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1.
Am J Cardiol ; 124(5): 723-728, 2019 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-31266594

RESUMO

Atrial fibrillation (AF) is one of the most common cardiovascular complications in patients hospitalized with community-acquired pneumonia (CAP). However, predisposing clinical factors associated with AF in CAP patients have not been fully elucidated. We enrolled 545 patients consecutively hospitalized for CAP. Data on demographic characteristics and co-morbidities were collected and all patients underwent ECG, echocardiography, and laboratory measurements. During the in-hospital stay, 9.5% of patients experienced a new episode of AF within 24 to 72 hours from admission. CAP patients who experienced AF had a higher indexed left atrial area (LAAi) and a higher proportion of concentric left ventricular hypertrophy than those not presenting AF. Univariate logistic regression analysis showed that hypertension, history of coronary heart disease, high Pneumonia Severity Index classes, history of paroxysmal AF, systolic heart failure, concentric left ventricular hypertrophy, and an enlarged LAAi were associated with a new episode of AF. A multivariable logistic analysis showed that history of paroxysmal AF (odds ratio [OR] 11.7; 95% confidence interval [CI] 5.8 to 23.7; p <0.001), enlarged LAAi (OR 5.4; 95% CI 2.5 to 11.9; p <0.001), and concentric left ventricular hypertrophy (OR 2.2; 95 CI 1.1 to 4.6; p = 0.034) remained independently associated with AF occurrence. In conclusion, in this large cohort of CAP patients, history of paroxysmal AF, enlarged LAAi, and concentric left ventricular hypertrophy are independent predictors of AF occurrence during the early stages of pneumonia.


Assuntos
Fibrilação Atrial/epidemiologia , Infecções Comunitárias Adquiridas/epidemiologia , Mortalidade Hospitalar/tendências , Hipertrofia Ventricular Esquerda/epidemiologia , Pneumonia Bacteriana/epidemiologia , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/terapia , Causas de Morte , Estudos de Coortes , Infecções Comunitárias Adquiridas/diagnóstico , Infecções Comunitárias Adquiridas/terapia , Comorbidade , Ecocardiografia/métodos , Eletrocardiografia/métodos , Hospitais Universitários , Humanos , Hipertrofia Ventricular Esquerda/diagnóstico , Hipertrofia Ventricular Esquerda/terapia , Itália , Modelos Logísticos , Pessoa de Meia-Idade , Análise Multivariada , Pneumonia Bacteriana/diagnóstico , Pneumonia Bacteriana/terapia , Prevalência , Prognóstico , Estudos Prospectivos , Medição de Risco , Índice de Gravidade de Doença , Distribuição por Sexo , Taxa de Sobrevida
2.
Jpn J Radiol ; 37(9): 642-650, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31301000

RESUMO

PURPOSE: To investigate the effects of renal denervation (RDN) on left ventricular (LV) mass, myocardial strain and diastolic function in patients with treatment-resistant arterial hypertension by cardiac magnet resonance imaging on a 12-month follow-up. MATERIALS AND METHODS: Sixteen patients (38% female) were examined before and 12 months after RDN. LV morphology and strain were analyzed. Diastolic function was determined by early (EPFR) and atrial peak filling rates (APFR) derived from differential volume-time-curve analysis. Clinical visits included 24-h ambulant blood pressure monitoring (ABPM). RESULTS: Twelve months after RDN LV mass decreased from 80 ± 21 g/m2 to 74 ± 20 g/m2 (P < 0.05). Global radial (35 ± 12% vs. 41 ± 10%, P < 0.05) and longitudinal strain improved (- 15 ± 4% vs. - 17 ± 3%, P < 0.05). Global circumferential strain (- 16 ± 5% vs. - 18 ± 4%, P = 0.12) remained unchanged. The parameter of diastolic LV function PFRR (EPFR/APFR) improved following RDN (0.9 ± 0.4 vs. 1.1 ± 0.5, P < 0.05). Individual changes of LV mass were associated with an increase of EPFR (r = - 0.54, P < 0.05) and a reduction of APFR by trend (r = 0.45, P = 0.08). Systolic ABPM showed a decrease by trend (152 mmHg vs. 148 mmHg, P = 0.08). CONCLUSIONS: After RDN we observed a reduction of LV mass, improvement of global strain and diastolic function.


Assuntos
Coração/fisiopatologia , Hipertensão/complicações , Hipertrofia Ventricular Esquerda/complicações , Rim/cirurgia , Imagem por Ressonância Magnética/métodos , Simpatectomia/métodos , Diástole , Feminino , Seguimentos , Ventrículos do Coração/diagnóstico por imagem , Humanos , Hipertrofia Ventricular Esquerda/diagnóstico por imagem , Hipertrofia Ventricular Esquerda/terapia , Rim/inervação , Masculino , Pessoa de Meia-Idade , Resultado do Tratamento
3.
Arch Cardiovasc Dis ; 112(4): 278-287, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30826269

