ABSTRACT
BACKGROUND: The importance of a serum creatinine increase, traditionally considered worsening renal function (WRF), during admission for acute heart failure has been recently debated, with data suggesting an interaction between congestion and creatinine changes. METHODS AND RESULTS: In post hoc analyses, we analyzed the association of WRF with length of hospital stay, 30-day death or cardiovascular/renal readmission and 90-day mortality in the PROTECT study (Placebo-Controlled Randomized Study of the Selective A1 Adenosine Receptor Antagonist Rolofylline for Patients Hospitalized With Acute Decompensated Heart Failure and Volume Overload to Assess Treatment Effect on Congestion and Renal Function). Daily creatinine changes from baseline were categorized as WRF (an increase of 0.3 mg/dL or more) or not. Daily congestion scores were computed by summing scores for orthopnea, edema, and jugular venous pressure. Of the 2033 total patients randomized, 1537 patients had both available at study day 14. Length of hospital stay was longer and 30-day cardiovascular/renal readmission or death more common in patients with WRF. However, these were driven by significant associations in patients with concomitant congestion at the time of assessment of renal function. The mean difference in length of hospital stay because of WRF was 3.51 (95% confidence interval, 1.29-5.73) more days (P=0.0019), and the hazard ratio for WRF on 30-day death or heart failure hospitalization was 1.49 (95% confidence interval, 1.06-2.09) times higher (P=0.0205), in significantly congested than nonsignificantly congested patients. A similar trend was observed with 90-day mortality although not statistically significant. CONCLUSIONS: In patients admitted for acute heart failure, WRF defined as a creatinine increase of ≥0.3 mg/dL was associated with longer length of hospital stay, and worse 30- and 90-day outcomes. However, effects were largely driven by patients who had residual congestion at the time of renal function assessment. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00328692 and NCT00354458.
Subject(s)
Creatinine/blood , Heart Failure/physiopathology , Heart Failure/therapy , Patient Readmission/statistics & numerical data , Acute Disease , Aged , Aged, 80 and over , Female , Heart Failure/diagnosis , Hospitalization/statistics & numerical data , Humans , Kidney/physiopathology , Male , Middle Aged , Prognosis , Proportional Hazards Models , Xanthines/pharmacologyABSTRACT
Con la finalidad de "saber qué hacer" en el ámbito de la urgencia de una insuficiencia cardíaca aguda y con el objetivo de optimizar las estrategias de diagnóstico y tratamiento en el primer contacto con un paciente que podría estar cursando esta patología, se presentan en este artículo, conceptos fundamentales sobre definiciones de esta patología, clasificaciones clínicas y hemodinámicas, manejos iniciales en diferentes escenarios (etapa pre hospitalaria, departamento de emergencia, ingreso a unidad coronaria) y finalmente, un algoritmo diagnóstico y terapéutico para la rápida toma de decisiones. Es nuestro objetivo que médicos generalistas, clínicos, internistas y/o cardiólogos, puedan en una forma organizada y eficiente optimizar el diagnóstico y manejo precoz de esta condición clínica que amenaza la calidad de vida y supervivencia.
Algorithm of acute heart failure Initial management: prehospital stage, emergency department, admission to coronary unit In order to "know what to do" in the area of acute heart failure and with the objective of optimizing diagnostic and treatment strategies in the first contact with a patient who might be attending this pathology, article, fundamental concepts on definitions of this pathology, clinical and hemodynamic classifications, initial management in different scenarios (prehospital stage, emergency department, coronary unit admission) and, finally, a diagnostic and therapeutic algorithm for rapid decision making. It is our goal that general practitioners, clinicians, internists and / or cardiologists, in an organized and efficient way, can optimize the diagnosis and early management of this life-threatening clinical condition.
