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1.
Card Electrophysiol Clin ; 14(4): 729-742, 2022 12.
Artículo en Inglés | MEDLINE | ID: mdl-36396189

RESUMEN

Ventricular fibrillation (VF) is a common cause of sudden cardiac death (SCD) and is unfortunately without a cure. Current therapies focus on prevention of SCD, such as implantable cardioverter-defibrillator (ICD) implantation and anti-arrhythmic agents. Significant progress has been made in improving our understanding and ability to target the triggers of VF, via advanced mapping and ablation techniques, as well as with autonomic modulation. However, the critical substrate for VF maintenance remains incompletely defined. In this review, we discuss the evidence behind the basic mechanisms of VF and review the current role of catheter ablation in patients with VF.


Asunto(s)
Ablación por Catéter , Fibrilación Ventricular , Humanos , Ablación por Catéter/métodos , Muerte Súbita Cardíaca/prevención & control , Antiarrítmicos
2.
J Interv Card Electrophysiol ; 65(1): 179-182, 2022 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-35579783

RESUMEN

BACKGROUND: As AF-associated morbidity and mortality are increasing, there is an acute need for improved surveillance and prevention strategies to reduce the impact of AF and related strokes. Specific echocardiographic parameters that can best predict future onset of AF within 3 months are lacking. METHODS: Twenty patients with AF, as identified by presence of ICD-9 diagnosis code, were compared with a control group of twenty age- and sex-matched patients selected from the same clinic population but without a diagnosis of AF. Transthoracic echocardiograms (TTE) obtained within 90 days prior to first documented AF episode (study group) or obtained closest to first clinic visit (control) were selected for review. RESULTS: Baseline characteristics, including age, BMI, presence of hypertension, hyperlipidemia, diabetes, and heart failure were comparable. Increased left atrial (LA) size (end systolic major axis in 2-chamber view: AF 4.62±0.03 vs control 3.79±0.21, P =0.03), increased mitral inflow (E/A ratio: AF 1.35±0.15 vs control 1.06±0.07, P =0.04), and reduced LA global longitudinal strain (AF -2.69±0.26 vs control - 3.59±0.31, P =0.04) were most closely associated with AF compared with the control group. Multivariate logistic regression was used to develop predictive models for AF onset. A combination of imaging and traditional clinical risk factors was the best AF prediction model with AUC of 0.94, which greatly exceeds the current best predictors published. From these parameters, we developed the SMASH2 scoring system for 90- day AF risk estimation. CONCLUSIONS: Risk factors for AF and early features of atrial cardiomyopathy including male sex, hypertension, LA enlargement, reduced mitral inflow, and reduced LA strain are powerful predictors of AF onset within 90 days, and may be used to prognosticate future AF risk.


Asunto(s)
Apéndice Atrial , Fibrilación Atrial , Hipertensión , Fibrilación Atrial/diagnóstico , Ecocardiografía/métodos , Atrios Cardíacos/diagnóstico por imagen , Humanos , Masculino
3.
Front Cardiovasc Med ; 7: 11, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32133372

RESUMEN

The most dreaded complication of atrial fibrillation is stroke, and 70-80% of patients with AF-related stroke die or become disabled. The mechanisms of thromboembolism in AF are multifactorial, with evidence demonstrating that all three criteria of Virchow's triad are satisfied in AF: abnormal stasis of blood, endothelial damage, and hypercoagulability. Mechanistic insights into the latter two limbs have resulted in effective stroke prophylactic therapies (left atrial appendage occlusion and oral anticoagulants); however, despite these advances, there remains an excess of stroke in the AF population that may be due, in part, to a lack of mechanistic understanding of atrial hypocontractility resulting in abnormal stasis of blood within the atrium. These observations support the emerging concept of atrial cardiomyopathy as a cause of stroke. In this Review, we evaluate molecular, translational, and clinical evidence for atrial cardiomyopathy as a cause for stroke from AF, and present a rationale for further investigation of this largely unaddressed limb of Virchow's triad in AF.

4.
Womens Health Rep (New Rochelle) ; 1(1): 463-467, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33786512

RESUMEN

Some women have underlying cardiovascular disease that leads to increased morbidity and mortality with pregnancy. These women may choose to terminate a pregnancy rather than face this increased risk. The optimal approach for pregnancy termination in women with cardiomyopathy is not well defined. We present two women with peripartum cardiomyopathy, both modified World Health Organization (mWHO) class IV and with elevated Cardiac Disease in Pregnancy (CARPREG II) pregnancy risk stratification scores who are at the highest risk for pregnancy continuation. Both underwent induced abortion, although the procedure was performed in very different settings. These cases illustrate factors that influence the mode and setting of pregnancy termination performance.

5.
Sci Rep ; 8(1): 16519, 2018 11 08.
Artículo en Inglés | MEDLINE | ID: mdl-30410044

RESUMEN

As mediators of intercellular communication, exosomes containing molecular cargo are secreted by cells and taken up by recipient cells to influence cellular phenotype and function. Here we have investigated the effects of exosomes in dystrophin-deficient (Dys) induced pluripotent stem cell derived cardiomyocytes (iCMs). Our data demonstrate that exosomes secreted from either wild type (WT) or Dys-iCMs protect the Dys-iCM from stress-induced injury by decreasing reactive oxygen species and delaying mitochondrial permeability transition pore opening to maintain the mitochondrial membrane potential and decrease cell death. The protective effects of exosomes were dependent on the presence of exosomal surface proteins and activation of ERK1/2 and p38 MAPK signaling. Based on our findings, the acute effects of exosomes on recipient cells can be initiated from exosome membrane proteins and not necessarily their internal cargo.


Asunto(s)
Distrofina/deficiencia , Exosomas/metabolismo , Células Madre Pluripotentes Inducidas/citología , Sistema de Señalización de MAP Quinasas , Mitocondrias/metabolismo , Miocitos Cardíacos/citología , Diferenciación Celular , Supervivencia Celular , Células Cultivadas , Distrofina/genética , Humanos , Células Madre Pluripotentes Inducidas/metabolismo , Potencial de la Membrana Mitocondrial , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Miocitos Cardíacos/metabolismo , Eliminación de Secuencia , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo
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