Comparison of continuous 24-hour and 14-day ECG monitoring for the detection of cardiac arrhythmias in patients with ischemic stroke or syncope.

BACKGROUND: Previous studies show that using 12-lead electrocardiogram (ECG) or 24-h ECG monitor for the detection of cardiac arrhythmia events in patients with stroke or syncope is ineffective. HYPOTHESIS: The 14-day continuous ECG patch has higher detection rates of arrhythmias compared with conventional 24-h ECG monitoring in patients with ischemic stroke or syncope. METHODS: This cross-sectional study of patients with newly diagnosed ischemic stroke or syncope received a 24-h ECG monitoring and 14-day continuous cardiac monitoring patch and the arrhythmia events were measured. RESULTS: This study enrolled 83 patients with ischemic stroke or syncope. The detection rate of composite cardiac arrhythmias was significantly higher for the 14-day ECG patch than 24-h Holter monitor (69.9% vs. 21.7%, p = .006). In patients with ischemic stroke, the detection rates of cardiac arrhythmias were 63.4% for supraventricular tachycardia (SVT), 7% for ventricular tachycardia (VT), 5.6% for atrial fibrillation (AF), 4.2% for atrioventricular block (AVB), and 1.4% for pause by 14-day ECG patch, respectively. The significant difference in arrhythmic detection rates were found for SVT (45.8%), AF (6%), pause (1.2%), AVB (2.4%), and VT (9.6%) by 14-day ECG patch but not by 24-h Holter monitor in patients with ischemic stroke or syncope. CONCLUSIONS: A 14-day ECG patch can be used on patients with ischemic stroke or syncope for the early detection of AF or other cardiac arrhythmia events. The patch can be helpful for physicians in planning medical or mechanical interventions of patients with ischemic stroke and occult AF.

Clinical outcomes of percutaneous coronary intervention with rotablation in patients with acute or recent myocardial infarction.

BACKGROUND: Although rotational atherectomy (RA) has been an accepted and widely used medical procedure for more than 15 years, the clinical outcomes of RA in high-risk populations remain elusive. Therefore, the purpose of this study was to investigate the safety and efficacy of RA for patients with acute or recent myocardial infarction (MI), and report the short- and long-term clinical outcomes in this population. METHODS: We enrolled patients undergoing percutaneous coronary intervention (PCI) and RA at two medical centers in Taiwan between January 2004 and December 2013. Individuals who suffered an acute MI within 30 days before RA were assigned to the MI group; the remaining subjects were assigned to the non-MI group. RESULTS: A total of 154 subjects were enrolled in our study, among them: 47 (30.5%) had an acute MI within 30 days of RA (MI group), and the remaining 107 (69.5%) patients without MI comprised the non-MI group. PCI and RA procedures were performed successfully in 150 patients. The 30-day and 1-year total death, MI, and major adverse cardiac event (MACE included all-cause death, MI, and clinical-driven target lesion revascularization) rates were 6.5%, 12.3%, and 15.6%, and 9.7%, 15.2%, and 30.5%, at the 30-day and 1-year follow-ups, respectively. MI was identified as an independent predictor for both 30-day MACE and total death (MACE, OR: 3.95, P = 0.006; total death, OR: 4.67, P = 0.043), and remained an independent predictor for 1-year total death and MI (total death, HR: 4.47, P = 0.007; MI, HR: 2.62, P = 0.016). CONCLUSION: Our study demonstrated the safety and efficacy of RA in patients with acute or recent MI, and identified MI as an independent predictor of both short- and long-term outcomes.

Rotablation in the treatment of high-risk patients with heavily calcified left-main coronary lesions.

OBJECTIVE: Heavily calcified left-main coronary diseases (LMCA) remain a formidable challenge for percutaneous interventions (PCI). This study was to investigate the safety and efficacy of using rotational atherectomy (RA) in treating such lesions in actual practice. METHODS: From February 2004 to March 2012, all consecutive patients who received RA for heavily-calcified LMCA lesions in our cath lab were enrolled. The relevant clinical and angiographic characteristics at the time of index PCI, as well as the clinical follow-up outcomes, were retrieved and analyzed. RESULTS: A total of 34 consecutive patients were recruited with a mean age 77.2 ± 10.2 years. There were 82.4% presented with acute coronary syndrome and 11.8% with cardiogenic shock. Chronic renal disease and diabetes were seen in 64.7% and 52.9%, respectively. Triple-vessel coronary disease was found in 76.5% of them. The mean SYNTAX score was 50 ± 15 and EuroSCORE II scale 5.6 ± 4.8. The angiographic success rate was 100% with a procedural success rate of 91.2%. The mean number of burrs per patient was 1.7 ± 0.5. Crossing-over stenting was used in 64.7%. Most stents were drug-eluting (67.6%). Intra-aortic ballon pump was used in 20.6% of the procedures. Three patients died during hospitalization, all due to presenting cardiogenic shock. No major complication occurred. Among 31 hospital survivors, the major adverse cardiac events (MACE) rate was 16.1%, all due to target lesion revascularization or target vessel revascularization. CONCLUSIONS: In high-surgical-risk elderly patients, plaque modification with RA in PCI of heavily-calcified LMCA could be safely accomplished with a minimal complication rate and low out-of-hospital MACE.

