ABSTRACT
BACKGROUND: Preservation of organ function and viability is a crucial factor for survival in cardiogenic shock (CS) patients. There is not information enough on cytoprotective substances that may delay organs damage in CS. We hypothesize that cytidine-5-diphosphocholine (CDP-choline) can act as a cytoprotective pharmacological measure that diminishes the target organ damage. So, we aimed to perform a review of works carried out in our institution to evaluate the effect of therapeutic cytoprotection of the CDP-choline. SUMMARY: CDP-choline is an intermediate metabolite in the synthesis of phosphatidylcholine. It is also a useful drug for the treatment of acute ischaemic stroke, traumatic brain injury, and neurodegenerative diseases and has shown an excellent pharmacological safety profile as well. We review our institution's work and described the cytoprotective effects of CDP-choline in experimental models of heart, liver, and kidney acute damage, where this compound was shown to diminish reperfusion-induced ventricular arrhythmias, oxidative stress, apoptotic cell death, inflammation, lactic acid levels and to preserve mitochondrial function. KEY MESSAGES: We propose that additional research is needed to evaluate the impact of cytoprotective therapy adjuvant to mitigate target organ damage in patients with CS.
Subject(s)
Cytidine Diphosphate Choline , Cytoprotection , Oxidative Stress , Shock, Cardiogenic , Cytidine Diphosphate Choline/pharmacology , Cytidine Diphosphate Choline/therapeutic use , Humans , Animals , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/metabolism , Shock, Cardiogenic/physiopathology , Oxidative Stress/drug effects , Apoptosis/drug effects , Myocardium/metabolism , Myocardium/pathologyABSTRACT
El shock cardiogénico posinfarto caracterizado por un estado de insuficiencia circulatoria sistémica requiere de un tratamiento precoz en vistas a restablecer la estabilidad hemodinámica y la función ventricular. Este consta de la reperfusión coronaria mediante revascularización miocárdica; en algunos casos es necesaria la utilización de dispositivos de asistencia ventricular. El ECMO venoarterial es un sistema de circulación extracorpórea que permite un soporte biventricular oxigenando la sangre y reintroduciéndola mediante un flujo continuo hacia la circulación arterial sistémica. El uso de dicho dispositivo en pacientes con shock cardiogénico ha mostrado una mejoría significativa de la sobrevida a 30 días en comparación con el uso del balón de contrapulsación intraaórtico. No obstante, sus potenciales complicaciones, como dificultad en el vaciamiento ventricular izquierdo, síndrome de Arlequín, sangrados e infecciones, hacen fundamental la formación y el trabajo en equipo del heart team. Un porcentaje no menor de estos pacientes presentarán una severa disfunción ventricular permanente, por lo que podrían ser candidatos a dispositivos de asistencia ventricular izquierda de larga duración tipo Heartmate III como puente al trasplante cardíaco, el cual ha mostrado resultados satisfactorios con una excelente sobrevida a mediano plazo.
Post-infarction cardiogenic shock characterized by a state of systemic circulatory failure requires early treatment in order to restore hemodynamic stability and ventricular function. This consists of coronary reperfusion through myocardial revascularization, requiring in some cases the use of ventricular assist devices. Veno-arterial ECMO is an extracorporeal circulation system that allows biventricular support by oxygenating the blood and reintroducing it through a continuous flow towards the systemic arterial circulation. The use of this device in patients with cardiogenic shock has shown a significant improvement in survival at 30 days compared to the use of intra-aortic balloon pump. However, its potential complications, such as difficulty in left ventricular emptying, Harlequin syndrome, bleeding and infections, make the training and teamwork of the heart team essential. A great percentage of these patients will present a severe permanent ventricular dysfunction, so they could be candidates for long-term mechanical circulatory support devices like Heartmate III as a bridge to transplant or myocardial recovery, or destination therapy, which has shown satisfactory results with excellent medium-term survival.
O choque cardiogênico pós-infarto caracterizado por um estado de insuficiência circulatória sistêmica requer tratamento precoce para restabelecer a estabilidade hemodinâmica e a função ventricular. Esta consiste na reperfusão coronariana por meio de revascularização miocárdica, necessitando, em alguns casos, do uso de dispositivos de assistência ventricular. A ECMO venoarterial é um sistema de circulação extracorpórea que permite o suporte biventricular oxigenando o sangue e reintroduzindo-o através de um fluxo contínuo para a circulação arterial sistêmica. O uso desse dispositivo em pacientes com choque cardiogênico mostrou melhora significativa na sobrevida em 30 dias em relação ao uso de contrapulsação com balão intra-aórtico. No entanto, suas potenciais complicações, como dificuldade de esvaziamento ventricular esquerdo, síndrome de Harlequin, sangramentos e infecções, tornam imprescindível o treinamento e o trabalho em equipe do time do coração. Não uma pequena porcentagem desses pacientes apresentará uma condição ventricular permanente grave, podendo ser candidatos a dispositivos de assistência ventricular esquerda de longa duração do tipo Heartmate III como ponte para o transplante cardíaco, que tem demonstrado resultados satisfatórios com excelente sobrevida em médio prazo.
