A potential evidence to explain the reason behind the devastating prognosis of coronary artery disease in uraemic patients: Renal insufficiency is associated with poor coronary collateral vessel development

Sezer, Murat; Özcan, Mustafa; Okçular, Irem; Elıtok, Ali; Umman, Sabahattin; Umman, Berrin; Tayyareci, Yelda; Olcay, Ayhan; Nişancí, Yílmaz; Bilge, Ahmet Kaya; Meriç, Mehmet

doi:10.1016/j.ijcard.2006.03.020

Cited by 30 publications

(19 citation statements)

References 38 publications

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“…The (nonsignificant) trend toward lower peak myocardial perfusion with increasing severity of CKD as well as the independent association between declining CrCl and greater loss of CFR that we observed during 1 year of follow-up raise the question of whether small declines in CFR and peak MBF begin in early CKD but become more pronounced and potentially more important as the severity and duration of CKD increases. In this regard, a study with longer follow-up might have had increased power to detect changes in myocardial perfusion over time This concept is supported by a recent angiographic study of patients with Ն80% stenosis of at least 1 coronary artery that found fewer collateral vessels in patients with a CrCl Ͻ80 mL/min than in patients with preserved renal function 25 and by experimental studies demonstrating reduced myocardial capillary densi- ties 10,12,26 in uremic animals and postmortem samples from individuals with end-stage renal disease. 13 Without pathological data, we are unable to determine whether an analogous loss of myocardial capillaries underlies the accelerated loss of CFR that we observed at 1 year in individuals with mild to moderate CKD.…”

Section: Discussionmentioning

confidence: 93%

Coronary Microvascular Function in Early Chronic Kidney Disease

Charytan

Shelbert

Carli

2010

Circ: Cardiovascular Imaging

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Background-Coronary microvascular dysfunction may underlie the high cardiovascular risk associated with chronic kidney disease (CKD), but the effects of CKD on coronary microvasculature function remain uncertain. Methods and Results-We assessed myocardial blood flow changes in mild-to-moderate CKD and analyzed the association between creatinine clearance (CrCl) and peak myocardial blood flow and coronary flow reserve (CFR) measured as the ratio of stress to rest perfusion at baseline and at 1 year in 435 nondiabetic individuals who underwent quantitative rest and pharmacological stress positron emission tomography imaging. At baseline, CFR was significantly associated with CrCl (␤ per 10 mL/min increase, 0.07; Pϭ0.001). Factors such as age and blood pressure accounted for this association, and it was not significant in adjusted analyses (␤ϭϪ0.02, Pϭ0.53). Peak flow was not associated with CrCl in either crude or adjusted analyses (␤ per 10 mL/minϭϪ0.02 mL/min per g, Pϭ0.29). Although change in peak flow at 1 year was similar in patients with and without CKD, CrCl was a strong and independent predictor of a higher rate of change in CFR, with a loss of 0.11 CFR units/y (95% confidence interval, 0.01 to 0.20) for each 10 mL/min drop in CrCl (Pϭ0.03). Conclusions-These findings demonstrate that mild-to-moderate CKD is not independently associated with a reduction in peak myocardial flow or CFR and suggests that microvascular changes are unlikely to explain the high cardiovascular mortality in mild to moderate CKD. Loss of CFR, however, may accelerate in mild to moderate CKD. Further studies are needed to determine whether these changes lead to more significant reductions that may reduce peak flows and CFR and contribute to cardiovascular risk in more severe CKD. (Circ Cardiovasc Imaging. 2010;3:663-671.)

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Section: Discussionmentioning

confidence: 93%

Coronary Microvascular Function in Early Chronic Kidney Disease

Charytan

Shelbert

Carli

2010

Circ: Cardiovascular Imaging

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“…Myocardial coronary flow reserve--a measure of microvascular supply and function—declines in parallel with glomerular filtration 14-17 , while coronary collateral vessels—whose presence reduces the risk of death in CAD 18, 19 — are 41% less abundant in individuals mild-moderate CKD than patients without CKD 20 . Similarly Left ventricular (LV) mass (see below), diastolic function and late gadolinium enhancement (a marker of myocardial scar/fibrosis) increase dramatically as GFR declines and are associated with risk of death 21-28 .…”

Section: Etiology Of Sudden Cardiac Death In Esrdmentioning

confidence: 99%

Is left ventricular hypertrophy a modifiable risk factor in end-stage renal disease

Charytan

2014

Current Opinion in Nephrology and Hypertension

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Purpose of Review Left ventricular hypertrophy (LVH) is common in ESRD and has been advocated as a therapeutic target. We review considerations for targeting LVH as a modifiable risk factor in ESRD. Recent Findings Pathologic myocardial changes underlying LVH provide an ideal substrate for the spread of arrhythmia and may be key contributors to the occurrence of sudden death in ESRD. LVH is present in 68-89% of incident hemodialysis patients and is frequently progressive, although regression is observed in a minority of patients. Higher degrees of baseline LVH as well as greater increases in left ventricular mass index over time are associated with decreased survival, but whether these association are causal remains uncertain. Several interventions including angiotensin blockade and frequent dialysis can reduce left ventricular mass index but whether the associated decrease in left ventricular mass index is associated with improves survival has not been definitively demonstrated. Summary LVH is a highly prevalent and reversible risk factor which holds promise as a novel therapeutic target in ESRD. Interventional trials are needed to provide additional evidence that LVH regression improves survival before prevention and reversal of LVH can be definitively adopted as a therapeutic paradigm in ESRD.

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“…Preinfarction angina has been shown to predict collateral formation, assessed by emergency coronary angiography [29] Poor collateral networks have been demonstrated in patients with diabetes mellitus [30] and renal disease [31]. Genetic variations in VEGF sensitivity could be demonstrated in cultured myocytes from patients with or without angiographically detected collaterals [21].…”

Section: Collateral Biologymentioning

confidence: 99%

CTO Pathophysiology: How Does this Affect Management?

Irving

2014

CCR

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Chronic total occlusion (CTO) pathophysiology has been described in a few, small studies using post mortem histology, and more recently, in vivo intravascular ultrasound (IVUS) to analyse the constituents of occluded segments. Recent improvements in equipment and techniques have revealed new insights into physical characteristics of occluded coronaries, which in turn enable predictable procedural success. The purpose of this review is to consider the published evidence describing CTO pathophysiology from the perspective of the hybrid algorithm approach to CTO PCI. Methods: Literature searches using “Chronic Occlusion”, “angioplasty”, and” pathology” as keywords. Further searches on “coronary” “collateral”, “Viability”. Bibliographies were scrutinised for further key publications in an iterative process. Papers describing animal models were excluded.

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A potential evidence to explain the reason behind the devastating prognosis of coronary artery disease in uraemic patients: Renal insufficiency is associated with poor coronary collateral vessel development

Cited by 30 publications

References 38 publications

Coronary Microvascular Function in Early Chronic Kidney Disease

Coronary Microvascular Function in Early Chronic Kidney Disease

Is left ventricular hypertrophy a modifiable risk factor in end-stage renal disease

CTO Pathophysiology: How Does this Affect Management?

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