Dilated Left Ventricle Research Articles

The additive role of cardiac CT in a patient with cardiogenic shock and suspected mechanical complication of myocardial infarction.

A 69-year-old woman with previous hypertension and type-2 diabetes was admitted to the emergency department with syncope, referring continuous chest pain in the last 4 days. At hospital admission, the patient was in cardiogenic shock. The initial electrocardiogram showed Q waves in the anterior wall and ST-segment elevation on the anterior, lateral, and inferior walls. A bedside echocardiogram was immediately performed (panels A and B; Supplementary data online, Video S1) which showed a dilated left ventricle (LV) with severe LV systolic dysfunction and akynesia of the mid-apical segments of all ventricular walls. The patient had pericardial effusion (PE) with images suggesting clots near to the right ventricle free wall, with tamponade criteria. Although no rupture of the LV wall was clearly visible on echocardiogram, there was a high clinical suspicion of this complication. Cardiac computed tomography (CT) angiography confirmed myocardial rupture at the distal segment of the anterior wall and a mild circumferential PE, with a fluid density suggestive of haematic content (panels C, D, and E; Supplementary data online, Video S2). The patient underwent emergent surgery (panel F; Supplementary data online, Video S3) to correct the LV free wall rupture.

Abstract 3208: Bone-derived TGF-ß release is associated with cardiac dysfunction due to oxidation of SR calcium gatekeepers, Ca2+ leak and mitochondrial dysfunction

Abstract Cancer patients with bone metastases are associated with cardiac dysfunction. Heart attack was observed in 3.8% of patients within 30 days of diagnosis. Here, we report that bone turnover marker β-CTX (P=0.002) and platelet-poor plasma TGF-ß (P=0.036) from patients with bone metastasis were significantly higher than those without bone metastasis. In patients, serum β-CTX concentration was positively correlated with TGF-ß (R2=0.67, P<0.0001). Excess TGF-ß release caused skeletal muscle weakness by oxidation of the sarcoplasmic reticulum (SR) Ca2+ ryanodine receptor (RyR), induction of SR and oxidative stress in breast cancer patients with bone metastasis. Thus, we hypothesized that the systemic effects of TGF-ß could have similar effects on cardiac muscle to induce heart failure. Mechanistically, we showed that TGF-β1 increased transcription of NADPH oxidases, aberrant Ca2+ signaling, SR stress and ROS production in adult cardiomyocytes. We tested this in a transgenic mouse model of Camurati-Engelmann Disease (CED) in which mutant TGF-ß1 (H222D) is overexpressed in osteoblasts and causes accelerated bone destruction. We found that CED mice had increased cardiac size, dilated left ventricle and reduced ejection fraction, by echocardiography, compared to littermate controls. This was associated with increased phosphorylation of Smad2/3, myocardial necrosis and fibrosis in cardiac tissues. Similarly, SR Ca2+ channel RyR2 and SERCA2 showed a significant increase in oxidation and nitrosylation and reduced binding of the stabilizing subunits as well as upregulated iNOS and NADPH oxidases consistent with depressed SR Ca2+ re-uptake, RyR-mediated Ca2+ leak and oxidative stress in CED mice left ventricular. Mitochondria isolated from ventricular samples showed increased mitochondrial Ca2+ overload, ROS production, release of apoptotic proteins, reduced mitochondrial DNA and ATP reproduction in CED mice. Thus, a feed-forward cycle of pathological Ca2+ handling is created between SR mitochondria, which underlies TGF-ß-driven cardiac muscle dysfunction. These findings are consistent with mitochondrial calcium toxicity induced by SR Ca2+ re-uptake and leak, and heart failure with reduced ATP production. The data suggest that excess TGF-ß release by pathological bone destruction could have significant impact on cardiac muscle to induce oxidative stress, SR Ca2+ leak and heart failure and could explain heart disease observed clinically with bone metastasis. Targeting this pathway may improve survival in patients with bone metastases. Citation Format: Lei Shi, Truc Kuo, Jade Martinez, Sukanya Suresh, Trupti Trivedi, Gabriel M. Pagnotti, Leah D. Guerra, Xu Cao, Theresa A. Guise. Bone-derived TGF-ß release is associated with cardiac dysfunction due to oxidation of SR calcium gatekeepers, Ca2+ leak and mitochondrial dysfunction [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3208.

The masquerade: What is the wide complex tachycardia?

A 19-year-old boy with rheumatic heart disease, post mitral valve replacement three years earlier, presented with recurrent episodes of palpitations. Sinus rhythm ECG showed left bundle branch block (LBBB). During symptoms, ECG showed regular wide complex tachycardia (WCT) at a rate of 140 beats per min (bpm) with QRS identical to sinus rhythm. Echocardiography revealed a dilated left ventricle with severely depressed systolic function. An electrophysiology study was performed. Four catheters - high right atrium, coronary sinus, right ventricle (RV), and multipolar catheter with close electrode spacing in the His region - were placed. The baseline His-Ventricle (HV) interval was 70 msec. Ventricular pacing showed central and decremental retrograde conduction. Clinical tachycardia at a rate of 140 bpm was initiated during atrial extra stimulus protocol with isoprenaline. The initiation and continuation of the tachycardia are shown (Figures1 and2). What is the best explanation for the arrhythmia seen? This article is protected by copyright. All rights reserved.

