Marina Pascual Izco

Frailty is a short-term prognostic marker in acute coronary syndrome of elderly patients:

Background: Frailty is a biological condition that reflects a state of decreased physiological reserve and vulnerability to stressors. The role of frailty in acute coronary syndrome patients has not been fully explored. Our study aims to assess the prevalence of frailty and its impact on in-hospital adverse outcomes of patients aged ⩾75 years admitted for acute coronary syndrome. Methods: This prospective, observational study included patients aged ⩾75 years admitted due to type 1 myocardial infarction in four tertiary hospitals. Frailty was assessed by the SHARE-FI index. The primary endpoint was the combination of in-hospital death or non-fatal myocardial (re)infarction. Secondary endpoints included the assessment of individual rates of (re)infarction, mortality, stroke, major bleeding and the combination of in-hospital death, (re)infarction and mortality. Results: A total of 202 patients were analysed. Frail patients (n=71, 35.1%) were older, more often women, had higher rates of comorbidities, and a higher risk profile according to GRACE, TIMI and CRUSADE scores at admission. The primary endpoint was significantly more frequent among frail patients (9.9% vs. 1.5%; P=0.006), as well as the combination of death, myocardial infarction and stroke (11.3% vs. 1.5%; P=0.002), driven mainly by a higher mortality rate (8.5% vs 0.8%; P=0.004). On multivariate analysis, frailty phenotype was an independent predictor of major adverse cardiac events (odds ratio 7.13; 95% confidence interval 1.43–35.42). Conclusions: Over one third of elderly patients with high-risk acute coronary syndrome are frail. Frailty phenotype is an important and independent prognostic marker in these patients.

Frailty predicts major bleeding within 30 days in elderly patients with Acute Coronary Syndrome

OBJECTIVE Bleeding in ACS patients is an independent marker of adverse outcomes. Its prognostic impact is even worse in elderly population. Current bleeding risk scores include chronological age but do not consider biologic vulnerability. No studies have assessed the effect of frailty on major bleeding. The aim of this study is to determine whether frailty status increases bleeding risk in patients with ACS. METHODS This prospective and observational study included patients aged ≥75years admitted due to type 1 myocardial infarction. Exclusion criteria were severe cognitive impairment, impossibility to measure handgrip strength, cardiogenic shock and limited life expectancy due to oncologic diseases. The primary endpoint was 30-day major bleeding defined as a decrease of ≥3g/dl of haemoglobin or need of transfusion. RESULTS A total of 190 patients were included. Frail patients (72, 37.9%) were older, with higher comorbidity features and with a higher CRUSADE score at admission. On univariate analysis, frailty predicted major bleeding during 30-day follow-up despite less frequent use of a P2Y12 inhibitor (66.2% vs 83.6%, p=0.007) and decreased catheterisation rate (69.4% vs 94.1%, p<0.001). Major bleeding was associated with increased all-cause mortality at day 30 (18.2% vs 2.5%, p<0.001). On multivariate analysis, frailty was an independent predictor for major bleeding. CONCLUSION Frailty phenotype, as a marker of biological vulnerability, is an independent predictor of major bleeding in elderly patients with ACS. Frailty can play an important role in bleeding risk stratification and objective indices should be integrated into routine initial evaluation of these patients.

Clinical Experience with Ivabradine in Acute Heart Failure

Objective: Ivabradine has been shown to improve symptoms and to reduce rehospitalization and mortality in patients with severe chronic heart failure (HF). Its indication in acute HF is not clear. Acute HF patients could also benefit from HR reduction, as myocardial consumption and oxidative stress are related to tachycardia. Moreover, beta-blockers are contraindicated in cardiogenic shock and should not be initiated with congestive signs. Accordingly, we evaluated the role of ivabradine in acute HF patients. Methods: This was a retrospective analysis of 29 consecutive patients treated for acute HF in the Cardiac ICU, and for whom ivabradine was initiated during hospitalization between January 2011 and January 2014. All patients were in sinus rhythm and had a heart rate (HR) >70 bpm. Catecholamine use was necessary in 16 patients (57.1%) during the hospitalization, in 14 (87.5%) of these before ivabradine treatment. Results: Systolic blood pressure showed no variation during the first 24 h of ivabradine administration or at discharge. HR showed an absolute reduction of 10 bpm at 6 h (p < 0.001), 11 bpm at 24 h (p = 0.004) and 19 bpm (p < 0.001) at discharge. No episodes of significant bradycardia or hypotension were recorded after starting the drug. Conclusions: HR reduction with ivabradine in acute HF is well tolerated. It represents an attractive option, especially when there is excessive catecholamine-related tachycardia; this should be appropriately evaluated in randomized trials.Objective: Ivabradine has been shown to improve symptoms and to reduce rehospitalization and mortality in patients with severe chronic heart failure (HF). Its ind

Frailty is an independent prognostic marker in elderly patients with myocardial infarction

Acute coronary syndrome (ACS) patients are increasingly older. Conventional prognostic scales include chronological age but do not consider vulnerability. In elderly patients, a frail phenotype represents a better reflection of biological age.