Subject(s)
Humans , Male , Middle Aged , Shock, Cardiogenic/therapy , Extracorporeal Membrane Oxygenation , Myocardial Infarction/complications , Shock, Cardiogenic/complications , Shock, Cardiogenic/drug therapy , Heart-Assist Devices , Treatment Outcome , Critical Care , Hemodynamic MonitoringSubject(s)
Humans , Male , Adult , Shock, Cardiogenic/diagnostic imaging , COVID-19/diagnosis , Myocarditis/diagnostic imaging , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/virology , Enalapril/administration & dosage , Bisoprolol/administration & dosage , COVID-19/complications , Heart Failure/drug therapy , Heart Failure/virology , Heart Failure/diagnostic imaging , Myocarditis/drug therapy , Myocarditis/virologyABSTRACT
La miocarditis es una enfermedad inflamatoria del miocardio. Las infecciones virales son la causa más común, aunque también puede deberse a reacciones de hipersensibilidad y de etiología autoinmunitaria, entre otras. El espectro clínico de la enfermedad es variado y comprende desde un curso asintomático, seguido de dolor torácico, arritmias y falla cardiaca aguda, hasta un cuadro fulminante. El término 'fulminante' se refiere al desarrollo de un shock cardiogénico con necesidad de soporte vasopresor e inotrópico o dispositivos de asistencia circulatoria, ya sea oxigenación por membrana extracorpórea o balón de contrapulsación intraaórtico. Cerca del 10 % de los casos de falla cardiaca por miocarditis corresponde a miocarditis fulminante. La miocarditis por influenza se considera una condición infrecuente; no obstante, su incidencia ha aumentado desde el 2009 a raíz de la pandemia de influenza por el virus AH1N1. Por su parte, la miocarditis por influenza de tipo B sigue siendo una condición infrecuente. Se describen aquí dos casos confirmados de miocarditis fulminante por el virus de la influenza B atendidos en un centro cardiovascular, que requirieron dispositivos de asistencia circulatoria mecánica.
Myocarditis is an inflammatory disease of the myocardium. Viral infections are the most common cause, although it can also be due to hypersensitivity reactions and autoimmune etiology, among other causes. The clinical spectrum of the disease is varied, from an asymptomatic course, followed by chest pain, arrhythmias, and acute heart failure, to a fulminant episode. The term fulminant refers to the development of cardiogenic shock with a need for vasopressor support and inotropic or assisted circulation devices either extracorporeal membrane oxygenation (ECMO) or intra-aortic counterpulsation balloon. About 10% of cases of heart failure due to myocarditis correspond to fulminant myocarditis. Influenza myocarditis has been considered an infrequent condition. However, its incidence has increased since 2009 as a result of the AH1N1 pandemic; otherwise, myocarditis due to the Influenza type B virus remains an infrequent entity. We describe the experience in a cardiovascular center of two confirmed cases of fulminant myocarditis due to influenza B that required circulatory assistance devices.
Subject(s)
Influenza B virus , Influenza, Human/complications , Myocarditis/etiology , Shock, Cardiogenic/etiology , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , Advanced Cardiac Life Support , Antiviral Agents/therapeutic use , Combined Modality Therapy , Emergencies , Extracorporeal Membrane Oxygenation , Fatal Outcome , Female , Hemofiltration , Humans , Influenza B virus/isolation & purification , Influenza, Human/drug therapy , Influenza, Human/virology , Intra-Aortic Balloon Pumping , Middle Aged , Myocarditis/diagnostic imaging , Oseltamivir/therapeutic use , Pericardial Effusion/etiology , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/therapy , Vasoconstrictor Agents/therapeutic use , Young AdultABSTRACT
Resumen La miocarditis es una enfermedad inflamatoria del miocardio. Las infecciones virales son la causa más común, aunque también puede deberse a reacciones de hipersensibilidad y de etiología autoinmunitaria, entre otras. El espectro clínico de la enfermedad es variado y comprende desde un curso asintomático, seguido de dolor torácico, arritmias y falla cardiaca aguda, hasta un cuadro fulminante. El término 'fulminante' se refiere al desarrollo de un shock cardiogénico con necesidad de soporte vasopresor e inotrópico o dispositivos de asistencia circulatoria, ya sea oxigenación por membrana extracorpórea o balón de contrapulsación intraaórtico. Cerca del 10 % de los casos de falla cardiaca por miocarditis corresponde a miocarditis fulminante. La miocarditis por influenza se considera una condición infrecuente; no obstante, su incidencia ha aumentado desde el 2009 a raíz de la pandemia de influenza por el virus AH1N1. Por su parte, la miocarditis por influenza de tipo B sigue siendo una condición infrecuente. Se describen aquí dos casos confirmados de miocarditis fulminante por el virus de la influenza B atendidos en un centro cardiovascular, que requirieron dispositivos de asistencia circulatoria mecánica.
Abstract Myocarditis is an inflammatory disease of the myocardium. Viral infections are the most common cause, although it can also be due to hypersensitivity reactions and autoimmune etiology, among other causes. The clinical spectrum of the disease is varied, from an asymptomatic course, followed by chest pain, arrhythmias, and acute heart failure, to a fulminant episode. The term fulminant refers to the development of cardiogenic shock with a need for vasopressor support and inotropic or assisted circulation devices either extracorporeal membrane oxygenation (ECMO) or intra-aortic counterpulsation balloon. About 10% of cases of heart failure due to myocarditis correspond to fulminant myocarditis. Influenza myocarditis has been considered an infrequent condition. However, its incidence has increased since 2009 as a result of the AH1N1 pandemic; otherwise, myocarditis due to the Influenza type B virus remains an infrequent entity. We describe the experience in a cardiovascular center of two confirmed cases of fulminant myocarditis due to influenza B that required circulatory assistance devices.
