Student survey after ten years of continuous blended teaching of echocardiography.

OBJECTIVE: To analyse the impact of 10 years of blended echocardiography teaching. METHODS AND RESULTS: A questionnaire was emailed to all medical doctors who graduated from the blended learning diploma in echocardiography developed by the University of Chile and taught by a team from Chile and Spain. One hundred and forty of the 210 students who graduated from the program between 2011 and 2020 completed the questionnaire: 53.57% were anaesthesiologists, and 26.42% were intensivists. More than 85% of respondents indicated that the online teaching met their expectations, and 70.2% indicated that the hands-on practice fulfilled the stated objectives. In a retrospective analysis using self-reported data, graduates reported that their use of transthoracic and transoesophageal echocardiography has increased from 24.29% to 40.71% and from 13.57% to 27.86%, repectively, after the programme compared to before the programme. They used echocardiography mainly in the perioperative period (56.7%) and during intensive care (32.3%), while only 11% of respondents used it in emergency care units. Nearly all (92.4%) respondents reported that the skills learned was very useful in their professional practice. CONCLUSIONS: Ten years after its launch, the blended learning diploma in echocardiography was well rated by graduate specialists, and is associated with a significant increase in the use of echocardiography in the perioperative period and during intensive care. The main challenges are to establish a longer period of practice and achieve greater implantation in emergency medicine.

Assessment of tricuspid annulus: anatomic and echocardiographic correlation.

Tricuspid regurgitation is associated with a poor outcome and its quantification remains a challenge. Tricuspid annulus dilatation is one of the parameters that influences clinical decision-making. The aim of this study was to compare the use of 2D transoesophageal echocardiography with surgical assessment for the measurement of the tricuspid annulus. Sixty-one cardiac patients (median age 64 years) were included in the study. Echocardiographic tricuspid annulus measurements were obtained from four chamber and transgastric short axis views and compared with the surgical measurements of this valve. The study was approved by the Ethics Committee of our institution. The tricuspid annulus measurements were obtained from the four chamber and the short axis views in 57 and 49 patients, respectively, while surgical measurement was performed in all 61 patients. Bland-Altman analysis of 49 tricuspid annulus-matched dimensions of the short axis view and surgical values showed a mean bias of 0.223 mm/m2, with limits of agreement of -5.86 to 6.31 mm/m2. Echocardiographic measurements of the tricuspid annulus dimension were accurate (90% sensitivity and 90% specificity for a four chamber view cut-off value ≥ 24.5 mm/m2, and 89% sensitivity and 97% specificity for a short axis view cut-off value ≥ 37.6 mm/m2, P < 0.0001; both cases) for detecting directly assessed annular dilatation by the surgeon in the operative field. Echocardiographic values of tricuspid annulus dimension have a good predictive value to detect surgically assessed annular dilatation and may help identify patients who require surgical tricuspid intervention.

[Ventricular contractility: Physiology and clinical projection]. / Contractilidad ventricular: Fisiología y proyección clínica.

The contractile state of the heart is the result of myocardial contractility, the intrinsic mechanism that regulates the force and the shortening of the ventricle and determines the ventricular ejection volume. However, the ejection volume is also modulated by ventricular preload (diastolic ventricular volume) and afterload (resistance to ejection). Accordingly, a decrease in contractility may be masked by changes in preload or afterload, maintaining a normal ejection volume and delaying the diagnosis of myocardial damage. Thus, it is necessary to develop a non-invasive method to measure contractility in the clinical practice. We review in this article the basic principles of cardiac contraction, the concept of contractility and its measurement with the ventricular pressure-volume loop, an experimental method that also measures most of the hemodynamic variables of the cardiac cycle including preload, afterload, ventricular work, ventricular lusitropy and arterial elastance. This method has been recently validated in cardiac patients and allows to evaluate the evolution of contractility in heart failure in a non invasive way. Although some modifications are still necessary, it will probably have an extensive use in practical cardiology in the near future.

Contractilidad ventricular: fisiología y proyección clínica / Ventricular contractility: physiology and clinical projection

The contractile state of the heart is the result of myocardial contractility, the intrinsic mechanism that regulates the force and the shortening of the ventricle and determines the ventricular ejection volume. However, the ejection volume is also modulated by ventricular preload (diastolic ventricular volume) and afterload (resistance to ejection). Accordingly, a decrease in contractility may be masked by changes in preload or afterload, maintaining a normal ejection volume and delaying the diagnosis of myocardial damage. Thus, it is necessary to develop a non-invasive method to measure contractility in the clinical practice. We review in this article the basic principles of cardiac contraction, the concept of contractility and its measurement with the ventricular pressure-volume loop, an experimental method that also measures most of the hemodynamic variables of the cardiac cycle including preload, afterload, ventricular work, ventricular lusitropy and arterial elastance. This method has been recently validated in cardiac patients and allows to evaluate the evolution of contractility in heart failure in a non invasive way. Although some modifications are still necessary, it will probably have an extensive use in practical cardiology in the near future.

