Subclinical Left Ventricular Systolic Dysfunction in Hospitalized Patients with COVID-19 by Strain: A 30-Day Echocardiographic Follow-Up.

Background and Objectives: Available studies confirm myocardial injury and its association with mortality in patients with COVID-19, but few data have been reported from echocardiographic studies. The aim of this study was to identify subclinical left ventricular dysfunction by global longitudinal strain (GLS) and its evolution in the short term in hospitalized patients with COVID-19. Materials and Methods: Thirty-one consecutive noncritical patients admitted for COVID-19 were included. Information on demographics, laboratory results, comorbidities, and medications was collected. Transthoracic echocardiograms were performed using a Philips Affinity 50, at the acute stage and at a 30-day follow-up. Automated left ventricular GLS was measured using a Philips Qlab 13.0. A GLS of <-15.9% was defined as abnormal. Results: The mean age was 65 ± 15.2 years, and 61.3% of patients were male. Nine patients (29%) had elevated levels of high-sensitivity troponin I. Left ventricular ejection fraction was preserved in all; however, 11 of them (35.5%) showed reduced GLS. These patients had higher troponin levels (median, 23.7 vs. 3.2 ng/L; p < 0.05) and NT-proBNP (median, 753 vs. 81 pg/mL; p < 0.05). The multivariate analysis revealed that myocardial injury, defined as increased troponin, was significantly associated with GLS values (coefficient B; p < 0.05). Follow-up at 30 days showed an improvement in GLS values in patients with subclinical left ventricular dysfunction (-16.4 ± 2.07% vs. -13.2 ± 2.40%; p < 0.01), without changes in the normal GLS group. Conclusions: Subclinical left ventricular dysfunction is common in noncritical hospitalized patients with COVID-19 (one in every three patients), even with preserved left ventricular ejection fraction. This impairment tends to be reversible on clinical recovery.

Clinical implications of nonsarcomeric gene polymorphisms in hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by cardiomyocyte hypertrophy and fibrosis. Although is an autosomal dominant trait, a group of nonsarcomeric genes have been postulated as modifiers of the phenotypic heterogeneity. MATERIAL AND METHODS: We prospectively recruited 168 HCM patients and 136 healthy controls from three referral centres. Patients and controls were clinically stable at entry in the study. Nine polymorphisms previously associated with ventricular remodelling were determined: I/D ACE, AGTR1(A1666C), CYP11B2(C344T), PGC1-α(G482S), COLIA1(G2046T), ADRB1(R389G), NOS3(G894T), RETN(-420C>G) and CALM3(-34T>A). Their potential influence on prognosis, assessed by hospital admissions, and their cause were recorded. RESULTS: The median follow-up time was 49·5 months. Allele and genotype frequencies did not differ between patients and controls. Thirty-six patients (21·5%) required urgent hospitalization (18·5% for heart failure, 22·2% for atrial arrhythmias, 11·1% for ventricular arrhythmias, 29·6% for ischaemic heart disease, 14·8% for stroke and 3·7% for other reasons) with a hospitalization rate of 8·75% per year. Multivariate analysis showed an independent predictive value for noncarriers of polymorphic COL1A1 allele [HR: 2·76(1·26-6·05), P = 0·011] and a trend in homozygous carriers of ADRB1 Arg389 variant [HR: 1·98(0·99-4·02); P = 0·057]. CONCLUSION: Our study suggests that COL1A1 polymorphism (2046G>T) is an independent predictor of prognosis in HCM patients supporting the importance of nonsarcomeric genes on clinical prognosis in HCM.

