Nuria Ribas

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).

Bioelectrical impedance vector analysis (BIVA) in stable and non-stable heart failure patients: A pilot study

a ICREC Research Group, Health Research Institute Germans Trias i Pujol, Badalona, Spain b Department of Electronic Engineering, Technical University of Catalonia, Barcelona, Spain c Cardiology Service, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain d Cardiology Service, Hospital Universitari Germans Trias i Pujol, Badalona, Spain e Department of Medicine, Universitat Autonoma de Barcelona, Barcelona, Spain

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.

Chronobiology of Death in Heart Failure

INTRODUCTION AND OBJECTIVES In the general population, heart events occur more often during early morning, on Mondays, and during winter. However, the chronobiology of death in heart failure has not been analyzed. The aim of this study was to determine the circadian, day of the week, and seasonal variability of all-cause mortality in chronic heart failure. METHODS This was an analysis of all consecutive heart failure patients followed in a heart failure unit from January 2003 to December 2008. The circadian moment of death was analyzed at 6-h intervals and was determined by reviewing medical records and by information provided by the relatives. RESULTS Of 1196 patients (mean [standard deviation] age, 69 [13] years; 62% male), 418 (34.9%) died during a mean (standard deviation) follow-up of 29 (21) months. Survivors were younger, had higher body mass index, left ventricular ejection fraction, glomerular filtration rate, hemoglobin and sodium levels, and lower Framingham risk scores, amino-terminal pro-B type natriuretic peptide, troponin T, and urate values. They were more frequently treated with angiotensin receptor blockers, beta-blockers, mineralocorticoids receptor antagonists, digoxin, nitrates, hydralazine, statins, loop diuretics, and thiazides. The analysis of the circadian and weekly variability did not reveal significant differences between the four 6-h intervals or the days of the week. Mortality occurred more frequently during the winter (30.6%) compared with the other seasons (P = .024). CONCLUSIONS All cause mortality does not follow a circadian pattern, but a seasonal rhythm in patients with heart failure. This finding is in contrast to the circadian rhythmicity of cardiovascular events reported in the general population.

Long-term outcome of transitory "reversible" complete atrio-ventricular block unrelated to myocardial ischemia.

fraction: comorbidities drive myocardial dysfunction and remodeling through coronarymicrovascular endothelial inflammation. J AmColl Cardiol 2013;62:263–71. [15] Sekhri V, Sanal S, DeLorenzo LJ, Aronow WS, Maguire GP. Cardiac sarcoidosis: a comprehensive review. Arch Med Sci 2011;7(4):546–54. [16] Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119(14):e391–479. [17] Baughman RP, Teirstein AS, Judson MA, et al. Clinical characteristics of patients in a case control study of sarcoidosis. Am J Respir Crit Care Med 2001;164:1885–9. [18] Quarta G, Holdright DR, Plant GT, et al. Cardiovascular magnetic resonance in cardiac sarcoidosis with MR conditional pacemaker in situ. J Cardiovasc Magn Reson 2011;13:26. [19] Fang L, Beale A, Ellims AH, et al. Associations between fibrocytes and postcontrast myocardial T1 times in hypertrophic cardiomyopathy. J Am Heart Assoc 2013;2(5): e000270.

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.