Oona Meroño

Iron deficiency is a key determinant of health-related quality of life in patients with chronic heart failure regardless of anaemia status

To evaluate the effect of iron deficiency (ID) and/or anaemia on health‐related quality of life (HRQoL) in patients with chronic heart failure (CHF).

Effects of Preoperative Intravenous Erythropoietin Plus Iron on Outcome in Anemic Patients After Cardiac Valve Replacement

Preoperative anemia is a risk factor for postoperative morbidity and in-hospital mortality in cardiac surgery. However, it is not known whether treatment of anemia before cardiac surgery by administering recombinant human erythropoietin (rhEPO) plus iron improves postoperative outcomes and decreases red blood cell transfusions in these patients. In 1998 a collection of consecutive data for patients who underwent valve replacement was initiated and the inclusion criterion was anemia. Treatment with rhEPO was given at a dose of 500 IU/kg/day every week for 4 weeks and the fifth dose 48 hours before valve replacement. During each rhEPO session, patients received intravenous iron sucrose supplementation. The intervention cohort (2006 to 2011) included 75 patients and the observation cohort was composed of 59 patients who did not receive any treatment (1998 to 2005). Multivariable logistic regression analysis showed that administration of combined therapy was independently associated with decreased postoperative morbidity (odds ratio [OR] 0.13, 95% confidence interval [CI] 0.03 to 0.59 p = 0.008) and in-hospital mortality (OR 0.16, 95% CI 0.28 to 0.95 p = 0.04) after adjusting for logistic European System for Cardiac Operative Risk Evaluation score, type of intervention, time of cardiopulmonary bypass, and year of surgery. Individually, this treatment also decreased postoperative renal failure (OR 0.23, 95% CI 0.06 to 0.88, p = 0.03). Rate of red blood cell transfusion decreased from 93% in the observation cohort to 67% in the intervention cohort as did days of hospitalization (median, 15 days, 10 to 27, versus 10 days, 8 to 14, respectively, p = 0.01 for all comparisons). In conclusion, administration of intravenous rhEPO plus iron in anemic patients before valve replacement improves postoperative survival, decreases blood transfusions, and shortens hospitalization.

Differences in neurohormonal activity partially explain the obesity paradox in patients with heart failure: The role of sympathetic activation

BACKGROUND Obese patients with chronic Heart Failure (HF) have better outcome than their lean counterparts, although little is known about the pathophysiology of this obesity paradox. Our aim was to evaluate the hypothesis that patients with chronic HF and obesity (defined as body mass index (BMI)≥30kg/m(2)), may have an attenuated neurohormonal activation in comparison with non-obese patients. METHODS AND RESULTS The present study is the post-hoc analysis of a cohort of 742 chronic HF patients from a single-center study evaluating sympathetic activation by measuring baseline levels of norepinephrine (NE). Obesity was present in 33% of patients. Higher BMI and obesity were significantly associated with lower NE levels in multivariable linear regression models adjusted for covariates (p<0.001). Addition to NE in multivariate Cox proportional hazard models attenuated the prognostic impact of BMI in terms of outcomes. Finally, when we explored the prognosis impact of raised NE levels (>70th percentile) carrying out a separate analysis in obese and non-obese patients we found that in both groups NE remained a significant independent predictor of poorer outcomes, despite the lower NE levels in patients with chronic HF and obesity: all-cause mortality hazard ratio=2.37 (95% confidence interval, 1.14-4.94) and hazard ratio=1.59 (95% confidence interval, 1.05-2.4) in obese and non-obese respectively; and cardiovascular mortality hazard ratio=3.08 (95% confidence interval, 1.05-9.01) in obese patients and hazard ratio=2.08 (95% confidence interval, 1.42-3.05) in non-obese patients. CONCLUSION Patients with chronic HF and obesity have significantly lower sympathetic activation. This finding may partially explain the obesity paradox described in chronic HF patients.

