Objectives: Identification of the cause of sudden cardiac death in deceased with structurally normal hearts is a long-standing challenge in forensic medicine. Current forensic methods in conventional autopsy, including newly introduced imaging techniques, fail to identify certain pathologies behind sudden cardiac death, especially in the young. We propose that diffusion tensor magnetic resonance imaging could be used to identify currently unidentifiable pathologies. There are, however, certain technical difficulties that prevent implementation as part of a standardised autopsy workflow. This technical note aims to illustrate a feasible workflow using diffusion tensor imaging as an adjunct to the conventional autopsy. Materials and methods: Two paediatric hearts were imaged for 1 h and 40 min using a 9.4T Agilent preclinical MRI system. A standard diffusion weighted 2D multi-slice spin-echo sequence was utilised using 6 isotropically distributed diffusion directions. One specimen was filled with a removable plastic polymer to improve the structural regularity of the heart. Results: Results were obtained from both hearts in a time efficient manner, whilst maintaining tissue integrity and permitted extraction and quantification of myocardial orientation. Tractography of both hearts correlated with results found from previous studies. Feedback from pathology staff was positive regarding including the DTMRI protocol. Conclusion: Diffusion tensor imaging can be integrated into the conventional autopsy workflow without disruption to the autopsy process. The plastic polymer improved the ease of analysis as compared to the specimen without a plastic polymer. Although the technique is not at present ready for use in the autopsy process, this note indicates that it could in future be a viable tool to aid identification of paediatric cardiac disease.

Despite intense investigation through centuries, there is still no scientific consensus on how to describe myocardial microarchitecture. This is mainly because the myocardium must be visualised in three dimensions, and with sufficiently high resolution to fully appreciate its complex nature. X-ray microtomography allows for exactly such visualisation. Using this technique, we herein provide a description of the ventricular mural architecture in a wide range of mammals. Myocardial biopsies from the left ventricle of a human, pig, rabbit, giraffe, elephant, and sei whale were imaged using X-ray microtomography after iodine staining. Aggregations of cardiomyocytes were segmented and visualised in three dimensions, permitting accurate assessment of their shape and orientation. It was possible to segment individual components of the overall mesh using the three-dimensional images in all the studied species. The myocardium is most accurately described as a complex hierarchical meshwork, with the cardiomyocyte as the smallest working unit. The cardiomyocytes are bound together by endomysium to form aggregates, which are themselves compartmented by perimysium. A high degree of variation in the shape of aggregation was found within each biopsy, but, most remarkably, significant differences were observed between species. Some bundles of aggregated cardiomyocytes stand out from the adjacent myocardium within the mesh due to a clear change in their orientation. We provide evidence that the mammalian ventricular myocardium is a complex meshwork of cardiomyocytes. This mesh, although continuous along its direction of contraction, is separated by perimysial clefts into aggregated entities most appropriately described as aggregates. When comparing between species, there is remarkable heterogeneity in this anatomical appearance. We found no evidence of the myocardium being ordered into a large individual band as previously described elsewhere.

The common hippopotamus (Hippopotamus amphibius) shares a common terrestrial ancestor with whales (Cetacea) and has independently evolved similar physiological adaptations to their aquatic lifestyle. Although several studies have explored the electrical signalling in whale hearts, the understanding of the conduction system and electrical activation of the hippopotamus heart remains sparse. We set out to map the conduction system within the hippopotamus heart and determine the sequence of electrical activation, including the mean electrical axis of ventricular activation. ECGs were recorded from three anaesthetized hippopotamuses. Histological samples were collected from two of these animals and from an additional animal. The hearts of the hippopotamuses constituted ∼0.3% of body mass and as in whales, the hearts were situated more cranially in the thoracic cavity compared to most terrestial mammals, and were spanning from the first to the fourth intercostal space. The network of Purkinje fibre strands extended deep into the ventricular walls and consisted of large, ovoid cells. Orthogonal ECG recordings revealed a mean electrical axis pointing towards the neck of the animal, indicating that electrical activation takes place in an apex-to-base direction.

