A nurse-led implantable loop recorder service is safe and cost effective.

INTRODUCTION: Implantable loop recorders (ILR) are predominantly implanted by cardiologists in the catheter laboratory. We developed a nurse-delivered service for the implantation of LINQ (Medtronic; Minnesota) ILRs in the outpatient setting. This study compared the safety and cost-effectiveness of the introduction of this nurse-delivered ILR service with contemporaneous physician-led procedures. METHODS: Consecutive patients undergoing an ILR at our institution between 1st July 2016 and 4th June 2018 were included. Data were prospectively entered into a computerized database, which was retrospectively analyzed. RESULTS: A total of 475 patients underwent ILR implantation, 271 (57%) of these were implanted by physicians in the catheter laboratory and 204 (43%) by nurses in the outpatient setting. Six complications occurred in physician-implants and two in nurse-implants (P = .3). Procedural time for physician-implants (13.4 ± 8.0 minutes) and nurse-implants (14.2 ± 10.1 minutes) were comparable (P = .98). The procedural cost was estimated as £576.02 for physician-implants against £279.95 with nurse-implants, equating to a 57.3% cost reduction. In our center, the total cost of ILR implantation in the catheter laboratory by physicians was £10 513.13 p.a. vs £6661.55 p.a. with a nurse-delivered model. When overheads for running, cleaning, and maintaining were accounted for, we estimated a saving of £68 685.75 was performed by moving to a nurse-delivered model for ILR implants. Over 133 catheter laboratory and implanting physician hours were saved and utilized for other more complex procedures. CONCLUSION: ILR implantation in the outpatient setting by suitably trained nurses is safe and leads to significant financial savings.

A multicentered evaluation of ablation at higher power guided by ablation index: Establishing ablation targets for pulmonary vein isolation.

BACKGROUND: Pulmonary vein isolation (PVI) using high power delivered by SmartTouch Surround Flow (STSF) catheters guided by ablation index (AI) was evaluated in a multicenter registry. METHODS: Patients with paroxysmal AF underwent PVI with STSF catheters using 30 W on the posterior wall and 40 W elsewhere. AI targets were 350 posterior walls and 450 elsewhere. Procedures were compared with controls using conventionally irrigated contact force-sensing catheters using conventional powers (25 W posterior wall and 30 W elsewhere) guided by force-time integral (no agreed targets). The waiting period of 30 minutes was observed before adenosine administration to assess acute pulmonary vein (PV) reconnection. RESULTS: One hundred patients from four centers were included: 50 patients in the high power ablation index (HPAI) group and 50 controls. Procedure time was 22% shorter in the HPAI group (156 [133.8-179] vs 199 [178.5-227] minutes; P < 0.001). Duration of the radiofrequency application was 37% shorter in the HPAI group (27.2 [21.5-35.8] vs 43.2 [35.1-52.1] minutes; P < 0.001). Acute PV reconnection was reduced (28 of 200 [14%] vs 48 of 200 [24%] veins; P = 0.015). Reconnection was predicted by a largest interlesion distance greater than 6 mm, a lesion with impedance drop less than 2.5 Ω, contact force less than 6 g, or less than 68% of the regional AI target (all P < 0.001). Freedom from atrial arrhythmia at 1 year off antiarrhythmic drugs after a single procedure was 78% in the HPAI group vs 64% in the control group ( P = 0.186). CONCLUSION: High-powered ablation guided by AI was safe and led to shorter procedure times with reduced acute PV reconnection compared with conventional ablation.

Disease Severity and Exercise Testing Reduce Subcutaneous Implantable Cardioverter-Defibrillator Left Sternal ECG Screening Success in Hypertrophic Cardiomyopathy.