Hyperkalemia Mimicking a Pattern of Brugada Syndrome

A 70-year-old patient with a history of hypertension and dyslipidemia was receiving treatment with enalapril, simvastatin, and hydrochlorothiazide. He was referred to our hospital for presyncope and suspected acute myocardial infarction in an anterior location. The first electrocardiogram (Fig. 1A) showed a saddlebag-type ST segment elevation in V1 to V3. Echocardiography excluded a segmental wall motion abnormality. Despite the patient’s advanced age and the absence of previous episodes of syncope or a family history of sudden death, the presumptive diagnosis was Brugada syndrome. The initial analyses showed creatinine 4.88 mg/dL, Na 127 mEq/L, K 7.53 mEq/L, pH 7.22, and troponin T <0.01 ng/mL. The patient was treated for hyperpotassemia and was hospitalized to investigate renal failure. Once the potassium concentration had normalized, a new electrocardiographic study was carried out (Fig. 1B), in which the Brugada pattern had disappeared. Nonetheless, a flecainide test was performed, with negative results. Various situations have been described in which an electrocardiographic pattern of Brugada syndrome is manifested, such as drug-related conditions, heart diseases, acute myocardial infarction with ST segment elevation, muscular dystrophy, and hypothermia. Although hyperpotassemia can display diverse manifestations on electrocardiography, a presentation mimicking a Brugada pattern is very unusual. Figure 1.

Clinical correlates and prognostic impact of impaired iron storage versus impaired iron transport in an international cohort of 1821 patients with chronic heart failure

AIMS To define iron deficiency in chronic heart failure (CHF), both, ferritin<100μg/L (indicating reduced iron storage) and transferrin saturation (TSAT)<20% (indicating reduced iron transport) are used. The aim of the study was to evaluate clinical outcomes and prognosis of either low ferritin or low TSAT in patients with CHF. METHODS AND RESULTS We evaluated the clinical impact of impaired iron storage (IIS) and impaired iron transport (IIT) either alone or in combination compared to patients with normal iron status (NIS), in an international cohort of 1821 patients with CHF with a mean age of 66±13years and mean left ventricular ejection fraction of 35%±15. Isolated IIS was observed in 219 patients (12%), isolated IIT in 454 (25%) and coexistence of both conditions (IIS+IIT) were seen in 389 (21%). In adjusted models we found that patients with IIS+IIT and patients with isolated IIT had higher NT-proBNP levels (OR 2.2 [1.6-3.1] and OR 2.1 [1.5-2.9] respectively) and worse quality of life (OR 1.8 [1.2-2.7] and OR 1.7 [1.2-2.5] respectively) compared with isolated IIS. Multivariate Cox analyses showed that IIS+IIT and isolated IIT were independently associated with all-cause mortality (OR 1.41 [1.06-1.86] and OR 1.47 [1.13-1.92] respectively). Patients with isolated IIS did not differ from NIS patients in terms of severity or outcomes. CONCLUSIONS Impaired iron transport alone or in combination with impaired iron storage is associated with worse clinical profile and increased risk of mortality in patients with CHF. Patients with isolated impaired iron storage may have a milder form of iron deficiency.

Iron Deficiency Is a Determinant of Functional Capacity and Health-related Quality of Life 30 Days After an Acute Coronary Syndrome.

BACKGROUND AND OBJECTIVES Iron deficiency (ID) is a prevalent condition in patients with ischemic heart disease and heart failure. Little is known about the impact of ID on exercise capacity and quality of life (QoL) in the recovery phase after an acute coronary syndrome (ACS). METHODS Iron status and its impact on exercise capacity and QoL were prospectively evaluated in 244 patients 30 days after the ACS. QoL was assessed by the standard EuroQoL-5 dimensions, EuroQoL visual analogue scale, and Heart-QoL questionnaires. Exercise capacity was analyzed by treadmill/6-minute walk tests. The effect of ID on cardiovascular mortality and readmission rate was also investigated. RESULTS A total of 46% of the patients had ID. These patients had lower exercise times (366±162 vs 462±155seconds; P<.001), metabolic consumption rates (7.9±2.9 vs 9.3±2.6 METS; P=.003), and EuroQoL-5 dimensions (0.76±0.25 vs 0.84±0.16), visual analogue scale (66±16 vs 72±17), and Heart-QoL (1.9±0.6 vs 2.2±0.6) scores (P<.05). ID independently predicted lower exercise times (OR, 2.9; 95%CI, 1.1-7.6; P=.023) and worse QoL (OR, 1.9; 95%CI, 1.1-3.3; P<.001) but had no effect on cardiovascular morbidity or mortality. CONCLUSIONS ID, a prevalent condition in ACS patients, results in a poorer mid-term functional recovery, as measured by exercise capacity and QoL.