Acute pulmonary embolism immediately after cesarean section despite dilatation of the left ventricle: a case report and literature review

Abstract Introduction Pulmonary embolism is a lethal complication during pregnancy and the puerperium. Compared with vaginal delivery, the risk of pulmonary disease is almost twice as high with cesarean section. However, diagnosing a pulmonary embolism can be challenging. Case presentation A 31-year-old nulliparous woman underwent cesarean section. Postoperatively, the patient suddenly developed dyspnea and dull pain in the left back region and cardiopulmonary function deteriorated rapidly. Venous ultrasonography confirmed thrombosis of the left common iliac vein. Transthoracic echocardiography revealed a normal right heart and a dilated left ventricle with a patent foramen ovale. An acute pulmonary embolism was confirmed by pulmonary angiography. Catheter-directed thrombus fragmentation and thrombolysis were then performed. Conclusion Dilated left ventricular echocardiography does not exclude postpartum acute pulmonary embolism. In extreme emergencies, when acute pulmonary embolism is the most likely diagnosis and life-threatening, catheter-directed angiography may be preferred over other approaches.

The association of Hs-Troponin I with cardiac dysfunction and structural changes in chronic heart failure with reduced ejection fraction patients

Introduction: Cardiomyocyte death is the key pathological feature of heart failure with reduced ejection fraction (HFrEF). One of the circulating markers which represent myocardial cell death is cardiac troponin. High sensitivity-troponin I (hs-TnI) has been validated as an acute coronary syndrome diagnostic criteria. But its value and role in chronic heart failure, specifically HFrEF, has been variable in different studies. The aim of this study was to determine whether hs-TnI, an indicator of cardiomyocyte injury, is associated with functional and structural changes in HFrEF patients. Methods: A hospital-based cross-sectional analytic study was conducted on 72 patients with stable chronic HFrEF between April and October 2022. All subjects underwent echocardiography (Philips EPIQ7 and Affinity 70) and hs-troponin I serum measurement (Abbott Architect assay). Spearman’s test was used to evaluate the correlation between hs-troponin I and left ventricular ejection fraction (LVEF), E/A ratio, left ventricular end-diastolic volume (LVEDV), tricuspid annular plane systolic excursion (TAPSE) and left atrial volume index (LAVI). Results: hs-TnI concentrations were quantifiable in all samples ranging from 10 to 280.9 pg/mL. hs-TnI was associated significantly with LVEF (r=-0.39; p<0.01), E/A ratio (r=0.328, p=0.01), and LVEDV (r=0.278, p=0.04). hs-TnI was not correlated with TAPSE and LAVI (r=0.241; p=0.07 and r=-0.13; p=0.429, respectively). The correlation between hs-troponin I with LVEF, E/A ratio and LVEDV proved that the degree of myocardial injury is directly associated with left ventricle (LV) systolic and diastolic dysfunction and also with LV dilatation. While it is not correlated with right ventricle (RV) systolic function. Hs-TnI may represent the injury in LV better than RV. Conclusion: These findings support the association of hs-TnI as a circulating marker of cardiomyocyte injury with LV dysfunction (systolic and diastolic) and dilatation in chronic HFrEF patients. This has expanded the role of hs-TnI in chronic heart disease.

Comparison of Hemodynamic Response between Patients with Systolic Heart Failure Differing in Serum Aldosterone Concentrations during and after a 6-Minute Walk Test.

Aldosterone regulates hemodynamics, including blood pressure (BP), and is involved in the development and progression of cardiovascular diseases, including systolic heart failure (HF). While exercise intolerance is typical for HF, neither BP nor heart rate (HR) have specific characteristics in HF patients. This study compares BP and HR profiles during and after standardized exercise between patients with systolic HF with either lower or higher aldosterone concentrations. We measured BP and HR in 306 ambulatory adults with systolic HF (left ventricular ejection fraction (LVEF) <50%) during and after a 6 min walk test (6MWT). All patients underwent a resting transthoracic echocardiography, and venous blood samples were collected for biochemical analyses. The patients were also divided into tertiles of serum aldosterone concentration: T1 (<106 pg/mL), T2 (106 and 263 pg/mL) and T3 (>263 pg/mL), respectively. Individuals from T1 and T2 were combined into T1-T2 as the reference group for comparisons with patients from T3. The individuals from T3 had significantly lower systolic, mean and diastolic BPs at rest, at the end and at 1 and 3 min post-6MWT recovery, as well as a more dilated left atrium and right ventricle alongside a higher concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP). Higher serum aldosterone concentration in HF patients with an LVEF < 50% is associated with a lower 6MWT BP but not an HR profile.

Anomalous origin of the left main coronary artery from the right pulmonary artery: a case report

