Involvement Of Left Ventricle Research Articles

Changes of biventricular contractile function depending on the types of left ventricular involvement in patients 1 year after COVID-19 pneumonia

Aim. To study the changes of biventricular contractile function depending on the types of left ventricular involvement according to the speckle tracking echocardiography (STE).Material and methods. Of the 380 patients from the Prospective Registry of People Survived COVID-19 Pneumonia, the study included 85 patients, which can be followed-up — 3 months (visit 1) and 12 months (visit 2) after COVID-19 pneumonia (men — 68,2%; mean age — 50,6±10,9 years).At visit 2, patients with diffuse left ventricle (LV) involvement according to STE (visual involvement of ≥4 segments of the same LV level) comprised group I (n=27), patients with regional LV involvement (≥3 segments corresponding to anterior, circumflex or right coronary arteries) — group II (n=39), patients without visual LV involvement — group III (n=19).Results. The groups were comparable in main clinical, functional and echocardiographic (conventional) parameters 3 and 12 months after COVID-19 pneumonia, with the exception of sex and body mass index. STE in group I showed a significant decrease in global longitudinal strain (GLS) (-18,0±2,0% at visit 1 and -16,9±1,4% at visit 2, p=0,025) and LS of all LV levels; in group II — an increase in right ventricular free wall strain (RV FWS) (-22,8±3,2% and -24,0±2,6%, respectively, p=0,006); in group III — an increase in GLS (-19,3±2,3% and -21,2±1,9%, p=0,005), LS of basal and medium LV levels, RV FWS (-23,3±2,9% and -25,0±3,0%, p=0,033). In group I, a significant increase in affected LV segments was revealed (7,0 [5,0;9,0] and 9,0 [7,0;10,0], p=0,010), while in group III there was a decrease in their number (5,0 [3,0;6,0] and 10,0 [1,0;2,0], p<0,001). According to logistic regression, LV basal LS at visit 1 (odds ratio 0,420; 95% confidence interval 0,273-0,644; p<0,001) had an independent association with diffuse LV involvement at visit 2. When it decreases, <15,8% sensitivity and the specificity of this model in predicting diffuse LV involvement was 74,1% and 74,1%, respectively (AUC=0,807; p<0,001).Conclusion. Patients with diffuse LV involvement according to STE are characterized by suppression of global biventricular contractile function during 1-year follow-up.

Scarring/arrhythmogenic cardiomyopathy.

The designation of 'arrhythmogenic cardiomyopathy' reflects the evolving concept of a heart muscle disease affecting not only the right ventricle (ARVC) but also the left ventricle (LV), with phenotypic variants characterized by a biventricular (BIV) or predominant LV involvement (ALVC). Herein, we use the term 'scarring/arrhythmogenic cardiomyopathy (S/ACM)' to emphasize that the disease phenotype is distinctively characterized by loss of ventricular myocardium due to myocyte death with subsequent fibrous or fibro-fatty scar tissue replacement. The myocardial scarring predisposes to potentially lethal ventricular arrhythmias and underlies the impairment of systolic ventricular function. S/ACM is an 'umbrella term' which includes a variety of conditions, either genetic or acquired (mostly post-inflammatory), sharing the typical 'scarring' phenotypic features of the disease. Differential diagnoses include 'non-scarring' heart diseases leading to either RV dilatation from left-to-right shunt or LV dilatation/dysfunction from a dilated cardiomyopathy. The development of 2020 upgraded criteria ('Padua criteria') for diagnosis of S/ACM reflected the evolving clinical experience with the expanding spectrum of S/ACM phenotypes and the advances in cardiac magnetic resonance (CMR) imaging. The Padua criteria aimed to improve the diagnosis of S/ACM by incorporation of CMR myocardial tissue characterization findings. Risk stratification of S/ACM patients is mostly based on arrhythmic burden and ventricular dysfunction severity, although other ECG or imaging parameters may have a role. Medical therapy is crucial for treatment of ventricular arrhythmias and heart failure. Implantable cardioverter defibrillator (ICD) is the only proven life-saving treatment, despite its significant morbidity because of device-related complications and inappropriate shocks. Selection of patients who can benefit the most from ICD therapy is one of the most challenging issues in clinical practice.

