S. Parnham

Impaired Myocardial Oxygenation Response to Stress in Patients With Chronic Kidney Disease

Background Coronary artery disease and left ventricular hypertrophy are prevalent in the chronic kidney disease (CKD) and renal transplant (RT) population. Advances in cardiovascular magnetic resonance (CMR) with blood oxygen level–dependent (BOLD) technique provides capability to assess myocardial oxygenation as a measure of ischemia. We hypothesized that the myocardial oxygenation response to stress would be impaired in CKD and RT patients. Methods and Results Fifty-three subjects (23 subjects with CKD, 10 RT recipients, 10 hypertensive (HT) controls, and 10 normal controls without known coronary artery disease) underwent CMR scanning. All groups had cine and BOLD CMR at 3 T. The RT and HT groups also had late gadolinium CMR to assess infarction/replacement fibrosis. The CKD group underwent 2-dimensional echocardiography strain to assess fibrosis. Myocardial oxygenation was measured at rest and under stress with adenosine (140 μg/kg per minute) using BOLD signal intensity. A total of 2898 myocardial segments (1200 segments in CKD patients, 552 segments in RT, 480 segments in HT, and 666 segments in normal controls) were compared using linear mixed modeling. Diabetes mellitus (P=0.47) and hypertension (P=0.57) were similar between CKD, RT, and HT groups. The mean BOLD signal intensity change was significantly lower in the CKD and RT groups compared to HT controls and normal controls (−0.89±10.63% in CKD versus 5.66±7.87% in RT versus 15.54±9.58% in HT controls versus 16.19±11.11% in normal controls, P<0.0001). BOLD signal intensity change was associated with estimated glomerular filtration rate (β=0.16, 95% CI=0.10 to 0.22, P<0.0001). Left ventricular mass index and left ventricular septal wall diameter were similar between the CKD predialysis, RT, and HT groups. None of the CKD patients had impaired global longitudinal strain and none of the RT group had late gadolinium hyperenhancement. Conclusions Myocardial oxygenation response to stress is impaired in CKD patients and RT recipients without known coronary artery disease, and unlikely to be solely accounted for by the presence of diabetes mellitus, left ventricular hypertrophy, or myocardial scarring. The impaired myocardial oxygenation in CKD patients may be associated with declining renal function. Noncontrast BOLD CMR is a promising tool for detecting myocardial ischemia in the CKD population.

Myocardial ischemia assessment in chronic kidney disease: challenges and pitfalls

Coronary artery disease is the leading cause of mortality and morbidity in the chronic kidney disease (CKD) population and often presents with atypical symptoms. Current diagnostic investigations of myocardial ischemia in CKD lack sensitivity and specificity or may have adverse effects. We present a case vignette and explore the challenges of diagnostic myocardial stress investigation in patients with CKD.

Preclinical alterations in cardiac energetics amongst sarcomere mutation carriers in hypertrophic cardiomyopathy

Background Hypertrophic cardiomyopathy (HCM) is characterised by reduced myocardial tissue oxygenation (assessed using blood oxygen level dependent (BOLD) CMR imaging) during stress, as well as reduced myocardial perfusion reserve (MPRI) due to coronary microvascular dysfunction. In HCM gene carriers without the HCM phenotype, it has been suggested that only oxygenation is impaired. [1] It remains unclear whether this relates to early cardiac remodelling/ diastolic dysfunction, or whether oxygen consumption is intrinsically altered with sarcomere mutations. We sought to assess the BOLD signal change during vasodilator stress in a homogenous group of MYPBC3 positive HCM patients (some with clinical HCM, and some with no phenotypic features of HCM), and normal controls.

Myocardial perfusion is impaired in asymptomatic patients post renal transplantation

Background Cardiovascular disease is one of the commonest causes of mortality post-renal transplantation (RT), often in patients with no known cardiac disease. The cardiac phenotype in these patients is not clearly defined. Multi-parametric cardiovascular magnetic resonance (CMR) imaging enables concurrent assessment of myocardial function, perfusion and irreversible injury. We hypothesized that myocardial perfusion reserve would be impaired in asymptomatic post-renal transplant patients when compared with hypertensive controls. Methods Twenty-two asymptomatic R Tp atients (3 months to 5 years post-transplant) with, no known history of ischemic heart disease) and 12 hypertensive controls underwent

