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Maternal obesity predisposes offspring (F1) to cardiovascular disease. To evaluate basal heart function and ischemia-reperfusion (IR) responses in F1 males and females of obese mothers, female Wistar rats (F0) were fed chow or an obesogenic (MO) diet from weaning through pregnancy and lactation. Non-sibling F1 males and females were weaned to chow at postnatal day (PND) 21 and euthanized at PND 550. Offspring of MO mothers (MOF1) rarely survive beyond PND 650. Hearts were immediately isolated from euthanized F1s and subjected to 30 min ischemia with 20 min reperfusion. Retroperitoneal fat, serum triglycerides, glucose, insulin, and insulin resistance were measured. Baseline left ventricular developed pressure (LVDP) was lower in male and female MOF1 than in controls. After global ischemia, LVDP in control (C) male and female F1 recovered 78 and 83%, respectively, while recovery in MO male and female F1 was significantly lower at 28 and 52%, respectively. Following the IR challenge, MO hearts showed a higher functional susceptibility to reperfusion injury, resulting in lower cardiac reserve than controls in both sexes. Female hearts were more resistant to IR. Retroperitoneal fat was increased in male MOF1 vs. CF1. Circulating triglycerides and insulin resistance were increased in male and female MOF1 vs. CF1. These data show that MO programming reduces F1 cardiac reserve associated with age-related insulin resistance in a sex-specific manner., (Copyright © 2024. Published by Elsevier Inc.)

The incidence of kidney disease is increasing worldwide. Acute kidney injury (AKI) can strongly favor cardio-renal syndrome (CRS) type 3 development. However, the mechanism involved in CRS development is not entirely understood. In this sense, mitochondrial impairment in both organs has become a central axis in CRS physiopathology. This study aimed to elucidate the molecular mechanisms associated with cardiac mitochondrial impairment and its role in CRS development in the folic acid-induced AKI (FA-AKI) model. Our results showed that 48 h after FA-AKI, the administration of N-acetyl-cysteine (NAC), a mitochondrial glutathione regulator, prevented the early increase in inflammatory and cell death markers and oxidative stress in the heart. This was associated with the ability of NAC to protect heart mitochondrial bioenergetics, principally oxidative phosphorylation (OXPHOS) and membrane potential, through complex I activity and the preservation of glutathione balance, thus preventing mitochondrial dynamics shifting to fission and the decreases in mitochondrial biogenesis and mass. Our data show, for the first time, that mitochondrial bioenergetics impairment plays a critical role in the mechanism that leads to heart damage. Furthermore, NAC heart mitochondrial preservation during an AKI event can be a valuable strategy to prevent CRS type 3 development.

There is increasing evidence that either ingested or produced fructose may have a role in metabolic syndrome. While not commonly considered a criterion for metabolic syndrome, cardiac hypertrophy is often associated with metabolic syndrome, and its presence carries increased cardiovascular risk. Recently it has been shown that fructose and fructokinase C (KHK) can be induced in cardiac tissue. Here we tested whether diet-induced metabolic syndrome causes heart disease associated with increased fructose content and metabolism and whether it can be prevented with a fructokinase inhibitor (osthole). Male Wistar rats were provided a control diet (C) or high fat/sugar diet for 30 days (MS), with half of the latter group receiving osthol (MS+OT, 40 mg/kg/d). The Western diet increased fructose, uric acid, and triglyceride concentrations in cardiac tissue associated with cardiac hypertrophy, local hypoxia, oxidative stress, and increased activity and expression of KHK in cardiac tissue. Osthole reversed these effects. We conclude that the cardiac changes in metabolic syndrome involve increased fructose content and its metabolism and that blocking fructokinase can provide cardiac benefit through the inhibition of KHK with modulation of hypoxia, oxidative stress, hypertrophy, and fibrosis.

Our work evaluated cardiac function and mitochondrial bioenergetics parameters in hearts from male Wistar rats subjected to the UUO model during 28 days of progression. We measured markers of kidney damage and inflammation in plasma and renal fibrosis by histological analysis and Western blot. Cardiac function was evaluated by echocardiography and proteins involved in cardiac damage by Western blot. Oxygen consumption and transmembrane potential were monitored in cardiac mitochondria using high-resolution respirometry. We also determined the activity of ATP synthase and antioxidant enzymes such as glutathione peroxidase, glutathione reductase, and catalase. Our results show that, although renal dysfunction is established in animals subjected to ureteral obstruction, cardiac function is maintained along with mitochondrial function and antioxidant enzymes activity after 28 days of injury evolution. Our results suggest that renocardiac syndrome might develop but belatedly in obstruction-induced renal damage, opening the opportunity for treatment to prevent this condition.

