Objectives
This study sought to perform a systematic review and meta-analysis to
understand the role of stress cardiac magnetic resonance imaging (CMR) in
assessing cardiovascular prognosis in patients with known or suspected
coronary artery disease (CAD).
Background
Although stress CMR is excellent for the diagnosis of obstructive
CAD, the prognostic value of stress CMR has been less well described.
Methods
PubMed, Cochrane CENTRAL, and metaRegister of Controlled Trials were
searched for stress CMR studies with >6 months of prognostic data.
Primary endpoints were cardiovascular death, myocardial infarction (MI), and
a composite outcome of cardiovascular death or MI during follow-up. Summary
effect estimates were generated with random-effects modeling, and annualized
event rates were assessed.
Results
Nineteen studies (14 vasodilator, 4 dobutamine, and 1 that used both)
involved a total of 11,636 patients with a mean follow-up of 32 months.
Patients had a mean age of 63 ± 12 years, 63% were male, and
26% had previous MI; mean left ventricular ejection fraction was 61
± 12%; and late gadolinium enhancement was present in
29% and ischemia in 32%. Patients with ischemia had a higher
incidence of MI (odds ratio [OR]: 7.7; p < 0.0001),
cardiovascular death (OR: 7.0; p < 0.0001), and the combined endpoint
(OR: 6.5; p < 0.0001) compared with those with a negative study. The
combined outcome annualized events rates were 4.9% for a positive
versus 0.8% for a negative stress CMR (p < 0.0001), 2.8%
versus 0.3% for cardiovascular death (p < 0.0001), and
2.6% versus 0.4% for MI (p < 0.0005). The presence of
late gadolinium enhancement was also significantly associated with a worse
prognosis.
Conclusions
A negative stress CMR study is associated with very low risk of
cardiovascular death and MI. Stress CMR has excellent prognostic
characteristics and may help guide risk stratification of patients with
known or suspected CAD.
Genetic studies have revealed the association between the ε2 allele of the apolipoprotein E (apoE) gene and greater risk of metabolic diseases. This study compared C57BL/6 mice in which the endogenous mouse gene has been replaced by the human APOE2 or APOE3 gene (APOE2 and APOE3 mice) to identify the mechanism underlying the relationship between ε2 and obesity and diabetes. In comparison with APOE3 mice, the APOE2 mice had elevated fasting plasma lipid and insulin levels and displayed prolonged postprandial hyperlipidemia accompanied by increased granulocyte number and inflammation 2 h after being fed a lipid-rich meal. In comparison with APOE3 mice, the APOE2 mice also showed increased adiposity when maintained on a Western-type, high-fat, high-cholesterol diet. Adipose tissue dysfunction with increased macrophage infiltration, abundant crown-like structures, and inflammation were also observed in adipose tissues of APOE2 mice. The severe adipocyte dysfunction and tissue inflammation corresponded with the robust hyperinsulinemia observed in APOE2 mice after being fed the Western-type diet. Taken together, these data showed that impaired plasma clearance of apoE2-containing, triglyceride-rich lipoproteins promotes lipid redistribution to neutrophils and adipocytes to accentuate inflammation and adiposity, thereby accelerating the development of hyperinsulinemia that will ultimately lead to advanced metabolic diseases.
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