Subject(s)
Female , Humans , Middle Aged , Young Adult , Influenza B virus , Shock, Cardiogenic/etiology , Influenza, Human/complications , Myocarditis/etiology , Antiviral Agents/therapeutic use , Influenza B virus/isolation & purification , Pericardial Effusion/etiology , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/therapy , Vasoconstrictor Agents/therapeutic use , Extracorporeal Membrane Oxygenation , Hemofiltration , Fatal Outcome , Combined Modality Therapy , Advanced Cardiac Life Support , Emergencies , Influenza, Human/drug therapy , Influenza, Human/virology , Oseltamivir/therapeutic use , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , Intra-Aortic Balloon Pumping , Myocarditis/diagnostic imagingABSTRACT
OBJETIVO: estudar o uso terapêutico do bloqueio da guanilato ciclase pelo azul de metileno em um modelo experimental de pancreatite aguda grave em suínos. MÉTODOS: a pancreatite aguda necrotizante foi induzida em porcos anestesiados por infusão ductal pancreática retrógrada de 1ml/kg de taurocolato de sódio a 5% e 8U/kg de enteroquinase. Três grupos foram estudados (n=5): controle (C), pancreatite (PA), "bolus" de azul seguido por pancreatite (AM+PA). Os dados incluíram enzimas séricas e do líquido abdominal, variáveis hemodinâmicas, hemogasometria arterial, volume de líquido abdominal, marcadores inflamatórios plasmáticos, nitrito/nitrato e mieloperoxidase e malondialdeído plasmático. Aplicou-se a análise de variância seguida do pós-teste de Bonferroni (p<0,05). RESULTADOS: os valores de amilase e lipase foram três e dez vezes mais elevados no grupo PA. A atividade da mieloperoxidase foi 50% superior no grupo PA. Os dados hemodinâmicos indicaram choque hipovolêmico precoce seguido de choque cardiogênico. Observou-se grave translocação de líquidos para a cavidade peritoneal. A nitrito/nitrato plasmática permaneceu inalterada. O grupo AM+PA teve aumento de cinco vezes do mieloperoxidase em comparação com o grupo C. CONCLUSÕES: a utilização de azul de metileno em suínos com pancreatite não demonstrou efeitos significativos sobre variáveis hemodinâmicas e inflamatórias. Seu uso terapêutico na pancreatite necro-hemorrágica pode ser inadequado e extremo cuidado deve ser tomado dado o aumento da peroxidação lipídica evidenciado pelo aumento dos valores do malondialdeído.
OBJECTIVE: To study the therapeutic application of guanylate cyclase inhibition by methylene blue in an experimental model of acute pancreatitis in pigs. METHODS: acute necrotizing pancreatitis was induced in anesthetized pigs by the retrograde infusion of 1 ml/kg of 5% sodium taurocholate and 8 U/kg enterokinase in the pancreatic duct. Three groups were studied (n = 5): control (C), pancreatitis (AP), and MB bolus followed by pancreatitis (MB+P). The data included serum and abdominal fluid enzymes, hemodynamic variables, arterial hemogasometry, abdominal fluid volume, inflammatory markers, plasma nitrite/nitrate (NOx), plasma myeloperoxidase (MPO) and plasma malondialdehyde (MDA). One- and two-way analysis of variance (ANOVA) was performed, followed by the Bonferroni test (p < 0.05). RESULTS: amylase and lipase were three and 10-fold higher in the AP group. Myeloperoxidase activity was 50% higher in the AP group. The hemodynamic data indicated early hypovolemic shock followed by cardiogenic shock. Severe fluid translocation to the peritoneal cavity was observed. Plasma NOx remained unchanged. The MB+P group had a five-fold increase in MDA compared with the C group. CONCLUSION: preemptive application of MB in pigs with AP demonstrated no significant effects on hemodynamic and inflammatory variables. The use of MB is inadequate in cases of exponential NO release, and extreme caution must be exercised, given the increase in lipid peroxidation based on the malondialdehyde dosage.
Subject(s)
Animals , Female , Guanylate Cyclase/antagonists & inhibitors , Methylene Blue/therapeutic use , Pancreatitis, Acute Necrotizing/complications , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/etiology , Analysis of Variance , Disease Models, Animal , Methylene Blue/pharmacology , Pancreatitis, Acute Necrotizing/enzymology , SwineABSTRACT
OBJECTIVE: To study the therapeutic application of guanylate cyclase inhibition by methylene blue in an experimental model of acute pancreatitis in pigs. METHODS: acute necrotizing pancreatitis was induced in anesthetized pigs by the retrograde infusion of 1 ml/kg of 5% sodium taurocholate and 8 U/kg enterokinase in the pancreatic duct. Three groups were studied (n = 5): control (C), pancreatitis (AP), and MB bolus followed by pancreatitis (MB+P). The data included serum and abdominal fluid enzymes, hemodynamic variables, arterial hemogasometry, abdominal fluid volume, inflammatory markers, plasma nitrite/nitrate (NOx), plasma myeloperoxidase (MPO) and plasma malondialdehyde (MDA). One- and two-way analysis of variance (ANOVA) was performed, followed by the Bonferroni test (p < 0.05). RESULTS: amylase and lipase were three and 10-fold higher in the AP group. Myeloperoxidase activity was 50% higher in the AP group. The hemodynamic data indicated early hypovolemic shock followed by cardiogenic shock. Severe fluid translocation to the peritoneal cavity was observed. Plasma NOx remained unchanged. The MB+P group had a five-fold increase in MDA compared with the C group. CONCLUSION: preemptive application of MB in pigs with AP demonstrated no significant effects on hemodynamic and inflammatory variables. The use of MB is inadequate in cases of exponential NO release, and extreme caution must be exercised, given the increase in lipid peroxidation based on the malondialdehyde dosage.
