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Acute myelogenous leukemia (AML) is one of the most common leukemias experienced in adults and conveys significant morbidity and mortality. While the traditional anthracycline based treatments of AML involves cytarabine, developments in alternatives (liposomal cytarabine, fludarabine, cladribine, azacitidine, decitabine), and targeted agents (midostaurin, gilteritinib, enasidenib, ivosidenib, gemtuzumab ozogamicin, and venetoclax) exist. Multiple cardiovascular adverse events, notably pericardial toxicity, have been observed in small studies; however, to date little is known about the comparative pericardial toxicity among these newer regimens. Due to the paucity of data, we sought to investigate the reported pericardial events and mortality associated with treatments for AML. Utilizing the Food and Drug Administration (FDA) Adverse Events Reporting System (FAERS), we identified all adverse events associated with FDA approved treatments for AML (2002-2022). Pericardial events were defined as pericarditis, pericardial effusion and tamponade. We excluded any individuals with age18 years old. Logistic regression was utilized to identify factors associated with pericardial events. Out of 94,262 reported adverse events, 675 pericardial toxicities were included (243 pericarditis, 479 tamponade). Pericardial events occurred less often in Cladribine (0.3%, P0.001), fludarabine (0.4%, P0.001), Venetoclax (0.3%, P0.001), enasidenib (0.3%, P value0.001), and ivosidenib (0.3%, P0.001) compared to Cytarabine (0.9%). Tamponade events occurred significantly less often in cladribine (0.1%, P0.001), fludarabine (0.4%, P = 0.001), enasidenib (0.1%, P = 0.006), ivosidenib (0.1%, P = 0.01), and venetoclax (0.1%, P0.001) compared to cytarabine 0.7%. After adjusting for age and sex, Cladribine (reporting odds ratio [ROR] 0.35 [95% CI 0.18-0.68], P = 0.008) and Fludarabine (ROR 0.65 [0.45-0.92], P = 0.03), venetoclax (ROR 0.57 [0.41-0.79], P0.001) remained significantly associated with lower incidence of reported pericardial events. While cytarabine has been the routinely used and/or drug of choice for induction chemotherapy for AML, alternatives like cladribine may have a greater safety profile regarding pericardial toxicities. Future studies should be directed at further investigating cardiovascular safety profiles of AML induction therapy.

Objectives The aim of this study was to determine the impact of invasive approaches and revascularization in patients with cocaine-associated non–ST-segment elevation myocardial infarction (NSTEMI). Background The role of invasive approaches in cocaine-associated NSTEMI is uncertain. Methods This retrospective cohort study identified 3,735 patients with NSTEMI and history of cocaine use from the Nationwide Readmissions Database from 2016 to 2017. Invasive approaches were defined as coronary angiography, percutaneous coronary intervention (PCI), and coronary artery bypass grafting (CABG). Revascularization was defined as PCI and CABG. The primary efficacy outcome was major adverse cardiac events (MACE), and the primary safety outcome was emergent revascularization. Nonadherence was identified using appropriate International Classification of Diseases-Tenth Revision codes. Two propensity-matched cohorts were generated (noninvasive vs. invasive and noninvasive vs. revascularization) through multivariate logistic regression. Results In the propensity score–matched cohorts, an invasive approach (hazard ratio [HR]: 0.72; 95% confidence interval [CI]: 0.56 to 0.92; p = 0.008) and revascularization (HR: 0.54; 95% CI: 0.40 to 0.73; p Conclusions Invasive approaches and revascularization for cocaine-associated NSTEMI are associated with lower morbidity. A history of medical nonadherence was not associated with a difference in morbidity but was associated with an increased risk for emergent revascularization with PCI.

When pericardial fluid accumulates and exceed the reserve volume of the pericardium or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may ensue, namely, cardiac tamponade (CT), characterised by the accumulation of pericardial fluid under pressure; constrictive pericarditis (CP), the result of scarring and loss of the normal elasticity of the pericardial sac; and effusive–constrictive pericarditis (ECP), characterised by the concurrence of a tense pericardial effusion and constriction of the heart by the visceral pericardium. Although relatively uncommon, prevalence estimates vary widely and depend on the nature of the cohorts studied, the methods used to diagnose ECP and the manner in which ECP is defined. Most cases of ECP are idiopathic, reflecting the frequency of idiopathic pericardial disease in general, and other causes include radiation, malignancy, chemotherapy, infection and postsurgical/iatrogenic pericardial disease. The diagnosis of ECP often becomes apparent when pericardiocentesis fails to decrease the right atrial pressure by 50% or to a level below 10 mm Hg. Important non-invasive diagnostic modalities include echocardiography, cardiac magnetic resonance and, to a lesser extent, cardiac CT. In cases with clear evidence of pericardial inflammation, a trial of an anti-inflammatory regimen is warranted. A complete pericardiectomy should be reserved for refractory symptoms or clinical evidence of chronic CP.

