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RESUMEN: La cardiomiopatía amiloide por transtiretina (CATTR) es una enfermedad caracterizada por depósito extracelular de fibrillas amiloides en el miocardio, a partir de transtiretina mal plegada, generando una miocardiopatía restrictiva. Esta proteína mal plegada puede tener origen hereditario o adquirido, siendo más frecuente en adultos mayores. La CA-TTR ha surgido como una causa subdiagnosticada de insuficiencia cardíaca con fracción de eyección preservada (IC FEp). El pilar fundamental para su diagnóstico es la alta sospecha clínica, basada en diversas banderas de alerta ya que la sintomatología que provoca suele ser inespecífica. Como veremos en esta revisión, el diagnóstico puede sustentarse con la cintigrafía ósea, reservando para situaciones particulares la toma de biopsia. Con el advenimiento de nuevas terapias que impactan en la sobrevida de esta enfermedad, el tiempo para realizar el diagnóstico certero y la diferenciación de otras causas de amiloidosis cardíaca como la de cadenas livianas, se ha tornado crucial.

Recently, we have witnessed major improvements in cancer treatment. Early diagnosis and development of new therapies have reduced cancer-related mortality. However, these new therapies, along with greater patient survival, are associated with an increase in untoward effects, particularly in the cardiovascular system. Although cardiotoxicity induced by oncologic treatments affects predominantly the myocardium, it can also involve other structures of the cardiovascular system, becoming one of the main causes of morbidity and mortality in those who survive cancer. The main objective of cardio-oncology is to achieve the maximum benefits of oncologic treatments while minimizing their deleterious cardiovascular effects. It harbors the stratification of patients at risk of cardiotoxicity, the implementation of diagnostic tools (imaging techniques and biomarkers) for early diagnosis, preventive strategies and early treatment options for the complications. Herein, we discuss the basic knowledge for the implementation of cardio-oncology units and their role in the management of cancer patients, the diagnostic tools available to detect cardiotoxicity and the present therapeutic options.

Ethnicity may affect graft longevity and recipient mortality after heart transplantation (HTx). We hypothesized that differences in ethnic origin between Arabs and Jews undergoing HTx in Israel may contribute to differences in long-term outcomes.The study population comprised all 254 patients who underwent HTx between 1991 and 2017 in a tertiary medical center located in the center of Israel. Patients were categorized as either Jews (226 patients, 89%) or Arabs (28 patients, 11%). The primary end point was cardiac allograft vasculopathy (CAV), secondary end points were cardiovascular (CV) mortality and the combined end point of CAV/CV mortality.In comparison with Jews, Arab patients were significantly younger (ave. age 42 vs. 50) and had shorter in-hospital stay (45 vs. 80 days). However, Kaplan-Meier survival analysis showed that at 10 years of follow-up CAV rates were significantly higher among Arabs (58%) compared with Jews (23%; log-rank P = 0.01) for the overall difference during follow-up. Similar results were shown for the separate end point of CV mortality and the combined end point of CAV/CV mortality. Multivariate analysis, which controlled for age, gender, statin treatment, and other potential confounders, showed that Arab recipient ethnic origin was associated with a significant 2.5-fold (p = 0.01) increase in the risk for CAV; a 4-fold increase in the risk for CV mortality (p = 0.001); and approximately 4-fold increase in the risk for the combined end point (p = 0.001). These findings were validated by propensity score analysis.Our data suggest that Arab ethnic origin is associated with a significantly increased risk for CAV and mortality following HTx. Suggested explanations contributing to ethnic disparities in Israel include socioeconomic, environmental and genetic factors. Further studies are required to evaluate whether more aggressive risk factor management in the Israeli Arab population following HTx would reduce CAV and CV mortality in this high-risk population. Increased awareness and early intervention of the Israeli healthcare system and cooperation with the Arab community is of paramount importance.

At present, heart failure (HF) is a worldwide problem, characterized by a high morbidity and mortality. In industrialized countries or regions, such as the United States, Canada, and western European countries, HF has a prevalence of 1.5% to 2.7%. Chile represents a growing economy in Latin America; however, the relatively high cost of more advanced therapies, in addition to other variables (ie, adequate and timely evaluation by HF specialists), makes access difficult for patients with HF. In this article, the authors review the principal difficulties in accessing advanced HF therapies in Chile, as a model of developing country.

Recently, we have witnessed major improvements in cancer treatment. Early diagnosis and development of new therapies have reduced cancer-related mortality. However, these new therapies, along with greater patient survival, are associated with an increase in untoward effects, particularly in the cardiovascular system. Although cardiotoxicity induced by oncologic treatments affects predominantly the myocardium, it can also involve other structures of the cardiovascular system, becoming one of the main causes of morbidity and mortality in those who survive cancer. The main objective of cardio-oncology is to achieve the maximum benefits of oncologic treatments while minimizing their deleterious cardiovascular effects. It harbors the stratification of patients at risk of cardiotoxicity, the implementation of diagnostic tools (imaging techniques and biomarkers) for early diagnosis, preventive strategies and early treatment options for the complications. Herein, we discuss the basic knowledge for the implementation of cardio-oncology units and their role in the management of cancer patients, the diagnostic tools available to detect cardiotoxicity and the present therapeutic options.

Systemic endothelial dysfunction and increased oxidative stress have been observed in pulmonary arterial hypertension (PAH). We evaluate whether oxidative stress and endothelial dysfunction are associated with acute pulmonary vascular bed response to an inhaled prostanoid in PAH patients.Fourteen idiopathic PAH patients and 14 controls were included. Oxidative stress was assessed through plasma malondialdehyde (MDA) levels and xanthine oxidase (XO) and endothelial-bound superoxide dismutase (eSOD) activity. Brachial artery endothelial-dependent flow-mediated vasodilation (FMD) was used to evaluate endothelial function. Hemodynamic response to inhaled iloprost was assessed with transthoracic echocardiography.PAH patients showed impaired FMD (2.8 ± 0.6 vs. 10.7 ± 0.6%, P.01), increased MDA levels and XO activity (0.6 ± 0.2 vs. 0.3 ± 0.2 μM, P.01 and 0.04 ± 0.01 vs. 0.03 ± 0.01 U/mL, P = .02, respectively) and decreased eSOD activity (235 ± 23 vs. 461 ± 33 AUC, P.01). Iloprost improved right cardiac output (3.7 ± 0.6 to 4.1 ± 1.2 L/min, P = .02) and decreased pulmonary vascular resistance (4.1 ± 1.1 to 2.9 ± 0.9 Wood U, P = .01). Changes in right cardiac output after prostanoid inhalation correlated significantly with baseline eSOD activity and FMD (Rho: 0.61, P.01 and Rho: 0.63, P = .01, respectively).PAH patients show increased systemic oxidative stress and endothelial dysfunction markers. Response to inhaled prostanoid is inversely related to both parameters.