Subject(s)
Guanylate Cyclase/antagonists & inhibitors , Methylene Blue/therapeutic use , Pancreatitis, Acute Necrotizing/complications , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/etiology , Analysis of Variance , Animals , Disease Models, Animal , Female , Methylene Blue/pharmacology , Pancreatitis, Acute Necrotizing/enzymology , SwineABSTRACT
INTERVENTIONS: Vasopressor therapy is required in septic shock to maintain tissue perfusion in the face of hypotension. Unfortunately, there are significant side effects of current vasopressors, and newer agents need to be developed. We recently discovered that ethyl gallate, a nonflavonoid phenolic antioxidant found in food substances, could reverse low mean arterial pressure found in an experimental model of septic shock due to inhibition of hydrogen peroxide signaling. In the present study, we compared the hemodynamic and biochemical effects of ethyl gallate vs. those of the commonly used vasopressor, norepinephrine, in a bacteremic canine model of Pseudomonas aeruginosa sepsis in two protocols. MEASUREMENTS AND MAIN RESULTS: We performed these studies in anesthetized and mechanically ventilated dogs. In the early treatment protocol, we infused P. aeruginosa until mean arterial pressure first decreased to â¼60 mm Hg (about 2-3 hrs), after which we stopped the infusion and randomly administered ethyl gallate or norepinephrine in respective groups. In the late treatment protocol, we administered ethyl gallate or norepinephrine after a sustained â¼5-hr decrease in mean arterial pressure to 60 mm Hg and continued the infusion for the duration of the experiment. We followed parameters for over 10 hrs after the initiation of P. aeruginosa in both groups. We measured stroke work, urine output, serum creatinine, among other parameters, and used serum troponin T as an index of myocardial injury. We found that in both protocols, ethyl gallate and norepinephrine improved mean arterial pressure and stroke work to similar extents over the duration of the study. Particularly in the late treatment protocol, ethyl gallate resulted in a lower heart rate, a lower troponin T, and a greater urine output as compared with norepinephrine (p < .05). CONCLUSIONS: These results suggest that phenolic antioxidants, such as ethyl gallate, that inhibit hydrogen peroxide signaling, may represent an alternative class of vasopressors for use in septic shock.
Subject(s)
Gallic Acid/analogs & derivatives , Norepinephrine/pharmacology , Pseudomonas Infections/drug therapy , Pseudomonas aeruginosa , Shock, Cardiogenic/drug therapy , Shock, Septic/drug therapy , Analysis of Variance , Animals , Disease Models, Animal , Dogs , Dose-Response Relationship, Drug , Drug Administration Schedule , Gallic Acid/pharmacology , Pseudomonas Infections/mortality , Random Allocation , Risk Assessment , Shock, Cardiogenic/diagnosis , Shock, Cardiogenic/mortality , Shock, Septic/microbiology , Shock, Septic/mortality , Survival Rate , Treatment OutcomeABSTRACT
Hantavirus pulmonary syndrome (HPS) is a severe disease characterized by a rapid onset of pulmonary edema followed by respiratory failure and cardiogenic shock. The HPS associated viruses are members of the genus Hantavirus, family Bunyaviridae. Hantaviruses have a worldwide distribution and are broadly split into the New World hantaviruses, which includes those causing HPS, and the Old World hantaviruses [including the prototype Hantaan virus (HTNV)], which are associated with a different disease, hemorrhagic fever with renal syndrome (HFRS). Sin Nombre virus (SNV) and Andes virus (ANDV) are the most common causes of HPS in North and South America, respectively. Case fatality of HPS is approximately 40%. Pathogenic New World hantaviruses infect the lung microvascular endothelium without causing any virus induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of HPS. This article briefly reviews the knowledge on HPS-associated hantaviruses accumulated since their discovery, less than 20 years ago.
Subject(s)
Genome, Viral , Hantaan virus/physiology , Hantavirus Pulmonary Syndrome/virology , Hemorrhagic Fever with Renal Syndrome/virology , Lung/virology , Orthohantavirus/physiology , Respiratory Insufficiency/virology , Shock, Cardiogenic/virology , Sin Nombre virus/physiology , Animals , Antiviral Agents/administration & dosage , Cricetinae , Europe , Orthohantavirus/pathogenicity , Hantavirus Pulmonary Syndrome/complications , Hantavirus Pulmonary Syndrome/drug therapy , Hantavirus Pulmonary Syndrome/epidemiology , Hantavirus Pulmonary Syndrome/pathology , Hemorrhagic Fever with Renal Syndrome/drug therapy , Hemorrhagic Fever with Renal Syndrome/epidemiology , Hemorrhagic Fever with Renal Syndrome/pathology , Humans , Lung/pathology , North America , Phylogeography , Respiratory Insufficiency/drug therapy , Respiratory Insufficiency/epidemiology , Respiratory Insufficiency/etiology , Respiratory Insufficiency/pathology , Ribavirin/administration & dosage , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/epidemiology , Shock, Cardiogenic/etiology , Shock, Cardiogenic/pathology , Sin Nombre virus/pathogenicity , South AmericaABSTRACT
OBJECTIVE: Cytomegalovirus (CMV) systemic disease and myocarditis in healthy persons is infrequently reported in the literature, although in increasing numbers in recent years. The importance of the recognition of the syndrome that usually has an initial picture of a mononucleosis like infection in an otherwise healthy person, is the available therapeutic agent, ganciclovir, that can cure the infectious disease. METHODS: We analyzed the clinical result of pulsotherapy with steroids in a patient with CMV myocarditis after 7 days of etiological treatment, with ganciclovir, intravenous vasodilators, and the conventional treatment for congestive heart failure. RESULTS: The clinical condition of the patient improved accordingly to the better function of the left ventricle, and the ganciclovir was kept for 21 days, most of it in an out patient basis. The patient was dismissed from the hospital, with normal myocardial function. CONCLUSION: Potentially curable forms of myocarditis, like M pneumoniae and CMV, for example, can have an initial disproportionate aggression to the myocardium, by the acute inflammatory reaction, that can by itself make worse the damage to the LV function. In our opinion, the blockade of this process by pulsotherapy with steroids can help in the treatment of these patients. We understand that the different scenario of immunosuppressive treatments for the possible auto immunity of the more chronic forms of the presumably post viral cardiomyopathy has been in dispute in the literature, and has stolen the focus from the truly acute cases.