Background The global pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused significant morbidity and mortality, not only through devastating lung injury, but also due to multiple malfunctions in the cardiovascular system. The primary aetiology is believed to be mediated through lung alveolar injury; however, a few published reports have linked SARS-CoV-2 to significant organ dysfunction, venous thrombo-embolism, and coagulopathy. In view of the fact that the utility of tissue plasminogen activator in this population is not well studied, we present this case of rapid improvement in oxygenation after successful lytic therapy for thrombus in transit in this patient with SARS-CoV-2. Case summary We discuss a patient admitted with SARS-CoV-2 pneumonia. Due to the development of dramatic hypoxia, he underwent echocardiography which demonstrated extensive thrombus in transit. He received successful thrombolytic therapy with tissue plasminogen activator, with subsequent improvement in oxygenation. The patient was successfully discharged home on 2 L of oxygen via nasal cannula, and continues to improve at follow-up with his cardiologist and primary care physician. Conclusion This case not only highlights embolic causes of hypoxia in SARS-CoV-2, but demonstrates the important utility of an echocardiogram and tissue plasminogen activator in this population.

Despite advances in cardiovascular imaging, the diagnosis of constrictive pericarditis remains challenging. A multimodality approach to the diagnosis of CP is essential to (a) fully assess the extent of pericardial thickening and calcification, (b) detect the functional and hemodynamic consequences of the constricting pericardium, and (c) implement the optimal management strategy in these often complex cases. This case-based review highlights the role and diagnostic ambiguities of multimodality imaging.

Constrictive pericarditis (CP) is the result of scarring and the consequent loss of pericardial elasticity, which constrains ventricular filling; attenuates of the inspiratory decrease in intrathoracic pressure that is normally transmitted to the cardiac chambers and enhances ventricular interaction. CP can occur after virtually any pericardial disease process. The aetiology varies widely depending on the population studied, with idiopathic and post-treatment (postoperative or post-radiation) causes being more common in developed countries and infectious aetiologies (tuberculous or purulent) being more prominent in developing countries. While echocardiography is the first-line diagnostic tool for suspected CP, invasive haemodynamic evaluation is sometimes necessary to confirm the diagnosis, particularly in those with suboptimal or non-diagnostic echocardiographic findings in whom imaging with cardiac magnetic resonance or cardiac CT is either unavailable or non-diagnostic. Cardiac catheterisation in patients with surgically confirmed CP shows the following time-honoured invasive diagnostic findings: an elevated mean right atrial pressure; an early diastolic dip followed by a plateau during diastasis (square root sign); diastolic equalisation of pressures and respiratory variation in the right ventricular and left ventricular (RV–LV) pressures (mirror image discordance). Classically, pulmonary arterial (PA) systolic pressure is mild (usually no greater than 50 mm Hg), a finding used to distinguish CP from its haemodynamic doppelganger, restrictive cardiomyopathy. Recently, elevated PA pressures owing to both isolated post-capillary pulmonary hypertension (PH) (ie, passive transmittal of elevated left-sided filling pressures) and combined pre-capillary and post-capillary pressures (ie, additional pulmonary vasoconstriction and pulmonary vascular remodelling) have been reported in patients with increased LV filling pressure, including CP.1 2 In these patient subsets, increased systolic PH has been associated with increased mortality and …

While the classical apical ballooning takotsubo cardiomyopathy (TC) was first reported in the 1990s, the rarer mid-ventricular and basal variants were not formally recognized until recently and they remain poorly understood. In this case report, we describe a 67-year-old woman who, during her hospitalization for a subarachnoid hemorrhage and subsequent readmission, experienced multiple complications, each of which resulted in a different variant of TC. To our knowledge, this is the first report of a single patient developing all three variants of TC.

Quadricuspid pulmonary valve is a rare entity that can be associated with pulmonary artery aneurysm. It is usually asymptomatic and diagnosed incidentally. Association with other congenital or acquired heart diseases has been reported. Echocardiography and gated CT angiography can provide useful functional and anatomic information that can help in the diagnosis and management.

Pericarditis is a rare but debilitating complication of cytarabine therapy. While echocardiography can aid with the diagnosis, cardiac MRI has superior accuracy in establishing the diagnosis. In this case, we describe a 65-year-old patient receiving cytarabine as part of induction chemotherapy for acute myeloid leukemia who developed acute pericarditis. Her cardiac MRI revealed pericardial edema on T2-weighted STIR imaging and pericardial late gadolinium enhancement which confirmed the diagnosis.