Algoritmo de insuficiência cardíaca aguda Manejo inicial: estágio pré-hospitalar, departamento de emergências, admissão à unidade coronária Para "saber o que fazer" na área de insuficiência cardíaca aguda e com o objetivo de otimizar estratégias de diagnóstico e tratamento no primeiro contato com um paciente que possa estar atendendo a esta patologia, artigo, conceitos fundamentais sobre definições desta patologia, classificações clínicas e hemodinâmicas, gerenciamento inicial em diferentes cenários (estágio pré-hospitalar, departamento de emergência, admissão da unidade coronária) e, finalmente, um algoritmo diagnóstico e terapêutico para a tomada de decisões rápidas. Nosso objetivo é que clínicos gerais, clínicos, internistas e / ou cardiologistas, de forma organizada e eficiente, possam otimizar o diagnóstico e o gerenciamento precoce desta condição clínica que ameaça a vida.
ABSTRACT
Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.
Subject(s)
Hypertension, Pulmonary/diagnosis , Adult , Female , Humans , Postpartum Period , Pregnancy , Rare Diseases/diagnosis , Young AdultABSTRACT
La presencia de hipertensión pulmonar (HP) en el embarazo es poco frecuente y conlleva un alto riesgo para madres e hijos. Existe escasa bibliografía relacionada al diagnóstico de la misma luego del parto. Se describen tres pacientes a quienes se diagnostica HP luego de cursar sus embarazos y partos libres de eventos. A pesar de desconocerse las causas, son varios los mecanismos propuestos, como la hipercoagulabilidad, la hipoxia placentaria o la embolia de líquido amniótico. Resulta difícil definir si la HP diagnosticada en el puerperio, corresponde a una HP en período asintomático que fue desenmascarada por el estrés fisiológico del parto o es una condición de reciente comienzo. A pesar de la falta de datos que avalen la ausencia de HP previa al embarazo en nuestras tres casos, el curso libre de eventos en sus embarazos, sin síntomas y con partos normales, indican que no padecían esta enfermedad hasta el momento del parto, y que la desarrollaron posteriormente. De haberla padecido antes se hubieran presentado síntomas previos al parto o en el puerperio inmediato, ya que las demandas hemodinámicas deterioran gravemente a un ventrículo con poca reserva.
Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.
Subject(s)
Humans , Female , Pregnancy , Adult , Young Adult , Hypertension, Pulmonary/diagnosis , Rare Diseases/diagnosis , Postpartum PeriodABSTRACT
La presencia de hipertensión pulmonar (HP) en el embarazo es poco frecuente y conlleva un alto riesgo para madres e hijos. Existe escasa bibliografía relacionada al diagnóstico de la misma luego del parto. Se describen tres pacientes a quienes se diagnostica HP luego de cursar sus embarazos y partos libres de eventos. A pesar de desconocerse las causas, son varios los mecanismos propuestos, como la hipercoagulabilidad, la hipoxia placentaria o la embolia de líquido amniótico. Resulta difícil definir si la HP diagnosticada en el puerperio, corresponde a una HP en período asintomático que fue desenmascarada por el estrés fisiológico del parto o es una condición de reciente comienzo. A pesar de la falta de datos que avalen la ausencia de HP previa al embarazo en nuestras tres casos, el curso libre de eventos en sus embarazos, sin síntomas y con partos normales, indican que no padecían esta enfermedad hasta el momento del parto, y que la desarrollaron posteriormente. De haberla padecido antes se hubieran presentado síntomas previos al parto o en el puerperio inmediato, ya que las demandas hemodinámicas deterioran gravemente a un ventrículo con poca reserva.(AU)
Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.(AU)
ABSTRACT
Pulmonary hypertension (PH) in pregnancy is a rare disorder that carries a high risk to mother and child, and as such, it is considered a contraindication to becoming pregnant. However, there are few published reports related to the diagnosis of this condition after delivery. We describe three PH cases diagnosed after their normal pregnancies and deliveries. Although the causes are unknown, several mechanisms such as hypercoagulation, placental hypoxia or amniotic fluid embolism have been considered as possible causes. It is difficult to define whether a PH diagnosed in the postpartum period, relates to an earlier asymptomatic PH period that was triggered by the physiological stress of labor or if it is a recently acquired condition. Despite the lack of data to support the absence of PH previous to pregnancy in our three patients, lack of events during this period, asymptomatic and normal deliveries, lead us to believe that they did not suffer this disease prior to pregnancy; considering that high hemodynamic demands impair a ventricle with little reserve, and its subsequent appearance at time of delivery.