CARDIAC SARCOIDOSIS: WHEN THE RIGHT VENTRICLE ISN’T RIGHT

CARDIAC SARCOIDOSIS: WHEN THE RIGHT VENTRICLE ISN’T RIGHT

C63 PHENOTYPE – GENOTYPE RELATIONSHIP IN ARRHYTHMOGENIC CARDIOMYOPATHY

Abstract Background Arrhythmogenic cardiomyopathy (ACM) is a primary disease of the myocardium with arrhythmic manifestations and fibro–fatty replacement either of the right (RV) or the left ventricle (LV) at the cardiac magnetic resonance (CMR). Over the last decade, different mutations in cardiac genes associated with heterogeneous phenotypes have been identified. Aim To investigate the genotype–phenotype relationships in ACM patients. Firstly, the phenotypic expression was defined in definite mutation carriers. Secondly, the prognostic significance of mutations was assessed across different phenotypes. Methods The study population included 281 patients with suspected ACM, based on family history, clinical and electrocardiographic evaluation, echocardiographic and CMR findings (Fig.1), studied at our Institution since 2012. All patients underwent genetic evaluation using Sanger sequencing and NGS of mutations in desmosomal (desmoplakin [DSP], plakophilin–2[PKP2], plakoglobin[JUP], desmoglein–2 [DSG2], desmocollin–2 [DSC2]) or non desmosomal genes. The composite endpoint included cardiac death, sustained and non–sustained ventricular tachycardia (VT), ventricular fibrillation (VF), appropriate defibrillator shock/antitachycardia pacing (ATP). Results The genetic test was positive in 113 patients (40%), 82 (73%) for desmosomal genes (41 DSP, 15 DSG2, 15 PKP2, 5 JUP, 6 DSC2), and 31 (27%) for non–desmosomal genes (4 titin, 2 TMEM 43, 2 lamin A/C, 23 others). Gene–positive compared to gene–negative (n = 168, 60%) patients showed a higher prevalence of LV ejection fraction (EF)<50% (14%vs.6%, p<0.011), LV and RV LGE (62%vs.46%, p < 0.001, 20%vs.12%, p<0.02), RV dilatation (27%vs.17%, p<0.041) (Table 1). DSG2 mutations were associated mainly to biventricular (7/15,46%) or RV involvement (4/15,26%), while DSP mutations to LV involvement (24/41,58%). During a median 36–month follow–up (IQ.range 12–56), 55 patients (19%) experienced the composite endpoint (35 non–sustained VT; 11 sustained VT – 3 ATP, 1 defibrillator–shock–; 9 VF, all treated by defibrillator–shock). At Kaplan–Meier analysis, DSP mutations were associated with the worst prognosis (Fig. 3). Conclusion Diverse genotypes were differently associated with LV dysfunction/LGE, RV dilatation/LGE. DSP mutations were associated with higher arrhythmic risk. Genetic screening may result in a better risk stratification, useful for clinical decision–making.

Diagnostic Challenges in Rare Causes of Arrhythmogenic Cardiomyopathy-The Role of Cardiac MRI.

Arrhythmogenic right ventricular dysplasia (ARVD) is a rare genetic condition of the myocardium, with a significantly high risk of sudden death. Recent genetic research and improved understanding of the pathophysiology tend to change the ARVD definition towards a larger spectrum of myocardial involvement, which includes, in various proportions, both the right (RV) and left ventricle (LV), currently referred to as ACM (arrhythmogenic cardiomyopathy). Its pathological substrate is defined by the replacement of the ventricular myocardium with fibrous adipose tissue that further leads to inadequate electrical impulses and translates into varies degrees of malignant ventricular arrythmias and dyskinetic myocardium movements. Particularly, the cardio-cutaneous syndromes of Carvajal/Naxos represent rare causes of ACM that might be suspected from early childhood. The diagnostic is sometimes challenging, even with well-established rTFC or Padua criteria, especially for pediatric patients or ACM with LV involvement. Cardiac MRI gain more and more importance in ACM diagnostic especially in non-classical forms. Furthermore, MRI is useful in highlighting myocardial fibrosis, fatty replacement or wall movement with high accuracy, thus guiding not only the depiction, but also the patient’s stratification and management.