Increased oxidative stress in heart failure (HF) leads to inflammation and endothelial dysfunction (ED). Both statins and allopurinol have known anti-oxidant properties, but their utility in HF has not been fully assessed.This investigation was a prospective, double-blind, double-dummy study, performed between March 2007 and June 2009. Seventy-four HF patients, with New York Heart Association (NYHA) Class II or III status and left ventricular ejection fraction (LVEF)40%, were included. Patients received placebo during 4 weeks and were then randomized to receive 4 weeks of either atorvastatin 20 mg/day plus placebo (ATV+PLA group) or atorvastatin 20 mg/day orally plus allopurinol 300 mg/day orally (ATV+ALLO group). Malondialdehyde (MDA), extracellular superoxide dismutase (ecSOD) activity and uric acid (UA) levels, among others, were determined at baseline and after 4 weeks of treatment. ED was assessed by flow-dependent endothelial-mediated vasodilation (FDD), and functional capacity by 6-minute walk test (6MWT).Thirty-two patients were randomized to ATV+PLA and 38 to ATV+ALLO. Mean age was 59 ± 2 years, 82% were male, and 22% had an ischemic etiology. Hypertension was present in 60% and diabetes in 15% of those studied. No significant differences were observed between baseline measurements and after placebo. After 4 weeks of treatment, both groups showed a significant decrease on MDA (0.9 ± 0.1 to 0.8 ± 0.1 and 1.0 ± 0.5 to 0.9 ± 0.1 μmol/liter, p = 0.88), UA (7.4 ± 0.4 to 6.8 ± 0.3 and 7.2 ± 0.4 to 5.0 ± 0.3 mg/dl, p0.01) and FDD (3.9 ± 0.2% to 5.6 ± 0.4% and 4.6 ± 0.3% to 7.1 ± 0.5%, p = 0.07) with increased ecSOD activity (109 ± 11 to 173 ± 13 and 98 ± 10 to 202 ± 16, U/ml/min, p = 0.41) and improved 6MWT (447 ± 18 to 487 ± 19 and 438 ± 17 to 481 ± 21 m, p = 0.83), with all values for ATV+PLA and ATV+ALLO, respectively; p-values are for comparison between groups after treatment.Short-term ATV treatment in heart failure (HF) patients reduces oxidative stress and improves FDD and functional capacity. These beneficial effects are not strengthened by the addition of allopurinol.

BACKGROUND: Pulmonary artery hypertension (PAH) is a progressive disease with high mortality. Major advances had been made in the treatment of this condition during the last decade. AIM: To characterize the clinical evolution and mortality of a cohort of Chilean patients. MATERIAL AND METHODS: Seventeen patients with PAH diagnosed in the last 10 years in two Chilean hospitals were enrolled. Measurements at diagnosis included hemodynamic variables and 6-minute walk test. The patients were followed clinically for 3 years and the observed mortality was compared with that predicted by the prognostic equation proposed by the historic registry of the National Institutes of Health (NIH). RESULTS: The mean age of patients was 45 years and 80% had an idiopathic PAH. The mean median pulmonary artery pressure was 57 ± 15 mmHg, the cardiac index was 2.4 ± 0.7 l/min/m² and the right atrial pressure was 12 ± 8 mmHg. The 6-minute walk distance was 348 ± 98 m. All patients received anticoagulants. Eighty two percent received ambrisentan, 12% received bosentan, 29% received iloprost and 24% sildenafil. At the end of follow-up only 3 patients had died, with an observed survival rate of 88, 82 and 82% at 1, 2 and 3 years, respectively. In contrast, the survival calculated according to the predictive formula of the NIH was 67, 56 and 45%, respectively. Among surviving patients, an improvement in exercise capacity was observed after one year (p < 0.05). CONCLUSIONS: The observed survival rate was significantly better than that estimated according to historical data. Furthermore, therapy was associated with an improvement in functional capacity after one year. This prognostic improvement is consistent with data of other contemporary registries published after the NIH Registry.

Background: Heart failure (HF) is characterized, among other features, by the development of alterations in myocardial energy metabolism, involving a decrease in glucose utilization and increased free fatty acid uptake by cardiomyocytes, associated with decreased deposits of high-energy phosphates (creatine phosphate/ creatine transporter). Magnetic resonance (MR) imaging allows a direct and noninvasive assessment of myocardial metabolites. Aim: To measure myocardial creatine and lipids by MR spectroscopy among patients with HF. Material and Methods: Cardiac MR spectroscopy (1.5 Tesla) with Hydrogen antenna and single voxel acquisition was performed in fve patients with non-ischemic heart failure, aged 58 ± 9.7 years, (60% males) and 5 healthy volunteers matched for age and sex. We analyzed the signals of creatine (Cr), lipids (L) and water (W) in the interventricular septum, establishing the water/lipid (W/L) and water/creatine (W/Cr) index to normalize the values obtained. Results: Among patients, left ventricular ejection fraction was 32 ± 6.9%, 60% were in functional capacity II, 60% had hypertension and one was diabetic. Spectroscopic curves showed a depletion of total Cr, evidenced by the W/ Cr index, among patients with heart failure, when compared with healthy controls (1.46 ± 1.21 and 5.96 ± 2.25 respectively, p < 0,05). Differences in myocardial lipid content, measured as the W/L index, were not significant (5.06 ± 2.66 and 1.80 ± 1.62 respectively, p = 0.08). Conclusions: Among patients with heart failure of non-ischemic etiology, there is a depletion of creatine levels measured by MR spectroscopy.