BACKGROUND: The features of the hypertrophic cardiomyopathy (HCM) ECG make it a challenge for subcutaneous implantable cardioverter-defibrillator (S-ICD) screening. We aimed to investigate the causes of screening failure at rest and on exercise to inform optimal S-ICD ECG vector development. METHODS AND RESULTS: One hundred and thirty-one HCM patients (age, 50±16 years; 92 males and 39 females) with ≥1 HCM risk factor for sudden death underwent S-ICD ECG screening at rest and on exercise. Fifty patients (38%) were ineligible for S-ICD because of screening failure in every lead vector: 33 (66%) failed in the supine position, 12 (24%) failed in the standing position, and 5 (10%) failed on exercise. In patients who could exercise and passed screening at rest, 31 (44%) had 1 vector safety, 16 (23%) had 2 vector safety, and 24 (33%) had 3 vector safety. Increased R:T wave ratio in the S-ICD screening ECG (odds ratio, 4.0; confidence interval, 3.0-5.3; P<0.001) was associated with screening failure, while R/T ratio <3 in aVF (odds ratio, 0.3; confidence interval, 0.12-0.69; P=0.006) and increasing age (odds ratio, 0.97; confidence interval, 0.95-0.99; P=0.03) was associated with reduced screening failure. European Society of Cardiology risk score was higher in those failing screening (risk score 5.5% [interquartile range, 3.2-8.7] in failed versus 4.5% [interquartile range, 2.9-7.4] in passed; P=0.04). CONCLUSIONS: HCM patients have a significant incidence of screening failure, which is determined primarily by the increased R:T ratio on the screening ECG and lead aVF. High-risk patients have an increased screening failure rate. Optimization of sensing algorithms is required to ensure that the highest risk HCM patients can benefit from S-ICD implantation.

Impact of electronegative low-density lipoprotein on angiographic coronary atherosclerotic burden.

OBJECTIVE: Low density lipoproteins (LDL) with an electronegative charge [LDL(-)] may cause endothelial injury. We assessed the association between serum LDL(-) levels and coronary artery disease (CAD) severity. METHODS: We prospectively enrolled patients with CAD angiographic evidence [stable angina (SA) or non-ST-elevation-acute coronary syndrome (NSTE-ACS)], or with normal coronary arteries (NCA). Baseline LDL(-) serum levels were measured in all patients. Angiographic CAD extent was assessed by using the Bogaty extent index, while CAD severity by evaluating the presence of multi-vessel disease. RESULTS: Forty-seven patients (age 61 ± 9 years, male sex 60%) were enrolled (17 SA, 15 NSTE-ACS and 15 NCA patients). LDL(-) levels were significantly higher in SA [21% (18-34) p = 0.0001] and NSTE-ACS [22% (18-28), p = 0.0001] as compared to NCA [6% (5-8)], without significant differences between SA and NSTE-ACS (p = 0.92). Multi-vessel disease patients had higher LDL(-) levels as compared to single-vessel disease patients (p = 0.002) but similar total LDL levels (p = 0.66). LDL(-) significantly correlated with extent index (r = 0.38, p = 0.03), while total LDL did not (p = 0.24). CONCLUSION: LDL(-) serum levels are associated with CAD angiographic severity and extent. This exploratory analysis should prime further larger studies in order to assess LDL(-) proatherogenic role.

CD4+CD28 null T lymphocytes are expanded in young women with polycystic ovary syndrome.

Women affected by polycystic ovary syndrome (PCOS) have an increased risk of cardiovascular disease. We demonstrated that women with PCOS showed an expansion of CD4(+)CD28(null) T cells, an aggressive population of T lymphocytes that has been recently associated with recurrent coronary instability and type 2 diabetes mellitus. This sheds new light on possible mechanisms responsible for the higher rate of cardiovascular disease among women with PCOS.

A case of early drug-eluting stent fracture.

Although stent fracture following femoro-popliteal intervention is well recognized, coronary stent fracture represents an underrecognized entity. Its incidence is low but it represents an important clinical entity as it may complicate with stent thrombosis causing acute coronary syndromes, or may predispose to instent restenosis. Although coronary stent fracture may involve both bare metal stents (BMS) and drug-eluting stents (DES), a recent analysis of the literature indicates that reports of stent fracture have increased since DES was introduced. Furthermore, chronic stretch at specific vessel sites as bends may lead to late occurrence of fracture. We present the case of a patient with a non-ST-segment elevation acute coronary syndrome caused by the early fracture of an everolimus-eluting stent (Xience®) implanted only three days before.