RESUMO

Fabry disease is an X-linked progressive multisystemic genetic sphingolipidosis caused by deficient activity of lysosomal α-galactosidase A. Men aged>30 years and women aged>40 years most often present with unexplained left ventricular hypertrophy, usually concentric and non-obstructive, but sometimes mimicking sarcomeric hypertrophic cardiomyopathy, particularly when isolated, as in the cardiac or late-onset variant of the disease. In hypertrophic cardiomyopathy cohorts, up to 1% of patients have been diagnosed with Fabry disease. Frequent cardiac symptoms include chronotropic incompetence, severe conduction disturbances and arrhythmias, heart failure and sudden death, and cardiovascular complications are currently the leading cause of death at a mean age of 55 years in men and 66 years in women. Complementary to screening for extracardiac manifestations, the initial cardiac evaluation should include long-duration electrocardiogram recordings, echocardiography and late gadolinium and T1 mapping magnetic resonance imaging. Abnormalities of a non-hypertrophied inferolateral wall at the base of the left ventricle (thinning, decreased strain, midwall fibrosis) and low native T1 signal on magnetic resonance imaging are evocative. Aggressive cardiac management may include the control of cardiovascular risk factors, anticoagulation, permanent cardiac pacing and/or an implantable cardioverter defibrillator device, while antiarrhythmics and beta-blockers should be used with caution. Specific therapy should be initiated at the earliest stage, when the first structural or functional cardiac abnormalities are detected, and should include enzyme replacement therapy (available since 2001) or chaperone therapy (available since 2016) (the use of which is limited to patients with Fabry disease and an amenable α-galactosidase A [GLA] gene mutation).


Assuntos
Cardiologia , Doença de Fabry , Hipertrofia Ventricular Esquerda , Adulto , Idoso , Cardiomiopatia Hipertrófica/diagnóstico , Diagnóstico Diferencial , Ecocardiografia , Eletrocardiografia , Terapia de Reposição de Enzimas , Doença de Fabry/diagnóstico , Doença de Fabry/mortalidade , Doença de Fabry/fisiopatologia , Doença de Fabry/terapia , Feminino , Humanos , Hipertrofia Ventricular Esquerda/diagnóstico , Hipertrofia Ventricular Esquerda/mortalidade , Hipertrofia Ventricular Esquerda/fisiopatologia , Hipertrofia Ventricular Esquerda/terapia , Imagem por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Prognóstico , Fatores de Risco , Função Ventricular Esquerda , Remodelação Ventricular
4.
J Cardiothorac Vasc Anesth ; 33(5): 1205-1213, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30416026

RESUMO

OBJECTIVE: To investigate whether prophylactic amiodarone infusion prevents ventricular fibrillation after aortic cross-clamp release and attenuates cytokine production in patients with left ventricular hypertrophy undergoing cardiac surgery. DESIGN: Prospective, randomized controlled trial. SETTING: A public hospital. PARTICIPANTS: The study comprised 68 patients undergoing aortic valve replacement for severe aortic stenosis. INTERVENTIONS: Patients were randomly assigned to receive a 150mg bolus then 30mg/h continuous infusion of amiodarone (amiodarone group) or a 1 mg/kg bolus then 1 mg/kg/h continuous infusion of lidocaine (lidocaine group). The primary outcome was the ventricular fibrillation incidence rate after aortic cross-clamp release. Secondary outcomes included perioperative serum interleukin-6 and tumor necrosis factor-alpha levels. MEASUREMENTS AND MAIN RESULTS: The ventricular fibrillation incidence rate was significantly lower in the amiodarone than in the lidocaine group (20.6% v 50%, relative risk 0.41; 95% confidence interval [CI] 0.20-0.86; p = 0.021). Interleukin-6 levels 1hour after aortic cross-clamp release and at intensive care unit admission were significantly lower in the amiodarone than in the lidocaine group (geometric mean [95% CI] 117.4pg/mL [87.1-158.4] v 339.5pg/mL [210.6-547.2]; p < 0.01 and 211.1pg/mL [162.8-73.6] v 434.1pg/mL [293.7-641.5]; p < 0.01, respectively). Tumor necrosis factor-alpha levels 1hour after aortic cross-clamp release were significantly lower in the amiodarone than in the lidocaine group (geometric mean [95% CI] 1.624pg/mL [1.359-1.940] v 2.283pg/mL [1.910-2.731]; p = 0.02). CONCLUSIONS: Amiodarone prevented reperfusion ventricular fibrillation in patients with left ventricular hypertrophy undergoing aortic valve replacement to a greater extent than did lidocaine. Furthermore, amiodarone inhibited postoperative interleukin-6 and tumor necrosis factor-alpha production.


Assuntos
Amiodarona/administração & dosagem , Antiarrítmicos/administração & dosagem , Estenose da Valva Aórtica/terapia , Implante de Prótese de Valva Cardíaca/tendências , Hipertrofia Ventricular Esquerda/terapia , Reperfusão Miocárdica/métodos , Fibrilação Ventricular/terapia , Idoso , Idoso de 80 Anos ou mais , Estenose da Valva Aórtica/fisiopatologia , Método Duplo-Cego , Feminino , Implante de Prótese de Valva Cardíaca/efeitos adversos , Humanos , Hipertrofia Ventricular Esquerda/fisiopatologia , Infusões Intravenosas , Masculino , Pessoa de Meia-Idade , Reperfusão Miocárdica/tendências , Profilaxia Pós-Exposição/métodos , Profilaxia Pós-Exposição/tendências , Estudos Prospectivos , Resultado do Tratamento , Fibrilação Ventricular/fisiopatologia
5.
Cardiovasc Res ; 115(1): 71-82, 2019 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-29931050

