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1.
J Atr Fibrillation ; 13(6): 20200474, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34950354

RESUMEN

BACKGROUND: Atrial fibrillation (AF) is a common comorbidity in patients with left ventricular assist devices (LVAD) with no defined guideline treatment strategy of rate versus rhythm control. The purpose of this study is to determine the effects of rate versus rhythm control for AF on the outcomes of patients with LVAD at our institution. METHODS: Consecutive patients who underwent LVAD implantation at St Vincent Hospital from January 1, 2015 to December 31, 2017 were retrospectively evaluated. Patients with AF were identified and divided into rate control or rhythm control groups. The primary outcome evaluated was a composite of death, heart failure admission, gastrointestinal bleed, ventricular tachycardia, cerebrovascular accident, hemolysis, and pump thrombosis. Secondary outcomes included the individual variables from the primary outcome. RESULTS: Out of 201 patients that underwent LVAD implantation, 81 had AF after implantation and were included with a median follow-up period of 384 days. The rate control group (n = 31; 38%) and the rhythm control group (n = 51; 62%) had no difference in composite outcomes (61% vs 59%, p = 0.83). When taken individually there was no difference in outcomes between the two groups. Thirteen patients underwent electrical cardioversion and successful conversion to normal sinus rhythm occurred in 71% of cases with a 60% recurrence rate. CONCLUSIONS: There was no difference in primary outcome between rate and rhythm control groups. These data suggest that maintenance of sinus rhythm may not be necessary in all patients with LVAD.

2.
JACC Case Rep ; 2(14): 2235-2239, 2020 Nov 18.
Artículo en Inglés | MEDLINE | ID: mdl-34317147

RESUMEN

A 55-year-old patient was found to have complete heart block during preoperative assessment. Cardiac magnetic resonance imaging revealed an interatrial mass suggestive of primary cardiac tumor. Extensive evaluation including intracardiac biopsy and finally open resection revealed lipomatous hypertrophy masquerading as tumor. (Level of Difficulty: Intermediate.).

3.
ASAIO J ; 64(6): 748-753, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29210772

RESUMEN

The aims of this analysis were to characterize the burden and timing of bleeding events in females versus males on left ventricular assist device (LVAD) support. A single-center retrospective review of 375 patients receiving continuous-flow LVADs was performed. Bleeding events included gastrointestinal, naso-oropharyngeal, gynecologic (GYN), intracranial hemorrhage (ICH), and mediastinal bleeding. Cox hazard ratios (HRs) [95% CI] and incident event rates for females versus males were calculated. Eighty-four females (22%) and 291 males (78%) received an LVAD. There were 189 patients with 406 bleeding events over a median 399 days of support. Two-year freedom from bleeding was 33 ± 6.2% in females and 46 ± 3.7% in males (p = 0.027). Correlates of bleeding included female sex (adjusted HR = 1.6 [1.1-2.2]) and older age (adjusted HR = 1.2 [1.1-1.3] per 10 years). There was no sex-associated difference in 30 day mediastinal bleeding (males 12%; females 16% at 30 days; overall p = 0.35), but incident event rates for overall bleeding and naso-oropharyngeal bleeding were higher in females (p < 0.05) and trends were noted in ICH (eppy: 0.06 male vs. 0.10 female, p = 0.14). Eight females (10%) experienced 12 GYN bleeding events; five required surgical intervention. In summary, females had a 60% higher hazard of bleeding than males with significant morbidity encountered from mucosa (including vaginal) bleeding. Future large device studies should be inclusive of sex-specific outcomes.


Asunto(s)
Corazón Auxiliar/efectos adversos , Hemorragia Posoperatoria/epidemiología , Hemorragia Posoperatoria/etiología , Adulto , Anciano , Femenino , Insuficiencia Cardíaca/cirugía , Humanos , Masculino , Persona de Mediana Edad , Modelos de Riesgos Proporcionales , Estudios Retrospectivos , Factores Sexuales
4.
Am J Physiol Heart Circ Physiol ; 309(11): H1793-812, 2015 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-26432837