Pericarditis is a rare but debilitating complication of cytarabine therapy. While echocardiography can aid with the diagnosis, cardiac MRI has superior accuracy in establishing the diagnosis. In this case, we describe a 65-year-old patient receiving cytarabine as part of induction chemotherapy for acute myeloid leukemia who developed acute pericarditis. Her cardiac MRI revealed pericardial edema on T2-weighted STIR imaging and pericardial late gadolinium enhancement which confirmed the diagnosis.

Background: Transcatheter aortic valve replacement (TAVR) may be an effective option for high-risk AR patients. Although international experiences of TAVR for AR are published, U.S. data is limited. The primary objective of this study was to investigate periprocedural and 30-days outcomes in terms of mortality and post-procedural complications in patients undergoing TAVR for AR using large national U.S. databases. Hypothesis: TAVR is a promising option in AR Methods: Study cohorts were derived from Nationwide Inpatient Sample (NIS) and Nationwide Readmissions Database (NRD) 2016-17. TAVR and AR were identified using ICD-10-CM-codes. The key outcomes were all-cause mortality, disabling stroke, valvular complications, complete heart block (CHB)/ permanent pacemaker placement (PPM), open heart surgery, acute kidney injury (AKI) requiring dialysis, and vascular complications. Multivariate logistic regression was used to adjust for confounders. Results: 915 patients from the NIS (male-71%, age 65-84.2%) and 822 patients from the NRD (male-69.3%, age 65-80.5%) underwent TAVR for AR. The median length of stay (LOS) was 4 days for both cohorts. In-hospital mortality was 2.7% in NIS and 30-day mortality was 3.3% in NRD. Disabling strokes were noted in 0.6% peri-procedurally and 1.8% at 30-days. Valve-related complications were 18-19% with paravalvular leak being the most common. Approximately 11% of patients developed CHB and/or needed PPM in both cohorts. In NRD, 2.2% of patients required dialysis for AKI, 1.5% developed vascular complications, and 0.6% required open-heart surgery within 30-days post-procedure. Anemia was predictive of increased overall complications and valvular complications, whereas, peripheral vascular disease was predictor of increased valvular complications and CHB/PPM. Conclusion: TAVR is a promising option in AR. Further studies are necessary for the expansion of TAVR as standard treatment in AR.

Introduction: Impact of an invasive approach in patients with cocaine associated non-ST-elevation myocardial infarction (CANSTEMI) is unknown. Hypothesis: To determine the effects of an invasive approach on patients with CANSTEMI. Methods: Nationwide Readmissions Database (NRD) from years 2016-2017 was utilized for hypothesis. We utilized ICD-10 CM codes I21.4 in primary diagnosis field and F14 in secondary fields to identify CANSTEMI. Coronary angiogram (CA) with or without percutaneous coronary intervention (PCI) was considered an invasive approach. The primary outcome was a composite of major adverse cardiac events (MACE) at one year. Secondary outcomes included all-cause mortality, MI readmission, stroke readmission, and emergent revascularization at one year. Cox-Proportional Hazard regression was used to adjust for demographic and comorbid confounders. Results: A total of 7,372 patients were identified of which 4,332 (58.8%) underwent invasive treatment. Patients with obesity, hyperlipidemia, tobacco use, and a personal and family history of CAD were more likely to undergo an invasive approach. Conversely, patients with CKD stage 3 or more and anemia were less likely to undergo invasive treatment. The primary outcome was significantly reduced with an invasive approach compared to a non-invasive approach. Similarly, all-cause mortality and MI readmission were also significantly reduced with an invasive approach. An invasive approach was associated with increased emergent revascularization compared to a noninvasive approach. On further stratification of an invasive approach, CA and PCI both were individually associated with improved MACE outcomes and PCI only was associated with increased emergent revascularization. Conclusions: In conclusion, an invasive approach with CA with or without PCI for CANSTEMI was associated with reductions in morbidity and mortality. PCI only was associated with an increase in emergent revascularization.

BACKGROUND Transcatheter aortic valve replacement (TAVR) can be an effective option for high-risk Aortic Regurgitation (AR) patients. Although international experiences of TAVR for AR are published, U.S. data are limited. This study sought to report the short-term outcomes of TAVR in AR in the U.S. POPULATION METHODS Study cohorts were derived from the Nationwide Inpatient Sample (NIS) and Nationwide Readmissions Database (NRD) 2016-17. TAVR and AR were identified using ICD-10-CM-codes. The key outcomes were all-cause mortality, disabling stroke, valvular complications, complete heart block (CHB)/permanent pacemaker placement (PPM), open-heart surgery, acute kidney injury (AKI) requiring dialysis, and vascular complications. Multivariate logistic regression was used to adjust for confounders. RESULTS 915 patients from the NIS (male-71%, age ≥65-84.2%) and 822 patients from the NRD (male-69.3%, age ≥65-80.5%) underwent TAVR for AR. The median length of stay (LOS) was 4 days for both cohorts. In-hospital mortality was 2.7%, and 30-day mortality was 3.3%. Disabling strokes were noted in 0.6% peri-procedurally and 1.8% at 30-days. Valve-related complications were 18-19% with paravalvular leak (4-7%) being the most common. Approximately 11% of patients developed CHB and/or needed PPM in both cohorts. In NRD, 2.2% of patients required dialysis for AKI, 1.5% developed vascular complications, and 0.6% required open-heart surgery within 30-days post-procedure. Anemia was predictive of increased overall complications and valvular complications, whereas peripheral vascular disease was a predictor of increased valvular complications and CHB/PPM. CONCLUSION TAVR is a promising option in AR. Further studies are necessary for the expansion of TAVR as the standard treatment in AR.