Anomalous origin of the left coronary from the right pulmonary artery (AOLCARPA) is an extremely rare anomaly, which has been reported in only a few patients worldwide [1] An 8-month-old male patient weighing 5.7 kg came to our hospital with chief complaints of tachypnea while feeding and failure to thrive. ECG of the patient showed sinus tachycardia. The patient had a heart rate of 140/min and saturation of 99% on room air. Chest radiograph showed cardiomegaly. Transthoracic echocardiography showed moderate mitral regurgitation, dilated left atrium and ventricle, severe left ventricular (LV) dysfunction, global LV hypokinesia with an LV ejection fraction of 15–20%. Flow pattern in the left anterior descending artery and the left circumflex artery was reversed and the right coronary artery (RCA) was dilated. The left main coronary artery (LMCA) origin was not clear. As the diagnosis was unclear, computed tomography coronary angiography (CTCA) was done to delineate the coronary anatomy, which showed an anomalous origin of LMCA from the right pulmonary artery (RPA) (Figs. 1 and 2Figs 1, 2). Blood investigations including complete blood count, and liver and kidney function tests were normal. Preoperative medication of the patient included digoxin, spironolactone, furosemide, and milrinone infusion. The patient was posted for corrective repair of anomalous origin of the left coronary artery from the RPA.Figure 1: Computed tomography coronary angiography showing left main coronary artery (LMCA) arising from the right pulmonary artery (RPA). PROX LAD, proximal left anterior descending artery.Figure 2: (a) Midesophageal (ME) ascending aortic short-axis (SAX) view showing retrograde flow from left main coronary artery (LMCA) to right pulmonary artery (RPA). (b) Midesophageal (ME) four-chamber view showing dilated left ventricle (LV) and mitral regurgitation jet. (c) Origin of LMCA from RPA. LPA, left pulmonary artery; Asc Aorta, ascending aorta.On the day of surgery, the patient was taken to the operating room. Preoperative inotropic support of intravenous infusion of milrinone 0.5 µg/kg/min was continued. After attaching a multiparameter monitor with a five-lead ECG, noninvasive blood pressure monitor, and a pulse oximeter, general anesthesia was induced with intravenous fentanyl 2 µg/kg, midazolam 0.1 mg/kg, vecuronium 0.1 mg/kg, and endotracheal intubation was done. Femoral artery was cannulated for invasive arterial blood pressure monitoring, and central venous catheter was inserted in the right internal jugular vein. Anesthesia was maintained with isoflurane and intermittent boluses of fentanyl and vecuronium. Intraoperative ventilation was instituted with the goals of avoiding hypocarbia, hyperoxia, and alkalosis. An FiO2 of 0.35 was kept with PaO2 targets of 80–100 mm Hg to maintain pulmonary vascular resistance End-tidal carbon dioxide (EtCO2) was maintained between 40 and 42 mm Hg. Pre-bypass transesophageal echocardiography (TOE) examination was carried out with a pediatric 9T probe (Vivid I, GE; Vingmed Ultrasound, Horten, Norway). ME ascending aorta short-axis view showed the origin of LMCA from RPA (Fig. 2a). Midesophageal four-chamber view showed dilated LV and moderate mitral regurgitation (Fig. 2b). Heparin 400 IU/kg was given, and cardiopulmonary bypass was instituted. Cardiopulmonary bypass was established using aortobicaval cannulation with looping of both pulmonary artery branches. Myocardial preservation was obtained with antegrade cold blood potassium cardioplegia into the aorta and main pulmonary artery. Under low pump flows, LMCA origin was identified originating from the RPA (Fig. 2c). Medial trap door was made in the aorta and LMCA was anastomosed to the aorta (coronary translocation). Posterior annuloplasty of the mitral valve was performed through the trans-septal approach. Weaning from the cardiopulmonary bypass was uneventful with minimal inotropic support (milrinone 0.5 µg/kg/min; Epinephrine 0.04 µg/kg/min). The chest was kept open with a sterile membrane cover electively and the patient was shifted to the pediatric ICU with stable hemodynamics. AOLCARPA is an extremely rare congenital coronary anomaly. Only 10–20% of neonates survive till adulthood, and it depends on the adequacy of LV perfusion through collaterals to LCA from RCA and the proportion of coronary steal from the LCA to pulmonary artery [2] Coronary angiogram is usually done to delineate the anatomy and for the diagnosis. In this case, the origin of LMCA could not be visualized on transthoracic echocardiography (TTE) leading to inconclusive diagnosis. CTCA delineated the exact anatomy and showed its origin from RPA. Intraoperative TOE examination also revealed it as a case of AOLCARPA. Anesthetic management of patients presenting with ALOCARPA includes rapid and smooth intubation, while avoiding swings in blood pressure and heart rate. A decrease in pulmonary vascular resistance is avoided by preventing hyperventilation, hyperoxia and hypocarbia [3] The aim is to maintain a PaO2 of 80–100 mm Hg and an EtCO2 of 40–45 mm Hg. Both reduction and increase in afterload can hamper RCA perfusion and stroke volume, respectively. An optimum preload is required to ensure adequate cardiac output. CTCA and TOE examinations are useful modalities for delineating the coronary anatomy and help in planning the perioperative surgical and anesthetic management of the patient.

Seizure-Induced Coma in Patient with Haemoglobin 1.3 gram per decilitre and MultiOrgan Dysfunction: A Rare Case Report

People of all ages are affected by anaemia which is a serious global health problem. Iron Deficiency Anaemia (IDA) seems to be the most commonly occurring type of anaemia in women. Elderly people with anaemia have higher morbidity and mortality. The purpose of treatment is to tackle the disorder’s underlying cause. Older people with persistent anaemia may need regular blood transfusions. The authors present a case report of a 55-year-old woman who visited the Emergency Department with primary complaints of convulsions and subsequent unconsciousness. She had generalised oedema and weakness since eight days. On examination she was afebrile with pulse 92 beats/min, Blood Pressure (BP) of 80 mmHg systolic. Laboratory results showed haemoglobin of 1.3 g/dL, increased White Blood Cells (WBC) and peripheral smear showed pencil-shaped cells and teardrop cells. Radiological investigation showed grade III renal parenchymal disease, cirrhosis of liver, gross ascites with bilateral pleural effusion, and splenic cyst. A 2D Echocardiography was done, which was suggestive of left ventricular hypertrophy, mild to moderate systolic dysfunction, along with dilated left ventricle. She was intubated in view of low Glasgow Coma Scale (GCS) and unconsciousness. On further stay in the hospital, she received blood transfusion. Hence, this case is a rare finding of severe anaemia.

