New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review.

This review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of ß-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans.

Rho-kinase pathway activation and apoptosis in circulating leucocytes in patients with heart failure with reduced ejection fraction.

BACKGROUND: Increased Rho-kinase activity in circulating leucocytes is observed in heart failure with reduced ejection fraction (HFrEF). However, there is little information in HFrEF regarding other Rho-kinase pathway components an on the relationship between Rho-kinase and apoptosis. Here, Rho-kinase activation levels and phosphorylation of major downstream molecules and apoptosis levels were measured for the first time both in HFrEF patients and healthy individuals. METHODS: Cross-sectional study comparing HFrEF patients (n = 20) and healthy controls (n = 19). Rho-kinase activity in circulating leucocytes (peripheral blood mononuclear cells, PBMCs) was determined by myosin light chain phosphatase 1 (MYPT1) and ezrin-radixin-moesin (ERM) phosphorylation. Rho-kinase cascade proteins phosphorylation p38-MAPK, myosin light chain-2, JAK and JNK were also analysed along with apoptosis. RESULTS: MYPT1 and ERM phosphorylation were significantly elevated in HFrEF patients, (3.9- and 4.8-fold higher than in controls, respectively). JAK phosphorylation was significantly increased by 300% over controls. Phosphorylation of downstream molecules p38-MAPK and myosin light chain-2 was significantly higher by 360% and 490%, respectively, while JNK phosphorylation was reduced by 60%. Catecholamine and angiotensin II levels were significantly higher in HFrEF patients, while angiotensin-(1-9) levels were lower. Apoptosis in circulating leucocytes was significantly increased in HFrEF patients by 2.8-fold compared with controls and significantly correlated with Rho-kinase activation. CONCLUSION: Rho-kinase pathway is activated in PMBCs from HFrEF patients despite optimal treatment, and it is closely associated with neurohormonal activation and with apoptosis. ROCK cascade inhibition might induce clinical benefits in HFrEF patients, and its assessment in PMBCs could be useful to evaluate reverse remodelling and disease regression.

Rho kinase cascade activation in circulating leukocytes in patients with diabetes mellitus type 2.

BACKGROUND: The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. METHODS: Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. RESULTS: Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. CONCLUSIONS: T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.

"Gigantic" biatrial myxoma with right heart functional impairment.

Cardiac myxomas are frequently located in the left or right atria, with multiple locations being rare. We report a 59-year-old healthy female with 5 months of cough and exertional dyspnea. A transthoracic echocardiography (TTE) exhibits a 9 × 5 cm nonpedunculated tumor arising from the interatrial septum (IAS) and inhabiting both atria, but was unable to depict the relation with the IAS. Transesophageal echocardiography exposes a single tumor crossing the IAS through an ostium secundum atrial septal defect (ASD) causing right heart functional impairment. Uneventful cardiac surgery allowed complete resection of the lesion and ASD closure. Pathology reported a myxoma.

Big thrombus "sitting" in an atrial septal aneurysm.

A 79 year-old-man presented three episodes of upper gastrointestinal bleeding and weight loss. Endoscopy revealed bleeding and extrinsic compression at the pyloric region. Computed tomography scan showed a pancreatic tumor, peritoneal carcinomatosis, vascular infiltration, and incidentally found a partially calcified hypodense lesion of 35 mm in the left atrium, suggesting a myxoma or a thrombus. Echocardiography revealed moderate left atrium enlargement, dilated left atrial appendage with spontaneous echo contrast, moderate dilatation and dysfunction of the left ventricle, ejection fraction was 39%, and an atrial septal aneurysm in which a piriform, mass of 35×33×25 mm, was "sitting," suggesting an organized thrombus.

[Large mitral annulus myxoma presenting with syncope: Report of one case]. / Síncope secundario a mixoma gigante del anillo mitral: Reporte de un caso.

