Importance of tricuspid regurgitation velocity threshold in risk assessment of pulmonary hypertension-long-term outcome of patients submitted to aortic valve replacement

Background: the upper physiological threshold for tricuspid regurgitation velocity (TRV) of 2.8 m/s proposed by the Pulmonary Hypertension (PH) guidelines had been questioned. The aim of this study was to evaluate the prognostic significance of preoperative PH in patients with aortic stenosis, long-term after valve replacement, using two different TRV thresholds (2.55 and 2.8 m/s). Methods: four hundred and forty four patients were included (mean age 73 ± 9 years; 55% male), with a median follow-up of 5.8 years (98% completed). Patients were divided into three PH probability groups according to guidelines (low, intermediate and high) for both thresholds (TRV ≤ 2.8 m/s and TRV ≤ 2.55 m/s), using right atrial area>18 cm2 and right ventricle/left ventricle ratio>1 as additional echocardiographic variables. Results: in patients with measurable TRV (n = 304), the low group mortality rate was 25% and 30%, respectively for 2.55 and 2.8 m/s TRV thresholds. The intermediate group with TRV > 2.55 m/s was an independent mortality risk factor (HR 2.04; 95% CI: 1.91 to 3.48, p = 0.01), in contrast to the intermediate group with TRV>2.8 m/s (HR 1.44; 95% CI: 0.89 to 2.32, p = 0.14). Both high probability groups were associated with an increased mortality risk, as compared to their respective low groups. When including all patients (with measurable and non-measurable TRV), both intermediate groups remained independently associated with an increased mortality risk: HR 1.62 (95% CI 1.11 to 2.35 p = 0.01) for the new cut-off point; and HR 1.43 (95% CI: 0.96 to 2.13, p = 0.07) for guidelines threshold. Conclusion: A TRV threshold of 2.55 m/s, together with right cavities measures, allowed a better risk assessment of patients with PH secondary to severe aortic stenosis, with or without tricuspid regurgitation

Left atrium assessment by speckle tracking echocardiography in cryptogenic stroke: seeking silent atrial fibrillation

Silent atrial fibrillation (AF) may be the cause of some cryptogenic strokes (CrS). The aim of the study was to analyse atrial size and function by speckle tracking echocardiography in CrS patients to detect atrial disease. Patients admitted to the hospital due to CrS were included prospectively. Echocardiogram analysis included left atrial ejection fraction (LAEF) and atrial strain. Insertable cardiac monitor was implanted, and AF was defined as an episode of ≥1 min in the first year after stroke. Left atrial enlargement was defined as indexed volume > 34 mL/m2. Seventy-five consecutive patients were included, aged 76 ± 9 years (arterial hypertension 75%). AF was diagnosed in 49% of cases. The AF group had higher atrial volume and worse atrial function: peak atrial longitudinal strain (PALs) 19.6 ± 5.7% vs. 29.5 ± 7.2%, peak atrial contraction strain (PACs) 8.9 ± 3.9% vs. 16.5 ± 6%, LAEF 46.8 ± 11.5% vs. 60.6 ± 5.2%; p < 0.001. AF was diagnosed in 20 of 53 patients with non-enlarged atrium, and in 18 of them, atrial dysfunction was present. The multivariate logistic regression analysis demonstrated an independent association between detection of AF and atrial volume, LAEF, and strain. Cut-off values were obtained: LAEF < 55%, PALs < 21.4%, and PACs < 12.9%. In conclusion, speckle tracking echocardiography in CrS patients improves silent atrial disease diagnosis, with or without atrial enlargement

Efficacy of a nurse-led lipid-lowering secondary prevention intervention in patients hospitalized for ischemic heart disease: A pilot randomized controlled trial

Background and aims: Lack of achievement of secondary prevention objectives in patients with ischaemic heart disease remains an unmet need in this patient population. We aimed at evaluating the six-month efficacy of an intensive lipid-lowering intervention, coordinated by nurses and implemented after hospital discharge, in patients hospitalized for an ischaemic heart disease event. Methods: Randomized controlled trial, in which a nurse-led intervention including periodic follow-up, serial lipid level controls, and subsequent optimization of lipid-lowering therapy, if appropriate, was compared with standard of care alone in terms of serum lipid-level control at six months after discharge. Results: The nurse-led intervention was associated with an improved management of low-density lipoprotein (LDL) cholesterol levels compared with standard of care alone: LDL cholesterol levels ⩽100 mg/dL were achieved in 97% participants in the intervention arm as compared with 67% in the usual care arm ( p value <0.001), the LDL cholesterol ⩽70 mg/dL target recommended by the 2016 European Society of Cardiology guidelines was achieved in 62% vs. 37% participants ( p value 0.047) and the LDL cholesterol reduction of ⩾50% recommended by the American College of Cardiology/American Heart Association in 2013 was achieved in 25.6% of participants in the intervention arm as compared with 2.6% in the usual care arm ( p value 0.007). The intervention was also associated with improved blood pressure control among individuals with hypertension. Conclusions: Our findings highlight the opportunity that nurse-led, intensive, post-discharge follow-up plans may represent for achieving LDL cholesterol guideline-recommended management objectives in patients with ischaemic heart disease. These findings should be replicated in larger cohorts