The Role of Frailty in Acute Coronary Syndromes in the Elderly

Background: Myocardial infarction (MI) patients are increasingly older, and common risk scores include chronological age, but do not consider chronic comorbidity or biological age. Frailty status reflects these variables and may be independently correlated with prognosis in this setting. Objective: This study investigated the impact of frailty on the prognosis of elderly patients admitted due to MI. Methods: This prospective and observational study included patients ≥75 years admitted to three tertiary hospitals in Spain due to MI. Frailty assessment was performed at admission using the Survey of Health, Ageing and Retirement in Europe Frailty Index (SHARE-FI) tool. The primary endpoint was the composite of death or non-fatal reinfarction during a follow-up of 1 year. Overall mortality, reinfarction, the composite of death, reinfarction and stroke, major bleeding, and readmission rates were also explored. Results: A total of 285 patients were enrolled. Frail patients (109, 38.2%) were older, with a higher score in the Charlson Comorbidity Index and with a higher risk score addressed in the GRACE and CRUSADE indexes. On multivariate analysis including GRACE, CRUSADE, maximum creatinine level, culprit lesion revascularization, complete revascularization, and dual antiplatelet therapy at discharge, frailty was an independent predictor of the composite of death and reinfarction (2.81, 95% CI 1.16–6.78) and overall mortality (3.07, 95% CI 1.35–6.98). Conclusion: Frailty is an independent prognostic marker of the composite of mortality and reinfarction and of overall mortality in patients aged ≥75 years admitted due to MI.

Inflammatory Pathways in Acute Myocardial Infarction: A Matter of Prime Importance

proliferative phase (day 5) after an ST-elevation MI in patients with adverse remodeling. In addition, compared with healthy subjects, in patients who remained free from adverse LV remodeling at follow-up, miRNA-155 expression was significantly suppressed during the same phase. There was also a positive correlation between miRNA-155 measured on day 5 and end-diastolic and end-systolic volumes after 6 months. There are several important aspects of this study. Firstly, this study identifies miRNA-155 as a marker of adverse remodeling in AMI, as suggested previously in animal models [3] . This biomarker could provide important prognostic information to enable adequate post-AMI follow-up, for the selection of pharmacological treatment, and for the scheduling of additional tests (e.g., echocardiograms or cardiac magnetic resonance imaging). Moreover, this study gives a rational explanation of the role of miRNA-155 during the different phases of myocardial inflammation. This physiological explanation helps to identify potential targets involved in adverse LV remodeling. This study also presents some weaknesses that should be pointed out. The sample is small, and the patients were exclusively male, so the study might be only considered as a hypothesis generator; its conclusions will need to be confirmed in larger studies including both male and female patients. In addition, although its results are concorInflammatory responses following acute myocardial infarction (AMI) have a decisive influence on left ventricular (LV) remodeling and the subsequent prognosis. LV remodeling in the infarct zone occurs in the first few days after AMI up to several months later, and involves apoptosis and inflammation. This response generates the myocardial scar and subsequent LV dilatation. Despite optimal pharmacological and surgical management of post-AMI patients, there remains a substantial incidence of LV dysfunction, so the need for more effective therapeutic strategies is evident. We describe the role of inflammation in this setting and its influence on adverse outcomes seems to increase every day. MicroRNAs, also known as miRNAs, a new class of small RNAs approximately 18–25 nucleotides in length, do not include the information encoding proteins, but they are involved in the regulation of gene expression at a posttranscriptional level. miRNAs were first described in Caenorhabditis elegans and are highly conserved among animals, humans, plants, and viruses [1] . The fact that their structure is conserved among species renders miRNAs easy-to-use biomarkers in translational investigation. In addition, miRNAs have recently emerged as inflammation markers in several cardiac pathologies, including AMI. In this issue of Cardiology, Latet et al. [2] report an increase in miRNA-155 (miRNA-155) expression in the Received: May 17, 2017 Accepted: May 17, 2017 Published online: June 16, 2017

Effects of Ivabradine on Heart Rate and Hemodynamic Parameters in a Swine Model of Cardiogenic Shock

