RESUMEN
BACKGROUND: There is a gradual progression from paroxysmal to persistent atrial fibrillation (AF) in humans. To elucidate the mechanism involved, the creation of an artificial atrial substrate to persist AF in mice was attempted.MethodsâandâResults:This study used wild type (WT) mice, but it is difficult to induce AF in them. A novel antegrade perfusion method from the left ventricle (LV) to enlarge both atria for artificial atrial modification was proposed in this study. Short duration AF was induced by burst pacing under this method. Optical mapping analysis revealed non-sustained focal type and meandering spiral reentrants after short duration AF. A tiny artificial substrate (~1.2 mm in diameter) was added in by laser irradiation to create a critical atrial arrhythmogenic substrate. Burst pacing was performed in a non-laser group (n=8), a circular-shape laser group (n=8), and a wedge-shaped dent laser group (n=8). We defined AF and atrial tachycardia (AT) as atrial arrhythmia (AA). Long-lasting AA was defined as lasting for ≥30 min. Long-lasting AA was observed in 0/8, 0/8, and 6/8 (75%) mice in each group. Optical mapping analysis revealed that the mechanism was AT with a stationary rotor around the irradiated margin. CONCLUSIONS: Regrettably, this study failed to reproduce persistent AF, but succeeded in creating an arrhythmic substrate that causes sustained AT in WT mice.
Asunto(s)
Fibrilación Atrial , Taquicardia Supraventricular , Animales , Fibrilación Atrial/etiología , Estimulación Cardíaca Artificial/efectos adversos , Modelos Animales de Enfermedad , Atrios Cardíacos , Humanos , RatonesRESUMEN
The indications for immune checkpoint inhibitors (ICIs) are expanding in cancer drug therapy, and while cardiac events associated with ICIs are often fatal, there are few reports regarding cardiac complications associated with long-term ICI therapy. We aimed to study cardiac complications in patients undergoing long-term ICI therapy. From the database of our local cardio-oncology unit, we enrolled patients with cancer undergoing ICI therapy for more than 6 months and for whom cardiologists continuously performed routine follow-ups. We defined the primary endpoint as discontinuation of ICI due to cardiac events. We also analyzed changes in cardiac biomarkers and echocardiographic parameters. We retrospectively analyzed 55 consecutive patients (43 males, mean age: 65 ± 11 years) treated with ICI therapy in our hospital between January 2017 and June 2021. None of the patients discontinued ICI therapy due to cardiac events more than 6 months after treatment was initiated. Among the participants, we observed four patients with elevated serum troponin I levels, seven patients with decreased global longitudinal strain values, and two patients with elevated plasma brain natriuretic peptide levels. No patient required drug intervention for these cardiac events; furthermore, there were no cases of clinically diagnosed myocarditis. In the present study, there were no cardiac events causing ICI discontinuation in patients undergo ICI therapy for more than 6 months.
