El síndrome de norte-sur, una complicación de la asistencia circulatoria con ECMO Venoarterial. Reporte de caso

We present the case of a 34-year-old male patient with a history of Marfan syndrome who was admitted to the emergency room for acute aortic regurgitation secondary to aneurysmal dilation of the ascending thoracic aorta. In the postoperative period, post-cardiotomy cardiogenic shock was documented, so circulatory support was initiated with peripheral Veno-Arterial ECMO, which developed hypoxemia due to bacterial pneumonia and data compatible with North-South syndrome. We present a review, non-conventional cannulation strategies and a diagnostic alternative for this entity.Presentamos el caso de un paciente masculino de 34 años con diagnóstico previo de síndrome de Marfan que ingresó por Insuficiencia aórtica aguda secundario a dilatación aneurismática de la aorta torácica ascendente. En el posoperatorio se documentó choque cardiogénico poscardiotomía por lo que se inició soporte circulatorio con ECMO venoarterial periférico, el cual desarrolló hipoxemia por neumonía bacteriana y datos compatibles con síndrome norte-sur. Presentamos una revisión, estrategias de canulación no convencional y una alternativa diagnóstica para esta entidad

Pacientes con infarto agudo de miocardio sin manifestaciones de COVID-19 pueden tener alta carga de trombo

Objetivo: Identificar las características clínicas y angiográficas de los pacientes con infarto agudo de miocardio con elevación del segmento ST (IAMCEST) sin manifestaciones clínicas de COVID-19 durante la pandemia y compararlos con los pacientes en el año previo. Métodos: Estudio observacional que incluyó 138 pacientes consecutivos que fueron hospitalizados por IAMCEST y que fueron tratados con angioplastía primaria (ACTP) sin manifestaciones clínicas de COVID-19 durante la pandemia de 2020. Se seleccionó a un grupo control de 175 pacientes con IAMCEST tratados con ACTP en el año previo a la pandemia. Resultados: Los pacientes atendidos durante la pandemia no tuvieron diferencias significativas en cuanto a las características clínicas, demográficas, comorbilidades, tiempo de retraso y localización del infarto. Además, no hubo diferencias entre ambos grupos en los niveles de CK-MB, NT-proBNP, marcadores de inflamación ni en la fracción de eyección del ventrículo izquierdo. En los pacientes sin COVID-19 tratados durante la pandemia encontramos mayor carga trombótica intracoronaria (trombo grado 5; 78.3% vs. 62.9%, respectivamente. p = 0.002). De igual manera, el uso de inhibidores de la glucoproteina IIB/IIIa (37.7% vs. 26.3%, p = 0.03) fue mayor. Conclusiones: Este studio demostró un aumento en la carga trombótica en los pacientes con IAMCEST sin manifestaciones clínicas de COVID-19 durante la pandemia al compararlos con los pacientes tratados por la misma patología en el año previo

Chagas Heart Disease: Beyond a Single Complication, from Asymptomatic Disease to Heart Failure

Chagas cardiomyopathy (CC), caused by the protozoan Trypanosoma cruzi, is an important cause of cardiovascular morbidity and mortality in developing countries. It is estimated that 6 to 7 million people worldwide are infected, and it is predicted that it will be responsible for 200,000 deaths by 2025. The World Health Organization (WHO) considers Chagas disease (CD) as a Neglected Tropical Disease (NTD), which must be acknowledged and detected in time, as it remains a clinical and diagnostic challenge in both endemic and non-endemic regions and at different levels of care. The literature on CC was analyzed by searching different databases (Medline, Cochrane Central, EMBASE, PubMed, Google Scholar, EBSCO) from 1968 until October 2022. Multicenter and bioinformatics trials, systematic and bibliographic reviews, international guidelines, and clinical cases were included. The reference lists of the included papers were checked. No linguistic restrictions or study designs were applied. This review is intended to address the current incidence and prevalence of CD and to identify the main pathogenic mechanisms, clinical presentation, and diagnosis of CC