RESUMO

Aims: Chronic heart failure is becoming increasingly prevalent and is still associated with a high mortality rate. Myocardial hypertrophy and fibrosis drive cardiac remodelling and heart failure, but they are not sufficiently inhibited by current treatment strategies. Furthermore, despite increasing knowledge on cardiomyocyte intracellular signalling proteins inducing pathological hypertrophy, therapeutic approaches to target these molecules are currently unavailable. In this study, we aimed to establish and test a therapeutic tool to counteract the 22 kDa calcium and integrin binding protein (CIB) 1, which we have previously identified as nodal regulator of pathological cardiac hypertrophy and as activator of the maladaptive calcineurin/NFAT axis. Methods and results: Among three different sequences, we selected a shRNA construct (shCIB1) to specifically down-regulate CIB1 by 50% upon adenoviral overexpression in neonatal rat cardiomyocytes (NRCM), and upon overexpression by an adeno-associated-virus (AAV) 9 vector in mouse hearts. Overexpression of shCIB1 in NRCM markedly reduced cellular growth, improved contractility of bioartificial cardiac tissue and reduced calcineurin/NFAT activation in response to hypertrophic stimulation. In mice, administration of AAV-shCIB1 strongly ameliorated eccentric cardiac hypertrophy and cardiac dysfunction during 2 weeks of pressure overload by transverse aortic constriction (TAC). Ultrastructural and molecular analyses revealed markedly reduced myocardial fibrosis, inhibition of hypertrophy associated gene expression and calcineurin/NFAT as well as ERK MAP kinase activation after TAC in AAV-shCIB1 vs. AAV-shControl treated mice. During long-term exposure to pressure overload for 10 weeks, AAV-shCIB1 treatment maintained its anti-hypertrophic and anti-fibrotic effects, but cardiac function was no longer improved vs. AAV-shControl treatment, most likely resulting from a reduction in myocardial angiogenesis upon downregulation of CIB1. Conclusions: Inhibition of CIB1 by a shRNA-mediated gene therapy potently inhibits pathological cardiac hypertrophy and fibrosis during pressure overload. While cardiac function is initially improved by shCIB1, this cannot be kept up during persisting overload.


Assuntos
Proteínas de Ligação ao Cálcio/metabolismo , Insuficiência Cardíaca/terapia , Hipertrofia Ventricular Esquerda/terapia , Miócitos Cardíacos/metabolismo , RNA Interferente Pequeno/metabolismo , Terapêutica com RNAi , Disfunção Ventricular Esquerda/terapia , Função Ventricular Esquerda , Remodelação Ventricular , Animais , Calcineurina/metabolismo , Proteínas de Ligação ao Cálcio/genética , Células Cultivadas , Modelos Animais de Doenças , Fibrose , Insuficiência Cardíaca/genética , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/fisiopatologia , Hipertrofia Ventricular Esquerda/genética , Hipertrofia Ventricular Esquerda/metabolismo , Hipertrofia Ventricular Esquerda/fisiopatologia , Masculino , Camundongos Endogâmicos C57BL , Miócitos Cardíacos/patologia , Fatores de Transcrição NFATC/metabolismo , Neovascularização Fisiológica , RNA Interferente Pequeno/genética , Ratos Sprague-Dawley , Transdução de Sinais , Disfunção Ventricular Esquerda/genética , Disfunção Ventricular Esquerda/metabolismo , Disfunção Ventricular Esquerda/fisiopatologia
6.
Prog Cardiovasc Dis ; 61(5-6): 446-455, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30408469

RESUMO

Left ventricular hypertrophy (LVH) was one of the earliest studied echocardiographic characteristics of the left ventricle. As the myriad of measurable metrics has multiplied over recent years, this reliable and relevant variable can often be overlooked. In this paper, we discuss appropriate techniques for accurate analysis, underlying pathophysiology, and the contributions from various risk factors. The prognostic implications of LVH on stroke, serious arrhythmias, and sudden cardiac death are reviewed. Finally, we examine the effect of therapy to reduce LVH and the resultant clinical outcomes.


Assuntos
Arritmias Cardíacas/etiologia , Morte Súbita Cardíaca/etiologia , Hipertrofia Ventricular Esquerda/complicações , Acidente Vascular Cerebral/etiologia , Função Ventricular Esquerda , Remodelação Ventricular , Arritmias Cardíacas/diagnóstico por imagem , Arritmias Cardíacas/fisiopatologia , Arritmias Cardíacas/terapia , Ecocardiografia , Humanos , Hipertrofia Ventricular Esquerda/diagnóstico por imagem , Hipertrofia Ventricular Esquerda/fisiopatologia , Hipertrofia Ventricular Esquerda/terapia , Valor Preditivo dos Testes , Prognóstico , Fatores de Risco , Acidente Vascular Cerebral/diagnóstico por imagem , Acidente Vascular Cerebral/fisiopatologia , Acidente Vascular Cerebral/terapia
7.
Semin Nephrol ; 38(6): 600-617, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30413254

RESUMO

Heart failure (HF) is a major comorbidity in patients with end-stage kidney disease (ESKD). The pathogenesis of HF in patients on renal replacement therapy represents the confluence of several traditional and nontraditional vascular risk factors, unique to the milieu of chronic kidney disease and the dialysis modality. The diagnosis of HF with ESKD is complicated by the background of frequent inevitable fluid shifts superimposed on underlying myocardial pump abnormalities and dialysis-induced myocardial stunning. A careful temporal assessment of symptoms and physical findings, cardiac imaging, hemodynamic data, and biomarkers help establish an accurate diagnosis of HF in ESKD. Accurate volume assessment and its tight management remains the cornerstone of treatment in HF in patients on dialysis. A multidisciplinary approach between the cardiologist and nephrologist in optimizing pharmacologic strategies for HF in this population, and dialysis-based options such as frequent dialysis, may help reduce the burden of HF in this vulnerable population. Finally, including patients with ESKD in clinical trials for HF therapies, and designing pragmatic trials that bring targeted strategies for HF into the daily clinical practice of dialysis, will shed light on the optimal management of the dual burden of cardiomyopathy and advanced kidney disease.


