To investigate the influence of CCBs on clopidogrel-mediated platelet inhibition.

Adenosine-5-diphosphate (ADP)-inducible platelet reactivity was assessed by light transmission aggregometry (LTA) and the VerifyNow P2Y12 assay in 162 patients after percutaneous intervention with stent implantation. Results in the fourth quartiles of both assays were considered as high on-treatment residual ADP-inducible platelet reactivity.

Patients with concomitant CCB therapy showed a significantly higher on-treatment platelet reactivity than patients without CCB medication (p=0.001 for both assays). Further, high on-treatment residual ADP-inducible platelet reactivity was significantly more common among patients currently taking CCBs (p=0.001 for LTA and p=0.004 for the VerifyNow P2Y12 assay). A multivariate regression analysis confirmed CCB therapy as an independent predictor of reduced clopidogrel-mediated platelet inhibition (p=0.006 for LTA and p=0.004 for the VerifyNow P2Y12 assay).

CCBs decrease clopidogrel-mediated platelet inhibition in patients undergoing angioplasty and stenting for cardiovascular disease.

Primary PCI with the Proxis system improves immediate microvascular flow post-procedure as measured by ST-segment resolution, which could result in better outcomes.

The ancillary CMR study included 206 STEMI patients who were enrolled in the PRoximal Embolic Protection in Acute myocardial infarction and Resolution of ST-Elevation (PREPARE) trial. CMR imaging was assessed between 4 and 6 months after the index procedure.

There were no significant differences in final infarct size (6.1 g/m² vs 6.3 g/m², p = 0.78) and left ventricular ejection fraction (50% vs 50%, p = 0.46) between both groups. Also, systolic wall thickening in the infarct area (44% vs 45%, p = 0.93) or the extent of transmural segments (8.3% of segments vs 8.3% of segments, p = 0.60) showed no significant differences. The incidence of major adverse cardiac and cerebral events at 6 months was similar in the Proxis and control group (8% vs 10%, respectively, p = 0.43).

Primary PCI with combined proximal embolic protection and thrombus aspiration in STEMI patients did not result in significant differences in final infarct size or left ventricular function at follow-up CMR. In addition, there was no difference in the incidence of major adverse cardiac and cerebral events at 6 months.

ISRCTN71104460.

OCT was used to measure the fibrous cap thickness of coronary artery atherosclerotic plaques in patients with acute myocardial infarction (AMI), unstable angina pectoris (UAP) and stable angina pectoris (SAP). Plasma levels of inflammatory factors including highly sensitive C-reactive protein (hs-CRP), IL-18 and tumour necrosis factor alpha (TNF) were detected by ELISA, and peripheral white blood cell (WBC) counts were performed. The results demonstrated that the plasma levels of inflammatory factors and WBC count were correlated inversely with fibrous cap thickness (r = –0.775 for hs-CRP, r = –0.593 for IL-18, r = –0.60 for TNF and r = –0.356 for WBC count). Patients with cap thickness less than 65 µm (defined to be thin cap fibroatheromas; TCFA) had higher plasma levels of inflammatory factors as well as WBC counts than those with thicker fibrous caps. Receiver operator characteristic (ROC) curves for hs-CRP, IL-18, TNF and WBC count, which displayed the capability of prediction about TCFA, showed the area under the curves were 0.95, 0.86, 0.79 and 0.70 (p<0.05), respectively. ROC curve analysis confirmed that an hs-CRP cut-off at 1.66 mg/l would detect TCFA with a sensitivity of 96% and a specificity of 90%, and was the strongest independent predictor of TCFA.

There is an inverse linear correlation between fibrous cap thickness and plasma levels of inflammatory markers. The plasma hs-CRP concentration is the strongest independent predictor of TCFA.

To test the hypothesis that ECP augments collateral function during a 1 min coronary balloon occlusion.

Twenty patients with chronic stable coronary artery disease were studied. Before and after 30 h of randomly allocated ECP (20 90 min sessions over 4 weeks at 300 mm Hg inflation pressure) or sham ECP (same setting at 80 mm Hg inflation pressure), the invasive collateral flow index (CFI, no unit) was obtained in 34 vessels without coronary intervention. CFI was determined by the ratio of mean distal coronary occlusive pressure to mean aortic pressure with central venous pressure subtracted from both. Additionally, coronary collateral conductance (occlusive myocardial blood flow per aorto-coronary pressure drop) was determined by myocardial contrast echocardiography, and brachial artery flow-mediated dilatation was obtained.

