Percutaneous closure of an aortic paravalvular leak via the transradial approach.

Percutaneous closure of aortic and mitral paraprosthetic leaks using the Amplatzer occluders (muscular ventricular septal defect occluder) is now a well recognized procedure although as "off label" use. Aortic paravalvular leak closure is usually carried out via transfemoral puncture, but problems with this approach include the need to stop warfarin and the inadequate length of standard delivery sheaths. We report the first case of percutaneous aortic paravalvular leak closure through the radial artery route.

A randomised controlled trial comparing the routine use of an Angio-Seal STS device strategy with conventional femoral haemostasis methods in a district general hospital.

Femoral artery closure devices reduce the time to haemostasis and ambulation. Most district general hospitals (DGHs) now perform day case angiography on site. The purpose of this study was to assess the Angio-Seal self-tightening suture (STS) device in comparison with manual compression in this environment. A prospective randomised controlled trial was undertaken comparing the Angio-Seal STS device with manual pressure recording complications, time from end of procedure and patient satisfaction in a DGH setting. Angiography lists of 206 patients undergoing day case diagnostic cardiac catheterisation with a five French sheath at a DGH were randomised by intention to treat to receive either manual compression or a six French Angio-Seal STS device. Time from sheath removal to mobilisation, complication rate and patient satisfaction were compared. There were no significant differences between the two groups in terms of demographics (manual compression: Angio-Seal; male (%) 58 vs. 57, age (years) 65.4 vs. 66.3, body mass index (kg/m(2)) 27.7 vs. 27.5). Despite randomisation, only 74 of 107 patients in the Angio-Seal group actually had a device deployed. Angio-Seal use was associated with significantly shorter times to mobilisation (87.6 vs. 144.1 min; p < 0.001), significantly less bruising (bruise size at 1 week (28.5 vs. 82.5 cm(3); p < 0.01) and no increase in vascular complications. In addition, patients were more satisfied with Angio-Seal devices in terms of length of immobility. The routine use of Angio-Seal closure devices result in earlier mobilisation, less bruising, increased patient satisfaction with no increase in other complications in comparison to manual pressure.

Cardiac resynchronisation therapy for heart failure.

Cardiac resynchronisation therapy (CRT) reduces symptoms and improves left ventricular function in chronic heart failure (CHF) patients with left ventricular systolic dysfunction and prolonged QRS duration. Recent studies have demonstrated a reduction in mortality associated with CRT. When combined with an implantable cardioverter defibrillator (ICD) reduction in mortality is likely to reduce further. Cardiac resynchronisation therapy is well tolerated and free from compliance issues and therefore should be considered for all suitable patients. Identifying patients who will derive maximum benefit requires further study and has health economic implications. We review here the CRT trial evidence as well as the implantation technique and complications. We also describe a case report where an intra-aortic balloon pump was used successfully as a bridge to CRT to treat a patient with end-stage heart failure.

Cardiac arrests at the Cenotaph.

This report describes the case histories of three veterans who suffered cardiac arrests at the 2005 Cenotaph Remembrance Parade. All three were successfully resuscitated and admitted to the St Thomas' Hospital Coronary Care Unit. They had internal cardioverter defibrillators (ICDs) inserted and remain well. All three plan to attend Remembrance ceremonies this year. We review the evidence between emotional stress and arrhythmias and the updated National Institute for Health and Clinical Excellence (NICE) guidelines for ICDs.

Antiplatelet therapy in cardiovascular disease.

Platelet activation and aggregation are considered to be central to arterial thrombus formation. Antiplatelet therapy is therefore important for both the treatment and prevention of cardiovascular disease. Aspirin, the most widely used antiplatelet agent, inhibits platelet cyclo-oxygenase and the conversion of arachidonic acid to the potent platelet agonist thromboxane A(2) but does not prevent platelet activation occurring via various signalling pathways that are independent of thromboxane A(2) release. Therefore a number of other compounds have been developed to complement aspirin's beneficial effect. These include the thienopyridines (clopidogrel and ticlopidine), dipyridamole, and the alpha(IIb)beta(3) (glycoprotein IIb/IIIa) receptor inhibitors.

Inhibition of ADP-induced intracellular Ca2+ responses and platelet aggregation by the P2Y12 receptor antagonists AR-C69931MX and clopidogrel is enhanced by prostaglandin E1.

P2Y(12) antagonists such as clopidogrel and AR-C69931MX inhibit aggregation by antagonizing the effects of ADP at P2Y(12) receptors on platelets. Agents such as PGE(1) also inhibit aggregation by stimulating adenylate cyclase to produce cAMP, which interferes with Ca(2+) mobilization within the cell. Since one facet of P2Y(12) receptors is that they mediate inhibition of adenylate cyclase by ADP, it might be expected that P2Y(12) antagonists would interact with PGE(1). We have explored the effects of PGE(1) and AR-C69931MX singly and in combination on ADP-induced intracellular Ca(2+) ([Ca(2+)](i)) responses and aggregation. PGE(1) alone caused parallel dose-dependent inhibition of [Ca(2+)](i) and aggregation responses. AR-C66931MX alone caused only partial inhibition of [Ca(2+)](i) despite a marked inhibitory effect on aggregation. Combinations of PGE(1) with AR-C66931MX were found to act in synergy to reduce both [Ca(2+)](i) and aggregation. This effect was confirmed in patients with acute coronary syndromes by studying the inhibitory effects of PGE(1) on [Ca(2+)](i) and aggregation before and after clopidogrel. In summary, we have shown that P2Y(12) antagonists interact with natural agents such as PGE(1) to provide more effective inhibition of [Ca(2+)](i) and platelet aggregation. This would contribute to the effectiveness of P2Y(12) antagonists as antithrombotic agents in man.