Asunto(s)
Antineoplásicos Inmunológicos , Miocarditis , Anciano , Antineoplásicos Inmunológicos/efectos adversos , Biomarcadores , Cardiotoxicidad/complicaciones , Cardiotoxicidad/tratamiento farmacológico , Femenino , Humanos , Inhibidores de Puntos de Control Inmunológico/efectos adversos , Masculino , Persona de Mediana Edad , Miocarditis/inducido químicamente , Miocarditis/diagnóstico , Péptido Natriurético Encefálico , Estudios Retrospectivos , Troponina IRESUMEN
Purulent pericarditis is a rare disease in the antibiotic era. The common pathogens of purulent pericarditis are gram-positive species such as Staphylococcus aureus. Streptococcus pneumoniae, Salmonella, Haemophilus, fungal pathogens/tuberculosis can also result in purulent pericarditis. We report an old male case of purulent pericarditis by Escherichia coli. He came to our hospital suffering from leg edema for 3 months. Echocardiography revealed the large amount of pericardial effusion, and he was admitted to test the cause of pericardial effusion without high fever, tachycardia, and shock vital signs. On the third day, he suddenly presented vital shock. We performed emergency cardiopulmonary resuscitation and pericardiocentesis. Appearance of pericardial effusion was hemorrhagic and purulent. The gram stain revealed remarkable E. coli invasion to pericardial space. Antibiotic therapy was immediately started; however, he died on sixth day with septic shock. The cytological examination of pericardial effusion suggested the invasion of malignant lymphoma to pericardium. This case showed subacute or chronic process of pericarditis without severe clinical and laboratory sings before admission. Nevertheless, bacterial purulent pericarditis usually shows acute clinical manifestation; the first process of this case was very silent. Immunosuppression of malignant lymphoma might make E. coli translocation from gastrointestinal tract to pericardial space, and bacterial pericarditis was progressed to purulent pericarditis. In the latter process, this case showed unexpected rush progression to death by sepsis from purulent pericarditis. Immediate pericardiocentesis should be performed for a prompt diagnosis of purulent pericarditis, and it might have improved the outcome of this case.
Asunto(s)
Infecciones por Escherichia coli/complicaciones , Linfoma/complicaciones , Derrame Pericárdico/etiología , Pericarditis/etiología , Anciano de 80 o más Años , Antibacterianos/uso terapéutico , Reanimación Cardiopulmonar/métodos , Progresión de la Enfermedad , Ecocardiografía , Electrocardiografía , Escherichia coli/aislamiento & purificación , Resultado Fatal , Humanos , Masculino , Derrame Pericárdico/microbiología , Derrame Pericárdico/terapia , Pericardiocentesis/métodos , Pericarditis/microbiología , Pericarditis/terapia , Pericardio/patología , Choque Séptico/etiología , Tomografía Computarizada por Rayos XRESUMEN
Left ventricular (LV) diastolic dysfunction is considered the main cause of heart failure with preserved ejection fraction (HFpEF). There have been few reports on the correlation between LV diastolic dysfunction and arterial stiffness in patients with clinical cardiovascular disease.This cross-sectional study enrolled 100 patients (67 men, 33 women; mean age, 70 years). All participants were diagnosed with cardiovascular disease. A total of 89 (89%) patients had coronary artery disease or HF. Patients with reduced EF and valvular disease were excluded. Arterial stiffness was assessed by the cardio-ankle vascular index (CAVI), and LV diastolic dysfunction was estimated using echocardiography. The patients were divided into two groups based on the median value of CAVI. In all patients the ratio of early diastolic transmitral flow velocity to early diastolic mitral annular velocity (E/e') was significantly higher in the high CAVI group than in the low CAVI group (15.5 ± 6.4 versus 12.5 ± 2.9, P = 0.003). In the HF subgroup, E/e' was also significantly higher in the high CAVI group than in the low CAVI group (17.2 ± 5.9 versus 13.0 ± 3.1, P = 0.026). In univariate regression analysis, CAVI was significantly associated with E/e' in all patients (ß = 0.28, P = 0.004) and in HF patients (ß = 0.4, P = 0.028). Also in multivariate analysis, CAVI remained as an independent predictive factor of E/e' (ß = 0.252, P = 0.037).A high CAVI was independently associated with LV diastolic dysfunction in patients with clinical cardiovascular disease. These results suggested that arterial stiffness contributed to the development of LV diastolic dysfunction.
