Depressed Left Ventricular Systolic Function Research Articles

6724 A Broken Heart Due to Excess Thyroid

Abstract Disclosure: R. Subramani: None. R. Subramani: None. V. Zeykan: None. Introduction: Tachycardia-induced cardiomyopathy related to thyrotoxicosis is an uncommon yet serious complication affecting fewer than 1% of individuals with hyperthyroidism. Restoring a euthyroid state can potentially reverse the abnormal cardiac structure and function. Here we report a case of tachycardia-induced cardiomyopathy secondary to thyrotoxicosis Case Summary: A 52-year-old woman with a history of hypertension presented with recent-onset exertional dyspnea, a nonproductive cough, and paroxysmal nocturnal dyspnea. On examination, she exhibited tachycardia (heart rate: 150/min), tachypnea, hypertension, and was afebrile. Physical findings included a mildly enlarged, firm, non-tender thyroid gland bilaterally, without exophthalmos or tremors. Auscultation revealed bilateral crackles in the left lower lung fields. Laboratory analysis revealed undetectable TSH (<0.02 uIU/mL), elevated free T4 (5.3 ng/dL), free T3 (16.30 pg/mL), thyroid stimulating immunoglobulin (TSI) at 216%, and NT proBNP at 8528 pg/mL. Neck ultrasound and CT confirmed diffuse enlargement of the thyroid gland. Transthoracic echocardiography (TTE) displayed severely depressed left ventricular systolic function, estimating an ejection fraction (EF) of 25-30%. Initial management involved intravenous beta-blockers for heart rate control, IV Lasix, and IV hydrocortisone. Subsequently, the patient received propylthiouracil, propranolol, and prednisone, resulting in symptomatic improvement. A follow-up TTE after 6 months revealed an improved EF of 50%. Discussion: The pathophysiologic mechanisms underlying thyrotoxic cardiomyopathy encompass several factors, including tachycardia-induced cardiomyopathy, direct myopathic effects induced by the T3 hormone, and concurrent autoimmune myocarditis associated with Graves' disease. Thyroid hormone exerts a comprehensive impact on nearly all tissue and organ systems, heightening basal metabolic rate and subsequently increasing preload, myocardial contractility, and cardiac output. While thyrotoxicosis-related congestive heart failure (CHF) is relatively uncommon among patients hospitalized for acute CHF, addressing hyperthyroidism and CHF through definitive treatment yields a more favorable prognosis compared to cases of acute CHF stemming from other etiologies. The intricate interplay of these mechanisms highlights the importance of a comprehensive approach in managing thyrotoxic cardiomyopathy, emphasizing the need for targeted interventions to address both the underlying thyroid dysfunction and associated cardiac manifestations. Presentation: 6/3/2024

High-output cardiac failure in the setting of iron deficiency anaemia: a case report.

We present a case of a child with high-output heart failure and severe iron deficiency anaemia-induced dilated cardiomyopathy managed with serial blood transfusions, preload and afterload reducing agents, inotropic therapies, and long-term iron supplementation. The complete resolution of echocardiogram findings of moderate enlargement of all cardiac chambers and moderately depressed left ventricular systolic function was achieved.

Diastolic function assessment with four-dimensional flow cardiovascular magnetic resonance using automatic deep learning E/A ratio analysis