Chagas disease is a chronic and potentially lethal disorder caused by the parasite Trypanosoma cruzi , and an effective treatment has not been developed for chronic Chagas disease. The objective of this study was to determine the effectiveness of a therapeutic DNA vaccine containing T. cruzi genes in dogs with experimentally induced Chagas disease through clinical, pathological, and immunological analyses. Infection of Beagle dogs with the H8 T. cruzi strain was performed intraperitoneally with 3500 metacyclic trypomastigotes/kg body weight. Two weeks after infection, plasmid DNA immunotherapy was administered thrice at 15-day intervals. The clinical (physical and cabinet studies), immunological (antibody and cytokine profiles and lymphoproliferation), and macro- and microscopic pathological findings were described. A significant increase in IgG and cell proliferation was recorded after immunotherapy, and the highest stimulation index (3.02) was observed in dogs treated with the pBCSSP4 plasmid. The second treatment with both plasmids induced an increase in IL-1, and the third treatment with the pBCSSP4 plasmid induced an increase in IL-6. The pBCSP plasmid had a good Th1 response regulated by high levels of IFN-gamma and TNF-alpha, whereas the combination of the two plasmids did not have a synergistic effect. Electrocardiographic studies registered lower abnormalities and the lowest number of individuals with abnormalities in each group treated with the therapeutic vaccine. Echocardiograms showed that the pBCSSP4 plasmid immunotherapy preserved cardiac structure and function to a greater extent and prevented cardiomegaly. The two plasmids alone controlled the infection moderately by a reduction in the inflammatory infiltrates in heart tissue. The immunotherapy was able to reduce the magnitude of cardiac lesions and modulate the cellular immune response; the pBCSP treatment showed a clear Th1 response; and pBCSSP4 induced a balanced Th1/Th2 immune response that prevented severe cardiac involvement. The pBCSSP4 plasmid had a better effect on most of the parameters evaluated in this study; therefore, this plasmid can be considered an optional treatment against Chagas disease in naturally infected dogs., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2020 Minerva Arce-Fonseca et al.)

Chagas disease (ChD) is considered an emerging disease in the USA and Europe. Trypanosoma cruzi genes encoding a trans -sialidase protein and an amastigote-specific glycoprotein were tested as vaccines in canine model. The aim for this study was determining the prophylactic effect of these genes in experimentally infected dogs by echocardiography evaluation to compare with our findings obtained by other techniques published previously. Low fractional-shortening values of non-vaccinated dogs suggested an impairment in general cardiac function. Low left ventricular ejection fraction values found in infected dogs suggested myocardial injury regardless of whether they were vaccinated. Low left ventricular diastolic/systolic diameters suggested that progressive heart damage or heart dilation could be prevented by DNA vaccination. Systolic peak time was higher in non-vaccinated groups, increasing vulnerability to malignant arrhythmias and sudden death. High left ventricular volume suggested a decrease in wall thickness that might lead to increased size of the heart cavity, except in the pBCSP plasmid-vaccinated dogs. There was an echocardiographic evidence of left ventricular dilation and reduction in systolic function in experimental chagasic dogs. Echocardiography allowed a more complete follow-up of the pathological process in the living patient than with other techniques like electrocardiography, anatomopathology, and histopathology, being the method of choice for characterizing the clinical stages of ChD.

Objectives: Left atrial disease is an independent risk factor for ischemic stroke and can be used to predict atrial fibrillation (AF). We examine whether left atrial enlargement (LAE) could predict stroke recurrence in patients with embolic stroke of undetermined source (ESUS)., Materials and Methods: Sixty-four patients with a confirmed diagnosis of ESUS were followed for a median of 22 months. Clinical data and echocardiogram findings were recorded. The echocardiogram interpretation was performed centrally and blindly. The Brown ESUS - AF score was used to categorize patients into high (human resource planning [HRP]: score > 2) and low-risk patients (non-HRP score 0-1). Stroke recurrence was the primary outcome., Results: The median age was 62 years (range: 22-85 years); and 33 (51.6%) were men. The median initial NIHSS score was three points (range: 0-27). Twelve (18.8%) patients were categorized as HRP. We found a significant tendency toward recurrence among HRP versus non-HRP patients. Three (25%) HRP versus 2 (3.8%) non-HRP experienced recurrence (OR: 8.3 95% CI 1.2-57; p=0.042); this association was related to severe atrial dilatation (OR: 14.5 95% CI 0.78-277, p = 0.02) and age > 75 years (OR: 12.7 95% CI 1.7-92.2, p = 0.03). We found no differences in recurrence in a univariate analysis., Conclusions: Patients with severe LAE who are 75 years old or older have a significant tendency to experience stroke recurrence., (Copyright: © 2020 Permanyer.)

Myocardial infarction (MI) initiates an inflammatory response that promotes both beneficial and deleterious effects. The early response helps the myocardium to remove damaged tissue; however, a prolonged later response brings cardiac remodeling characterized by functional, metabolic, and structural pathological changes. Current pharmacological treatments have failed to reverse ischemic-induced cardiac damage. Therefore, our aim was to study if clofibrate treatment was capable of decreasing inflammation and apoptosis, and reverse ventricular remodeling and MI-induced functional damage. Male Wistar rats were assigned to (1) Sham coronary artery ligation (Sham) or (2) Coronary artery ligation (MI). Seven days post-MI, animals were further divided to receive vehicle (V) or clofibrate (100 mg/kg, C) for 7 days. The expression of IL-6, TNF-α, and inflammatory related molecules ICAM-1, VCAM-1, MMP-2 and -9, nuclear NF-kB, and iNOS, were elevated in MI-V. These inflammatory biomarkers decreased in MI-C. Also, apoptotic proteins (Bax and pBad) were elevated in MI-V, while clofibrate augmented anti-apoptotic proteins (Bcl-2 and 14-3-3ε). Clofibrate also protected MI-induced changes in ultra-structure. The ex vivo evaluation of myocardial functioning showed that left ventricular pressure and mechanical work decreased in infarcted rats; clofibrate treatment raised those parameters to control values. Echocardiogram showed that clofibrate partially reduced LV dilation. In conclusion, clofibrate decreases cardiac remodeling, decreases inflammatory molecules, and partly preserves myocardial diameters.