Myocardial perfusion is impaired in renal transplant and liver transplant patients

Methods We conducted a prospective study of 25 renal transplant (RT) recipients, 8 liver transplant (LT) recipients without previous CKD history and 7 controls with hypertension (HT). The transplant recipients were asymptomatic and had no previous ischaemic heart disease or revascularisation or systolic heart failure. The pre-transplant workup of the RT and LT were negative for haemodynamically significant epicardial coronary artery stenosis. Diabetes mellitus history between RT, LT and HT controls were not statistically different. Myocardial function, late-gadolinium enhancement and first-pass perfusion was assessed semiquantitatively at rest and under stress. The MPRI was calculated as the ratio of perfusion during adenosine-induced hyperemia to the rest perfusion. The RT and LT patients underwent whole-heart non-contrast magnetic resonance coronary angiography (MRCA) to assess the presence of proximal to mid epicardial coronary artery disease.

Myocardial oxygenation is impaired in advanced chronic kidney disease and renal transplant patients

Background Coronary artery disease (CAD) and left ventricular hypertrophy are prevalent in the chronic kidney disease (CKD) and renal transplant population. Advances in cardiovascular magnetic resonance (CMR) with the blood oxygen level-dependent (BOLD) technique provides unprecedented capability to assess myocardial oxygenation as a measure of ischaemia. We hypothesised that myocardial oxygenation would be reduced in advanced CKD and renal transplant patients and may provide a novel strategy for assessing myocardial ischaemia. Methods We prospectively studied 20 advanced CKD subjects (8 dialysis group with median eGFR 9.5 (range 5-37) ml/ min and 12 CKD group with median eGFR 14 (range 818) ml/min), 8 renal transplant (RT) recipients with median eGFR 74.5 (range 57-114) ml/min and 7 hypertensive (HT) controls with median eGFR 107 (range 57144) ml/min. All patients were asymptomatic for CAD and none had prior history of CAD. All groups had cine and BOLD CMR at 3T, and RT and HT groups also had late gadolinium CMR to assess infarction/replacement fibrosis. CKD group additionally underwent 2D echocardiography strain to assess fibrosis. Myocardial oxygenation was measured at rest and under stress with adenosine (140 µg/kg/min) using BOLD Signal Intensity (SI). Analyses were performed using linear mixed models. Results

Reduced myocardial perfusion in post renal transplant population is not associated with aortic stiffness

Background Objective: The purpose of this study was to assess central (aortic) vascular dysfunction in post renal transplant patients by high-resolution cardiovascular magnetic resonance imaging (CMR). Background: Renal transplant recipients are at increased risk of cardiovascular (CV) disease. The cardiac phenotype in post-transplant recipients is not well defined. A recent study suggested myocardial perfusion is impaired in renal transplant patients irrespective of the degree of left ventricular hypertrophy [1].We hypothesized that post transplant patients have persistently increased aortic stiffness, and that it could be correlated with reduced myocardial perfusion.

Myocardial oxygenation is reduced in end-stage renal failure: a novel blood oxygen level dependant (BOLD)-cardiac MRI study

Background Cardiovascular disease is the leading cause of mortality and morbidity in end-stage renal failure (ESRF) population, mostly from coronary artery disease (CAD). Majority of CAD in ESRF patients is asymptomatic and current cardiac stress imaging modalities are sub-optimal as risk predictors. Advances in cardiovascular magnetic resonance (CMR) with the novel blood oxygen level-dependent (BOLD) technique provides unprecedented capability to assess regional myocardial deoxygenation. We hypothesized that myocardial oxygenation would be reduced in ESRF patients and may form a novel strategy to assess myocardial ischemia. Methods Sixteen chronic renal failure (CRF) patients (7 on dialysis, 9 pre-dialysis) with no known history of CAD underwent CMR scanning at 3.0 T. Given known reductions in BOLD signals in hypertrophied myocardium, we also assessed a control group of HT patients with no history of CAD (n = 6) Myocardial function, rest and stress BOLD was performed. To measure oxygenation, using a T2-prepared BOLD sequence, myocardial Signal Intensity (SI) was measured at adenosine stress (140 μg/ kg/min) and at rest (corrected to RR interval). Comparison of myocardial SI analyses were performed using multivariate linear regression. Results