BackgroundDiastolic left ventricular dysfunction is a powerful contributor to the symptoms and prognosis of patients with heart failure. In patients with depressed left ventricular systolic function the EA ratio is the first step to defining the grade of diastolic dysfunction. Doppler echocardiography is the preferred imaging technique for diastolic function assessment, while CMR is less established as a method. Previous 4D Flow-based studies have looked at the EA ratio proximally to the mitral valve, requiring manual interaction. In this study we compare an automated, deep learning-based, and two semiautomated approaches for 4D Flow CMR-based EA ratio assessment to conventional, gold standard echo-based methods. MethodsNinety-seven subjects with chronic ischemic heart disease underwent a cardiac echo followed by an MRI investigation. 4D Flow-based EA ratio values were computed using three different approaches; two semi-automated, assessing the EA ratio by measuring the inflow velocity (MVvel) and the inflow volume (MVflow) at the mitral valve plane, and one fully automated, creating a full LV segmentation using a deep learning-based method within which the EA ratio could be assessed without constraint to the mitral plane (LVvel). ResultsMVvel, MVflow, and LVvel EA ratios were strongly associated with Echo EA ratio (R2= 0.60, 0.58, 0.72). LVvel peak E and A showed moderate association to Echo peak E and A, while MVvel values were weakly associated. MVvel and MVflow EA ratios were very strongly associated with LVvel (R2= 0.84, 0.86). MVvel peak E was moderately associated with LVvel, while peak A showed strong association (R2= 0.26, 0.57). Discussion and ConclusionPeak E, peak A and EA ratio are integral to the assessment of diastolic dysfunction and may expand the utility of CMR studies in patients with cardiovascular disease. While underestimation of absolute peak E and A velocities was noted, the EA ratio measured with all three 4D Flow methods was strongly associated with the gold standard Doppler echocardiography. The automatic, deep learning-based method performed best, with the most favorable runtime of ~40seconds. As both semiautomatic methods associated very strongly to LVvel, they could be employed as an alternative for estimation of EA ratio.

A normal and particularly small (

The left atrium (LA) size can change due to cardiac pathologies like heart failure and aging. While the link between LA enlargement and left ventricular (LV) dysfunction is acknowledged, this study aims to assess the negative predictive value of normal LA size concerning the severity of LV systolic function in a large cohort undergoing diagnostic echocardiography. This retrospective cohort study, conducted at the University of California, Irvine Medical Center from 1984 to 1998, aimed to elucidate the negative predictive value of normal LA size measured by M-mode and two-dimensional echocardiography in a large cohort undergoing diagnostic assessment. In the analysis of 22,390 echocardiograms, 55.1% exhibited normal LA size (<40 mm), while 44.9% showed abnormal LA size (≥40 mm). Within the normal LA size group, only 2.4% demonstrated abnormal LV systolic function, with 1.1% mildly depressed, 0.7% moderately depressed, and 0.6% severely depressed LV function. The negative predictive value of normal LA size for abnormal LV systolic function was calculated at 97.5%, rising to 99.3% and 99.4% for moderate or severely decreased LV systolic function, respectively. In patients with small LA size (<35 mm), moderate to severely depressed LV systolic function was observed in only 0.8%, with severe LV systolic dysfunction in 0.3%, yielding an overall prevalence of 1.5% for all systolic dysfunction in the small LA size group. Our findings underscore the clinical significance of normal LA size as a reliable indicator of preserved LV function.

Incidentally induced atrial fibrillation during programmed electrical stimulation in patients with depressed left ventricular systolic function after an acute myocardial infarction: a CARISMA substudy

Abstract Background The aim of this study was to investigate the clinically significant value of incidentally induced atrial fibrillation (AF) during programmed electrical stimulation (PES) in patients with left ventricular systolic dysfunction (≤40%) after an acute myocardial infarction (MI). Methods In this study we included 231 patients from the Cardiac Arrhythmias and RIsk Stratification after Myocardial InfArction (CARISMA) study. These patients were identified 3-21 days after being diagnosed with an MI, had left ventricular ejection fraction ≤40% and had no prior history of AF. They all received an implantable cardiac monitor (ICM) and were continuously monitored for cardiac arrhythmias for 2 years. A PES was performed 6 weeks post-MI with pacing from the right atrium and coronary sinus for induction of SVT and from the ventricular apex and outflow tract with up to three extra stimuli for induction of VT. Induction of AF was unwanted but reported if this incidentally occurred. Results AF was induced in 34 patients (15%) during the PES of which 10 (29%) later developed AF. A total of 61 patients (26%) developed AF within 2-years follow-up and the overall risk of AF was not significantly increased in patients with PES induced AF compared to patients without inducible AF (HR 1.6, P=0.14), however, the risk of AF ≤188 days post-MI was slightly increased (HR 3.0, P=0.01). The risk of bradyarrhythmia (HR=0.2, P=0.07), ventricular arrhythmias (HR=0.7, P=0.77) and MACE (HR 0.5, P=0.28) was reduced in patients with inducible AF compared to patients without inducible AF. Conclusions Incidentally induced AF during an electrophysiological study in post-MI patients was relatively frequent (15%) but was not associated with a higher risk of atrial fibrillation, other cardiac brady- or tachy-arrhythmias or major cardiac events. Even though the short-term risk for AF slightly increased, this does not seem to justify anticoagulation treatment or intensified follow-up in these patients.