Aim Human Immunodeficiency Virus (HIV) patients commonly experience dyspnea for which an immediate cause may not be always apparent. In this prospective cohort study of HIV patients with exercise limitation, we use cardiopulmonary exercise testing (CPET) coupled with exercise cardiovascular magnetic resonance (CMR) to elucidate etiologies of dyspnea. Methods and results Thirty-four HIV patients on antiretroviral therapy with dyspnea and exercise limitation (49.7 years, 65% male, mean absolute CD4 count 700) underwent comprehensive evaluation with combined rest and maximal exercise treadmill CMR and CPET. The overall mean oxygen consumption (VO2) peak was reduced at 23.2 ± 6.9 ml/kg/min with 20 patients (58.8% of overall cohort) achieving a respiratory exchange ratio > 1. The ventilatory efficiency (VE)/VCO2 slope was elevated at 36 ± 7.92, while ventilatory reserve (VE: maximal voluntary ventilation (MVV)) was within normal limits. The mean absolute right ventricular (RV) and left ventricular (LV) contractile reserves were preserved at 9.0% ± 11.2 and 9.4% ± 9.4, respectively. The average resting and post-exercise mean average pulmonary artery velocities were 12.2 ± 3.9 cm/s and 18.9 ± 8.3 respectively, which suggested lack of exercise induced pulmonary artery hypertension (PAH). LV but not RV delayed enhancement were identified in five patients. Correlation analysis found no relationship between peak VO2 measures of contractile RV or LV reserve, but LV and RV stroke volume correlated with PET CO2 (p = 0.02, p = 0.03). Conclusion Well treated patients with HIV appear to have conserved RV and LV function, contractile reserve and no evidence of exercise induced PAH. However, we found evidence of impaired ventilation suggesting a non-cardiopulmonary etiology for dyspnea.

Due to limited real-world data, the aim of this study was to explore the impact of catheter ablation (CA) for atrial fibrillation (AF) in heart failure (HF). This retrospective cohort study identified 119,694 patients with AF and HF from the Nationwide Readmissions Database (NRD) from 2016 to 2017. Propensity-matching was generated using demographics, comorbidities, hospital and other characteristics through multivariate logistic regression. Greedy's propensity score match (1:15) algorithm was used to create matched data. The primary end point was a composite of HF readmission and mortality at 1 year. Secondary outcomes include HF readmission, mortality, AF readmission, and any-cause readmission at 1 year. Of the 119,694 patients, 63,299 had HF with reduced ejection fraction (HFrEF), and 56,395 had HF with preserved ejection fraction (HFpEF). In the overall HFrEF cohort, the primary outcome was similar (HR, 95% confidence interval, p-value) (1.01, 0.91 to 1.13, 0.811). AF readmission (0.41, 0.33 to 0.49,0.001) and any readmission (0.87, 0.82 to 0.93,0.001) were reduced with CA. In the propensity-matched HFrEF cohort, results were unchanged (primary outcome: 1.10, 0.95 to 1.27, 0.189; AF readmission: 0.46, 0.36 to 0.59,0.001; any readmission: 0.89, 0.82 to 0.98, 0.015). In the overall HFpEF cohort, the primary outcome was similar (0.90, 0.78 to 1.04, 0.154). AF readmission was reduced with CA (0.54, 0.44 to 0.65,0.001). In the propensity-matched HFpEF cohort, results were unchanged (primary outcome 1.10, 0.92 to 1.31, 0.289; AF readmission 0.44, 0.33 to 0.57,0.001). CA did not reduce mortality and HF readmission at one year irrespective of the type of HF, but significantly reduce readmission due to AF.

Venoarterial (VA) extracorporeal membrane oxygenation (ECMO) support is an increasingly used temporizing therapy for patients with refractory cardiogenic shock. Contrast-enhanced echocardiography plays a critical role in the diagnosis and management of diseases that precipitate severe cardiac failure. In this case report, we describe a previously healthy 60-year-old woman who presented with dyspnea on exertion, and whose hospital course was complicated by ventricular fibrillation, emergent coronary artery bypass surgery (CABG), and ECMO support. Her contrast-enhanced ECMO images demonstrated a unique pattern of opacification of three of the four cardiac chambers, which led to a diagnosis of severe aortic insufficiency.

