Impact of renal denervation on quality of life (How does renal denervation contribute to improving hypertension treatment affected by poor medication adherence?).

The US Food and Drug Administration has approved renal denervation (RDN) as a new treatment option for hypertension (HT) because it not only has antihypertensive effects but also improves the quality of blood pressure (BP) reduction. RDN is expected to be increasingly used in clinical practice in the future. This review summarizes the impact of RDN on quality of life (QOL). Although the treatment of HT aims to improve life prognosis, the use of antihypertensive agents can impair QOL because of adverse effects and lifestyle changes associated with long-term medication use. Consequently, poor adherence to antihypertensive agents is a common problem and may be the most important issue affecting patient QOL. In RDN trials in patients taking antihypertensive agents, approximately 40% of patients had poor adherence to the drugs. Poor adherence is often the cause of resistant hypertension. Therefore, RDN should be well suited to treating HT and improving QOL. Studies have shown that approximately 30% of HT patients prefer RDN to drug treatment. Patients who prefer RDN are typically male and younger and have high BP, poor adherence, and a history of adverse effects of antihypertensive agents. We hope that RDN will improve not only life prognosis but also QOL in HT patients because of its benefits for adherence. Furthermore, we expect that in the future, RDN will be used in other sympathetic nervous system-related diseases, such as heart failure, atrial fibrillation, and sleep apnea syndrome.

Serial intravascular ultrasound assessment of very late stent thrombosis after sirolimus-eluting stent placement.

PURPOSE: In-stent restenosis has been decreasing through the introduction of drug-eluting stents (DES). On the other hand, adverse events such as very late stent thrombosis (VLST) and late catch-up phenomenon can occur especially with sirolimus-eluting stents (SES, first-generation DES) in long-term follow-up. However, the precise mechanisms underlying VLST have not been well investigated in vivo. METHODS AND RESULTS: From 2004 to 2010, 2034 SES were implanted in 1656 patients and caused eight VLST (0.48% per patient) at Fukuoka Tokushukai Medical Center. Of these, serial intravascular ultrasound (IVUS) images (post-stent implantation and at the time of VLST onset) were obtained from three patients with VLST. Comparing them with eight control patients with SES implanted, the vascular reactivity of VLST patients was analyzed. Eight VLST happened 50 ± 15 months after stent implantation and three of the eight patients with VLST had not taken aspirin daily. There were no differences in minimum stent area, maximum external elastic membrane (EEM) area, and stent edge (distal and proximal) EEM area in post-procedural IVUS images. Compared with the control group patients, ΔEEM area (10.6 ± 3.4mm(2) vs. 1.7 ± 1.9 mm(2), p=0.01) and vessel expansion ratio (185.6 ± 40.3% vs. 112.0 ± 12.1%, p=0.01) were significantly greater in the VLST group based on the greater peri-stent plaque expansion (262.1 ± 72.8% vs. 118.7 ± 21.2%, p=0.01). CONCLUSION: Our serial IVUS study showed that the vascular positive remodeling after SES implantation is one of the most probable morphological mechanisms for VLST development.

Percutaneous coronary intervention strategy for acute coronary syndrome caused by spontaneous coronary artery dissection for relieving ongoing ischemia-Case series and literature review.

Although spontaneous coronary artery dissection (SCAD) is one of the causes of acute coronary syndrome (ACS) or sudden cardiac death, its standard management, especially primary percutaneous coronary intervention (PCI) in ACS patients with ongoing ischemia, has not been established. We experienced three ACS patients with SCAD who were treated with a different strategy of primary PCI. Each PCI strategy led to different clinical and procedural results. We describe here such PCI strategies and results, and also discuss the literature regarding primary PCI strategies for SCAD-induced ACS patients with ongoing ischemia. .