Coronary atherosclerotic burden in patients with infection by CagA-positive strains of Helicobacter pylori.

OBJECTIVES: Cytotoxic associated gene-A (CagA)-positive strains of Helicobacter pylori emerged as a possible atherosclerotic stimulus. Nevertheless, whether CagA-positivity is associated with more extensive or severe atherosclerotic coronary burden has never been studied. METHODS: Forty consecutive patients with coronary artery disease (CAD) and twenty consecutive patients with normal coronary arteries undergoing coronary angiography were enrolled. All patients underwent evaluation of classical atherogenic risk factors and assessment of anti-urease B and anti-CagA antibodies titer. Either the severity of coronary stenosis (stenosis score) or the extent of coronary atherosclerosis (extent score) was evaluated in CAD patients. RESULTS: The anti-CagA antibody titer was significantly higher in patients with CAD as compared with normal coronary arteries patients [85 (10-108.75) vs. 47.3 (17-64) RU/ml, P=0.02], whereas there were no differences in anti-urease B titer between the two groups. A significant correlation was found between anti-CagA antibody titer and extent score (R=0.35, P=0.03), whereas stenosis score was similar (R=0.25, P=0.11). On the contrary, no significant correlation was found between anti-urease B antibody titer and either extent or stenosis score. Moreover, CagA-positive patients had a more extensive CAD (P=0.029) when compared with CagA-negative patients. Interestingly, whereas serum glucose, LDL levels, anti-urease B, and anti-CagA antibodies were predictors of extent score at univariate analysis, at multivariate analysis anti-CagA antibody titer only was an independent predictor of the extent of coronary atherosclerosis (B=0.051, standard error of B=0.042, P=0.04). CONCLUSION: These results support the association between CagA-positive H. pylori infection and coronary atherosclerotic burden. Further studies are needed to better elucidate the mechanism by which CagA-positive strains may promote atherosclerosis.

Eosinophil cationic protein: A new biomarker of coronary atherosclerosis.

AIMS: Coronary atherosclerosis is a chronic inflammatory disease, but different inflammatory biomarkers may reflect different phases of atherosclerotic plaque evolution. We aimed at assessing the role of eosinophil cationic protein (ECP), a sensitive marker of eosinophil activation, and C-reactive protein (CRP) in coronary artery disease (CAD). METHODS AND RESULTS: Consecutive anginal patients with angiographic evidence of CAD [stable angina (SA) or non-ST-elevation acute coronary syndrome (NSTE-ACS)], or with angiographically normal coronary arteries (NCA) were enrolled. The severity of CAD was graded according to Bogaty's score and coronary lesion morphology was defined as smooth or complex. Baseline ECP and high sensitivity CRP were measured in all patients. Of 198 patients (64 + or - 10 years, male 74%), 91 had SA, 57 had NSTE-ACS and 50 had NCA. ECP levels were significantly higher in SA [30 microg/L (13.8-46.9), p<0.001] and NSTE-ACS [21.8 microg/L (5.5-46.3), p=0.016] compared to NCA [9.7 microg/L (6.1-13.6)], without significant difference between SA and NSTE-ACS (p=0.45). CRP levels were significantly higher in NSTE-ACS [2.38 mg/L (1.11-11.94)] compared to SA [1.48 mg/L (0.82-2.83), p=0.03], and NCA [1.09 mg/L (0.8-2.1), p<0.001], without significant difference between SA and NCA (p=0.20). The addition of ECP to main cardiovascular risk factors improved the area under the curve from 0.88 to 0.92, p=0.007 for the angiographic diagnosis of CAD; further addition of CRP increased the area to 0.94, p=0.014. At multiple linear regression analysis ECP levels independently predicted CAD severity (p=0.001), whereas CRP levels independently predicted lesion complexity (p=0.01). CONCLUSIONS: Our study shows that ECP is a marker of CAD and that different inflammatory biomarkers reflect different phases of atherosclerotic plaque evolution.

Predictive value of C-reactive protein after drug-eluting stent implantation.