The 2020 "Padua Criteria" for Diagnosis and Phenotype Characterization of Arrhythmogenic Cardiomyopathy in Clinical Practice.

Arrhythmogenic Cardiomyopathy (ACM) is a heredo-familial cardiac disease characterized by fibro-fatty myocardial replacement and increased risk of sudden cardiac death. The diagnosis of ACM can be challenging due to the lack of a single gold-standard test: for this reason, it is required to satisfy a combination of multiple criteria from different categories including ventricular morpho-functional abnormalities, repolarization and depolarization ECG changes, ventricular arrhythmias, tissue characterization findings and positive family history/molecular genetics. The first diagnostic criteria were published by an International Task Force (ITF) of experts in 1994 and revised in 2010 with the aim to increase sensitivity for early diagnosis. Limitations of the 2010 ITF criteria include the absence of specific criteria for left ventricle (LV) involvement and the limited role of cardiac magnetic resonance (CMR) as the use of the late gadolinium enhancement technique for tissue characterization was not considered. In 2020, new diagnostic criteria (“the Padua criteria”) were proposed. The traditional organization in six categories of major/minor criteria was maintained. The criteria for identifying the right ventricular involvement were modified and a specific set of criteria for identifying LV involvement was created. Depending on the combination of criteria for right and LV involvement, a diagnosis of classic (right dominant) ACM, biventricular ACM or left-dominant ACM is then made. The article reviews the rationale of the Padua criteria, summarizes the main modifications compared to the previous 2010 ITF criteria and provides three examples of the application of the Padua criteria in clinical practice.

Right ventricular dysfunction parallels left ventricular functional involvement in women with breast cancer experiencing subclinical cardiotoxicity

Abstract Funding Acknowledgements Type of funding sources: None. Background Cancer therapy related cardiac toxicity disease (CRCTD) of the left ventricle (LV)can influence the outcome of oncologic patients. Little is known on CRCTD related right ventricular (RV)dysfunction even though RV involvement has been proven to be a remarkable prognosticator in heart failure. Purpose To analyse parallel changes in LV and RV function occurring during the course of cancer therapy in women affected by breast cancer by using both standard and speckle tracking echocardiography. Methods Fifty Her-2 positive breast cancer women (age = 53.6 ± 11.7 years) underwent sequential cancer therapy protocol including anthracycline (ANT) epirubicine + cyclophosphamide (4 cycles) followed by a total amount of 18 cycles with trastuzumab (TRZ) + paclitaxel. A complete echo-Doppler exam, including LV and RV global longitudinal strain (GLS)as well as RV septal and free wall longitudinal strain (SLS and FWLS respectively) assessment, was performed at baseline, after ANT end and after TRZ completion. Patients with overt heart failure and LV ejection fraction < 50%, coronary artery disease,atrial fibrillation, hemodinamically significant valve disease and inadequate echo were excluded. Overt CRCTD was defined according guidelines and both subclinical LV and RV CRCTD as a LV and RV GLS drop from baseline >15%. Results None of the patients experienced overt CTCRD but 6 patients (14%) showed subclinical LV dysfunction and 33 (66%) had a significant drop of RV longitudinal function.The comparison of standard echo-Doppler exam at baseline and after ANT and TRZ completion did not show significant changes of LV and RV systolic and diastolic parameters. Conversely, a progressive significant reduction of RV GLS (p < 0.002 after TRZ), SLS and FWLS and, with a lower extent, of LV GLS (p < 0.02 after TRZ) was observed after ANT and TRZ completion (Figure). Percentage reduction in RV GLS (DRV GLS) from baseline to ANT end correlated with LV GLS both at EC end (r=-0.40, p = 0.006) and after TRZ completion (r=-0.62, p < 0.0001). Conclusions Detrimental cardiac effects of cancer therapy involve both LV and RV systolic longitudinal function. Progressive RV dysfunction is evident through ANT and TRZ treatment. Early RV dysfunction parallels LV involvement and predicts subsequent LV subclinical dysfunction. A comprehensive LV and RV longitudinal function assessment might better predict the onset of CRCTD in breast cancer patients. Abstract Figure.

