Analyses were performed on 5532 patients with ST-elevation myocardial infarction from the Assessment of Pexelizumab in Acute Myocardial Infarction trial. The primary objective of this analysis was to ascertain the relation between red blood cell transfusion and 90-day mortality in patients with recent myocardial infarction. We initially determined the baseline and in-hospital predictors of transfusion (multivariable logistic regressions) and subsequently assessed the association between transfusion and mortality using a series of Cox proportional hazards regression combined to a landmark analyses. A total of 213 patients (3.9%) received a transfusion. Transfusion remained significantly associated with mortality [hazards ratio = 2.16 (1.20–3.88)], despite adjustment for baseline characteristics, in-hospital co-interventions, and for propensity of receiving a transfusion. Among patients who survived to hospital discharge, however, the hazard of death was not different in patients treated with transfusion.

Transfusion is associated with 90-day mortality in acute myocardial infarction treated with primary percutaneous coronary intervention. Although transfusion may be causally related to mortality, it is likely that at least part of the association is due to confounding. This association illustrates the complex relationship between transfusion, bleeding, and mortality and underscores the need for further research to understand the relationship between transfusion and clinical outcomes.

Patients with CAD were identified in the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease (APPROACH) registry between January 2001 and March 2006. Analyses were conducted separately by treatment strategy [medical management only, percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG)]. Patients were grouped according to six BMI categories. Multivariable-adjusted hazard ratios (HRs) for mortality were calculated using the Cox regression with the referent group for all analyses being normal BMI (18.5–24.9 kg/m²). The cohort included 31 021 patients with a median follow-up time of 46 months. In the medically managed only group, BMIs of 25.0–29.9 and 30.0–34.9 kg/m² were associated with significantly lower mortality compared with normal BMI patients (adjusted HR 0.72; 95% CI 0.63–0.83 and adjusted HR 0.82; 95% CI 0.69.0–0.98, respectively). In the CABG group, BMI of 30.0–34.9 kg/m² had the lowest risk of mortality (adjusted HR 0.75; 95% CI 0.61–0.94), whereas in the PCI group, BMI of 35.0–39.9 kg/m² had the lowest risk of mortality (adjusted HR 0.65; 95% CI 0.47–0.90). Patients who were overweight or have mild or moderate obesity were also more likely to undergo revascularization procedures compared with those with normal BMI, despite having lower risk coronary anatomy.

A paradoxical association between BMI and survival exists in patients with established CAD irrespective of treatment strategy. Patients with obesity may be presenting earlier and receiving more aggressive treatment compared with those with normal BMI.

Seventy-six HCM mutation carriers from 32 families identified by predictive DNA testing underwent cardiac evaluation including history, examination, electrocardiography, Doppler echocardiography, exercise testing, and 24 h Holter monitoring. The published diagnostic criteria for HCM in adult members of affected families were used to diagnose HCM. Thirty-three (43%) men and 43 (57%) women with a mean age of 42 years (range 16–79) were examined; in 31 (41%) HCM was diagnosed. Disease penetrance was age related and men were more often affected than women (P = 0.04). Myosin Binding Protein C (MYBPC3) mutation carriers were affected at higher age than Myosin Heavy Chain (MYH7) mutation carriers (P = 0.01). Risk factors for SCD were present in affected and unaffected carriers.

Hypertrophic cardiomyopathy was diagnosed in 41% of carriers. Disease penetrance was age dependent, warranting repeated cardiologic evaluation. The MYBPC3 mutation carriers were affected at higher age than MYH7 mutation carriers. Risk factors for SCD were present in carriers with and without HCM. Follow-up studies are necessary to evaluate the effectiveness of risk stratification for SCD in this population.

This was a cohort study, with prospective data collection. We studied 1380 patients, referred to a cardiomyopathy clinic in London, UK [mean age 42 years (SD 15); 62% male; mean follow-up 54 (SD 49) months]. Patients underwent two-dimensional and Doppler echocardiography, upright exercise testing, and Holter monitoring. Twenty-seven patients [mean age 40 (SD 14) years (18–64); 22 (81.5%) male] had NSVT (24) or ventricular fibrillation (VF) (3) during exercise. During exercise, 13 (54.2%) had more than one run of NSVT (maximum 5) with a mean heart rate of 221 (SD 48) b.p.m. Patients with exercise NSVT/VF had more severe hypertrophy (22.6 vs. 19.5 mm, P = 0.009) and larger left atria (47.3 vs. 43.7 mm, P = 0.03). Male gender was significantly associated with exercise NSVT/VF [22 (81.5%) vs. 832 (61.5%), P = 0.03]. Eight (29.6%) of the exercise NSVT/VF patients died or had a cardiac event (SD/ICD discharge/transplant) compared with 150 (11.1%) patients without exercise NSVT/VF, P = 0.008. Patients with NSVT/VF had a 3.73-fold increase in risk of SD/ICD discharge (HR 95% CI: 1.61–8.63, P = 0.002). Exercise NSVT alone was associated with a 2.82-fold increased risk (HR 95% CI: 1.02–7.75, P = 0.049). In multivariable analysis with other risk markers, exercise NSVT/VF (but not NSVT alone) was independently associated with an increased risk of SD/ICD [HR 3.14 (95% CI: 1.29–7.61, P = 0.01)].

