Left Ventricular Damage Research Articles

J waves reaching to equal or more than 2 of 3 LV inferior wall leads may predict the presence of organized myocardial fibrotic or fat change in survivors of ventricular fibrillation

Abstract Funding Acknowledgements Type of funding sources: None. Background The distribution of J waves and the presence of organized left ventricular (LV) myocardial damage may be related in survivors of ventricular fibrillation (VF). Purpose To predict the presence of organized myocardial damage such as fibrotic or fat change on cardiac computed tomography (CT) using the distribution of J waves in survivors of VF. Methods We conducted a retrospective analysis of 21 survivors of VF (17 males; mean age, 61 ± 14 years) that were implanted with a cardioverter defibrillator and underwent cardiac CT. Results On ECG, 4 patients had atrial fibrillation and 15 had J waves. On CT, 13 patients had organized LV myocardial fibrotic and/or fat change in myocardium. The mean corrected QT interval was 453 ± 30 and 429 ± 48 msec in patients with and without myocardial fibrotic and/or fat change, respectively (P = 0.182). The distribution of J waves was as follows: 5 had J waves in II, III and aVF leads (one had myocardial fibrotic and/or fat change) and 2 had J waves in III lead (one had myocardial fibrotic and/or fat change). One patient each had J waves in V1 lead; V1,2 leads; II, III, aVF and V1-3 leads; I, III, aVF and V1 leads; II, III, aVF, aVL and V1-6 leads; II, III, aVF and V4,5 leads; II, III, aVF and V2-5 leads; and III and aVF leads. The first one did not have myocardial fibrotic and/or fat change and the remaining 6 had myocardial fibrotic and/or fat change. If the J waves reached to ≥1 of 3 LV inferior wall leads (II, III, aVF leads) (N = 13), 10 (77%) had LV myocardial fibrotic and/or fat change. If not (N = 8), 3(38%) had LV myocardial fibrotic and/or fat change (P = 0.071). If the J waves reached ≥2 of 3 LV inferior wall leads (N = 11), 9 (82%) had LV myocardial fibrotic and/or fat change. If not (N = 10), 4 (40%) had LV myocardial fibrotic and/or fat change (P = 0.049). If the J waves reached all three LV inferior wall leads (N = 10), 8 (80%) had LV myocardial fibrotic and/or fat change. If not (N = 11), 5 (46%) had LV myocardial fibrotic and/or fat change (P = 0.104). Conclusions In survivors of VF, if the J waves reached ≥2 of 3LV inferior wall leads, the frequency of organized LV myocardial fibrotic and/or fat change was significantly higher than those without. Furthermore, the distribution of J waves and the presence of myocardial fibrotic and/or fat change on CT may predict VF. Abstract Figure. CT fibrosis in VF survivors with HCM

Primary prevention of chronic anthracycline cardiotoxicity with ACE inhibitor is temporarily effective in rabbits, but benefits wane in post-treatment follow-up.

Angiotensin-converting enzyme inhibitors (ACEis) have been used to treat anthracycline (ANT)-induced cardiac dysfunction, and they appear beneficial for secondary prevention in high-risk patients. However, it remains unclear whether they truly prevent ANT-induced cardiac damage and provide long-lasting cardioprotection. The present study aimed to examine the cardioprotective effects of perindopril on chronic ANT cardiotoxicity in a rabbit model previously validated with the cardioprotective agent dexrazoxane (DEX) with focus on post-treatment follow-up (FU). Chronic cardiotoxicity was induced by daunorubicin (DAU; 3 mg/kg/week for 10 weeks). Perindopril (0.05 mg/kg/day) was administered before and throughout chronic DAU treatment. After the completion of treatment, significant benefits were observed in perindopril co-treated animals, particularly full prevention of DAU-induced mortality and prevention or significant reductions in cardiac dysfunction, plasma cardiac troponin T (cTnT) levels, morphological damage, and most of the myocardial molecular alterations. However, these benefits significantly waned during 3 weeks of drug-free FU, which was not salvageable by administering a higher perindopril dose. In the longer (10-week) FU period, further worsening of left ventricular function and morphological damage occurred together with heart failure (HF)-related mortality. Continued perindopril treatment in the FU period did not reverse this trend but prevented HF-related mortality and reduced the severity of the progression of cardiac damage. These findings contrasted with the robust long-lasting protection observed previously for DEX in the same model. Hence, in the present study, perindopril provided only temporary control of ANT cardiotoxicity development, which may be associated with the lack of effects on ANT-induced and topoisomerase II β (TOP2B)-dependent DNA damage responses in the heart.

Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension

Treatment of hypertension-mediated cardiac damage with left ventricular (LV) hypertrophy (LVH) and heart failure remains challenging. To identify novel targets, we performed comparative transcriptome analysis between genetic models derived from stroke-prone spontaneously hypertensive rats (SHRSP). Here, we identified carboxypeptidase X 2 (Cpxm2) as a genetic locus affecting LV mass. Analysis of isolated rat cardiomyocytes and cardiofibroblasts indicated Cpxm2 expression and intrinsic upregulation in genetic hypertension. Immunostaining indicated that CPXM2 associates with the t-tubule network of cardiomyocytes. The functional role of Cpxm2 was further investigated in Cpxm2-deficient (KO) and wild-type (WT) mice exposed to deoxycorticosterone acetate (DOCA). WT and KO animals developed severe and similar systolic hypertension in response to DOCA. WT mice developed severe LV damage, including increases in LV masses and diameters, impairment of LV systolic and diastolic function and reduced ejection fraction. These changes were significantly ameliorated or even normalized (i.e., ejection fraction) in KO-DOCA animals. LV transcriptome analysis showed a molecular cardiac hypertrophy/remodeling signature in WT but not KO mice with significant upregulation of 1234 transcripts, including Cpxm2, in response to DOCA. Analysis of endomyocardial biopsies from patients with cardiac hypertrophy indicated significant upregulation of CPXM2 expression. These data support further translational investigation of CPXM2.

Гендерні та вікові особливості ремоделювання серця у хворих із постінфарктним кардіосклерозом, цукровим діабетом 2-го типу та ожирінням

У статті було визначено гендерні та вікові особливості ремоделювання серця у хворих із постінфарктним кардіосклерозом, цукровим діабетом (ЦД) 2-го типу й ожирінням.Із цією метою проведено обстеження 295 хворих із постінфарктним кардіосклерозом. Гендерні та вікові особливості ремоделювання серця у 215 хворих із постінфарктним кардіосклерозом, цукровим діабетом 2-го типу та ожирінням порівнювали з такими у хворих, які не мали діабету й ожиріння (група порівняння (n = 80)). Усі хворі з постінфарктним кардіосклерозом були розподілені на групи залежно від наявності ЦД 2-го типу (перша група (n = 68)), ожиріння (друга група (n = 76)) та їх поєднаного перебігу (третя група (n = 71)). Усі групи були порівнянні за віком (64,38 ± 1,08; 64,87 ± 1,98; 65,13 ± 1,43 та 63,47 ± 1,28 року відповідно). Верифікацію діагнозу проводили на підставі чинних критеріїв. Усім хворим проводили загальноклінічні та інструментальні обстеження. Ехокардіографічні дослідження проводили за стандартною методикою Х. Фейгенбаума на ультразвуковому апараті RADMIR (Ultima PRO 30) (Харків, Україна).Гендерний аналіз показав вірогідне збільшення розмірів лівого шлуночка та лівого передсердя на тлі більш вираженого зниження систолічної функції у чоловіків із постінфарктним кардіосклерозом, ЦД 2-го типу та ожирінням порівняно з жінками незалежно від віку. У хворих похилого віку спостерігалися такі самі зміни, як у хворих середнього віку. У всіх обстежених хворих виявлялося порушення геометричної адаптації, із них концентричний тип ремоделювання був переважно в осіб жіночої статі, в обстежених чоловіків частіше траплялося ексцентричне ремоделювання лівого шлуночка.Таким чином, у жінок валідними факторами, що визначають тяжкість ураження міокарда лівого шлуночка і перебігу хронічної серцевої недостатності на тлі перенесеного інфаркту міокарда, є ЦД 2-го типу, надлишкова маса тіла й перевага сприятливого концентричного типу ремоделювання лівого шлуночка зі збереженою його систолічною функцією. Тоді як у чоловіків ремоделювання міокарда має менш сприятливий перебіг зі збільшенням розмірів лівого шлуночка та лівого передсердя на тлі більш вираженого зниження систолічної функції.

Abstract 13802: J Waves Observed in More Than 3 Electrocardiographic Leads Predict the Presence of Organized Myocardial Fibrotic or Fat Change in Non Ischemic Survivors of Ventricular Fibrillation