Cardiovascular diseases (CVDs) are one of the leading causes of death in patients over 60years with Huntington's disease (HD). Here, we investigated if age-related oxidative stress (OS) is a relevant factor to develop cardiac damage in an in vivo model of striatal neurodegeneration induced by 3-nitropropionic acid (3-NP). We also evaluated the potential effect of tert-butylhydroquinone (tBHQ) to increase the Nrf2-regulated antioxidant response in hearts from adult and aged rats intoxicated with 3-NP. Our results showed that 3-NP-treatment did not induce cardiac dysfunction, neither in adult nor in aged rats. However, at the cellular level, adult animals showed higher susceptibility to 3-NP-induced damage than aged rats, which suggest that chronic oxidative stress ongoing during aging might have induced an hormetic response that probably prevented from further 3-NP damage. We also found that the oxidative unbalance concurs with unresponsiveness of the Nrf2-mediated antioxidant response in old animals., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The catabolism and structure of high-density lipoproteins (HDL) may be the determining factor of their atheroprotective properties. To better understand the role of the kidney in HDL catabolism, here we characterized HDL subclasses and the catabolic rates of apo A-I in a rabbit model of proteinuria. Proteinuria was induced by intravenous administration of doxorubicin in New Zealand white rabbits (n = 10). HDL size and HDL subclass lipids were assessed by electrophoresis of the isolated lipoproteins. The catabolic rate of HDL-apo A-I was evaluated by exogenous radiolabelling with iodine-131. Doxorubicin induced significant proteinuria after 4 weeks (4.47 ± 0.55 vs. 0.30 ± 0.02 g/L of protein in urine, P < 0.001) associated with increased uremia, creatininemia, and cardiotoxicity. Large HDL2b augmented significantly during proteinuria, whereas small HDL3b and HDL3c decreased compared to basal conditions. HDL2b, HDL2a, and HDL3a subclasses were enriched with triacylglycerols in proteinuric animals as determined by the triacylglycerol-to-phospholipid ratio; the cholesterol content in HDL subclasses remained unchanged. The fractional catabolic rate (FCR) of [(131)I]-apo A-I in the proteinuric rabbits was faster (FCR = 0.036 h(-1)) compared to control rabbits group (FCR = 0.026 h(-1), P < 0.05). Apo E increased and apo A-I decreased in HDL, whereas PON-1 activity increased in proteinuric rabbits. Proteinuria was associated with an increased number of large HDL2b particles and a decreased number of small HDL3b and 3c. Proteinuria was also connected to an alteration in HDL subclass lipids, apolipoprotein content of HDL, high paraoxonase-1 activity, and a rise in the fractional catabolic rate of the [(131)I]-apo A-I.

Background: Torrent-Guasp explains the structure of the ventricular myocardium by means of a helical muscular band. Our primary purpose was to demonstrate the utility of echocardiography in human and porcine hearts in identifying the segments of the myocardial band. The second purpose was to evaluate the relation of the topographic distribution of the myocardial band with some post-myocardial infarction ruptures., Methods: Five porcine and one human heart without cardiopathy were dissected and the ventricular myocardial segments were color-coded for illustration and reconstruction purposes. These segments were then correlated to the conventional echocardiographic images. Afterwards in three cases with post-myocardial infarction rupture, a correlation of the topographic location of the rupture with the distribution of the ventricular band was made., Results: The human ventricular band does not show any differences from the porcine band, which confirms the similarities of the four segments; these segments could be identified by echocardiography. In three cases with myocardial rupture, a correlation of the intra-myocardial dissection with the distribution of the ventricular band was observed., Conclusions: Echocardiography is helpful in identifying the myocardial band segments as well as the correlation with the topographic distribution of some myocardial post-infarction ruptures.

Purpose: The pathogenic mechanisms leading to cardiovascular disorders in patients with chronic kidney disease have not been clearly established, although increased oxidative stress has been pointed out as a potential cause. Therefore, as cardiovascular events are still the first cause of death in patients with chronic kidney disease and traditional drugs or therapies rarely have effects on cardiac complications, we sought to determine the effect of curcumin in treating cardiac dysfunction in rats with established chronic renal disease., Methods and Results: Treatment consisted in daily administration of curcumin (120 mg/kg/day) dissolved in 0.05% carboxymethylcellulose via oral gavages during 30 days, beginning from day 30 after 5/6 nephrectomy (5/6Nx). Cardiac function, markers of oxidative stress, activation of PI3K/Akt/GSK3β and MEK1/2-ERK1/2 pathway, metalloproteinase-II (MMP-2) content, overall gelatinolytic activity, ROS production and mitochondrial integrity were evaluated after 1-month treatment. Curcumin restored systolic blood pressure, diminished interventricular and rear wall thickening, decreased left ventricle dimension at end-systole (LVSd) and restored ejection fraction in nephrectomized rats. Also, it diminished metalloproteinase-II levels and overall gelatinase activity, decreased oxidative stress and inhibited the mitochondrial permeability transition pore opening., Conclusion: Our findings suggest that curcumin might have therapeutic potential in treatment of heart disease in patients with established CKD by attenuating oxidative stress-related events as cardiac remodeling, mitochondrial dysfunction and cell death.