Background: Pulmonary Arterial Hypertension (PAH) is characterized by endothelial dysfunction and vascular remodeling. Several lines of experimental evidence indícate that oxidative stress plays an important role in the pathogenesis of PAH. The role of oxidative stress and its relation with peripheral endothelial function and pulmonary vascular response to vasodilators remains unknown. Aim: To evalúate whether systemic oxidative stress and endothelial dysfunction markers are associated with the response of the pulmonary vascular bed to inhaled vasodilators in PAH patients. Methods: Cross-sectional study Fourteen patients with PAH and 14 age and gender-matched controls were in-cluded. Systemic oxidative stress was assessed through plasma malondialdehyde (MDA), xanthine oxidase (eXO) levéis and endothelial-bound superoxide dis-mutase (eSOD) activity Brachial artery endothelial-de-pendent flow-mediated vasodilation (FDD) was used to evalúate endothelial function. Right ventricular function and pulmonary vascular bed reactivity to inhaled vasodilators was determined with echocardiography in PAH patients. Results: Compared to controls, PAH patients showed impaired FDD (2.8 ± 0.6 vs 10.7% ± 0.6, p< 0.01), increased MDA and eXO levéis (0.61 ± 0.17 vs 0.34 ± 0.15μM, p

Increased serum uric acid has been identified as an independent risk factor for cardiovascular disease. However, because of its antioxidant capacity, uric acid may play a beneficial role in endothelial function. This paradoxical relationship between uric acid and endothelial function in chronic heart failure patients remains poorly understood. Thirty-eight chronic heart failure patients (New York Heart Association functional class II-III, mean age 58+/-10 years and mean left ventricular ejection fraction 25+/-8%) and twelve age-and-sex-matched healthy controls were studied. Chronic heart failure patients showed higher uric acid levels (7.3+/-2.3 mg/dL vs. 6.1+/-0.2 mg/dL, p

OBJECTIVE To evaluate the effects of glucose-insulin-potassium (GIK) therapy on infarct size and left ventricular function when used as an adjuvant therapy to primary angioplasty. DESIGN Prospective, randomized, double-blind, placebo-controlled study. SETTING Cardiac intensive care unit at a university hospital. PATIENTS Thirty-seven patients with acute myocardial infarction for whom primary angioplasty was indicated. INTERVENTIONS Eligible patients were randomized by a blinded pharmacist to GIK solution (30% glucose in water with insulin 50 U/L, and KCl 40 mM/L) vs. placebo at 1.5 mL/kg/hr for 24 hrs. MEASUREMENTS AND MAIN RESULTS Tc 99m sestamibi myocardial scintigraphy was performed at admission and at 3 months. Primary end points were the changes in left ventricular ejection fraction (LVEF) and the size of salvaged myocardium. Baseline clinical characteristics were similar in both groups. At the 3-month follow-up, a significant overall decrease in infarct size (37 +/- 16% vs. 12 +/- 10%, p

O stress has been implicated in the pathogenesis of chronic heart failure (HF). Different studies have shown that reactive oxygen species are produced in the failing myocardium, causing injury in cardiac myocytes.1–3 Different factors classically associated with cardiomyocyte dysfunction and death in chronic HF, such as increased plasma catecholamine levels, are well-known stimuli for the generation of reactive oxygen species.4 In patients with advanced chronic HF at rest, the circulating norepinephrine concentrations are much higher, generally 2 to 3 times the level found in normal subjects.5,6 During comparable levels of exercise, much greater elevations in circulating norepinephrine occur in patients with chronic HF than in normal subjects. However, despite the increase in norepinephrine with exercise, patients with chronic HF had an attenuated heart rate response to exercise; this finding has been attributed to postsynaptic desensitization of the -adrenergic receptor pathway.7 A relation between cardiac exercise capacity and oxidative stress determined by malondialdehyde (MDA) plasma levels, a marker of lipid peroxidation, has been proposed.8 Experimental data also suggest that hydrogen peroxide may attenuate the -adrenoceptor– linked signal transduction in the heart by changing the functions of Gs proteins and the catalytic subunit of the adenylyl cyclase.9 In the present study we investigated the association between MDA plasma levels, catecholamines at peak exercise, and impaired heart rate response to exercise in patients with chronic HF. • • • We enrolled 27 patients with chronic HF secondary to coronary heart disease (n 15) or idiopathic dilated cardiomyopathy (n 12). They fulfilled the following criteria: (1) chronic stable HF in New York Heart Association functional classes II to IV; (2) ability to complete a symptom-limited treadmill exercise test; (3) evidence of left ventricular (LV) dilation and LV ejection fraction 40% as determined by radionuclide-gated pool scan; and (4) treatment with diuretics, digitalis, and vasodilators. We excluded patients with (1) coronary artery bypass surgery, angioplasty, or myocardial infarction in the last 6 months; (2) chronic angina; (3) uncontrolled hypertension (systolic blood pressure 160 mm Hg or diastolic blood pressure 90 mm Hg); (4) hypertensive myocardiopathy; (5) change in maintenance therapy or use of blockers in the last 2 months; (6) implanted pacemaker; (7) significant valvular disease; and (8) presence of other conditions that affect determination of oxidative stress status, such as renal insufficiency (plasma creatinine 2 mg/dl), autoimmune diseases, neoplasia, advanced liver or pulmonary disease, and acute or chronic inflammation. All patients signed an informed consent approved by our institutional review board and ethics committee. For clinical assessment we used New York Heart Association functional class and the Mahler et al10 clinical score (range 0 to 12 points), which evaluates the severity of dyspnea. The score depends on ratings for 3 different categories: functional impairment, magnitude of task, and magnitude of effort. Dyspnea is rated in 5 degrees from 0 (severe) to 4 (unimpaired) for each category. The ratings for each of the 3 categories are added to form the score. LV end-diastolic and LV end-systolic diameters were determined by Doppler 2-dimensional echocardiography, and LV ejection fraction was determined by radionuclide ventriculography. Each patient performed a 6-minute corridor walk test and a maximal exercise test with gas exchange. Plasma norepinephrine and epinephrine specimens were collected from an indwelling venous line after patients had been in the supine position in a quiet room for 30 minutes. Measurements were repeated at maximal exercise. Determination of catecholamines was performed by high-performance liquid chromatography using a commercial kit (Chromsystems Instruments & Chemicals GmbH, Munchen, Germany). The interand intra-assay coefficients were 6% and 5%, respectively. The ratio of the increment in heart rate divided by the increment in norepinephrine from From the Department of Cardiovascular Diseases, Faculty of Medicine, P. Catholic University of Chile; and the Departments of Biochemistry and Molecular Biology and Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, Faculty of Medicine and the FONDAP Center for Molecular Studies of the Cell, University of Chile, Santiago, Chile. Dr. Castro was supported in part by Grant FONDECYT 1010992, Santiago; and Dr. Lavandero was supported in part by Grant FONDAP 15010006, Santiago, Chile. Dr. Castro’s address is: Department of Cardiovascular Diseases, Faculty of Medicine, P. Catholic University of Chile, Marcoleta 367, Santiago, Chile. E-mail: pcastro@med.puc.cl. Manuscript received January 23, 2003; revised manuscript received and accepted April 7, 2003.