We report a 23-year-old woman, with three recent exertional syncopes. Transthoracic (TTE) and transesophageal (TEE) echocardiography found a large heterogeneous mass (38 x 35 mm) arising from the posterior mitral annulus, protruding in systole through the left ventricular outflow tract (LVOT). Heart MRI confirmed the echocardiography findings, suggesting a cardiac myxoma. Cardiac surgery accomplished the complete resection of the lesion, confirming a mass arising from the posterior mitral annulus and preserving mitral anatomy and function. Pathology was positive for a myxoma. Uneventful evolution allowed the discharge of the patient at the fifth postoperative day. Control TTE discarded any complication.

[Spontaneous rupture of tricuspid valve papillary muscle in pulmonary hypertension secondary to HIV infection. Report of one case]. / Rotura espontánea de válvula tricúspide en un paciente con hipertensión pulmonar secundaria a VIH.

Acute primary tricuspid regurgitation (TR) secondary to papillary muscle rupture is an extremely rare clinical situation. We report a 42-year-old male with pulmonary artery hypertension (PAH) secondary to HIV infection, who presented with an acute TR due to spontaneous papillary muscle rupture. He remained in cardiogenic shock despite therapy with inotropic drugs and pulmonary vasodilator therapy. He was subjected to a tricuspid valve replacement. In the postoperative period the patient had severe PAH, which was successfully controlled with inhaled nitric oxide. Tricuspid valve replacement and adjunctive use of pulmonary vasodilator therapy can be a life saving and useful approach in this condition.

[Infective endocarditis caused by Listeria monocytogenes: review of the literature and a case report]. / Endocarditis infecciosa por Listeria monocytogenes: revisión de la literatura a partir de un caso clínico.

Infective endocarditis caused by Listeria monocytogenesis an extremely rare but usually aggressive disease. We have seen in recent years an increase in age of onset of this disease and a predilection for patients with valvular disease, especially prosthetic valve. The treatment of choice is ampicillin, which is combined with gentamicin for synergy. It is known that even with treatment the mortality is very high and higher than in other types of bacterial endocarditis. With optimal therapy, that is medical-surgical, mortality has declined significantly in recent years. We presents a review of the literature and a clinical case of a patient with a febrile syndrome diagnosed as a infective endocarditis caused by L. monocytogenestreated medically with successful outcome to date.

Assessment of left atrial function in hypertrophic cardiomyopathy and athlete's heart: a left atrial myocardial deformation study.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a common cause of sudden death in athletes and differentiating this condition from the nonpathological "athlete's heart" remains a challenge. The development of pathological left ventricular hypertrophy (LVH) is associated with left atrial (LA) dilatation and dysfunction. LA strain and strain rate by two-dimensional (2D) speckle tracking are novel indices of LA function and might contribute to differentiate physiological from pathological LVH among athletes with underdiagnosed HCM. METHODS: We evaluated 20 patients with nonobstructive HCM, 20 highly trained athletes and 20 healthy controls matched for age, gender, and body surface area. All patients underwent a transthoracic echocardiogram with evaluation of LA strain: s-wave (LASs); and strain rate: s-wave (LASRs) and a-wave (LASRa). RESULTS: LV mass index, LA volume index, and ejection fraction were comparable between patients with HCM and athletes. Patients with HCM had a significantly lower LASs (19 + 8% vs. 43 + 8%, P < 0.01), LASRs (0.7 + 0.2 s-1 vs. 1.6 + 0.2 s-1, P < 0.01), and LASRa (-0.8 + 0.1 s-1 vs. -1.4 + 0.3 s-1, P < 0.01) compared to athletes. Among hypertrophic subjects, independent predictors of hypertrophy related to HCM were LASs and E/é ratio. CONCLUSIONS: LA myocardial deformation is significantly impaired in patients with HCM compared to athletes and healthy controls. LA strain and strain rate assessed by 2D speckle tracking should be incorporated in the evaluation of trained athletes with LVH and LA dilatation.

Markedly increased Rho-kinase activity in circulating leukocytes in patients with chronic heart failure.