BACKGROUND:Cardiac diffusion tensor imaging (cDTI) is an emerging technique for microstructural characterization of the heart and has shown clinical potential in a range of cardiomyopathies. However, there is substantial variation reported for in vivo cDTI results across the literature, and sensitivity of cDTI to differences in imaging sites, scanners, acquisition protocols, and post-processing methods remains incompletely understood. METHODS:SIGNET is a prospective multi-center, observational study in traveling and non-traveling healthy volunteers. The study was initiated by the executive board of the Society of Cardiovascular Magnetic Resonance (SCMR) Cardiac Diffusion Special Interest Group (SIG) as a follow-up to a previous multi-center study on phantom validation of cardiac DTI and a recently published SCMR consensus statement on cardiac diffusion MRI. The study has been developed by the Project Management Committee in consultation with the SCMR cardiac diffusion SIG, which includes international experts in cardiac diffusion MRI. To date, more than 20 international institutions have engaged with the study, including sites that are new to cardiac DTI, making this the largest collaborative effort in the field. DISCUSSION:SIGNET will provide important information about the key sources of variation in cardiac DTI. This will help rationalize strategies for addressing and minimizing such variation. Harmonization of protocols in this and future studies will underpin efforts to translate cardiac DTI for clinical application.

Although pig-to-baboon cardiac xenotransplantation has become increasingly successful, challenges remain in its clinical translation, particularly in addressing xenograft overgrowth. While several causes can be managed through genetic modifications and hemodynamic control, growth persists. Research on myocardial architecture and interspecies variation is limited. This study employs diffusion tensor imaging to probe the orientation of cardiomyocytes and their aggregations and aims to investigate whether these parameters may act as intrinsic factors, contributing to xenograft overgrowth in a setting of extrinsic hemodynamic mismatch. Five pig and five baboon ex-vivo hearts were compared by cardiac diffusion tensor magnetic resonance imaging. Myocardial architecture was assessed by quantifying helical, intrusion and E3-angles in left ventricle, septum and right ventricle. Notable differences were found in E3-angles of the left ventricle. The E3 angle was closer to 0° throughout the baboon myocardium. The epicardial E3-angle differed by -9°, midwall by -17.1°, and endocardial by -23.7° The myocardial architecture observed in baboon hearts may support a greater contractional deformation, potentially reflecting an enhanced contractile potential as compared to the porcine heart. Further ex- and in-vivo investigation of both pre- and post-transplantation animals is warranted to assess the exact functional implications of these myocardial architecture differences.

An intricate meshwork of trabeculations lines the luminal side of cardiac ventricles. Compaction, a developmental process, is thought to reduce trabeculations by adding them to the neighboring compact wall which is then enlarged. When pig, a plausible cardiac donor for xenotransplantation, is compared to human, the ventricular walls appear to have fewer trabeculations. We hypothesized the trabecular volume is proportionally smaller in pig than in human. Macroscopically, we observed in 16 pig hearts that the ventricular walls harbor few but large trabeculations. Close inspection revealed a high number of tiny trabeculations, a few hundred, within the recesses of the large trabeculations. While tiny, these were still larger than embryonic trabeculations and even when considering their number, the total tally of trabeculations in pig was much fewer than in human. Volumetrics based on high-resolution MRI of additional six pig hearts compared to six human hearts, revealed the left ventricles were not significantly differently trabeculated (21.5 versus 22.8%, respectively), and the porcine right ventricles were only slightly less trabeculated (42.1 vs 49.3%, respectively). We then analyzed volumetrically 10 pig embryonic hearts from gestational day 14-35. The trabecular and compact layer always grew, as did the intertrabecular recesses, in contrast to what compaction predicts. The proportions of the trabecular and compact layers changed substantially, nonetheless, due to differences in their growth rate rather than compaction. In conclusion, processes that affect the trabecular morphology do not necessarily affect the proportion of trabecular-to-compact myocardium and they are then distinct from compaction.