Abstract 12011: A Case of Emphysematous Pyelonephritis With Use of Empagliflozin

Background: SGLT2i improve cardiovascular (CV) outcome in patients with HFrEF with or without diabetes (DM). Although recent trials and metanalysis have showed improve renal outcomes with SGLT-2i, one should be aware of the potential serious adverse effects with this group of medications including life threatening UTI. Case: 50-year-old female with history of type 2 DM presented with septic shock due to bilateral (B/L) pyelonephritis, with no associated renal calculi. CT of the abdomen also revealed emphysematous pyelonephritis of the left kidney. Few days later, patient went into PEA requiring intubation with return of spontaneous circulation within 4 minutes of advanced cardiac life support. Patient was extubated subsequently later on during her hospitalization. Work up for PEA revealed depressed left ventricular systolic function with an EF of 25-29% with no wall motion abnormality. Patient also developed decompensated HFrEF with development of b/l pleural effusion and generalized anasarca. Cardiology was consulted for management of her cardiomyopathy. She was recommended coronary angiography but she declined. Therefore, Patient was started on guideline direct medical therapy for HF with metoprolol succinate, lisinopril and spironolactone. Due to recent evidence of SGLT-2i improving CV outcomes in patients with HFrEF, it was also recommended to start SGLT-2i. Discussion: On further reviewing regarding use of SGLT-2i and association with UTI, we found a case report causing emphysematous pyelonephritis with use of canagliflozin. Medication reconciliation done at the time of discharge revealed that patient was recently initiated on empagliflozin three months prior to her admission. Therefore, it was speculated that her emphysematous pyelonephritis could be one of the rare complications of SGLT-2i since no other etiologies was noted per urological workup and we decided not to continue SGLT-2i. A search of FAERS from March 2013 through October 2014 identified 19 cases of urosepsis reported with the SGLT2 inhibitors (canagliflozin [n=10] and dapagliflozin [n=9]). All cases resulted in hospitalization. No deaths were reported. Clinicians should be aware of potential life-threatening UTI which may occur with SGLT-2i use.

Cardiac dysfunction and final outcome in correlation with serum cortisol level in active pulmonary tuberculosis: A single-center experience

Introduction: Although cardiac involvement is extremely rare in tuberculosis (TB), cardiac dysfunction is not uncommon. We have studied the prevalence of cardiac dysfunction in pulmonary TB with special emphasis on echocardiography, serum cortisol, and its correlation in cases with unstable cardiorespiratory parameters. Methods: A prospective observational and interventional study conducted in Pulmonary Medicine, MIMSR Medical College and Venkatesh Chest Hospital, Latur, India during July 2015 to December 2020, which included 800 cases of active pulmonary TB confirmed microscopically or with GeneXpert MTB/RIF, documented MTB genome in respiratory specimens’ sputum/induced sputum and bronchoscopy-guided bronchial wash, or bronchoalveolar lavage whenever necessary. Cases with known risk factors for cardiac disease and taking cardiac medicines and cases with pericardial effusion were excluded from study. Disproportionate tachycardia and tachypnea with or without shock and hypoxia were the key entry point criteria in this study. Chest radiograph, pulse oximetry, electrocardiography (ECG), sputum examination, cardiac enzyme studies (creatine phosphokinase MB [CPK-MB] and cardiac troponins), serum cortisol test, and echocardiography are done in all study cases during enrollment at 2 and 6 months of treatment with anti-TB medicines. Statistical analysis was carried out by chi-square test. Observations and analysis: Of the 800 cases with active pulmonary TB, cardiac dysfunction was documented in 26% cases, 44% were females, and 56% cases were older than 50 years. Echocardiographic abnormalities were documented such as global hypokinesia in 62% cases; depressed left ventricular systolic and diastolic function in 44 and 28% cases, respectively; dilated right atrium and right ventricle in 32% cases; and pulmonary hypertension in 6% cases. Serum cortisol level was significantly lower in cases with cardiac dysfunction (P &lt; 0.00001). Hypoxia had significant association with right and left heart dysfunction (P &lt; 0.00001). Cachexia, anemia, and hypoalbuminemia were documented to have significant association with cardiac dysfunction (P &lt; 0.00001). Treatment outcome showed significant improvement in cardiac function (P &lt; 0.00001). Coronary angiography did not show significant coronary artery lesions, and computed tomography (CT) pulmonary angiography did not show pulmonary embolism. Conclusion: Cardiac dysfunction in active pulmonary TB is underestimated and less evaluated routinely; disproportionate tachycardia and tachypnea with or without shock are clinical indicators to suspect early, especially in cases with risk factors such as advanced pulmonary TB on chest radiograph, cachexia with body mass index (BMI) &lt;18, advanced age, females, cases with anemia, and hypoalbuminemia. Echocardiography shows “global hypokinesia” as a predominant cardiac dysfunction in study cases, and right or left heart dysfunction depends on with or without hypoxia, respectively. Serum cortisol measurement will help in majority of the cases and a proportionate number of cases were having associated adrenal suppression.

