2. • EL PRESENTE CASO TIENE FINES
ACADÉMICOS Y DE REVISIÓN DE TEMAS.
3. PACIENTE DE SEXO FEMENINO
86 AÑOS DE EDAD
AMA DE CASA
•MOTIVO DE CONSULTA:
“ESTA MAS AHOGADA Y SE LE INFLAMARON
LAS PIERNAS”
4. ENFERMEDAD ACTUAL
1 MES DE EVOLUCIÓN DE DETERIORO DE LA CLASE FUNCIONAL,
DISNEA, DISNEA PAROXISTICA NOCTURNA Y ORTOPNEA.
ADICIONALMENTE REFIERE EDEMA PROGRESIVO EN MIEMBROS
INFERIORES Y APARICION DE EQUIMOSIS EN MIEMBROS SUPERIORES .
PACIENTE TRAE REPORTE DE ECOCARDIOGRAMA TRANSTORACICO 22
JULIO 2015:
FEVI 44%, CARDIOPATIA ISQUEMICA, ESCLEROSIS VALVULAR AORTICA,
CALCIFICACION DEL ANILLO MITRAL, MODERADA DILATACION DE LA
AURICULA IZQUIERDA, HIPERTENSION PULMONAR LEVE CON
DILATACION DE CAVIDADES DERECHA SECUNDARIA.
5. ANTECEDENTES
HTA, ACV ISQUEMICO HACE 5 AÑOS, EPOC OXIGENO REQUIRIENTE,
SAHOS, INSUFICIENCIA CARDIACA CONGESTIVA, ANTECEDENTE DE
ANTICOAGULACION CON WARFARINA SIN INDICACION CLARA (CON
ESTUDIO HOLTER HACE UN AÑO SIN EVIDENCIA DE FA)
ESPIRONOLACTONA 25 MG AL DIA
LOSARTAN 50 MG VO CADA12 HORAS
NIFEDIPINO 30 MG AL DIA
FUROSEMIDA 40 MG AL DIA
ATORVASTATINA 40 MG AL DIA
CARVEDILOL 6.25 MG CADA 12 HORAS
FAQUECTOMIA BILATERAL
TÓXICOS: COCINO CON LEÑA POR 30AÑOS.
6. EXAMEN FISICO
FC : 88 LPM FR: 24 RPM TA: 120/80 MMHG SO2: 70%
REGULARES CONDICIONES GENERALES, ALERTA, AFEBRIL, CON
CIANOCIS PERIBUCAL
CREPITOS DE PREDOMINIO EN HEMITORAX DERECHO. RUIDOS
CARDIACOS RITMICOS NO DEFICIT DE PULSO, NO SOPLOS.
EDEMA EN MIEMBROS INFERIORES GRADO II
7. PARACLINICOS DE INGRESO:
PT 17.5 CONTROL 14.3 INR 1.27 PTT 33.3 CONTROL 30
HEMOGRAMA PLAQUETAS 137000 LEUCOS 12100 NEUTROFILOS 73.9 %
LINFOCITOS 13.7 MONOCITOS 12.10 % HB 15.9 HCTO 49.9
CL 98.8 K 4.28 NA 139.9
CREAT 1.58 BUN 35.8 GASES ARTERIALES FIO2 0.2 SAT 90.9 PH 7.3 PCO2
37.3 MM HG HB 15.9 HCO3 22.4 MMOL/L BB 46.1 EB -2.3
GLUCOSA 133
UROANALISIS PH 5.0 NITRITOS POSITIVOS PROTEINAS 75 MG/DL GLUCOSA
NORMAL CETONAS NEGA UROBILINOGENO NEG ERITROCITOS 50 U/L
BACTERIAS +++ C EPITELIALES 2 LEUCOCITOS 60 HEMATIES 10
8. EKG CON RITMO SINUSAL, FC 77LPM, SIN HALLAZGOS QUE
SUGIERAN ISQUEMIA AGUDA.
RX DE TORAX :
INFILTRADOS ALVEOLARES RETROCARDIACOS,
CARDIOMEGALIA CON VELAMIENTO ANGULO COSTOFRENICO
IZQUIERDO, SIN SIGNOS FRANCOS DE CONSOLIDACION, NO
BRONCOGRAMA AEREO.
