다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

ABI
: ankle–brachial index
ACCORD
: Action to Control Cardiovascular Risk in Diabetes
ADVANCE
: Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation
AGREE
: Appraisal of Guidelines Research and Evaluation
AHA
: American Heart Association
apoA1
: apolipoprotein A1
apoB
: apolipoprotein B
CABG
: coronary artery bypass graft surgery
CARDS
: Collaborative AtoRvastatin Diabetes Study
CCNAP
: Council on Cardiovascular Nursing and Allied Professions
CHARISMA
: Clopidogrel for High Athero-thrombotic Risk and Ischemic Stabilisation, Management, and Avoidance
CHD
: coronary heart disease
CKD
: chronic kidney disease
COMMIT
: Clopidogrel and Metoprolol in Myocardial Infarction Trial
CRP
: C-reactive protein
CURE
: Clopidogrel in Unstable Angina to Prevent Recurrent Events
CVD
: cardiovascular disease
DALYs
: disability-adjusted life years
DBP
: diastolic blood pressure
DCCT
: Diabetes Control and Complications Trial
ED
: erectile dysfunction
eGFR
: estimated glomerular filtration rate
EHN
: European Heart Network
EPIC
: European Prospective Investigation into Cancer and Nutrition
EUROASPIRE
: European Action on Secondary and Primary Prevention through Intervention to Reduce Events
GFR
: glomerular filtration rate
GOSPEL
: Global Secondary Prevention Strategies to Limit Event Recurrence After MI
GRADE
: Grading of Recommendations Assessment, Development and Evaluation
HbA1c
: glycated haemoglobin
HDL
: high-density lipoprotein
HF-ACTION
: Heart Failure and A Controlled Trial Investigating Outcomes of Exercise TraiNing
HOT
: Hypertension Optimal Treatment Study
HPS
: Heart Protection Study
HR
: hazard ratio
hsCRP
: high-sensitivity C-reactive protein
HYVET
: Hypertension in the Very Elderly Trial
ICD
: International Classification of Diseases
IMT
: intima-media thickness
INVEST
: International Verapamil SR/Trandolapril
JTF
: Joint Task Force
LDL
: low-density lipoprotein
Lp(a)
: lipoprotein(a)
LpPLA2
: lipoprotein-associated phospholipase 2
LVH
: left ventricular hypertrophy
MATCH
: Management of Atherothrombosis with Clopidogrel in High-risk Patients with Recent Transient Ischaemic Attack or Ischaemic Stroke
MDRD
: Modification of Diet in Renal Disease
MET
: metabolic equivalent
MONICA
: Multinational MONItoring of trends and determinants in CArdiovascular disease
NICE
: National Institute of Health and Clinical Excellence
NRT
: nicotine replacement therapy
NSTEMI
: non-ST elevation myocardial infarction
ONTARGET
: Ongoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial
OSA
: obstructive sleep apnoea
PAD
: peripheral artery disease
PCI
: percutaneous coronary intervention
PROactive
: Prospective Pioglitazone Clinical Trial in Macrovascular Events
PWV
: pulse wave velocity
QOF
: Quality and Outcomes Framework
RCT
: randomized clinical trial
RR
: relative risk
SBP
: systolic blood pressure
SCORE
: Systematic Coronary Risk Evaluation Project
SEARCH
: Study of the Effectiveness of Additional Reductions in Cholesterol and
SHEP
: Systolic Hypertension in the Elderly Program
STEMI
: ST-elevation myocardial infarction
SU.FOL.OM3
: SUpplementation with FOlate, vitamin B6 and B12 and/or OMega-3 fatty acids
Syst-Eur
: Systolic Hypertension in Europe
TNT
: Treating to New Targets
UKPDS
: United Kingdom Prospective Diabetes Study
VADT
: Veterans Affairs Diabetes Trial
VALUE
: Valsartan Antihypertensive Long-term Use
VITATOPS
: VITAmins TO Prevent Stroke
VLDL
: very low-density lipoprotein
WHO
: World Health Organization

### 1.1 Introduction

Atherosclerotic cardiovascular disease (CVD) is a chronic disorder developing insidiously throughout life and usually progressing to an advanced stage by the time symptoms occur. It remains the major cause of premature death in Europe, even though CVD mortality has …

/pdf/european-guidelines-on-cardiovascular-disease-prevention-in-4z4nw4311i.pdf

European Guidelines on Cardiovascular Disease Prevention in Clinical Practice (Version 2012)

ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation : The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC).