Introduction: There is an increasing focus on the prevention of secondary injuries following traumatic spinal cord injury (TSCI), especially through improvement of spinal cord perfusion and immunological modulation. Such therapeutic strategies require translational and controlled animal models of disease progression of the acute phases of human TSCI. Research question: Is it possible to establish a 72-h sedated porcine model of incomplete thoracic TSCI, enabling controlled use of continuous, invasive, and non-invasive modalities during the entire sub-acute phase of TSCI? Material and methods: A sham-controlled trial was conducted to establish the model, and 10 animals were assigned to either sham or TSCI. All animals underwent a laminectomy, and animals in the TSCI group were subjected to a weight-drop injury. Animals were then kept sedated for 72 h. The amount of injury was assessed by ex-vivo measures MRI-based fiber tractography, histology and immunohistochemistry. Results: In all animals, we were successful in maintaining sedation for 72 h without comprising vital physiological parameters. The MRI-based fiber tractography showed that all TSCI animals revealed a break in the integrity of spinal neurons, whereas histology demonstrated no transversal sections of the spine with complete injury. Notably, some animals displayed signs of secondary ischemic tissue in the cranial and caudal sections. Discussion and conclusions: This study succeeded in producing a porcine model of incomplete TSCI, which was physiologically stable up to 72 h. We believe that this TSCI model will constitute a potential translational model to study the pathophysiology secondary to TSCI in humans.

Background: Principal strain (PS) analysis quantifies three-dimensional myocardial deformation using threedimensional speckle-tracking echocardiography. It defines both the amplitude and direction of the principal myocardial contraction, expressed as PS, and a perpendicular secondary strain of lower intensity. The aims of this study were to apply PS analysis to describe the contractile pattern in the single right ventricle (SRV) functioning as a systemic chamber in hypoplastic left heart syndrome, compared with the normal left ventricle (LV) and right ventricle (RV), and to compare SRV function using conventional echocardiographic evaluations.Methods: Fifty-four post-Fontan patients with hypoplastic left heart syndrome and age-matched control subjects (normal LV, n = 64; normal RV, n = 48) underwent computation of PS lines, ejection fraction (EF), end diastolic volume indexed to body surface area, PS, secondary strain, circumferential strain, and longitudinal strain. The PS lines were compared between groups. Linear regressions with coefficient determination (R2) of strains, fractional area change, and tricuspid annular plane systolic excursion with EF and end-diastolic volume index were assessed in SRV. Additionally, the hypoplastic left heart syndrome cohort was equally divided into two groups with higher and lower EFs, followed by comparison of all parameters.Results: The pattern of PS lines demonstrated a left-handed direction in the anterior free wall, a right-handed direction in the posterior free wall, and a circumferential direction in the medial wall in SRV. In contrast, in the normal LV, the principal contraction is in the circumferential direction, whereas in the normal RV, it is predominantly longitudinal. The R2 values for PS, secondary strain, and circumferential strain on EF were high (0.88, 0.72, and 0.90, respectively), whereas the R2 value for longitudinal strain was comparable with that for fractional area change (0.56 and 0.55). All parameters were independent of end-diastolic volume index. PS lines in the higher EF group showed a more circumferential orientation than in the lower EF group in SRV.Conclusion: PS analysis provides a unique functional map of SRV contraction. This map differs from corresponding maps of the normal LV and RV. This may be helpful in understanding the mechanisms of SRV function, although future longitudinal studies are needed. (J Am Soc Echocardiogr 2023;36:878-87.)

The risk of traumatic injury in football has been suggested to be affected by field conditions. This study, therefore, aimed to investigate whether near surface water content of the football field, influenced the risk of traumatic injuries during a youth football tournament.

