First, anti-cTnI and anti-cTnT antibody titres were measured in sera from 272 patients with dilated- (DCM) and 185 with ischaemic- (ICM) cardiomyopathy. Secondly, 108 patients with acute myocardial infarction (AMI) were included for a follow-up study. Heart characteristics were determined by magnetic resonance imaging 4 days and 6–9 months after AMI. Altogether in 7.0% of patients with DCM and in 9.2% with ICM, an anti-cTnI IgG antibody titre ≥1:160 was measured. In contrast, only in 1.7% of patients with DCM and in 0.5% with ICM, an anti-cTnT IgG antibody titre ≥1:160 was detected. Ten out of 108 patients included in the follow-up study were tested positive for cTnI-Ab with IgG Ab titres ≥1:160. TnI-Ab negative patients showed a significant increase in left ventricular ejection fraction (LVEF) and stroke volume 6–9 months after AMI. In contrast, there was no significant increase in LVEF and stroke volume in TnI-Ab positive patients.

We demonstrate for the first time that the prevalence of cTnI-Abs in patients with AMI has an impact on the improvement of the LVEF over a study period of 6–9 months.

Sixty patients with angiographically documented CAD and a history of arterial hypertension were randomized in a double-blinded fashion to pravastatin (PRAV, 40 mg/day, n = 30) or PRAV plus irbesartan (PRAV+IRB, 40 mg/day+300 mg/day, n = 30) and were treated for 3 months. Blood pressure (BP) and cholesterol fractions were determined at baseline and after 3 months. SPLA₂ activity as primary endpoint, sPLA₂-IIA protein, oxLDL levels, and high-sensitivity (hs)-C-reactive protein were measured by an enzyme-linked immunabsorbent assay. In both treatment groups, systolic BP levels and circulating HDL and LDL levels were reduced to the same extent. The combined treatment of PRAV+IRB significantly decreased sPLA₂-IIA activity and sPLA₂-IIA-protein concentration compared with PRAV treatment alone (P < 0.05). In addition, PRAV+IRB significantly reduced oxLDL levels compared with PRAV treatment alone (P < 0.05). This effect was independent of changes in LDL cholesterol levels.

These findings are consistent with the notion that the combined treatment of pravastatin with irbesartan reduced sPLA₂-IIA-activity, sPLA₂-IIA-protein concentration, and oxLDL in patients with CAD suggesting a novel anti-atherogenic effect by combining AT₁-receptor blockade with statin treatment.

We used data from the PRIME Study, a prospective cohort of 9758 asymptomatic middle-aged men recruited in Northern Ireland and France between 1991 and 1993. A nested case–control study was established with the baseline plasma sample of 269 incident cases and 538 matched controls. Odds ratios (ORs) for SA and ACS were estimated by conditional logistic regression analysis. After 5 years of follow-up, 107 incident SA and 162 ACS cases were validated. After adjustment for traditional risk factors, higher circulating levels of hs-CRP, ICAM1, interleukin 6 and interleukin 18 were equally predictive of SA and ACS (all P-values of OR comparison >0.05). In contrast, elevated levels of fibrinogen, von Willebrand factor, and possibly higher level of D-dimers and lower level of tissue factor pathway inhibitor were associated with ACS only. The comparison of the ORs showed a statistically significant difference for von Willebrand factor only [OR_{4th vs. 1st quartile} = 2.99 (1.49–6.02) for ACS vs. 0.80 (0.33–1.94) for SA; P_{z test} = 0.02].

This is the first population-based study suggesting that higher levels of circulating haemostatic markers and of von Willebrand factor, in particular, are significantly more predictive of incident ACS than SA.

Patients with de novo coronary lesions in native vessels were randomly assigned to receive a BP stent, a PF stent or a PP stent. The primary endpoint was in-stent late lumen loss at follow-up angiogram.

A total of 605 patients were enrolled: 202 patients received BP stents, 202 were treated with PP stents, and 201 received PF stents. Repeat angiography was available for 492 patients (81.3%). Mean late lumen loss at 6–8-month angiographic follow-up was 0.17 ± 0.45 mm in the BP stent group, 0.23 ± 0.46 mm in the PP cohort, and 0.47 ± 0.56 mm in the PF stent group. The BP stent met pre-specified criteria for non-inferiority (P < 0.001), whereas the PF stent did not (P = 0.94). There were no differences in safety outcomes.

Both BP and PF stents have a 1-year safety profile similar to that of the PP stent. Whereas the PF stent provided an inferior efficacy, the BP stent is at least as effective as the PP stent in terms of anti-restenotic efficacy.

OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) collected data on 48 612 patients from 259 hospitals. Characteristics, treatments, and outcomes were compared for current/recent smokers vs. those without current/recent smoking, and multivariable regression analyses with adjustment for hospital clustering were performed. There were 7743 (15.9%) smokers, 39 126 (80.5%) non-smokers, and 1743 (3.6%) missing. Smokers were younger, had similar renal function, but lower ejection fraction. The risk of in-hospital mortality was less in smokers (2.3 vs. 3.9%, P < 0.001). After extensive covariate adjustment, smokers still had lower in-hospital mortality risk OR (odds ratio) 0.70, 95% CI (confidence interval) 0.56–0.88, P = 0.002. Post-discharge, smokers (n = 998) had similar mortality risk (6.7 vs. 8.4%, P = 0.29) compared with those without current/recent smoking.

Smokers hospitalized with HF had lower risk adjusted in-hospital mortality and similar early post-discharge mortality compared with non-smokers. The residual association of smoking and better prognosis, the ‘smoker’s paradox’, was not fully explained by measured covariates.

We monitored 266 patients with anterior MI. Echocardiographic studies were performed at hospital discharge, at 3 months, and at 1 year following hospitalization for MI. A clinical follow-up examination was performed after 3 years. Left ventricular remodelling was documented by an increase in LV end-diastolic volume after 1 year. Left ventricular end-diastolic and end-systolic volumes did not differ with age for all time points studied. Left ventricular remodelling was observed in 31, 26, 34, and 34% of patients <48, 48–57, 58–71, and >71 years of age, respectively. The 3 year heart-failure hospitalization rates were 1.9, 1.5, 11.0, and 20.3% for patients <48, 48–57, 58–71, and >71 years of age, respectively. Hospitalization for heart failure was more frequent in older patients.

We found that age was a major determinant of subsequent re-hospitalization for heart failure. However, we found no significant association between age and the LV remodelling process.

Thirty-five patients underwent cine and delayed contrast-enhanced cardiovascular magnetic resonance (deCMR) for the quantitative assessment of regional and global LV functions and segmental extent of hyperenhancement (SEH). Function was assessed 1 month before and 3, 6, and 24 ± 12 months after revascularization, and temporal changes were related to baseline extent of hyperenhancement. The likelihood of functional improvement was inversely related to the SEH during the entire follow-up: at the end of the study period, segments with 1–25, 26–50, 51–75, and 76–100% SEH were 2, 5, 11, and 86 times, respectively, less likely to have functional improvement than segments without hyperenhancement (multilevel analysis, P < 0.001). Although improvement continued over the whole study period in all SEH groups, the time course was significantly more delayed in segments with more extensive hyperenhancement at baseline (multilevel analysis, P < 0.001).

In patients with chronic ischaemic LV dysfunction, improvement of dysfunctional but viable myocardium can be considerably delayed. Both the likelihood and the time course of long-term functional improvement are related to the baseline amount of scar, as visualized by deCMR.

In total, 340 consecutive patients (182 men, 55 ± 12 years) without a history of CAD who were referred for MSCT angiography were included in the study. Based on patient characteristics and the referral reason for MSCT angiography, patients were classified as having a low, intermediate, or high pre-test likelihood of CAD. Patients were evaluated for the presence of coronary artery calcium as well as the presence of atherosclerosis. Overall, 157 (46%) patients did not have coronary artery calcium and 133 (40%) patients had a completely normal MSCT angiogram. In 58% of the patients with low pre-test likelihood, no coronary atherosclerosis was observed when compared with 33 and 17% of the patients with intermediate and high pre-test likelihood, respectively.

MSCT ruled out coronary atherosclerosis in 40–46% of patients without known CAD who were referred for MSCT. Accordingly, in patients with low-to-intermediate pre-test likelihood, MSCT may be an attractive modality to exclude coronary atherosclerosis and may prevent unnecessary additional functional testing or invasive angiography.

In 480 subjects enrolled in a family-based population study (50.5% women; mean age, 50.5 years; 37.2% hypertensive), we measured: (i) end-systolic longitudinal strain and peak-systolic SR from the basal portion of the LV inferior and inferolateral free walls; (ii) radial deformation of the LV inferolateral wall. Longitudinal (mean, 22.9%) and radial (59.2%) strain and longitudinal (1.31 s^–1) and radial (3.40 s^–1) SR decreased with age (P ≤ 0.007). Longitudinal and radial strain independently decreased (P ≤ 0.006) with relative wall thickness (RWT), longitudinal strain with the waist-to-hip ratio, and radial strain with body weight. In contrast, LV ejection fraction increased (P ≤ 0.0001) with age and RWT. Longitudinal and radial stain rate increased with heart rate (P ≤ 0.05). In healthy subgroup (n = 236), the fifth percentiles were 18.4 and 44.3%, and 0.99 and 2.43 s^–1, for longitudinal and radial strain and SR, respectively.