The use and clinical outcomes of rotablation in challenging cases in the drug-eluting stent era.

BACKGROUND: Rotational atherectomy (RA) has been advocated in the bare metal stent (BMS) era but is underused now due to technique demands and nonsuperior outcomes. The aim of this study was to evaluate the procedural and clinical outcomes of patients with very complex, severely calcified coronary lesions treated by RA and drug-eluting stents (DESs) in our current percutaneous coronary intervention (PCI) practice in a region where RA use has been limited by lack of insurance reimbursement. METHODS: From March 2004 to November 2010, all consecutive patients who required RA treatment for severely calcified de novo lesions of native coronary arteries followed by DES implantation were queried from the cath lab database and recruited. Their clinical and angiographic characteristics at the index PCI were analyzed and completed by a thorough review of the medical charts. RESULTS: A total of 67 consecutive patients with 71 very complex, heavily calcified coronary lesions treated with RA plus DES were recruited. Of these patients, 64% presented with acute coronary syndrome, 9.0% with cardiogenic shock, 43.3% with chronic renal failure, and 50.7% with diabetes. Multiple-vessel diseases were found in 92.5% of our patients, and the average coronary artery calcification (CAC) score was 3.6±1.4. Of the coronary lesions, 26.7% were either balloon-uncrossable or balloon-undilatable. The angiographic success rate was 100% with one non-Q myocardial infarction. Five patients (7.5%) died in hospital, all initially presenting with extensive myocardial infarction and/or cardiogenic shock. The out-of-hospital major adverse cardiac event was 17.9% at the mean follow-up of 23.2 months (range: 5-86), primarily due to high target-lesion revascularization and target-vessel revascularization rates of 10.4% and 10.4%, respectively. Only one (1.5%) probable subacute stent thrombosis was observed in the follow-up. CONCLUSION: RA with DES implantation in very complex, heavily calcified coronary lesions can achieve very low complication and low out-of-hospital major adverse cardiac event rates even in high-risk patients despite use limited by lack of insurance reimbursement. The study results convince us to sustain and even broaden the use of this novel, but underused, device in the DES era.

Mechanism of hypoxia-induced GCM1 degradation: implications for the pathogenesis of preeclampsia.

Preeclampsia is a major pregnancy-specific disorder affecting 5-7% of pregnancies worldwide. Although hypoxia caused by incomplete trophoblast invasion and impaired spiral arterial remodeling is thought to be a major cause of preeclampsia, how hypoxia affects placental development remains uncertain. GCM1 (glial cells missing homolog 1) is a transcription factor critical for placental development. In preeclampsia, GCM1 and its target genes syncytin 1 and placental growth factor, important for syncytiotrophoblast formation and placental vasculogenesis, are all decreased. Here we present evidence that GCM1 is a major target of hypoxia associated with preeclampsia. We show that hypoxia triggers GCM1 degradation by suppressing the phosphatidylinositol 3-kinase-Akt signaling pathway, leading to GSK-3beta activation. Activated GSK-3beta phosphorylates GCM1 on Ser322, which in turn recruits the F-box protein FBW2, leading to GCM1 ubiquitination and degradation. Importantly, the GSK-3beta inhibitor LiCl prevented hypoxia-induced GCM1 degradation. Our study identifies a molecular basis for the disrupted GCM1 transcription network in preeclampsia and provides a potential avenue for therapeutic intervention.

Ubiquitin-conjugating enzyme UBE2D2 is responsible for FBXW2 (F-box and WD repeat domain containing 2)-mediated human GCM1 (glial cell missing homolog 1) ubiquitination and degradation.

Glial cell missing homolog 1 (GCM1) is an important transcription factor regulating placental cell fusion. Recently, we have demonstrated that GCM1 is a labile protein and that the F-box protein FBXW2 (F-box and WD repeat domain containing 2) mediates GCM1 ubiquitination for proteasomal degradation. Multiple factors are involved in the ubiquitin-proteasome degradation system. Therefore, in order to better understand the mechanism regulating GCM1 stability, we further isolated and characterized the E2 ubiquitin-conjugating enzyme responsible for FBXW2-mediated ubiquitination of GCM1 in this study. We prepared and screened a variety of E2 proteins in an in vitro ubiquitination assay system for GCM1 and found that UBE2D2 is required for the SCF(FBXW2) E3 ligase in regulation of GCM1 ubiquitination. We also demonstrated that the enzyme activity of UBE2D2 is required for GCMa ubiquitination and for association with the SCF(FBXW2) complex. Moreover, knocking down UBE2D2 expression by RNA interference not only suppressed FBXW2-mediated GCM1 ubiquitination, but also prolonged the half-life of GCM1 in vivo. Our results suggest that UBE2D2 is a functional E2 protein which, together with FBXW2, regulates GCM1 stability in the placenta.