The left ventricular ejection fraction does not accurately predict exercise capacity or symptom severity and has a limited role in predicting prognosis in heart failure. A better method of assessing ventricular performance is needed to aid understanding of the pathophysiological mechanisms and guide management in conditions such as heart failure. In this study, we propose two novel measures to quantify myocardial performance, the global longitudinal active strain energy (GLASE) and its density (GLASED) and compare them to existing measures in normal and diseased left ventricles. GLASED calculates the work done per unit volume of muscle (energy density) by combining information from myocardial strain and wall stress (contractile force per unit cross sectional area). Magnetic resonance images were obtained from 183 individuals forming four cohorts (normal, hypertension, dilated cardiomyopathy, and cardiac amyloidosis). GLASE and GLASED were compared with the standard ejection fraction, the corrected ejection fraction, myocardial strains, stroke work and myocardial forces. Myocardial shortening was decreased in all disease cohorts. Longitudinal stress was normal in hypertension, increased in dilated cardiomyopathy and severely decreased in amyloid heart disease. GLASE was increased in hypertension. GLASED was mildly reduced in hypertension (1.39 ± 0.65 kJ/m 3 ), moderately reduced in dilated cardiomyopathy (0.86 ± 0.45 kJ/m 3 ) and severely reduced in amyloid heart disease (0.42 ± 0.28 kJ/m 3 ) compared to the control cohort (1.94 ± 0.49 kJ/m 3 ). GLASED progressively decreased in the hypertension, dilated cardiomyopathy and cardiac amyloid cohorts indicating that mechanical work done and systolic performance is severely reduced in cardiac amyloid despite the relatively preserved ejection fraction. GLASED provides a new technique for assessing left ventricular myocardial health and contractile function.

Mechanical unloading of the left ventricle reduces infarct size after acute myocardial infarction by reducing cardiac work. Left ventricular veno-occlusive unloading reduces cardiac work and may reduce ischemia and reperfusion injury. In a porcine model of myocardial ischemia–reperfusion injury we randomized 18 pigs to either control or veno-occlusive unloading using a balloon engaged from the femoral vein into the inferior caval vein and inflated at onset of ischemia. Evans blue and 2,3,5-triphenyltetrazolium chloride were used to determine the myocardial area at risk and infarct size, respectively. Pressure–volume loops were recorded to calculate cardiac work, left ventricular (LV) volumes and ejection fraction. Veno-occlusive unloading reduced infarct size compared with controls (Unloading 13.9 ± 8.2% versus Control 22.4 ± 6.6%; p = 0.04). Unloading increased myocardial salvage (54.8 ± 23.4% vs 28.5 ± 14.0%; p = 0.02), while the area at risk was similar (28.4 ± 6.7% vs 27.4 ± 5.8%; p = 0.74). LV ejection fraction was preserved in the unloaded group, while the control group showed a reduced LV ejection fraction. Veno-occlusive unloading reduced myocardial infarct size and preserved LV ejection fraction in an experimental acute ischemia–reperfusion model. This proof-of-concept study demonstrated the potential of veno-occlusive unloading as an adjunctive cardioprotective therapy in patients undergoing revascularization for acute myocardial infarction.

Background Pulmonary hypertension is a significant risk factor in patients undergoing surgery. The combined effects of general anaesthesia and positive pressure ventilation can aggravate this condition and cause increased pulmonary blood pressures, reduced systemic blood pressures and ventricular contractility. Although perioperative use of inotropic support or vasopressors is almost mandatory for these patients, preference is disputed. In this study, we investigated the effects of norepinephrine and dobutamine and their ability to improve the arterio-ventricular relationship and haemodynamics in pigs suffering from chronic pulmonary hypertension. Method Pulmonary hypertension was induced in five pigs by banding the pulmonary artery at 2–3 weeks of age. Six pigs served as controls. After 16 weeks of pulmonary artery banding, the animals were re-examined under general anaesthesia using biventricular conductance catheters and a pulmonary artery catheter. After baseline measurements, the animals were exposed to both norepinephrine and dobutamine infusions in incremental doses, with a stabilising period in between the infusions. The hypothesis of differences between norepinephrine and dobutamine with incremental doses was tested using repeated two-way ANOVA and Bonferroni multiple comparisons post-test. Results At baseline, pulmonary artery-banded animals had increased right ventricular pressure (+ 39%, p = 0.04), lower cardiac index (− 23% p = 0.04), lower systolic blood pressure (− 13%, p = 0.02) and reduced left ventricular end-diastolic volume (− 33%, p = 0.02). When incremental doses of norepinephrine and dobutamine were administered, the right ventricular arterio-ventricular coupling was improved only by dobutamine ( p < 0.05). Norepinephrine increased both left ventricular end-diastolic volume and left ventricular contractility to a greater extent ( p < 0.05) in pulmonary artery-banded animals. While the cardiac index was improved equally by norepinephrine and dobutamine treatments in pulmonary artery-banded animals, norepinephrine had a significantly greater effect on mean arterial pressure ( p < 0.05) and diastolic arterial pressure ( p < 0.05). Conclusion While norepinephrine and dobutamine improved cardiac index equally, it was obtained in different manners. Dobutamine significantly improved the right ventricular function and the arterio-ventricular coupling. Norepinephrine increased systemic resistance, thereby improving arterial pressures and left ventricular systolic function by maintaining left ventricular end-diastolic volume.