Assuntos
Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/terapia , Hipertrofia Ventricular Esquerda/etiologia , Falência Renal Crônica/complicações , Miocárdio/patologia , Diálise Renal , Biomarcadores/sangue , Líquidos Corporais , Cardiomiopatias/etiologia , Cardiomiopatias/patologia , Fatores de Crescimento de Fibroblastos/sangue , Fibrose , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/etiologia , Humanos , Hipertrofia Ventricular Esquerda/sangue , Hipertrofia Ventricular Esquerda/terapia , Hipotensão/etiologia , Falência Renal Crônica/fisiopatologia , Falência Renal Crônica/terapia , Diálise Renal/efeitos adversos , Diálise Renal/métodos
9.
Mol Genet Metab ; 124(2): 143-151, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-29747997

RESUMO

Fabry disease is a hereditary disorder that occurs due to the reduction or absence of alpha-galactosidase A activity, which leads to cardiac involvement including left ventricular hypertrophy (LVH). Enzyme replacement therapy (ERT) provides better patient outcomes by preventing serious complications. However, there have been very few studies on the long-term effects of ERT on the cardiac manifestations in Japanese Fabry patients. We retrospectively analyzed the data from the medical records of 42 Fabry patients (male, n = 17; female, n = 25) who were followed at Jikei University Hospital, and in whom the long-term effects of ERT could be evaluated (median follow-up period: male, 11 years; female, 8 years). The slope of the left ventricular mass (LVM) increase was 3.02 ±â€¯3.41 g/m2/year in males and 1.69 ±â€¯2.73 g/m2/year in females. In a subgroup analysis, the slopes of males with and without LVH did not differ to a statistically significant extent; however, the slope in female patients without LVH was significantly smaller than that of female patients with LVH. We then compared our data to the natural historical data that have previously been reported. In comparison to the previously reported data, we found a significant reduction in the LVM changes (g/height2.7/year) of patients who received long-term ERT (male, 4.07 ±â€¯1.03 to 1.25 ±â€¯1.39; female, 2.31 ±â€¯0.81 to 0.78 ±â€¯1.23). Long-term ERT effectively prevents LVH in Fabry patients. This effect was also observed in the patients with LVH prior to the initiation of ERT.


Assuntos
Terapia de Reposição de Enzimas , Doença de Fabry/complicações , Hipertrofia Ventricular Esquerda/terapia , alfa-Galactosidase/administração & dosagem , Adulto , Ecocardiografia , Doença de Fabry/enzimologia , Feminino , Humanos , Hipertrofia Ventricular Esquerda/enzimologia , Hipertrofia Ventricular Esquerda/etiologia , Masculino , Prognóstico , Estudos Retrospectivos , alfa-Galactosidase/metabolismo
10.
J Am Heart Assoc ; 7(11)2018 05 27.
Artigo em Inglês | MEDLINE | ID: mdl-29807890

RESUMO

BACKGROUND: Longer QRS duration (QRSd) improves, but increased left ventricular (LV) end-diastolic volume (LVEDV) reduces, efficacy of cardiac resynchronization therapy (CRT). QRSd/LVEDV ratios differ between sexes. We hypothesized that in the EchoCRT (Echocardiography Guided Cardiac Resynchronization Therapy) trial enrolling patients with heart failure with QRSd <130 ms, those with larger LVEDV would deteriorate but those with the highest QRSd/LVEDV would improve with CRT. METHODS AND RESULTS: Primary outcome in patients (n=787, 72% men, 93% New York Heart Association class III, QRSd <130 ms, LV ejection fraction ≤35%, LV dilation and dyssynchrony) randomized to CRT-ON or CRT-OFF and followed up for 19 months was compared according to LVEDV (height indexed) or QRSd/LVEDV ratio, in multivariable analysis. Structural remodeling was assessed echocardiographically 6 months after implantation. Patients with baseline LVEDV higher than or equal to median worsened with CRT (death/heart failure hospitalization: CRT-ON versus CRT-OFF, 35.2% versus 24.5% [hazard ratio, 1.64; 95% confidence interval, 1.11-2.42; P=0.012]), but those with LVEDV lower than median remained unaffected. Patients with the highest QRSd/LVEDV ratio improved with CRT (death/heart failure hospitalization in top quartile: 20.9% in CRT-ON [n=91] versus 28.3% in CRT-OFF [n=106] [hazard ratio, 0.64; 95% confidence interval, 0.34-1.24; P=0.188], versus the remaining quartiles: 31.7% in CRT-ON [n=300] versus 24.8% in CRT-OFF [n=290] [hazard ratio, 1.47; 95% confidence interval, 1.07-2.02; P=0.016], test for interaction P=0.046). QRSd and dyssynchrony were similar between groups. The 3-way test for interaction indicated no sex-specific effects. However, numerically, men with LVEDV higher than or equal to median accounted for worse outcomes of CRT-ON. Women, with the highest QRSd/LVEDV ratio exhibited significant reverse remodeling. CONCLUSION: CRT has opposite effects among patients with heart failure with QRSd <130 ms according to LV size: worsening outcomes in patients with larger LV, but inducing beneficial effects in those with smaller LV. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00683696.