BACKGROUND: The small guanosine triphosphatase Rho and its target Rho-kinase have significant roles in experimental remodeling and ventricular dysfunction, but no data are available on Rho-kinase activation in patients with heart failure (HF). We hypothesized that, in patients with chronic HF, Rho-kinase in circulating leukocytes is activated and related to left ventricular (LV) remodeling and dysfunction. METHODS: Accordingly, Rho-kinase activity, assessed by the levels of phosphorylated to total myosin light chain phosphatase 1 (MYPT1-P/T) in circulating leukocytes, and echocardiographic LV function data were compared between patients with HF New York Heart Association functional class II or III due to systolic dysfunction (n = 17), healthy controls (n = 17), and hypertensive patients without HF (n = 17). RESULTS: In the control subjects, mean MYPT1-P/T ratio was 1.2 ± 0.2 (it was similar in the hypertensive patients without HF), whereas in patients with HF, it was significantly increased by >100-fold (P < .001). Both MYPT1-P/T and log MYPT1-P/T ratios were inversely correlated with ejection fraction (r = -0.54, P < .03 and r = -0.86, P < .001, respectively). Furthermore, in patients with HF with LV end-diastolic diameter <60 mm, MYPT1-P/T ratio was 35.8 ± 18.1, whereas it was significantly higher in patients with LV diameter ≥60 mm (P < .05). CONCLUSIONS: Rho-Kinase activity is markedly increased in patients with stable chronic HF under optimal medical treatment, and it is associated with pathologic LV remodeling and systolic dysfunction. Mechanisms of Rho-kinase activation in patients with HF, its role in the progression of the disease, and the direct effect of Rho-kinase inhibition need further investigation.

Left atrial dysfunction is a predictor of postcoronary artery bypass atrial fibrillation: association of left atrial strain and strain rate assessed by speckle tracking.

BACKGROUND: Even though atrial fibrillation (AF) is the most common arrhythmia after coronary artery bypass grafting (CABG), its etiology remains poorly understood. Several factors are linked to postoperative AF (POAF), including advanced age and systemic inflammation. However, left atrial (LA) contractile dysfunction has not been evaluated in the perioperative scenario. AIM: To evaluate LA function through strain and strain rate in patients with coronary artery disease undergoing CABG and its correlation with POAF. METHODS: We studied 70 patients undergoing CABG in sinus rhythm at the time of surgery. Preoperative echocardiography with evaluation of LA strain and strain rate by speckle tracking was performed. The occurrence of POAF was evaluated by continuous monitoring. Baseline and postoperative C-reactive protein (CRP) levels were measured to evaluate systemic inflammation. RESULTS: After 1-week follow-up 26% of subjects developed AF. LA strain s wave (LASs) and LA strain rate s (LASRs) and a wave (LASRa) were significantly decreased in patients who developed POAF: LASs (10 ± 1% vs. 24 ± 1%, P < 0.001), LASRs (0.6 ± 0.1 sec(-1) vs. 1.2 ± 0.1 sec(-1) , P < 0.001), LASRa (-0.6 ± 0.1 sec(-1) vs. -1.8 ± 0.1 sec(-1) , P < 0.001). LASRs, LASRa, age, and LA volume were independent predictors of POAF. CRP at baseline was similar irrespective of POAF development. CONCLUSIONS: LA dysfunction, evaluated by strain and strain rate is an independent predictor of POAF and contributes to classic risk factors like age and atrial volume.

Reverse Remodeling in Human Heart Failure after Cardiac Resynchronization Therapy Is Associated With Reduced RHO-Kinase Activation.