Objective The aim of the study was to study the feasibility, safety, and efficacy of transesophageal echocardiography–guided intraoperative left ventricular lead placement via a video-assisted thoracoscopic surgery approach in patients with failed conventional biventricular pacing. Methods Twelve patients who could not have the left ventricular lead placed conventionally underwent epicardial left ventricular lead placement by video-assisted thoracoscopic surgery. Eight patients had previous chest surgery (66%). Operative positioning was a modified far lateral supine exposure with 30-degree bed tilt, allowing for groin and sternal access. To determine the optimal left ventricular location for lead placement, the left ventricular surface was divided arbitrarily into nine segments. These segments were transpericardially paced using a handheld malleable pacing probe identifying the optimal site verified by transesophageal echocardiography. The pacing leads were screwed into position via a limited pericardiotomy. Results The video-assisted thoracoscopic surgery approach was successful in all patients. Biventricular pacing was achieved in all patients and all reported symptomatic benefit with reduction in New York Heart Association class from III to I–II ( P = 0.016). Baseline ejection fraction was 23 ± 3%; within 1-year follow-up, the ejection fraction increased to 32 ± 10% ( P = 0.05). The mean follow-up was 566 days. The median length of hospital stay was 7 days with chest tube removal between postoperative days 2 and 5. Conclusions In patients who are nonresponders to conventional biventricular pacing, intraoperative left ventricular lead placement using anatomical and functional characteristics via a video-assisted thoracoscopic surgery approach is effective in improving heart failure symptoms. This optimized left ventricular lead placement is feasible and safe. Previous chest surgery is no longer an exclusion criterion for a video-assisted thoracoscopic surgery approach.

The pericardium consists of a visceral mesothelial monolayer (epicardium) that reflects over the great vessels and joins an outer, relatively inelastic fibrous parietal layer of organized collagen and elastin fibers, between which is a potential space that normally contains up to 50 mL of plasma filtrate. Although not essential for life, the pericardium serves important albeit subtle functions in the euvolemic healthy individual that become increasingly important in hypervolemic states and conditions in which the heart enlarges acutely. The pericardial functions can be divided into the mechanical, reflex, membranous, metabolic, ligamentous.

This review examines the current status of measuring left atrial mechanical functions and the ability of atrial functional analysis to predict cardiovascular outcomes. Increasing data support the use of echocardiography, computed tomography, and cardiac magnetic resonance in this regard. This review will discuss the various techniques used to assess left atrium reservoir, conduit, and booster pump functions and will focus on their ability to predict cardiovascular events in general and referral populations, and in patients with atrial fibrillation and other heart diseases.

Prolylcarboxypeptidase (PRCP) is a carboxypeptidase that cleaves angiotensin II (AngII) forming Ang(1-7). The impact of genetic PRCP deficiency on AngII metabolism, blood pressure (BP), kidney histology, and cardiac phenotype was investigated in two lines of PRCP-deficient mice: KST302 derived in C57BL/6 background and GST090 derived in FVB/N background. The GST090 line had increased mean arterial pressure (MAP) (113.7 ± 2.07 vs. WT 105.0 ± 1.23 mmHg; p 0.01) and left ventricular hypertrophy (LVH) (ratio of diastolic left ventricular posterior wall dimension to left ventricular diameter 0.239 ± 0.0163 vs. WT 0.193 ± 0.0049; p 0.05). Mice in the KST302 line also had mild hypertension and LVH. Cardiac defects, increased glomerular size, and glomerular mesangial expansion were also observed. After infusion of AngII to mice in the KST302 line, both MAP and LVH increased, but the constitutive differences between the gene trap mice and controls were no longer observed. Plasma and cardiac AngII and Ang(1-7) were not significantly different between PRCP-deficient mice and controls. Thus, PRCP deficiency is associated with elevated blood pressure and cardiac alterations including LVH and cardiac defects independently of systemic or cardiac AngII and Ang(1-7). An ex vivo assay showed that recombinant PRCP, unlike recombinant ACE2, did not degrade AngII to form Ang(1-7) in plasma at pH 7.4. PRCP was localized in α-intercalated cells of the kidney collecting tubule. The low pH prevailing at this site and the acidic pH preference of PRCP suggest a role of this enzyme in regulating AngII degradation in the collecting tubule where this peptide increases sodium reabsorption and therfore BP. However, there are other potential mechanisms for increased BP in this model that need to be considered as well. PRCP converts AngII to Ang(1-7) but only at an acidic pH. Global PRCP deficiency causes heart and kidney alterations and a moderate rise in BP. PRCP is abundant in the kidney collecting tubules, where the prevailing pH is low. In collecting tubules, PRCP deficiency could result in impaired AngII degradation. Increased AngII at this nephron site stimulates Na reabsorption and increases BP.Prolylcarboxypeptidase (PRCP) converts AngII to Ang (1-7) but only at an acidic pH. Global PRCP deficiency causes heart and kidney alterations and a moderate rise in BP. PRCP is abundant in the kidney collecting tubules, where the prevailing pH is low. In collecting tubules, PRCP deficiency could result in impaired AngII degradation. Increased AngII at this nephron site stimulates Na reabsorption and increases BP.

