Manejo de la disfagia en pacientes con antecedente de infección severa por COVID-19 / Manejo de la disfagia en pacientes con antecedente de infección severa por COVID-19

de la deglución, los cuales representan todas las alteraciones del proceso fisiológico encargado de llevar el alimento desde la boca al esófago y después al estómago, salvaguardando siempre la protección de las vías respiratorias. OBJETIVO. Definir el manejo óptimo, de la disfagia en pacientes con antecedente de infección severa por COVID-19. METODOLOGÍA. Se realizó una revisión de la literatura científica en las bases de datos PubMed y Elsevier que relacionan el manejo de la disfagia y pacientes con antecedente de infección severa por SARS-CoV-2. Se obtuvo un universo de 134 artículos que cumplieron los criterios de búsqueda. Se seleccionaron 24 documentos, para ser considerados en este estudio. RESULTADOS. La incidencia de disfagia posterior a infección severa por SARS-CoV-2 fue del 23,14%, siendo la disfagia leve la más frecuente 48,0%. Los tratamientos clínicos más empleados en el manejo de la disfagia fueron rehabilitación oral y cambio de textura en la dieta en el 77,23% de los casos, mientras que el único tratamiento quirúrgico empleado fue la traqueotomía 37,31%. Un 12,68% de pacientes recuperó su función deglutoria sin un tratamiento específico. La eficacia de los tratamientos clínicos y quirúrgicos en los pacientes sobrevivientes de la infección severa por SARS-CoV-2 fue del 80,68%, con una media en el tiempo de resolución de 58 días. CONCLUSIÓN. La anamnesis es clave para el diagnóstico de disfagia post COVID-19. El tratamiento puede variar, desde un manejo conservador como cambios en la textura de la dieta hasta tratamientos más invasivos como traqueotomía para mejorar la función deglutoria.

INTRODUCTION. The difficulty to swallow or dysphagia is included within the problems of swallowing, which represent all the alterations of the physiological process in charge of carrying the food from the mouth to the esophagus, and then to the stomach, always taking into account the protection of the airways. OBJECTIVE. To define the optimal management, both clinical and surgical, for the adequate treatment of dysphagia produced as a consequence of severe SARS-CoV-2 infection. METHODOLOGY. A review of the scientific literature was carried out using both PubMed and Elsevier databases, which relate the management of dysphagia and patients with a history of severe SARS-CoV-2 infection. RESULTS. The incidence of dysphagia following severe SARS-CoV-2 infection was of 23,14%, with mild dysphagia being the most frequent 48,00%. The most frequently used clinical treatments for dysphagia management were oral rehabilitation and change in dietary texture in 77,23% of cases, while tracheotomy was the only surgical treatment used 37,31%. A total of 12,68% of patients recovered their swallowing function without specific treatment. The efficacy of clinical and surgical treatments in survivors of severe SARS-CoV-2 infection was 80,68%, with a mean resolution time of 58 days. CONCLUSION. An adequate medical history is key to the diagnosis of post-COVID-19 dysphagia. Treatment can range from conservative management such as changes in diet texture to more invasive treatments such as tracheotomy to improve swallowing function.

Smoking induces long-lasting effects through a monoamine-oxidase epigenetic regulation.

BACKGROUND: Postulating that serotonin (5-HT), released from smoking-activated platelets could be involved in smoking-induced vascular modifications, we studied its catabolism in a series of 115 men distributed as current smokers (S), never smokers (NS) and former smokers (FS) who had stopped smoking for a mean of 13 years. METHODOLOGY/PRINCIPAL FINDINGS: 5-HT, monoamine oxidase (MAO-B) activities and amounts were measured in platelets, and 5-hydroxyindolacetic acid (5-HIAA)--the 5-HT/MAO catabolite--in plasma samples. Both platelet 5-HT and plasma 5-HIAA levels were correlated with the 10-year cardiovascular Framingham relative risk (P<0.01), but these correlations became non-significant after adjustment for smoking status, underlining that the determining risk factor among those taken into account in the Framingham risk calculation was smoking. Surprisingly, the platelet 5-HT content was similar in S and NS but lower in FS with a parallel higher plasma level of 5-HIAA in FS. This was unforeseen since MAO-B activity was inhibited during smoking (P<0.00001). It was, however, consistent with a higher enzyme protein concentration found in S and FS than in NS (P<0.001). It thus appears that MAO inhibition during smoking was compensated by a higher synthesis. To investigate the persistent increase in MAO-B protein concentration, a study of the methylation of its gene promoter was undertaken in a small supplementary cohort of similar subjects. We found that the methylation frequency of the MAOB gene promoter was markedly lower (P<0.0001) for S and FS vs. NS due to cigarette smoke-induced increase of nucleic acid demethylase activity. CONCLUSIONS/SIGNIFICANCE: This is one of the first reports that smoking induces an epigenetic modification. A better understanding of the epigenome may help to further elucidate the physiopathology and the development of new therapeutic approaches to tobacco addiction. The results could have a larger impact than cardiovascular damage, considering that MAO-dependent 5-HT catabolism is also involved in addiction, predisposition to cancer, behaviour and mental health.

