To determine the risk of new onset of HF and dysrhythmias among women after a prior MPS-affected pregnancy.

A retrospective cohort study was carried out of 1 130 764 individual women with a delivery in Ontario between 1992 and 2009, excluding those with cardiac or thyroid disease 1 year before delivery. The risk of a composite outcome of a hospitalisation for HF or an atrial or ventricular dysrhythmia was compared in women with and without MPS, starting 1 year after delivery.

75 242 individuals (6.7%) experienced a MPS. After a median duration of 7.8 years, the composite outcome occurred in 148 women with MPS (2.54 per 10 000 person-years) and 1062 women without MPS (1.28 per 10 000 person-years) (crude HR=2.00, 95% CI 1.68 to 2.38). The mean age at composite outcome was 37.8 years. The HR was 1.61 (95% CI 1.35 to 1.91) after adjustment for demographic characteristics, diabetes, obesity, dyslipidaemia and drug dependence or tobacco use, as well as coronary artery disease or thyroid disease >1 year after delivery. The adjusted HRs were minimally reduced by further adjusting for chronic hypertension (1.51, 95% CI 1.26 to 1.80) and were higher in women with MPS plus preterm delivery and poor fetal growth (2.42, 95% CI 1.25 to 4.67).

Women with MPS are at higher risk of premature HF and dysrhythmias, especially when perinatal morbidity is present.

112 patients with STEMI undergoing primary PCI were evaluated. LVR was defined as a ≥20% increase in the left ventricular end-diastolic volume at 6-month follow-up assessed using echocardiogram as compared with that at discharge. Blood samples were obtained for glucose, N-terminal pro-brain natriuretic peptide, troponin T (TnT), matrix metalloproteinase 9, procollagen type-I N-terminal propeptide and high-sensitivity C reactive protein (hs-CRP).

24 patients (21%) developed LVR. Higher levels of maximum TnT, and matrix metalloproteinase 9 and hs-CRP at discharge, were detected as independent risk factors for LVR (OR 1.310, p=0.03; OR 1001, p=0.04; OR 1.040, p=0.04, respectively). Both TnT and hs-CRP showed significant ability to distinguish patients who developed LVR from those who did not, being the values that yielded the greatest sensitivity and specificity as follows: TnT 7.0 μg/l (73%, 84%), hs-CRP 30 mg/l (59%, 85%).

Myocardial necrosis, as measured by released TnT, and inflammation state evident due to circulating levels of CRP are factors that may play a major role in the development of LVR following STEMI treated with primary PCI.

A systematic review was performed to better define subgroups amenable to appendage closure.

The English scientific literature was searched using Pubmed through to March 1, 2011. Reference lists of relevant and review articles were screened to retrieve additional articles.

Studies were only included if they described the location of thrombus in left atrium. Case reports and case series describing less than 10 thrombi were excluded.

Two reviewers independently extracted data and assessed quality of each study.

A total of 34 studies reporting on the location of atrial thrombus in patients with AF were included: 17 in valvular AF, 10 non-valvular AF and 8 in mixed valvular and non-valvular AF. Atrial thrombi were located outside the LAA in 56% (95% CI 53, 60) of valvular AF, 22% (95% CI 19, 25) in mixed cohorts and 11% (95% CI 6, 15) non-valvular AF. In non valvular AF, the studies with higher proportion of thrombi in the left atrial cavity had non-anticoagulated patients and a greater proportion of ventricular dysfunction and history of stroke.

The location of atrial thrombus in patients with AF is dependent on the underlying substrate. In valvular AF, more than half the thrombi are located in the left atrial cavity. In the non-valvular AF group, a smaller proportion of thrombi were located outside the appendage. However, in certain subgroups (ie. non anti-coagulated, left ventricular dysfunction or prior stroke) the chances of left atrial cavity thrombus are higher.

To conduct a prospective observational longitudinal study in order to measure the impact of cigarette smoking on on-clopidogrel platelet reactivity (OPR).

From the prospective CROSS-VERIFY cohort, 810 subjects with repeated measurement of OPR at least 1 month apart were analysed. With smoking status ascertained at two time points, baseline and follow-up, study subjects were categorised into never smokers (n=628), smoking quitters (n=77) and persistent smokers (n=105). Dependent variables included OPR measured by the VerifyNow assay and the percentage of subjects with high OPR (HOPR).