Asunto(s)
Insuficiencia Cardíaca/fisiopatología , Rigidez Vascular/fisiología , Disfunción Ventricular Izquierda/fisiopatología , Anciano , Anciano de 80 o más Años , Índice Tobillo Braquial , Arterias , Velocidad del Flujo Sanguíneo/fisiología , Estudios Transversales , Diástole , Femenino , Insuficiencia Cardíaca/complicaciones , Humanos , Masculino , Persona de Mediana Edad , Análisis de Regresión , Volumen Sistólico/fisiología , Disfunción Ventricular Izquierda/complicaciones , Disfunción Ventricular Izquierda/diagnósticoRESUMEN
Ras-related small G-protein Rad plays a critical role in generating arrhythmias via regulation of the L-type Ca(2+) channel (LTCC). The aim was to demonstrate the role of Rad in intracellular calcium homeostasis by cardiac-Specific dominant-negative suppression of Rad. Transgenic (TG) mice overexpressing dominant-negative mutant Rad (S105N Rad TG) were generated. To measure intracellular Ca(2+) concentration ([Ca(2+)]i), we recorded [Ca(2+)]i transients and Ca(2+) sparks from isolated cardiomyocytes using confocal microscopy. The mean [Ca(2+)]i transient amplitude was significantly increased in S105N Rad TG cardiomyocytes, compared with control littermate mouse cells. The frequency of Ca(2+) sparks was also significantly higher in TG cells than in control cells, although there were no significant differences in amplitude. The sarcoplasmic reticulum Ca(2+) content was not altered in the S105N Rad TG cells, as assessed by measuring caffeine-induced [Ca(2+)]i transient. In contrast, phosphorylation of Ser(2809) on the cardiac ryanodine receptor (RyR2) was significantly enhanced in TG mouse hearts compared with controls. Additionally, the Rad-mediated RyR2 phosphorylation was regulated via a direct interaction of Rad with protein kinase A (PKA).
Asunto(s)
Arritmias Cardíacas/genética , Calcio/metabolismo , Proteínas Quinasas Dependientes de AMP Cíclico/metabolismo , Canal Liberador de Calcio Receptor de Rianodina/metabolismo , Proteínas ras/genética , Potenciales de Acción/efectos de los fármacos , Animales , Arritmias Cardíacas/metabolismo , Arritmias Cardíacas/fisiopatología , Cafeína/farmacología , Señalización del Calcio , Proteínas Quinasas Dependientes de AMP Cíclico/genética , Regulación de la Expresión Génica , Ratones , Ratones Transgénicos , Mutación , Miocardio/metabolismo , Miocardio/patología , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , Fosforilación , Cultivo Primario de Células , Canal Liberador de Calcio Receptor de Rianodina/genética , Retículo Sarcoplasmático/efectos de los fármacos , Retículo Sarcoplasmático/metabolismo , Proteínas ras/deficienciaRESUMEN
Background: Trastuzumab, an anti-human epidermal growth factor receptor 2 (HER2) monoclonal antibody, is a specific first-line treatment for patients with HER2-positive cancers. Cardiac dysfunction is among the most problematic adverse events associated with trastuzumab. Although regular echocardiographic screening is recommended for early detection of cardiac damage, few reports have investigated the validity of echocardiographic screening in chemotherapy. Therefore, the aim of this study was to determine whether a GLS-guided management approach could reduce cardiotoxicity and discontinuation of trastuzumab chemotherapy. MethodsâandâResults: To evaluate the usefulness of global longitudinal strain (GLS)-guided cardioprotective interventions, we retrospectively analyzed 67 patients treated with trastuzumab who underwent structured echocardiographic assessments before and after 1, 3, and 6 courses of trastuzumab administration. If a >15% relative decrease in GLS was identified, cardioprotective agents were administered. Thirty (44.8%) patients had breast cancer; the remaining patients had salivary gland cancer. The median observation period for the intervention group was 304 days from the initial evaluation. Nineteen (28.4%) patients exhibited a >15% relative decrease in GLS, and consequently received cardioprotective agents. The incidence of trastuzumab discontinuation for cardiogenic reasons was significantly lower among patients receiving GLS-guided interventions than among those not receiving the intervention (2.4% vs. 24.0%; P=0.009). The incidence of a subsequent decline in left ventricular ejection fraction was lower among patients receiving the intervention than among those not receiving the intervention (4.8% vs. 24.0%; P=0.04). Conclusions: GLS-guided cardioprotective intervention significantly decreased the incidence of trastuzumab discontinuation.