Relationship of circulating biomarkers of inflammation and hemostasis with preclinical atherosclerotic burden in nonsmoking hypercholesterolemic men.

BACKGROUND: Relations of mediators of inflammation and hemostasis with preclinical atherosclerosis have been poorly analyzed. The aim of this study was to test potential associations of these blood markers with indicators of cardiovascular risk and atherosclerotic burden in asymptomatic, nonsmoking, hypercholesterolemic men. METHODS: A total of 87 men underwent cardiovascular risk assessment by means of 10-year Framingham risk calculation (median 9%) and atherosclerotic burden evaluation by means of ultrasonographic measurement of common carotid intima-media thickness and assessment of atherosclerotic plaques at three arterial sites (three-site plaques). RESULTS: Of the markers C-reactive protein, tumor necrosis factor-alpha, interleukin-10, factor VIIc, fibrinogen, plasminogen activator inhibitor-activator, soluble intercellular adhesion molecule-1, soluble P-selectin (sP-selectin), and von Willebrand factor, only sP-selectin was positively and independently associated with high Framingham risk score (>9%) (71.7 +/- 3.6 ng/mL, n = 33 v 59.6 +/- 2.8, n = 54; mean +/- SEM; P < .05) and with three-site plaques (75.4 +/- 5.7 ng/mL, n = 14 v 62.0 +/- 2.5, n = 73; P < .05). After adjustment for all of the above markers and for cardiovascular risk factors, odd ratios of having high Framingham risk and three-site plaques were 3.38 (1.43 to 10.21) and 5.23 (1.74 to 23.52) respectively, per 1-standard deviation increase in sP-selectin. CONCLUSIONS: These results confirm that among several hemostasis and inflammation mediators, only sP-selectin blood level was associated with preclinical atherosclerosis. It might confer to sP-selectin measurement a clinical usefulness for detecting and managing high cardiovascular risk in primary prevention.

Circulating leukocyte-derived microparticles predict subclinical atherosclerosis burden in asymptomatic subjects.

OBJECTIVE: To clarify circulating microparticles (MP) relationships with preclinical atherosclerosis. METHODS AND RESULTS: In 216 subjects without cardiovascular disease, we assessed: (1) annexin V-positive, platelet-derived, endothelium-derived and leukocyte-derived circulating MP by capture on annexin V, anti-GPIb, anti-CD105, and anti-CD11a antibody-coated wells, respectively; (2) Framingham risk, metabolic syndrome, and low-grade inflammation by risk factors measurement including hsCRP; and (3) subclinical atherosclerosis by ultrasound examination of carotid, abdominal aorta, and femoral arteries. Number of sites with plaque ranged from 0 to 3 and plaque burden was classified into 0 to 1 or 2 to 3 sites disease. Leukocyte-derived MP level was higher in the presence than in the absence of moderate to high Framingham risk (P<0.05), metabolic syndrome (P<0.01), high C-reactive protein (CRP) (P<0.05), or 2- to 3-sites disease (P<0.01), and correlated positively with number of metabolic syndrome components (P<0.001), tertiles of fibrinogen (P<0.001), and number of diseased sites (P<0.01). In multivariate analysis, 2- to 3-sites disease was independently associated with leukocyte-derived MP level (P<0.05), Framingham risk (P<0.001), and metabolic syndrome (P<0.01). None of the other MP types correlated with risk markers or atherosclerosis. CONCLUSIONS: Leukocyte-derived MP, identified by affinity for CD11a, are increased in subjects with ultrasound evidence of subclinical atherosclerosis, unveiling new directions for atherosclerosis research.

Differential associations of statin and fibrate treatment with carotid arterial remodeling.

