Association of coronary heart disease with age‐adjusted aortocoronary calcification in patients with familial hypercholesterolaemia

Jensen, Jesper Møller; Gerdes, Lars Ulrik; Jensen, Henrik Kjærulf; Christiansen, T.; Brorholt-Petersen, Jens Uffe; Færgeman, Ole

doi:10.1046/j.1365-2796.2000.00630.x

Cited by 12 publications

(8 citation statements)

References 33 publications

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“…VC is probably primarily due to abnormal mineral metabolism that is seen in renal failure (141)(142)(143)(144)(145), perhaps through a complex process involving osseous metaplasia of the vascular wall components (118,119,146). Associations of calcium/phosphorus/parathyroid hormone dysregulation with CVD and concerns that coronary artery calcification may beget coronary artery occlusive disease (147)(148)(149)(150) argue for an important role of VC in the CVD epidemic in ESRD (84,151).…”

Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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D uring the past several decades, the advent and refinement of maintenance dialysis and kidney transplantation have essentially eliminated kidney failure per se as a cause of death in developed countries. However, as patients survive many years after the development of renal failure, comorbidities develop, progress, and ultimately cause death in these individuals. Cardiovascular disease (CVD) has ranked prominent among these comorbidities, accounting for nearly half of the deaths (1). All along the continuum of chronic kidney disease (CKD)-from microalbuminuria to ESRD-a higher risk for CVD has been observed (see Epidemiology of CVD in CKD). In fact, individuals with early CKD are more likely to die of CVD than to develop ESRD (2,3). Then, among those who survive to ESRD, the all-cause CVD mortality in patients with ESRD is many-fold higher than in the general population (4). Unfortunately, the reasons for the association of CKD with CVD are not clearly understood, and the role of various clinical interventions in stemming the CVD epidemic are not well defined. Complicating the issue is the potential variation in the pathophysiology and clinical behavior of CVD through the stages of CKD.3-Hydroxyl-3-methylglutaryl CoA reductase inhibitors (statins) and other lipid-lowering drugs (LLD) have been clearly demonstrated to lessen the morbidity and mortality of CVD in the general population; therefore, there is hope that the use of these drugs may likewise help patients with CKD (In addition, it has been theorized that dyslipidemia may contribute to the progression of CKD, such that LLD may prove to slow CKD progression.) Nevertheless, given differences in epidemiology and pathophysiology of CVD in CKD, there are reasons to question whether the cardiovascular benefits of LLD that are observed in the general population will also be realized in the CKD population. It is widely acknowledged that the current medical literature provides insufficient data to guide the use of LLD in the CKD population, in large part because renal insufficiency has been an exclusion criterion for most of the randomized, controlled studies that have addressed this issue. Although consensus-based guidelines on the treatment of dyslipidemias in individuals with CKD and with kidney transplants have been published by the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) Work Groups, the nephrology and cardiology communities recognize the urgent need for high-quality clinical studies on this issue, and this has fueled the publication of subgroup analyses of previous large studies in the general population and the launching of large-scale clinical trials in the CKD population, as summarized in Table 1. To provide the reader with a better appreciation of the important issues that are germane to management of dyslipidemia in CKD, this article (1) briefly summarizes the literature on the benefits of LLD in the general population, (2) demonstrates the limited involvement of individuals with CKD in the studies in the ge...

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Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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“…Arterial wall calcification is common in patients with familial hypercholesterolemia, a genetic disorder of cholesterol metabolism. [3][4][5] Several studies have identified the relationship between the serum level of low-density lipoprotein cholesterol (LDL-C) and arterial wall calcification; moreover, lipid-lowering therapy using 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has been reported to inhibit the progression of arterial wall calcification. 6,7 In patients receiving long-term hemodialysis, elevated serum triglyceride (TG) levels and reduced high-density lipoprotein cholesterol (HDL-C) levels are risk factors for coronary artery calcification.…”

mentioning

confidence: 99%

“…Most of the previous studies used the "calcium score" determined by CT as a semiquantitative index of calcification of the aorta or coronary arteries. [3][4][5][6][7] However, the calcium score may not accurately reflect subtle changes in calcium deposit levels. To accurately quantify the degree of calcium deposition, we developed an image color analysis software program that can automatically determine the percentages of calcified volume against whole vascular volume (%ACV) using plain CT. 9 We previously reported a strong correlation between %ACV and aortic calcification dimension in aortas of autopsy specimens, the latter of which was determined using soft X-ray photographs.…”

mentioning

confidence: 99%

Pulse Pressure Is an Independent Predictor for the Progression of Aortic Wall Calcification in Patients With Controlled Hyperlipidemia