Right ventricular dysfunction parallels left ventricular functional involvement in women with breast cancer experiencing subclinical cardiotoxicity

Abstract Background Cancer therapy related cardiac toxicity disease (CRCTD) of the left ventricle (LV)can influence the outcome of oncologic patients. Little is known on CRCTD related right ventricular (RV)dysfunction even though RV involvement has been proven to be a remarkable prognosticator in heart failure. Purpose To analyse parallel changes in LV and RV function occurring during the course of cancer therapy in women affected by breast cancer by using both standard and speckle tracking echocardiography. Methods Fifty Her-2 positive breast cancer women (age = 53.6±11.7 years) underwent sequential cancer therapy protocol including anthracycline (ANT) epirubicine + cyclophosphamide (4 cycles) followed by a total amount of 18 cycles with trastuzumab (TRZ) + paclitaxel. A complete echo-Doppler exam, including LV and RV global longitudinal strain (GLS)as well as RV septal and free wall longitudinal strain (SLS and FWLS respectively) assessment, was performed at baseline, after ANT end and after TRZ completion. Patients with overt heart failure and LV ejection fraction <50%, coronary artery disease,atrial fibrillation, hemodinamically significant valve disease and inadequate echo were excluded. Overt CRCTD was defined according guidelines and both subclinical LV and RV CRCTD as a LV and RV GLS drop from baseline >15%. Results None of the patients experienced overt CTCRD but 6 patients (14%) showed subclinical LV dysfunction and 33 (66%) had a significant drop of RV longitudinal function.The comparison of standard echo-Doppler exam at baseline and after ANT and TRZ completion did not show significant changes of LV and RV systolic and diastolic parameters. Conversely, a progressive significant reduction of RV GLS (p<0.002 after TRZ), SLS and FWLS and, with a lower extent, of LV GLS (p<0.02 after TRZ) was observed after ANT and TRZ completion (Figure). Percentage reduction in RV GLS (DRV GLS) from baseline to ANT end correlated with LV GLS both at EC end (r=−0.40, p=0.006) and after TRZ completion (r=−0.62, p<0.0001). Conclusions Detrimental cardiac effects of cancer therapy involve both LV and RV systolic longitudinal function. Progressive RV dysfunction is evident through ANT and TRZ treatment. Early RV dysfunction parallels LV involvement and predicts subsequent LV subclinical dysfunction. A comprehensive LV and RV longitudinal function assessment might better predict the onset of CRCTD in breast cancer patients. LV and RV strain during cancer therapy Funding Acknowledgement Type of funding source: None

Right Heart Involvement in Patients with Sarcoidosis

The left ventricle (LV) is affected in 20-25% of patients with sarcoidosis and its involvement is associated with morbidity and mortality. However, effects of sarcoidosis on the right ventricle (RV) are not well documented. Our aims were to investigate the prevalence of RV dysfunction in patients with sarcoidosis and determine whether it is predominantly associated with direct cardiac involvement, severity of lung disease, or pulmonary hypertension (PH). We identified 50 patients with biopsy-proven extra-cardiac sarcoidosis and preserved LV function, who underwent echocardiography, pulmonary function (PF) testing, and cardiovascular magnetic resonance. RV function was quantified by free wall longitudinal strain. Tricuspid valve Doppler and estimated right atrial pressure were used to estimate systolic pulmonary artery pressure. Myocardial late gadolinium enhancement was considered diagnostic for cardiac sarcoidosis and assumed to involve both ventricles. Of the 50 patients, 28 (56%) had RV dysfunction, 4 with poorly defined PF status. Of the remaining 24 patients, 16 (67%) had lung disease, 8 (33%) had PH, and 10 (42%) had LV involvement. Ten patients had greater than one of these findings, and 4 had all 3. In contrast, in 4/24 patients (17%), RV dysfunction could not be explained by these mechanisms, despite severely reduced RV strain. In conclusion, RV dysfunction is common in patients with sarcoidosis and is usually associated with either direct LV involvement, lung disease, or PH, but may occur in the absence of these mechanisms, suggesting the possibility of isolated RV involvement and underscoring the need for imaging protocols that would include RV strain analysis.