An intensive, structured, mobile devices-based healthcare intervention to optimize the lipid-lowering therapy improves lipid control after an acute coronary syndrome

Aims: despite the evidence, lipid-lowering treatment (LLT) in secondary prevention remains insufficient, and a low percentage of patients achieve the recommended LDL cholesterol (LDLc) levels by the guidelines. We aimed to evaluate the efficacy of an intensive, mobile devices-based healthcare lipid-lowering intervention after hospital discharge in patients hospitalized for acute coronary syndrome (ACS). Methods and results: ambiespective register in which a mobile devices-based healthcare intervention including periodic follow-up, serial lipid level controls, and optimization of lipid-lowering therapy, if appropriate, was assessed in terms of serum lipid-level control at 12 weeks after discharge. A total of 497 patients, of which 462 (93%) correctly adhered to the optimization protocol, were included in the analysis. At the end of the optimization period, 327 (70.7%) patients had LDLc levels ≤ 70 mg/dL. 40% of patients in the LDLc ≤ 70 mg/dL group were upgraded to very-high intensity lipid-lowering ability therapy vs. 60.7% in the LDLc > 70 mg/dL group, p < 0.001. Overall, 38.5% of patients had at least a change in their LLT. Side effects were relatively infrequent (10.7%). At 1-year follow-up, LDLc levels were measured by the primary care physician in 342 (68.8%) of the whole cohort of 497 patients. In this group, 71.1% of patients had LDLc levels ≤ 70 mg/dL. Conclusion: an intensive, structured, mobile devices-based healthcare intervention after an ACS is associated with more than 70% of patients reaching the LDLc levels recommended by the clinical guidelines. In patients with LDLc measured at 1-year follow-up, 71.1% had LDLc levels ≤ 70 mg/dL

Association between norepinephrine levels and abnormal iron status in patients with chronic heart failure: is iron deficiency more than a comorbidity?

Background Mechanisms underlying iron homeostasis dysregulation in patients with chronic heart failure remain unsettled. In cardiomyocyte models, norepinephrine may lead to intracellular iron depletion, but the potential association between catecholamines (sympathetic activation markers) and iron metabolism biomarkers in chronic heart failure is unknown. Methods and Results In this cross-sectional analysis, we studied the association between plasma norepinephrine levels and serum iron status biomarkers indicating iron storage (ferritin), iron transport (transferrin saturation), and iron demand (soluble transferrin receptor) in a prospective cohort of 742 chronic heart failure patients (mean age, 72±11 years; 56% male). Impaired iron status was defined as ferritin 0.05). Adjusted norepinephrine marginal means were significantly higher in patients with impaired iron status compared with those with normal iron status (528 pg/mL [505-551] versus 482 pg/mL [448-518], respectively; P=0.038). Conclusions In chronic heart failure patients, increased sympathetic activation estimated with norepinephrine levels is associated with impaired iron status and, particularly, dysregulation of biomarkers suggesting impaired iron transport and increased iron demand. Whether the relationship between norepinephrine and iron metabolism is bidirectional and entails causality need to be elucidated in future research

Socioeconomic status and prognosis of patients with ST-elevation myocardial infarction managed by the emergency-intervention "Codi IAM" network

Background: despite the spread of ST-elevation myocardial infarction (STEMI) emergency intervention networks, inequalities in healthcare access still have a negative impact on cardiovascular prognosis. The Family Income Ratio of Barcelona (FIRB) is a socioeconomic status (SES) indicator that is annually calculated. Our aim was to evaluate whether SES had an effect on mortality and complications in patients managed by the "Codi IAM" network in Barcelona. Methods: this is a cohort study with 3,322 consecutive patients with STEMI treated in Barcelona from 2010 to 2016. Collected data include treatment delays, clinical and risk factor characteristics, and SES. The patients were assigned to three SES groups according to FIRB score. A logistic regression analysis was conducted to estimate the adjusted effect of SES on 30-day mortality, 30-day composite cardiovascular end point, and 1-year mortality. Results: the mean age of the patients was 65 ± 13% years, 25% were women, and 21% had diabetes mellitus. Patients with low SES were younger, more often hypertensive, diabetic, dyslipidemic (p < 0.003), had longer reperfusion delays (p < 0.03) compared to participants with higher SES. Low SES was not independently associated with 30-day mortality (OR: 0.95;9 5% CI: 0.7-1.3), 30-day cardiovascular composite end point (OR: 1.03; 95% CI: 0.84-1.26), or 1-year all-cause mortality (HR: 1.09; 95% CI: 0.76-1.56). Conclusion: although the low-SES patients with STEMI in Barcelona city were younger, had worse clinical profiles, and had longer revascularization delays, their 30-day and 1-year outcomes were comparable to those of the higher-SES patients