et al. 2004

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Abstract-Recent epidemiological studies suggested that calcifications of the aorta and the coronary arteries are important predictors for cardiovascular morbidity and mortality. However, the relation between blood pressure components and the progression of vascular wall calcification has remained unclear. We quantified calcium deposits in the abdominal aorta as the percentage of aortic calcification volume (%ACV) using computed tomography in patients with hyperlipidemia. Those who had aortic calcification were treated with lipid-lowering agents and followed-up for Ͼ2 years (6.3Ϯ3.2 years). The relationship between the components of blood pressure and the increase in %ACV per year (⌬%ACV/year) was assessed in subjects in whom serum lipid levels were well controlled during the follow-up periods. An age-and sex-adjusted correlation analysis showed that ⌬%ACV/year was significantly correlated to body mass index (rϭ0. Key Words: hypertension Ⅲ calcium Ⅲ aorta Ⅲ pulse Ⅲ imaging Ⅲ risk factors C alcification in the aorta and coronary arteries is a strong predictor for cardiovascular morbidity and mortality. 1,2 Previous studies have shown the close relationships between arterial wall calcification and abnormal serum lipid levels. Arterial wall calcification is common in patients with familial hypercholesterolemia, a genetic disorder of cholesterol metabolism. [3][4][5] Several studies have identified the relationship between the serum level of low-density lipoprotein cholesterol (LDL-C) and arterial wall calcification; moreover, lipid-lowering therapy using 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has been reported to inhibit the progression of arterial wall calcification. 6,7 In patients receiving long-term hemodialysis, elevated serum triglyceride (TG) levels and reduced high-density lipoprotein cholesterol (HDL-C) levels are risk factors for coronary artery calcification. 8 These studies suggested that abnormal serum lipid levels promote calcium deposition in the arterial wall.Several studies have examined the influence of hypertension on the progression of arterial wall calcification. In these studies, antihypertensive therapy has been shown to inhibit the formation of calcified lesions, suggesting that hypertension promotes calcium deposition in the arterial wall. 9 -11 However, it remains undetermined which blood pressure (BP) component, ie, systolic BP (SBP), diastolic BP (DBP), mean BP (MBP), or pulse pressure (PP) is responsible for the accelerated formation of calcification, probably because the abnormal serum lipid levels may have made it difficult to assess the effect of BP alone on the formation of calcified lesions.Computed tomography (CT) is a useful tool to evaluate the level of arterial wall calcification. Most of the previous studies used the "calcium score" determined by CT as a semiquantitative index of calcification of the aorta or coronary arteries. [3][4][5][6][7] However, the calcium score may not accurately reflect subtle changes in calcium deposit levels. To accurat...

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“…Jensen et al found that age-adjusted calcium scores still increased slightly with age, suggesting that coronary calcification is a self-perpetuating process 12) . His diagnostic model for the prediction of CAD in FH patients based on cholesterol-year scores was the weakest model in his study, more than his model based on a combination of traditional risk factors, including age, sex, smoking, hypertension, untreated cholesterol, and BMI.…”

Section: Discussionmentioning

confidence: 99%

“…CCS is recommended to estimate the risk of coronary events in asymptomatic individuals, particularly those with intermediate risks, but high prognostic and diagnostic values were also shown in high-risk patients 10) . To date, only a few studies are available that report about CCS in patients with FH [11][12][13] . percutaneous transluminal coronary angioplasty, angina, wall motion abnormalities on an echocardiogram, or positive results of exercise testing which was performed on all patients with results of CCS above 100.…”

Section: Introductionmentioning

confidence: 99%

Assessment of Subclinical Atherosclerosis Using Computed Tomography Calcium Scores in Patients with Familial and Nonfamilial Hypercholesterolemia

Gałąska

Kulawiak-Gałąska

Węgrzyn

et al. 2016

JAT

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Aim:The aim of this study was to compare coronary calcium scores and aortic calcium scores between patients with severe hypercholesterolemia having a DNA-based diagnosis of FH (FH group) versus patients with severe hypercholesterolemia without the FH gene mutation (NFH group). Method: A total of 89 FH and 50 NFH patients underwent CT with coronary and thoracic aorta calcium scoring. Their CCS and TCS in ascending aorta (TCSasc) and descending aorta (TCSdesc) were determined and compared between the two patient groups. Results: TCSasc was significantly higher in the FH group when compared to the NFH group (30.6 59 vs 4.7 13.4, p 0.001. After adjusting for age, sex, smoking, blood pressure, history of diabetes mellitus and LDL cholesterol levels, FH gene mutation was an independent risk factor of having non-zero TCSasc 3.6 (95% CI, 1.4 -9.5, p 0.01), high TCSasc 9.6 (95% CI, 2.4 -38.2, p 0.01) and high CCS of 4.1 (95% CI, 1.2 -13.2. p 0.05). Conclusion: We found that when computed tomography calcium scores were used as an assessment, patients with familial hypercholesterolemia displayed an increased burden of ascending aorta atherosclerosis when compared to patients with nonfamilial severe hypercholesterolemia. This phenomenon appears to be more dependent on the presence of FH genotype than hypercholesterolemia itself. See

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Association of coronary heart disease with age‐adjusted aortocoronary calcification in patients with familial hypercholesterolaemia

Cited by 12 publications

References 33 publications

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Pulse Pressure Is an Independent Predictor for the Progression of Aortic Wall Calcification in Patients With Controlled Hyperlipidemia

Assessment of Subclinical Atherosclerosis Using Computed Tomography Calcium Scores in Patients with Familial and Nonfamilial Hypercholesterolemia

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