Cardiovascular disease and chimeric antigen receptor cellular therapy.

Chimeric antigen receptor T-cell (CAR T) therapy is a revolutionary personalized therapy that has significantly impacted the treatment of patients with hematologic malignancies refractory to other therapies. Cytokine release syndrome (CRS) is a major side effect of CAR T therapy that can occur in 70–90% of patients, with roughly 40% of patients at grade 2 or higher. CRS can cause an intense inflammatory state leading to cardiovascular complications, including troponin elevation, arrhythmias, hemodynamic instability, and depressed left ventricular systolic function. There are currently no standardized guidelines for the management of cardiovascular complications due to CAR T therapy, but systematic practice patterns are emerging. In this review, we contextualize the history and indications of CAR T cell therapy, side effects related to this treatment, strategies to optimize the cardiovascular health prior to CAR T and the management of cardiovascular complications related to CRS. We analyze the existing data and discuss potential future approaches.

Early Manifestation of Clozapine-Induced Cardiotoxicity: Detection, Pathophysiology, and Management

Schizoaffective disorder, bipolar type is a chronic mental health disorder that may manifest as mania. Clozapine is effective in treating acute mania and in achieving mood stabilization. However, on rare occasions, the use of clozapine has been associated with cardiotoxicity. Here, we present a case of a 31-year-old man who at baseline is known to have schizoaffective disorder, bipolar type, and cannabis dependence and was admitted to our hospital with a psychotic relapse. He was treated with clozapine, uptitrated to a maximum daily dose of 200mg twice daily by day 10. Thereafter he became febrile and experienced malaise, myalgias, and chest pain. He was noted on electrocardiogram to have sinus tachycardia without ischemic changes. In this context, he had a troponin leak, increased white blood cell count, serologies and cultures were negative and chest x-ray revealed no acute disease of the chest. Due to the suspicion of clozapine-induced cardiotoxicity, a transthoracic echocardiogram was done, which revealed mildly depressed left ventricular (LV) systolic function without pericardial effusion. Thereafter, clozapine was withdrawn and switched to lithium. Additionally, the cardioselective, metoprolol tartrate was initiated. Within 36-48 hours, he had resolution of symptoms and remained cardiovascularly stable. Clozapine uncommonly causes cardiotoxicity and early features may be non-specific. Awareness of this and recognizing early features aids in reducing the associated cardiovascular morbidity and mortality.

Prevalence of left ventricular thrombus formation after mitral valve edge-to-edge repair

The prevalence of left ventricular (LV) thrombus formation following percutaneous mitral valve edge-to-edge repair (TMVR) with the MitraClip system is unclear. Decreased total stroke volume and perfusion of the LV apex after mitral valve repair may facilitate thrombus formation especially in the context of reduced LV function. LV thrombus may cause disabling stroke or other thromboembolic events in this elderly and multimorbid patient cohort. Analyses of the prevalence of and risk factors for left ventricular thrombus formation in patients treated with the MitraClip system due to severe mitral valve regurgitation. All discharge and follow-up transthoracic echocardiographic examinations up to 6 months of 453 consecutive patients treated with the MitraClip system were screened for the presence of LV thrombus. Prevalence of LV thrombus formation was 1.1% (5/453). Importantly, LV thrombi were exclusively found in patients with severely depressed left ventricular systolic function (LV-EF < 30%), comprising a prevalence of 4.4% in this subgroup (5/113). Importantly, two of these patients were under active DOAC therapy with Rivaroxaban and Apixaban, respectively. Apart from LV-EF, we did not identify other factors that might have facilitated LV thrombus formation. LV thrombus formation following percutaneous mitral valve repair occurred exclusively in patients with severely depressed LV-EF. As two patients developed LV thrombus despite of DOAC therapy, anticoagulation with a Vitamin K antagonist should be considered in patients with an indication for oral anticoagulation following TMVR.