Background: Reverse remodeling is a clinically relevant endpoint in heart failure with reduced ejection fraction (HFrEF). Rho-kinase (ROCK) signaling cascade activation correlates with cardiac remodeling and left ventricular (LV) systolic dysfunction in HFrEF patients. Cardiac resynchronization therapy (CRT) is effective in HFrEF, especially when there is a left bundle block, as this treatment may stimulate reverse remodeling, thereby improving quality of life and prolonging survival for patients with this severe condition. Here, we evaluate the hypothesis that ROCK activation is reduced after effective CRT in HFrEF. Methods: ROCK activation in circulating leukocytes was evaluated in 28 HFrHF patients, using Western blot (myosin light chain phosphatase subunit 1 phosphorylation, MYPT1p/t), before and three months after initiation of CRT. LV systolic function and remodeling were assessed by echocardiography. Results: Three months after CRT, LV ejection fraction increased an average of 14.5% (p < 0.001) in 13 patients (responders), while no change was observed in 15 patients (non-responders). End-systolic diameter decreased 16% (p < 0.001) in responders, with no change in non-responders. ROCK activation in PBMCs decreased 66% in responders (p < 0.05) but increased 10% in non-responders (NS). LV end-diastolic diameter was also 5.2 mm larger in non-responders vs. responders (p = 0.058). LV ejection fraction, systolic diameter, and ROCK activation levels were similar in both groups at baseline. Conclusion: In HFrEF patients, 3 months of effective CRT induced reverse myocardial remodeling, and ROCK activation was significantly decreased in circulating leukocytes. Thus, decreased ROCK activation in circulating leukocytes may reflect reverse cardiac remodeling in patients with heart failure.

Effect of Early Normotension with Olmesartan on Rho-kinase Activity in Hypertensive Patients.

BACKGROUND: Angiotensin II is a potent activator of the Rho-kinase (ROCK) pathway, through which it exerts some of its adverse vasoconstrictor effects. Clinical evidence on the effects of blocking the angiotensin II receptor 1 on ROCK activity in hypertensive patients is scarce. OBJECTIVE: To demonstrate that ROCK activity in peripheral blood mononuclear cells (PMBCs) in patients with essential hypertension is reduced earlier than previously observed, along with blood pressure (BP) lowering on treatment with olmesartan. METHODS: Prospective pilot open study; 17 hypertensive patients were treated with progressive olmesartan doses starting with 20 mg qd. BP was measured at 3, 6 and 9 weeks after treatment initiation. If treatment failed to normalize BP after 3 weeks, olmesartan dose was increased to 40 mg qd, and if still hypertensive after 6 weeks, 12.5 mg of hydrochlorothiazide qd was added. ROCK activity was measured at baseline and 9 weeks after treatment as myosin phosphatase target subunit 1 phosphorylation (MYPT1-p/T ratio) in PBMC. RESULTS: Mean baseline BP was 162 ± 4.9/101 ± 2.4 mmHg. After 9 weeks of treatment, both systolic and diastolic BP were reduced by 41 and 22 mmHg, respectively (p<0.05). Mean pretreatment MYPT1- p/T ratio in PMBCs was significantly reduced by 80% after 9 weeks with olmesartan (p<0.01). CONCLUSION: Normotension achieved after 9 weeks in 82% of the patients treated with olmesartan was associated with a significant reduction of ROCK activity in PBMC.

Estenosis mitral con calcificación severa del anillo mitral: reemplazo mitral con prótesis OnX Conform en posición supraanular / Mitral stenosis with severe annular calcification: mitral valve replacement with an OnX Conform prosthesis in a supra annular position

Abstract A 68-year-old man previously subjected to radiotherapy had a prior aortic valve replacement due de radiation induced calcification of the aortic valve. Presently the patient developed severe calcification of the mitral valve ring leading to critical mitral valve stenosis. A supra annular implantation of an On X Conform valve was successfully achieved. The clinical course was uneventful, and the echocardiographic evaluation demonstrated a normal function of the valve. Different alternatives for the surgical management of this complication are discussed.

Increased rho-kinase activity in hypertensive patients with left ventricular hypertrophy.