OBJECTIVE. The presence of intramyocardial hemorrhage (IMH) is frequent in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PPCI). We aim for the presence IMH using cMRI in patients who presented AMI and did not undergo PPCI or thrombolysis. Cardiac magnetic resonance has proven to be a highly sensitive method for detect its presence in the ischemic damaged tissue. MATERIAL AND METHODS. Patients admitted with diagnosis of ST elevation myocardial infarction > 24 h after initial presentation and without reperfusion therapy were enrolled in the study. All patients underwent cardiac magnetic resonance for detecting edema, microvascular obstruction and intramyocardial hemorrhage, followed by coronary angiography. RESULTS. Seven male patients, with median age of 53 years, were enrolled. Cardiac magnetic resonance showed that all patients had microvascular obstruction and edema. Two of them had intramyocardial hemorrhage in association with spontaneous reperfusion demonstrated by angiography. CONCLUSION. The results of our study show that in patients with acute myocardial infarction, intramyocardial hemorrhage occurs not only after therapeutic, but also after spontaneous reperfusion. This is the first time that its presence is demonstrated by cardiac magnetic resonance.

Castrated rats of either sex were used in this work, and sex hormones of their own gender or cross-sex hormones were administered for 4 months. Animals were then put through 5 min of myocardial ischemia followed by a 5-min reperfusion injury. Electrocardiographic recordings were made and serum was obtained. Sex hormone levels were measured. Cardiac frequency was calculated, arterial pressure was determined, and the levels of lactate dehydrogenase (LDH), creatinine kinase (CK), and thiobarbituric acid reactive species (TBARs) were analyzed. Proinflammatory cytokine levels were measured in homogenized hearts; besides this, five hearts of each experimental group were obtained and fixed for histopathologic analysis. In male rats with estradiol replacement, the incidence of tachyarrhythmias and CK levels were higher when compared to the rest of the animals. Their cytokine levels were also elevated when compared to the group that received testosterone. Estradiol replacement protected female rats from variations in all of the parameters evaluated, whereas testosterone did not show a protective effect. In the presence of testosterone, the incidence of tachyarrhythmia was higher and TBARs, cytokines, CK, and LDH levels were also elevated. The results shown reinforce the idea that cross-sex hormone administration can damage the cardiovascular system.