Ventricular arrhythmia during symptom limited exercise is rare in patients with hypertrophic cardiomyopathy, but is associated with an increased risk of sudden cardiac death.

The study was designed as a prospective randomized cross-over trial with each physician completing a 24 h (h) OCD and a 24 h control period including a regular 8 h non-OCD. Thirty healthy physicians with a median age of 33.5 years (range 29.0–45.0) were analysed. Twenty-four hours ECG and BP monitoring were performed and participants were instructed to fill out an event diary and perform a 24 h urine collection. Furthermore, blood was drawn before and after OCD and control day. Twenty-four hours ECG showed a higher rate of ventricular premature beats (VPB) during early morning hours (VPB 0–6 h, 0.5 vs. 0.0, P = 0.047) and increased low-frequency normalized units (29.3 vs. 25.5, P = 0.050) during night shift when compared with respective control night at home. During OCD, BP monitoring revealed a greater diastolic BP throughout 24 h (83.5 vs. 80.2 mmHg, P = 0.025) as well as during night-time (75.4 vs. 73.0, P = 0.028) associated with a higher rate of systolic BP more than 125 mmHg during sleep time. Tumour necrosis factor alpha concentrations increased significantly during night shift (0.76 vs. 0.05 pg/mL, P = 0.045). Urinary noradrenaline excretion was greater during OCD when compared with control day (46.0 vs. 36.0 µg/24 h, P = 0.007).

Our results highlight the association of OCD with an increased risk profile for cardiovascular disease. In addition to the acute effects observed, frequent night-calls over a longer period possibly elicit sustained alterations in cardiovascular homeostasis.

A prospective study included patients without previous diagnosis of diabetes that were referred for PCI between November 2005 and May 2006. Major cardiac events were registered after admission and during 12 months of follow-up, and oral glucose tolerance was tested at 15 days after hospital discharge. Six hundred and sixty-two consecutive patients were referred to our hospital for PCI. The distribution of the glycometabolic state of the entire population was (95% CI): known diabetes 28.8% (25.2–32.6), newly detected diabetes 16.2% (13.1–19.8), impaired glucose tolerance 24.5% (20.8–28.5), impaired fasting glucose 1% (0.4–2.4), and normal glucose regulation 29.5% (25.5–33.7). In a multivariable analysis, the presence of newly detected diabetes was not an independent predictor of cardiac events after 1 year of follow-up.

The prevalence of diabetes in patients who underwent PCI was very high (45%), 35% of which was patients with newly detected diabetes. In our series newly detected diabetes was not an independent predictor of outcome at 12 months. Nevertheless, this finding requires independent confirmation in other series to draw general conclusions on the whole spectrum of percutaneous interventions.

In 432 patients (59% male, age 58 ± 11 years) referred for cardiac evaluation owing to suspected coronary artery disease (CAD), CS and 64-slice MSCTA were performed. The following events were combined in a composite endpoint: all-cause mortality, non-fatal infarction, and unstable angina requiring revascularization. CS was 0 in 147 (34%) patients, CS 1–99 was present in 122 (28%), CS 100–399 in 75 (17%), CS 400–999 in 56 (13%), and CS ≥ 1000 in 32 (7%). MSCTA was normal in 133 (31%) patients, MSCTA 30–50% stenosis was observed in 190 (44%), and MSCTA ≥50% stenosis in 109 (25%). During follow-up [median 670 days (25th–75th percentile: 418–895)], an event occurred in 21 patients (4.9%). After multivariate correction for CS, MSCTA ≥ 50% stenosis, the number of diseased segments, obstructive segments, and non-calcified plaques were independent predictors with an incremental prognostic value to CS.

MSCTA provides additional information to CS regarding stenosis severity and plaque composition. This additional information was shown to translate into incremental prognostic value over CS.