During the last few decades, with the evolution of techniques and materials and the increasing experience of operators, percutaneous coronary interventions (PCI) have become an equally efficient alternative to coronary artery bypass grafts for the treatment of most coronary stenoses. Bare-metal stent implantation represented a major step forward, compared with plain old balloon angioplasty (POBA), by improving the immediate angiographic success. However, the incidence of in-stent restenosis (ISR) remained unacceptably high. Development of the drug-eluting stent (DES) significantly improved the outcome of PCI by dramatically abating the rate of ISR and reducing the incidence of target lesion revascularization. However, ISR has not been eliminated and the persistence of metal vessel scaffolding also raises concern regarding the occurrence of late or very late stent thrombosis. POBA and stent implantation have been shown to induce a local and systemic inflammatory response, whose magnitude is associated with worse clinical outcome, and they increase the risk of ISR. C-reactive protein, a marker of systemic inflammation, has been demonstrated to predict clinical and angiographic outcome after POBA or bare-metal stent implantation. However, conflicting data regarding the prognostic value of C-reactive protein following DES implantation are available. In this paper, we review the literature regarding the clinical and pathophysiological association between inflammation and prognosis after DES implantation and suggest some possible therapeutic approaches to reduce inflammatory burden with the aim to improve clinical and angiographic outcome after PCI.

Effect of chronic Aspirin therapy on angiographic thrombotic burden in patients admitted for a first ST-elevation myocardial infarction.

Myocardial no-reflow may negate the benefit of urgent coronary revascularization in patients with acute ST-elevation myocardial infarction (STEMI). Among its pathogenetic mechanisms, distal embolization is of prominent importance and several studies have shown that a high coronary thrombotic burden is associated with distal embolization. We aimed at assessing predictors of angiographic thrombus grade in patients undergoing primary percutaneous coronary intervention. Ninety-one patients (62 +/- 12 years old, 79% men) presenting for a first STEMI and undergoing urgent coronary angiography within 12 hours from onset of symptoms were consecutively included in the study. Thrombus grade was evaluated by angiography according to the Gibson score and patients were allocated to the high thrombus grade (HTG; score 4 to 5) group or to the low thrombus grade (score 0 to 3) group. Variables predicting angiographic thrombus grade were assessed among clinical, angiographic, procedural, and laboratory data. Sixty-four patients (61 +/- 12 years old, 78% men) presented with HTG, whereas 27 patients (63 +/- 10 years old, 80% men) presented with low thrombus grade. Patients an HTG showed a significantly higher white blood cell count (12.5 +/- 4.8 vs 10.5 +/- 2.9, p = 0.015). Aspirin and beta-blocker therapy before admission were less frequently taken in the HTG group (5% vs 26% and 7% vs 23%, respectively, p = 0.01 and p = 0.03). At multivariate analysis, lack of previous therapy with aspirin was the only independent predictor of an HTG (odds ratio 6.14, 95% confidence interval 1.09 to 34.67, p = 0.04). In conclusion, previous aspirin therapy is associated with a decrease in angiographic thrombus grade in patients with STEMI treated with primary percutaneous coronary intervention, thus further priming efforts for appropriate use of aspirin in primary prevention of a first STEMI.

[Association between ethanol intake and ischemic heart disease]. / Rapporti tra etanolo e cardiopatia ischemica.

Most world populations consume alcoholic beverages. Ethanol may have both protective and harmful effects on health depending on the amount and way of consumption. An extensive body of data shows concordant J or U-shaped associations between alcohol intake and a variety of adverse health outcomes, including coronary heart disease, diabetes, hypertension, congestive heart failure, stroke, and all-cause mortality. In particular, moderate ethanol consumption is associated with cardioprotective benefits such as lower cardiovascular risk and mortality, probably mediated by beneficial effects on inflammation, lipids, and coagulation. In contrast, binge and/or heavy drinking results in proportional worsening of outcomes, increasing cardiovascular events and mortality. This harmful effect has been recently associated with the blockade of ischemic preconditioning mediated by high doses of ethanol. In this review, we highlight the recent epidemiological and experimental evidences regarding the specific benefits and risks of ethanol in the setting of ischemic heart disease.