BACKGROUND: The effects of statins on intima-media thickness (IMT) are well documented, whereas those of fibrates are unknown. Therefore we compared IMT under treatment with each class of drugs. METHODS: We studied a cohort of consecutive dyslipidemic subjects treated with statin (n = 291) or fibrate (n = 82) drugs. Fibrate-treated subjects were matched with the same number of statin-treated subjects to obtain two subgroups of similar demographic and risk factors including LDL cholesterol. Common carotid far wall IMT and lumen diameter were measured by ultrasonography. RESULTS: In the entire study population, IMT was greater in the fibrate group than in the statin group (P < .001), even after adjustment for LDL cholesterol and other covariates (P < .05). In the matched groups, IMT was greater in fibrate group than in the statin group (P < .01), even after adjustment for LDL cholesterol and other covariates including treatment duration (P < .01). The IMT correlated positively with treatment duration in the fibrate group (P < 0.05) but not in the statin group. In addition, IMT correlated positively with carotid lumen diameter in both the fibrate and statin groups (P < .05, P < .01) but with a lower slope in the former (P < .05). CONCLUSIONS: In this study fibrate treatment was associated with greater IMT, steeper IMT-time relationship, and lower compensatory carotid enlargement than was statin treatment. These differences were not explained by differences in LDL cholesterol.

Differences between markers of atherogenic lipoproteins in predicting high cardiovascular risk and subclinical atherosclerosis in asymptomatic men.

OBJECTIVE: As main markers of atherogenic lipoproteins, apolipoprotein B (apoB), non-HDL cholesterol (non-HDLC), and LDL cholesterol (LDLC) do not seem equipotent to predict cardiovascular complications, we have compared simultaneously their capacity to predict high cardiovascular risk and subclinical atherosclerosis in a primary prevention population. METHODS: In 723 asymptomatic men, we measured apoB, non-HDLC, and LDLC, and we determined concomitantly coronary heart disease (CHD) risk equivalent defined by National Cholesterol Education Program guidelines, ultrasound-assessed extra-coronary plaques at multiple sites, and electron beam computed tomography-assessed high coronary calcium. RESULTS: Odds ratios (95% confidence interval) per standard deviation of apoB, non-HDLC, and LDLC of having: (i) CHD risk equivalent were 1.90 (1.53-2.37), 1.78 (1.43-2.21), 1.47 (1.19-1.81); (ii) extra-coronary plaques were 1.37 (1.16-1.61), 1.31 (1.11-1.56), 1.19 (1.01-1.39); (iii) high coronary calcium were 1.35 (1.09-1.68), 1.33 (1.07-1.64), 1.26 (1.01-1.39), respectively. Risk factors and treatment did not confound the above associations, except triglycerides for which adjustment weakened the risk predictions of lipids and annihilated lipids differences in predicting CHD risk equivalent and atherosclerosis markers. CONCLUSIONS: ApoB was the best predictor, non-HDLC the second best predictor, and LDLC the poorest predictor of high cardiovascular risk and subclinical extra-coronary and coronary atherosclerosis, and triglycerides participated to these differences.

Comparison of new ultrasound index with laser reference and viscosity indexes for erythrocyte aggregation quantification.

We have previously established new ultrasonic indexes for erythrocyte aggregation using a Couette device, and validated them toward the Rayleigh's theory and reproducibility. Two hydrodynamic protocols were applied on various suspensions and their aggregation degrees were characterized by: 1. for the decreasing shear rates protocol: the power P(US) at the nominal frequency of the transducer used; 2. for the kinetic protocol: aggregation times (latency and half-rise times), variation between initial disaggregated state (Vo) and final aggregated state (V(inf)) and AI(US), which is the integral of the kinetic curve over time. The objective of the present study was to demonstrate the ability of these indexes to characterize the aggregation dynamics of suspensions with various levels of aggregation induced by concentrations of dextran 70 kD (Dx) of 10, 20 and 40 g/L added to washed red cells resuspended in saline solution. The results showed a maximum of backscattered power (P(US)) for Dx = 40 g/L with the decreasing shear rates protocol. We measured a final aggregation level (V(inf)), a minimal aggregation time (T(m)) and a maximal value of AI(US) for Dx = 40 g/L with the aggregation kinetics protocol. On the other hand, viscosity is increased with dextran concentration. These evolutions of the ultrasound (US) indexes and viscosity with dextran concentrations are consistent with literature reports. In addition, a particularly interesting phenomenon of US backscattering enhancement was observed for kinetics with no null final shear rate, which has never before been reported in such a precise manner. By another way, each of the dextran suspensions was tested on the laser erythroaggregometer that is presently considered as the "gold standard" method for erythrocyte characterization. The laser indexes (aggregation time T(a), aggregation indexes AI(10s) and AI(60s)), deduced from a kinetic protocol, have similar significance to the US ones. Statistical comparisons have been done between laser and ultrasonic indexes and significant correlations (0.001 < p < 0.01) were obtained. The set of results allowed us to conclude that ultrasonic indexes are suitable markers for the erythrocyte aggregation.