9. IDX: Falla cardiaca descompensada
RESTRICCION HIDRICA
O2 POR CN A 2 LT POR MIN
FUROSEMIDA 10 mg IV CADA 6 HORAS
ESPIRONOLACTONA 12.5 mg AL DIA
LOSARTAN 50 mg CADA 12 HORAS
NIFEDIPINO 30 mg AL DIA
ATORVASTATINA 40 mg DIA
CARVEDILOL 6.25 mg CADA 12 HORAS
S/S ECOCARDIOGRAMA TRANSTORACICO
10. EVOLUCION SEGUNDO DIA
ECOCARDIOGRAMA
1- CARDIOMIOPATIA HIPERTROFICA EXCENTRICA CON FUNCION
VENTRICULAR MODERADAMENTE COMPROMETIDA FEVI 37%
2- DISFUNCION DIASTOLICA TIPO TRASTORNO DE LA RELAJACION.
3- AURICULOMEGALIA IZQUIERDA
4- SIGNOS INDIRECTOS DE HIPERTENSION PULMONAR
HEMOGRAMA LEUCOCITOS 11450 NEUTROFILOS 72 % LINFOCITOS
12.2 % HB 15.1 HCTO 46.4 PLAQUETAS 126000
CL 97.8 CREAT 1.68 BUN 34.9 K 3.83 NS 138.9
11. • SE SOLICITA TAC DE TORAX SIMPLE POR IMAGEN DE
OCUPACION ALVEOLAR RETROCARDIACA EN RX DE TORAX.
O2 POR CN A 2 LT POR MIN
SSN 30 CC HORA IV
FUROSEMIDA 10 mg IV CADA 6 HORAS
ESPIRONOLACTONA 12.5 mg AL DIA
LOSARTAN 50 mg CADA 12 HORAS
NIFEDIPINO 30 mg AL DIA
ATORVASTATINA 40 mg DIA
CARVEDILOL 6.25 mg CADA 12 HORAS
ENOXAPARINA 40 MG SC CADA DIA
ASPIRINA 100 MG CADA DIA
CEFUROXIMA 750 MG C 8 HORAS IV
12. TERCER DIA DE EVOLUCION
CL 98.7 CREATININA 2.22 BUN 51.3 K 3.74 NA 138.3
TAC DE TORAX:
1-POSIBLE PROCESO NEUMÓNICO EN EL LÓBULO INFERIOR
IZQUIERDO CON PEQUEÑO DERRAME PLEURAL ASOCIADO.
2-ZONAS DE DISMINUCIÓN DE LA TRANSPARENCIA MAL
DEFINIDAS EN EL LÓBULO SUPERIOR IZQUIERDO DE ASPECTO
RESIDUAL.
3-CARDIOPATÍA DILATADA Y EXTENSA CALCIFICACIÓN
ATEROMATOSA DE LAS ARTERIAS CORONARIAS.
AMPICILINA/SULBACTAM 3 G IV CADA 6 HORAS
13. CUARTO DIA DE EVOLUCION
SODIO 140 POTASIO 4.0 CLORO 99 CREATININA 2.75 BUN 62
HB 14.9 HTCO 45 PLAQ 174.000 LEUCOS 13960 NEUTROFILOS
DE 13110 PREVIOS DE 11530
SE DECIDE AJUSTAR ANTIBIOTICO Y MANEJO PARA FALLA
CARDIACA
SE REALIZAN PARACLINICOS DE CONTROL A LAS DOCE HORAS
QUE MUESTRAN:
LACTATO 1.0 CL 100.6 CREATININA 4.24 BUN 89.6 K 4.23
NA 140.5 PCR 124.5 MG/L
14. 1. FALLA CARDIACA DESCOMPENSADA ESTADIO C NYHA IV
STEVENSON B FEVI 37%
1.1 SINDROME CARDIORENAL TIPO 2
2. FALLA RENAL CRONICA AGUDIZADA AKIN 3
3. EPOC GOLD C
4. HIPERTENSION ARTERIAL
5. SAHOS
6. ANTECEDENTE ACV HACE 5 AÑOS
•SE SUSPENDE FUROSEMIDA, ESPIRONOLACTONA, Y LOSARTAN
•REMISION CUIDADOS INTERMEDIOS
PASO DE CATETER VENOSO CENTRAL PARA OPTIMIZACION DE
REANIMACION, Y BOLOS DE CAPACITANCIA CON AUMENTO DE
VOLUMEN ARTERIAL EFECTIVO
17. DEFINICION
• Síndrome complejo que resulta de una
alteración en la función o en la estructura
del llenado ventricular, o en la fracción de
eyección (FE)
• Disnea, fatiga, intolerancia al ejercicio,
retención de líquidos, congestión pulmonar
y esplacnica y/o edema periférico
YANCY, CW et al. 2013 ACCF/AHA Heart
Failure Guideline
23. DESCOMPENSACION AGUDA - FALLA
CARDIACA
• Primera causa de hospitalización - < 65 años
• 3000 muertes al año por Falla cardiaca
• 12 % descompensación
MICHAEL C. SCOTT, MD a,b, MICHAEL E. WINTERS, MDa.