BACKGROUND: There is experimental evidence on the role of Rho-kinase (ROCK) activation in cardiac hypertrophy but no information on its role in human hypertension and left ventricular hypertrophy (LVH). We hypothesized that ROCK activity is higher in hypertensive patients with LVH compared with hypertensive patients without LVH. METHODS: We conducted a cross-sectional study comparing untreated hypertensive patients with (n = 41) and without LVH (n = 46) determined by echocardiography with a healthy normotensive control group (n = 51). Measurements included LV mass, dimensions, and function and ROCK activity determined in circulating leukocytes by measuring Western blot levels of phosphorylated to total myosin light chain phosphatase 1 (MYPT1-p/t). RESULTS: Compared with normotensive subjects, MYPT1-p/t was significantly increased by 4.5-fold in the hypertensive patients without LVH and by 9-fold in the hypertensive patients with LVH. Compared with the hypertension without LVH group, MYPT1-p/t was significantly increased by 2-fold in the hypertension with LVH gorup. In patients with eccentric LVH, the mean MYPT1-p/t ratio was significantly higher by 4-fold compared with hypertensive patients without eccentric LVH. Patients with an E/e' ratio ≥15 (n = 6) showed a higher MYPT1-p/t ratio (by 26%) compared with patients with a lower E/e' ratio (P ≤ 0.01). CONCLUSIONS: ROCK activity is higher in hypertensive patients with LVH compared with hypertensive patients without LVH, and it is further increased when eccentric LVH is present. Thus, in hypertension, ROCK activation is related to pathological cardiac remodeling and might have a role as an LVH marker.

Biomarcadores de fibrosis y función ventricular derecha en maratonistas con distinto grado de entrenamiento: estudio en la maratón de Santiago / Fibrosis and right ventricular function biomarkers in marathon runners: a study at the Santiago, Chile marathon

Resumen: Introducción: Atletas altamente entrenados muestran cambios cardíacos estructurales como adaptación a la sobrecarga, producto del ejercicio repetitivo y extenuante. Se han evidenciado elevación de biomarcadores de remodelado y fibrosis miocárdica posterior al ejercicio intenso en atletas. Sin embargo, el comportamiento de estos biomarcadores según el nivel de entrenamiento previo no se ha evaluado. Objetivo: Investigar biomarcadores de fibrosis y función ventricular derecha en maratonistas con distinto nivel de entrenamiento previo. Métodos: Se incluyeron 36 maratonistas hombres, sanos, que completaron 42 km en la maratón de Santiago. Se dividieron según entrenamiento previo en dos grupos, Grupo 1 (G1): ≥100 km/semana y Grupo 2 (G2): <100 km/semana. Se realizó ecocardiografía transtorácica y se evaluaron niveles plasmáticos de galectina-3 y del propéptido amino terminal del procolágeno tipo III (PIIINP) en la semana previa a la carrera e inmediatamente posterior a ésta. Resultados: Posterior a la maratón, la función sistólica del ventrículo derecho disminuyó en el grupo G2 junto con un aumento significativo de los niveles plasmáticos de PIIIPNP (61±16 a 94±24 ng/mL, p=0,01). Estos cambios no se observaron en el grupo G1 (65 ± 11 a 90±29 ng/mL, p=0,10). Los niveles plasmáticos de galectina-3 aumentaron significativamente en ambos grupos posterior al ejercicio (6,8±2,2 a 19,7±4,9 ng/mL, p 0,012 y 6,0±1,1 a 19,4 ± 5,9 ng/mL, p 0,01) en los grupos G1 y G2, respectivamente). Conclusiones: Atletas con menor grado de entrenamiento, presentan posterior a una maratón un significativo aumento de productos de degradación del colágeno (PIIIPNP) asociado a disminución de la función del ventrículo derecho. Los niveles de galectina-3 plasmática aumentan significativamente en ambos grupos post-esfuerzo independiente del entrenamiento previo.

