Pooled analysis from the ISAR-SWEET, SMART-2, ISAR-REACT and REACT-2 trials

The study included 4847 patients with coronary artery disease (CAD) undergoing PCI after pre-treatment with 600 mg of clopidogrel. The primary outcome was one-year mortality. The combined incidence of death, myocardial infarction and target lesion revascularisation was the secondary outcome.

Based on the median value of CRP (2.3 mg/l), patients were divided into two groups: the high-CRP group (n = 2448) and the low-CRP group (n = 2399). During one year, there were 141 deaths (5.8%) in the high-CRP group compared with 51 deaths (2.1%) in the low-CRP group (OR = 2.77, 95% CI 2.04 to 3.77; p<0.001). The incidence of major adverse cardiac events (MACE) was 28% in the high-CRP group compared with 25% in the low-CRP group (OR = 1.13, 95% CI 1.01 to 1.26; p = 0.034). The Cox proportional hazards model showed that high CRP was an independent predictor of one-year mortality (hazard ratio 2.20, 95% CI 1.54 to 3.15; p<0.001 for CRP level >2.3 mg/l vs CRP level <=2.3 mg/l). No significant interaction was observed between CRP level and abciximab regarding one-year mortality (p = 0.08) or MACE (p = 0.68).

In patients with CAD undergoing PCI after pretreatment with 600 mg of clopidogrel, baseline CRP level predicts one-year mortality and MACE. Abciximab therapy did not confer any particular beneficial effect in patients with a higher inflammatory burden.

Prospective cohort study.

University hospital.

119 patients (44% with ischaemic and 56% non-ischaemic aetiology) who underwent CRT.

Clinical follow-up for 39 (24) months.

Cardiovascular mortality, HF and cardiovascular hospitalisation were compared by Kaplan-Meier curves between the two groups, followed by Cox regression analysis for prognostic predictor(s).

41 (34%) patients died, in whom cardiovascular causes were identified in 32 (27%) patients. The ischaemic group had a higher cardiovascular mortality (log-rank ² = 4.293, p = 0.038) and cardiovascular hospitalisation (log-rank ² = 5.123, p = 0.024) when compared with the non-ischaemic group, though no difference was found in HF hospitalisation (log-rank ² = 0.019, p = 0.892). At three months, left ventricular reverse remodelling occurred in 52% of the ischaemic group and 55% of the non-ischaemic group (² = 0.128, p = 0.720). By Cox regression analysis, ischaemic aetiology and absence of reverse remodelling at three months were independent predictors of cardiovascular mortality (HR = 2.698, p = 0.032; HR = 3.541, p = 0.030) and cardiovascular hospitalisation (HR = 1.905, p = 0.015; HR = 2.361, p = 0.004). Furthermore, these two factors had an incremental value in predicting cardiovascular mortality when compared with either alone (left ventricular reverse remodelling, log-rank ² = 10.275 vs 6.311, p = 0.05; Ischaemic aetiology, log-rank ² = 10.275 vs 4.293, p<0.05).

Ischaemic aetiology of HF is an independent predictor of higher cardiovascular mortality and hospitalisation after CRT. This may implicate the progressive nature of coronary heart disease leading to a worse outcome despite similar short-term benefits of CRT.

In 14 patients with severe postinfarction heart failure, 93 (14)x106 autologous bone marrow cells were percutaneously injected in the infarction border zone. LV ejection fraction (LVEF), LV dyssynchrony and echocardiographic global strain were assessed at baseline and 3 months in patients and in a non-randomised control group of 10 patients with a history of infarction who developed heart failure and were treated medically.

No periprocedural complications occurred during bone marrow cell injection. At 3 months mean (SD) LVEF increased from 23 (8)% to 27 (9)% (p = 0.02) and global strain improved from –7.7 (4.7)% to –8.5 (4.9)% (p = 0.04). In patients with >=5% improvement in LVEF after bone marrow cell injection, global strain improved from –8.7 (4.6)% to –10.6 (4.5)% (p<0.01). Global strain remained unchanged in patients with <5% improvement in LVEF (–6.6 (4.9)% vs –6.4 (4.5)%, p = NS). The relation between the increase in LVEF and improvement in global strain was significant (r = 0.84, p<0.01). In patients with >=5% improvement in LVEF, LV dyssynchrony decreased from 173 (64) ms to 116 (64) ms (p = 0.01). In patients with <5% improvement in LVEF, LV dyssynchrony remained unchanged (155 (67) ms vs 177 (81) ms, p = NS). The correlation between improvement in LVEF and reduction in LV dyssynchrony was good (r = –0.77, p<0.01). In the control group, LVEF, global strain and LV dyssynchrony did not improve.

Bone marrow cell injection improves LVEF in patients with severe postinfarction heart failure. The improvement in LVEF was related to reduced LV dyssynchrony and increased global strain.

To assess the appropriateness of this practice by comparing CVD event rates of patients with and without prior CVD, over and above risk predicted by standard CVD risk factors.