At baseline, current smokers showed significantly lower OPR compared with never smokers, with no significant differences in OPR between future quitters and future persistent smokers within current smokers. While the OPR of never smokers and persistent smokers did not change significantly during the follow-up, the mean OPR of quitters increased significantly by 19 P2Y12 reaction units (p=0.013). The frequency of HOPR showed similar results, with an 8–10% increase in smoking quitters in contrast to no significant changes in never and persistent smokers. Both mean OPR and the frequency of HOPR showed a linear inverse relationship with the amount of smoking.

Enhanced clopidogrel response in smokers is reversed after smoking discontinuation, suggesting a causal relationship in addition to the previously reported association between smoking and enhanced clopidogrel response.

Clinical study.

Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.

Twenty-four patients with a single HCM-causing mutation D175N in the α-tropomyosin gene and 17 control subjects.

Endomyocardial biopsy samples taken from the patients with HCM were compared with matched myocardial autopsy specimens. Levels of high-sensitivity C-reactive protein (hsCRP) and proinflammatory cytokines were measured in patients and controls. Myocardial late gadolinium enhancement (LGE) in cardiac MRI (CMRI) was detected.

Endomyocardial samples in patients with HCM showed variable myocyte hypertrophy and size heterogeneity, myofibre disarray, fibrosis, inflammatory cell infiltration and nuclear factor kappa B (NF-B) activation. Levels of hsCRP and interleukins (IL-1β, IL-1RA, IL-6, IL-10) were significantly higher in patients with HCM than in control subjects. In patients with HCM, there was a significant association between the degree of myocardial inflammatory cell infiltration, fibrosis in histopathological samples and myocardial LGE in CMRI. Levels of hsCRP were significantly associated with histopathological myocardial fibrosis. hsCRP, tumour necrosis factor α and IL-1RA levels had significant correlations with LGE in CMRI.

A variable myocardial and systemic inflammatory response was demonstrated in patients with HCM attributable to an identified sarcometric mutation. Inflammatory response was associated with myocardial fibrosis, suggesting that myocardial fibrosis in HCM is an active process modified by an inflammatory response.

Recurrent pericarditis prevention is a major management goal that may reduce morbidity and management costs. Although empiric anti-inflammatory therapy is considered the mainstay of treatment, no specific drug has been proven to be efficacious for prevention but colchicine.

Controlled clinical studies were searched in several databases and were included provided they focused on the pharmacologic primary or secondary prevention of pericarditis. We performed a meta-analysis including studies primary outcome, adverse events, and drug withdrawal.

From the initial sample of 127 citations, five controlled clinical trials were finally included (795 patients): three studies were double-blind randomised controlled trials, and two studies were open-label randomised controlled trials. Trials followed patients for a mean of 13 months. Meta-analytic pooling showed that colchicine use was associated with a reduced risk of pericarditis during follow-up (RR=0.40, 95% CI 0.30 to 0.54, p for effect <0.001, p for heterogeneity = 0.95, I²=0%) either for primary or secondary prevention without a significant higher risk of adverse events compared with placebo (RR=1.22, 95% CI 0.71 to 2.10, p for effect 0.48, p for heterogeneity = 0.44, I²=0%), but more cases of drug withdrawals (RR=1.85, 95% CI 1.04 to 3.29, p for effect 0.04, p for heterogeneity = 0.42, I²=0%). Gastrointestinal intolerance is the most frequent side effect (mean incidence 8%), but no severe adverse events were recorded.

Available evidence suggests that colchicine is safe and efficacious for the primary and secondary prevention of pericarditis.

To summarise the evidence about the effectiveness of LUCAS.

Searches of 4 electronic databases, reference lists of included studies, review articles, clinical guidelines, and the manufacturer's web site. No language restrictions were applied. Date of last search: September 2011.

All studies, of any design, comparing mechanical chest compression using LUCAS with manual chest compression, with human or animal subjects. Studies published only as abstracts were included. Manikin studies, and case reports or case series, were excluded.

Data were extracted on study methodology and outcomes, including return of spontaneous circulation, survival, injuries caused by resuscitation, and physiological parameters.