Utilities and Limitations of Cardiac Magnetic Resonance Imaging in Dilated Cardiomyopathy.

Dilated cardiomyopathy (DCM) is one of the most common types of non-ischemic cardiomyopathy. DCM is characterized by left ventricle (LV) dilatation and systolic dysfunction without coronary artery disease or abnormal loading conditions. DCM is not a single disease entity and has a complex historical background of revisions and updates to its definition because of its diverse etiology and clinical manifestations. In cases of LV dilatation and dysfunction, conditions with phenotypic overlap should be excluded before establishing a DCM diagnosis. The differential diagnoses of DCM include ischemic cardiomyopathy, valvular heart disease, burned-out hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, and non-compaction. Cardiac magnetic resonance (CMR) imaging is helpful for evaluating DCM because it provides precise measurements of cardiac size, function, mass, and tissue characterization. Comprehensive analyses using various sequences, including cine imaging, late gadolinium enhancement imaging, and T1 and T2 mapping, may help establish differential diagnoses, etiological work-up, disease stratification, prognostic determination, and follow-up procedures in patients with DCM phenotypes. This article aimed to review the utilities and limitations of CMR in the diagnosis and assessment of DCM.

Increased Epicardial Adipose Tissue (EAT), Left Coronary Artery Plaque Morphology, and Valvular Atherosclerosis as Risks Factors for Sudden Cardiac Death from a Forensic Perspective.

Background: In sudden cardiac deaths (SCD), visceral adipose tissue has begun to manifest interest as a standalone cardiovascular risk factor. Studies have shown that epicardial adipose tissue can be seen as a viable marker of coronary atherosclerosis. This study aimed to evaluate, from a forensic perspective, the correlation between body mass index (BMI), heart weight, coronary and valvular atherosclerosis, left ventricular morphology, and the thickness of the epicardial adipose tissue (EAT) in sudden cardiac deaths, establishing an increased thickness of EAT as a novel risk factor. Methods: This is a retrospective case-control descriptive study that included 80 deaths that were autopsied, 40 sudden cardiac deaths, and 40 control cases who hanged themselves and had unknown pathologies prior to their death. In all the autopsies performed, the thickness of the epicardial adipose tissue was measured in two regions of the left coronary artery, and the left ventricular morphology, macro/microscopically quantified coronary and valvular atherosclerosis, and weight of the heart were evaluated. Results: This study revealed a higher age in the SCD group (58.82 ± 9.67 vs. 53.4 ± 13.00; p = 0.03), as well as a higher incidence in females (p = 0.03). In terms of heart and coronary artery characteristics, there were higher values of BMI (p = 0.0009), heart weight (p &lt; 0.0001), EAT of the left circumflex artery (LCx) (p &lt; 0.0001), and EAT of the left anterior descending artery (LAD) (p &lt; 0.0001). In the multivariate analysis, a high baseline value of BMI (OR: 4.05; p = 0.004), heart weight (OR: 5.47; p &lt; 0.001), EAT LCx (OR: 23.72; p &lt; 0.001), and EAT LAD (OR: 21.07; p &lt; 0.001) were strong independent predictors of SCD. Moreover, age over 55 years (OR: 2.53; p = 0.045), type Vb plaque (OR: 17.19; p &lt; 0.001), mild valvular atherosclerosis (OR: 4.88; p = 0.002), and moderate left ventricle dilatation (OR: 16.71; p = 0.008) all act as predictors of SCD. Conclusions: The data of this research revealed that higher baseline values of BMI, heart weight, EAT LCx, and EAT LAD highly predict SCD. Furthermore, age above 55 years, type Vb plaque, mild valvular atherosclerosis, and left ventricle dilatation were all risk factors for SCD.

PS-C30-13: GESTATIONAL HYPERTENSION AND PERIPARTUM CARDIOMYOPATHY: EPIDEMIOLOGICAL, CLINICAL AND EVOLUTIONARY PROFILE IN THE REFERENCE HOSPITALS OF YAOUNDE