Myocarditis Following mRNA COVID-19 Vaccine.

A growing number of adolescents are being diagnosed with acute myocarditis following mRNA COVID-19 vaccinations. This case describes an adolescent who presented to the emergency department with chest pain and tachycardia following the Pfizer-BioNTech COVID-19 vaccination. Point-of-care ultrasound was performed prior to the return of laboratory studies and revealed depressed left ventricular systolic function. Point-of-care ultrasound may be a tool used to rapidly diagnose or risk stratify patients with potential post-COVID-19 vaccine myocarditis.

Reversible left ventricular noncompaction caused by hypertensive hydrocephalus: a pediatric case report

BackgroundLeft ventricular noncompaction cardiomyopathy (LVNC) is characterized by prominent ventricular trabeculations on cardiovascular imaging. Acquired reversible LVNC has not been reported in pediatrics without a genetic background.Case presentationA 9-year-old girl with a ventriculoperitoneal (VP) shunt for neonatal posthemorrhagic hydrocephalus was referred due to exacerbation of hydrocephalus caused by VP shunt dysfunction. Transthoracic echocardiography (TTE) revealed depressed left ventricular (LV) systolic function and thick prominent trabeculae in the LV, predominantly in the apex, suggesting LVNC. Following treatment with extraventricular drainage for hydrocephalus, prominent trabeculation of the LV was diminished on TTE within 3 months. Genetic testing using next-generation sequencing was performed, and no significant variants were identified.ConclusionsWe revealed for the first time a pediatric case of reversible LVNC without genetic predisposition. This case report provides valuable information on the pathogenesis of acquired LVNC and suggests that detailed evaluation is required to elucidate the diagnosis of this wide spectrum of etiologic–pathogenetic disorders.

A facilitated home-based cardiac rehabilitation intervention for people with heart failure and their caregivers: a research programme including the REACH-HF RCT

A facilitated home-based cardiac rehabilitation intervention for people with heart failure and their caregivers: a research programme including the REACH-HF RCT

Deficiency in gp91Phox (NOX2) Protects against Oxidative Stress and Cardiac Dysfunction in Iron Overloaded Mice

The role of NADPH oxidase subunit, gp91phox (NOX2) in development of oxidative stress and cardiac dysfunction due to iron (Fe)-overload was assessed. Control (C57BL/6J) and gp91phox knockout (KO) mice were treated for up to 8 weeks with Fe (2.5 mg/g/wk, i.p.) or Na-dextran; echocardiography, plasma 8-isoprostane (lipid peroxidation marker), cardiac Fe accumulation (Perl’s staining), and CD11b+ (WBCs) infiltrates were assessed. Fe caused no adverse effects on cardiac function at 3 weeks. At 6 weeks, significant declines in left ventricular (LV) ejection fraction (14.6% lower), and fractional shortening (19.6% lower) occurred in the Fe-treated control, but not in KO. Prolonging Fe treatment (8 weeks) maintained the depressed LV systolic function with a trend towards diastolic dysfunction (15.2% lower mitral valve E/A ratio) in controls but produced no impact on the KO. Fe-treatment (8 weeks) caused comparable cardiac Fe accumulation in both strains, but a 3.3-fold elevated plasma 8-isoprostane, and heightened CD11b+ staining in controls. In KO mice, lipid peroxidation and CD11b+ infiltration were 50% and 68% lower, respectively. Thus, gp91phox KO mice were significantly protected against oxidative stress, and systolic and diastolic dysfunction, supporting an important role of NOX2-mediated oxidative stress in causing cardiac dysfunction during Fe overload.

Electrical Storm in ChagasCardiomyopathy: Clinical Predictors, Outcome, and Arrhythmic Characteristics ina Prospective Registry.