La puntuación CHADS2 como predictor de riesgo de ictus en ausencia de fibrilación auricular en pacientes hipertensos de 65 o más años / The CHADS2 score to predict stroke risk in the absence of atrial fibrillation in hypertensive patients aged 65 years or older

Introducción y objetivos: La puntuación CHADS2 es una demostrada herramienta fundamental para identificar el riesgo cardioembólico, fundamentalmente el ictus, de pacientes con fibrilación auricular no valvular, con el propósito de indicar la terapia anticoagulante. El objetivo del presente estudio es analizar la utilidad de dicha puntuación para pacientes hipertensos sin fibrilación auricular conocida en una zona mediterránea. Métodos: Se incluyó a 887 pacientes hipertensos de edad ≥ 65 años, no anticoagulados y sin fibrilación auricular, que acudieron a la consulta médica. Se recogieron los principales factores de riesgo, la historia cardiovascular, el tratamiento farmacológico, una analítica básica y un electrocardiograma y se calculó la puntuación CHADS2 (insuficiencia cardiaca, hipertensión, edad ≥ 75 años, diabetes mellitus e ictus previo o accidente isquémico transitorio). Se realizó un seguimiento clínico con recogida de los ingresos hospitalarios por ictus o accidente isquémico transitorio. La mediana del seguimiento fue 804 días. Resultados: La media de edad era 72,5 ± 5,7 años, con el 46,6% de varones, el 27,8% de diabéticos y el 8,6% de fumadores. Durante el seguimiento, 40 pacientes fueron ingresados por ictus o accidente isquémico transitorio (4,5%). El análisis de supervivencia libre de eventos mostró diferencias significativas en función de la puntuación CHADS2 (log rank test, p < 0,001). En el análisis multivariable, el tabaquismo y un CHADS2 ≥ 3 fueron predictores independientes de ictus o accidente isquémico transitorio. Conclusiones: La puntuación CHADS2 puede ser una herramienta útil para identificar el riesgo de ictus o accidente isquémico transitorio de los pacientes hipertensos sin fibrilación auricular conocida (AU)

Introduction and objectives: The CHADS2 score is a proven, essential tool for estimating cardioembolic risk (mainly stroke) in patients with nonvalvular atrial fibrillation, with the purpose of determining the indication for anticoagulant therapy. In this study we analyzed the use of CHADS2 in hypertensive patients without known atrial fibrillation in a Mediterranean population. Methods: The study included 887 hypertensive patients aged 65 years or older without atrial fibrillation or anticoagulant therapy, who attended a medical consultation. Data on the patients’ main risk factors, cardiovascular history, and medication were collected, basic laboratory analyses and electrocardiography were performed, and the CHADS2 score (heart failure, hypertension, age ≥ 75 years, diabetes mellitus, and previous stroke or transient ischemic attack) was calculated. A clinical follow-up was carried out, recording hospital admissions for a stroke or transient ischemic attack. The median duration of follow-up was 804 days. Results: Mean age was 72.5 (SD,5.7) years, 46.6% were men, 27.8% had diabetes, and 8.6% were smokers. During follow-up, 40 patients were hospitalized for a stroke or transient ischemic attack (4.5%). The event-free survival analysis showed significant differences according to the CHADS2 score (log rank test, P < .001). On multivariate analysis, smoking and CHADS2 ≥3 were independent predictors of stroke or transient ischemic attack. Conclusions: The CHADS2 may be useful for estimating the risk of stroke or transient ischemic attack in hypertensive patients without known atrial fibrillation (AU)

La importancia de la estratificación de riesgo de muerte súbita en la miocardiopatía hipertrófica / Importance of sudden cardiac death risk stratification in hypertrophic cardiomyopathy

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The CHADS2 Score to Predict Stroke Risk in the Absence of Atrial Fibrillation in Hypertensive Patients Aged 65 Years or Older.