Studies on the role of apoptosis after transient myocardial ischemia: genetic deletion of the executioner caspases-3 and -7 does not limit infarct size and ventricular remodeling.

Although it is widely accepted that apoptosis may contribute to cell death in myocardial infarction, experimental evidence suggests that adult cardiomyocytes repress the expression of the caspase-dependent apoptotic pathway. The aim of this study was to analyze the contribution of caspase-mediated apoptosis to myocardial ischemia-reperfusion injury. Cardiac-specific caspase-3 deficient/full caspase-7-deficient mice (Casp3/7DKO) and wild type control mice (WT) were subjected to in situ ischemia by left anterior coronary artery ligation for 45 min followed by 24 h or 28 days of reperfusion. Heart function was assessed using M-mode echocardiography. Deletion of caspases did not modify neither infarct size determined by triphenyltetrazolium staining after 24 h of reperfusion (40.0 ± 5.1 % in WT vs. 36.2 ± 3.6 % in Casp3/7DKO), nor the scar area measured by pricosirius red staining after 28 days of reperfusion (41.1 ± 5.4 % in WT vs. 44.6 ± 8.7 % in Casp3/7DKO). Morphometric and echocardiographic studies performed 28 days after the ischemic insult revealed left ventricular dilation and severe cardiac dysfunction without statistically significant differences between WT and Casp3/7DKO groups. These data demonstrate that the executioner caspases-3 and -7 do not significantly contribute to cardiomyocyte death induced by transient coronary occlusion and provide the first evidence obtained in an in vivo model that argues against a relevant role of apoptosis through the canonical caspase pathway in this context.

Exercise preconditioning of myocardial infarct size in dogs is triggered by calcium.

We showed that exercise induces early and late myocardial preconditioning in dogs and that these effects are mediated through nicotinamide adenine dinucleotide phosphate reduced form (NADPH) oxidase activation. As the intracoronary administration of calcium induces preconditioning and exercise enhances the calcium inflow to the cell, we studied if this effect of exercise triggers exercise preconditioning independently of its hemodynamic effects. We analyzed in 81 dogs the effect of blocking sarcolemmal L-type Ca channels with a low dose of verapamil on early and late preconditioning by exercise, and in other 50 dogs, we studied the effect of verapamil on NADPH oxidase activation in early exercise preconditioning. Exercise reduced myocardial infarct size by 76% and 52% (early and late windows respectively; P < 0.001 both), and these effects were abolished by a single low dose of verapamil given before exercise. This dose of verapamil did not modify the effect of exercise on metabolic and hemodynamic parameters. In addition, verapamil blocked the activation of NADPH oxidase during early preconditioning. The protective effect of exercise preconditioning on myocardial infarct size is triggered, at least in part, by calcium inflow increase to the cell during exercise and, during the early window, is mediated by NADPH oxidase activation.

Disfunción cognitiva después de cirugía cardiaca: Saturación cerebral e índice biespectral: estudio longitudinal / Neuropsychological dysfunction after cardiac surgery: Cerebral saturation and bispectral index: A longitudinal study

Background: Neuropsychological dysfunction is a major cause of morbidity and mortality after cardiac surgery. Aim: To evaluate if intraoperative cerebral desatu-ration and depth of anesthesia measured by bispectral index are related to postoperative cognitive dysfunction in cardiac surgery. Material and Methods: Prospective study in patients undergoing elective cardiac surgery with cardiopulmonary bypass. A comprehensive neuropsychological assessment was applied preoperatively and 3 months after surgery. Postoperative dysfunction was defined as a decrease of at least one standard deviation in two or more neuropsychological tests. Cerebral oxygenation and bispectral index were continuously recorded and corrected throughout surgery. Cerebral oxygenation data were analyzed by the mean value and at three thresholds: 50%, 40% and < 25% of the basal value. Bispectral index was analyzed at threshold of 45. Results: Fifty-six patients were initially enrolled and 48 completed the study. Nine of these (18.8 %) presented postoperative cognitive dysfunction. Mean cerebral saturation and bispectral index data were not different among the patients with or without cognitive dysfunction. There was no association between cerebral desaturation and bispectral index with changes in neurocognitive tests or with length of stay in the intensive care unit. A significant but weak correlation was found between baseline Ray-neurocognitive score and intensive care unit stay (rho = -0.46; P = 0.001). Conclusions: We did not find a significant association between cerebral desaturation and depth of anesthesia with postoperative cognitive decline in this population of patients.