22 papers reporting 16 separate studies were included. There was one randomised trial, nine cohort studies, 2 before/after studies and 4 animal studies. No meta-analyses were performed because of high risk of bias and heterogeneity in the study designs. Animal studies suggested an advantage to LUCAS in terms of physiological parameters, but human studies did not suggest an advantage in ROSC or survival. Existing evidence is low quality because most studies were small and many were poorly reported.

There is insufficient evidence to make any recommendations for clinical practice. Large scale, high quality randomised trials of LUCAS are needed. Studies that have so far been published only as abstracts should be reported fully.

Abciximab represents a cornerstone in the treatment of STEMI patients undergoing primary PCI. Intracoronary abciximab bolus administration has been proposed as an alternative strategy to the standard intravenous route. However, whether intracoronary abciximab effectively improves clinical outcomes compared with standard route remains unknown.

Individual data of 1198 patients enrolled in five trials were entered into the pooled analysis. The primary endpoint of the study was the occurrence of all-cause death and reinfarction at 30-day follow-up. Secondary endpoints were all-cause death, reinfarction and target-vessel revascularisation (TVR).

No significant heterogeneity was found across trials. Compared with the intravenous route, intracoronary abciximab administration significantly reduced the risk of the composite of death and reinfarction (HR 0.52, 95% CI 0.29 to 0.94; p=0.03), death (HR 0.44, 95% CI 0.20 to 0.95; p=0.04) and TVR (HR 0.53, 95% CI 0.29 to 0.99; p=0.045), without a significant impact on the risk of reinfarction (HR 0.54, 95% CI 0.24 to 1.21; p=0.13). However, after correction for baseline differences, only the composite of death/reinfarction and death remained significant.

In STEMI patients undergoing primary PCI, intracoronary abciximab administration, when compared with the intravenous standard route, can improve short-term clinical outcomes mainly by reducing the risk of death.

Serum calcium and phosphate were measured in a cohort of initially 1206 patients undergoing a 3 week rehabilitation programme after an acute cardiovascular event and subsequently being followed-up for 8 years. Multivariate Cox regression was employed to assess the association of quartiles and continuous levels of calcium and phosphate with secondary cardiovascular events and all-cause mortality.

No significant risk elevations were observed for secondary cardiovascular event incidence in models adjusted for a variety of potential confounders. High calcium levels, however, were strongly associated with mortality risk in adjusted models (HR_Q4vsQ1=2.39 (1.22 to 4.66)). In additional multivariable analyses, the calcium/albumin ratio was predictive for all-cause mortality (HR_Q4vsQ1=2.66 (1.35 to 5.22)) and marginally predictive for cardiovascular event incidence (HR_Q4vsQ1=1.74 (1.00 to 3.05)).

Calcium and the ratio of calcium with albumin, its major binding protein, were strongly associated with all-cause mortality among patients with coronary heart disease. The underlying mechanisms and the clinical implications of these findings deserve further study.

Prospective cross-sectional study in tertiary health care setting.

Thirty-six CoAs (age 16±1 years; neonatal surgery only: n=16; surgery and/or stent implantation: n=20) and 37 age-matched controls were examined by very-high resolution ultrasound, echocardiography and applanation tonometry.

CoA was associated with increased right arm systolic BP (p<0.001), intima-media thickness (IMT) in the common carotid (p<0.001), right brachial (p<0.05) and radial (p<0.05) arteries and ascending aortic stiffness (p<0.05). Carotid IMT correlated positively with age at first intervention (r=0.36, p<0.05). With left subclavian flap type repair, left arm systolic BP (p<0.001) and left brachial (p<0.001), radial (p<0.001) and ulnar (p<0.05) arterial IMTs were all reduced. When adjusted for BP, body mass index, age and gender, only carotid IMT (p<0.001) and LV-mass (p=0.013) of stented patients, as well as left arm arterial IMTs (p<0.01) in subclavian flap type repair patients remained different from controls. The significant associations of stented patients disappeared after adjustment for later patient age at intervention (median 8.7 vs 0.03 years, p<0.001). Residual arm-leg BP gradients correlated positively with carotid and brachial IMT.

CoA repair in early childhood is associated with increased preductal arterial IMT, LV mass and ascending aortic stiffness in adolescents. The more pronounced cardiovascular abnormalities after CoA stent implantation are likely related to the older patient age at the time of intervention.