Background Previous studies have suggested that neointimal growth and strut coverage is reduced in patients with acute coronary syndrome (ACS) that receive metallic stents.
We present a case of iatrogenic aortocoronary dissection sustained during routine percutaneous coronary intervention for stable angina. Careful wiring of the true lumen and stent implantation to seal ...off the dissection flap prevented immediate complications, and computed tomography aortography guided a conservative approach to manage the residual aortic dissection. (Level of Difficulty: Intermediate.)
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We sought to determine whether right ventricular stunning could be detected after supply (during coronary balloon occlusion BO) and supply/demand ischemia (induced by rapid pacing RP during ...transcatheter aortic valve replacement) in humans.
Ten subjects with single-vessel right coronary artery disease undergoing percutaneous coronary intervention with normal ventricular function were studied in the BO group. Ten subjects undergoing transfemoral transcatheter aortic valve replacement were studied in the RP group. In both, a conductance catheter was placed into the right ventricle, and pressure volume loops were recorded at baseline and for intervals over 15 minutes after a low-pressure BO for 1 minute or a cumulative duration of RP for up to 1 minute. Ischemia-induced diastolic dysfunction was seen 1 minute after RP (end-diastolic pressure mm Hg: 8.1±4.2 versus 12.1±4.1,
<0.001) and BO (end-diastolic pressure mm Hg: 8.1
4.0 versus 8.7±4.0,
=0.03). Impairment of systolic and diastolic function after BO remained at 15-minutes recovery (ejection fraction %: 55.7±9.0 versus 47.8±6.3,
<0.01; end-diastolic pressure mm Hg: 8.1±4.0 versus 9.2±3.9,
<0.01). Persistent diastolic dysfunction was also evident in the RP group at 15-minutes recovery (end-diastolic pressure mm Hg: 8.1±4.1 versus 9.9±4.4,
=0.03) and there was also sustained impairment of load-independent indices of systolic function at 15 minutes after RP (end-systolic elastance and ventriculo-arterial coupling mm Hg/mL: 1.25±0.31 versus 0.85±0.43,
<0.01).
RP and right coronary artery balloon occlusion both cause ischemic right ventricular dysfunction with stunning observed later during the procedure. This may have intraoperative implications in patients without right ventricular functional reserve.
Registry data have suggested higher than anticipated rates of scaffold thrombosis following bioresorbable vascular scaffold (BVS) implantation. We examined early neointimal growth and strut coverage ...in BVS to ascertain whether this was affected by clinical presentation.
Patients undergoing optical coherence tomography (OCT)-guided BVS implantation, either for stable angina (SA) or acute coronary syndrome (ACS), were recruited to this observational study. Repeat OCT was performed at follow-up (median 74 days), and scaffolds analysed at 1 mm longitudinal intervals for scaffold/flow area, scaffold apposition, neointimal growth and strut coverage. Twenty-nine BVS were included in the analysis (62% implanted following ACS). There were no differences in baseline patient/lesion characteristics. All BVS achieved >90% predicted scaffold area with only 1.64% of struts classified as incompletely apposed, compared with 0.47% at follow-up (p=0.006). Reductions in mean scaffold (-4.0%, p=0.01) and flow (-8.4%, p<0.001) areas were observed at follow-up, with larger reductions in mean flow area in stable patients (-14.5±14.2 vs. -4.9±7.9%, p=0.03). ACS patients had reduced neointimal growth (0.51±0.18 vs. 0.87±0.37 mm2, p=0.002), and increased percentage of uncovered struts (2.68±1.67 vs. 1.43±0.87%, p=0.015).
Early neointimal growth and strut coverage are reduced following ACS in patients receiving BVS. These results may, in part, explain the high rates of ST in registry data.
Glucagon-like peptide-1-(7-36) amide (GLP-1) is a human incretin hormone responsible for the release of insulin in response to food. Pre-clinical and human physiological studies have demonstrated ...cardioprotection from ischemia-reperfusion injury. It can reduce infarct size, ischemic left ventricular dysfunction, and myocardial stunning. GLP-1 receptor agonists have also been shown to reduce infarct size in myocardial infarction. The mechanism through which this protection occurs is uncertain but may include hijacking the subcellular pathways of ischemic preconditioning, modulation of myocardial metabolism, and hemodynamic effects including peripheral, pulmonary, and coronary vasodilatation. This review will assess the evidence for each of these mechanisms in turn. Challenges remain in successfully translating cardioprotective interventions from bench-to-bedside. The window of cardioprotection is short and timing of cardioprotection in the appropriate clinical setting is critically important. We will emphasize the need for high-quality, well-designed research to evaluate GLP-1 as a cardioprotective agent for use in real-world practice.
We present a case of iatrogenic aortocoronary dissection sustained during routine percutaneous coronary intervention for stable angina. Careful wiring of the true lumen and stent implantation to seal ...off the dissection flap prevented immediate complications, and computed tomography aortography guided a conservative approach to manage the residual aortic dissection. (
Level of Difficulty: Intermediate.
)
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