Background: Peripartum cardiomyopathy (PPCM) is a primary dilated cardiomyopathy responsible for congestive heart failure that occurs in the last two months of pregnancy or during the first five months of postpartum. It is a rare pathology with unknown etiologies. Nevertheless, several etiopathogenic factors such as an history of gestational hypertension, black race, multiparity and poverty have been incriminated. However, the epidemiological and clinical data on peripartum cardiomyopathy are little known in Cameroon, thus justifying our descriptive study. Methodology: We carried out a prospective descriptive study over a period of six months. It was conducted in six reference hospitals in Yaounde. The study population was made of pregnant women with dyspnoea and women who had given birth with dyspnoea. Were included all pregnant or postpartum women (from the 32nd WA to the 5th months of postpartum) who had a LVEF &lt; 45% and/or a SF &lt; 30% associated or not with left ventricle dilation. They were placed on treatment with a follow-up over 3 months, where they had a second cardiac ultrasound to highlight the evolutionary profile. Results: We enrolled 10 patients from 26 women who were pregnant or had given birth and presented with dyspnoea within 6 months. The average age was 25.9 ± 4.9 years (range: 16–33 years). The average parity was 1.6 ± 1.17 (extreme 0–3). Multiparas were the most represented. The history of gestational hypertension was the main predisposing factor found (50%); followed by multiparity (30%), the notion of twin pregnancy and advanced maternal age (20%). Heart failure was the clinical expression in 60% of cases. Sinus tachycardia was constant; followed by signs of left ventricular hypertrophy and repolarization disorders on ECG assessment. The echocardiographic pattern depicted a hypokinetic dilated cardiomyopathy (mean LVEDD 61.2 ± 8.6 mm) with an average systolic function of 27.1 ± 10.6%. The main complications were acute pulmonary edema (60%), thromboembolic events including pulmonary embolism (10%), ischemic stroke (10%) and one death (10%). The treatment mostly based on the use of diuretics, ACE inhibitors, beta-blockers, Aldactone (1/3 of the patients) without forgetting the anticoagulation made with Rivaroxaban(n = 4) for some and aspirin (n = 6); and bromocriptine (initiated in 3 patients). Conclusion: PPCM is a cause of heart failure during pregnancy. It primarily arises during the postpartum period regardless of maternal age. It is a serious disease due to its (important morbi-mortality rate) and its complications, both hemodynamic and thromboembolic.\

The prognostic value of single photon emission computed tomography (SPECT) myocardial perfusion imaging is independent of left ventricular size.

Many variables have been shown to impact accuracy and prognostic power of myocardial perfusion imaging (MPI); however, effects of left ventricular size have not been extensively studied. In particular, perfusion defects in smaller hearts could be overlooked due to partial volume averaging, potentially reducing the prognostic power of MPI. We determined stress total perfusion deficit (TPD) and rest end diastolic volume (REDV) from single photon emission computed tomography (SPECT) MPI in consecutive patients without pathologically dilated left ventricles. Area under the curve (AUC) and Cox regression analysis were used to assess prediction of subsequent major adverse cardiac events [MACE-death, hospitalized acute myocardial infarction (AMI), hospitalized unstable angina, late revascularization]. Analyses were stratified by sex and REDV tertile. The analytic population included 2,503 patients (965 men and 1,538 women). Outcomes were assessed over an average of 6.4±2.3 years. MACE was observed in 254 (26.3%) of 965 men and 261 (17.0%) of 1,538 women. Stress TPD showed significant AUCs for stratifying MACE risk regardless of sex and REDV tertile (all P<0.05). In Cox regression analysis, increasing stress TPD (but not REDV) was associated with MACE in both men and women. There was no significant TPD*REDV interaction. In conclusion, we found the prognostic power of SPECT MPI to be independent of left ventricular size.

Computed Tomography-Chest in COVID-19 Pneumonia and cardiac failure: An Imaging Enigma

BACKGROUND- Computed tomography (CT) of the chest is an efficient tool to assess COVID-19 pneumonia. Nevertheless, imaging characteristics that overlap with cardiogenic pulmonary edema are not infrequent. CT chest characteristics pose challenges for which additional transthoracic echocardiography is an additional invaluable simple tool to aid in the diagnosis. In this article, we present the CT chest findings of patients with only covid-19 pneumonia, isolated heart failure, and combined covid-19 pneumonia and heart failure. Methods- This study included 120 patients in a tertiary care hospital in South India with dyspnoea and SP02 ≤ 95% between April 2021 to March 2022 who were subjected to chest CT imaging and transthoracic echocardiography and the results were analyzed. Isolated COVID-19 (n=60), isolated heart failure (n=39), and combined covid-19 pneumonia and heart failure (n-21) were identified depending on the CT chest imaging features. Results- There was no statistical difference in the imaging findings like ground glass opacities, crazy pavementpatternswithCOVID-19pneumonia, HF, and also in combined (covid 19 + cardiac failure )groups. However, in HF patients, diffuse patterns were more common than in COVID-19 pneumonia, which was statistically significant (p=0.001). Notably, CT images in HF patients were more likely to have interlobular septal thickening (ILST)(p=0.001) cardiomegaly (p=0.001), increased artery-to-bronchus ratio (p=0.0001), and bilateral pleural effusion (p=0.0001 ), and pericardial effusion (p=0.0001 ) Conclusion- Chest CT is an indispensable tool in the early diagnosis of COVID-19 pneumonia.CT chest features overlap, and separating COVID-19 pneumonia from heart failure is not always easy. Yet, certain specific CT features may suggest heart failure over covid -19 pneumonia. In HF patients, thickening of the interlobular septa, increased artery-to-bronchus ratio, cardiomegaly, and bilateral pleural effusion, pericardial effusion are more common. Additional transthoracic echo showing dilated left ventricle with reduced ejection fraction is an additional key to aid diagnosis.