RESUMEN
Background: Immune checkpoint inhibitors (ICIs) are a central part of cancer therapy; however, cardiac complications, such as myocarditis, have the potential for significant morbidity and mortality. Within this population, the clinical significance of longitudinal strain (LS) remains unknown. Objectives: This study sought to define the changes in LS in ICI-treated patients, and their associations with high-sensitivity troponin I (hsTnI) and myocarditis. Methods: We conducted a retrospective cohort study of patients who received ICIs at our hospital from April 2017 to September 2021. All patients underwent echocardiography and blood sampling at standardized time intervals. We measured the changes in global and regional LS before and after ICI administration. Age- and sex-adjusted Cox regression analysis was used to evaluate the association between LS and elevations in hsTnI and myocarditis. Results: In a cohort of 129 patients with a median follow-up period of 170 (IQR: 62-365) days; 6 and 18 patients had myocarditis and hsTnI elevation, respectively. In an age- and sex-adjusted Cox proportional hazards model, an early relative worsening of ≥10% in the basal and mid LS and ≥15% in global LS was associated with hsTnI elevation. Relative reductions in LS were not significantly associated with myocarditis; however, 4 of the 6 patients with myocarditis had relative reduction of ≥10% in the basal LS. Conclusions: An early worsening in the global and regional LS was associated with increased hsTnI in patients receiving ICIs. Assessment of LS early after ICI administration should be further studied as a strategy for risk stratification of ICI-treated patients.
RESUMEN
Failure of the right ventricle plays a critical role in any type of heart failure. However, the mechanism remains unclear, and there is no specific therapy. Here, we show that the right ventricle predominantly expresses alternative complement pathway-related genes, including Cfd and C3aR1. Complement 3 (C3)-knockout attenuates right ventricular dysfunction and fibrosis in a mouse model of right ventricular failure. C3a is produced from C3 by the C3 convertase complex, which includes the essential component complement factor D (Cfd). Cfd-knockout mice also show attenuation of right ventricular failure. Moreover, the plasma concentration of CFD correlates with the severity of right ventricular failure in patients with chronic right ventricular failure. A C3a receptor (C3aR) antagonist dramatically improves right ventricular dysfunction in mice. In summary, we demonstrate the crucial role of the C3-Cfd-C3aR axis in right ventricular failure and highlight potential therapeutic targets for right ventricular failure.
Asunto(s)
Insuficiencia Cardíaca , Disfunción Ventricular Derecha , Animales , Complemento C3/genética , Convertasas de Complemento C3-C5 , Factor D del Complemento , Insuficiencia Cardíaca/genética , Ratones , Ratones Noqueados , Remodelación VentricularRESUMEN
BACKGROUND: Conventional diuretic therapy such as loop diuretics is a cornerstone of the treatment for heart failure (HF). Diuretic response is an important factor in determining resistance to HF therapy and has been shown to be associated with subsequent clinical outcome. Tolvaptan (TVP), a vasopressin V2 receptor antagonist, has a favorable profile in terms of rapid fluid removal and less aggravation of renal function. We hypothesized that the response to TVP might be associated with the subsequent clinical outcome. METHOD: In this single-center retrospective study, 148 consecutive HF patients who were administered TVP from 2014 through 2018 [age 79 (69-86) years, male 89 (60%)] were included. Ninety-six patients were divided into TVP responder [N = 39 (41%)] and non-responder groups based on the cut-off value of gained urine output (+ 93 ml/mg TVP /day) on the day after TVP was introduced. RESULTS: Early TVP introduction (p = 0.012) and lower dose of loop diuretics (p = 0.043) were predictors of TVP responder. For 2 years after discharge, TVP responders showed more favorable outcomes regarding the primary endpoint defined as the composite of all-cause death and HF readmission (p = 0.034, log-rank test) and HF readmission (p = 0.005). A multivariable Cox model analysis revealed that TVP responder was an independent predictor of the primary endpoint (hazard ratio 0.48, p = 0.041). TVP responders had a lower number of HF readmissions over a 1-year period (p = 0.002). TVP response was independently associated with the number of HF readmissions (p = 0.015). The proportion of patients with an extended period between discharge and HF readmission after TVP administration was higher in responders than non-responders (67% vs. 23%, p = 0.006). These associations of TVP response and post-discharge outcomes were more evident in patients who continued TVP after discharge. CONCLUSION: TVP response can be indicative of subsequent clinical outcomes and may be informative when considering advanced care planning.