Curcumin, a natural pigment with antioxidant activity obtained from turmeric and largely used in traditional medicine, is currently being studied in the chemoprevention of several diseases for its pleiotropic effects and nontoxicity. In chronic renal failure, the pathogenic mechanisms leading to cardiovascular disorders have been associated with increased oxidative stress, a process inevitably linked with mitochondrial dysfunction. Thus, in this study we aimed at investigating if curcumin pretreatment exerts cardioprotective effects in a rat model of subtotal nephrectomy (5/6Nx) and its impact on mitochondrial homeostasis. Curcumin was orally administered (120mg/kg) to Wistar rats 7 days before nephrectomy and after surgery for 60 days (5/6Nx+curc). Renal dysfunction was detected a few days after nephrectomy, whereas changes in cardiac function were observed until the end of the protocol. Our results indicate that curcumin treatment protects against pathological remodeling, diminishes ischemic events, and preserves cardiac function in uremic rats. Cardioprotection was related to diminished reactive oxygen species production, decreased oxidative stress markers, increased antioxidant response, and diminution of active metalloproteinase-2. We also observed that curcumin's cardioprotective effects were related to maintaining mitochondrial function. Aconitase activity was significantly higher in the 5/6Nx + curc (408.5±68.7nmol/min/mg protein) than in the 5/6Nx group (104.4±52.3nmol/min/mg protein, P<0.05), and mitochondria from curcumin-treated rats showed enhanced oxidative phosphorylation capacities with both NADH-linked substrates and succinate plus rotenone (3.6±1 vs 1.1±0.9 and 3.1±0.7 vs 1.2±0.8, respectively, P<0.05). The mechanisms involved in cardioprotection included both direct antioxidant effects and indirect strategies that could be related to protein kinase C-activated downstream signaling., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Postconditioning (PostC) cardioprotection has been related to up-regulation of survival kinases; however, the efficacy of PostC and the role of ERK1/2 (extracellular signal-regulated kinase 1/2) remain to be substantiated in hypertension states that may produce "pathologic remodeling." Therefore, in this work we compared PostC effect and assessed the role of ERK1/2 activation in a model of hypertensive dilated cardiomyopathy (DCM), versus normal (Sham) and compensated hypertrophy (CH) models., Methods and Results: Rats were subjected to angiotensin II administration until development of cardiovascular diseases. Then, isolated hearts underwent ischemia followed by PostC and reperfusion. PostC maintained the double product in all groups. PostC reduced infarct size from 36.16 ± 3% to 9.8% ± 2.2 in Sham, from 37.5 ± 2.4% to 12 ± 3% in CH, and from 40 ± 2.4% to 11.55 ± 3% in DCM. Inhibition of the mitogen-activated protein kinase kinase (MEK)/ERK1/2 pathway had different effects on PostC-conferred cardioprotection in the evaluated groups. Interestingly, although phosphatidylinositol-3-kinase activation was negligible in PostC DCM hearts, we observed Akt activation., Conclusions: PostC confers cardioprotection through alternative survival pathways in normal and CH hearts, and cardiac function recovery in DCM relies mainly on MEK/ERK1/2 cascade. Down-regulation of phosphatidylinositide 3-kinase does not affect the cardioprotective response in DCM, because MEK/ERK1/2 cascade may convey direct Akt activation, strengthening downstream signaling., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Potentially fatal cardiac rupture is a complication of myocardial infarction (MI), which can appear in the first hours of the acute event and during the course of the first week. The intramyocardial dissecting hematoma might appear as a component of the rupture during the evolution process. The description of the myocardium as a helical muscular band facilitates the explanation of the fiber dissection. With echocardiography, it is possible to diagnose intramyocardial dissecting hematomas (IDH), determine its location, progression, potential complications, and in some cases its reabsorption. It is necessary to search for neocavitations in the infarcted myocardium and identify the intramyocardial edge that surrounds the defect, as well as the flow inside the myocardial dissection, the pathway of the dissection, and its communication with ventricular cavities, and also to look for the complete or partial reabsorption of the cavitary image. The greater the myocardial dissection is, the worse the prognosis. If the dissecting hematoma is confined to the apical segments, it is more likely to reabsorb spontaneously. Tissue characterization with magnetic resonance during an acute myocardial infarction allows identification of reperfusion injuries with altered microcirculation and intramyocardial hemorrhage (IMH). It is necessary to search for IMH in reperfused patients with ventricular arrhythmias, stunned myocardium, and no reflow. These patients may develop an increased stiffness in the infarcted wall and a major likelihood to develop a parietal rupture. Everything seems to indicate that we are facing the same physiopathological process which can be characterized by 2 complementary imaging methods, echocardiography and magnetic resonance., (© 2012, Wiley Periodicals, Inc.)

Heart failure is one of the most prevalent diseases in industrialized countries. Up to 30% of the patients with advanced heart failure present disturbances in intra-ventricular conduction, and this produce asynchrony of ventricular contractility, leading to further deterioration in heart function. Cardiac resynchronization (TRC) is an increasingly important therapeutic option for a subgroup of patients with heart failure. Several methods have been show to be useful in study the mechanical asynchrony. However, there are discrepancies between the results of the different methods. The echocardiography provides the best parameters in predicting a good response.

Subepicardial aneurysms (SEA) are an infrequent and serious form of subacute cardiac rupture complicating myocardial infarction. An early diagnosis and surgical repair may be life saving. SEA comprise an abrupt interruption of the myocardium, with a narrow neck and thin wall containing only the epicardium. It may progress to fatal cardiorrhexis. We describe the echocardiographic evolution of this type of cardiac rupture and the contribution of contrast-enhanced echocardiography. A possible pathophysiological mechanism is proposed.

Background: In large necropsy studies dissecting intramyocardial hematoma (DIH) with serpiginous tracts across the myocardial fibers has been reported in both the septum and the left ventricle free wall., Methods: We studied 15 patients admitted to the hospital with acute myocardial infarction (AMI) in which DIH was demonstrated by either transthoracic and/or transesophageal and confirmed intraoperatively or by necropsy., Results: In nine patients the hemorrhagic dissection was predominantly in the septum and in the remaining it was in the free wall of the left ventricle (LV). Myocardial infarction involved the left ventricular inferior wall in two, and the anterior wall in 13 patients. The overall mortality was 47%, and in the group with septal hematoma it reached to 78%. Echocardiography disclosed the various acoustic densities of the evolving intramyocardial hematoma, its extension through the hemorrhagic dissection, its spontaneous reabsorption, as well as its communication with the ventricular cavities., Conclusions: Echocardiography is the method of choice for the noninvasive diagnosis of patients with suspected myocardial rupture and intramyocardial dissection postmyocardial infarction.

The study involved 63 patients with an echocardiographic, surgical and histopathologic diagnosis of cardiac myxoma who were seen over a period of 20 years. Tumor recurrence or relapse was documented in five of these patients (7.9%), 3 of whom had a confirmed diagnosis of Carney complex, while one other patient had a probable diagnosis. Genetic studies demonstrated abnormalities in the PRKAR1A gene on chromosome 17 in 2 patients and their immediate family. In 11 of the 58 patients who did not experience relapse of the myxoma, genetic studies failed to show any abnormality. In conclusion, the possible presence of the Carney complex should be investigated in patients with multiple myxomas or with a cardiac myxoma whose location is atypical.