Massive Left Ventricular Thrombus in the Setting of COVID-19–Induced Systemic Thrombi

A 58-year-old White man with no known medical history initially presented to the emergency department for fatigue and was ultimately diagnosed with COVID-19. He was in stable condition and discharged to quarantine at home. He returned to the emergency department 2 weeks later with a chief report of progressive pain and swelling of his legs. Initial vitals were remarkable for a heart rate of 115/minute. Physical examination revealed edematous and erythematous lower extremities with weeping wounds. Laboratory workup was remarkable for a white blood cell count of 12.7 × 1,000/μL, platelet count of 81 × 1,000/μL, troponin I level of 0.678 ng/mL, brain natriuretic peptide level of 4,000 pg/mL, C-reactive protein level of 121 mg/L, lactate level of 3.7 mmol/L, and international normalized ratio of 1.5.Chest computed tomographic angiography revealed acute emboli of subsegmental pulmonary arteries of the left upper, middle, and lower lobes (Fig. 1). Echocardiogram revealed a severely dilated left ventricle with apical akinesis and an ejection fraction of 10% to 15%. Large, layered thrombi were seen in the apex of the left and right ventricles (Fig. 2). Duplexes of the lower extremities showed acute occlusive calf vein thrombi in the right posterior tibial and bilateral peroneal veins. Arteries were patent in both lower extremities. Venous duplex of the right upper extremity revealed acute superficial venous thrombi in the right basilic and cephalic veins. Cardiac magnetic resonance imaging was performed to assess viability, which revealed significant transmural scarring and a large thrombus (8 × 6 × 5 cm) occupying the mid- and complete apical left ventricle cavity (Fig. 3). Multiple small thrombi in the right ventricle apex were seen.Given the thrombocytopenia on presentation, there was concern for disseminated intravascular coagulation; however, with such extensive clot burden, the patient was started on a heparin drip. Four days later, he sustained a cardiac arrest secondary to venous thromboembolism. Upon achieving return of spontaneous circulation, he was taken for left heart catheterization, which revealed severe triple-vessel disease. Cardiothoracic surgery was consulted, but it was determined that the patient to be too high risk to undergo coronary artery bypass graft or operative thrombectomy. Ultimately, his clinical status deteriorated, and the patient along with family proceeded with comfort measures.SARS-CoV-2 infection primarily affects the lower respiratory tract, but there are reports of COVID-19–induced cardiac complications, including acute coronary syndromes, arrythmias, myocarditis, and thrombosis.1 Venous thromboembolism is reported to occur in approximately 30% of patients with COVID-19, but intracardiac thrombus in very rare.2 Cardiac thrombus should be considered in the diagnosis of COVID-19 in patients presenting with chest pain and leg swelling.

Peripartum Cardiomyopathy Due to Gestational Hypertension and Tocolytic Therapy

Introduction: Peripartum cardiomyopathy (PPCM) is a rare and sometimes fatal systolic heart failure that affects women during late pregnancy or the early postpartum period. Risk factors contributing to this condition are: advanced maternal age, multiparity, administration of tocolytic agents, underlying cardiac disease, iatrogenic volume overload, preeclampsia, hypertension and In patients with gestational hypertension (GH) and other risk factors close monitoring is mandatory during pregnancy as well as in the postpartum period. Case report: A 38 year- old patient previously treated for endometriosis, infertility and GH was transferred from the Clinic of Gynecology due to diagnosed congestive heart failure. Five days prior admission she gave birth to her first child. Prior delivery she was treated with tocolytic therapy. She received methyldopa due to GH, that was abruptly discontinued after her delivery. Echocardiography on admission revealed moderately reduced left ventricular systolic function with an ejection fraction (EF) of 37% with dilated left ventricle (LV) and pulmonary artery hypertension (PAH) secondary to left ventricular failure. During hospitalization the patient was with signs of volume overload, but with well response on parenteral diuretic therapy. She was additionally treated with guideline recommended heart failure therapy. The controlled echocardiography showed improvement of the left ventricular function with an EF of 42%. Conclusion: PPCM is a rare condition with high morbidity and mortality. An LVEF &lt;30%, marked LV dilatation, LV end-diastolic diameter &gt;6.0 cm, and RV involvement are associated with adverse outcomes. Although delivery of the fetus and the placenta trigger resolution of symptoms and recovery to the nonpregnant state of various organism, the contrary happens with blood pressure. Its peaking time is three to six days after delivery. Hypertension medication must not be immediately terminated. Prolonged tocolytic therapy are a risk factor for PPCM due to causing decreased baroreflex sensitivity Patients with risk factors should be closely monitored for eventual cardiac complications.

938 ARRHYTHMOGENIC CARDIOMYOPATHY IN A PATIENT CARRYING A PATHOGENIC LMNA VARIANT

Abstract Background Lamin A (LMNA) protein is one of the main constituents of the nuclear lamina. Pathogenic variants of LMNA gene have been demonstrated to be linked to a wide spectrum of disorders, including cardiac diseases. The first reported heart disease linked to LMNA was dilated cardiomyopathy (DCM), in a form typically characterized by the presence of conduction disorders and high incidence of sudden cardiac death (SCD) disrespectfully of left ventricular systolic function. Genetic variants of the same gene have been associated with Arrhythmogenic Cardiomyopathy (ACM), but its putative role as disease causing gene is still debated. Case summary a man with positive familial history for DCM presented to the Emergency Department because of palpitations. The electrocardiogram showed first degree AV-block, complete right bundle branch block and low QRS voltages on limb leads. Cardiac magnetic resonance revealed severe dilatation of the right ventricle with wall motion abnormalities in keeping with ACM, associated with mild dilatation and moderate dysfunction of left ventricle. The genetic test identified a pathogenic variant in LMNA. Moreover, non-sustained ventricular tachycardias were present on the ECG Holter. According to international guidelines on SCD prevention, the patient underwent ICD implantation, with one appropriate ICD discharge on a sustained ventricular tachycardia episode after few months. Discussion LMNA pathogenic variants can lead to a broad spectrum of cardiac manifestations, including Arrhythmogenic Cardiomyopathy. A genetic test should be considered if there is a familial cardiomyopathy associated with conduction disorders, in order to achieve a proper risk stratification for sudden death.