INTRODUCTION AND OBJECTIVES: The CHADS2 score is a proven, essential tool for estimating cardioembolic risk (mainly stroke) in patients with nonvalvular atrial fibrillation, with the purpose of determining the indication for anticoagulant therapy. In this study we analyzed the use of CHADS2 in hypertensive patients without known atrial fibrillation in a Mediterranean population. METHODS: The study included 887 hypertensive patients aged 65 years or older without atrial fibrillation or anticoagulant therapy, who attended a medical consultation. Data on the patients' main risk factors, cardiovascular history, and medication were collected, basic laboratory analyses and electrocardiography were performed, and the CHADS2 score (heart failure, hypertension, age ≥ 75 years, diabetes mellitus, and previous stroke or transient ischemic attack) was calculated. A clinical follow-up was carried out, recording hospital admissions for a stroke or transient ischemic attack. The median duration of follow-up was 804 days. RESULTS: Mean age was 72.5 (SD,5.7) years, 46.6% were men, 27.8% had diabetes, and 8.6% were smokers. During follow-up, 40 patients were hospitalized for a stroke or transient ischemic attack (4.5%). The event-free survival analysis showed significant differences according to the CHADS2 score (log rank test, P < .001). On multivariate analysis, smoking and CHADS2 ≥3 were independent predictors of stroke or transient ischemic attack. CONCLUSIONS: The CHADS2 may be useful for estimating the risk of stroke or transient ischemic attack in hypertensive patients without known atrial fibrillation.

Identification and confirmation of haptoglobin as a potential serum biomarker in hypertrophic cardiomyopathy using proteomic approaches.

INTRODUCTION: Aiming at identifying biomarkers for hypertrophic cardiomyopathy (HCM), the serum proteome was explored through a two-dimensional gel-based proteomic approach (2D-DIGE) coupled with mass spectrometry and database interrogation. METHODS: Serum samples from 20 male HCM patients and their sex- and age-matched controls were cleaned from interfering components. Patients and controls were pooled in five matched groups with the same age, and proteins extracts from each pool were labelled with cyanine dyes. Then, gel images were analysed using a fluorescence scanner and proteins were identified. Tryptic peptides were analysed by capillary reversed-phase liquid chromatography coupled online with tandem mass spectrometry (MS/MS). RESULTS: Four different proteins were observed to be differentially expressed between HCM patients and their matched controls. Of them, decreases in haptoglobin levels were confirmed to be associated with HCM in an independent set of 181 consecutive HCM patients from our monographic clinic and 114 controls with similar age and sex using a nephelometer-based technique. Moreover, a significant negative correlation was observed between haptoglobin and subaortic gradient, thus highlighting the role of haptoglobin in HCM. CONCLUSION: All these observations point out the utility of the 2D-DIGE proteomic strategy for the identification of serum proteins indicative of the presence of cardiac injury.

Growth differentiation factor-15, a novel biomarker related with disease severity in patients with hypertrophic cardiomyopathy.

BACKGROUND: The growth differentiation factor 15 (GDF-15) has been shown up-regulated in stress conditions and to have regulatory actions in myocyte hypertrophy. We hypothesized that GDF-15 could be related to disease severity and functional status in patients with hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: We performed a study which includes 102 consecutive outpatient HCM subjects, 73% males, aged 47.1±14.6 years. A complete history and clinical examination was performed, including 12-lead electrocardiogram, echocardiography, symptom-limited treadmill exercise, 24-hour ECG-Holter monitoring, and magnetic resonance with Gadolinium. Several biomarkers, associated with myocardial remodeling and damage, were compared to GDF-15 levels. The assays were performed with commercial ELISAs or standardized methods when available. There was a significant association between GDF-15 levels and comorbidities, being higher in hypertension (p=0.001), diabetes (p=0.030), atrial fibrillation (p=0.012), dyspnea (p=0.020) and NYHA≥II functional class (p=0.037). GDF-15 levels were positively correlated with clinical variables (age, worse exercise capacity and mild renal dysfunction) and biomarkers of interstitial remodeling, such as metalloproteinase-2 (r: 0.40; p=0.009), N-terminal pro-B-type natriuretic peptide (r: 0.28; p=0.049), high-sensitivity troponin T (r: 0.30; p=0.003) and von Willebrand factor (r: 0.33; p=0.001). Multivariate analysis was assessed to estimate the involvement of these different factors in the GDF-15 levels, confirming the independent implication of severe dyspnea and functional status. CONCLUSIONS: The present results show that higher levels of GDF-15 are associated to conditions of severe disease in HCM. Hence, GDF-15 is suggested as a novel marker related to the severity and could represent a further useful tool in monitoring functional capacity of HCM patients.