This study of patients with Chagas heart disease (CHD) with an implantable cardioverter-defibrillator (ICD) for secondary prevention of sudden cardiac death sought to compare the characteristics of those with or without electrical storm (ES) during long-term follow-up. ES is a common problem in patients with CHD harboring an ICD, but data on clinical predictors and outcomes are limited. The authors retrospectively evaluated 110 patients with CHD with a mean follow-up of 1,949 ± 1,271days. Demographic, clinical, arrhythmia characteristics, ICD treatment, and death data were collected. Descriptive statistics included mean ± SD and Fisher exact tests used for comparisons. A p value<0.05 was considered significant. The ES group (n = 57; 43 men; age 62 ± 10 years) and the non-ES group (n = 53; 43 men; age 57 ± 14 years) had similar baseline demographic and clinical parameters, but left ventricular ejection fraction was higher in the ES group (44 ± 14% vs. 37 ± 14%; p=0.02) and QRS duration was shorter (109 ± 35ms vs. 134 ± 36ms; p=0.0027). Mortality rates were comparable in the 2 groups (odds ratio: 1.2; 95% confidence interval: 0.79 to 1.85; p=0.44). The ES group presented 116 ES (2.03 ±1.47, 1 to 6). A total of 2,953 (61%) arrhythmic events required ICD therapy. No deaths occurred directly caused by ES, but clinical triggers were reported in 20 patients. ES is frequent in CHD but in itself does not carry a worse prognosis in this study population and was not associated with a more depressed left ventricular systolic function or a longer QRS.

Asymptomatic Left Ventricle Systolic Dysfunction.

Heart failure is a common debilitating illness, associated with significant morbidity and mortality, rehospitalisation and societal costs. Current guidelines and position statements emphasise the management of patients with overt symptomatic disease, but the increasing prevalence of congestive heart failure underscores the need to identify and manage patients with early left ventricular dysfunction prior to symptom onset. Asymptomatic left ventricular systolic dysfunction (ALVSD), classified as stage B heart failure, is defined as depressed left ventricular systolic function in the absence of clinical heart failure. Early initiation of therapies in patients with presumed ALVSD has been shown to lead to better outcomes. In this article, the authors clarify issues surrounding the definition and natural history of ALVSD, outline clinical tools that may be of value in identifying patients with ALVSD and highlight potential opportunities for future investigations to better address aspects of our understanding of this complex syndrome.

Ventricular Dysfunction in the Case of the Sever Fetal Aortic Stenosis – the Role of Speckle-tracking

Abstract Congenital aortic stenosis (AS) occurs in around 0.2–0.5% of newborns, and its clinical severity is quite variable. Some of the newborns with AS require urgent medical care: prostaglandin infusion, balloon aortic valvuloplasty, or surgical intervention. Despite having a severe clinical evolution in neonates, the prenatal diagnosis of congenital AS is quite low. We present the case of a fetus with critical AS, who had been prenatally diagnosed at 35 weeks of gestation, via fetal cardiac ultra-sound. The echocardiographic parameters revealed a severely depressed left ventricular systolic function, with dilated chambers, and a severe aortic stenosis. Offline speckle-tracking analysis was performed in order to aid in deciding the optimal methods and timing of delivery. Left ventricular analysis revealed a severely impaired global longitudinal strain of 2.1%, left ventricular ejection fraction 18.4%, increased LV volumes, while the right ventricular function was only mildly depressed. Therefore, the decision was to delay the premature delivery, and the fetus was born at a gestational age of 38 weeks, in a hospital with a neonatal cardiovascular surgery department. The patient had undergone surgical repair of the cardiac anomaly at 3 days after birth.