OBJECTIVE To evaluate the oxidative stress status and the modification with glucose-insulin-potassium (GIK) therapy in patients with acute myocardial infarction undergoing primary percutaneous transluminal coronary angioplasty. DESIGN Prospective, randomized, double-blinded, placebo-controlled study. SETTING Cardiac intensive care unit at the university hospital. PATIENTS Twenty patients were randomized to GIK solution (30% glucose in water with insulin 50 IU/L, and KCl 40 mM) vs. placebo (normal saline) at 1.5 mL/kg/hr for 24 hrs. The control group was 15 healthy volunteers with no heart disease. INTERVENTIONS Eligible patients were randomized by a blinded pharmacist, patients with acute myocardial infarction were treated by primary percutaneous transluminal coronary angioplasty and randomized to GIK or placebo (saline solution). Primary angioplasty was successful in nine of ten patients (90%) and ten of ten patients (100%) in the GIK and placebo groups, respectively. Nine (100%) and six (60%) patients from GIK and placebo groups, respectively, underwent stent implantation. MEASUREMENTS AND MAIN RESULTS We determined plasma levels of lipid peroxidation estimated by the malondialdehyde assay, superoxide dismutase, glutathione peroxidase, and catalase erythrocyte activities at admission and 0.5 and 24 hrs after angioplasty. Baseline determinations were compared with a control group (n = 15). Baseline clinical characteristics and time to treatment (4.5 +/- 3.5 hrs) were similar between groups. Angioplasty success rate (Thrombolysis in Myocardial Infarction [TIMI] 3 flow with residual stenosis < or = 30%) was 90% and 100% in GIK and placebo groups, respectively. Patients with acute myocardial infarction had an increase of malondialdehyde at baseline (2.9 +/- 1.7 vs. 1.1 +/- 0.3 microM, p

A 32-year-old man infected with HIV presented to the emergency department of our hospital reporting pain, coldness, paresthesias, and cyanosis in both feet and hands. The symptoms had started 3 days before, with lower extremities claudication at 200 m, which progressed to rest pain the day of admission; it was worse on the right foot. He was on chronic antiretroviral therapy with 300 mg QID tenofovir (Viread), 300 mg BID abacavir (Ziagen), and two 200/50 mg BID lopinavir/ritonavir (Kaletra). His CD4 cell count was 245 cells/mm and his HIV viral load was 45 copies/mL. When directly interviewed, the patient remembered that he had taken a single dose of ergotamine (1 mg) for migraine 24 hours before the onset of symptoms. He denied any recent drug intake. On examination, his 4 extremities were cold, cyanotic, and pulseless (Figure 1A). Only femoral pulses were weakly palpable. Plethysmography revealed bilateral multilevel ischemia, with severe proximal disease …

Background— Identification of coronary ischemia may enable targeted diagnostic and therapeutic strategies for acute heart failure. We determined the risk of 30-day mortality associated with ischemic ECG abnormalities in patients with acute heart failure. Methods and Results— Among 8772 patients (53.4% women, median 78 years [Q1, Q3: 68,84]) presenting with acute heart failure to 86 hospital emergency departments in Ontario, Canada, Q-waves, T-wave inversion, or ST-depression were present in 51.8% of subjects. However, presence of ST-depression was the only finding associated with 30-day mortality with adjusted odds ratio 1.24 (95% confidence interval [CI], 1.02–1.50). Using continuous net reclassification improvement, addition of ST-depression to the Emergency Heart failure Mortality Risk Grade model reclassified 16.9% of patients overall, and 29.3% of those with a history of ischemic heart disease (both P c -statistic 0.801), with 0.57% mortality rate in the lowest risk decile. Adjusted odds ratios for 30-day mortality were 2.81 (95% CI, 1.48–5.31; P =0.002) in quintile 2, 7.41 (95% CI, 4.13–13.30; P P P P Conclusions— Presence of ST-depression on the ECG reclassified risk of 30-day mortality in patients with acute heart failure, identifying both high- and low-risk subsets.

Radionuclide isotopic ventriculography with phase analysis was performed in 30 patients with stable heart failure (HF), determining left ventricular (LV) and interventricular contraction synchrony at baseline and after 6 months of treatment with maximal tolerated doses of carvedilol. Patients with HF had significant ventricular dyssynchrony compared with a normal population. The 50th percentile of patients with the greatest dyssynchrony at baseline showed significant improvement in ventricular synchrony after receiving carvedilol, and this was correlated positively with a reduction in end-diastolic LV volumes.

