RESUMEN
Few studies have evaluated the effects of pulmonary arterial hypertension therapies on pericardial effusion. We evaluated hemodynamics, echocardiograms, and outcomes for 119 parenteral prostanoid-treated patients. We discovered an increased frequency of pericardial effusions posttreatment, and that a moderate-large pericardial effusion at initiation, but not at 1st follow-up, was significantly associated with mortality.
RESUMEN
BACKGROUND: In ≈25% of patients with heart failure and reduced left-ventricular ejection fraction, right-ventricular (RV), and left-ventricular (LV) filling pressures are discordant (ie, one is elevated while the other is not). Whether clinical assessment allows detection of this discordance is unknown. We sought to determine the agreement of clinically versus invasively determined patterns of ventricular congestion. METHODS: In 156 heart failure and reduced LV ejection fraction subjects undergoing invasive hemodynamic assessment, we categorized patterns of ventricular congestion (no congestion, RV only, LV only, or both) based on clinical findings of RV (jugular venous distention) or LV (hepatojugular reflux, orthopnea, or bendopnea) congestion. Agreement between clinically and invasively determined (RV congestion if right atrial pressure [RAP] ≥10 mm Hg and LV congestion if pulmonary capillary wedge pressure [PCWP] ≥22 mm Hg) categorizations was the primary end point. RESULTS: The frequency of clinical patterns of congestion was: 51% no congestion, 24% both RV and LV, 21% LV only, and 4% RV only. Jugular venous distention had excellent discrimination for elevated RAP (C=0.88). However, agreement between clinical and invasive congestion patterns was poor, к=0.44 (95% CI, 0.34-0.55). While those with no clinical congestion usually had low RAP and PCWP (67/79, 85%), over one-half (24/38, 64%) with isolated LV clinical congestion had PCWP <22 mm Hg, most (5/7, 71%) with isolated RV clinical congestion had PCWP ≥22 mm Hg, and ≈one-third (10/32, 31%) with both RV and LV clinical congestion had elevated RAP but PCWP <22 mm Hg. CONCLUSIONS: While clinical examination allows accurate detection of elevated RAP, it does not allow accurate detection of discordant RV and LV filling pressures.
Asunto(s)
Insuficiencia Cardíaca/fisiopatología , Presión Esfenoidal Pulmonar/fisiología , Volumen Sistólico/fisiología , Disfunción Ventricular Izquierda/fisiopatología , Hemodinámica/fisiología , Humanos , Masculino , Persona de Mediana Edad , Examen Físico/métodos , Función Ventricular Izquierda/fisiología , Presión Ventricular/fisiologíaAsunto(s)
Insuficiencia Cardíaca , Arteria Pulmonar , Humanos , Presión Esfenoidal Pulmonar , Hemodinámica , DisneaAsunto(s)
Insuficiencia Cardíaca Sistólica/fisiopatología , Flujo Pulsátil/fisiología , Pared Torácica/irrigación sanguínea , Insuficiencia de la Válvula Tricúspide/fisiopatología , Venas/fisiopatología , Anciano de 80 o más Años , Fibrilación Atrial/complicaciones , Fibrilación Atrial/fisiopatología , Disnea/etiología , Edema/etiología , Insuficiencia Cardíaca Sistólica/complicaciones , Insuficiencia Cardíaca Sistólica/diagnóstico por imagen , Humanos , Venas Yugulares , Masculino , Examen Físico , Pronóstico , Insuficiencia de la Válvula Tricúspide/diagnóstico por imagen , Presión VenosaRESUMEN
Prior exposure to social disruption stress (SDR) exacerbates both the acute and chronic phase of Theiler's murine encephalomyelitis virus infection (TMEV; [Johnson, R.R., Storts, R., Welsh, T.H., Jr., Welsh, C.J., Meagher, M.W., 2004. Social stress alters the severity of acute Theiler's virus infection. J. Neuroimmunol. 148, 74--85; Johnson, R.R., Prentice, T.W., Bridegam, P., Young, C.R., Steelman, A.J., Welsh, T.H., Welsh, C.J.R., Meagher, M.W., 2006. Social stress alters the severity and onset of the chronic phase of Theiler's virus infection. J. Neuroimmunol. 175, 39--51]). However, the neuroimmune mechanism(s) mediating this effect have not been determined. The present study examined whether stress-induced increases in the proinflammatory cytokine interleukin-6 (IL-6) contributes to the adverse effects of SDR on acute TMEV infection. Experiment 1 demonstrated that SDR increases central and peripheral levels of IL-6 and that this effect is reversed by intracerebral ventricular infusion of neutralizing antibody to IL-6 prior to each of six SDR sessions. Although SDR reduced the sensitivity of spleen cells to the anti-inflammatory effects of corticosterone, the neutralizing antibody to IL-6 did not alter this effect. To investigate whether stress-induced increases in IL-6 contribute to the exacerbation of acute TMEV infection, Experiment 2 examined whether intracerebral administration of neutralizing antibody to IL-6 during SDR would prevent the subsequent exacerbation of acute TMEV infection. Experiment 3 then replaced the social stress with intracerebral infusion of IL-6 to assess sufficiency. As expected, prior exposure to SDR subsequently increased infection-related sickness behaviors, motor impairment, CNS viral titers, and CNS inflammation. These deleterious effects of SDR were either prevented or significantly attenuated by intracerebral infusion of neutralizing antibody to IL-6 during the stress exposure period. However, infusion of IL-6 alone did not mimic the adverse effects of SDR. We conclude that IL-6 is necessary but not sufficient to exacerbate acute TMEV infection.