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1.
Intern Emerg Med ; 10(8): 965-72, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26037394

RESUMO

Renal dysfunction (RD) and venous congestion are related and common in heart failure (HF). Studies suggest that venous congestion may be the primary driver of RD in HF. In this study, we sought to investigate retrospectively the relationship between common measures of renal function with caval congestion and mortality among outpatients with HF and RD. We reviewed data from 103 HF outpatients (45 males, mean age 74 years, ejection fraction 41.8 ± 11.6 %) with estimated glomerular filtration rate (eGFR) of < 60 ml/min in a single centre. During an ambulatory visit, all patients underwent blood test and ultrasonography of the inferior vena cava (IVC). Caval congestion was defined as IVC with both dilatation and impaired collapsibility. The best values of renal metrics in predicting caval congestion were determined with receiver-operating characteristic analysis. The BUN/Cr ratio is moderately correlated with IVC expiratory maximum diameter (r = 0.31, p < 0.0007). In a multiple logistic regression model, BUN/Cr > 25.5 (adjusted OR 2.98, p 0.015) and eGFR ≤ 45.8 (adjusted OR 5.38, p 0.002) identify patients at risk for caval congestion; a BUN/Cr > 23.7 was the best predictor of impaired collapsibility (adjusted OR 4.41, p 0.001). a BUN/Cr > 25.5 (HR 2.19, 95 % CI 1.21-3.94, p < 0.001) and NYHA class 3 (HR 2.91, 95 % CI 1.60-5.31, p < 0.0005) were independent risk factors associated with all-cause death during a median follow-up of 31 months. In outpatients with HF and RD, a higher BUN/Cr and lower eGFR are reliable renal biomarkers for caval congestion. The BUN/Cr is associated with long-term mortality and may help to stratify HF severity.


Assuntos
Nitrogênio da Ureia Sanguínea , Creatinina/sangue , Insuficiência Cardíaca/mortalidade , Hiperemia/diagnóstico por imagem , Insuficiência Renal/complicações , Veia Cava Inferior/diagnóstico por imagem , Idoso , Biomarcadores/sangue , Feminino , Taxa de Filtração Glomerular , Insuficiência Cardíaca/sangue , Humanos , Itália , Masculino , Estudos Retrospectivos , Fatores de Risco
3.
Intern Emerg Med ; 8(3): 221-8, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-21594682

RESUMO

Congestive heart failure (CHF) worsening is a worldwide cause of rehospitalization and mortality, specially during the early period after hospitalization. Fluid accumulation plays a key role in the pathophysiology of both acute heart decompensation and disease progression. The effective use of drugs to maintain restored clinical stabilization in recently discharged patients is a difficult task, and it relies on matching the most appropriately tailored therapy to specific clinical profiles. However, no successful treatment has been shown to reduce post-discharge readmission. We evaluated in a case-control study the effectiveness of an early and personalized congestion-guided ambulatory program on medium-term (6 months) compensation in recently discharged CHF patients. Group A (22 patients) underwent a post-discharge close follow-up consisting of: an early clinic visit within 10 days; a second visit within 10 days after the first; and the other visits at month 1, 2, 3 after discharge. Controls (Group B, 21 patients) underwent a conventional ambulatory follow-up only at month 1, 2, 3 after discharge. The ambulatory approach in both groups was based on the monitoring of signs/symptoms of congestion and body weight, body hydration estimation by using bioelectrical impedance analysis (BIA) and laboratory data. This assessment was finalized to tailor furosemide and daily fluid intake at each visit to eliminate clinical or instrumental evidence of persistent congestion relieving the signs and symptoms. At 6 months, Group A was associated with a better clinical compensation (improved hydration state, lower BNP levels and congestion score), an improved quality of life, and reduced re-hospitalizations. We conclude that in CHF the early and personalized ambulatory follow-up based on congestion-guided treatment is effective to optimize management and maintain clinical stability in the post-discharge period.


Assuntos
Assistência Ambulatorial/organização & administração , Diuréticos/uso terapêutico , Hidratação , Furosemida/uso terapêutico , Insuficiência Cardíaca/terapia , Idoso , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Alta do Paciente , Fatores de Tempo , Resultado do Tratamento
4.
Am J Ther ; 2011 Jan 18.
Artigo em Inglês | MEDLINE | ID: mdl-21248622

RESUMO

Propafenone is a membrane-stabilizing agent belonging to a subgroup of the Vaughan Williams class I antidysrhythmic agents, structurally resembling propranolol and characterized by weaker beta-blocking activity. Despite respiratory complications having been reported as examples of side effects, very few reports have been published in the literature.We describe the case of an elderly woman with a history of hypertension and allergy to Parietaria, grass, olive, mites, and with periodic asthmatic manifestations, for whom the administration of oral propafenone for recurrent supraventricular dysrhythmia was associated with the sudden onset of severe bronchostenosis.A 78-year-old woman was frequently admitted to the Emergency Department for a recurrent supraventricular tachycardia, which was treated initially with veramapil and thereafter with ivabradin. During her last visit to the cardiologist, she was prescribed propafenone (150 mg, 3 times a day) in place of ivabradin. After the administration of the second dose on the first day of the therapy, the patient began to complain of the onset of progressively severe dyspnea at rest. In the Emergency Department, respiratory auscultation showed diffuse rhonchi, wheezing, and rales; and arterial pressure was 200/100 mm Hg. Hemogasanalysis revealed hypoxemia, respiratory acidosis with 83% of O2-saturation. Emergency treatment with O2 therapy, methylprednisolone intravenous, furosemide, and then salbutamol was also started; the electrocardiogram only showed sinusal tachycardia. Results of laboratory examinations, including a white cell count and cardiac enzymes, were within the normal range. The patient achieved good respiratory function, after a period of 3 days.This report describes that even a relatively small dose of oral propafenone after commencing treatment can have a severe effect in exacerbating the obstruction of the airways in a susceptible subject. The likely mechanisms are an allergic reaction or a direct bronchospastic effect. Considering the recognized asthmogenicity of propafenone due to beta-blocker activity, we suggest that the cardiologist always refer to the patient's medical history before prescribing this drug, which is capable of producing notable side effects in predisposed individuals, beginning the eventual administration in the hospital setting. The use of bronchial provocation test allows the selection of inclined patients, thus reducing the risk of bronchospasm.

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