Background Ventricular dyssynchrony is a common finding in patients with heart failure (HF), especially in the presence of conduction delays. The loss of ventricular synchrony leads to progressive impairment of contractile function, which may be explained in part by segmental abnormalities of myocardial metabolism. However, the association of these metabolic disarrangements with parameters of ventricular dyssynchrony and electrocardiography (ECG) findings has not yet been studied. Methods Our aim was to determine the correlation between the presence of left bundle branch block (LBBB) with left ventricular (LV) mechanical synchrony assessed by multiple-gated acquisition scan (MUGA) and with patterns of 18-fluorodeoxyglucose ( 18 FDG) uptake in patients with non-ischemic heart failure. Twenty-two patients with non-ischemic cardiomyopathy, LV ejection fraction (LVEF) ≤45% and New York Heart Association (NYHA) Functional Class II or III symptoms under standard medical therapy were included, along with 10 healthy controls matched for age and gender. A 12-lead ECG was obtained to measure the length of the QRS. Mechanical LV synchrony was assessed by MUGA using phase analysis. All patients and controls underwent positron emission tomography with 18 FDG to determine the distribution of myocardial glucose uptake. The standard deviation of peak 18 FDG uptake was used as an index of metabolic heterogeneity. Student's t -test and Pearson's correlation were used for statistical analysis. Results The mean age of the patients with HF was 54 ± 12 years and 72% were male. The length of the QRS was 129 ± 31 milliseconds and LBBB was present in 9 patients. Patients with HF had decreased LV 18 FDG uptake compared with controls (7.56 ± 3.36 vs 11.63 ± 4.55 standard uptake value; p = 0.03). The length of the QRS interval correlated significantly with glucose uptake heterogeneity ( r = 0.62; p = 0.002) and mechanical dyssynchrony ( r = 0.63; p = 0.006). HF patients with LBBB showed marked glucose uptake heterogeneity compared with HF patients without LBBB (41.4 ± 10 vs 34.7 ± 4.9 ml/100 g/min, respectively; p = 0.01). Conclusions Patients with non-ischemic heart failure exhibit a global decrease in myocardial glucose uptake. Within this group, subjects who also have LBBB exhibit a marked heterogeneity in segmental glucose uptake, which directly correlates with QRS duration.

Complications and mortality of heart failure are high, despite the availability of several forms of treatment. Uric acid, the end product of purine metabolism would actively participate in the pathophysiology of heart failure. However, there is no consensus about its action in cardiovascular disease. Serum uric acid would have a protective antioxidant activity. This action could help to reduce or counteract the processes that cause or appear as a result of heart failure. However, these protective properties would vanish in the intracellular environment or in highly hydrophobic areas such as atherosclerotic plaques and adipose tissue. This review discusses the paradoxical action of uric acid in the pathophysiology of heart failure.

Heart failure (HF) is characterized, among other features, by the development of alterations in myocardial energy metabolism, involving a decrease in glucose utilization and increased free fatty acid uptake by cardiomyocytes, associated with decreased deposits of high-energy phosphates (creatine phosphate/creatine transporter). Magnetic resonance (MR) imaging allows a direct and noninvasive assessment of myocardial metabolites.To measure myocardial creatine and lipids by MR spectroscopy among patients with HF.Cardiac MR spectroscopy (1.5 Tesla) with Hydrogen antenna and single voxel acquisition was performed in five patients with non-ischemic heart failure, aged 58 ± 9.7 years, (60% males) and 5 healthy volunteers matched for age and sex. We analyzed the signals of creatine (Cr), lipids (L) and water (W) in the interventricular septum, establishing the water/lipid (W/L) and water/creatine (W/Cr) index to normalize the values obtained.Among patients, left ventricular ejection fraction was 32 ± 6.9%, 60% were in functional capacity II, 60% had hypertension and one was diabetic. Spectroscopic curves showed a depletion of total Cr, evidenced by the W/ Cr index, among patients with heart failure, when compared with healthy controls (1.46 ± 1.21 and 5.96 ± 2.25 respectively, p0,05). Differences in myocardial lipid content, measured as the W/L index, were not significant (5.06 ± 2.66 and 1.80 ± 1.62 respectively, p = 0.08).Among patients with heart failure of non-ischemic etiology, there is a depletion of creatine levels measured by MR spectroscopy.

hyperglycemia at admission has been associated to an adverse prognosis in patients with ST-segment elevation acute myocardial infarction (STE-MI). However, its impact over the results of reperfusion therapies in patients with STEMI is still a matter of controversy.to determine the impact of admission hyperglycemia on hospital and long term mortality, according to the method of reper-fusion utilized in patients with STEMI.prospective registry of 1,634 consecutive patients aged 60 ± 12 years (77% male), from 3 participating hospitals in the Chilean Registry of Myocardial Infarction (GEMI). We evaluated demographic, clinical and laboratory variables, reperfusion method used, hospital and long term mortality. The impact of hyperglycemia on hospital and long term mortality was evaluated by a logistic regression analysis and Cox risk, respectively, adjusted by Thrombolysis in Myocardial Infarction (TIMI) risk score.twenty four percent of patients were diabetics and in 45%, the infarct was located on the anterior wall. The mean TIMI risk score was 3.2 ± 2.4. Hyperglycemia at entry was associated to a greater hospital and long term mortality, independently of the reperfusion strategy utilized. Primary angioplasty was associated to a greater benefit, compared to thrombolysis among hyperglycemic patients with an odds ratio: 2.9, 95% confi dence intervals: 1.0-8.0 and a hazard ratio of 2.9, 95% confi dence intervals: 1.44-5.88, independently of a previous history of diabetes mellitus and TIMI risk score.in patients with STEMI, admission hyperglycemia is associated with a worse prognosis which was significantly improved with primary angioplasty compared to thrombolysis, independently of the admission TIMI risk score.

Background: Hyperglycemia at admission has been associated to an adverse prognosis in patients with ST-segment elevation acute myocardial infarction (STE-MI). However, its impact over the results of reperfusion therapies in patients with STEMI is still a matter of controversy. Aim: To determine the impact of admission hyperglycemia on hospital and long term mortality, according to the method of reper-fusion utilized in patients with STEMI. Material and Methods: Prospective registry of 1,634 consecutive patients aged 60 ± 12 years (77% male), from 3 participating hospitals in the Chilean Registry of Myocardial Infarction (GEMI). We evaluated demographic, clinical and laboratory variables, reperfusion method used, hospital and long term mortality. The impact of hyperglycemia on hospital and long term mortality was evaluated by a logistic regression analysis and Cox risk, respectively, adjusted by Thrombolysis in Myocardial Infarction (TIMI) risk score. Results: Twenty four percent of patients were diabetics and in 45%, the infarct was located on the anterior wall. The mean TIMI risk score was 3.2 ± 2.4. Hyperglycemia at entry was associated to a greater hospital and long term mortality, independently of the reperfusion strategy utilized. Primary angioplasty was associated to a greater benefit, compared to thrombolysis among hyperglycemic patients with an odds ratio: 2.9, 95% confi dence intervals: 1.0-8.0 and a hazard ratio of 2.9, 95% confi dence intervals: 1.44-5.88, independently of a previous history of diabetes mellitus and TIMI risk score. Conclusions: In patients with STEMI, admission hyperglycemia is associated with a worse prognosis which was significantly improved with primary angioplasty compared to thrombolysis, independently of the admission TIMI risk score.

