resonance imaging on late gadolinium enhancement to predict cardiovascular events

“…Novel CMR techniques to detect diffused myocardial fibrosis, including native T1 mapping, have proven the association with aortic stiffness [12] , [38] . However, prognostic data regarding these techniques combined with aortic stiffness requires further evaluation and may play a significant role in the near future.…”