Invasive Phenoprofiling of Acute-Myocardial-Infarction-Related Cardiogenic Shock

Background: Studies had previously identified three cardiogenic shock (CS) phenotypes (cardiac-only, cardiorenal, and cardiometabolic). Therefore, we aimed to understand better the hemodynamic profiles of these phenotypes in acute myocardial infarction-CS (AMI-CS) using pulmonary artery catheter (PAC) data to better understand the AMI-CS heterogeneity. Methods: We analyzed the PAC data of 309 patients with AMI-CS. The patients were classified by SCAI shock stage, congestion profile, and phenotype. In addition, 24 h hemodynamic PAC data were obtained. Results: We identified three AMI-CS phenotypes: cardiac-only (43.7%), cardiorenal (32.0%), and cardiometabolic (24.3%). The cardiometabolic phenotype had the highest mortality rate (70.7%), followed by the cardiorenal (52.5%) and cardiac-only (33.3%) phenotypes, with significant differences (p p = 0.001) and pulmonary capillary wedge pressure (p = 0.01) were higher in the cardiometabolic and cardiorenal phenotypes. Cardiac output, index, power, power index, and cardiac power index normalized by right atrial pressure and left-ventricular stroke work index were lower in the cardiorenal and cardiometabolic than in the cardiac-only phenotypes. We found a hazard ratio (HR) of 2.1 for the cardiorenal and 3.3 for cardiometabolic versus the cardiac-only phenotypes (p p p = 0.011) and ∆congestion (p = 0.028). These scores independently predicted mortality. Conclusions: Accurate patient prognosis and treatment strategies are crucial, and phenotyping in AMI-CS can aid in this effort. PAC profiling can provide valuable prognostic information and help design new trials involving AMI-CS

The prognostic importance of the angiotensin II/angiotensin-(1–7) ratio in patients with SARS-CoV-2 infection

Background: Information about angiotensin II (Ang II), angiotensin-converting enzyme 2 (ACE2), and Ang-(1–7) levels in patients with COVID-19 is scarce. Objective: To characterize the Ang II–ACE2–Ang-(1–7) axis in patients with SARS-CoV-2 infection to understand its role in pathogenesis and prognosis. Methods: Patients greater than 18 years diagnosed with COVID-19, based on clinical findings and positive RT-PCR test, who required hospitalization and treatment were included. We compared Ang II, aldosterone, Ang-(1–7), and Ang-(1–9) concentrations and ACE2 concentration and activity between COVID-19 patients and historic controls. We compared baseline demographics, laboratory results (enzyme, peptide, and inflammatory marker levels), and outcome (patients who survived versus those who died). Results: Serum from 74 patients [age: 58 (48–67.2) years; 68% men] with moderate (20%) or severe (80%) COVID-19 were analyzed. During 13 (10–21) days of hospitalization, 25 patients died from COVID-19 and 49 patients survived. Compared with controls, Ang II concentration was higher and Ang-(1–7) concentration was lower, despite significantly higher ACE2 activity in patients. Ang II concentration was higher and Ang-(1–7) concentration was lower in patients who died. The Ang II/Ang-(1–7) ratio was significantly higher in patients who died. In multivariate analysis, Ang II/Ang-(1–7) ratio greater than 3.45 (OR = 5.87) and lymphocyte count ⩽0.65 × 10 3 /µl (OR = 8.43) were independent predictors of mortality from COVID-19. Conclusion: In patients with severe SARS-CoV-2 infection, imbalance in the Ang II–ACE2–Ang-(1–7) axis may reflect deleterious effects of Ang II and may indicate a worse outcome

Cardiac myosin activation with omecamtiv mecarbil in systolic heart failure

BACKGROUND The selective cardiac myosin activator omecamtiv mecarbil has been shown to improve cardiac function in patients with heart failure with a reduced ejection fraction. Its effect on cardiovascular outcomes is unknown. METHODS We randomly assigned 8256 patients (inpatients and outpatients) with symptomatic chronic heart failure and an ejection fraction of 35% or less to receive omecamtiv mecarbil (using pharmacokinetic-guided doses of 25 mg, 37.5 mg, or 50 mg twice daily) or placebo, in addition to standard heart-failure therapy. The primary outcome was a composite of a first heart-failure event (hospitalization or urgent visit for heart failure) or death from cardiovascular causes. RESULTS During a median of 21.8 months, a primary-outcome event occurred in 1523 of 4120 patients (37.0%) in the omecamtiv mecarbil group and in 1607 of 4112 patients (39.1%) in the placebo group (hazard ratio, 0.92; 95% confidence interval [CI], 0.86 to 0.99; P = 0.03). A total of 808 patients (19.6%) and 798 patients (19.4%), respectively, died from cardiovascular causes (hazard ratio, 1.01; 95% CI, 0.92 to 1.11). There was no significant difference between groups in the change from baseline on the Kansas City Cardiomyopathy Questionnaire total symptom score. At week 24, the change from baseline for the median N-terminal pro-B-type natriuretic peptide level was 10% lower in the omecamtiv mecarbil group than in the placebo group; the median cardiac troponin I level was 4 ng per liter higher. The frequency of cardiac ischemic and ventricular arrhythmia events was similar in the two groups. CONCLUSIONS Among patients with heart failure and a reduced ejection, those who received omecamtiv mecarbil had a lower incidence of a composite of a heart-failure event or death from cardiovascular causes than those who received placebo. (Funded by Amgen and others; GALACTIC-HF ClinicalTrials.gov number, NCT02929329; EudraCT number, 2016 -002299-28.)