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Table 1. Participant characteristics according to presence or absence of all-cause mortality and CVD hospitalization end-points.

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Table 2. Age and sex-adjusted rates of all-cause mortality and CVD hospitalization by quartile of serum lipids.

Age-adjusted mortality rates (deaths/10,000 person-years) showed a significant positive association with the TG/HDL-C ratio and an inverse association with TC, HDL-C and LDL-C. Regarding the risk of hospitalization for CHD, a significant positive association was observed in non-HDL-C minus LDL-C, TG, TC/HDL-C ratio and TG/HDL-C ratio, and an inverse relationship with TC, HDL-C and LDL-C. For hospitalization due to stroke, there was a significant positive association with LDL-C, non-HDL-C minus LDL-C, TG, TC/HDL-C ratio and TG/HDL-C ratio, and an inverse association with HDL-C. After further adjustment for other cardiovascular risk factors, however, the association of elevated TC and LDL-C levels and CHD hospitalization was no longer significant, either in the relative or additive scales (Tables mintamp;berry Mules white odyLWSul8
and 4 ). For stroke, however, the association with LDL-C remained significant in fully adjusted models. The rate ratio and rate differences (95% CI) for all–cause mortality and CVD hospitalization after a 3.2-year follow-up comparing the 75 th versus 25 th percentile of lipid biomarkers concentrations are shown in the S1 Table , with consistent findings. Jimmy choo Cloth Lace Ups S2BGur
shows the fully adjusted dose-response association between lipid values and risk of mortality and hospitalization due to CHD and stroke. A sensitivity analysis was performed in participants according to current lipid-lowering treatment ( S1 Fig ), but no relevant differences were found between groups.

Fig 1. Age and sex-adjusted rates ratios for all-cause mortality and CVD hospitalization by serum lipid levels.

Models are adjusted for age, sex, smoking status (never, former, current), obesity (no, yes), diabetes (no, yes), hypertension (no, yes), chronic kidney disease (no, yes), anti-hypertensive medication (no, yes), glucose lowering medication (no, yes), lipid-lowering medication (no, yes). Models for specific lipid biomarkers have been additionally adjusted as follows: 1) Total-cholesterol is further adjusted by HDL ≤ 40 for men and ≤ 50 for women (no, yes); 2) HDL-cholesterol is further adjusted by LDL.C ≥ 130 mg/dL (no, yes); 3) Non-HDL-cholesterol is further adjusted by HDL ≤ 40 for men and ≤ 50 for women (no, yes); 4) LDL-cholesterol is further adjusted by HDL ≤ 40 for men and ≤ 50 for women (no, yes); 5) Non-HDL minus LDL-cholesterol is further adjusted by HDL ≤ 40 for men and ≤ 50 for women (no, yes) and LDL-C ≥ 130 mg/dL (no, yes); 6) Triglycerides is further adjusted by total cholesterol > 200 mg/dL (no, yes) and HDL ≤ 40 for men and ≤ 50 for women (no, yes); 7) Total cholesterol/HDL is further adjusted by total cholesterol (mg/dL); and 7) Triglycerides/HDL is further adjusted by total cholesterol (mg/dL).


Incidence of myocardial infarction and myocardial injury stratified by age in unselected consecutive hospital inpatients with myocardial necrosis. Reproduced from Shah . 6

Whether adoption of high-sensitivity troponin assays and the 99th centile for diagnosis of myocardial infarction translates into improvements in clinical outcomes for patients with suspected acute coronary syndrome is being evaluated in a stepped wedge cluster randomised trial across Scotland (High-STEACS, NCT: 01852123). If increased sensitivity does not impinge on specificity for the diagnosis of type 1 myocardial infarction, then these assays will improve patient outcomes through better targeting of therapies for coronary artery disease. However, if increased sensitivity leads to poor specificity, then patients may be misdiagnosed and given inappropriate cardiac medications with potentially detrimental outcomes. This trial will establish whether the introduction of high-sensitivity assays into routine clinical practice is detrimental or beneficial to patient management and outcomes; a fundamental and critical assessment for the modern definition of acute myocardial infarction.

Outcomes of myocardial injury and type 2 myocardial infarction

Patients with type 2 myocardial infarction or myocardial injury have poor clinical outcomes, worse than those patients with type 1 myocardial infarction, with one in three patients dead at 1 year. 6 In a prospective study of patients with acute coronary syndrome (n=2818), Stein found an increased risk of death in those with an adjudicated diagnosis of type 2 versus type 1 myocardial infarction at 30 days (13.6% vs 4.9%, p<0.0001) and at 1 year (23.9% vs 8.6%, p<0.0001). 31 Another single-centre study by El-Haddad reported mortality rates 6.9 times greater in type 2 versus type 1 myocardial infarction at 1 year. 32

Sarkisian reviewed 3762 patients who underwent cardiac troponin testing on clinical indication. Patients with acute myocardial injury were at significantly greater risk of all-cause mortality than those with myocardial infarction at a median follow-up of 3.2 years (59% vs 39%, p<0.0001 by log-rank test). In a subgroup analysis, they demonstrate no difference in risk for all-cause mortality between patients with type 2 myocardial infarction or myocardial injury (adjusted hazard ratio (HR) 1.28, 95% CI 0.97 to 1.65). 41 More recently, we extended follow-up in our cohort of consecutive unselected hospital inpatients, 6 demonstrating 60% of patients with type 2 myocardial infarction and 75% of patients with myocardial injury were dead at 5 years. Vanessa Bruno Leather Sandal hZP2jLb
Whether it is possible to improve outcomes in these patients through therapeutic intervention is currently unknown.