2015. Congestive Heart Failure;Emerg Med Clin N Am
24. FALLA CARDIACA DESCOMPENSADA
• Mas que un exceso de volumen
intravascular
• Compromiso
CARDIACO
VASCULAR
MICHAEL C. SCOTT, MD a,b, MICHAEL E. WINTERS, MDa.
2015. Congestive Heart Failure;Emerg Med Clin N Am
25. Compromiso cardiaco
• Insuficiencia cardiaca crónica
• Exceso de volumen intravascular (no
adherencia dieta/tto, compromiso renal)
• Edema pulmonar y periférico
MICHAEL C. SCOTT, MD a,b, MICHAEL E. WINTERS, MDa.
2015. Congestive Heart Failure;Emerg Med Clin N Am
26. Compromiso vascular
• Aumento abrupto de vasoconstricción
• Aumento de Postcarga
Eje renina angiotensina aldosterona-
Simpatico
• DESCOMPENSACION AGUDA
MICHAEL C. SCOTT, MD a,b, MICHAEL E. WINTERS, MDa.
2015. Congestive Heart Failure;Emerg Med Clin N Am
34. • Disminución precarga y postcarga
• IECAs (Postcarga)
• Diuréticos (Sobrecarga de líquidos)
Tipo asa
• Inotrópicos (shock cardiogenico)
35. DIURETICOS
OJO GASTO URINARIO, SIGNOS Y SINTOMAS DE CONGESTION
AJUSTE DE DIURETICOS (electrolitos, función renal)
YANCY, CW et al. 2013 ACCF/AHA Heart Failure Guideline
36. CONTINUACION TERAPIA CRONICA
BB A BAJAS DOSIS – PACIENTE ESTABLE HEMODINAMICAMENTE
OJO IECAs, ARAII,ANTAGONISTAS ALDOSTERONA – FUNCION
RENAL
YANCY, CW et al. 2013 ACCF/AHA Heart Failure Guideline
43. DEFINICION
• Alteración de la función renal durante el
tratamiento de falla cardiaca
descompensada
• Terapia para falla cardiaca descompensada
limitada por disminución en la función renal
PETRA NIJST & WILFRIED MULLENS. 2014. The Acute Cardiorenal Syndrome:
Burden and Mechanisms of Disease. Curr Heart Fail Rep. 11: 453-462
44. SINDROME CARDIORENAL
• Reto terapéutico (IATROGENIA)
• creatinina - TFG
• Falla cardiaca Insuficiencia renal
PETRA NIJST & WILFRIED MULLENS. 2014. The Acute Cardiorenal Syndrome:
Burden and Mechanisms of Disease. Curr Heart Fail Rep. 11: 453-462
45. FISIOPATOLOGIA
PETRA NIJST & WILFRIED MULLENS. 2014. The Acute Cardiorenal Syndrome:
Burden and Mechanisms of Disease. Curr Heart Fail Rep. 11: 453-462
46. CLASIFICACION
PETRA NIJST & WILFRIED MULLENS. 2014. The Acute Cardiorenal Syndrome:
Burden and Mechanisms of Disease. Curr Heart Fail Rep. 11: 453-462
47. SCR TIPO 1
PETRA NIJST & WILFRIED MULLENS. 2014. The Acute Cardiorenal Syndrome:
Burden and Mechanisms of Disease. Curr Heart Fail Rep. 11: 453-462
48. SCR TIPO 2
PETRA NIJST & WILFRIED MULLENS. 2014. The Acute Cardiorenal Syndrome:
Burden and Mechanisms of Disease. Curr Heart Fail Rep. 11: 453-462
49. TRATAMIENTO SCR TIPO 1
• Diuréticos
• Vasodilatadores
• Vaptanos
• Inotropicos
FRANCOIS ROUBILLE a,h MARION MORENA. 2014. Pharmacologic
Therapies for Chronic and Acute Decompensated Heart Failure; Specific
Insights on Cardiorenal Syndromes. Blood Purif. 37 (suppl 2): 20-33
50. DIURETICOS
• Diminución de congestión vascular
• Pilar tratamiento - Manejo insuficiencia
cardiaca
• Asa – Tiazidas – Ahorradores K –
Antagonistas aldosterona (bloqueo
neurohormonal)
FRANCOIS ROUBILLE a,h MARION MORENA. 2014. Pharmacologic Therapies for
Chronic and Acute Decompensated Heart Failure; Specific Insights on Cardiorenal
Syndromes. Blood Purif. 37 (suppl 2): 20-33
51. DIURETICOS
• Diuréticos de ASA
• Bloqueo reabsorción de Na – Porción
ascendente asa de henle
• Rápida absorción: 30 min VO – IV Inmediata
• Furosemida, torasemida, bumetanida
FRANCOIS ROUBILLE a,h MARION MORENA. 2014. Pharmacologic Therapies for
Chronic and Acute Decompensated Heart Failure; Specific Insights on Cardiorenal
Syndromes. Blood Purif. 37 (suppl 2): 20-33