Serum levels of high-sensitivity troponin T: a novel marker for cardiac remodeling in hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by inappropriate hypertrophy, small-vessel coronary artery disease, myocyte disarray, and increased interstitial fibrosis. High-sensitivity troponin T (hs-TnT) could be a reliable indicator of myocardial remodeling, a proposed prognostic marker in HCM. Therefore we hypothesized that increased hs-TnT levels are related to different variables associated with myocardial remodeling, such as the presence of fibrosis assessed with cardiac magnetic resonance imaging (MRI). METHODS AND RESULTS: We included 95 hemodynamically stable HCM patients, 72 male, aged 45.7 ± 14.2 years, and 45 healthy control subjects with similar age and gender. A complete history and clinical examination was performed, including 12-lead electrocardiogram (ECG), echocardiography, 24-hour ECG-Holter monitoring, symptom-limited treadmill exercise test, and late gadolinium enhancement in cardiac MRI. Risk factors for sudden death were evaluated. A blinded cardiac MRI was performed with late gadolinium enhancement study. Serum hs-TnT levels were assayed. A high proportion (42%) of hemodynamically stable patients studied showed increased levels of hs-TnT. The hs-TnT levels were raised in patients with severe dyspnea: New York Heart Association (NYHA) functional class ≥3 (P = .020), outflow obstruction (P = .013), systolic dysfunction (P = .037), abnormal blood pressure response (P = .036), and presence of gadolinium enhancement (P = .021). The hs-TnT levels correlated positively with the maximum left ventricular wall thickness (r = 0.47; P < .001), left atrial diameter (r = 0.36, P = .014), and outflow gradient (r = 0.28; P = .008). CONCLUSIONS: A high proportion of hemodynamically stable patients show increased levels of hs-TnT. We observed that raised hs-TnT serum levels are associated with different conditions related to the severity of the disease.

Plasma levels of von Willebrand factor are increased in patients with hypertrophic cardiomyopathy.

UNLABELLED: Hypertrophic cardiomyopathy (HCM) is characterised by inappropriate hypertrophy, small-vessel coronary artery disease, myocyte disarray and increased interstitial fibrosis. Microvascular dysfunction is a common finding in HCM and its extent has been proposed as an important prognostic marker. Plasma von Willebrand factor (vWf) is an established marker of endothelial damage or dysfunction; however it has scarcely been studied in HCM. We hypothesised that vWf could be raised in patients with HCM and be related to different variables associated with severity of HCM. METHODS: We included 124 HCM patients, 93 males, aged 48+/-15 years, 59 healthy control subjects with similar age and sex and 20 patients with ischemic heart disease but clinical stability for the last 6 months. A complete history and clinical examination was performed, including 12-lead electrocardiogram, echocardiography, 24 hours ECG-Holter monitoring, and symptom limited treadmill exercise test. Risk factors for sudden death were evaluated. A blinded cardiac MRI was performed with late enhanced study with Gadolinium. Plasma vWf levels were assayed by commercial ELISA. RESULTS: Patients showed higher levels of vWf (140.0+/-65.0 UI/ml vs 105.0+/-51.0 UI/ml, p<0.001) even after adjusting for ABO blood group. vWf levels were found raised in patients with severe functional class (168.4+/-65.9 UI/mL vs 132.4+/-60.7 UI/mL, p=0.020), atrial fibrillation (175.8+/-69.4 UI/mL vs 133.0+/-59.0 UI/mL, p=0.005), hypertension (161.4+/-60.8 vs 128.9+/-60.5, p=0.010) obstruction (153.9+/-67.9 vs 128.2+/-57.4 UI/mL, p=0.046) and non sustained ventricular tachycardia (159.3+/-59.1 vs 133.0+/-63.0, p=0.049). vWf correlated with age (r:0.26; p=0.006) and obstruction (r:0.22; p=0.021). CONCLUSIONS: We show, for the first time, patients with HCM present significantly raised levels of vWf. These are associated with different conditions related to the severity of the disease.