Cardiogenic shock (CS) after myocardial infarction is associated with elevated mortality. There are few specific treatment options. Catecholamine administration may worsen tachycardia because decreased tissue perfusion may lead to reduced ventricular efficiency and increased oxygen consumption. Preliminary data indicate that ivabradine may offer a benefit in situations of severe tachycardia and shock, probably as a result of lower oxygen consumption and oxidative stress, although the hemodynamic effects of the drug in this context are unknown. For this reason, prior to administration of the drug in a clinical setting, we deemed it appropriate to study whether ivabradine administration may induce hemodynamic changes in a porcine model of CS after myocardial infarction. Ten female large white pigs (mean weight, 32.8 [2.2] kg) were included. The animals were anesthetized with propofol and fentanyl and the anterior descending artery was occluded for 45 minutes by inflation of an angioplasty balloon. To simulate CS after infarction, noradrenalin, dobutamine, and saline solution were administered until a postreperfusion heart rate (HR) of 90 bpm and a pulmonary wedge pressure > 18 mmHg were achieved. Amiodarone was also administered at the same dose in both study groups to prevent ventricular fibrillation, which is a frequent occurrence in porcine models of acute ischemia. Hemodynamic parameters (blood pressure, HR, cardiac output, pulmonary artery pressure, pulmonary wedge pressure, and central venous pressure) were monitored with Swan-Ganz catheters inserted into the aorta via the carotid and jugular approach. After balloon deflation, each animal was stabilized for 15 minutes prior to subsequent open-label randomization to the control group (n = 5) or ivabradine group (n = 5). Ivabradine was administered intravenously as a slow intravenous bolus at a dose of 0.3 mg/kg and was diluted in distilled water at a concentration 12 mg/mL. The placebo group received the equivalent volume of saline solution. The aforementioned hemodynamic parameters were then measured at 15-minute intervals after infusion of drug/placebo. The study variables are expressed as mean SD. The means were compared with the Student t test for independent data with a normal distribution and with the Fisher-Pitman test for independent variables with a nonparametric distribution. Ivabradine administration was associated with a significant decrease in HR (Figure 1; median [confidence interval] absolute reduction in HR at 15 minutes, 21 [21 to 25] vs –1 [–5 to 0] bpm; P = .04), with no change in blood pressure, pulmonary artery pressure, or cardiac output. Tidal volume significantly increased in the ivabradine group (Figure 2; tidal volume at 15 minutes, 63.7 [5.7] vs 43.7 [7.5] mL; P < .01). However, the decrease in HR was not accompanied by a reduction in pulmonary wedge pressure, and an increase in central venous pressure was observed compared with the control group (Figure 1). The numerical differences recorded in the 2 groups before administration of the study drug were not significant for any variables. Although findings indicative of the efficacy and safety of ivabradine in acute heart failure after infarction have been reported, the hemodynamic impact of reducing HR in CS is not known. Our results are in agreement with those of Bakkehaug et al. in a porcine model of CS. The model used by those authors, however, was more invasive than ours—medial sternotomy was performed—and is thus less readily applicable in clinical practice. An additional consideration, at least as important as the type of model, is that the animals in that study were not randomized; rather, the animals were their own control. An effect of spontaneous improvement occurring after induction of ischemia and reperfusion of the infarction cannot therefore be ruled out. In conclusion, ivabradine administered in a porcine model of CS induced by ischemia/reperfusion can reduce HR without significantly compromising cardiac output and can therefore increase tidal volume. However, this reduction in HR does not appear to reduce filling pressures. Before randomized clinical studies are conducted, we believe broader knowledge is required, in particular with a view to establishing whether this pharmacological strategy is of any value in reducing oxidative stress and myocardial damage in CS after myocardial infarction.

General Aspects of Transthoracic 3D-Echo

3D TTE has been one of the biggest advances in ultrasound technology. To obtain large volumes with adequate frame rate is the major challenge in 3D TTE. There are several methods of data acquisition in 3D TTE. To assess left ventricular function, it is better to choose full volume acquisition. To evaluate mitral or aortic valves, choose zoom acquisition. There are also various methods of 3D image display: slice rendering allows accurate measurements of chamber dimensions, valve areas and regurgitant jets. Cropping is very useful to remove anatomical structures to focus exclusively on the target anatomy. Apical four-chamber is the preferred view to 3D TTE left ventricle (LV) data acquisition. 3D TTE enables complete assessment of right ventricle (RV) geometry including the inflow, apex and outflow tract. 3D TTE may be superior to 2D TTE techniques diagnosing complex mitral valve disease. It enables “en face” visualization of the mitral valve from LV and LA perspectives. Parasternal long and short axis, apical and the subcostal views are the preferred to display the tricuspid valve (TV). 3D TTE aortic valve (AV) area measurement is more precise than the 2D TEE approach. 3DE short-axis view allows real AV orifice planimetry. 3D TTE has proved to be a useful tool in Congenital Heart disease (CHD) in three specific areas: improved understanding of the anatomy of the CHD, quantification of volumes and ventricular function, especially of the right ventricle and guiding therapeutic interventions.

Aortitis With Associated Left Main Coronary Artery Stenosis: Role of Cardiac Computed Tomography

We report on a 49-year-old man who presented to the emergency department with progressive angina. Echocardiography displayed severe aortic regurgitation and aortic valve thickening. The suspected diagnosis was acute aortic syndrome. Cardiac computed tomography showed circumferential thickening of the aortic wall and left main coronary artery ostial stenosis. Histologic examination showed diffuse aortic inflammation. No damage of any other organ or vascular structure was reported, and the final diagnosis was nonspecific aortitis. Differential diagnosis, prognosis, and therapeutic strategies are discussed.