/pdf/2015-esc-guidelines-for-the-management-of-acute-coronary-6did6h5nxk.pdf

2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC)

2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC)

/pdf/2017-esc-guidelines-for-the-management-of-acute-myocardial-14hhjrfylv.pdf

2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC).

DOI:10.1097/MOL.0000000000000557 LDL cholesterol (LDL-C) plays a robust causal role in atherosclerotic coronary heart disease (CHD). However, this relationship might not be so straightforward for atherosclerosis in other territories like the brain, for instance in large vs. small artery occlusive disease leading to ischemic stroke, or the aorta, particularly abdominal aortic aneurysms (AAA). Furthermore, there still controversy, in the absence of definitive results from robust intervention studies, as to whether triglyceride-rich lipoproteins (TGRL), HDL and lipoprotein(a) [Lp(a)] are each causal in atherosclerosis across diverse vascular beds. Fortunately, recent Mendelian randomization studies add information to the controversial epidemiologic associations of these lipoproteins with CHD and nonCHD atherosclerosis, and these findings might have implications for future interventional studies [1 & ]. Hindy et al. [2 && ] found that genetically elevated LDL-C was associated with ischemic stroke arising from large artery atherosclerosis but not with small artery occlusive or cardioembolic stroke in 16 851 cases and 32 473 controls. Of interest, genetically elevated HDL cholesterol (HDL-C) was associated with a reduced risk of small artery occlusion stroke but not the other two stroke subtypes. No association was encountered between genetically elevated triglyceride levels and any type of stroke. These new studies therefore suggest a causal role of LDL-C elevation in atherothrombotic large artery stroke but neither with small vessel disease nor with cerebral embolism. Statins and PCSK9 inhibitors reduce both LDL-C and atherothrombotic ischemic stroke, essentially confirming causality for this association. Harrison et al. [3 && ] reported in 4914 cases and 48 002 controls that genetic elevations of either LDLC or triglyceride were independently associated with greater odds ratios for AAA. On the other hand, genetically elevated HDL-C had an inverse association with AAA. Thus, the evidence suggests that elevated LDL-C or triglyceride may be causally implicated with AAA. However, despite that intensive LDLC reduction can reduce low-extremity peripheral artery disease, as recently seen by PCSK9 inhibition

Mendelian randomization causally link lipoproteins to systemic atherosclerosis and help design clinical trials for the future of lipidology.

Statins are a class of cholesterol-lowering drugs that inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Anti-inflammatory and antioxidant properties, as well as improvement of endothelial function and plaque stabilization have also been proposed as parts of the pleiotropic effects of statins. Specialized pro-resolving mediators (SPMs) are endogenous lipid-derived molecules originating from ω-6 and ω-3 polyunsaturated fatty acids, such as arachidonic, docosahexaenoic and eicosapentaenoic acid that trigger and modulate the resolution of inflammation. Impaired SPM biosynthesis can lead to excessive or chronic inflammation and is implicated in the pathogenesis of several diseases. Exogenous administration of SPMs, including lipoxin, maresin, protectin, have been shown to improve both bacterial and viral infections, mainly in preclinical models, thus minimizing inflammation. Statin-triggered-SPM production in several in vitro and in vivo models may represent another anti-inflammatory pathway involving these drugs. This commentary discusses scientific publications on the effects of statins on SPMs and the resolution of inflammation process. 

Effects of statins on specialized pro-resolving mediators: An additional pathway leading to resolution of inflammation.