ABSTRACT
BACKGROUND: A high incidence of Achilles tendinopathy--tendinitis or rupture--has been observed after quinolone treatment in lung and kidney transplant patients. In the absence of relevant published data, we aimed to determine its incidence, clinical features, risk factors and outcome among heart graft recipients. METHODS: We studied the clinical records of all adult heart transplant patients who were prescribed quinolones at our center between August 1995 and September 2006. Achilles tendinopathy had been diagnosed clinically, with ultrasound assessment when necessary. In all cases, quinolone treatment had been terminated upon diagnosis of tendinopathy. RESULTS: During this period, quinolones had been given on 242 occasions to 149 heart transplant patients (33 women, 116 men). Achilles tendinopathy developed on 14 occasions (5.8%; 95% confidence interval: 2.8% to 8.7%), affecting 13 men and 1 woman (mean age: 62 years). Three cases involved tendon rupture, and bilateral tendinopathy was present in 8 cases. The median time between the start of treatment and onset of symptoms was 2.5 days, with 12 patients being asymptomatic 2 months after drug withdrawal. Independent risk factors for tendinopathy were renal dysfunction (p = 0.03) and increased time between transplantation and treatment (p = 0.005). Incidence was not influenced by the type, dose or previous administration of quinolones, or by the immunosuppressive regimen. CONCLUSIONS: Quinolone-related Achilles tendinopathy is frequent among heart transplant patients, especially in the presence of renal dysfunction or lengthy post-transplantation survival. If no alternative anti-bacterial therapy is available for high-risk patients, close clinical surveillance should be warranted.
Subject(s)
Achilles Tendon , Graft Rejection/drug therapy , Heart Transplantation , Quinolones/adverse effects , Tendinopathy/epidemiology , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Prognosis , Quinolones/therapeutic use , Retrospective Studies , Risk Factors , Tendinopathy/chemically inducedABSTRACT
INTRODUCTION AND OBJECTIVES: Data on chronic anemia following heart transplantation (HT) are scarce and contradictory. Our aims were to determine the prevalence of chronic anemia after HT, to identify predisposing factors for the condition at 12 months, and to evaluate its influence on medium-term and long-term survival. METHODS: Retrospective analysis of patients who underwent HT between 1991 and 2005 (n=457). Chronic anemia was defined as a hemoglobin level <12 g/dL. RESULTS: The prevalence of post-HT chronic anemia was 75.5% at 1 month, 31% at 12 months, and 26.2% at 120 months. The condition was significantly more prevalent among women than men. Predisposing factors for chronic anemia 1 year post-HT were mild-to-moderate chronic renal failure (i.e., creatinine level >1.5 mg/dL; odds ratio [OR]=2.8; 95% confidence interval [CI], 1.5-5.0), female sex (OR=6.4; 95% CI, 3.1-13.2), and immunosuppression with mycophenolate mofetil compared with azathioprine (OR=2.6;, 95% CI, 1.4-4.8). The prevalence of chronic anemia 12 months after HT was independent of the donor's sex, the recipient's age, the etiology of the recipient's heart failure, diabetes mellitus, mild-to-moderate graft rejection, cytomegalovirus infection, and angiotensin-converting enzyme inhibitor treatment. The presence of chronic anemia 12 months after HT did not influence either long-term survival (mean, 11.5 years with chronic anemia vs. 13.0 years without) or actuarial survival. CONCLUSIONS: Post-HT chronic anemia is common, but improves with time and treatment. Predisposing factors for the condition 1 year post-HT include chronic renal failure, female sex, and immunosuppression with mycophenolate mofetil. The presence of chronic anemia does not appear to influence long-term survival.