CFI changed from 0.125 (0.073; interquartile range) at baseline to 0.174 (0.104) at follow-up in the ECP group (p=0.006), and from 0.129 (0.122) to 0.111 (0.125) in the sham ECP group (p=0.14). Baseline to follow-up change of coronary collateral conductance was from 0.365 (0.268) to 0.568 (0.585) ml/min/100 mm Hg in the ECP group (p=0.072), and from 0.229 (0.212) to 0.305 (0.422) ml/min/100 mm Hg in the sham ECP group (p=0.45). There was a correlation between the flow-mediated dilatation change from baseline to follow-up and the corresponding CFI change (r=0.584, p=0.027).

ECP appears to be effective in promoting coronary collateral growth. The extent of collateral function improvement is related to the amount of improvement in the systemic endothelial function.

The Scottish Health Survey provided cross-sectional data on 3921 asymptomatic members of the general population aged 40–74 years. We undertook simulation models of five screening strategies: mass screening, targeted screening of deprived communities, targeted screening of family members and combinations of the latter two.

To identify one individual at high risk of premature cardiovascular disease using mass screening required 16.0 people to be screened at a cost of £370. Screening deprived communities targeted 17% of the general population but identified 45% of those at high risk, and identified one high-risk individual for every 6.1 people screened at a cost of £141. Screening family members targeted 28% of the general population but identified 61% of those at high risk, and identified one high-risk individual for every 7.4 people screened at a cost of £170. Combining both approaches enabled 84% of high risk individuals to be identified by screening only 41% of the population. Extending targeted to mass screening identified only one additional high-risk person for every 58.8 screened at a cost of £1358.

Targeted screening strategies are less costly than mass screening, and can identify up to 84% of high-risk individuals. The additional resources required for mass screening may not be justified.

Patients (New York Heart Association class III–IV) scheduled for mitral annuloplasty (n=9) or ventricular restoration (n=10) and patients with normal left ventricular function undergoing coronary artery bypass grafting (n=12) were instrumented with pressure-conductance catheters to measure pressure–volume loops before and after surgery. Data obtained during vena cava occlusion provided directly measured EDPVRs. Baseline end-diastolic pressure (P_m) and volume (V_m) were used for single-beat prediction of EDPVRs. Root-mean-squared error (RMSE) between measured and predicted EDPVRs, was 2.79±0.21 mm Hg. Measured versus predicted end-diastolic volumes at pressure levels 5, 10, 15 and 20 mm Hg showed tight correlations (R²=0.69–0.97). Bland–Altman analyses indicated overestimation at 5 mm Hg (bias: pre-surgery 44 ml (95% CI 29 to 58 ml); post-surgery 35 ml (23 to 47 ml)) and underestimation at 20 mm Hg (bias: pre-surgery –57 ml (–80 to –34 ml); post-surgery –13 ml (–20 to –7.0 ml)). End-diastolic volumes were significantly different between groups and between conditions, but these differences were not dependent on the method (ie, measured versus predicted). RMSEs were not different between groups or conditions, nor dependent on V_m or P_m, indicating that EDPVR prediction was equally accurate over a wide volume range.

Single-beat EDPVRs obtained from hearts spanning a wide range of sizes and conditions accurately predicted directly measured EDPVRs with low RMSE. Single-beat EDPVR indices correlated well with directly measured values, but systematic biases were present at low and high pressures. The single-beat method facilitates less invasive EDPVR estimation, particularly when coupled with emerging non-invasive techniques to measure pressures and volumes.

Retrospective database review.

RTP was utilised in 254 DSE and TESE patients being examined for the presence of significant CAD. A continuous infusion of 3% Definity (Lantheus Medical Imaging) was used for all studies, and contrast replenishment (MCR), plateau intensity (PMCE) and wall motion (WM) were examined for the detection of CAD.

Sensitivity/specificity/accuracy to detect CAD.

For DSE, the sensitivity of myocardial perfusion (MP) imaging with RTP was 85%, which was significantly higher than WM analysis (72%; p<0.05). The improvement in sensitivity with MP analysis during DSE was primarily the result of better detection of left anterior descending disease. MP sensitivity during TESE was significantly better than MP sensitivity during DSE (98% versus 85%; p<0.05), and WM sensitivity during TESE was better than WM sensitivity during DSE (89% versus 72%; p<0.05). The improvement in WM sensitivity during TESE was due to detection of subendocardial wall thickening abnormalities in 48% of the patients with induced subendocardial perfusion defects.

Myocardial perfusion imaging with RTP improves the detection of CAD during both DSE and TESE. During TESE, the subendocardial perfusion defects improve WM sensitivity by delineating subendocardial WM abnormalities.