Background Accurate measurement of the cholesterol within lipoprotein(a) (Lp[a]‐C) and its contribution to low‐density lipoprotein cholesterol (LDL‐C) has important implications for risk assessment, diagnosis, and treatment of atherosclerotic cardiovascular disease, as well as in familial hypercholesterolemia. A method for estimating Lp(a)‐C from particle number using fixed conversion factors has been proposed (Lp[a]‐C from particle number divided by 2.4 for Lp(a) mass, multiplied by 30% for Lp[a]‐C). The accuracy of this method, which theoretically can isolate “Lp(a)‐free LDL‐C,” has not been validated. Methods and Results In 177 875 patients from the VLDbL (Very Large Database of Lipids), we compared estimated Lp(a)‐C and Lp(a)‐free LDL‐C with measured values and quantified absolute and percent error. We compared findings with an analogous data set from the Mayo Clinic Laboratory. Error in estimated Lp(a)‐C and Lp(a)‐free LDL‐C increased with higher Lp(a)‐C values. Median error for estimated Lp(a)‐C <10 mg/dL was −1.9 mg/dL (interquartile range, −4.0 to 0.2); this error increased linearly, overestimating by +30.8 mg/dL (interquartile range, 26.1–36.5) for estimated Lp(a)‐C ≥50 mg/dL. This error relationship persisted after stratification by overall high‐density lipoprotein cholesterol and high‐density lipoprotein cholesterol subtypes. Similar findings were observed in the Mayo cohort. Absolute error for Lp(a)‐free LDL‐C was +2.4 (interquartile range, −0.6 to 5.3) for Lp(a)‐C<10 mg/dL and −31.8 (interquartile range, −37.8 to −26.5) mg/dL for Lp(a)‐C≥50 mg/dL. Conclusions Lp(a)‐C estimations using fixed conversion factors overestimated Lp(a)‐C and subsequently underestimated Lp(a)‐free LDL‐C, especially at clinically relevant Lp(a) values. Application of inaccurate Lp(a)‐C estimations to correct LDL‐C may lead to undertreatment of high‐risk patients.

https://www.ahajournals.org/doi/pdf/10.1161/JAHA.121.023136

Assessing the Accuracy of Estimated Lipoprotein(a) Cholesterol and Lipoprotein(a)‐Free Low‐Density Lipoprotein Cholesterol

Safety of statin treatment in children with familial hypercholesterolemia: Filling the gaps.

Chapters of the PCSK9 story book. In Chapter I, proprotein convertase subtilisin kexin type 9 (PCSK9), initially named as neural apoptosis-regulated convertase 1 or NARC-1, was characterized and described as highly expressed in the liver by Seidah et al.3 The role of NARC-1 in cholesterol homeostasis was not known. In Chapter II, two seminal studies demonstrated that gain-of-function and loss-of-function genetic variants in the PCSK9 gene resulted in elevated and reduced LDL-cholesterol (LDL-C) levels, respectively.4,5 In Chapter III, once the role of PCSK9 in cholesterol homeostasis was established, monoclonal antibodies (mAbs) against PCSK9 were successfully developed with an efficacy of ∼40–60% in LDL-C reduction.6–9 In Chapter IV, outcome studies with two PCSK9 mAbs, evolocumab and alirocumab, showed a 15% reduction in major atherosclerotic cardiovascular events (MACE) in secondary prevention patients on mAbs relative to placebo.10,11 In Chapter V, RNA-directed therapies are emerging. The small interfering RNA against the PCSK9 mRNA promotes a 50% reduction in LDL-C levels with 2–3 injections per year.15 In Chapter VI, the current study suggests a 26% reduction in MACE with inclisiran on an exploratory analysis, but outcome studies are ongoing (Chapter VII).14 

Raul D. Santos

Papers

Mendelian randomization causally link lipoproteins to systemic atherosclerosis and help design clinical trials for the future of lipidology.

Effects of statins on specialized pro-resolving mediators: An additional pathway leading to resolution of inflammation.

Assessing the Accuracy of Estimated Lipoprotein(a) Cholesterol and Lipoprotein(a)‐Free Low‐Density Lipoprotein Cholesterol

Safety of statin treatment in children with familial hypercholesterolemia: Filling the gaps.

Cholesterol lowering with inclisiran: a new chapter in the PCSK9 story book.