¿Existe un efecto beneficioso a largo plazo con el tratamiento con marcapasos de la miocardiopatía hipertrófica obstructiva severa? / Does pacemaker implantation provide long-term benefits in severe obstructive hypertrophic cardiomyopathy?

Introducción y objetivos. Alrededor de un 25% de los pacientes con MCH obstructiva permanecen sintomáticos a pesar de una correcta medicación. Algunos pueden beneficiarse del implante de un marcapasos. El objetivo fue valorar el efecto del marcapasos en la modificación del gradiente en el tracto de salida del ventrículo izquierdo (TSVI), grosor máximo del ventrículo izquierdo (VI) y en la capacidad funcional. Métodos. A 72 pacientes con MCH obstructiva y síntomas incapacitantes se les implantó un marcapasos. Se realizó un examen clínico, una ecocardiografía (61 pacientes) y una ergometría (34 pacientes) antes y después de la implantación del marcapasos. Resultados. La capacidad funcional subjetiva, estimada según la clasificación de la NYHA, mejoró en el 43,1% de los pacientes, aunque no lo hizo la estimada mediante ergometría. Se observó una reducción significativa del gradiente subaórtico (mediana, 87 [intervalo intercuartílico, 61,5-115,2] frente a 30 [18-54,5] mmHg; p < 0,001) y del grosor máximo del VI (22,1 ± 4,5 frente a 19,8 ± 3,6 mm; p = 0,001). En el análisis univariable, el sexo femenino (OR = 3,43; p = 0,020) y la clase funcional III/IV (OR = 4,17; p = 0,009) se asociaron a una mejoría clínica. En el análisis multivariable, sólo la clase funcional III/IV mantuvo la significación (OR = 3,12; p = 0,048). Conclusiones. La implantación de marcapasos en pacientes con MCH obstructiva con síntomas incapacitantes disminuye el gradiente obstructivo del TSVI y el grosor máximo del VI, pero sólo el 43,1% consigue una mejoría clínica subjetiva, siendo una clase funcional más avanzada el único factor predictor de mejoría (AU)

Introduction and objectives. About 25% of patients with obstructive hypertrophic cardiomyopathy (HCM) remain symptomatic despite optimal medical treatment. Some may benefit from pacemaker implantation. The aim of this study was to determine the effect of pacemaker implantation on the left ventricular outflow tract (LVOT) gradient, the maximum thickness of the left ventricle, and functional capacity. Methods. In total, 72 patients with obstructive HCM and incapacitating symptoms underwent pacemaker implantation. Clinical examination, echocardiography (in 61 patients) and treadmill testing (in 34 patients) were performed before and after implantation. Results. Subjective functional capacity, as assessed using the New York Heart Association (NYHA) classification, improved in 43.1% of patients, but treadmill testing showed no change. There were significant reductions in subaortic gradient, from a median of 87.0 mmHg (interquartile range [IQR] 61.5-115.2 mmHg) to 30.0 mmHg (IQR 18.0-54.5 mmHg; P < .001), and maximum left ventricular thickness, from 22.1±4.5 mm to 19.8±3.6 mm (P=.001). Univariate analysis identified two factors associated with clinical improvement: female sex (odds ratio [OR]=3.43; P=.020) and functional class III/IV (OR=4.17; P=.009). On multivariate analysis, only functional class III/IV remained a significant predictor (OR=3.12; P=.048). Conclusions. In patients with obstructive HCM and incapacitating symptoms, pacemaker implantation reduced the LVOT gradient and the maximum left ventricular thickness, but only 43.1% of patients experienced clinical improvement. The only factor predictive of improvement was advanced NYHA functional class (AU)

Gadolinium-enhanced cardiovascular magnetic resonance and exercise capacity in hypertrophic cardiomyopathy.