Subject(s)
Cytomegalovirus Infections/drug therapy , Myocarditis/drug therapy , Shock, Cardiogenic/drug therapy , Adult , Anti-Bacterial Agents/therapeutic use , Antihypertensive Agents/therapeutic use , Antiviral Agents/therapeutic use , Ganciclovir/therapeutic use , Glucocorticoids/therapeutic use , Humans , Injections, Intravenous , Male , Myocarditis/virology , Prednisone/therapeutic use , Shock, Cardiogenic/etiology , Teicoplanin/therapeutic useABSTRACT
OBJECTIVE: Cytomegalovirus (CMV) systemic disease and myocarditis in healthy persons is infrequently reported in the literature, although in increasing numbers in recent years. The importance of the recognition of the syndrome that usually has an initial picture of a mononucleosis like infection in an otherwise healthy person, is the available therapeutic agent, ganciclovir, that can cure the infectious disease. METHODS: We analyzed the clinical result of pulsotherapy with steroids in a patient with CMV myocarditis after 7 days of etiological treatment, with ganciclovir, intravenous vasodilators, and the conventional treatment for congestive heart failure. RESULTS: The clinical condition of the patient improved accordingly to the better function of the left ventricle, and the ganciclovir was kept for 21 days, most of it in an out patient basis. The patient was dismissed from the hospital, with normal myocardial function. CONCLUSION: Potentially curable forms of myocarditis, like M pneumoniae and CMV, for example, can have an initial disproportionate aggression to the myocardium, by the acute inflammatory reaction, that can by itself make worse the damage to the LV function. In our opinion, the blockade of this process by pulsotherapy with steroids can help in the treatment of these patients. We understand that the different scenario of immunosuppressive treatments for the possible auto immunity of the more chronic forms of the presumably post viral cardiomyopathy has been in dispute in the literature, and has stolen the focus from the truly acute cases.
OBJETIVO: Doença sistêmica por citomegalovírus (CMV) com miocardite em pessoas saudáveis é raramente referida na literatura, apesar de em maior número em anos recentes. A importância do reconhecimento da síndrome, que usualmente tem um quadro inicial "mononucleosis like" em uma pessoa sadia é a disponibilidade do agente terapêutico ganciclovir, que pode curar a infecção. MÉTODOS: Nós analisamos o resultado da pulsoterapia com esteróides em um paciente com miocardite por CMV, após 7 dias de tratamento etiológico com ganciclovir, vasodilatadores intravenosos e o tratamento convencional para insuficiência cardíaca congestiva. RESULTADOS: A condição clínica do paciente melhorou com a melhor função do ventrículo esquerdo e o ganciclovir foi mantido por 21 dias após alta hospitalar.A função miocárdica retornou ao normal. CONCLUSÃO: Formas curáveis de miocardites como M pneumonia e CMV, por exemplo, podem ter uma agressão grave ao miocárdio por uma ação inflamatória que pode piorar a função cardíaca. Em nossa opinião, o bloqueio deste processo pela pulsoterapia com esteróides pode auxiliar no tratamento destes pacientes. Entendemos que existe um cenário diferente de tratamento com imunossupressores para possível agressão auto-imune das formas mais crônicas de cardiomiopatias dilatadas e isso está em disputa na literatura, talvez mudando o foco dos casos realmente agudos.
Subject(s)
Adult , Humans , Male , Cytomegalovirus Infections/drug therapy , Myocarditis/drug therapy , Shock, Cardiogenic/drug therapy , Anti-Bacterial Agents/therapeutic use , Antihypertensive Agents/therapeutic use , Antiviral Agents/therapeutic use , Ganciclovir/therapeutic use , Glucocorticoids/therapeutic use , Injections, Intravenous , Myocarditis/virology , Prednisone/therapeutic use , Shock, Cardiogenic/etiology , Teicoplanin/therapeutic useABSTRACT
This 63 years old man presented to the emergency room with chest pain of more than 12 hours duration. The initial electrocardiogram showed as ST segment elevation inferior and right ventricular infarction. He developed signs and symptoms consistent with cardiogenic shock, followed by life threatening ventricular fibrillation and cardiac arrest. After repeated cardio-respiratory resuscitations and successful cardiac defibrillation, thrombolytic therapy was administered followed by clinical and hemodynamic improvements. One-week later cardiac catheterization and coronary arteriography were performed. The study showed 93% obstructive lesion in the proximal right coronary artery, an angioplasty was performed and a stent was placed. After appropriate re-adjustment of medical therapy, the patient was discharged and followed in the outpatient clinic. Although the time frame to administer thrombolytic therapy was over the 12 hours window as suggested by the AHA guidelines1, the potential risks benefits in the casepresented justifed the used of fibrinolytic therapy. Considering the multiple complications that the patient presented, fibrinolytic therapy needs to be considered even after 12 hours of symptoms initiation, particularly when facilities for primary percutaneous coronary interventions are not readily available.