Aortic prosthetic valve endocarditis is often a challenging disease process that carries high morbidity and mortality. Echocardiography is widely used to identify infected valves and associated complications. One major complication of an infection involving the aortic annulus is dehiscence of the prosthetic valve from the aortic root and is usually associated with paravalvular regurgitation. Here, we present a rare case of complete prosthetic valve dehiscence without paravalvular regurgitation on transthoracic and transesophageal echocardiography.

Myocardial contusion and aortic injury are well-known cardiac complications of blunt chest trauma, but valvular injury is rare. Traumatic valve injuries most commonly involve the aortic valve, with isolated mitral valve injury being quite rare. We report a case of acute severe mitral regurgitation due to ruptured chordae tendineae requiring surgical repair following a motor vehicle accident.

To review the current status of measuring left atrial functions with echocardiography and the ability of atrial functional analysis to predict cardiovascular outcomes. An increasing body of data suggests that left atrium (LA) function assessed with echocardiography provides incremental prognostic information in general and referral populations, and in patients with atrial fibrillation, stroke, heart failure, and ischemic and valvular heart disease. In addition to volumetric analysis and spectral and tissue Doppler, deformational (strain and strain rate) imaging has most recently been used to assess LA reservoir, conduit, and booster pump functions and predict cardiovascular events. Studies of LA function provide new insights into the contribution of LA performance to cardiovascular disease and are promising tools for predicting cardiovascular events in healthy subjects and patients with heart disease. However, robust clinical outcome data from large prospective outcome trials are needed to confirm the incremental predictive ability of these LA functional measures before they are widely accepted.

Purpose of review To summarize recent literature on the use of left atrial strain in the diagnosis and management of patients with heart failure. Recent findings Left atrial dysfunction is a hallmark of diastolic dysfunction and heart failure, in particular, heart failure with preserved ejection fraction (HFpEF). Recently, myocardial deformation analysis via strain and strain rate measurements have been applied to the left atrium. These measurements have been shown to aid in the diagnosis of heart failure and be accurate predictors of cardiac pressures, diastolic dysfunction, exercise performance, and clinical outcomes such as cardiac hospitalizations and mortality. However, limitations related to the technical aspect of accurately imaging and tracking the thin-walled left atrium and the current lack of consensus on 'normal' reference values remain. Summary Left atrial strain represents a novel, noninvasive technique to aid in the diagnosis, prognosis, and management of patients with heart failure. Although it is not yet a part of routine clinical practice, the measurement has significant promise within this population pending further validation.

Background Left ventricular non-compaction cardiomyopathy (LVNCC) is a rare disease that starts in utero and may progress to heart failure (HF), sometimes requiring orthotopic heart transplantation (OHT). There are limited data addressing characteristics of LVNCC patients that require OHT and their outcomes. We therefore sought to investigate the characteristics and outcomes of LVNCC patients treated with OHT. Methods We queried the United Network for Organ Sharing (UNOS) database for all patients listed for OHT with LVNCC as the primary heart failure etiology between 2000 and 2013. We examined their characteristics at listing and outcomes after OHT and compared the findings with those of patients with idiopathic cardiomyopathy (IDCMP). Results We identified 113 patients (43 adults and 70 pediatrics) with LVNCC of 45,298 patients (0.25% overall, 0.11% of adults and 1.0% of pediatrics) listed for OHT in this time period. Most were male children with mean age at listing of 16.9 years. Compared with the overall IDCMP cohort, patients with LVNCC were younger, had higher use of inotropes and extracorporeal membrane oxygenation (ECMO), and were more often listed as UNOS Status 1A with shorter waiting time. However, when adjusted for age, gender and ethnicity, these differences disappeared. During transplant listing, 8 (7.9%) died, 5 (5.0%) improved and avoided transplant, 3 (3.0%) became too sick for transplant and 78 (77.2%) underwent OHT. There was a non-significant trend toward longer cardiac allograft survival in patients with LVNCC (10.6 vs 9.4 years; log-rank test, p = 0.068). Patients with LVNCC had similar outcomes to other IDCMP patients, except for more post-transplant infections (50.0% vs 21.6%, p Conclusions LVNCC patients undergoing heart transplantation are mostly pediatric and predominantly bridged to transplant with inotropes or ECMO. Despite having more post-transplant infections, their survival is similar to that of other IDCMP patients.