There is an increased incidence of celiac disease in patients with idiopathic dilated cardiomyopathy. We report a 4 7 year-old female presenting with heart failure secondary to dilated cardiomyopathy of unknown etiology. During the five months following the first hospitalization the patient had multiple hospital admissions due to decompensate heart failure. Due to a history of intermittent diarrhea and weight loss, a celiac disease was suspected. Antiendomysial antibodies were positive and there was a villous atrophy in duodenal mucosa. A gluten free diet was started with a concomitant recovery of her functional capacity. After one month of gluten free diet a new echocardiogram showed a normal left ventricle and systolic function.

The aortic arch aneurysm is a complex disease with a growing incidence in our population. We report a 64 year-old female with an atherosclerotic aortic arch aneurysm with a maximum diameter of 9.4 cm and evidence of contained rupture. We performed a complete aortic arch replacement in a single period of 100 minutes of circulatory arrest with deep hypothermia and brain protection with anterograde cerebral perfusion through the right axillary artery. The patient had a complete recovery without evidence of neurological damage and was extubated on the next morning. One year later, the patient is asymptomatic and the peri-aortic haematoma was completely reabsorbed.

El tema del efecto del estres sobre las personas quetrabajan con personas, es motivo de reflexion y estudiodesde los anos 70. Muchos de los profesionalesdedicados al cuidado de otros, estan siendoconsiderados profesionales en riesgo de enfermar enel ejercicio de su quehacer, a este sindrome se ledenomina Burnout.El Burnout, que en espanol puede ser traducidocomo “agotamiento” -“fundirse”, “quemarse”- se hadescrito como “la respuesta patologica a estresores

There is an increased incidence of celiac disease in patients with idiopathic dilated cardiomyopathy. We report a 4 7 year-old female presenting with heart failure secondary to dilated cardiomyopathy of unknown etiology. During the five months following the first hospitalization the patient had multiple hospital admissions due to decompensate heart failure. Due to a history of intermittent diarrhea and weight loss, a celiac disease was suspected. Antiendomysial antibodies were positive and there was a villous atrophy in duodenal mucosa. A gluten free diet was started with a concomitant recovery of her functional capacity. After one month of gluten free diet a new echocardiogram showed a normal left ventricle and systolic function.

The aortic arch aneurysm is a complex disease with a growing incidence in our population. We report a 64 year-old female with an atherosclerotic aortic arch aneurysm with a maximum diameter of 9.4 cm and evidence of contained rupture. We performed a complete aortic arch replacement in a single period of 100 minutes of circulatory arrest with deep hypothermia and brain protection with anterograde cerebral perfusion through the right axillary artery. The patient had a complete recovery without evidence of neurological damage and was extubated on the next morning. One year later, the patient is asymptomatic and the peri-aortic haematoma was completely reabsorbed.

Introducción: El aumento en la actividad de la xantina-oxidasa unida al endotelio (XOec) puede participar como un importante mediador de la disfunción endotelial en la insuficiencia cardíaca crónica (IC). Las estatinas son capaces de reducir el estrés oxidativo y restaurar la disfunción endotelial a través de mecanismos independientes de la reducción del colesterol. Sin embargo, el efecto de estos fármacos en la actividad de XOec es completamente desconocido. Nosotros estudiamos la hipótesis que atorvastatina durante 8 semanas reduce la actividad de XOec de manera independiente de los cambios en el colesterol. Metodología: Un total de 25 pacientes con IC (Fracción de eyección < 40 % y Clase funcional NYHA ll-lll) recibieron placebo por 4 semanas, seguido por 8 semanas de atorvastatina 20 mg por día. Muestras de sangre fueron recolectadas basalmente, 4 semanas y 12 semanas. La actividad de XOec y los niveles de ácido úrico fueron medidos por espectrofotometría. Resultados: El tratamiento con atorvastatina, pero no el placebo, redujo la actividad de ecXO (p Conclusión: El efecto beneficioso a corto plazo de la atorvastatina en relación a la mejoría de la función endotelial demostrado en estudios previos, estaría asociado a una disminución en la actividad de XOec de una manera independiente a los cambios en el colesterol, lo que sugiere la presencia de un nuevo efecto pleiotrópico de las estatinas.

We investigated the clinical response of chronic heart failure patients with beta(2)-adrenergic receptor Gln(27)-->Glu polymorphism treated for 6 months with carvedilol, a alpha/beta-antagonist with antioxidant properties. The 6-min. walk test, the left ventricular ejection fraction, heart rate, plasma norepinephrine and malondialdehyde, a stress oxidative marker, concentrations were evaluated at baseline and after treatment for 6 months with carvedilol in 33 stable chronic heart failure patients with the Gln(27)-->Glubeta(2)-adrenergic receptor polymorphism. Carvedilol significantly increased the left ventricular ejection fraction, while decreasing the heart rate and malondialdehyde plasma concentrations in chronic heart failure patients with the Glu(27)beta(2)-adrenergic receptor allele. There were however, no significant changes in patients with the Gln(27)beta(2)-adrenergic receptor variant.