In recent decades, investigators have strived to describe and quantify the orientation of the cardiac myocytes in an attempt to classify their arrangement in healthy and diseased hearts. There are, however, striking differences between the investigations from both a technical and methodological standpoint, thus limiting their comparability and impeding the drawing of appropriate physiological conclusions from the structural assessments. This review aims to elucidate these differences, and to propose guidance to establish methodological consensus in the field. The review outlines the theory behind myocyte orientation analysis, and importantly has identified pronounced differences in the definitions of otherwise widely accepted concepts of myocytic orientation. Based on the findings, recommendations are made for the future design of studies in the field of myocardial morphology. It is emphasised that projection of myocyte orientations, before quantification of their angulation, introduces considerable bias, and that angles should be assessed relative to the epicardial curvature. The transmural orientation of the cardiomyocytes should also not be neglected, as it is an important determinant of cardiac function. Finally, there is considerable disagreement in the literature as to how the orientation of myocardial aggregates should be assessed, but to do so in a mathematically meaningful way, the normal vector of the aggregate plane should be utilised.

The principal aim of this study was to evaluate changes in systolic function in the single right ventricle (SRV), during progression of the same patient through the three stages of surgical repair for hypoplastic left heart syndrome and during a 5-year follow-up. We hypothesize that, SRV global longitudinal strain (GLS) will be low during 3 stages of repair even in stable patients. We retrospectively evaluated 140 echocardiograms in 20 patients with HLHS (ages 0–11.3 years), before and after 3 stages of surgical palliation. Five-year follow-up data were available in all 20 patients. Controls with structurally normal hearts and in the same age group were used for comparison. We utilized speckle-tracking imaging for assessment of SRV segmental and global longitudinal and circumferential strains, from previously acquired 4-chamber and mid-cavity short-axis views prior to and within 1–3 months of each surgical stage. Longitudinal strain (LS) remained low through all 3 stages of repair and during follow-up. The pre-Fontan stage demonstrated significant interstage improvement compared to the post-Glenn stage despite similar volume status. Global LS was (− 15.6 ± 4.5% after Fontan surgery and remained similar (− 15.32 ± 3.2%) 5 years later. The SRV also showed increased dominance of circumferential strain compared to the normal RV, where the longitudinal deformation was dominant. In SRV, longitudinal strain may be a useful clinical index for evaluating both segmental and global function in an objective manner. Due to lack of significant clinical deterioration over a 10-year period, we speculate that a “lower-than-normal” longitudinal strain may be used as an objective measure of SRV function in clinically stable patients, particularly after the Fontan operation. Compensatory mechanisms where the longitudinal pattern of contraction switches to a more circumferential pattern, may play a role in asymptomatic patients with HLHS.

In heart failure, myocardial overload causes vast metabolic changes that impair cardiac energy production and contribute to deterioration of contractile function. However, metabolic therapy is not used in heart failure care. We aimed to investigate the interplay between cardiac function and myocardial carbohydrate metabolism in a large animal heart failure model. Using magnetic resonance spectroscopy with hyperpolarized pyruvate and magnetic resonance imaging at rest and during pharmacological stress, we investigated the in-vivo cardiac pyruvate metabolism and contractility in a porcine model of chronic pulmonary insufficiency causing right ventricular volume overload. To assess if increasing the carbohydrate metabolic reserve improves the contractile reserve, a group of animals were fed dichloroacetate, an activator of pyruvate oxidation. Volume overload caused heart failure with decreased pyruvate dehydrogenase flux and poor ejection fraction reserve. The animals treated with dichloroacetate had a larger contractile response to dobutamine stress than non-treated animals. Further, dichloroacetate prevented myocardial hypertrophy. The in-vivo metabolic data were validated by mitochondrial respirometry, enzyme activity assays and gene expression analyses. Our results show that pyruvate dehydrogenase kinase inhibition improves the contractile reserve and decreases hypertrophy by augmenting carbohydrate metabolism in porcine heart failure. The approach is promising for metabolic heart failure therapy.