Asunto(s)
Cuidados Posteriores , Insuficiencia Cardíaca , Anciano , Antagonistas de los Receptores de Hormonas Antidiuréticas , Benzazepinas , Insuficiencia Cardíaca/tratamiento farmacológico , Humanos , Masculino , Alta del Paciente , Estudios Retrospectivos , TolvaptánRESUMEN
BACKGROUND: Oxidative posttranslational modifications (OPTM) impair the function of Sarcoplasmic/endoplasmic reticulum (SR) calcium (Ca2+) ATPase (SERCA) 2 and trigger cytosolic Ca2+ dysregulation. We investigated the extent of OPTM of SERCA2 in patients with non-ischemic cardiomyopathy (NICM). METHODS AND RESULTS: Endomyocardial biopsy (EMB) was obtained in 40 consecutive patients with NICM. Total expression and OPTM of SERCA2, including sulfonylation at cysteine-674 (S-SERCA2) and nitration at tyrosine-294/295 (N-SERCA2), were examined by immunohistochemical analysis. S-SERCA2 increased in the presence of late gadolinium enhancement on cardiac magnetic resonance imaging. S-SERCA2/SERCA2 and N-SERCA2/SERCA2 correlated with cardiac fibrosis evaluated by Masson's trichrome staining of EMB. SERCA2 expression modestly increased in parallel with an upward trend in OPTM of SERCA2 with aging. This tendency became prominent only in patients aged >65â¯years. OPTM of SERCA2 positively correlated with brain natriuretic peptide (BNP) values only in patients aged ≤65â¯years. Composite major adverse cardiac events (MACE) increased more in the high OPTM group of younger patients; however, MACE-free survival was similar irrespective of the extent of OPTM in older patients. CONCLUSIONS: OPTM of SERCA2 correlate with myocardial fibrosis in NICM. In younger patients, OPTM of SERCA2 correlate with elevated BNP and increased composite MACE.
RESUMEN
In patients with newly diagnosed AV block and/or ventricular tachycardia, cardiac sarcoidosis should always be considered in the differential diagnosis. In addition to the pacemaker implant, cardiac resynchronization therapy (CRT) should be selected for severe heart failure patients who have class III or IV heart failure, LVEF Asunto(s)
Arritmias Cardíacas/diagnóstico
, Arritmias Cardíacas/terapia
, Cardiomiopatías/diagnóstico
, Cardiomiopatías/terapia
, Sarcoidosis/diagnóstico
, Sarcoidosis/terapia
, Arritmias Cardíacas/complicaciones
, Cardiomiopatías/complicaciones
, Humanos
, Sarcoidosis/complicaciones
RESUMEN
Disorders of L-type Ca2+ channels can cause severe cardiac arrhythmias. A subclass of small GTP-binding proteins, the RGK family, regulates L-type Ca2+ current (I(Ca,L)) in heterologous expression systems. Among these proteins, Rad (Ras associated with diabetes) is highly expressed in the heart, although its role in the heart remains unknown. Here we show that overexpression of dominant negative mutant Rad (S105N) led to an increase in I(Ca,L) and action potential prolongation via upregulation of L-type Ca2+ channel expression in the plasma membrane of guinea pig ventricular cardiomyocytes. To verify the in vivo physiological role of Rad in the heart, a mouse model of cardiac-specific Rad suppression was created by overexpressing S105N Rad, using the alpha-myosin heavy chain promoter. Microelectrode studies revealed that action potential duration was significantly prolonged with visible identification of a small plateau phase in S105N Rad transgenic mice, when compared with wild-type littermate mice. Telemetric electrocardiograms on unrestrained mice revealed that S105N Rad transgenic mice had significant QT prolongation and diverse arrhythmias such as sinus node dysfunction, atrioventricular block, and ventricular extrasystoles, whereas no arrhythmias were observed in wild-type mice. Furthermore, administration of epinephrine induced frequent ventricular extrasystoles and ventricular tachycardia in S105N Rad transgenic mice. This study provides novel evidence that the suppression of Rad activity in the heart can induce ventricular tachycardia, suggesting that the Rad-associated signaling pathway may play a role in arrhythmogenesis in diverse cardiac diseases.