[Neuropsychological dysfunction after cardiac surgery: Cerebral saturation and bispectral index: A longitudinal study]. / Disfunción cognitiva después de cirugía cardiaca: Saturación cerebral e índice biespectral: estudio longitudinal.

BACKGROUND: Neuropsychological dysfunction is a major cause of morbidity and mortality after cardiac surgery. AIM: To evaluate if intraoperative cerebral desaturation and depth of anesthesia measured by bispectral index are related to postoperative cognitive dysfunction in cardiac surgery. MATERIAL AND METHODS: Prospective study in patients undergoing elective cardiac surgery with cardiopulmonary bypass. A comprehensive neuropsychological assessment was applied preoperatively and 3 months after surgery. Postoperative dysfunction was defined as a decrease of at least one standard deviation in two or more neuropsychological tests. Cerebral oxygenation and bispectral index were continuously recorded and corrected throughout surgery. Cerebral oxygenation data were analyzed by the mean value and at three thresholds: 50%, 40% and < 25% of the basal value. Bispectral index was analyzed at threshold of 45. RESULTS: Fifty-six patients were initially enrolled and 48 completed the study. Nine of these (18.8 %) presented postoperative cognitive dysfunction. Mean cerebral saturation and bispectral index data were not different among the patients with or without cognitive dysfunction. There was no association between cerebral desaturation and bispectral index with changes in neurocognitive tests or with length of stay in the intensive care unit. A significant but weak correlation was found between baseline Ray-neurocognitive score and intensive care unit stay (rho = -0.46; P = 0.001). CONCLUSIONS: We did not find a significant association between cerebral desaturation and depth of anesthesia with postoperative cognitive decline in this population of patients.

Late cardiac preconditioning by exercise in dogs is mediated by mitochondrial potassium channels.

We previously showed that exercise induces myocardial preconditioning in dogs and that early preconditioning is mediated through mitochondrial adenosine triphosphate-sensitive potassium channels. We decided to study if late preconditioning by exercise is also mediated through these channels. Forty-eight dogs, surgically instrumented and trained to run daily, were randomly assigned to 4 groups: (1) Nonpreconditioned dogs: under anesthesia, the coronary artery was occluded during 1 hour and then reperfused during 4.5 hours. (2) Late preconditioned dogs: similar to group 1, but the dogs run on the treadmill for 5 periods of 5 minutes each, 24 hours before the coronary occlusion. (3) Late preconditioned dogs plus 5-hydroxydecanoate (5HD): similar to group 2, but 5HD was administered before the coronary occlusion. (4) Nonpreconditioned dogs plus 5HD: similar to group 1, but 5HD was administered before the coronary occlusion. Infarct size (percent of the risk region) decreased by effect of exercise by 56% (P < 0.05), and this effect was abolished with 5HD. 5HD by itself did not modify infarct size. Exercise did not induce myocardial ischemia, and the hemodynamics during ischemia-reperfusion period did not differ among groups. These effects were independent of changes in collateral flow to the ischemic region. We concluded that late cardiac preconditioning by exercise is mediated through mitochondrial adenosine triphosphate-sensitive potassium channels.

Calpain translocation and activation as pharmacological targets during myocardial ischemia/reperfusion.

Calpains contribute to reperfusion-induced myocardial cell death. However, it remains controversial whether its activation occurs during ischemia or reperfusion. We investigated the regulation and time-course of calpain activation secondary to transient ischemia and the efficacy of its inhibition at reperfusion as a therapeutic strategy to limit infarct size. In isolated rat hearts (Sprague-Dawley), ischemia induced a time-dependent translocation of m-calpain to the membrane that was not associated with calpain activation as assessed by proteolysis of its substrate alpha-fodrin. Translocation of calpain was dependent on Ca(2+) entry through reverse mode Na(+)/Ca(2+)-exchange and was independent of acidosis. Calpain activation occurred during reperfusion, but only after intracellular pH (pHi) normalization, and was not prevented by inhibiting its translocation during ischemia with methyl-beta-cyclodextrin. The intravenous infusion of MDL-28170 in an in vivo rat model with transient coronary occlusion during the first minutes of reperfusion resulted in a reduction of infarct size (43.9+/-3.9% vs. 60.2+/-4.7, P=0.046, n=18) and alpha-fodrin degradation. These results suggest that (1) Ca(2+)-induced calpain translocation to the membrane during ischemia is independent of its activation, (2) intracellular acidosis inhibits calpain activation during ischemia and pHi normalization allows activation upon reperfusion, and (3) calpain inhibition at the time of reperfusion appears as a potentially useful strategy to limit infarct size.