Subject(s)
Chest Pain/etiology , Fibrinolytic Agents/administration & dosage , Myocardial Infarction/complications , Shock, Cardiogenic/etiology , Thrombolytic Therapy , Ventricular Fibrillation/etiology , Adrenergic beta-Antagonists/therapeutic use , Angioplasty, Balloon, Coronary , Contraindications , Coronary Stenosis/complications , Coronary Stenosis/therapy , Dopamine/therapeutic use , Drug Therapy, Combination , Electrocardiography , Fibrinolytic Agents/therapeutic use , Fluid Therapy , Heart Block/drug therapy , Heart Block/etiology , Humans , Male , Middle Aged , Myocardial Infarction/drug therapy , Myocardial Infarction/therapy , Myocardial Reperfusion/methods , Nitroglycerin/therapeutic use , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/therapy , Stents , Time Factors , Ventricular Fibrillation/drug therapyABSTRACT
PURPOSE: Study hemodynamic pattern and lipoperoxidation during methylene blue (MB) treatment on taurocholate - enterokinase induced acute pancreatitis (AP). METHODS: Thirty pigs were equally divided in control group; MB group; AP group; MB previous AP group; and MB after 90 min of induced AP group. MB was given iv in a bolus dose (2 mg.kg-1) followed by maintenance dose (2 mg.kg-1.h-1). Hemodynamic parameters were recorded continuously during 180 min by Swan-Ganz catheter. Blood samples were taken every 60 min to determine arterial and venous nitrate, malondialdehyde (MDA) and amylase. Pancreatic tissue was removed for histopathologic study. RESULTS: In AP group MBP and CO decreased over time 33% (p<0.05) and 52% (p<0.05), respectively. In MB previous induced-AP group, there was 70 minutes delay (p<0.05) to decrease MBP and CO. In MB group arterial and venous nitrite decreased (p<0.05) over time. MB infusion increased (p>0.05) serum MDA when associated to AP. After induced AP, MB did not reverse MBP and CO decrease. There was no difference in serum amylase and necro-hemorrhagic findings with MB treatment. CONCLUSIONS: In this taurocholate-induced AP model MB treatment delayed hemodynamic shock and decreases serum nitrate levels but increases serum MDA levels. No volemic replacement was done and it may have been a mitigated factor to a poor tissue perfusion and impairment microcirculation. Further investigations are needed to elucidate MB treatment role during AP treatment.
Subject(s)
Enzyme Inhibitors/therapeutic use , Hemodynamics/drug effects , Lipid Peroxidation/drug effects , Methylene Blue/therapeutic use , Pancreatitis/drug therapy , Shock, Cardiogenic/drug therapy , Acute Disease , Animals , Biomarkers/blood , Cholagogues and Choleretics , Disease Models, Animal , Drug Evaluation, Preclinical , Enteropeptidase , Male , Malondialdehyde/blood , Nitrates/blood , Pancreatitis/chemically induced , Pancreatitis/physiopathology , Shock, Cardiogenic/physiopathology , Swine , Taurocholic Acid , Time FactorsABSTRACT
PURPOSE: Study hemodynamic pattern and lipoperoxidation during methylene blue (MB) treatment on taurocholate - enterokinase induced acute pancreatitis (AP). METHODS: Thirty pigs were equally divided in control group; MB group; AP group; MB previous AP group; and MB after 90 min of induced AP group. MB was given iv in a bolus dose (2mg.kg-1) followed by maintenance dose (2 mg.kg-1.h-1). Hemodynamic parameters were recorded continuously during 180 min by Swan-Ganz catheter. Blood samples were taken every 60 min to determine arterial and venous nitrate, malondialdehyde (MDA) and amylase. Pancreatic tissue was removed for histopathologic study. RESULTS: In AP group MBP and CO decreased over time 33 percent (p<0.05) and 52 percent (p<0.05), respectively. In MB previous induced-AP group, there was 70 minutes delay (p<0.05) to decrease MBP and CO. In MB group arterial and venous nitrite decreased (p<0.05) over time. MB infusion increased (p>0.05) serum MDA when associated to AP. After induced AP, MB did not reverse MBP and CO decrease. There was no difference in serum amylase and necro-hemorrhagic findings with MB treatment. CONCLUSIONS: In this taurocholate-induced AP model MB treatment delayed hemodynamic shock and decreases serum nitrate levels but increases serum MDA levels. No volemic replacement was done and it may have been a mitigated factor to a poor tissue perfusion and impairment microcirculation. Further investigations are needed to elucidate MB treatment role during AP treatment.(AU)
OBJETIVO: estudar o perfil hemodinâmico e a lipoperoxidação durante o tratamento com azul de metileno (AM) de pancreatite aguda (PA) induzida por taurocolato-enteroquinase. MÉTODOS: Trinta porcos foram igualmente divididos em: grupo controle, grupo AM; grupo PA; grupo AM prévio à PA; grupo AM após 90 minutos após a indução da PA. O AM foi administrado sob a forma de bolus EV (2mg.kg-1) seguido por dose de manutenção (2 mg.kg-1.h-1). Os parâmetros hemodinâmicos foram registrados continuamente durante 180 min com auxílio de cateter de Swan-Ganz. Amostras sanguíneas foram colhidas a cada 60 min para a determinação arterial e venosa de nitrato, malondialdeido (MDA) and amilase. Removeu-se tecido pancreático para estudo histopatológico. RESULTADOS: No grupo PA a pressão arterial media (PAM) e o débito cardíaco (DC) diminuíram respectivamente 33 por cento (p<0.05) e 52 por cento (p<0.05) no decorrer do tempo. No grupo AM prévio à indução da PA ocorreu 70 minutes de demora (p<0.05) para as diminuições da PAM e DC. No grupo AM houve diminuição temporal do nitrato arterial e venoso (p<0.05). A infusão de AM aumentou os valores de MDA sérico quando associado a PA (p>0.05). Após a indução da PA a infusão de AM não reverteu as quedas da PA e DC. Não houve diferenças nos níveis de amilase sérica e achados histológicos com o tratamento com o azul de metileno. CONCLUSÕES: No presente modelo de PA induzida por taurocolato o AM retardou o desenvolvimento do choque circulatório, diminuiu os níveis de nitrato mas aumentou os níveis de MDA. Não se realizou nenhum tipo de reposição volêmica que poderia melhorar a perfusão tecidual e melhora da microcirculação. Investigações adicionais são necessárias para elucidar o papel terapêutico do AM no tratamento da PA aguda.(AU)