Asunto(s)
Canales de Calcio Tipo L/fisiología , Corazón/fisiología , Síndrome de QT Prolongado/metabolismo , Síndrome de QT Prolongado/fisiopatología , Taquicardia Ventricular/metabolismo , Taquicardia Ventricular/fisiopatología , Proteínas ras/antagonistas & inhibidores , Proteínas ras/fisiología , Potenciales de Acción/genética , Sustitución de Aminoácidos/genética , Animales , Línea Celular , Cobayas , Humanos , Síndrome de QT Prolongado/genética , Ratones , Ratones Transgénicos , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/fisiología , Taquicardia Ventricular/genética , Proteínas ras/genéticaRESUMEN
Sarcoidosis is a multisystem granulomatous disorder of unknown etiology. The annual incidence of systemic sarcoidosis is estimated at 10-20 per 100,000 individuals. Owing to the recent advances in imaging modalities, cardiac sarcoidosis (CS) is diagnosed more frequently. The triad of CS includes conduction abnormality, ventricular tachycardia, and heart failure. Atrial and ventricular arrhythmias are caused by either inflammation or scar formation. Inflammation should be treated with immunosuppression and antiarrhythmic agents and scar formation should be treated with antiarrhythmics and/or ablation, in addition to implantable cardioverter defibrillator (ICD) implantation, if necessary. Ablation can provide a good outcome, but it might require bipolar ablation if the critical portion is located mid-myocardium. Late recurrence might be caused by reactivation of sarcoidosis, which would need to be evaluated by positron emission tomography-computed tomography imaging. Risk of sudden cardiac death (SCD) in patients with advanced atrioventricular block is not low, and ICD implantation could be considered instead of a pacemaker. For risk stratification for SCD, late gadolinium enhancement by cardiac magnetic resonance imaging or program stimulation is often used.
RESUMEN
BACKGROUND: Periodic echo-based screening to detect early stages of a rare complication of dasatinib, pulmonary arterial hypertension (PAH), is inefficient and weakens the potential benefit of dasatinib as a potent drug for chronic myelogenous leukemia (CML). This study aimed to identify the predisposing factors of DASA-PAH to stratify high-risk patients for dasatinib-induced PAH (DASA-PAH). METHODS: Sixty consecutive adult patients who received dasatinib were enrolled in this case-control study. We defined DASA-PAH when at least one of the following four criteria was met: (1) recent electrocardiographic changes indicating right ventricular pressure overload, (2) estimated systolic pulmonary arterial pressure > 40 mmHg measured by Doppler echocardiography; (3) computed tomography (CT)-measured pulmonary artery to aorta diameter (PaD/AoD) ratio > 1; and (4) mean pulmonary arterial pressure > 25 mmHg and pulmonary artery wedge pressure < 15 mmHg measured by right heart catheterization. RESULTS: We identified 13 patients with DASA-PAH among 59 patients analyzed. Baseline PaD/AoD ratios of patients who developed DASA-PAH (PH group) were significantly larger than those who did not (NPH group). A dramatic rise in PaD/AoD ratio after dasatinib treatment was observed. Interestingly, the EUTOS score and spleen size were significantly smaller in the PH than in the NPH group. CONCLUSION: High baseline PaD/AoD ratio and low EUTOS score were associated with DASA-PAH development. The spleen might play a protective role against DASA-PAH.