52. DOSIS DIURETICO DE ASA
G.MICHAEL FELKER, MD, M.H.S, KERRY L. LEE, N. 2011. Diuretic Strategies
in Patiens with Acute Decompensated Heart Failure. N Engl J Med. 364: 797-
805
53. G.MICHAEL FELKER, MD, M.H.S, KERRY L. LEE, N. 2011. Diuretic Strategies
in Patiens with Acute Decompensated Heart Failure. N Engl J Med. 364: 797-805
54. VASODILATADORES
• Nitratos – nitropusiato
• Disminución de precarga y postcarga
Reducción trabajo ventricular – aumento
volumen latido y gasto cardiaco
Para pacientes con presión arterial elevada
FRANCOIS ROUBILLE a,h MARION MORENA. 2014. Pharmacologic Therapies for
Chronic and Acute Decompensated Heart Failure; Specific Insights on Cardiorenal
Syndromes. Blood Purif. 37 (suppl 2): 20-33
55. NESIRITIDE
• Forma recombinante de BNP
• Dilatación arteriola aferente y disminución
reabsorción de Na
• Disminución precarga, postcarga, y
resistencia vascular pulmonar
• Altera función renal y aumento mortalidad
56. VAPTANOS
• ANTAGONISTAS RECEPTORES Vasopresina
• Excreción H2O libre de electrolitos
• Falla cardiaca, SIADH, Cirrosis hepática
(hiponatremia dilucional)
RUEDIGER W. LEHRICH, MD, DAVID I. ORTIZ-MELO. Role of
Vaptans in the Management of Hyponatremia. Am J Kidney Dis. 62 (2):
364-376
57. RUEDIGER W. LEHRICH, MD, DAVID I. ORTIZ-MELO. Role of Vaptans in
the Management of Hyponatremia. Am J Kidney Dis. 62 (2): 364-376
58. RUEDIGER W. LEHRICH, MD, DAVID I. ORTIZ-MELO. Role of Vaptans
in the Management of Hyponatremia. Am J Kidney Dis. 62 (2): 364-376
61. LEVOSIMENDAN
• Ca sensibilizador – aumenta afinidad de
Troponina C por el Ca
• Estabilización de complejo TnC-Ca
• Inhibiendo Troponina I – acelera la unión
actina miosina
MORENO N, et al. 2015. Levosimendan; The current situation and new
prospectos. Rev Port Cardio
62. LEVOSIMENDAN
• Acción depende de niveles de Ca
intracelulares
No altera relajación ventricular
• Activación canales K dependientes de ATP
en musculo liso vascular
Hiperpolarización y vasodilatación vascular
63. LEVOSIMENDAN
• t ½ 1 hora – Duración de efecto por días
• Metabolizado en intestino (OR-1855) y
posteriormente acetilada en hígado para
formar OR-1896 (t ½ 80 horas)
• No efecto rebote
MORENO N, et al. 2015. Levosimendan; The current situation and new
prospectos. Rev Port Cardio
64. LEVOSIMENDAN
Falla cardiaca aguda – Función renal
•Disminución parámetros hemodinámicos y
síntomas
•NO aumenta consumo O2 miocárdico, ni
produce arritmias (hipocalemia e
hipotensión)
65. MORENO N, et al. 2015. Levosimendan; The current situation and new
prospectos. Rev Port Cardio
66. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI. Levosimendan
improves renal function in acute decompensated heart failure; possible underlying
mechanisms
67. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI. Levosimendan
improves renal function in acute decompensated heart failure; possible underlying
mechanisms
68. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI. Levosimendan
improves renal function in acute decompensated heart failure; possible underlying
mechanisms
69. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI. Levosimendan
improves renal function in acute decompensated heart failure; possible underlying
mechanisms
70. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI. Levosimendan
improves renal function in acute decompensated heart failure; possible underlying
mechanisms
71. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI. Levosimendan
improves renal function in acute decompensated heart failure; possible underlying