Assuntos
Terapia de Ressincronização Cardíaca , Sistema de Condução Cardíaco/fisiopatologia , Insuficiência Cardíaca/terapia , Ventrículos do Coração/fisiopatologia , Hipertrofia Ventricular Esquerda/terapia , Função Ventricular Esquerda , Remodelação Ventricular , Potenciais de Ação , Idoso , Terapia de Ressincronização Cardíaca/efeitos adversos , Terapia de Ressincronização Cardíaca/mortalidade , Ecocardiografia , Eletrocardiografia , Feminino , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/mortalidade , Insuficiência Cardíaca/fisiopatologia , Frequência Cardíaca , Ventrículos do Coração/diagnóstico por imagem , Humanos , Hipertrofia Ventricular Esquerda/diagnóstico , Hipertrofia Ventricular Esquerda/mortalidade , Hipertrofia Ventricular Esquerda/fisiopatologia , Masculino , Pessoa de Meia-Idade , Medição de Risco , Fatores de Risco , Fatores Sexuais , Fatores de Tempo , Resultado do Tratamento
11.
Atherosclerosis ; 274: 206-211, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29800790

RESUMO

BACKGROUND AND AIMS: Left ventricular hypertrophy (LVH), assessed by electrocardiogram (ECG), is associated with increased risk for stroke. However, few studies that evaluated whether ECG-detected LVH predicts ischemic stroke severity and outcome. We aimed to evaluate these associations. METHODS: We prospectively studied 922 patients consecutively admitted with acute ischemic stroke (age 79.6 ±â€¯6.9 years). Stroke severity was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). Severe stroke was defined as NIHSS≥5. LVH was evaluated with the Sokolow-Lyon index and the Cornell voltage-duration product criteria in an ECG obtained at admission. The outcome was assessed with dependency at discharge (modified Rankin scale 2-5) and in-hospital mortality. RESULTS: Independent predictors of severe stroke were age (relative risk (RR) per year 1.07, 95% confidence interval (CI) 1.03-1.11, p<0.001), female gender (RR 0.36, 95% CI 0.17-0.76, p<0.01), atrial fibrillation (RR 2.07, 95% CI 1.30-3.29, p<0.005), chronic kidney disease (RR 2.38, 95% CI 1.04-5.44, p<0.05), heart rate (RR per 1/min 1.02, 95% CI 1.01-1.04, p<0.005), glucose levels (RR 1.012, 95% CI 1.006-1.018, p<0.001), high-density lipoprotein cholesterol levels (RR 0.976, 95% CI 0.960-0.993, p<0.005) and LVH defined according to the Cornell voltage-duration product criteria (RR 2.08, 95% CI 1.12-3.86, p<0.05). Independent predictors of dependency at discharge were age (RR per year 1.08, 95% CI 1.03-1.13, p<0.001), past smoking (RR versus no smoking 0.42, 95% 0.19-0.89, p<0.05), history of ischemic stroke (RR 2.13, 95% CI 1.23-3.71, p<0.01) and NIHSS at admission (RR 1.48, 95% CI 1.35-1.63, p<0.001). Independent predictors of in-hospital mortality were glucose levels (RR 1.014, 95% CI 1.003-1.025, p<0.05), NIHSS at admission (RR 1.29, 95% CI 1.19-1.41, p<0.001) and LVH according to the Cornell voltage-duration product criteria (RR 4.95, 95% CI 1.09-22.37, p<0.05). CONCLUSIONS: LVH according to the Cornell voltage-duration product criteria appears to be associated with more severe stroke and with higher in-hospital mortality in patients with acute ischemic stroke.


Assuntos
Isquemia Encefálica/mortalidade , Eletrocardiografia , Mortalidade Hospitalar , Hipertrofia Ventricular Esquerda/diagnóstico , Acidente Vascular Cerebral/mortalidade , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Isquemia Encefálica/diagnóstico , Isquemia Encefálica/fisiopatologia , Isquemia Encefálica/terapia , Comorbidade , Avaliação da Deficiência , Feminino , Nível de Saúde , Humanos , Hipertrofia Ventricular Esquerda/mortalidade , Hipertrofia Ventricular Esquerda/fisiopatologia , Hipertrofia Ventricular Esquerda/terapia , Masculino , Admissão do Paciente , Valor Preditivo dos Testes , Prognóstico , Estudos Prospectivos , Medição de Risco , Fatores de Risco , Fatores Sexuais , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/fisiopatologia , Acidente Vascular Cerebral/terapia , Fatores de Tempo
12.
Medicine (Baltimore) ; 97(20): e10813, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29768383

RESUMO

RATIONALE: Infantile-onset hypertrophic cardiomyopathy (HCMP) should be considered a largely genetic condition, although its onset is most often triggered by infection. Very long chain acyl-CoA dehydrogenase (VLCAD) deficiency is a rare autosomal recessive inborn error of mitochondrial fatty acid ß-oxidation that often causes severe cardiomyopathy and/or sudden death during the neonatal period. PATIENT CONCERNS: Herein, we report an infant with VLCAD deficiency who presented with severe cardiac manifestations, including massive pericardial effusion and HCMP. The subject's older sister died of unknown causes at three days of age; however, the subject exhibited a normal tandem mass-spectrometry profile during the neonatal period. DIAGNOSES: During her later cardiac presentation, the subject's C-14 and C-18 levels became elevated, and she was determined, via the conducted molecular analysis, to harbor a novel homozygous frameshift mutation (c.103_112dup) in ACADVL. INTERVENTIONS: After VLCAD deficiency diagnosis, the subject was treated with the administration of a medium chain triglyceride formula and fluid therapy. OUTCOMES: The subject's cardiac status was markedly improved by the dietary intervention and fluid therapy. LESSONS: This report highlights that genetic mutations should be investigated as possible causes of infantile-onset HCMP, and that early diagnosis and intervention can prevent mortality for patients with VLCAD deficiency.