The distinction between type 2 myocardial infarction and myocardial injury may, however, be clinically important, as it has been demonstrated that patients classified as having a type 2 myocardial infarction are twice as likely as those with myocardial injury to be readmitted with a type 1 myocardial infarction in 1 year. 6 This potentially important observation suggests that a proportion of patients with type 2 myocardial infarction may benefit from further investigation and treatment for coronary artery disease. Selection of patients for further investigation requires a greater understanding of the clinical features that identify those patients at increased risk of future acute coronary events and a better understanding of the mechanisms of myocardial injury in this setting.

Pragmatic classification of patients with myocardial injury and infarction

We believe there remains scope for clarification of the diagnostic criteria for type 2 myocardial infarction and myocardial injury and that this is necessary to encourage clinicians to adopt the classification proposed in the universal definition. This clinical classification acknowledges the central role of coronary artery disease in the pathogenesis of myocardial infarction.

For example, while a patient with a submassive pulmonary embolism and an elevation in cardiac troponin may have both chest pain and an abnormal electrocardiogram, a diagnosis of type 2 myocardial infarction is unhelpful. The diagnosis is pulmonary embolism and acute myocardial injury due to hypoxia or right ventricular strain; coronary investigations and secondary prevention are not indicated.

The term type 2 myocardial infarction should, in our opinion, be used exclusively in patients with acute myocardial injury where coronary artery disease has contributed and where there may be opportunities to improve outcomes through coronary revascularisation or medical therapy. Selection of patients with acute myocardial injury for further investigation will depend on the nature of primary illness and the patient's probability of having coronary artery disease.

For example, a patient with chronic kidney disease who presents with a community-acquired pneumonia may have persistently elevated cardiac troponin concentrations. The subsequent development of chest pain and ischaemic changes on the electrocardiogram with a temporal rise in serum cardiac troponin concentrations may be due to hypoxia, tachycardia or hypotension, with the acute illness representing a ‘physiological stress test’ identifying otherwise quiescent stable coronary artery disease. The initial diagnosis is ‘acute myocardial injury’, and the need for further investigation for coronary artery disease should be guided by an assessment of cardiovascular risk. In patients with a low probability of coronary artery disease, further cardiac investigations may not be necessary. In patients with an intermediate or high probability, imaging to identify those with coronary artery disease should be considered. Should these investigations confirm the presence of coronary artery disease without evidence of plaque rupture, the diagnosis of type 2 myocardial infarction would be appropriate and secondary prevention should be considered.

Until prospective studies have been performed that define the mechanism of myocardial injury in consecutive patients presenting with an alternative acute illness, clinicians will need to rely on clinical judgement to evaluate the likelihood of coronary artery disease.

We propose a simple decision framework for the initial investigation strategy to determine the aetiology of myocardial injury and identify those with coronary artery disease who may benefit from secondary prevention ( figure 3 ).

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Figure 1

The proposed role of adiponectin in renal pathophysiology and the interplay between adiponectin and renal injury. AMPK, AMP-activated protein kinase; ADIPOR1, adiponectin receptor 1. A full colour version of this figure is available at

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In steady-state subjects, in whom plasma adiponectin levels do not change over time, urinary adiponectin excretion rate (as assessed by the ratio urinary adiponectin:urinary creatinine) equates with adiponectin production rate in adipose tissue – hepatic adiponectin excretion rate. The urinary adiponectin excretion rate has been reported to be positively correlated with UAE and negatively with GFR ( Reiss Bradley Clae Leather Sneakers in Light Pink Mens GjtM58q9
, Fujita et al . 2006 , Roger Vivier 45MM POLLY SUEDE ANKLE BOOTS njOD9zdMD
). The positive relationship between urinary adiponectin excretion rate and UAE has been shown to strengthen with increasing UAE; this association has been found to exist mainly in patients with macroalbuminuria (UAE >300 mg/24 h) or microalbuminuria (UAE between 30 and 300 mg/24 h) and less consistently in subjects with normoalbuminuria ( Koshimura et al . 2004 , Fujita et al . 2006 , Jorsal et al . 2013 ). Thus, in patients with increased UAE or decreased GFR, the adiponectin production rate – hepatic adiponectin excretion rate – appears to be increased. This elevation could be attributed to an increased rate of adiponectin production, because adiponectin expression and adiponectin protein content in visceral as well as subcutaneous adipose tissue were found to be increased in patients with end-stage renal disease ( Martinez Cantarin et al . 2013 ). Studies investigating the possible modulation of hepatic adiponectin excretion rate in patients with renal disease are lacking, and thus further studies investigating this issue are needed. Taking into account the renoprotective properties of adiponectin mentioned earlier, a plausible explanation for the upregulation of adipose tissue adiponectin production in patients with albuminuria or decreased GFR is that adiponectin production in adipose tissue and secretion into the bloodstream is enhanced via an as yet unknown mechanism to mitigate renal injury. Consistently, Ohashi et al . (2007) found that adiponectin accumulated in the glomeruli and interstitium of the remnant kidney of WT mice to counteract for the subtotal nephrectomy-induced renal injury. In addition, serum adiponectin levels have been found to be positively correlated with urinary levels of markers of renal tubulointerstitial injury in diabetics, such as N -acetylglucosaminidase and MCP1 ( Fujita et al . 2006 ). Moreover, exposure of proximal tubular cells to recombinant adiponectin has been reported to result in decreased MCP1 secretion ( Shen et al . 2008 ).

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