The purpose of this paper is to review current approaches to the diagnosis and treatment of pericardial effusions and cardiac tamponade. Recent recommendations from the American Society of Echocardiography and the European Society of Cardiology have refined our approaches to the patient with pericardial effusion and cardiac tamponade, but significant knowledge gaps remain. New diagnostic and triage strategies have been proposed, and recent data have advanced our ability to assess the presence and size of a pericardial effusion, assess its hemodynamic impact, and establish its cause. Despite these recent findings, there is a paucity of evidence-based data to guide the management of pericardial effusion and cardiac tamponade. While the first-line function of echocardiography in managing these disorders is unquestioned, there are increasing niche roles for multimodality imaging.

> Form follows function—this has been misunderstood. Form and function should be one, joined in a spiritual union. > > —Frank Lloyd Wright Left atrial (LA) remodeling refers to the spectrum of pathophysiological changes in atrial structure and mechanical function and the electric, ionic, and molecular milieu of the LA that most often occurs in response to stresses imposed by conditions such as hypertension, heart failure, diabetes mellitus, and obesity. Remodeling is initially adaptive, but when it occurs in response to a chronic pathological stimulus (as opposed to remodeling of the athlete’s heart), it often becomes maladaptive and associated with an increased risk of cardiovascular events and mortality.1 Remodeling forms the basis of atrial cardiomyopathy, defined recently by a multisociety, expert consensus statement as any complex of structural, architectural, contractile, or electrophysiological changes affecting the atria with the potential to produce clinically relevant manifestations.2 See Article by Oliver et al LA structural remodeling is the complex phenotypic expression that results from changes in LA size, shape,3 and architecture and alterations in the cardiomyocyte, fibroblast, and noncollagen infiltrative compartments of the atrium.2 LA enlargement, which is simple to measure, is the default clinical hallmark of structural remodeling that occurs most often in response to LA pressure and volume overload; in the absence of atrial fibrillation, mitral valvular disease, and high cardiac output states, it is an excellent biomarker for the presence and severity of left ventricular (LV) diastolic dysfunction.4 Moreover, LA enlargement portends a poor prognosis in a variety of cardiovascular diseases.1 Indices of LA size are also markers of cardiovascular risk in the general population.5,6 The strength of the association between atrial remodeling as determined by increased maximal indexed LA volume (LAVi) and cardiovascular risk reported in the literature is influenced by the nature …

The author examines the ability of left atrial size and function to predict cardiovascular outcomes. Data are sufficient to recommend evaluation of left atrial volume in certain populations, and although analysis of atrial reservoir, conduit, and booster pump function trails in that regard, the gap is rapidly closing. In this state-of-the-art paper, the author reviews the methods used to assess left atrial size and function and discusses their role in predicting cardiovascular events in general and referral populations and in patients with atrial fibrillation, cardiomyopathy, ischemic heart disease, and valvular heart disease.

The term "post-cardiac injury syndromes" includes post-myocardial infarction pericarditis, post-pericardiotomy syndrome, and post-traumatic pericarditis (iatrogenic, i.e. after percutaneous coronary or intracardiac interventions, such as pacemaker lead insertion, radiofrequency ablation, or non-iatrogenic, i.e. following blunt or penetrating trauma). All these conditions represent different clinical conditions characterized by an initial cardiac injury involving the pericardium/myocardium and/or pleura and the subsequent inflammatory syndrome ranging from simple, uncomplicated pericarditis to more complicated cases with pleuropericarditis, cardiac tamponade or massive pleural effusion. The etiopathogenesis is presumed to be immune-mediated in predisposed individuals that develop autoreactive reactions following the initial traumatic event. Treatment is essentially based on empirical anti-inflammatory therapy and adjunctive colchicine, which has been shown to be safe and efficacious for the prevention of pericarditis.

Aims The transcription factor hexamethylene-bis-acetamide-inducible protein 1 (HEXIM1) regulates myocardial vascularization and growth during cardiogenesis. Our aim was to determine whether HEXIM1 also has a beneficial role in modulating vascularization, myocardial growth, and function within the adult heart. Methods and results To achieve our objective, we created and investigated a mouse line wherein HEXIM1 was re-expressed in adult cardiomyocytes to levels found in the foetal heart. Our findings support a beneficial role for HEXIM1 through increased vascularization, myocardial growth, and increased ejection fraction within the adult heart. HEXIM1 re-expression induces angiogenesis, that is, essential for physiological hypertrophy and maintenance of cardiac function. The ability of HEXIM1 to co-ordinate processes associated with physiological hypertrophy may be attributed to HEXIM1 regulation of other transcription factors (HIF-1-α, c-Myc, GATA4, and PPAR-α) that, in turn, control many genes involved in myocardial vascularization, growth, and metabolism. Moreover, the mechanism for HEXIM1-induced physiological hypertrophy appears to be distinct from that involving the PI3K/AKT pathway. Conclusion HEXIM1 re-expression results in the induction of angiogenesis that allows for the co-ordination of tissue growth and angiogenesis during physiological hypertrophy.