Assuntos
Acil-CoA Desidrogenase de Cadeia Longa/deficiência , Mutação da Fase de Leitura , Hipertrofia Ventricular Esquerda/etiologia , Erros Inatos do Metabolismo Lipídico/diagnóstico , Erros Inatos do Metabolismo Lipídico/genética , Doenças Mitocondriais/diagnóstico , Doenças Mitocondriais/genética , Doenças Musculares/diagnóstico , Doenças Musculares/genética , Derrame Pericárdico/etiologia , Acil-CoA Desidrogenase de Cadeia Longa/genética , Diagnóstico Tardio , Feminino , Hidratação , Humanos , Hipertrofia Ventricular Esquerda/terapia , Lactente , Erros Inatos do Metabolismo Lipídico/complicações , Erros Inatos do Metabolismo Lipídico/terapia , Doenças Mitocondriais/complicações , Doenças Mitocondriais/terapia , Doenças Musculares/complicações , Doenças Musculares/terapia , Derrame Pericárdico/terapia , Triglicerídeos/uso terapêutico
13.
Clin Chim Acta ; 484: 47-51, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-29758204

RESUMO

BACKGROUND: Left ventricular hypertrophy (LVH) is one of the most common cardiac abnormalities in patients with end-stage renal disease. Hippuric acid (HA), a harmful uremic toxin, is known to be elevated in patients with uremia, and serum HA levels are associated with neurological symptoms, metabolic acidosis, and accelerated renal damage associated with chronic kidney disease. However, the pathophysiological role of HA in patients with uremia remains unclear. We investigated the association between serum HA levels and echocardiographic measurements in patients undergoing hemodialysis (HD) treatment. METHODS: Eighty consecutive patients treated at a single HD center (44 males, 36 females; mean age 66 y, mean HD duration 6 y) were included in this study. Comprehensive echocardiography was performed after HD. Blood samples were obtained before HD. RESULTS: Pearson's correlation analysis revealed that serum HA levels were positively correlated with diastolic blood pressure, serum creatinine, left ventricular mass index, end diastolic interventricular septal thickness, left ventricular end-diastolic diameter, left ventricular end systolic diameter, end systolic left ventricular posterior wall thickness, and left atrium diameter, and negatively correlated with age. Furthermore, the HD patients with LVH had higher median serum HA levels than those without LVH (34.2 vs. 18.1 µg/ml, p = 0.003). Multiple logistic regression analysis revealed that HA was independently associated with LVH even after adjusting for known biomarkers. Moreover, the receiver operator characteristics curve of HA showed that a HA level of >26.9 µg/ml was associated with LVH. CONCLUSIONS: HA was significantly associated with LVH. HA could be a novel biomarker of left ventricular overload, which is closely associated with an increased risk of death in HD patients.


Assuntos
Hipuratos/efeitos adversos , Hipertrofia Ventricular Esquerda/terapia , Diálise Renal , Idoso , Biomarcadores/sangue , Ecocardiografia , Feminino , Hipuratos/administração & dosagem , Hipuratos/sangue , Humanos , Hipertrofia Ventricular Esquerda/sangue , Hipertrofia Ventricular Esquerda/diagnóstico , Masculino
14.
Am J Nephrol ; 47(3): 208-217, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29621747

RESUMO

BACKGROUND: Regression of left ventricular hypertrophy (LVH) is feasible with more frequent hemodialysis (HD). We aimed to ascertain pathways associated with regression of left ventricular mass (LVM) in patients enrolled in the Frequent HD Network (FHN) trials. METHODS: This was a post hoc observational cohort study. We hypothesized LVH regression with frequent HD was associated with a different cardiovascular biomarker profile. Regressors were defined as patients who achieved a reduction of more than 10% in LVM at 12 months. Progressors were defined as patients who had a minimum of 10% increase in LVM at 12 months. RESULTS: Among 332 randomized patients, 243 had biomarker data available. Of these, 121 patients did not progress or regress, 77 were regressors, and 45 were progressors. Mean LVM change differed between regressors and progressors by -65.6 (-74.0 to -57.2) g, p < 0.001. Regressors had a median (interquartile range) increase in dialysis frequency (from 3.0 [3.0-3.0] to 4.9 [3-5.7] per week, p = 0.001) and reductions in pre-dialysis systolic (from 149.0 [136.0-162.0] to 136.0 [123.0-152.0] mm Hg, p < 0.001) and diastolic (from 83.0 [71.0-91.0] to 76.0 [68.0-84.0] mm Hg, p < 0.001) blood pressures. Klotho levels increased in regressors versus progressors (76.9 [10.5-143.3] pg/mL, p = 0.024). Tissue inhibitors of metalloproteinase (TIMP)-2 levels fell in regressors compared to progressors (-7,853 [-14,653 to -1,052] pg/mL, p = 0.024). TIMP-1 and log (brain natriuretic -peptide [BNP]) levels also tended to fall in regressors. Changes in LVM correlated inversely with changes in klotho (r = -0.24, p = 0.014). -Conclusions: Markers of collagen turnover and changes in klotho levels are potential novel pathways associated with regression of LVH in the dialysis population, which will require further prospective validation.