Subject(s)
Animals , Male , Enzyme Inhibitors/therapeutic use , Hemodynamics , Lipid Peroxidation , Methylene Blue/therapeutic use , Pancreatitis/drug therapy , Shock, Cardiogenic/drug therapy , Acute Disease , Biomarkers/blood , Drug Evaluation, Preclinical , Enteropeptidase , Malondialdehyde/blood , Nitrates/blood , Pancreatitis/physiopathology , Shock, Cardiogenic/physiopathology , Swine , Taurocholic AcidABSTRACT
PURPOSE: Study hemodynamic pattern and lipoperoxidation during methylene blue (MB) treatment on taurocholate - enterokinase induced acute pancreatitis (AP). METHODS: Thirty pigs were equally divided in control group; MB group; AP group; MB previous AP group; and MB after 90 min of induced AP group. MB was given iv in a bolus dose (2mg.kg-1) followed by maintenance dose (2 mg.kg-1.h-1). Hemodynamic parameters were recorded continuously during 180 min by Swan-Ganz catheter. Blood samples were taken every 60 min to determine arterial and venous nitrate, malondialdehyde (MDA) and amylase. Pancreatic tissue was removed for histopathologic study. RESULTS: In AP group MBP and CO decreased over time 33 percent (p<0.05) and 52 percent (p<0.05), respectively. In MB previous induced-AP group, there was 70 minutes delay (p<0.05) to decrease MBP and CO. In MB group arterial and venous nitrite decreased (p<0.05) over time. MB infusion increased (p>0.05) serum MDA when associated to AP. After induced AP, MB did not reverse MBP and CO decrease. There was no difference in serum amylase and necro-hemorrhagic findings with MB treatment. CONCLUSIONS: In this taurocholate-induced AP model MB treatment delayed hemodynamic shock and decreases serum nitrate levels but increases serum MDA levels. No volemic replacement was done and it may have been a mitigated factor to a poor tissue perfusion and impairment microcirculation. Further investigations are needed to elucidate MB treatment role during AP treatment.
OBJETIVO: estudar o perfil hemodinâmico e a lipoperoxidação durante o tratamento com azul de metileno (AM) de pancreatite aguda (PA) induzida por taurocolato-enteroquinase. MÉTODOS: Trinta porcos foram igualmente divididos em: grupo controle, grupo AM; grupo PA; grupo AM prévio à PA; grupo AM após 90 minutos após a indução da PA. O AM foi administrado sob a forma de bolus EV (2mg.kg-1) seguido por dose de manutenção (2 mg.kg-1.h-1). Os parâmetros hemodinâmicos foram registrados continuamente durante 180 min com auxílio de cateter de Swan-Ganz. Amostras sanguíneas foram colhidas a cada 60 min para a determinação arterial e venosa de nitrato, malondialdeido (MDA) and amilase. Removeu-se tecido pancreático para estudo histopatológico. RESULTADOS: No grupo PA a pressão arterial media (PAM) e o débito cardíaco (DC) diminuíram respectivamente 33 por cento (p<0.05) e 52 por cento (p<0.05) no decorrer do tempo. No grupo AM prévio à indução da PA ocorreu 70 minutes de demora (p<0.05) para as diminuições da PAM e DC. No grupo AM houve diminuição temporal do nitrato arterial e venoso (p<0.05). A infusão de AM aumentou os valores de MDA sérico quando associado a PA (p>0.05). Após a indução da PA a infusão de AM não reverteu as quedas da PA e DC. Não houve diferenças nos níveis de amilase sérica e achados histológicos com o tratamento com o azul de metileno. CONCLUSÕES: No presente modelo de PA induzida por taurocolato o AM retardou o desenvolvimento do choque circulatório, diminuiu os níveis de nitrato mas aumentou os níveis de MDA. Não se realizou nenhum tipo de reposição volêmica que poderia melhorar a perfusão tecidual e melhora da microcirculação. Investigações adicionais são necessárias para elucidar o papel terapêutico do AM no tratamento da PA aguda.
Subject(s)
Animals , Male , Enzyme Inhibitors/therapeutic use , Hemodynamics/drug effects , Lipid Peroxidation/drug effects , Methylene Blue/therapeutic use , Pancreatitis/drug therapy , Shock, Cardiogenic/drug therapy , Acute Disease , Biomarkers/blood , Cholagogues and Choleretics , Disease Models, Animal , Drug Evaluation, Preclinical , Enteropeptidase , Malondialdehyde/blood , Nitrates/blood , Pancreatitis/chemically induced , Pancreatitis/physiopathology , Swine , Shock, Cardiogenic/physiopathology , Taurocholic Acid , Time FactorsABSTRACT
OBJECTIVE: To determine the impact of the intra-aortic balloon pump in the mortality due to cardiogenic shock post-acute myocardial infarction. METHODS: In a two-year period, 292 patients with acute myocardial infarction were admitted to the coronary intensive care unit, 40 were included in the study. Afterwards, patients were divided in two groups: early cardiogenic and late cardiogenic shock, and they were assigned randomly and blind to treatment with inotropics and inotropics plus intra-aortic balloon pump. RESULTS: There were significant differences in the measurements of pulmonary wedge pressure (20.4 +/- 1.6 vs 24.4 +/- 1.50, p = 0.0004) and the cardiac index (2.06 +/- 0.7 vs 1.65 +/- 0.18, p = 0.0002) between the two groups. The late cardiogenic shock group showed an increased mortality (25.9% vs 61.5%, p < 0.05). Patients treated with inotropics + balloon, in both early and late shock groups, showed a reduction in mortality of 66% and 69%, respectively. CONCLUSIONS: The use of the intra-aortic balloon pump in the treatment of cardiogenic shock post acute myocardial infarction reduces the mortality when associated with the use of inotropics and reperfusion.