Between 2002 and 2007 CVD risk assessments were generated using a web-based Framingham risk prediction algorithm in routine primary care. Individual risk profiles were subsequently linked to national hospitalisation and death records. Observed and predicted (Framingham) CVD risk were compared in patients with and without prior CVD.

35 760 patients were assessed including 10.4% with prior CVD. Of 1216 first CVD events during an average follow-up of 2.05 years, 42% occurred in those with prior CVD. Among those without prior CVD, the predicted Framingham five-year CVD risk was similar to the observed risk extrapolated to five years; in the highest Framingham risk band (>20% five-year risk), observed risk was 25.3%. Among those with prior CVD the observed risk extrapolated to five years rose from 21.7% in the lowest Framingham risk band (<5%) to 49% in the highest (>20%).

Patients with prior CVD have five-year CVD risks approximately 20% higher, in absolute terms than patients without prior CVD, after accounting for standard risk factors. Almost half the CVD events occurred in those with prior CVD. These patients should be the highest priority for intensive preventive management in primary care.

Case–control study.

Non-invasive Cardiology and Cardiac Surgery Department.

Eighty-nine patients with ATAA and varying degrees of FAR undergoing surgery, 40 age-matched patients with ATAA without aortic regurgitation and 20 normal control subjects.

Doppler and two-dimensional transoesophageal echocardiography.

Vena contracta (VC) of aortic regurgitant jet, diastolic tented area and coaptation height (CH) of aortic valve leaflets, aortic dimension indexes—Valsalva sinus, sinotubular junction (STJ), tubular tract, annulus (A), STJ/A ratio.

When VC was used, a wide range of FAR was seen (mean (SD) 5.59 (2.59) mm, ranging from 2 to 13 mm). Of the variables tested, the most strongly associated with FAR severity in multivariate analysis was diastolic leaflet tenting, measured as CH (R² = 0.69) (sensitivity 98%, specificity 95% using a cut-off value of CH >=1.1 cm). In turn, the diastolic leaflet tenting was strongly identified by the STJ/A ratio (sensitivity 87%, specificity 71% using a cut-off value of STJ/A >1.66).

The diastolic tenting of aortic leaflets is strongly related to FAR severity in patients with ATAA. The mismatch of STJ/A is significantly associated with diastolic leaflet tenting and its correlated valve regurgitation, independently of the actual ATAA dimension. These findings provide new insight into the mechanism of FAR arising from ATAA.

16 COPD patients (GOLD stages II–IV) underwent right heart catheterisation at rest and during exercise. In this group and eight age-matched controls resting and exercise right ventricular SV, end-diastolic volume (RVEDV) and end-systolic volume (RVESV) were assessed by magnetic resonance imaging (MRI). The exercise protocol during both measurements consisted of 3 minutes of cycling in supine position at 40% of maximal workload.

In all patients mean Ppa increased significantly in response to exercise (21 (8) vs 33 (11) mm Hg, p<0.01), whereas pulmonary vascular resistance did not change. In the patient group, RVEDV (129 (42) vs 135 (42) ml, p<0.05) and SV (63 (13) vs 69 (14) ml, p<0.05) increased significantly from rest to exercise, but RVESV and RV ejection fraction remained unaltered. In contrast, in healthy controls SV is augmented (81 (22) vs 101 (28) ml, p<0.05) by both increased RVEDV (123 (33) vs 134 134) ml, p<0.05) and reduced RVESV (37 (9) vs 27 (10) ml, p<0.05). Resting mean Ppa was related to SV during exercise (r = –0.59, p<0.02).

As a consequence of unaltered pulmonary vascular resistance to exercise in COPD patients, Ppa increases and SV response to exercise is limited and results from an increased preload only. Ppa at rest predicts exercise SV.

We review the effectiveness of right ventricular outflow tract (RVOT) stenting in the symptomatic young infant with TOF.

Clinical, echocardiographic, angiographic and haemodynamic data were reviewed for nine patients who underwent 11 RVOT stenting procedures from October 1994 to August 2007.

The pulmonary valve was deemed unsalvageable in all patients (median valve diameter 3.7 mm (range 2.7–4.2), Z-score –6.7 (range –9.7 to –5.4). RVOT stenting improved arterial oxygen saturation from a median of 73% (60–85%) to 94% (90–98%) (p = 0.008). Median Z-score for the left pulmonary artery increased from –4.9 (–7.8 to –2.4) before stent implantation to –1.5 (–4.2 to –0.2) (p = 0.02) before surgical repair. Median Z-score for the right pulmonary artery increased from –3.7 (–6.8 to –1.9) to –0.8 (–2.5 to 0.1) (p = 0.008). Median Nakata index increased from 56 mm²/m² (21–77) to 150 mm²/m² (123–231) (p = 0.008). There were no procedural complications. Six patients have undergone successful repair. There were no deaths.

In the symptomatic young infant with TOF, stenting of the RVOT provides a safe and effective management strategy, improving arterial oxygen saturation and encouraging pulmonary artery growth.