Beta adrenergic receptors (AR) are highly polymorphic and important regulators of cardiovascular homeostasis. Among these, beta1 and beta2 AR regulate cardiac contractility and frequency and are important pharmacological targets.To evaluate genotype and gene-gene interaction between beta1-AR Arg389Gly and beta2-AR Arg16Gly, Gln27Glu and Thr164Ile polymorphisms, as risk factors for HF.Eighty chronic HF patients and eighty-eight controls matched by age and sex were genotyped for beta1-AR Arg389Gly, beta2-AR Arg16Gly, Gln27Glu and Thr164Ile polymorphisms.The presence of beta2-AR Glu allele was a risk predictor for HF (odds ratio (OR) = 2.81; 95% confidence intervals (CI) = 1.49-5.31). Interactions that increased the risk for HF were found in patients carrying at least one of the beta2-AR Glu and beta2-AR Gly allele (OR = 3.81; 95% CI = 1.50-0.70) and beta2-AR Glu and beta1-AR Gly allele combination (OR = 5.51; 95% CI = 2.19-13.86). Furthermore, the frequency of beta2-AR Glu allele was higher among patients with a history of acute myocardial infarction (with infarction: 0.534, without: 0.313, p = 0.01).Beta2-AR Glu allele could be a risk predictorfor HF. This risk could be enhanced by the additional presence of beta2-AR Gly16 or beta1-AR Arg389 alleles. The frequency of beta2-AR Gln27 Glu allele was higher among patients with a history of myocardial infarction.

Primary angioplasty is the most effective treatment of ST-segment elevation acute myocardial infarction (STEMI). However, its worldwide implementation is difficult to obtain. Therefore thrombolysis continues to be the treatment most commonly used.To evaluate in-hospital and long term mortality of patients with STEMI treated with thrombolysis or angioplasty, in three hospitals participating in the Chilean National Registry of Acute MI (GEMI group).Registry of 1,634 consecutive patients with STEMI admitted between 2002 and 2006. Risk was stratified using the Thrombolysis in Myocardial Infarction (TIMI) Risk Score. Hospital and log term mortalities were adjusted using logistic and Cox regression models.Fifty nine percent of patients (967 patients aged 60+/-12 years, 77% males) were subjected to reperfusion therapies, 28% with primary angioplasty and 72% with thrombolysis. Hospital mortality rates among patients treated with thrombolysis and angioplasty were 10.9% and 5.6% (p =0.01), respectively The figures for long term mortality were 20.4% and 9.7%, respectively (p0.01). Multivariate analysis confirmed the lower mortality among subjects treated with angioplasty, with an odds ratio (OR) in favor of angioplasty of 8.5 (95% confidence intervals (CI) 3-35) for in hospital mortality and of 4.7 (95% CI 2.6-8.3) for long term mortality. The higher benefits of angioplasty were observed in males, in the elderly and in patients with a TIMI score over3.Hospital and long term mortality of patients with STEMI was lower among those treated with primary angioplasty. This treatment is most beneficial among males, in the elderly and in patients with a TIMI score3 .

Background: ß adrenergic receptors (AR) are highly polymorphic and important regulators of cardiovascular homeostasis. Among these, ß1 and ß2 AR regulate cardiac contractility and frequency and are important pharmacological targets. Aim: To evaluate genotype and gene-gene interaction between ß1-AR Arg389Gly and ß2-AR ArglSGly GlnZ7Gly and Thrl 64Ile polymorphisms, as risk factors for HF. Material and methods: Eighty chronic HF patients and eighty-eight controls matched by age and sex were genotyped for ß1 -AR Arg389Gly ß2-AR ArgWGly, GlnZ7Glu and Thr164Ile polymorphisms. Results: The presence of ß2-AR Glu afiele was a risk predictor for HF (odds ratio (OR) =2.81; 95% confidence intervals (CI) =1.49-5.31). Interactions that increased the risk for HF were found in patients carrying at least one of the ß2-AR Glu and ß2-AR Gly allele (OR =3.81; 95% CI =1.50-0.70) and ß2-AR Glu and ß1 -AR Gly allele combination (OR =5.51; 95% CI =2.19-13.86). Furthermore, the frequency of ß2-AR Glu allele was higher among patients with a history ofacute myocardial infarction (with infarction: 0.534, without: 0.313, p =0.01). Conclusions: ß2-AR Glu allele could be a risk predictor for HF. This risk could be enhanced by the additional presence of ß2-AR GlyW or ß1-AR Arg389 alleles. The frequency of ß2-AR Gln27 Glu allele was higher among patients with a history of myocardial infarction.

In chronic heart failure (CHF), endothelial dysfunction (ED) is a consequence of an imbalance of vascular tone regulating substances. The relationship between ED and inflammation has not been fully investigated.To assess the association between inflammation and ED in CHF.Forty two patients aged 56+/-14 years (80% male) with a CHF in functional capacity II-III (New York Heart Association) and an ejection fraction (FE)40% were consecutively studied. Patients were classified according to the presence or absence of ED, evaluated by reactive vasodilation measured by ultrasound, after brachial artery compression. Circulating levels of highly sensitive C reactive protein (usCRP), tumor necrosis factor a (TNFá) and interleukin-6 (IL-6) were determined by ELISA. A group of 15 healthy subjects of similar age, were studied as controls.Sixty seven percent of patients had ED. Compared to controls, patients with CHF had higher usCRP (0.58+/-0.4 and 4.9+/-7.1 mg/dl respectively, p0.01) and IL-6 (1.38+/-0.06 and 3.1+/-1.7 mg/dl respectively, p0.01). Compared to patients without ED, patients with CHF and ED had higher levels of usCRP (3.0+/-0.4 and 6.0+/-5.7 mg/dl respectively, p0.01) and TNFá (0.31+/-0.26 and 1.0+/-1.1 pg/ml, p =0.02). No differences in IL-6 were found between CHF groups.In CHF patients, the presence of ED was associated with increased levels of inflammatory markers.

Background: Primary angioplasty is the most effective treatment of ST-segment elevation acute myocardial infarction (STEMI). However, its worldwide implementation is difficult to obtain. Therefore thrombolysis continues to be the treatment most commonly used. Aim: To evaluate inhospital and long term mortality of patients with STEMI treated with thrombolysis or angioplasty, in three hospitals participating in the Chilean National Registry of Acute MI (GEMIgroup). Material and tnethods: Registry of 1,634 consecutive patients with STEMI admited between 2002 and 2006. Risk was stratified using the Thrombolysis in Myocardial Infarction (TIMI) Risk Score. Hospital and log term mortalities were adjusted using logistic and Cox regression models. Results: Fifty nine percent of patients (967 patients aged 60±12 years, 77% males) were subjected to reperfusion therapies, 28% with primary angioplasty and 72% with thrombolysis. Hospital mortality rates among patients treated with thrombolysis and angioplasty were 10.9% and 5.6% (p =0.01), respectively The figures for long term mortality were 20.4% and 9.7%, respectively (p 3. Conclusions: Hospital and long term mortality of patients with STEMI was lower among those treated with primary angioplasty. This treatment is most beneficial among males, in the elderly and in patients with a TIMI score >3 .