Pathophysiology and Risk Stratification of Sudden Cardiac Death in Ischemic Heart Disease

Sudden cardiac death accounts for approximately 360,000 annually in the United States and is the cause of half of all cardiovascular deaths. Ischemic heart disease is the major cause of death in the general adult population. Sudden cardiac death can be due to arrhythmic or non-arrhythmic cardiac causes, for example, myocardial rupture. Arrhythmic sudden cardiac death may be caused by ventricular tachyarrhythmia (ventricular tachycardia/ventricular fibrillation) or pulseless electrical activity/asystole. The majority of research in risk stratification centers on ventricular tachyarrhythmias simply because of the availability of a successful management strategy, the implantable cardioverter/ defibrillator. Currently the main criterion of primary defibrillator prophylaxis is the presence of organic heart disease and depressed left ventricular systolic function assessed as left ventricular ejection fraction. However, only one third of eligible patients benefit from the implantable defibrillator, resulting in significant redundancy in the use of the device. The cost to the health care system of sustaining this approach is substantial. Further, the current low implantation rate among eligible population probably reflects a perceived low benefit-to-cost ratio of the device. Therefore, attempts to optimize the selection process for primary implantable defibrillator prophylaxis are paramount. The present report will review the most recent pathophysiology and risk stratification strategies for sudden cardiac death beyond the single criterion of depressed ejection fraction. Emphasis will be placed on electrophysiological surrogates of conduction disorder, dispersion of repolarization, and autonomic imbalance, which represent our current understanding of the electrophysiological mechanisms that underlie the initiation of ventricular tachyarrhythmias. Further, factors that modify arrhythmic death, including noninvasive risk variables, biomarkers, and genomics will be addressed. These factors may have great utility in predicting sudden cardiac arrhythmic death in the general public.

Unplanned Readmissions After Acute Myocardial Infarction: 1-Year Trajectory Following Discharge From a Safety Net Hospital.

Financial penalties rendered by the Centers for Medicare and Medicaid Services have brought about new challenges for safety net hospitals that serve a vulnerable patient population with risk factors associated with high readmission rates. Our goal was to determine the 1-year trajectory of unplanned readmissions in post-myocardial infarction (MI) patients, and to identify factors associated with readmission. A total of 261 acute MI patients admitted from April 2015 to April 2016 were evaluated in a multidisciplinary cardiology clinic within 10 days of hospital discharge and baseline characteristics and medical comorbidities were collected. Readmission and mortality data were obtained at 1 year through chart review and telephone follow-up. At 1 year, there were 90 (34%) unplanned readmissions of which half were for noncardiac diagnoses. Of these, 69 patients (77%) were readmitted once, 16 (18%) were readmitted twice, 2 (2%) were readmitted 3 times, and 3 (3%) were readmitted 4 times over the subsequent year. Cardiac causes of 1-year readmission included recurrent MI in 23 (9%) and decompensated heart failure in 18 (7%) patients. Depressed left ventricular systolic function (hazard ratio, 2.23; 95% confidence interval, 2.00-2.44; P = 0.0003) and diabetes mellitus (hazard ratio, 1.60; 95% confidence interval, 1.38-1.82; P = 0.029) were associated with a significantly higher risk of readmission at 1 year. Following acute MI, patients are readmitted for cardiac and noncardiac diagnoses well beyond the 30-day mark. This is likely a function of the vulnerability of the patient population rather than a reflection of the medical care provided. More frequent surveillance may attenuate this problem.

Clinical manifestations, diagnosis, and treatment of ischemic mitral regurgitation: a review.

Ischemic mitral regurgitation (IMR) is a frequent complication after acute myocardial infarction (AMI) associated with a worse prognosis. The pathophysiological mechanisms of IMR are not fully understood, but it is known to be a complex process in which ventricular remodelling is the main causal factor. The various imaging techniques in cardiology and echocardiography fundamentally have contributed significantly to clarify the mechanisms that cause and progressively aggravate IMR. At present, different therapeutic options, the most important of which are cardio-surgical, address this problem. Nowadays the improvement in cardiac surgery and transcatheter therapies, have shown a therapeutic advance in IMR management. IMR is a predictor of poor prognosis in patients with heart failure and depressed left ventricular (LV) systolic function. However, it remains controversial whether mitral regurgitation (MR) in these patients is a consequence of dilation and dysfunction of the LV, or whether it contributes to worsening the prognosis of the ventricular dysfunction. Given that echocardiography has a fundamental reference role in the identification, graduation of severity and evaluation of the therapeutics used in the treatment of MR, we are going to focus on it over the rest of the imaging techniques. In contrast to primary MR the benefits of mitral surgery in patients with secondary MR are uncertain. Therefore, we will comment fundamentally on the role of mitral surgery in patients with IMR, with an update of the different surgical interventions available, without forgetting to mention the other therapeutic options currently available.