INTRODUCTION AND OBJECTIVES: Using gadolinium-enhanced cardiovascular magnetic resonance, it is possible to evaluate the presence of myocardial fibrosis in hypertrophic cardiomyopathy. Classical disease markers are weak predictors of functional disability in affected patients. Our objective was to study the relationship between the degree of myocardial fibrosis observed by cardiac magnetic resonance and exercise capacity. METHODS: We performed cardiac magnetic resonance, echocardiography, exercise testing and Holter monitoring, along with the usual clinical assessments, in 98 patients (age, 46.3+/-15.4 years, 71.4% male) referred from two specialist hypertrophic cardiomyopathy clinics. Cardiac magnetic resonance assessment included quantifying the degree of fibrosis (i.e., the percentage of the myocardium showing enhancement) 10 min after gadolinium infusion. Symptom-limited exercise testing was used to determine exercise capacity (in metabolic equivalent [MET] units). In 71 patients, the basal N-terminal probrain natriuretic peptide (NT-proBNP) level was also measured. RESULTS: Late enhancement was observed on cardiac magnetic resonance in 67 (68.4%) patients. These patients had a lower exercise capacity (8.04+/-3.56 MET vs. 10.41+/-3.57 MET; P=.003). There was an inverse correlation between the percentage of fibrosis and exercise capacity (r=-0.21; P=.044). The best predictor of exercise capacity was the logarithm of the NT-proBNP level (r=-0.5; P< .0001). Multivariate analysis confirmed that age, a history of atrial fibrillation, the basal NT-proBNP level and the presence of fibrosis were independent predictors of exercise capacity (r2 for the model=0.47). CONCLUSIONS: The observation of areas of late gadolinium enhancement on cardiac magnetic resonance was independently associated with poor exercise capacity in patients with hypertrophic cardiomyopathy.

Factor VII -323 decanucleotide D/I polymorphism in atrial fibrillation: implications for the prothrombotic state and stroke risk.

UNLABELLED: There are limited data on the influence of genetic polymorphisms in atrial fibrillation (AF) stroke risk. We hypothesized that a functional haemostatic polymorphism, that is, the factor VII -323 Del/Ins polymorphism, would influence the prothrombotic state associated with AF, as well as stroke risk. Other functional polymorphisms were also tested. METHODS: We performed a cross-sectional study of 119 AF patients, who were compared to 96 patients with stroke secondary to AF. In the first patient group, we analysed plasma prothrombin fragment 1+2 levels (F1+2, an index of thrombin generation) to reflect the prothrombotic state of AF. RESULTS: AF patients carrying the -323 Ins allele had lower plasma F1+2 levels (P=0.015). After multivariate analysis adjusted by age, sex and clinical risk factors, advanced age and 807C/T polymorphism of glycoprotein Ia (GPIa) gene were associated with higher risk of ischaemic stroke (OR: 1.06; P=0.003 and OR: 1.91; P=0.025), whilst FVII Ins -323 allele was associated with lower stroke risk (OR: 0.41; P=0.017). CONCLUSION: FVII -323 Ins allele may modulate the prothrombotic state associated with AF. Despite the small sample size, we found that FVII Ins -323 allele could be associated with a lower stroke risk in AF, whereas the 807C/T polymorphism may increase the risk.