Transesophageal echocardiography has advantages over transthoracic technique in defining morphology of atrial structures. Even though real time three-dimensional echocardiographic imaging is a reality, the off-line reconstruction technique usually allows to obtain higher spatial resolution images. The purpose of this study was to explore the accuracy of off-line three-dimensional transesophageal echocardiography in a spectrum of atrial septal defects by comparing them with representative anatomic specimens.

Hypertrophic cardiomyopathy (HCM) was first described more than a century ago; the characteristic finding is an inappropriate myocardial hypertrophy, occurring in the absence of an obvious cause. Determination of the exact site of the hypertrophy and of the obstruction of the left ventricular outflow tract, in asymmetric septal hypertrophy, establishes which is the best treatment strategy. Forty-one-year-old man with a history of recurrent palpitations without any other symptomatology. The initial electrocardiogram (EKG) showed sinus rhythm with evidence of ventricular left hypertrophy and unspecific changes in ventricular repolarization. The transthoracic echocardiogram showed HCM and mitral regurgitation. The electrophysiological study, under treatment with amiodarone, did not induce ventricular arrhythmias. The 10-years evolution of the EKG showed changes of variable degrees associated with the hypertrophy and systolic overload of the left ventricle. The echocardiographic three-dimensional reconstruction in the long axis revealed the dynamic obstruction of the left ventricular outflow tract. In the hemodynamic study, the existence of a subaortic gradient confirmed the diagnosis and showed an increase of the gradient at the post-extrasystolic beat (Brockenbrough-Braunwald phenomenon). The echocardiographic three-dimensional reconstruction defines more accurately the exact site of the septal hypertrophy and its hemodynamic consequences.

Echocardiography occupies an excellent place in the field of valvular heart disease study. Its presence is being increased in the catheterism and surgery rooms as well as in the intensive cares units. The ultrasound machines development has improved its technology and echocardiographic diagnoses has a greater repercussion in clinical decisions every time. The greater challenge than appears to us is to be able to have prepared enough professionals that know the tool, the physiopathology, the therapeutics modalities, and who can apply and take advantage of the new technological developments for a better cardiological practice.

Acute coronary syndromes involving the right side of the heart are associated with increased mortality, a complex clinical course, and lengthy hospitalization, as well as with frequent mechanical and electrical complications. It is important that the signs and symptoms associated with the spread of ischemic disease to the right heart chambers are recognized so that the patient can be given appropriate treatment, which can improve short-term and long-term prognosis. The purpose of this review was to summarize key aspects of the diagnosis, prognosis and treatment of this condition.

Intramyocardial dissecting hematoma is a form of subacute cardiac rupture complicating acute myocardial infarction. Initially contained within the myocardial wall, the hematoma may expand, rupture into adjacent structures, or spontaneously resolve. However, long-term follow-up is unknown because clinical and serial imaging data are lacking. The purpose of this study was to characterize the early and late myocardial wall changes after transmural myocardial infarction using serial ultrasound examinations of the infarct-related segments. Clinical, electrocardiographic, and echocardiographic features of 8 patients (7 men, mean age 59 years) who presented with acute myocardial infarction and echocardiographically documented intramyocardial dissecting hematoma were analyzed. All patients had precordial echocardiography and 6 underwent transesophageal echocardiography. Differentiating hematoma from trabeculations, thrombus, or pseudoaneurysm was done with contrast and color flow Doppler. Seven patients presented with S-T elevation in V1 to V4, and in 3 the elevation extended to V5, V6, I, and aVL. One patient presented with S-T elevation in II, III, aVF, V3R, and V4R. The most striking feature was persistent S-T elevation of more than 72 hours in all patients. Hematoma consisted of a cysticlike, echolucent cavity variable in size, adjacent to severely hypokinetic or dyskinetic infarct-related segments. Hematoma acoustic characteristics depended on time of evolution. Two patients underwent elective revascularization and the rest were medically treated. Two patients died and 6 were alive at the mean follow-up of 12 months. In conclusion, persistent S-T elevation is an important clue in suggesting intramyocardial dissecting hematoma, which is confirmed by its unique ultrasound appearance. Serial echocardiography is useful in determining its evolving nature, and may guide outcome.

The case of a 16-years old female patient with left atrial myxoma and cerebral embolism is reported. She was subjected to surgical excision of the mass. At 40 months of follow-up she initiates with dyspnea and an aortic murmur is detected. The transthoracic and transesophageal echocardiographic analysis revealed the presence of three tumors: in the left atrium, left and right ventricle. The myxoma of the left ventricle obstructs the aortic valve. We discuss the usefulness of bi-and three-dimensional echocardiography as initial diagnostic method.