Abstracts: Introduction: Highly trained athletes show structural cardiac changes as adaptation to overload. Rise in remodeling biomarkers and myocardial fibrosis after intense exercise in athletes has been evidenced; however, the behavior of these biomarkers according to pre-competition training level has not been evaluated. Objective: To evaluate fibrosis biomarkers levels and right ventricle function in marathon runners according to their previous training level, in the period prior to a marathon race and immediately after it. Methods: Thirty-six healthy male marathon runners were included. Subjects were grouped according to their previous training level: Group 1 (G1): ≥100 km/week and Group 2 (G2): <100 km/week. Transthoracic echocardiography along with plasmatic levels of galectin-3 and amino terminal propeptide of type III procollagen (PIIINP) were measured one week previous and immediately after the marathon. Results: Post-effort right ventricle systolic function decreased in G2, together with a significant elevation of PIIIPNP (61±16 to 94±24 ng/mL, p=0.01). These changes were not observed in G1 (from 65±11 to 90±29 ng/mL, p=0.10). Plasma galectin-3 increased significantly in both groups immediately post-exercise (6.8±2.2 to 19.7±4.9 ng/mL, p=0.012, and 6.0±1.1 to 19.4±5.9 ng/mL, p=0.01, in G1 and G2. respectively). Conclusion: Less trained athletes evidenced higher post marathon levels of PIIIPNP which is associated with a decreased global right ventricle function. Plasma galectin-3 levels increased significantly after intense exertion regardless of the intensity of previous training.

Insuficiencia aórtica severa aguda, aspectos diagnósticos de la ecocardiografía: a propósito de un caso clínico / Acute severe aortic regurgitacion echocardiography features: clinical case and review

Resumen: La insuficiencia aórtica severa aguda (IASA) constituye una emergencia quirúrgica; sus principales causas son la endocarditis infecciosa y la disección aórtica. Existen tres hallazgos ecocardiográficos distintivos de dicha patología, que ayudan al diagnóstico y manejo que son: el cierre prematuro de la válvula mitral (CPVM), la insuficiencia mitral diastólica (IMD) y la apertura prematura de la válvula aórtica (APVA). Estos elementos reflejan el severo aumento de la presión de fin de diástole del ventrículo izquierdo (PFDVI) y, si bien son específicos, no son únicos de dicha patología. A continuación, se reporta el caso de un paciente con IASA. Hombre de 36 años, sin antecedentes, consulta por estado infeccioso asociado a insuficiencia cardíaca aguda. Ingresa en shock cardiogénico y la ecocardiografía muestra: ventrículo izquierdo severamente dilatado con función sistólica conservada, dilatación leve de la aurícula izquierda y una endocarditis de válvula aórtica trivalvar asociado a insuficiencia severa. Se identifica, además, la presencia de CPVM y de IMD hallazgos que evidenciaban la severidad de la lesión y lo agudo de la presentación. Se realizó un recambio valvular aórtico de urgencia con una prótesis biológica con buena evolución postoperatoria.

Abstracts: Severe acute aortic regurgitation (SAAR) constitutes a surgical emergency. Its main causes are infective endocarditis and aortic dissection. Three echocardiographic hallmarks aid in its diagnosis and management, namely: premature opening of the aortic valve (POAV), premature mitral valve closure (PMVC) and diastolic mitral regurgitation (DMR), findings that reflect the great increase in left ventricular end-diastolic pressure. Also, these findings are distinctive but not unique to SAAR. We report a 36-year-old male, without past medical history that refers three weeks of malaise, fever and heart failure. At the emergency department, the patient evolved to cardiogenic shock being admitted to the coronary unit. A transthoracic and transesophageal echocardiography revealed a severely dilated left ventricle with normal systolic function, a mild left atrium enlargement and endocarditis of a trileaflet aortic valve with severe regurgitation. Furthermore, PMVC and DMR were identified, findings that portrayed the severe and acute presentation of the disease. A surgical aortic valve replacement was performed uneventfully, and the patient discharged in good conditions.