Abstract 15314: Left Ventricular Dysfunction in Children and Adolescents With Arrhythmogenic Right Ventricular Cardiomyopathy

Background: Involvement of the left ventricle (LV) is increasingly recognized in adults with arrhythmogenic right ventricular cardiomyopathy (ARVC) but it is unclear whether LV function is compromised in children with this condition. The aim of this study was examine myocardial contractility in pediatric patients with suspected ARVC. Methods: For this retrospective study, patients with a work-up for ARVC were classified into ‘no’, ‘possible’, ‘borderline’ or ‘definite’ ARVC according to the revised Task Force Criteria (rTFC). Ventricular size and function as well as LV myocardial strain and torsion were measured by cardiac magnetic resonance (CMR). Results: A total of 142 patients were enrolled, of whom 58 (41%) had no, 32 (23%) possible, 29 (20%) borderline and 23 (16%) definite ARVC. The groups were similar in age at CMR. With higher rTFC score, z scores (Z) of right ventricular (RV) ejection fraction (EF) were lower (p<0.001) while z-RV end diastolic volume (EDV) and z-LV EDV were larger (p=0.002 and 0.013, respectively). LV EF did not differ between rTFC categories. Global circumferential strain (GCS) of the LV was lower in patients in higher rTFC categories (p=0.018). Z-LVEDV correlated with z-RVEDV (r2 = 0.69, p<0.001) and z- LVEF correlated with z-RVEF (r2 = 0.55, p <0.001). Z-LVEF and z-RVEF correlated with LV GCS (r2 = 0.48, p<0.001 and r2 = 0.46, p<0.001, respectively) and torsion (r2 = 0.21, p=0.032 for both). Forty-two patients had a follow-up CMR, after a median interval of 2.6 years (0.4- 8.4). The rate of deterioration of LV or RV EF or EDV did not differ between rTFC categories. A more rapid increase of z-RVEDV was associated with a faster decline in z-RVEF (r2 = -0.383, p=0.004) and z-LVEF (r2 = -0.45, p=0.001). A decline of z-LVEF over time correlated with that of z-RVEF (r2 = 0.60, p<0.001) and z-LVEDV increase correlated with z-RVEDV increase (r2 = 0.84, p<0.001). Conclusion: LV myocardial dysfunction is present in young patients with suspected or confirmed ARVC. Quantification of myocardial mechanics with CMR may be a useful tool to detect early LV involvement in ARVC. Progressive LV dysfunction and enlargement appear to parallel those of the RV.

Echocardiographic Hypertrabeculated/Non-compacted Right Ventricle Accompanied by Atrial Septal Defect and Anomalous Pulmonary Vein Connection

Myocardial noncompaction (NC) is a disorder of the embryonic endomyocardial morphogenesis frequently associated with congenital cardiac abnormalities. NC predominantly affects the left ventricle (LV). Right ventricle (RV) NC may occur in association with LV involvement or in isolation. A 47-year-old woman was admitted for atrial septal defect closure. Transthoracic echocardiography revealed hypertrabeculation of the RV apex, consisting of multiple deep recesses with the entrance of blood flow in color Doppler imaging, suggestive of isolated RV hypertrabeculation/NC. The RV and right atrium (RA) were enlarged, and systolic pulmonary arterial pressure was slightly increased. Our patient's associated abnormalities were atrial septal defect (superior sinus venosus type), anomalous connection of the right upper pulmonary vein to the junction of the superior vena cava and the RA, and large patent foramen ovale. Association between atrial septal defect and partial anomalous pulmonary vein connection and isolated hypertrabeculated/noncompacted RV should be considered by cardiologists.