We explored the early signs of LV systolic dysfunction in a general population, using tissue Doppler imaging technique. LV strain and SR decrease with age, body weight, central obesity, and RWT. Our current study resulted in the proposal for diagnostic thresholds for strain and SR, based on a healthy subgroup recruited via random sampling of the population.

The impact of recent and long-term fish consumption and EPA+DHA intake on (sudden) coronary death was investigated in the Zutphen Study, a cohort of 1373 men born between 1900 and 1920, and examined repeatedly between 1960 and 2000. Hazard ratios were obtained from time-dependent Cox regression models. The associations between long-term fish consumption, EPA+DHA intake, and (sudden) coronary death were stronger than those of recent consumption. Long-term fish consumption was inversely associated (borderline significant) with coronary heart disease (CHD) death; however, the strength of the association decreased from age 50 [HR: 0.32 (95% CI: 0.13–0.80)] until age 80 [HR: 1.34 (0.58–3.12)]. For men with a daily EPA+DHA intake from fish below 250 mg compared with no intake, CHD death risk was reduced to the same extent as for men with a daily intake above 250 mg (P-value for trend: 0.27). Moreover, long-term fatty-fish consumption lowered the risk of sudden coronary death [HR: 0.46 (0.27–0.78)].

The strength of the association between long-term fish consumption and CHD death decreased with increasing age. Fatty-fish consumption lowered sudden coronary death risk. There was no clear dose–response relationship between EPA+DHA intake and (sudden) coronary death.

RCTs of HRT were identified. Event rates for cerebrovascular disease [stroke, TIA (transient ischaemic attack)], CHD (myocardial infarction, unstable angina, sudden cardiac death), and VTE (pulmonary embolism, deep vein thrombosis) were analysed. Sensitivity analyses were performed by type of HRT (mono vs. dual) and subject age. 31 trials (44 113 subjects) were identified. HRT was associated with increases in stroke (odds ratio, OR, 1.32, 95% confidence intervals, CI, 1.14–1.53) and VTE (OR 2.05, 95% CI 1.44–2.92). In contrast, CHD events were not increased (OR 1.02, 95% CI 0.90–1.11). Ordinal analyses confirmed that stroke severity was increased with HRT (OR 1.31, 95% CI 1.12–1.54). Although most trials included older subjects, age did not significantly affect risk. The addition of progesterone to oestrogen doubled the risk of VTE.

HRT is associated with an increased risk of stroke, stroke severity, and VTE, but not of CHD events. Although most trials studied older patients, increased risk was not related to age. Combined HRT increases the risk of VTE compared with oestrogen monotherapy.

The angioplasty was performed in 99 consecutive patients aged 36 days to 32.6 years (median 268 days). Recoarctation to descending aorta diameter ratio increased from 0.44 (0.35/0.50) to 0.66 (0.57/0.77), P < 0.001. Systolic gradient was reduced from 34.0 (26.0/44.75) to 15.0 (8.25/27.0) mmHg, P < 0.001. In seven patients (7.1%) the procedure was ineffective. One patient (1%) with heart failure died within 24 h after a successful angioplasty and in another (1%) an intimal abruption necessitated surgical revision. The follow-up ranged up to 20.7 years (median 8.1 years). Actuarial probability of survival 20.7 years after the procedure was 0.91, and of reintervention-free survival was 0.44. Older age at the angioplasty was associated with a higher incidence of reinterventions (hazard ratio 1.057; 95% confidence interval 1.012–1.103; P = 0.010). The type of surgery and the recoarctation anatomy did not influence the outcome. In 69 patients aneurysm formation was studied by high-sensitive methods with only one positive finding per 462 patient-years.

Angioplasty is safe and effective regardless of the type of surgery used and the recoarctation anatomy. Older age at the angioplasty is associated with a higher incidence of reinterventions.

Various models of AS (plates and biological valves) were studied in an in vitro circuit. Valve areas were calculated with the Doppler continuity equation and the Gorlin formula. Systolic systemic pressures were increased from 80 to 200 mmHg while flow rates were maintained constant. In addition, a computational fluid dynamics (CFD) model was constructed to test the effect of systemic pressures on pressure gradient and valve area estimates.

When systemic pressure was raised, pressure gradients as well as valve areas did not change (mean difference 3.4 ± 1.8 mmHg, range 0.4–6.8 mmHg; mean difference 0.01 ± 0.03 cm², range –0.02 to 0.05 cm²). By multivariable analysis, neither valve area nor pressure gradient were independently affected by systemic pressure. In addition, CFD analysis revealed no effect of systemic pressure on pressure gradient and valve area.

Our results suggest that blood pressure itself does not directly affect pressure gradients and valve area estimates in AS. Thus, when observed in vivo, these changes are most likely due to afterload-related variations of ejection fraction and, therefore, flow rate.