Characterization of the Nodal Slow Pathway in Patients With Nodal Reentrant Tachycardia: Clinical Implications for Guiding Ablation

INTRODUCTION AND OBJECTIVES Nodal slow pathway ablation is the treatment of choice for nodal reentrant tachycardia. No demographic, anatomic, or electrophysiologic variables have been reported to predict an exact location of the slow pathway in the atrioventricular node or its proximity to the fast pathway. The purpose of this study was to analyze these variables. METHODS The study prospectively included 54 patients (17 men; mean age, 55 [16] years) who had undergone successful slow pathway ablation. The refractory periods of both pathways and their differential conduction time were measured, and calculations were performed to obtain the distance from the His-bundle region (location of the fast pathway) to the coronary sinus ostium (to estimate the anteroposterior length of the triangle of Koch) and to the slow pathway area. RESULTS The differential conduction time (139 [98] ms) did not correlate with the His-coronary sinus distance (19 [6] mm; P=.6) or the His-slow pathway distance (14 [4] mm; P=.4). When the His-coronary sinus distance was larger, the His-slow pathway distance was also larger (r=0.652; P<.01) and the anatomic correlation between the triangle dimensions and the separation between the two pathways was confirmed. In patients older than 70 years, smaller triangle sizes and a shorter distance between both pathways were observed (P<.001). CONCLUSIONS A greater anteroposterior dimension of the triangle of Koch is associated with a slow-pathway location farther from the fast pathway. In elderly patients the two pathways are closer together (higher risk of atrioventricular block).

Brugada Phenocopy Emerging as a New Concept. Response

The authors appreciate the interest in the case report we published in Revista Española de Cardiologı́a concerning the observation of the Brugada electrocardiographic (ECG) pattern in a patient with hyperkalemia. We likewise welcome the introduction of the concept of phenocopy, an expression with which our finding is compatible.We also consider it opportune to stress that both the latest consensus on ECG diagnosis of Brugada syndrome and the introduction of the term phenocopy are more recent than the online publication of our case report in 2011. The definitions of the ECG patterns that are typical of Brugada syndrome and those that mimic this syndrome in the presence of serum electrolyte disturbances were introduced subsequent to our publication. It is important to highlight reasons for attributing the changes observed in the ECG to hyperkalemia rather than to the acidosis and hyponatremia also observed in our patient. Reports of Brugada phenocopy associated with hyponatremia and acidosis have described the development of pseudo J waves in the QRS complex and ST segment depression in leads other than right precordial leads. These are precisely the features that differentiate this ECG pattern from type 1 Brugada pattern. Other possible causes (hyperglycemia, drugs, fever, and myocardial ischemia) were ruled out in the case discussed in our report. We appreciate any contribution that aids in the understanding of the mechanisms involved in the induction of ECG patterns mimicking Brugada syndrome (phenocopies) and other patterns, such as early repolarization, which can also be associated with the risk of sudden cardiac death. Finally, we agree with Dr. Anselm on the importance of performing a challenge test with flecainide to rule out Brugada syndrome. Until the prognosis of patients presenting with Brugada phenocopy has been established, it is advisable to perform pharmacological challenge tests and, if appropriate, to induce ventricular arrhythmias by means of an electrophysiological study.