Archive for December, 2016

30 Day Myocardial Infarction and Cardiac Death post surgery after previous PCI

Egholm et al report on the 30 day event rates of myocardial infarction/cardiac death/all cause mortality in patients with prior PCI (<1 month, 1-2 month.2-12 month intervals PCI to surgery). Data was from National Registry. The control group was patients without ischemic heart disease. An hazard for myocardial infarction and cardiac death for those with PCI within 1 month of surgery was demonstrated.



Guidelines recommend postponing surgery for at least 6 months after treatment with a drug-eluting stent by percutaneous coronary intervention (DES-PCI).


The goal of this study was to evaluate the surgical risk associated with DES-PCI compared with that in nonstented patients without ischemic heart disease (IHD).


Between 2005 and 2012, a total of 22,590 patients underwent DES-PCI in western Denmark. By
record-linking the Western Denmark Heart Registry and the Danish National Patient Register, we evaluated 4,303 DES-PCI–treated patients with a surgical procedure and compared them with a control group of patients without previous IHD undergoing similar surgical procedures (n ¼ 20,232). Events of interest were myocardial infarction (MI), cardiac death, and all-cause mortality within 30 days after surgery.


Surgery in DES-PCI–treated patients was associated with an increased risk of MI (1.6% vs. 0.2%; odds ratio[OR]: 4.82; 95% confidence interval [CI]: 3.25 to 7.16) and cardiac death (1.0% vs. 0.2%; OR: 5.87; 95% CI: 3.60 to 9.58) but not all-cause mortality (3.1% vs. 2.7%; OR: 1.12; 95% CI: 0.91 to 1.38). When stratified for time from PCI to surgery, only surgery within the first month was associated with a significant increased risk of events.


Patients requiring surgery within 12 months after DES-PCI had an increased risk of MI and cardiac death compared with patients without IHD. The increased risk was only present within the first month after DES-PCI, suggesting that surgery might be undertaken earlier than currently recommended.


Causes of Death in Atrial Fibrillation

Gomez-Outez et al report on the causes of death in patients with atrial fibrillation. The authors systematically searched for randomized clinical trials comparing “direct” oral anticoagulants (DOAC) versus warfarin. An editorialis available here.



Oral anticoagulation reduces the risk of mortality in atrial fibrillation (AF), but examination
of the causes of death is essential to design new strategies to further reduce the high mortality rates observed in this population.


The authors sought to analyze and compare causes of death in patients receiving direct oral
anticoagulants (DOAC) or warfarin for prevention of stroke and systemic embolism (SE) in AF.
METHODS The authors systematically searched for randomized trials of DOAC versus warfarin for prevention of stroke/SE in AF. The main outcome was mortality and independently adjudicated specific causes of death. The authors used the random effects model of meta-analysis to combine the studies.


71,683 patients from 4 trials were included (134,046 patient-years of follow-up). A total of 6,206 patients (9%) died during follow-up. Adjusted mortality rate was 4.72%/year (95% confidence interval [CI]: 4.19 to 5.28). Cardiac deaths accounted for 46% of all deaths, whereas nonhemorrhagic stroke/SE and hemorrhage related deaths represented 5.7% and 5.6% of the total mortality, respectively. Compared with patients who were alive, those who died had more frequent history of heart failure (odds ratio [OR]: 1.75; 95% CI: 1.25 to 2.44), permanent/persistent AF (OR: 1.38; 95% CI: 1.25 to 1.52) and diabetes (OR: 1.37; 95% CI: 1.11 to 1.68); were more frequently male (OR: 1.24; 95% CI: 1.13 to 1.37) and older (mean difference 3.2 years; 95% CI: 1.6 to 4.8); and had a lower creatinine clearance (9.9 ml/min; 95% CI: 11.3 to 8.4). There was a small, but significant, reduction in all-cause mortality with the DOAC versus warfarin (difference 0.42%/year; 95% CI: 0.66 to 0.18), mainly driven by a reduction in fatal bleedings.


In contemporary AF trials, most deaths were cardiac-related, whereas stroke and bleeding
represented only a small subset of deaths. Interventions beyond anticoagulation are needed to further reduce mortality in AF.


Physician Burnout

Panagioti et al report a systematic review and meta-analysis of interventions directed towards preventing physician burnout. There is some evidence to support the existence of effective strategies and for an enhancement if strategies are organizational.


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Alcohol and Atrial Fibrillation

Voskoboinik et al review the relationship between alcohol and atrial fibrillation. This is an interesting and useful paper.


Area: Height Ratio in Patients With Proximal Ascending Aortic Dilation and Trileaflet Aortic Valve

Masri et al report an observational longitudinal study of patients with proximal dilation of the ascending aorta and trileaflet aortic valves. The authors report the relationship between ascending aortic area to height ration (as assessed by CT or MRI) and clinical outcome.



In patients with a dilated proximal ascending aorta
and trileaflet aortic valve, we aimed to assess (1) factors independently
associated with increased long-term mortality and (2) the incremental
prognostic utility of indexing aortic root to patient height.