Ventricular septal rupture (VSR), which can complicate an acute myocardial infarction (MI), carries a high mortality rate. Because precordial and transesophageal echocardiography can identify the type of rupture and assess right ventricular (RV) function at the patient's bedside, we examined the prognostic significance of echocardiographic patterns in postinfarct VSR by postulating that complex rupture and RV involvement carry a worse prognosis. Seventeen patients (10 men; mean age 66 years) who had confirmed postinfarct VSR underwent precordial and transesophageal echocardiography followed by coronary angiography. Serial 12-lead and right precordial leads were also available. Type of septal rupture was classified as simple or complex based on autopsy-proved echocardiographic criteria. Three patients had inferior wall MI and 14 had anterior wall MI. ST-segment elevation persisted >72 hours in all 3 patients who had inferior wall MI and in 12 who had anterior wall MI. Segmental wall motion abnormalities helped in detecting the left ventricular entry site, and use of unconventional views superimposed with color flow Doppler provided the RV exit site. RV function was better appreciated with transesophageal echocardiography. Two patients who had inferior wall MI and 7 who had anterior wall MI had complex ruptures. All 3 patients who had inferior wall MI and 7 who had anterior wall MI had electrocardiographic and echocardiographic evidence of RV involvement. Mortality rate was higher in patients who had complex rupture (78% vs 38%, p <0.001) and in those who had RV extension (71% vs 29%, p <0.001). In conclusion, persistent ST elevation is a common finding in patients who have postinfarct VSR. Complex VSR and RV involvement are significant determinants of clinical outcome.

The case of a patient with cardiac rupture following a myocardial infarction is presented. The rupture led to the formation of a ventricular pseudoaneurysm that was occupied by a thrombus that sealed the breakthrough point. The patient has survived without surgical treatment during the last 5 years.

The way in which microbubbles (MB) increase the acoustic signal of blood was discovered incidentally during a hemodynamic study 30 years ago. Since then, new techniques and materials have been developed, looking for possible applications. Stability of MB has been increased, their size has been diminished, and interactions between MB and ultrasound have been understood. In this paper, we show the ways in which MB have been demonstrated or, at least, suggested to be useful in the fields of cardiological diagnosis and treatment.

Objective: The aim of this study is to evaluate the effect of trimetazidine (TMZ) on myocardial systolic dysfunction resulting from an isolated episode of induced coronary ischemia., Methods: In a double-blinded randomized design we studied 13 mongrel anesthetized dogs of either sex (6 of them treated with oral TMZ previously). The anterior descending coronary artery was totally occluded during 15 minutes followed by 60 minutes of reperfusion. Global and regional cardiac variables were recorded in control and ischemic areas., Results: There were no significant differences between TMZ and placebo series with respect to global cardiac function variables. Both series showed no significant variations in global variables during the ischemia-reperfusion process. The shortening fraction in the ischemic area fell significantly during the ischemic period in both TMZ and placebo series reaching dyskinetic values. Myocardial contractility dysfunction persisted after 60 minutes of reperfusion in both series with no significant differences (41% vs 50% placebo)., Conclusions: Contrary to shorter and repeated occlusion periods, myocardial contractility recovery after a complete episode of ischemia did not show significant differences between TMZ-treated and placebo series.

The utilization of intracardiac echocardiography (ICE) is a recent alternative in the control of procedures in the Cath Lab. In this paper we presents the results of a pilot study, in 10 patients submitted to total correction of its congenital heart disease, in who the analysis of the surgical results was done in base to the application of intracardiac echocardiography in operations room. In all the patients it was possible to obtain adequate images with ICE, there was a case false negative, a Total anomalous return Pulmonary Veins, in whom there not indentified a obstruction in right pulmonary veins flow. We conclude that ICE is a good alternative in the evaluation of surgical results.

Three-dimensional echocardiography is becoming an important tool within the diagnostic arsenal in cardiovascular diseases. This study provides, in an easy way, a new dynamic and functional point of view of the anatomy of the heart and of the vascular tree. This review describes its principles, discusses its indications, and its place within clinical evaluations. Its capabilities. Advantages in relation with other imaging methods, its current situation and, of course, its own limitations are also commented.

Williams-Beurer syndrome is an unusual genetic alteration associated with congenital heart defects. We present the capabilities of three-dimensional echocardiography in the study of the cardiopathy associated with this syndrome.

Background: The role of the right atrium in adaptation to the hemodynamic changes produced by extension of myocardial infarction (MI) of the left ventricular inferior wall to the right ventricle is fundamental., Hypothesis: The aim of this study was analyze a group of patients with MI with extension of right chambers, and particularly right atrial alterations, by transesophageal echocardiography and to correlate it with clinical and angiographic variables., Methods: Thirty patients with right ventricular (RV) MI involving obstruction of the right coronary artery without stenosis of the left coronary artery were included; 18 underwent early reperfusion. Transesophageal echocardiography was performed on all within 5 days of coronary angiography. Follow-up was continued from hospitalization to the present., Results: When patients with right atrial ischemia were compared with those with normal right atrium, the RV wall movement score was significantly greater in the group with right atrial ischemia, severe RV dilatation was more frequent, and association with proximal occlusion of the artery responsible for the MI, as well as absence of right atrial branches and poor collateral circulation, were significant. Hospitalization was more prolonged in this group, and there was a higher incidence of arrhythmias, complete atrioventricular block, and mortality., Conclusions: Right atrial ischemia associated with RV infarction leads to a higher incidence of complications and higher mortality. Transesophageal echocardiography is a safe, reproducible technique that provides detailed anatomic information about right chambers and aids in the determination of prognosis and therapeutic decisions.