Asunto(s)
Antineoplásicos/efectos adversos , Aorta/diagnóstico por imagen , Presión Arterial , Angiografía por Tomografía Computarizada , Dasatinib/efectos adversos , Hipertensión Pulmonar/diagnóstico por imagen , Inhibidores de Proteínas Quinasas/efectos adversos , Arteria Pulmonar/diagnóstico por imagen , Anciano , Aorta/fisiopatología , Presión Arterial/efectos de los fármacos , Estudios de Casos y Controles , Cateterismo de Swan-Ganz , Ecocardiografía Doppler , Femenino , Humanos , Hipertensión Pulmonar/inducido químicamente , Hipertensión Pulmonar/fisiopatología , Masculino , Persona de Mediana Edad , Valor Predictivo de las Pruebas , Pronóstico , Arteria Pulmonar/efectos de los fármacos , Arteria Pulmonar/fisiopatología , Presión Esfenoidal Pulmonar , Medición de Riesgo , Factores de Riesgo , Bazo/diagnóstico por imagen , Factores de TiempoRESUMEN
The management of chronic disseminated intravascular coagulation (DIC) caused by aortic dissection has not yet been established. Even in cases where surgical correction is performed, therapeutic control of systemic hemorrhaging is still required. We herein report the successful treatment of a case of aortic dissection with a patent false lumen using tranexamic acid for acute exacerbation of chronic DIC. Oral administration of 1,500 mg tranexamic acid per day stabilized the coagulative and fibrinolytic parameters and relieved bleeding tendencies with no side effects. Heparin was administered periodically for the management of hemodialysis. This favorable result continued for up to 3 years.
Asunto(s)
Antifibrinolíticos/uso terapéutico , Aneurisma de la Aorta/complicaciones , Disección Aórtica/complicaciones , Coagulación Intravascular Diseminada/tratamiento farmacológico , Ácido Tranexámico/uso terapéutico , Anciano , Enfermedad Crónica , Femenino , Humanos , Resultado del TratamientoRESUMEN
BACKGROUND: d-ROMs test developed to determine the degree of individual oxidative stress may predict cardiovascular events. METHODS AND RESULTS: 265 patients (204 men, 61 women; age, 65±13years) who had been treated for cardiovascular disease were divided evenly by quartile of baseline d-ROMs levels, and were followed up. During the observation periods of 2.66±1.47years, there were 14 (5%) deaths, 8 (3%) cardiovascular deaths, 13 (5%) major adverse cardiovascular events (MACEs), and 51 (19%) all cardiovascular events including heart failure, cardiovascular surgery, and revascularization. Log-rank tests demonstrated that the patients in the 4th quartile (d-ROMsâ§395.00U.CARR) had a higher incidence rate of cardiovascular death than those in the 2nd quartile (d-ROMs 286.00-335.00, p=0.022). In multivariate Cox regression analysis, even after adjustment for age, sex, coronary risk factors, C-reactive protein, and renal function, high d-ROMs was a risk factor for all-cause death [adjusted HR of 4th vs. 1st quartile, 10.791 (95% confidence interval 1.032-112.805), p=0.047], and all cardiovascular events [HR of 4th vs. 1st quartile, 2.651 (95% confidence interval 1.138-6.177), p=0.024]. CONCLUSIONS: Our results suggest that d-ROMs is a useful oxidative stress marker to assess prognosis and risk of further cardiovascular events.