Subject(s)
Anemia/epidemiology , Anemia/etiology , Heart Transplantation/adverse effects , Anemia/therapy , Causality , Chronic Disease , Female , Humans , Male , Middle Aged , Prevalence , Prognosis , Retrospective Studies , Survival Rate , Time FactorsABSTRACT
Introducción y objetivos. La información disponible sobre anemia crónica (AC) en pacientes con trasplante cardiaco (TC) es escasa y discordante. Nuestro objetivo fue estudiar la prevalencia de AC en pacientes post-TC, factores predisponentes de AC a 12 meses y su significado pronóstico a medio y largo plazo. Métodos. Análisis retrospectivo de pacientes con TC entre 1991 y 2005 (n = 457). AC fue definida como hemoglobina < 12 g/dl. Resultados. La prevalencia de AC post-TC fue del 75,5% a 1 mes, el 31% a los 12 meses y el 26,2% a los 120 meses, significativamente más prevalente en mujeres que en varones. Factores predisponentes de AC a 12 meses: insuficiencia renal crónica (IRC) leve-moderada (creatinina > 1,5 mg/dl) (odds ratio [OR] = 2,8; intervalo de confianza [IC] del 95%, 1,5-5); sexo femenino (OR = 6,4; IC del 95%, 3,1-13,2), e inmunosupresión con micofenolato mofetilo (MMF) respecto a azatioprina (OR = 2,6; IC del 95%, 1,4-4,8). La prevalencia de AC 1 año tras el TC no se relacionó con el sexo del donante, la edad del receptor, la cardiopatía del receptor, la diabetes mellitus, el rechazo leve o moderado del injerto (≥ 3A), infección por citomegalovirus o tratamiento con inhibidores de la enzima de conversión de angiotensina. Tener AC a 1 año del TC no supuso diferencias en la supervivencia a largo plazo (tiempo de vida medio con AC, 11,5 años y sin AC, 13 años) ni en la supervivencia actuarial. Conclusiones. La AC post-TC es un problema frecuente que mejora con el tiempo y el tratamiento. La IRC, el sexo femenino y la inmunosupresión con MMF predisponen a AC a los 12 meses del TC. Tener AC no parece influir en la supervivencia a largo plazo (AU)
Introduction and objectives. Data on chronic anemia following heart transplantation (HT) are scarce and contradictory. Our aims were to determine the prevalence of chronic anemia after HT, to identify predisposing factors for the condition at 12 months, and to evaluate its influence on medium-term and long-term survival. Methods. Retrospective analysis of patients who underwent HT between 1991 and 2005 (n=457). Chronic anemia was defined as a hemoglobin level 1.5 mg/dL; odds ratio [OR]=2.8; 95% confidence interval [CI], 1.55.0), female sex (OR=6.4; 95% CI, 3.113.2), and immunosuppression with mycophenolate mofetil compared with azathioprine (OR=2.6;, 95% CI, 1.44.8). The prevalence of chronic anemia 12 months after HT was independent of the donor's sex, the recipient's age, the etiology of the recipient's heart failure, diabetes mellitus, mild-to-moderate graft rejection, cytomegalovirus infection, and angiotensin-converting enzyme inhibitor treatment. The presence of chronic anemia 12 months after HT did not influence either long-term survival (mean, 11.5 years with chronic anemia vs. 13.0 years without) or actuarial survival. Conclusions. Post-HT chronic anemia is common, but improves with time and treatment. Predisposing factors for the condition 1 year post-HT include chronic renal failure, female sex, and immunosuppression with mycophenolate mofetil. The presence of chronic anemia does not appear to influence long-term survival (AU)