The ability to visualize with dynamic 3D views the images obtained from the 2D study was the obviously next step in the evolution of echocardiography. Today, thanks to the technological evolution, the capability of obtaining and processing images with computers support has emerged with a great potential. Three-dimensional echocardiography facilitates spatial recognition of intracardiac structures, is surpassing the experimental phase quickly and its accuracy has been validated in vivo.

The adequate study of the left atrial appendage is an echocardiographic challenge. The purpose of this study was to assess the ability of 3-dimensional echocardiography in reconstructing this potentially complex structure.

Background: Infective endocarditis (IE) occurs with significant frequency in patients with congenital heart disease. The complications leading to increased morbidity and mortality may be detected by echocardiographic examination. This study was undertaken in order to identify echocardiographic findings that influence the outcome of patients with congenital heart disease and IE., Methods: Twenty-five patients with an average age of 28 years were selected and divided into two groups according to evolution. Group I included patients who survived the infectious process, while Group II included patients who died during hospitalization or after release., Results: Aortic valve disease was the most frequent anomaly. The clinical finding of most relevance for evolution during hospitalization was heart failure. Acute kidney failure and multiple organ failure from sepsis were the most common complications in patients who died. Echocardiograms established the diagnosis in all cases. Transesophageal studies revealed all periaortic abscesses., Conclusions: Echocardiography makes it possible to identify and evaluate complications associated with elevated morbidity and mortality in patients with congenital heart disease and IE.

We evaluated the hemodynamic response of patients with chronic aortic regurgitation and decreased ejection fraction (EF), mean value +/- SD (37 +/- 9), to dobutamine stress echocardiography (DSE). Eleven patients were studied with DSE. Nine patients were in New York Heart Association (NYHA) Class II and two in NYHA Class III. Ten patients received medical treatment in the only other periodic evaluation. With DSE in nine patients, a significant decrease in left ventricular end-diastolic and end-systolic diameters (LVEDD and LVESD) as well as LV end-diastolic and end-systolic volumes (LVEDV and LVESV) was documented in comparison to resting values. EF and fractional shortening (FS) improved significantly with DSE. Systolic wall stress (SWS) and pulmonary arterial systolic pressure (PASP) did not change. Average follow-up was 6.7 months. Three patients underwent valve replacement with mechanical prostheses. Two of them are in NYHA Class I and the other died of LV failure 3 days after surgery. One patient deteriorated beyond surgical treatment and was in NYHA Class II. The other seven patients remain in NYHA Class II and await valve replacement. In patients with chronic aortic regurgitation and depressed EF, the variables relevant to myocardial reserve appear to be EF, FS, LVEDD, LVESD, LVEDV, and LVESV.

We present the 2-dimensional findings and 3-dimensional reconstruction of images from an 18-year-old patient with unroofed coronary sinus, persistent left superior vena cava, a common atrium with levoisomerism, ventricular septal defect, and double-outlet right ventricle. The left superior vena cava showed continuity with the floor of the coronary sinus. Diagnosis of the constellation of anomalies established by transesophageal reconstruction clarified the continuity of the coronary sinus with left superior vena cava and atrial wall.

Cor triatriatum dexter is an unusual cardiac abnormality with division between the sinus and primitive atrial portions of the right atrium. Three-dimensional echocardiography is a novel technique that defines this entity.

The echocardiographic findings of an intramyocardial dissecting hematoma that formed after an extensive acute myocardial infarction of the anterior wall of a 42-year- old man are described. Serial transesophageal studies were used to construct 3-dimensional images that clarified the participation of various myocardial layers that surrounded the dissecting hematoma. The patient was successfully treated with intra-aortic balloon counterpulsation and subsequently coronary artery bypass grafting. Intramyocardial dissecting hematoma is a rare complication of acute infarction; differential diagnosis must be made with pseudoaneurysm by establishing integrity of epicardium and with intracavitary thrombosis by identifying the endomyocardial layer surrounding the neoformation and associated wall movement.

Unlabelled: The potential cardioembolic sources for ischemic stroke in patients younger than 40 years could be asymptomatic. The purpose of this study is to justify routine implementation of transesophageal echocardiography (TEE) in the study of young patients with ischemic stroke., Material and Methods: 34 patients younger than 40 years with ischemic stroke were studied with TEE complemented with contrast study, looking for potential cardioembolic sources or intracardiac shunts., Results: 19 patients were male and 15 female with ages between 18-40 years (average 31 years). None had cardiac signs or symptoms. Eleven anomalies were detected in 20 patients (58.8%); of these, only 3 were considered as probably coursing with cardioembolic sources: patent foramen ovale (PFO), mitral valve prolapse, and ventricular enlargement, which were found in 12 patients (35.29%). In patients with cardiovascular anomalies, we found a hypercoagulable state, associated in eight patients with PFO (four patients), two with valvular thickening, and two with valvular nodules., Conclusions: In patients younger than 40 years with ischemic stroke, TEE is useful in detecting direct and indirect cardiac sources of embolism, even in those patients with unsuspected cardiac disease.

Fifty-four percent of left atrial appendages have two lobes. The number ranges from one to four lobes. We describe three patients with accessory lobes of the left atrial appendage studied with multiplanar transesophageal echocardiography (TEE). In one patient there was evidence of thrombi in the accessory lobe.