Hipertrofia ventricular izquierda con patrón de strain característico / Left ventricular hypertrophy with a characteristic strain pattern

Abstracts: A 68 year-old male, with no past medical history, presented progressive shortness of breath on exertion and leg edema during the previous year. Trans-thoracic echocardiography depicted; severe left ventricular hypertrophy with mild systolic dysfunction (LVEF 50% biplane Simpson's method), severe diastolic dysfunction and moderate left atrial enlargement. Left ventricular myocardial deformation imaging by two-dimensional speckle-tracking was paramount for elucidating the differential diagnosis.

Insuficiencia aórtica sistólica: un fenómeno singular / Systolic aortic regurgitation: a remarkable event

La insuficiencia aórtica consiste en el reflujo diastólico de sangre desde la aorta hacia el ventrículo izquierdo, sus mecanismos son múltiples y su magnitud queda determinada por: el área del orificio regurgitante, el gradiente diastólico entre la aorta y el ventrículo izquierdo y la duración de la diástole. En contraposición a esto la insuficiencia aórtica sistólica (IAS) es un fenómeno inusual, con escasos reportes y con una fisiopatología particular. Reportamos tres casos clínicos que ilustran los mecanismos de la IAS. CASO 1: Hombre 54 años, consulta por palpitaciones y disnea, la ecocardiografía transtorácica (ETT) objetiva hipertrofia ventricular izquierda leve con buena función y una valvulopatía aórtica degenerativa con insuficiencia leve, durante el examen se registran ex-trasístoles ventriculares aislados asociado a IAS. CASO 2: Hombre de 61 años con diagnóstico de miocardiopatía dilatada no isquémica en estadio D. Su ETT basal evidencia severa dilatación y disfunción ventricular izquierda (FEVI 19%, DTD 90 mm), insuficiencia mitral funcional severa e insuficiencia aórtica leve. Por dependencia a infusión de inótropos se implanta en Marzo del 2016 un dispositivo de asistencia ventricular izquierda HeartWa-re, en control ambulatorio el dispositivo funcionaba normalmente y el ETT objetiva una significativa disminución de los diámetros del ventrículo izquierdo (DTD 70 mm) una válvula aórtica con apertura intermitente asociado a una IAS en rango leve a moderado. CASO 3: Mujer de 82 años con insuficiencia cardíaca y severa disfunción y dilatación ventricular izquierda, se hospitaliza por infección respiratoria, un ETT muestra insuficiencia mitral funcional severa asociado a IAS moderada.

Aortic regurgitation is a diastolic event in which blood from the aorta regurgitates back to the left ventricle, with several possible mechanisms. Its magnitude is determined by: the regurgitant orifice area, the diastolic gradient between the aorta and the left ventricle and the duration of diastole. In contrast, systolic aortic regurgitation (SAR) is an unusual phenomenon with few cases reported in the literature and with a particular pathophysiology. We report three cases of SAR that illustrate its mechanisms. CASE 1: 54 years-old hypertensive male, refers dyspnea associated with irregular heartbeatsTrans-thoracic echocardiography (TTE) revealed a mild left ventricular hypertrophy with normal function along with a degenerative aortic valve that presented mild regurgitation, isolated premature ventricular contractions were frequently observed associated with mild SAR. CASE 2. 61 years-old diabetic male, with a long history of stage D dilated non ischemic cardiom-yopathy. His last TTE was remarkable for a severe left ventricular dilatation and dysfunction (LVEF 19%, EDD 90 mm), severe functional mitral regurgitation, mild aortic regurgitation and pulmonary hypertension (SPAP 60 mmHg) along with right ventricular dysfunction. Because of inotrope infusion dependency a left ventricular assist device (LVAD) Heartware was implanted. At six months outpatient control, LVAD presented normal function parameters and TTE showed significant reduction in left ventricle diameters (EDD 70 mm) along with mild to moderate SAR. CASE 3: 82 year-old female, longstanding heart failure with severe LV dilatation and dysfunction (LVEF 15%), admitted for a respiratory infection, TTE showed moderate SAR along with functional severe mitral regurgitation.