Late stent collapse identified with OCT - An underdiagnosed mechanism of restenosis?

Very late stent recoil is a rare albeit recognized phenomenon leading to subsequent in-stent restenosis. Angiography alone may not be adequate in making the diagnosis, and intravascular imaging with optical coherence tomography (OCT) is far superior in confirming the diagnosis and guiding subsequent management. We describe a case with interesting coronary angiogram and OCT images demonstrating very rare diagnosis of the late stent collapse. These images provide a valuable insight into a novel mechanism responsible for late target lesion failure. These images highlight the importance of modern intra-coronary imaging techniques in understanding the mechanisms underlying target-lesion failure, and guiding appropriate management.

The impact of routine and intravascular ultrasound-guided high-pressure postdilatation after drug-eluting stent deployment: the STent OPtimization (STOP) study.

OBJECTIVES: Drug-eluting stent (DES) implantations with low final cross-sectional area (CSA) are associated with adverse clinical outcomes. However, there is no guidance to facilitate optimal stent deployment (SD). The stent optimization (STOP) study was performed to assess DES routine postdilatation (PD) following implantation with intravascular ultrasound (IVUS) guidance. METHODS: Forty-eight patients were included in this single-center prospective study. All DESs were deployed at 16 atm for 20 seconds and underwent routine non-compliant balloon PD (minimum 20 atm for 10 seconds). IVUS performed after SD (blinded) and PD (unblinded) measured CSA at 4 stent reference points. Optimal deployment was defined as distal and proximal stent CSA ≥60% distal and proximal reference CSA; mid and minimum stent CSA ≥70% of distal reference CSA. All per-protocol criteria were required to define optimal SD. Suboptimally deployed DESs underwent further PD with IVUS guidance (IVPD). RESULTS: Fifty-two lesions were treated in 48 patients. CSA increased by 20% following PD. STOP criteria were only achieved in 21% of DESs after SD compared to 54% after PD. IVPD was performed in 20 DESs, which increased CSA by a further 21%. STOP criteria were eventually attained in 81% cases (P<.001 for all comparisons). CONCLUSION: DES deployment leads to suboptimal deployment, which can be optimized by routine PD. IVUS identifies DES implantations that benefit from further PD. Optimizing final DES-CSA may have longterm clinical benefits, although a randomized study is required.

Spironolactone has antiarrhythmic activity in ischaemic cardiac patients without cardiac failure.

OBJECTIVES: To examine whether endogenous aldosterone can cause either arrhythmias (and some of their underlying mechanisms) or endothelial dysfunction in patients with coronary artery disease (CAD) but without heart failure. BACKGROUND: Aldosterone blockade has been shown to reduce the incidence of sudden death in patients with heart failure. This could be caused by a reduction in arrhythmias or in coronary events. Whether either effect also occurs in other cardiac patients without heart failure is currently unknown. METHOD: We performed a randomized, placebo-controlled, double-blind crossover study on 98 patients with CAD but without heart failure on standard therapy, comparing 12.5-50 mg/day spironolactone (3 months) with placebo. Endothelial function was assessed by bilateral forearm venous occlusion plethysmography. Ventricular extrasystoles, procollagen III N-terminal peptide (PIIINP) and QT interval length were used to represent arrhythmias and their determinants. RESULTS: Spironolactone produced a highly significant 75% reduction in ventricular extrasystoles (median 192, range 48-744) on placebo compared with spironolactone (median 48, range 19.2-288, P < 0.003). Spironolactone also decreased the QT interval from a mean of 440 +/- 28 to a mean of 425 +/- 25 (P < 0.001) and a collagen marker (PIIINP) from a mean of 3.6 +/- 0.9 to a mean of 3.0 +/- 0.8 (P < 0.001), but did not significantly change endothelial dysfunction or heart rate variability. CONCLUSION: These results suggest that despite conventional therapy, endogenous aldosterone can be an arrhythmogenic influence in patients with CAD, but without heart failure. The possible mechanisms are that aldosterone promotes myocardial fibrosis and lengthens the QTc interval as well as decreasing potassium in CAD patients without heart failure.

Aldosterone blockade over and above ACE-inhibitors in patients with coronary artery disease but without heart failure.

Recent evidence points to a role for the renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of atherosclerosis and its complications, including acute angina pectoris. Two large trials in heart failure have clearly demonstrated that blocking aldosterone improves mortality and that this benefit occurs over and above standard therapy with angiotensin-converting enzyme (ACE) inhibitors. The question that naturally arises from these landmark studies is whether aldosterone blockade would produce the same benefits in patients with coronary artery disease (CAD) but no heart failure. There are three reasons to believe this might be the case. Firstly, angiotensin II (Ang II) and aldosterone produce similar biological effects and Ang II withdrawal has been shown to benefit patients with angina; aldosterone blockade may therefore follow in the footsteps of ACE inhibitors, as it did in heart failure, and produce benefits in vascular patients without heart failure. Secondly, one of the main mechanisms which is thought to be responsible for the benefit of aldosterone blockade in the Randomised ALdactone Evaluation Study (RALES) and Eplerenone Post-AMI Heart Failure Survival Study (EPHESUS), is that it improves endothelial/vascular function and endothelial/vascular dysfunction is the fundamental abnormality in angina pectoris. Finally, aldosterone blockade has been shown to reduce atherosclerosis in animal studies of atherosclerosis without heart failure, which are analogous to CAD patients.