Right Ventricular Function in Cardiovascular Disease, Part II

Right ventricular (RV) function may be impaired in pulmonary hypertension (PH), congenital heart disease (CHD), and coronary artery disease and in patients with left-sided heart failure (HF) or valvular heart disease. In recent years, many studies have demonstrated the prognostic value of RV function in cardiovascular disease. In the past, however, the importance of RV function has been underestimated. This perception originated from studies on open-pericardium dog models and from the observation that patients may survive without a functional subpulmonary RV (Fontan procedure). In the 1940s, studies using open-pericardium dog models showed that cauterization of the RV lateral wall did not result in a decrease in cardiac output or an increase in systemic venous pressure.1–3 As was later demonstrated, the open-pericardium model did not take into account the complex nature of ventricular interaction. In 1982, Goldstein and colleagues2 showed that RV myocardial infarction (RVMI) in a closed-chest dog model led to significant hemodynamic compromise. These findings were further supported by clinical studies demonstrating an increased risk of death, arrhythmia, and shock in patients with RVMI.4 The study of the RV is a relatively young field. In 2006, the National Heart, Lung, and Blood Institute identified RV physiology as a priority in cardiovascular research.5 The goal of this review is to present a clinical perspective on RV physiology and pathobiology. In the first article of the series, the anatomy, physiology, embryology, and assessment of the RV were discussed. In this second part, we discuss the pathophysiology, clinical importance, and management of RV failure. RV failure is a complex clinical syndrome that can result from any structural or functional cardiovascular disorder that impairs the ability of the RV to fill or to eject blood. The cardinal clinical manifestations of RV failure are (1) fluid retention, which may lead …

Role of cardiovascular magnetic resonance imaging in arrhythmogenic right ventricular dysplasia.

Arrhythmogenic right ventricular dysplasia (ARVD) is a genetic cardiomyopathy characterized clinically by ventricular arrhythmias and progressive right ventricular (RV) dysfunction. The histopathologic hallmark is fibro-fatty replacement of RV myocardium. It is inherited in an autosomal pattern with variable penetrance. ARVD is unique in that it most commonly presents in young, otherwise healthy and highly athletic individuals. The cause of ARVD is not well-known but recent evidence suggests strongly that it is a disease of desmosomal dysfunction. The disease involvement is not limited only to the RV as left ventricle (LV) has also been reportedly affected. Diagnosis of ARVD is challenging and is currently based upon a multi-disciplinary work-up of the patient as defined by the Task Force. Currently, implanted cardioverter defibrillators (ICD) are routinely used to prevent sudden death in patients with ARVD. Cardiovascular MR is an important non-invasive diagnostic modality that allows both qualitative and quantitative evaluation of RV. This article reviews the genetics of ARVD, current status and role of CMR in the diagnosis of ARVD and LV involvement in ARVD.

Individualized versus standardized analysis of ambulatory blood pressure profile: relationship with left ventricular characteristics.

Objective To determine whether the use of patients' individual awake/asleep patterns instead of fixed day/night intervals would influence the correlations between blood pressure values and left ventricular morpho-functional characteristics. We enrolled 167 never-treated hypertensives (clinic blood pressures >160 mmHg systolic or 90 mmHg diastolic, or both): 32 had 24h blood pressures <130/80 mmHg [white-coat hypertensives (WCH)] and 135 had 24h blood pressures >130 mmHg systolic or 80 mmHg diastolic, or both (hypertensives). Each patient underwent left ventricular echocardiographic examination and 24h ambulatory blood pressure monitoring, evaluated twice, using standard day/night intervals (daytime 0700-2200 h, night-time 2200-0700 h) and using the patient's individual awake/asleep pattern (an individualized scheme). Daytime and night-time blood pressures in WCH and daytime and night-time diastolic blood pressures in hypertensives were not affected by choice of using individualized or standard intervals; daytime systolic blood pressure in hypertensives was significantly higher and night-time systolic blood pressure lower with individualized intervals. The non-dippers (nocturnal decrease in blood pressure <10% of daytime blood pressure) were 31 hypertensives and six WCH with standard day/night intervals and 25 hypertensives and four WCH with individualized intervals; nocturnal falls in systolic and diastolic blood pressures were significantly greater with individualized intervals for both groups. Left ventricular hypertrophy was present in 68 hypertensives and seven WCH; left ventricular systolic function was normal in all and left ventricular diastolic function was impaired in 53 hypertensives and seven WCH. Left ventricular characteristics of WCH were not correlated to blood pressure parameters; left ventricular mass index of hypertensives was directly correlated to 24h, daytime and night-time systolic blood pressures, whereas left ventricular diastolic function was inversely correlated to night-time systolic and diastolic blood pressures. The correlations were not affected by choice of using individual awake/asleep patterns. Timing day and night in an individualized way seems to improve the evaluation of nocturnal fall in blood pressure, but does not improve the ability to predict the left ventricle's involvement with ambulatory blood pressure monitoring.