BackgroundEarly detection of heart failure is important for timely treatment. During development of heart failure adaptive, intracellular processes that evolve prior to macro‐anatomic pathology could provide an early signal of impending heart failure. Therefore, metabolic alterations following cardiac dysfunction would appear early in disease progression. We hypothesised that metabolic imaging with hyperpolarised magnetic resonance can detect early development of heart failure before conventional echocardiography detects cardiac dysfunction.Methods and ResultsFive 8.5 kg piglets were subjected to pulmonary banding and subsequently examined by [1‐13C]pyruvate hyperpolarisation, conventional magnetic resonance imaging, echocardiography, and blood samples every four weeks for 16 weeks. They were compared with a weight matched, healthy control group. Conductance catheter examination at the end of the study showed impaired right ventricular systolic function along with compromised left ventricular diastolic function. After 16 weeks we saw a significant decrease in the left ventricular conversion ratio of pyruvate/bicarbonate from 0.13 (0.04) in controls to 0.07 (0.02) in animals with pulmonary banding, and a significant increase in the lactate/bicarbonate ratio to 3.47 (1.57) versus 1.34 (0.81) in controls. NT‐proBNP was increased by more than 300%, while cardiac index was reduced to 2.8 (0.95) l/min/m2 versus 3.9(0.95)in controls. Echocardiography revealed no changes.ConclusionHyperpolarisation detected a shift towards anaerobic metabolism in early stages of right ventricular dysfunction as evident by an increased lactate/bicarbonate ratio. Dysfunction was confirmed with conductance catheter assessment, but could not be detected by echocardiography. Hyperpolarisation holds a promising future in clinical assessment of heart failure in both acquired and congenital heart disease.Support or Funding InformationThe study is funded by the Danish Children Heart Foundation.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The three-dimensional rearrangement of the right ventricular (RV) myocardium during cardiac deformation is unknown. Previous in-vivo studies have shown that myocardial left ventricular (LV) deformation is driven by rearrangement of aggregations of cardiomyocytes that can be characterised by changes in the so-called E3-angle. Ex-vivo imaging offers superior spatial resolution compared with in-vivo measurements, and can thus provide novel insight into the deformation of the myocardial microstructure in both ventricles. This study sought to describe the dynamic changes of the orientations of the cardiomyocytes in both ventricles brought upon by cardiac contraction, with particular interest in the thin-walled RV, which has not previously been described in terms of its micro-architecture. The hearts of 14 healthy 20 kg swine were excised and preserved in either a relaxed state or a contracted state. Myocardial architecture was assessed and compared between the two contractional states by quantification of the helical, transmural and E3-angles of the cardiomyocytes using high-resolution diffusion tensor imaging. The differences between the two states of contraction were most pronounced in the endocardium where the E3-angle decreased from 78.6° to 24.8° in the LV and from 82.6° to 68.6° in the RV. No significant change in neither the helical nor the transmural angle was found in the cardiomyocytes of the RV. In the endocardium of the LV, however, the helical angle increased from 35.4° to 47.8° and the transmural angle increased from 3.1° to 10.4°. The entire myocardium rearranges through the cardiac cycle with the change in the orientation of the aggregations of cardiomyocytes being the predominant mediator of myocardial wall thickening. Interestingly, differences also exist between the RV and LV, which helps in the explanation of the different physiological capabilities of the ventricles.

Measuring vital signs is central to medical practice, but they are difficult to monitor in awake laboratory animals. We examined the feasibility of a noninvasive device for telemetric assessment of respiration rate, heart rate, temperature and movement in pigs. Awake piglets were monitored continuously for 31 h (interquartile range, 7) before (n = 4) and after (n = 3) surgery. Data quality was sufficient for determination of all parameters. We conclude that continuous, noninvasive monitor- ing of pigs is possible by using the evaluated device.