Assuntos
Biomarcadores/sangue , Hipertrofia Ventricular Esquerda/terapia , Falência Renal Crônica/complicações , Diálise Renal , Adulto , Estudos de Coortes , Feminino , Humanos , Hipertrofia Ventricular Esquerda/sangue , Falência Renal Crônica/sangue , Falência Renal Crônica/terapia , Masculino , Pessoa de Meia-Idade , Ensaios Clínicos Controlados Aleatórios como Assunto , Indução de Remissão
15.
JACC Heart Fail ; 6(5): 364-375, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29655825

RESUMO

Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiomyopathy, manifesting as left ventricular hypertrophy in the absence of a secondary cause. The genetic underpinnings of HCM arise largely from mutations of sarcomeric proteins; however, the specific underlying mutation often remains undetermined. Patient presentation is phenotypically diverse, ranging from asymptomatic to heart failure or sudden cardiac death. Left ventricular hypertrophy and abnormal ventricular configuration result in dynamic left ventricular outflow obstruction in most patients. The goal of therapeutic interventions is largely to reduce dynamic obstruction, with treatment modalities spanning lifestyle modifications, pharmacotherapies, and septal reduction therapies. A small subset of patients with HCM will experience sudden cardiac death, and risk stratification remains a clinical challenge. This paper presents a clinical update for diagnosis, family screening, clinical imaging, risk stratification, and management of symptoms in patients with HCM.


Assuntos
Cardiomiopatia Hipertrófica Familiar/terapia , Cardiomiopatia Hipertrófica Familiar/diagnóstico por imagem , Cardiomiopatia Hipertrófica Familiar/genética , Cardiotônicos/uso terapêutico , Morte Súbita Cardíaca/etiologia , Diagnóstico Precoce , Ecocardiografia , Previsões , Marcadores Genéticos/genética , Testes Genéticos , Estilo de Vida Saudável , Coração Auxiliar , Humanos , Hipertrofia Ventricular Esquerda/terapia , Angiografia por Ressonância Magnética , Ilustração Médica , Mutação/genética , Linhagem , Medição de Risco , Fatores de Risco , Síncope/etiologia , Obstrução do Fluxo Ventricular Externo/etiologia
16.
Heart Surg Forum ; 21(2): E090-E095, 2018 Mar 06.
Artigo em Inglês | MEDLINE | ID: mdl-29658865

RESUMO

OBJECTIVES: Ventricular pacemaker stimulation may cause deterioration of hemodynamics in patients with left-ventricular hypertrophy following aortic valve replacement. Since the diastolic function is often impaired, it remains unclear which heart rate best optimizes cardiac output. Low heart rates are suggested to treat impaired diastolic function chronically, but it is possible that cardiac output may be augmented by increasing the heart rate in patients with a fixed stroke volume (SV). The aim of this study is the identification of the best pacing mode and heart rate for the surrogate parameter SV and cardiac index(CI) in patients with left ventricular hypertrophy. METHODS: Various pacemaker stimulation modes and different heart rates, as well as their influence on hemodynamics, were tested following aortic valve replacement in 48 patients with severe left-ventricular hypertrophy (Intraventricular septum (IVS)>1.5 cm) and aortic stenosis. SV and cardiac output were recorded by pulse curve analysis. Four modes of stimulation (right ventricular pacemaker stimulation (DDDright), left ventricular pacemaker stimulation (DDDleft), biventricular pacemaker stimulation (DDDbi), atrial pacemaker stimulation (AAI)) were documented at five different rates (60, 80, 100, 120, 140 beats/min) and three different postoperative time points (intraoperatively, 3h and 24h postoperatively). RESULTS: The highest CI was found at linear rates between 60 to 140bpm. AAI was the best mode of stimulation in the majority of cases (35%), but in others, either left, right and/or biventricular stimulation was found to be better (15%). SV showed a u-shaped trend with a peak at 100 beats/min. CONCLUSION: An increase in the heart rate does not lead to a notable drop in SV postoperatively in left-ventricular hypertrophy; hence a rise in cardiac output can be anticipated up to a rate of 100 beats/min. A standardized response in terms of an ideal pacemaker stimulation mode could not be identified.


Assuntos
Estenose da Valva Aórtica/cirurgia , Valva Aórtica/cirurgia , Estimulação Cardíaca Artificial/métodos , Próteses Valvulares Cardíacas , Hemodinâmica/fisiologia , Hipertrofia Ventricular Esquerda/terapia , Idoso , Idoso de 80 Anos ou mais , Estenose da Valva Aórtica/complicações , Estenose da Valva Aórtica/diagnóstico , Eletrocardiografia , Feminino , Humanos , Hipertrofia Ventricular Esquerda/etiologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Masculino
17.
Circulation ; 137(2): 184-196, 2018 01 09.
Artigo em Inglês | MEDLINE | ID: mdl-29311349

RESUMO

A series of hemodynamic and pathological responses occur in chronic aortic regurgitation, which eventually result in myocardial fibrosis and irreversible left ventricular dysfunction. According to guidelines, valvular surgery is recommended with the development of symptoms, left ventricular systolic dysfunction, or left ventricular dilatation. The optimal timing of surgical intervention has recently been questioned with documentation of irreversible myocardial damage resulting in incomplete left ventricular recovery and adverse clinical outcomes after surgery. Recognizing the shortcomings of the guidelines, we performed a comprehensive review on the novel diagnostic methods that have been shown to improve the detection of subclinical ventricular dysfunction in chronic aortic regurgitation and to improve prediction of outcomes.