Anesthetic considerations in pediatric renal autotransplantation

BackgroundRenal autotransplantation is a complex procedure involving reimplantation of the renal artery and vein at a different site. Anesthetic management of renal autotransplant is challenging because of associated morbidities and intraoperative hemodynamic changes.Case presentationWe present a case of a 14-month-old male who had severe hypertension and cardiomyopathy due to renal artery stenosis. Echocardiography reported dilated left atrium and left ventricle, moderate to severe left ventricular systolic dysfunction, and a left ventricular ejection fraction of 30%. The renal artery and renal vein were anastamosed to the great vessels. Anesthetic management included maintaining normal baseline diastolic pressure, systemic vascular resistance, and preload and avoiding tachycardia. Milrinone infusion was used.ConclusionsAnesthetic management was challenging as adequate perfusion pressures had to be maintained while keeping the patient hemodynamically stable.

1121 USE OF IMPELLA 5.0 AS BRIDGE TO LVAD IN CARDIOGENIC SHOCK: REPORT OF TWO CASES

Abstract Background Left ventricle assist devices (LVAD) are an option in end stage heart failure (HF) as bridge to or alterative to heart transplantation. Adequate compensation of patient is key to obtain a good outcome. We report two cases of Impella 5.0 bridge to LVAD in patients with cardiogenic shock (CS) in which intra-aortic balloon pump (IABP) failed to obtain hemodynamic stability. Case series A) A 60 years old man developed CS after anterior myocardial infarction treated with primary PCI of left main coronary artery. At presentation patient was hypotensive with signs of hypoperfusion and pulmonary congestion: systemic blood pressure (SBP) 80/60 mmHg despite inotropic drugs, blood lactates 4 mmol/l, urine output of last 6 hours 0,4 ml/kg/h (INTERMACS 2). Echocardiography showed severe left ventricle disfunction with LVEF 15%, severe mitral regurgitation (MR) and sPAP 45 mmHg. Therefore, IABP was implanted. Right heart catheterization (RHC) showed pulmonary hypertension and high filling pressure with reduced cardiac output and increased pulmonary vascular resistance (mPAP 39 mmHg, CPWP 28 mmHg, CO 3 l/min, PVR 3.7 uW, PAPi 2.8); X-ray chest showed persistence of pulmonary congestion. After 9 days on IABP, patient underwent Impella 5.0 implant through right axillary artery as bridge to durable LVAD. Pulmonary artery catheter (PAC) monitoring showed reduction of pulmonary hypertension with mPAP 35 mmHg and CPWP 17 mmHg and chest X-ray documented improvement of lung congestion. Bedside rehabilitation was started. Two weeks later patient underwent LVAD HM3 implantation as destination therapy. The patient was discharge home on post-operative day 55. B) After subacute myocardial infarction with three-vessels disease, a 53 y.o. man developed severe congestive HF with severe left ventricular disfunction and was referred to our institution for evaluation. RHC showed pulmonary hypertension with pre-capillary component not reversible after enoximone test, contraindicating heart transplantation. Therefore, patient was candidate to receive LVAD as bridge strategy. Echocardiography at admission showed dilated and hypokinetic left ventricle (EDV 200 ml, LVEF 17% severe MR, sPAP 60 mmHg) and dilated and hypokinetic RV. During hospitalization the patient experienced CS with SBP 62/45 mmHg, 6-hours urine output of 1,4 ml/kg/h and blood lactates 8.3 mmol/l (INTERMACS 1) so femoral IABP was implanted. RHC was repeated both without IABP support (mPAP 37 mmHg, PCWP 28 mmHg, CO 1.4 l/min, CI 0.9 l/min/m2) and with IABP support (mPAP 32 mmHg, PCWP 18 mmHg, CO 2.15 l/min, CI 1.4 l/min/m2). During the following stay he developed S. Aureus sepsis requiring prolonged antibiotic therapy. Expecting a long time before LVAD, axillary Impella 5.0 was implanted in order to unload the LV and allow early patient mobilization. Subsequent PAC monitoring showed improvement of pulmonary hypertension and cardiac index (mPAP 24 mmHg, PCWP 9 mmHg, CO 5.1 l/min with Impella flow 4.2 l/min, CI 3.2 l/min/m2). After 11 days, patient received LVAD HVAD with uneventful course and was discharged on post-operative day 22. Conclusions Impella 5.0 is a surgically implanted intravascular microaxial blood pump that delivers up to 5 l/min of blood from LV to aorta, leading to improved perfusion and more efficient LV unloading. In patients with CS this can help to obtain better decongestion, RV recovery, and favorable preconditioning before LVAD implant. Moreover, axillary access allows better patient mobilization preventing cachexia after long time hospitalization.