Matrix metalloproteinases and tissue remodeling in hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is defined by the presence of unexplained left ventricular hypertrophy, myocyte disarray, and interstitial fibrosis. An increase in extracellular matrix produces interstitial fibrosis, by raised amounts of collagen type I/III. Regions of myocardial late gadolinium enhancement by cardiac magnetic resonance (CMR) represented increased myocardial collagen. Regarding the role of matrix metalloproteinases (MMPs) in myocardial remodeling and subsequent fibrosis, the aim of our study was to explore the relation between MMP system and myocardial late gadolinium enhancement by CMR (as expression of image-documented fibrosis) and N-terminal pro-brain natriuretic peptide (NT-proBNP) (as a marker of cardiac overload) in HCM. METHODS: We included 67 HCM patients (44 men aged 49 +/- 14 years) and were compared to 58 controls with similar age and sex. Risk factors for sudden death were recorded. A blinded CMR was performed with gadolinium. Matrix metalloproteinase 1, MMP-2, and MMP-9 plasma levels were assayed by enzyme-linked immunosorbent assay. Serum samples were used for measurement of NT-proBNP. RESULTS: In patients, >50% of MMP-1 values were below the lowest limit of detection of the technique. Raised levels of MMP-2, MMP-9, and NT-proBNP were observed in HCM patients (all P < .01). Matrix metalloproteinase 2 was associated with dyspnea (P = .049) and correlated with MMP-9 (r = 0.28, P = .025) and NT-proBNP (r = 0.39, P = .001). Matrix metalloproteinase 9 was associated with the presence of gadolinium enhancement in CMR (P = .001) and correlated with NT-proBNP (r = 0.52, P < .001). NT-proBNP was also associated with gadolinium enhancement (P = .006). Both MMP-2 and MMP-9 correlated negatively with exercise capacity (metabolic equivalent units), (r = -0.36 and r = -0.42 respectively, both P < .01). On multivariate analysis (adjusted by sudden death risk factors and echocardiographic markers), only MMP-9 was associated with fibrosis (P = .011). CONCLUSIONS: Matrix metalloproteinase 9 is independently associated with gadolinium enhancement on CMR in patients with hypertrophic cardiomyopathy, suggesting that the MMP system has an important role in cardiac remodeling and fibrosis in this condition.

Cardiorresonancia magnética con gadolinio y capacidad de esfuerzo en la miocardiopatía hipertrófica / Gadolinium-Enhanced Cardiovascular Magnetic Resonance and Exercise Capacity in Hypertrophic Cardiomyopathy

Introducción y objetivos. La cardiorresonancia magnéticacon gadolinio permite estudiar la fibrosis miocárdicaen la miocardiopatía hipertrófica. Los marcadores clásicos de la enfermedad predicen débilmente la limitación funcional de estos pacientes. Nuestro objetivo es estudiar la relación entre la fibrosis en la cardiorresonancia magnética y la capacidad de ejercicio.Métodos. Se realizó cardiorresonancia magnética, ecocardiografía, ergometría y Holter, junto con la valoración clínica habitual, a 98 pacientes procedentes de dos consultas especializadas de miocardiopatía hipertrófica (edad, 46,3 ± 15,4 años; el 71,4% varones). El estudio de cardiorresonancia magnética incluyó cuantificación de fibrosis (porcentaje de miocardio realzado) 10 min tras la inyección de gadolinio. Mediante ergometría limitada por síntomas, se determinó la capacidad de esfuerzo (MET). En 71 pacientes se obtuvieron además concentraciones plasmáticas basales de NT-proBNP.Resultados. Presentaron áreas de realce tardío en lacardiorresonancia magnética 67 (68,4%) pacientes. Estospacientes tenían peor capacidad de esfuerzo (8,04 ± 3,56frente a 10,41 ± 3,57 MET; p = 0,003). Se observó correlación negativa entre el porcentaje de fibrosis y los MET alcanzados (r = –0,21; p = 0,044). El mejor predictor de capacidad de esfuerzo fue el logNT-proBNP (r = –0,5; p <0,0001). El análisis multivariado confirmó que la edad, los antecedentes de fibrilación auricular, las concentraciones basales de NT-proBNP y la fibrosis son predictores independientes de la capacidad de esfuerzo (r2 del modelo = 0,47).Conclusiones. La presencia de áreas de realce tardíocon gadolinio en la cardiorresonancia magnética se asociade forma independiente con una peor capacidad deesfuerzo en pacientes con miocardiopatía hipertrófica