Assuntos
Insuficiência da Valva Aórtica/diagnóstico por imagem , Hipertrofia Ventricular Esquerda/diagnóstico por imagem , Miocárdio/patologia , Disfunção Ventricular Esquerda/diagnóstico por imagem , Função Ventricular Esquerda , Remodelação Ventricular , Idoso , Insuficiência da Valva Aórtica/complicações , Insuficiência da Valva Aórtica/fisiopatologia , Insuficiência da Valva Aórtica/terapia , Doenças Assintomáticas , Fármacos Cardiovasculares/uso terapêutico , Doença Crônica , Progressão da Doença , Diagnóstico Precoce , Feminino , Fibrose , Implante de Prótese de Valva Cardíaca , Humanos , Hipertrofia Ventricular Esquerda/etiologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Hipertrofia Ventricular Esquerda/terapia , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Recuperação de Função Fisiológica , Fatores de Tempo , Tempo para o Tratamento , Resultado do Tratamento , Disfunção Ventricular Esquerda/etiologia , Disfunção Ventricular Esquerda/fisiopatologia , Disfunção Ventricular Esquerda/terapia , Função Ventricular Esquerda/efeitos dos fármacos , Remodelação Ventricular/efeitos dos fármacos
18.
Hypertension ; 71(3): 429-436, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29378853

RESUMO

Limited information exists on the longitudinal association between the left ventricular (LV) structure and function and future cognitive impairment and dementia in a large population without clinically recognized cardiovascular disease at baseline. The aim of the present study was to investigate the association between cardiac structure and function and risk of dementia and cognitive impairment in the MESA (Multi-Ethnic Study of Atherosclerosis) cohort. Measures of LV structure and function were determined using magnetic resonance imaging at baseline in 4999 participants free of clinically diagnosed cardiovascular disease and dementia. Probable incident clinical dementia was ascertained from hospitalization discharge records. Cognitive function was evaluated using tests addressing global cognitive function, processing speed, and memory. Associations of measures of LV structure and function with the incidence of clinically diagnosed dementia and cognitive performance were evaluated using Cox proportional hazard regression models adjusted for demographics, cardiovascular risk factors, and cardiovascular events. During a median follow-up of 12 years, 130 probable incident dementia cases were documented. Higher LV mass index (hazard ratio, 1.01; 95% confidence interval, 1.00-1.02) and LV mass-to-volume ratio (hazard ratio, 2.37; 95% confidence interval, 1.25-4.43) were independently associated with incident dementia and impaired cognitive function. Measures of LV function were not associated with risk of dementia or cognitive impairment. In conclusion, in a multiethnic cohort of participants without clinically detected cardiovascular disease and dementia at baseline, LV hypertrophy and concentric remodeling were independently associated with incident dementia and cognitive impairment.


Assuntos
Disfunção Cognitiva/epidemiologia , Disfunção Cognitiva/fisiopatologia , Demência/epidemiologia , Grupos Étnicos/estatística & dados numéricos , Hipertrofia Ventricular Esquerda/diagnóstico por imagem , Hipertrofia Ventricular Esquerda/epidemiologia , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Disfunção Cognitiva/diagnóstico , Estudos de Coortes , Bases de Dados Factuais , Demência/fisiopatologia , Feminino , Seguimentos , Humanos , Hipertrofia Ventricular Esquerda/terapia , Incidência , Imagem Cinética por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Valor Preditivo dos Testes , Modelos de Riscos Proporcionais , Estudos Retrospectivos , Medição de Risco , Índice de Gravidade de Doença , Distribuição por Sexo , Estados Unidos/epidemiologia , Remodelação Ventricular/fisiologia
20.
Life Sci ; 189: 8-17, 2017 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-28893641

RESUMO

AIMS: HIIT (high-intensity interval training) has the potential to reduce cardiometabolic risk factors, but the effects on cardiac remodeling and local RAS (renin-angiotensin system) in mice fed high-fat or high-fructose diets still need to be fully addressed. MAIN METHODS: Sixty male C57BL/6 mice (12weeks old) were randomly divided into three groups, control (C), High-fat (HF), or High-fructose diet (HRU) and were monitored for eight weeks before being submitted to the HIIT. Each group was randomly assigned to 2 subgroups, one subgroup was started on a 12-week HIIT protocol (T=trained group), while the other subgroup remained non-exercised (NT=not-trained group). KEY FINDINGS: HIIT reduced BM and systolic blood pressure in high-fat groups, while enhanced insulin sensitivity after high-fat or high-fructose intake. Moreover, HIIT reduced left ventricular hypertrophy in HF-T and HFRU-T. Notably, HIIT modulated key factors in the local left ventricular renin-angiotensin-system (RAS): reduced protein expression of renin, ACE (Angiotensin-converting enzyme), and (Angiotensin type 2 receptor) AT2R in HF-T and HFRU-T groups but reduced (Angiotensin type 1 receptor) AT1R protein expression only in the high-fat trained group. HIIT modulated ACE2/Ang (1-7)/Mas receptor axis. ACE2 mRNA gene expression was enhanced in HF-T and HFRU-T groups, complying with elevated Mas (Mas proto-oncogene, G protein-coupled receptor) receptor mRNA gene expression after HIIT. SIGNIFICANCE: This study shows the effectiveness of HIIT sessions in producing improvements in insulin sensitivity and mitigating LV hypertrophy, though hypertension was controlled only in the high-fat-fed submitted to HIIT protocol. Local RAS system in the heart mediates these findings and receptor MAS seems to play a pivotal role when it comes to the amelioration of cardiac structural and functional remodeling due to HIIT.


Assuntos
Treinamento Intervalado de Alta Intensidade , Hipertrofia Ventricular Esquerda/terapia , Resistência à Insulina/fisiologia , Sistema Renina-Angiotensina/fisiologia , Remodelação Ventricular/fisiologia , Angiotensina I/metabolismo , Animais , Pressão Sanguínea/fisiologia , Dieta Hiperlipídica , Frutose , Regulação da Expressão Gênica/fisiologia , Hipertensão/terapia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fragmentos de Peptídeos/metabolismo , Peptidil Dipeptidase A/metabolismo , Distribuição Aleatória , Receptor Tipo 2 de Angiotensina/metabolismo , Renina/metabolismo
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