Background: In chronic heart failure (CHF), endothelial dysfunction (ED) is a consequence of an imbalance of vascular tone regulating substances. The relationship between ED and inflammation has not been fully investigated. Aim: To assess the association between inflammation and ED in CHF. Material and methods: Forty two patients aged 56±14 years (80% male) with a CHF in functional capacity II-III (New York Heart Association) and an ejection fraction (FE)

Background Increased oxidative stress, a common feature in chronic heart failure, has been associated with inflammation, endothelial dysfunction, and extracellular matrix degradation. Statins have known anti-inflammatory and anti-oxidant effects; however, their role in chronic heart failure is still controversial. Methods This was a prospective study of 38 patients with stable systolic chronic heart failure. Patients received a 4-week placebo course, followed by atorvastatin 20 mg/day for 8 weeks. Oxidative stress, inflammation and remodeling markers, brachial artery flow-mediated vasodilation, and 6-minute walk test were evaluated at baseline, 4, and 8 weeks. Results Mean age was 58 ± 12. Mean left ventricular ejection fraction was 27% ± 12%. No significant differences were observed between measurements at baseline and after placebo. Atorvastatin induced a significant decrease of matrix metalloproteinase-9 activity, high-sensitivity C-reactive protein, tumor necrosis factor-α, interleukin-6, and malondialdehyde, and a significant increase of endothelial superoxide dismutase activity when compared with placebo. No differences in tissue inhibitor of matrix metalloproteinase and matrix metalloproteinase-2 activities were observed. Atorvastatin use was associated with an improved flow-dependent brachial vasodilation and exercise capacity in the 6-minute walk test. Conclusions In chronic heart failure patients, atorvastatin therapy is associated with a decrease of inflammation and extracellular matrix remodeling, improving both endothelial function and exercise capacity.

Primary pulmonary hypertension (PPH) is a progressive disease leading to right heart failure and death. Right heart catherization and maximal or submaximal tests are employed to assess the course of the disease. A neurohormonal parameter such as pro-brain natriuretic peptide (BNP) would be helpful in the assessment of these patients.To study the correlation of BNP with functional status and non-invasive hemodynamic determinations in patients with PPH.Twelve patients (mean age: 48 years; 58% female) were evaluated with 6 minutes walk distance test (6-min WT), plasma BNP, systolic pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR) and cardiac output (CO) determined by echocardiogram. Plasma BNP levels were compared with normal subjects.BNP levels were increased in PPH patients (1270+/-547 vs 48+/-8 pg/ml, p-value0.01). Mean PAPs was 82+/-27 mmHg and the mean distance walked in 6 minutes was 407+/-113 meters. BNP levels were positively correlated with PVR (r=0.58, p-value=0.006) and negatively correlated with 6-min WT (r=-0.83, p-value0.001). No correlation was found between BNP levels, PAPs and CO.In PPH patients, BNP levels are increased and correlate with functional class and PVR. Follow-up studies are needed to evaluate the role of BNP as a marker of progression and therapeutic response in PPH patients.

Background: Primary pulmonary hipertension (PPH) is a progressive disease leading to right heart failure and death. Right heart catherization and maximal or submaximal tests are employed to assess the course of the disease. A neurohormonal parameter such as pro-brain natriuretic peptide (BNP) would be helpful in the assessment of these patients. Aim: To study the correlation of BNP with functional status and non-invasive hemodynamic determinations in patients with PPH. Material and methods: Twelve patients (mean age: 48 years; 58% female) were evaluated with 6 minutes walk distance test (6-min WT), plasma BNP, systolic pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR) and cardiac output (CO) determined by echocardiogram. Plasma BNP levels were compared with normal subjects. Results: BNP levels were increased in PPH patients (1270±547 vs 48±8 pg/ml, p-value

Background: Our previous studies suggest that the increase in heart rate from rest to peak exercise is reduced in patients with chronic heart failure (CHF) and this is associated with increased oxidative stress, as determined by malondialdehyde (MDA) plasma levels. Aim: To investigate the effects of carvedilol on the heart rate response to exercise and oxidative stress in patients with CHF. Methods and results: Thirty stable NYHA classes II—III CHF patients received carvedilol therapy for 6 months, at a mean maintenance dose of 25 mg (range 6.25—50 mg/day). After treatment, the patients showed a significant improvement in their functional NYHA class (p=0.013), increased left ventricular ejection fraction (LVEF) (24±1.4% to 31±2.3%, p=0.003) and 6-min walk distance (499±18 to 534±18 m, p=0.03), without changes in the peak VO2. At baseline, norepinephrine (NE) plasma levels increased with exercise (510±51 to 2513±230 pg/mL, p

Introduction and objective. Carvedilol is an antioxidant and adrenergic antagonist with demonstrated benefits in terms of mortality from heart failure (HF). The aim of the present study was to evaluate clinical parameters, left ventricular function, oxidative stress levels, and neurohumoral status at baseline and after 6 months of treatment with carvedilol in patients with chronic HF. Patients and method. Thirty patients with chronic HF that was stable without beta-blocker treatment were included. Functional class was II or III, and left ventricular ejection fraction (LVEF) was

We reported a case of a 30-year-old Hispanic patient with a history of idiopathic pulmonary arterial hypertension (PAH). A baseline catheterisation showed a mean pulmonary artery pressure (PAP) of 58 mm Hg, capillary wedge pressure of 14 mm Hg, cardiac index of 2.7 l/min/m2 and pulmonary vascular resistance of 7.5 WU, with no response to adenosine. A pulmonary CT scan ruled out thromboembolism or significant abnormalities (such as glass opacities, septal lines or mediastinal node enlargement commonly seen in venocclusive disease1); albumin macroaggregate lung perfusion scan showed normal perfusion without significant intrapulmonary shunt (IPS). He was started on diuretics, oxygen and sildenafil 25 mg three times a day. Despite treatment, dyspnoea worsened and 2 months later the patient was referred …