Subject(s)
Intra-Aortic Balloon Pumping , Myocardial Infarction/complications , Shock, Cardiogenic/mortality , Shock, Cardiogenic/therapy , Aged , Cardiotonic Agents/administration & dosage , Cardiotonic Agents/therapeutic use , Coronary Care Units , Data Interpretation, Statistical , Electrocardiography , Female , Humans , Male , Middle Aged , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/etiology , Time FactorsABSTRACT
Propósito del trabajo: Determinar el impacto del balón intra-aórtico de contrapulsación en la mortalidad por choque cardiogénico postinfarto agudo del miocardio. Método: 292 pacientes con infarto agudo del miocardio ingresaron a la unidad de cuidados intensivos coronarios en el período comprendido de febrero de 2001 a febrero del 2003, de los cuales 40 cumplieron los criterios de inclusión y exclusión, posteriormente fueron divididos en 2 grupos: choque cardiogénico temprano y tardío, se les asignó al azar y de forma ciega a recibir tratamiento a base de inotrópicos aislados e inotrópicos más balón intra-aórtico de contrapulsación. Resultados: Se observaron diferencias significativas en ambos grupos en los valores de la presión en cuña de la pulmonar (20.4 ± 1.6 vs 24.4 ± 1.50, p = 0.0004) y el índice cardíaco (2.06 ± 0.7 vs 1.65 ± 0.18, p = 0.0002). El grupo de choque tardío presentó una mayor mortalidad (25.9% vs 61.5%, p < 0.05), los pacientes que recibieron apoyo con balón mostraron una disminución en la mortalidad del 66% y 69% en choque temprano y tardío respectivamente. Conclusiones: El uso del balón intra-aórtico de contrapulsación en los pacientes que desarrollan choque cardiogénico post IAM disminuye la mortalidad, como coadyuvante con el uso de inotrópicos y angioplastía primaria.
Objective: To determine the impact of the intra-aortic balloon pump in the mortality due to cardiogenic shock post-acute myocardial infarction. Methods: In a two-year period, 292 patients with acute myocardial infarction were admitted to the coronary intensive care unit, 40 were included in the study. Afterwards, patients were divided in two groups: early cardiogenic and late cardiogenic shock, and they were assigned randomly and blind to treatment with inotropics and inotropics plus intra-aortic balloon pump. Results: There were significant differences in the measurements of pulmonary wedge pressure (20.4 ± 1.6 vs 24.4 ± 1.50, p = 0.0004) and the cardiac index (2.06 ± 0.7 vs 1.65 ± 0.18, p = 0.0002) between the two groups. The late cardiogenic shock group showed an increased mortality (25.9% vs 61.5%, p < 0.05). Patients treated with inotropics + balloon, in both early and late shock groups, showed a reduction in mortality of 66% and 69%, respectively. Conclusions: The use of the intra-aortic balloon pump in the treatment of cardiogenic shock post acute myocardial infarction reduces the mortality when associated with the use of inotropics and reperfusion. (Arch Cardiol Mex 2005; 75: 260-266).
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Intra-Aortic Balloon Pumping , Myocardial Infarction/complications , Shock, Cardiogenic/mortality , Shock, Cardiogenic/therapy , Coronary Care Units , Cardiotonic Agents/administration & dosage , Cardiotonic Agents/therapeutic use , Data Interpretation, Statistical , Electrocardiography , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/etiology , Time FactorsABSTRACT
Vasopressin is secreted by the neurohypophysis influenced by many variables; among them the most important and known is the osmotic pressure (osmotic regulation) of body fluid. Other factors that modify this hormone's secretion are changes in blood volume and blood pressure, which contribute significantly to hemodynamic recovery. Vasopressin receptors are located in different sites, and their stimulation generate also generates different physiological responses. The receptors are of two types, V1 and V2. The usefulness of exogenous vasopressin has been proven in many clinical situations, refractory cardiac arrest, septic shock, vasodilator shock, postcardiotomy shock, and vasoplegic shock, with promising results. At present, enough scientific support exists for the use of this antidiuretic hormone (vasopressin) in clinical practice.
Subject(s)
Heart Arrest/drug therapy , Shock, Cardiogenic/drug therapy , Shock, Septic/drug therapy , Vasopressins/therapeutic use , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/physiopathology , Hemodynamics/physiology , Humans , Receptors, Vasopressin/physiology , Vasopressins/metabolism , Vasopressins/physiologyABSTRACT
Vasopressin is secreted by the neurohypophysis influenced by many variables; among them the most important and known is the osmotic pressure (osmotic regulation) of body fluid. Other factors that modify this hormone's secretion are changes in blood volume and blood pressure, which contribute significantly to hemodynamic recovery. Vasopressin receptors are located in different sites, and their stimulation generate also generates different physiological responses. The receptors are of two types, V1 and V2. The usefulness of exogenous vasopressin has been proven in many clinical situations, refractory cardiac arrest, septic shock, vasodilator shock, postcardiotomy shock, and vasoplegic shock, with promising results. At present, enough scientific support exists for the use of this antidiuretic hormone (vasopressin) in clinical practice.