Background: Conflicting evidence exists on the ideal choice of non-invasive pharmacologic stress imaging for coronary artery disease (CAD) diagnosis in patients with left bundle branch block (LBBB). The aim of this meta-analysis is to compare data that examine the sensitivity and specificity of non-invasive pharmacologic stress imaging in patients with LBBB for obstructive CAD diagnosis. Methods: We performed a literature search in MEDLINE, embase.com and Cochrane (CENTRAL) without publication type or language restrictions. Both pharmacologic stress echocardiography (SE) and nuclear myocardial perfusion imaging (MPI) searches were restricted to the period between January 2004 and review time. Exclusion criteria included studies that lacked sensitivity and specificity data. The primary objective was to compare the sensitivities and specificities of all pharmacologic SE, MPI, myocardial contrast echocardiography (MCE), stress cardiac magnetic resonance (CMR) and positron emission tomography (PET) for identifying significant CAD in patients with LBBB. Results: 10 studies met the inclusion criteria for analysis. The sensitivity and specificity odds ratio of MCE was 92% (95% CI 81-97%), 93% (95% CI 86- 97%); Dobutamine (D)-CMR 64% (95% CI 42-82%), 94% (95% CI 85-98%); pharmacologic SE 73% (95% CI 55-86%), 84% (95% CI 75-91%); and pharmacologic MPI 83% (95% CI 72-91%), 56% (95% CI 42-70%). Conclusion: MCE and D-CMR appear to have improved diagnostic accuracy in comparison to pharmacologic SE and MPI in patients with LBBB. Additional MCE and D-CMR studies are warranted given their potential to become the non-invasive gold standard for the diagnosis of CAD in this population.

Background: Despite the American Society of Echocardiography recommendation to use left atrial volume indexed for body surface area (LAVI) for quantification of left atrial size, a variety of methods are used in clinical practice. Our objectives were to evaluate the accuracy of M-mode and two-dimensional (2D) echocardiographic LA size estimates to LAVI and to determine their ability to predict left ventricular diastolic dysfunction. Methods: In 150 consecutive patients, LA diameter (LAD), LA diameter indexed for body surface area (LADI), LA area in the apical two- and four-chamber views (LAA 2c and LAA 4c), biplane area–length LA volume (LAV), and LAVI were obtained. The accuracy of these methods to quantify LA enlargement by LAVI, correlation with clinical parameters, and ability to act as a surrogate for diastolic dysfunction were determined using Pearson correlation coefficients along with univariate and multiple logistic analysis. Results: The true degree of LA size (with LAVI as standard) was identified by LAD in 45%, LADI in 42%, LAA 4c in 43%, and LAA 2c in 41%. All methods showed positive correlation with age, E/E′, mitral regurgitation, and right atrial size and negative correlation with ejection fraction. LAVI was the strongest method to predict any (c = 0.655, P = 0.012) or moderate–severe (P = 0.856 and P < 0.001) diastolic dysfunction. All methods have greater capacity to identify moderate or severe diastolic dysfunction than any degree of diastolic dysfunction alone. Conclusions: One-dimensional and 2D methods inaccurately quantify LA size and are inferior to LAVI to predict diastolic dysfunction. (Echocardiography 2012;29:379-384)

Background— Decreased expression of cardiac myosin binding protein C (cMyBPC) as a result of genetic mutations may contribute to the development of hypertrophic cardiomyopathy (HCM); however, the mechanisms that link cMyBPC expression and HCM development, especially contractile dysfunction, remain unclear. Methods and Results— We evaluated cardiac mechanical function in vitro and in vivo in young mice (8–10 weeks of age) carrying no functional cMyBPC alleles (cMyBPC −/− ) or 1 functional cMyBPC allele (cMyBPC ± ). Skinned myocardium isolated from cMyBPC −/− hearts displayed significant accelerations in stretch activation cross-bridge kinetics. Cardiac MRI studies revealed severely depressed in vivo left ventricular (LV) magnitude and rates of LV wall strain and torsion compared with wild-type (WT) mice. Heterozygous cMyBPC ± hearts expressed 23±5% less cMyBPC than WT hearts but did not display overt hypertrophy. Skinned myocardium isolated from cMyBPC ± hearts displayed small accelerations in the rate of stretch induced cross-bridge recruitment. MRI measurements revealed reductions in LV torsion and circumferential strain, as well reduced circumferential strain rates in early systole and diastole. Conclusions— Modest decreases in cMyBPC expression in the mouse heart result in early-onset subtle changes in cross-bridge kinetics and in vivo LV mechanical function, which could contribute to the development of HCM later in life.