El control lipídico óptimo es difícil de conseguir. Se evalúa el cumplimiento previo de los objetivos de la Sociedad Europea de Cardiología para el control del colesterol unido a lipoproteínas de baja densidad (cLDL) de los pacientes que ingresaron por síndrome coronario agudo.Se midió el cLDL en ayunas de 3.164 pacientes ingresados entre 2010 y 2017 y se analizó la frecuencia de un control adecuado, con objetivos según el riesgo cardiovascular individual, y los predictores de control inadecuado.La mediana de cLDL fue 104 (80-130) mg/dl. La mayoría de los pacientes tenían un riesgo cardiovascular alto o muy alto y solo el 34,2% tenía un cLDL dentro del objetivo recomendado para su nivel de riesgo. Se apreció un pequeño aumento en la consecución de los objetivos de cLDL a lo largo del periodo estudiado. El control adecuado de cLDL se relacionó inversamente con el riesgo de los pacientes. La dislipemia, el tabaquismo, la diabetes mellitus o un índice de masa corporal ≥ 25 fueron predictores independientes de un control lipídico inadecuado, mientras que el tratamiento previo con estatinas se asoció con un control apropiado.Poco más de un tercio de los pacientes ingresados por síndrome coronario agudo tiene valores de cLDL al ingreso acordes con los objetivos recomendados. Hay un amplio campo de mejora en prevención primaria y secundaria, especialmente para los pacientes con exceso de peso u otros factores de riesgo cardiovascular.Optimal lipid control is difficult to attain. We assessed preadmission achievement of the European Society of Cardiology targets for low-density lipoprotein-cholesterol (LDL-C) control in patients admitted for acute coronary syndrome.Fasting LDL-C levels were measured in 3164 patients admitted between 2010 and 2017. We assessed the frequency of adequate LDL-C control, with targets defined according to individual cardiovascular risk, and the predictors of inadequate control.The median LDL-C value was 104 (80-130) mg/dL. Most patients had high or very high cardiovascular risk and only 34.2% had LDL-C levels below the recommended target for their estimated risk. Achievement of LDL-C goals increased moderately throughout the study period. Adequate LDL-C control was inversely associated with patient risk. Dyslipidemia, active smoking, diabetes mellitus, and body mass index ≥ 25 were independent predictors of inadequate lipid control, while ongoing statin therapy was associated with adequate control.Only slightly more than one third of patients admitted for acute coronary syndrome meet recommended LDL-C targets on admission. There is broad scope for improvement in primary and secondary prevention, especially among patients who are overweight or have other cardiovascular risk factors.

The manner of packing together of the cardiomyocytes within the walls of the cardiac ventricles has now been investigated for over half a millennium. In 1669, Lower dissected the ventricular mass, likening the arrangement to skeletal musculature, in the form of a myocardial band extending between the right and left atrioventricular junctions. Pettigrew subsequently showed obvious helical arrangements to be evident within the ventricular walls, but emphasised that the cardiomyocytes were attached to each other, and could not justifiably be compared with skeletal cardiomyocytes. Torrent-Guasp then reactivated the notion that the ventricular mass was formed of a solitary band. Unlike Lower, he dissected the band as extending between the pulmonary to the aortic roots. Multiple investigations conducted using gross dissection and histology, and more recently diffusion tensor magnetic resonance imaging and computed tomographic analysis, have shown an absence of any anatomical boundaries within the walls that might permit the mass uniformly to be dissected so as to reveal the band. A response to a recent letter to the Journal, nonetheless, claimed that the dissections had been validated by clinicians interpreting the findings so as to provide an explanation for ventricular cardiodynamics, arguing that the findings provided a suitable anatomical model for this purpose. Anatomical models, however, are of no value unless they are anatomically correct. In this review, therefore, we summarise the evidence showing that the cardiomyocytes making up the ventricular walls, rather than forming a ventricular myocardial band, are instead aggregated together to form a three-dimensional myocardial mesh.