mechanisms
72. FRANCESCO FEDELE *+, NOEMÍ BRUNO, BRUNO BRASOLINI.
Levosimendan improves renal function in acute decompensated heart failure;
possible underlying mechanisms
73. SERELAXIN
• Forma recombinante de RELAXIN-2
• Vasodilatación, antioxidativo
• Reducción resistencia vascular renal y
sistémica (Preclinicos)
• Mejoría síntomas – Mortalidad 180 días
(EC)
ANNA ISOTTA CASTRINIA, VALENTINA CARUBELLIa. 2015. Serelaxin a
novel treatment for acute heart failure. Expert Rev. Clin. Pharmacol. 8 (5), 549-
557
74. FRANCOIS ROUBILLE a,h MARION MORENA. 2014. Pharmacologic Therapies
for Chronic and Acute Decompensated Heart Failure; Specific Insights on
Cardiorenal Syndromes. Blood Purif. 37 (suppl 2): 20-33
75. TRATAMIENTO SCR TIPO 2
• Mecanismo SCR TIPO 2
Activación crónica de RAAS y sistema
nervioso simpático
Por volumen arterial bajo y congestión
venosa
• IECAs – B Bloqueadores (seleccionados)
76. FRANCOIS ROUBILLE a,h MARION MORENA. 2014. Pharmacologic Therapies for
Chronic and Acute Decompensated Heart Failure; Specific Insights on Cardiorenal
Syndromes. Blood Purif. 37 (suppl 2): 20-33
77. CONCLUSIONES
• Dar tratamiento pero ajustar según
necesidad y efectos adversos
• Uso agresivo de diuréticos (SIN APORTE
LEV) – Deterioro función renal
• IECAs, ARA – Cardioprotectores pero
también hay alteración renal
Notes de l'éditeur
1. Traditionally, worsening renal function in HF had been attributed
to low-output failure or hypotension resulting in renal
hypoperfusion [18, 26]. Inadequate RBF prompts renin release
by the juxtaglomerular cells of the afferent arterioles
through low-flow states in the ascending limb of the loop of
Henle and pressure-sensing baroreceptors Activation of the
renin-angiotensin-aldosterone cascade will lead to afferent
and efferent arteriolar vasoconstriction and thereby decreasing
GFR
2. A rise in CVP can diminish RBF through backward transmission
of venous pressure. The raised CVP might distend the
venules surrounding the distal ends of the tubules so that the
lumen of the tubule can be obliterated [39, 40]. Also, since the
kidneys are encapsulated organs, increased central venous
pressure could cause an increase in renal interstitial pressure
further attenuating RBF [40, 41]. Moreover, angiotensin II
(AT II) concentrations increase with increasing renal venous
pressure [36, 42]. This will lead to a further fall in GFR and
will increase sympathetic system activity
BLOOD PRESURE
that changes in systemic blood
pressure during ADHF treatment, due to aggressive vasoactive
and diuretic therapy, are another strong hemodynamic determinant
of dynamic renal function
4. PRESION INTRABDOMINAL
Elevated IAP results in an indirect increase in central
venous pressures as well as directly “compressing” the kidneys
(and thus increase renal pressure), both leading to reduction
in RBF
5. SRAA
Renin-angiotensin-aldosterone system (RAAS) upregulation
in HF is a (mal)adaptive response to altered hemodynamics
and sympathetic signalling. Moreover, neurohormonal factors
are more stimulated in the presence of reduced renal function
[52, 53] and in the presence of congestion [54]. Renin, AT II,
and aldosterone cause both systemic and renal vasoconstriction
(i.e., hemodynamic effects) and therefore reduce RBF and
enhance tubular sodium reabsorption
Furthermore,
high levels of AT II directly contributes to intrinsic
kidney damage since AT II upregulates cytokines
transforming growth factor-β, tumor necrosis factor-α nuclear
factor-κB, and interleukin-6 and stimulates fibroblasts,
resulting in cell growth, inflammation, and fibrotic damage
in the renal parenchyma
SISTEMA NERVIOSO SIMPATICO
renal sympathetic overdrive in renal dysfunction
through RAAS upregulation, mechano- and chemoreflex activation
and endothelial dysfunction with decreased bioavailability
of nitric oxide (NO) [58]. Moreover, SNS overactivity
leads to direct renal afferent and efferent arteriolar vasoconstriction
and renin release, both leading to decreasing RBF
and ultimately GFR. Beta-blockers may counteract the negative
effects of chronic renal SNS activation
ESTRES OXIDATIVO
Neurohormones
are strong precipitants and mediators of an oxidative
