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1 itative rather than qualitative estimates of residual risk.
2 es as a novel marker of or target to address residual risk.
3 ntially to the disease burden and perpetuate residual risk.
4 to identify unique HFrEF subgroups with high residual risk.
5 redictor of incident events and biomarker of residual risk.
6 om VLDL and chylomicrons, contribute to this residual risk.
7 rapy, Lp(a) was a significant determinant of residual risk.
8 novel therapies are required to reduce this residual risk.
9 C, apolipoprotein B, or ratios in predicting residual risk.
10 stions about its value for stratification of residual risk.
11 few treatments are documented to reduce this residual risk.
12 Lipoprotein(a) levels may influence residual risk.
13 e clinical biomarker to identify patients at residual risk.
14 allow better estimation of carrier rates and residual risks.
15 essential to sustain these gains and address residual risks.
16 nt to 40% or higher (HFimpEF) may still face residual risks.
17 g hold incremental predictive information on residual risk after acute coronary syndrome beyond that
19 goal of this study was to determine whether residual risk after high-dose statin therapy for primary
21 tic techniques enables the estimation of the residual risk after the consumption of a product that un
22 s in medium- and high-risk patients, and the residual risk after these cut points were 0.2% for low-r
23 ng strategies with a second test to identify residual risk among those deemed low risk by the first t
24 innovative clinical trial designs to address residual risk and identify novel therapeutic targets.
26 mbined cholesterol and inflammatory risk, no residual risk, and isolated residual cholesterol risk.
29 erol with statins, there remains significant residual risk as evidenced by incident and recurrent car
31 dictor of future cardiovascular events as is residual risk assessed by low-density lipoprotein choles
34 admission, there should be consideration for residual risk based on the LDL/HDL ratio, following stro
35 to study therapeutic approaches that address residual risk beyond LDL-C reduction to promote plaque s
37 lipoproteins (TRLs) represents an important residual risk factor for cardiovascular and chronic kidn
39 ency, PIK3CA mutations do not seem to affect residual risk following treatment with endocrine therapy
40 ological characteristics that differentiated residual risk for cardiovascular death or heart failure
41 LDL-C as the primary target of therapy, yet residual risk for cardiovascular disease (CVD) among sta
42 pective on some of these salient issues: the residual risk for disease progression after sustained vi
43 educed ejection fraction (HFrEF) have a high residual risk for heart failure hospitalizations and car
44 te coronary syndromes (NSTE-ACS) are at high residual risk for long-term cardiovascular (CV) mortalit
45 patients on MRA therapy may remain at a high residual risk for poor outcomes even on MRA therapy.
46 tor-positive breast cancer have considerable residual risk for recurrence after completing 5 years of
47 lity that HDL modification could address the residual risk has brought renewed focus on an old HDL-ra
48 The pursuit of novel therapies to target the residual risk has focused on raising the levels of high-
50 with proper risk mitigation strategies; the residual risk, however, should be weighed carefully agai
52 festyle counseling more effective; assessing residual risk in a treated patient; diagnosing and treat
55 ide-rich lipoproteins (TRLs) are a source of residual risk in patients with atherosclerotic cardiovas
59 is unknown whether Lp(a) is a determinant of residual risk in the setting of low low-density lipoprot
61 States, there is a need to better integrate residual risk into cardiovascular disease (CVD) risk str
64 candidate genes that may contribute to this residual risk is the endothelial nitric oxide synthase (
65 recognition of the role of inflammation as a residual risk marker of adverse outcomes for coronary ar
66 Lp(a) levels, possibly contributing to the "residual risk" noted in outcomes trials and at the bedsi
67 nt for 10 years) would lead to expected mean residual risk of 14.6% (A; ARR 2.6%) or 13.9% (B; ARR 3.
68 ol in identifying statin-treated patients at residual risk of all-cause mortality and myocardial infa
69 but not LDL cholesterol, are associated with residual risk of all-cause mortality and myocardial infa
71 nchmark TTR to achieve further mitigation of residual risk of bleeding and enhance haemocompatibility
72 in Lp(a) concentrations were associated with residual risk of cardiovascular disease (adjusted hazard
74 iovascular disease and MetS have substantial residual risk of cardiovascular events despite statin th
75 ognised in nephrology, could help to explain residual risk of cardiovascular events in the general po
76 e anti-inflammatory medication to target the residual risk of cardiovascular events in the secondary
77 oduction of these therapeutics, an important residual risk of CKD progression and cardiovascular deat
78 eutic strategies, there remains an extensive residual risk of clinical events, particularly in high-r
80 ant associations of a similar magnitude with residual risk of CVD were found for on-treatment LDL-C,
86 eening for HIV, HCV, and HBV has reduced the residual risk of infectious-window-period donations, suc
87 patients with cardiovascular disease have a residual risk of ischaemic events despite receiving anti
90 tion and lowering cholesterol, a significant residual risk of major atherosclerotic complication rema
92 ovascular treatment goals is associated with residual risk of mortality and cardiovascular outcomes i
93 n the association between Lp(a) and the high residual risk of myocardial infarction, providing suppor
97 s clopidogrel/aspirin can further reduce the residual risk of stroke recurrence in patients with posi
98 thogen-reduction technologies to address the residual risk of TAS as well as the potential risk of th
99 HCV infections annually and has reduced the residual risk of transfusion-transmitted HIV-1 and HCV t
100 nd kidney events when used individually, the residual risks of these events remain high across major
102 the cardiovascular-metabolic component, and residual risk persists despite healthy lifestyles and tr
104 individuals with established CHD, to improve residual risk prediction and identify novel drug targets
107 C declined over the 3 years, but substantial residual risk remained in the third year, leading to 90.
109 sures can mitigate mortality rates; however, residual risk remains even at speeds of 10 knots or less
112 scular events by about 25-35%, a substantial residual risk remains, leading to a search for additiona
116 tion we observed between RCB and a patient's residual risk suggests that prospective evaluation of RC
117 DL particle number may be a better marker of residual risk than chemically measured HDL-C or apoA-I.
118 o estimated the potential risk reduction and residual risk that can be achieved if patients reach gui
119 ts a promising candidate to address the high residual risk that persists in ACS patients receiving gu
120 A1/2 pathogenic variant (PV) carriers have a residual risk to develop peritoneal carcinomatosis (PC).