RESUMEN

A growing number of extreme climate events are occurring in the setting of ongoing climate change, with an increase in both the intensity and frequency. It has been shown that ambient temperature challenges have a direct and highly varied impact on cardiovascular health. With a rapidly growing amount of literature on this issue, we aim to review the recent publications regarding the impact of cold and heat on human populations with regard to cardiovascular disease (CVD) mortality/morbidity while also examining lag effects, vulnerable subgroups, and relevant mechanisms. Although the relative risk of morbidity/mortality associated with extreme temperature varied greatly across different studies, both cold and hot temperatures were associated with a positive mean excess of cardiovascular deaths or hospital admissions. Cause-specific study of CVD morbidity/mortality indicated that the sensitivity to temperature was disease-specific, with different patterns for acute and chronic ischemic heart disease. Vulnerability to temperature-related mortality was associated with some characteristics of the populations, including sex, age, location, socioeconomic condition, and comorbidities such as cardiac diseases, kidney diseases, diabetes, and hypertension. Temperature-induced damage is thought to be related to enhanced sympathetic reactivity followed by activation of the sympathetic nervous system, renin-angiotensin system, as well as dehydration and a systemic inflammatory response. Future research should focus on multidisciplinary adaptation strategies that incorporate epidemiology, climatology, indoor/building environments, energy usage, labor legislative perfection, and human thermal comfort models. Studies on the underlying mechanism by which temperature challenge induces pathophysiological response and CVD await profound and lasting investigation.


Asunto(s)
Aclimatación , Regulación de la Temperatura Corporal , Enfermedades Cardiovasculares/etiología , Sistema Cardiovascular/fisiopatología , Cambio Climático , Frío , Fiebre/complicaciones , Calor , Hipotermia/complicaciones , Estaciones del Año , Animales , Enfermedades Cardiovasculares/metabolismo , Enfermedades Cardiovasculares/mortalidad , Enfermedades Cardiovasculares/fisiopatología , Sistema Cardiovascular/metabolismo , Fiebre/metabolismo , Fiebre/mortalidad , Fiebre/fisiopatología , Humanos , Hipotermia/metabolismo , Hipotermia/mortalidad , Hipotermia/fisiopatología , Medición de Riesgo , Factores de Riesgo
5.
Arterioscler Thromb Vasc Biol ; 30(12): 2518-27, 2010 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-20864666

RESUMEN

OBJECTIVE: To evaluate the role of early-life exposure to airborne fine particulate matter (diameter, <2.5 µm [PM(2.5)]) pollution on metabolic parameters, inflammation, and adiposity; and to investigate the involvement of oxidative stress pathways in the development of metabolic abnormalities. METHODS AND RESULTS: PM(2.5) inhalation exposure (6 h/d, 5 d/wk) was performed in C57BL/6 mice (wild type) and mice deficient in the cytosolic subunit of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p47(phox) (p47(phox-/-)) beginning at the age of 3 weeks for a duration of 10 weeks. Both groups were simultaneously fed a normal diet or a high-fat diet for 10 weeks. PM(2.5)-exposed C57BL/6 mice fed a normal diet exhibited metabolic abnormalities after exposure to PM(2.5) or FA for 10 weeks. Consistent with insulin resistance, these abnormalities included enlarged subcutaneous and visceral fat contents, increased macrophage infiltration in visceral adipose tissue, and vascular dysfunction. Ex vivo-labeled and infused monocytes demonstrated increased adherence in the microcirculation of normal diet- or high-fat diet-fed PM(2.5)-exposed mice. p47(phox-/-) mice exhibited an improvement in parameters of insulin resistance, vascular function, and visceral inflammation in response to PM(2.5). CONCLUSIONS: Early-life exposure to high levels of PM(2.5) is a risk factor for subsequent development of insulin resistance, adiposity, and inflammation. Reactive oxygen species generation by NADPH oxidase appears to mediate this risk.


Asunto(s)
Inflamación/inducido químicamente , Grasa Intraabdominal/enzimología , NADPH Oxidasas/metabolismo , Obesidad/inducido químicamente , Material Particulado/toxicidad , Grasa Subcutánea/enzimología , Adiposidad , Factores de Edad , Envejecimiento , Animales , Aorta Torácica/fisiopatología , Glucemia/metabolismo , Células Cultivadas , Quimiotaxis de Leucocito , Grasas de la Dieta , Modelos Animales de Enfermedad , Inflamación/enzimología , Inflamación/genética , Inflamación/inmunología , Inflamación/fisiopatología , Mediadores de Inflamación/sangre , Exposición por Inhalación , Insulina/sangre , Resistencia a la Insulina , Grasa Intraabdominal/inmunología , Grasa Intraabdominal/fisiopatología , Macrófagos/inmunología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , NADPH Oxidasas/deficiencia , NADPH Oxidasas/genética , Obesidad/enzimología , Obesidad/genética , Obesidad/inmunología , Obesidad/fisiopatología , Tamaño de la Partícula , Fosforilación , Especies Reactivas de Oxígeno/metabolismo , Factores de Riesgo , Grasa Subcutánea/fisiopatología , Vasoconstricción , Vasodilatación
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