We studied consecutive patients with a dilated aortic root (≥4
cm) that underwent echocardiography and gated contrast-enhanced thoracic
aortic computed tomography or magnetic resonance angiography between
2003 and 2007. A ratio of aortic root area over height was calculated
(cm2/m) on tomography, and a cutoff of 10 cm2/m was chosen as abnormal,
on the basis of previous reports. All-cause death was recorded.


The cohort comprised 771 patients (63 years [interquartile range,
53–71], 87% men, 85% hypertension, 51% hyperlipidemia, 56% smokers).
Inherited aortopathies, moderate to severe aortic regurgitation, and severe
aortic stenosis were seen in 7%, 18%, and 2%, whereas 91% and 54% were
on β-blockers and angiotensin-converting enzyme inhibitors, respectively.
Aortic root area/height ratio was ≥10 cm2/m in 24%. The Society of
Thoracic Surgeons score and right ventricular systolic pressure were 3.3±3
and 31±7 mm Hg, respectively. At 7.8 years (interquartile range, 6.6–8.9),
280 (36%) patients underwent aortic surgery (76% within 1 year) and 130
(17%) died (1% in-hospital postoperative mortality). A lower proportion of
patients in the surgical (versus nonsurgical) group died (13% versus 19%,
P<0.01). On multivariable Cox proportional hazard analysis, aortic root area/
height ratio (hazard ratio, 4.04; 95% confidence interval [CI], 2.69–6.231)
was associated with death, whereas aortic surgery (hazard ratio, 0.47;
95% CI, 0.27–0.81) was associated with improved survival (both P<0.01).
For longer-term mortality, the addition of aortic root area/height ratio ≥10
cm2/m to a clinical model (Society of Thoracic Surgeons score, inherited
aortopathies, hypertension, hyperlipidemia, medications, aortic regurgitation,
and right ventricular systolic pressure), increased the c-statistic from 0.57
(95% CI, 0.35–0.77) to 0.65 (95% CI, 0.52–0.73) and net reclassification
index from 0.17 (95% CI, 0.02–0.31) to 0.23 (95% CI, 0.04–0.34), both
P<0.01. Of the 327 patients with aortic root diameter between 4.5 and 5.5
cm, 44% had an abnormal aortic root area/height ratio, of which 78% died.


In patients with dilated aortic root and trileaflet aortic
valve, a ratio of aortic root area to height provides independent and
improved stratification for prediction of death.


Genetic variation of PCSK9 and Type 2 Diabetes Mellitus

Schmidt et al report a mendelian randomization study assessing the relationship between PCSK9 genetic variants and the risk of type 2 diabetes mellitus. Mendelian randomization is a technique that uses genetic variants (“randomized by nature”) that are plausibly related to a predictor of interest as instrumental variables in models with other confounders included. See concept diagram below:
The authors use this technique to quantify the association between PCSK9 genetic variants and type 2 diabetes mellitus.



Statin treatment and variants in the gene encoding HMG-CoA reductase are associated with reductions in both the concentration of LDL cholesterol and the risk of coronary heart disease, but also with modest hyperglycaemia, increased bodyweight, and modestly increased risk of type 2 diabetes, which in no way off sets their substantial benefits. We sought to investigate the associations of LDL cholesterol-lowering PCSK9 variants with type 2 diabetes and related biomarkers to gauge the likely effects of PCSK9 inhibitors on diabetes risk.


In this mendelian randomisation study, we used data from cohort studies, randomised controlled trials, case control studies, and genetic consortia to estimate associations of PCSK9 genetic variants with LDL cholesterol,
fasting blood glucose, HbA1c, fasting insulin, bodyweight, waist-to-hip ratio, BMI, and risk of type 2 diabetes, using a standardised analysis plan, meta-analyses, and weighted gene-centric scores.


Data were available for more than 550 000 individuals and 51 623 cases of type 2 diabetes. Combined analyses of four independent PCSK9 variants (rs11583680, rs11591147, rs2479409, and rs11206510) scaled to 1 mmol/L lower
LDL cholesterol showed associations with increased fasting glucose (0·09 mmol/L, 95% CI 0·02 to 0·15), bodyweight (1·03 kg, 0·24 to 1·82), waist-to-hip ratio (0·006, 0·003 to 0·010), and an odds ratio for type diabetes of 1·29 (1·11 to 1·50). Based on the collected data, we did not identify associations with HbA1c (0·03%, –0·01 to 0·08), fasting insulin (0·00%,
–0·06 to 0·07), and BMI (0·11 kg/m², –0·09 to 0·30).


PCSK9 variants associated with lower LDL cholesterol were also associated with circulating higher fasting glucose concentration, bodyweight, and waist-to-hip ratio, and an increased risk of type 2 diabetes. In trials of PCSK9 inhibitor drugs, investigators should carefully assess these safety outcomes and quantify the risks and benefits of PCSK9 inhibitor treatment, as was previously done for statins.