694 DRUG INDUCED KIDNEY INFARCTION: A CASE REPORT

Abstract Isotretinoin (ISO) is a synthetic analog of vitamin A. Notwithstanding the well-known long-term efficacy in the treatment of severe resistant cystic acne, ISO induces several side effects too. Dyslipidemia, increased liver enzymes, as well as reduction of biotidinase have been already reported [1]. Homocysteine (HCY), a sulfur-containing amino acid, is recycled into methionine by a transmethylation reaction requiring folate and vitamin B12. Given that during ISO treatment elevated liver enzymes (SGOT, SGPT) are often observed, it has been hypothesized that iatrogenic liver dysfunction could affect cystathionine-b-synthase, an enzyme involved in HCY metabolism, [2]. Several studies have highlighted that elevated plasma HCY concentrations are associated with an increased risk of premature occlusive vascular disease. We hereby report a case of drug-induced kidney infarction after ISO therapy. A previously healthy 18-year-old male, on therapy with 40 mg/die isotretinoin for acne, was admitted to the Emergency Unit for abdominal pain, nausea and vomiting and dyspnea. A trans-thoracic echocardiogram showed dilated and hypocontractile left ventricle. During the hospitalization he had a total body CT that showed the presence of an ischemic lesion on left kidney without other pathological findings. He started therapy with 12 IU/kg UFH as soon as a surgical emergency was excluded. Subsequently, he underwent a coronary angiogram that resulted unremarkable. Cardiac MRI showed extensive delayed gadolinium late enhancement with intramural linear pattern. In the hypothesis of drug-induced vasculitis, an extensive serological testing was performed. Elevation of serum liver enzymes (SGOT, SGPT), CRP, LDH was found. Mutations on MTHFR gene and Leiden Factor were not detected, neither alteration in coagulation parameters. Finally the dosage of plasmatic HCY resulted over the range of normality and ISO was discontinued. The patient was discharged on optimized medical therapy for heart failure. He is currently managed as outpatient. HCY levels could be found elevated in patients with ischemic events during ISO treatment. Given the widespread use of this drug for acne, it could be reasonable to dose HCY in patients with suspected liver dysfunction. Physicians should be aware of this scenario and should act swiftly to avoid uneventful outcomes. [1] Schulpis KH et al. Elevated plasma homocysteine levels in patients on isotretinoin therapy for cystic acne. Int J Dermatol. 2001 Jan;40(1):33-6. [2] Polat M, et al. Plasma homocysteine level is elevated in patients on isotretinoin therapy for cystic acne: a prospective controlled study. J Dermatolog Treat. 2008;19(4):229-32.

142 ADVANCED HEART FAILURE IN PATIENTS WITH ARRHYTHMOGENIC CARDIOMYOPATHY

Abstract Background Arrhythmogenic Cardiomyopathy (ACM) is a primary disease of the heart muscle, characterized by fibro-fatty myocardial replacement. Improvements in the clinical diagnosis and antiarrhythmic therapy, including the use of the defibrillator (ICD) and endo-epicardial catheter ablation, have increased the survival of these patients, who experience late complications such as advanced heart failure, which sometimes requires cardiac transplantation. Aim of the study To evaluate clinical, instrumental and genetic features of patients affected with ACM who developed heart failure (HF) and to sought for possible predictive factors of HF. Methods From the entire cohort of probands and family members followed at the Cardiomyopathy unit of our University (555 patients), 34 patients (29%), both probands (n= 26, 77%) and family members who experienced HF (6%) were selected (24 males, 71%). Their anamnestic, clinical, and instrumental data were compared with those without episodes of HF (n-HF). Results The mean age at diagnosis in HF cohort was 45.2 (±18) years. In 14 patients (41%) HF was the first symptom that led to diagnosis. According to 2010 TFC 30 patients (88%) had a definite diagnosis of ACM. The most frequently observed phenotype was the biventricular ACM (n=27, 79%). A disease-related genetic variant was found in 18 (53%) and DSP was the more common disease-gene, accounting for 24% of cases. The mean duration of follow-up was 12.6 (±11.0) years (min-max, 1-20 years). During this period a total of 14 subjects (41.2%) experienced life-threatening arrhythmias (LTA), while 13 patients (38.2%) died, of whom 11 (84.6%) because of refractory HF. Eighteen patients (53%) underwent cardiac transplantation (mean age 43±17 years), approximately 4 (±3.5) years after the onset of symptoms. Comparison with the n-HF cohort of ACM patients showed a significant difference on presence of T-wave inversion (TWI) in V1-V3 (p=0.001), TWI in V4-V6 (p=0.010), low QRS voltages both in precordial and limb leads (both p&amp;lt;0.001) and presence of left bundle-branch block and right bundle-branch block (both p&amp;lt;0.001). Regarding CMR, HF cohort was characterized by a significantly more dilated right and left ventricle EDV (both p&amp;lt;0.001), EF reduction (both p&amp;lt;0.001), presence of wall motion alterations (respectively, p=0.007 and p&amp;lt;0.001) and LGE (respectively, p=0.002 and p=0.005) compared to n-HF group. Regarding outcomes evaluation, the HF group showed more frequently LTA (HF=41.2% vs n-HF 21.5%, p=0.008). Finally, the presence of right bundle-branch block at ECG (OR=20.562, CI 1.884-224.413, p=0.013) and of impaired RV ejection fraction (OR=0.821, CI 0.719-0.937, p=0.004) were found to be independent predictors of HF. Conclusions Heart failure is a rare complication in patients affected with ACM, with a prevalence of 6% in our study. The mean age of onset of HF was 45.2 (±18) years. Furthermore, 18 patients (53%) had an unfavorable progression to heart transplantation. The presence of right bundle branch block at ECG and an impaired CMR RV-EF were found to be predictors of HF. Our results suggest the importance of scheduling a close follow-up in ACM patients who show initial signs and/or symptoms of HF, taking into consideration the fast rate of progression to refractory HF, once established.