injury cascade that leads to widespread endothelial dysfunction,
inflammation, and cell death in the heart and kidneys. AT
II seems to be particularly important in this process, exerting
many deleterious effects through the activation of NADPH
oxidase and NADH oxidase. AT II activates these two enzymes
within vascular smoothmuscle cells, cardiac myocytes,
and renal tubular epithelial cells, generating superoxide, a
reactive oxygen species
EN RESUMEN
In essence, all the agents tried to improve
RBF—hence GFR—by increasing cardiac output (inotropes,
vasodilators), decreasing congestion (diuretics, ultrafiltration,
vaptans), and lowering renal vascular resistance (rolofylline,
serelaxin, nesiritide, renal denervation, etc.). However, none of
the current studied therapeutic strategies have proven beneficial
effects on outcome.
DOSE STUDY
the Diuretic
Optimization Strategies Evaluation (DOSE), a large prospective
double-blind randomized trial, evaluated diuretic
dose and strategy in ADHF [26] . The trial randomized
308 ADHF patients to intravenous furosemide given as
twice-daily boluses or continuous infusion, with either a
low or high dose. No significant difference was found in
global assessment of symptoms or change in serum creatinine
over 72 h with diuretic administration by bolus or
continuous infusion or with a low- versus a high-dose
strategy. However, patients with a higher-dose strategy
had a significantly more favorable outcome regarding relief
of dyspnea, change in weight, and net fluid loss, but
with a greater risk of serum creatinine increasing by &gt;0.3
mg/dl within 72 h. This would suggest that the strategy of
using higher doses of diuretics in ADHF on admission to
hospital is likely to more rapidly control fluid retention
and to relieve symptoms with a slightly higher risk of renal
dysfunction not affecting outcome
The cardio-renal syndrome plays a critical role in acute heart failure (HF). Levosimendan, an inodilator drug, has
a positive but controversial effect on kidney. Our aim was to evaluate its effects on both renal and systemic
haemodynamic parameters as well as on renal function, explaining the possible mechanisms involved.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Methods
and results
From April 2007, 29
consecutive patients admitted to our Department with acute decompensated
HF and renal impairment were enrolled in the study. All
patients were randomized according to a 2:1 scheme to receive either
a 10 min i.v. loading dose of levosimendan (6 μg/kg) followed by
an infusion (0.1 μg/kg/min) for 24 h, or placebo.
Patients with acute decompensated HF, moderate renal impairment, wedge pressure &gt;20mmHg and EF &lt;40% were
eligible. Twenty-one patients were randomized to infusion of levosimendan or placebo, on top of standard therapy.
Systemic haemodynamic parameters (wedge and cardiac output) were evaluated at baseline and at 8, 16, 24, 48,
and 72 h. An intravascular renal artery Doppler exam was performed at baseline, after levosimendan bolus, and 1 h
thereafter. Renal blood flow, glomerular filtration rate (GFR), cystatin C, blood urea nitrogen (BUN), urinary output,
sodium excretion, and plasma sodium were measured. The effect of levosimendan was beneficial and significantly
different from placebo on several renal and cardiac parameters. Specifically, the levosimendan and placebo group
exhibited significantly different changes over time in GFR (P =0.037), renal blood flow (P =0.037), and renal artery
diameter (P =0.033), with ensuing improvements in serum levels of BUN (P =0.014), creatinine (P =0.042), and
cystatin C (P =0.05). Concomitantly, levosimendan provided a significant increase in urine output up to 72 h (P =0.02).
These beneficial results on renal parameters were accompanied by similarly significant and favourable changes in
cardiac index (P =0.029) and PCWP (P &lt;0.001).
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Conclusion Levosimendan, in acute decompensated HF, has an immediate renoprotective effect, mediated by an increase in renal
blood flow, due to a selective renal arterial and venous vasodilating action.