Introduction and objectives. Using gadoliniumenhancedcardiovascular magnetic resonance, it ispossible to evaluate the presence of myocardial fibrosis in hypertrophic cardiomyopathy. Classical disease markersare weak predictors of functional disability in affectedpatients. Our objective was to study the relationshipbetween the degree of myocardial fibrosis observed bycardiac magnetic resonance and exercise capacity.Methods. We performed cardiac magnetic resonance,echocardiography, exercise testing and Holter monitoring,along with the usual clinical assessments, in 98 patients(age, 46.3±15.4 years, 71.4% male) referred from twospecialist hypertrophic cardiomyopathy clinics. Cardiacmagnetic resonance assessment included quantifying thedegree of fibrosis (i.e., the percentage of the myocardium showing enhancement) 10 min after gadolinium infusion. Symptom-limited exercise testing was used to determine exercise capacity (in metabolic equivalent [MET] units). In 71 patients, the basal N-terminal probrain natriuretic peptide (NT-proBNP) level was also measured.Results. Late enhancement was observed on cardiacmagnetic resonance in 67 (68.4%) patients. Thesepatients had a lower exercise capacity (8.04±3.56 METvs. 10.41±3.57 MET; P=.003). There was an inversecorrelation between the percentage of fibrosis andexercise capacity (r=–0.21; P=.044). The best predictor of exercise capacity was the logarithm of the NT-proBNPlevel (r=–0.5; P<.0001). Multivariate analysis confirmedthat age, a history of atrial fibrillation, the basalNT-proBNP level and the presence of fibrosis wereindependent predictors of exercise capacity (r2 for themodel=0.47).Conclusions. The observation of areas of lategadolinium enhancement on cardiac magnetic resonancewas independently associated with poor exercise capacityin patients with hypertrophic cardiomyopathy

Prevalence of fabry disease in a cohort of 508 unrelated patients with hypertrophic cardiomyopathy.

OBJECTIVES: We aimed to study the prevalence of Fabry disease (FD) in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: There are limited and controversial data about the prevalence of FD in patients with HCM. METHODS: We screened the plasma alpha-galactosidase A activity from 508 unrelated patients with HCM (328 men, 180 women, ages 58 +/- 16 years). Patients with low activity (0% to 30% of the normal control in men, and 0% to 50% in women) underwent genetic study of the GLA gene. RESULTS: We found low plasma activity in 15 patients (3%). Three men had GLA mutations (0.9%): S238N (novel) in 2 and E358del (described) in 1. Two women had described mutations (1.1%): L89P and A143T. Three unrelated men had the D313Y variant previously associated with enzyme pseudo-deficiency. Two women had polymorphisms that did not segregate with the disease in their families. Five women (activity 39% to 47%) had no sequence variants. The familial studies allowed the diagnosis of 14 carriers: 6 women without Fabry manifestations, 3 women with cardiomyopathy, 2 men with renal and cardiac disease, 1 man with microhematuria, 1 woman with first-degree atrioventricular block, and a 32-year-old woman with only renal disease. CONCLUSIONS: By means of a screening based on genotyping of patients with low plasma enzymatic activity, the prevalence of FD in our population of HCM is 1% (0.9% in men and 1.1% in women). This diagnosis is relevant, because it allows the identification of disease carriers that might benefit from enzyme replacement therapy.

Antiplatelet versus anticoagulant therapies in advanced age: an unfinished task.

We have read with great interest a retrospective cohort study recently published by Blich and Gross. In our opinion, this article renews the controversy of the best antithrombotic therapy in patients with AF. The use of anticoagulant treatment to prevent the occurrence of stroke in patients with AF is supported by several randomized controlled clinical trials. Aspirin is also effective in preventing stroke in AF, but both direct and indirect comparisons with oral anticoagulation suggest less effectiveness. However, very probably these patients are quite different than those seen in the clinical practice. The role of antiplatelet therapy is not completely established, and the selection between aspirin or warfarin in advanced age remains an unfinished task.