Introduction: The distribution of J waves and the presence of organized left ventricular (LV) myocardial damage may be related in non ischemic survivors of ventricular fibrillation (VF). Hypothesis: We hypothesize that the distribution of J waves can predict the presence of myocardial damage such as fibrotic or fat change in non ischemic survivors of VF. Methods: We conducted a retrospective analysis of 16 survivors of VF (12 males; 60±15 years) without any histories of previous myocardial infarction and underwent cardiac CT in which no significant coronary stenosis were observed and/or MRI before implantation of a cardioverter defibrillator. Results: On ECG, 3 patients had atrial fibrillation and 12 had J waves. On CT and/or MRI, 7 patients had organized LV myocardial fibrotic and/or fat change. The mean corrected QT interval was 451±47 and 415±5 msec in patients with and without J waves (P=0.147) and 458±32 and 429±48 msec in patients with and without myocardial fibrotic and/or fat change (P=0.202), respectively. The distribution of J waves was presented in the table. Presence of the J waves observed more than 3 ECG leads (N=4) and presence of myocardial fibrotic and/or fat change (N=7) significantly correlated each other in the Fisher's exact test (P=0.019). Presence of myocardial fibrotic and/or fat change were significantly greater in patients with J waves observed more than 3 ECG leads than those with J waves observed less than 4 ECG leads (100% vs 25%, P=0009). Presence of J waves observed more than 3 ECG leads were also significantly greater in patients with myocardial fibrotic and/or fat change than those without (57% vs 0%, P=0009). Conclusions: In non ischemic survivors of VF, if J waves were observed more than 3 ECG leads, the frequency of LV myocardial fibrotic and/or fat change was significantly higher than those without. The distribution and numbers of ECG leads with J waves and the presence of myocardial fibrotic and/or fat change may be useful to predict non ischemic VF.

A Flow Sensor-Based Suction-Index Control Strategy for Rotary Left Ventricular Assist Devices.

Rotary left ventricular assist devices (LVAD) have emerged as a long-term treatment option for patients with advanced heart failure. LVADs need to maintain sufficient physiological perfusion while avoiding left ventricular myocardial damage due to suction at the LVAD inlet. To achieve these objectives, a control algorithm that utilizes a calculated suction index from measured pump flow (SIMPF) is proposed. This algorithm maintained a reference, user-defined SIMPF value, and was evaluated using an in silico model of the human circulatory system coupled to an axial or mixed flow LVAD with 5–10% uniformly distributed measurement noise added to flow sensors. Efficacy of the SIMPF algorithm was compared to a constant pump speed control strategy currently used clinically, and control algorithms proposed in the literature including differential pump speed control, left ventricular end-diastolic pressure control, mean aortic pressure control, and differential pressure control during (1) rest and exercise states; (2) rapid, eight-fold augmentation of pulmonary vascular resistance for (1); and (3) rapid change in physiologic states between rest and exercise. Maintaining SIMPF simultaneously provided sufficient physiological perfusion and avoided ventricular suction. Performance of the SIMPF algorithm was superior to the compared control strategies for both types of LVAD, demonstrating pump independence of the SIMPF algorithm.

Staging cardiac damage in aortic valve disease: one size fits all?

Abstract Background Nowadays, in patients with aortic regurgitation (AR), aortic valve surgery is indicated when severe and symptomatic or those with depressed LVEF. However, clinical outcomes of patients with significant aortic regurgitation are not influenced by these factors only. Recently, a new staging system for severe aortic stenosis has been proposed by Généreux on the basis of the extent of anatomic and functional cardiac damage. If this model could be applicable to an unselected significant AR population has not been tested. Purpose The aim of our study was to evaluate the prevalence of the different stages of extra-aortic valvular cardiac damage by the application of Généreux staging and its impact on prognosis in a large, real world cohort of significant AR patients. Methods This study retrospectively analysed the clinical, Doppler echocardiographic and outcome data in patients with grade III or greater AR between January 2014 and September 2019. According to the extent of cardiac damage on echocardiography, patients were classified as Stage 0 (no cardiac damage), Stage 1 (left ventricular damage), Stage 2 (mitral valve or left atrial damage), Stage 3 (tricuspid valve or pulmonary artery vasculature damage) or Stage 4 (right ventricular damage). Exclusion criteria were severe aortic stenosis and previous valve repair or replacement. The primary end-point was all-cause mortality. Results A total of 572 patients, aged 70.1±13.9 years, 294 (51.3%) men were enrolled. One third of patients were in NYHA I. Based on the proposed classification, 82 patients (14.3%) were classified in stage 0, 130 (22.7%) in stage 1, 276 (48.2%) in stage 2, 68 (11.8%) in stage 3 and 17 (3.0%) in stage 4. Median follow-up time was 3.3±1.9 years. There was a progressive increase in mortality rates according to staging: 8.5% in stage 0, 10.8% in stage 1, 24.9% in stage 2, 42.6% in stage 3 and 52.9% in stage 4 (p<0.001). On multivariable analysis, the extent of cardiac damage was independently associated with excess mortality (HR 1.69, 95% CI 1.29 to 2.21) Conclusion Our study demonstrated that this new staging system studied for aortic stenosis also provides increased prognostic value to patients with significant aortic regurgitation. This staging system can be helpful to identify the degree of extra-aortic valvular cardiac damage and to optimize the time of valvular intervention. Further prospective studies are needed to confirm the benefit of the applicability of this model in clinical practice. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Centro Hospitalar Vila Nova de Gaia / Espinho Distribution of stages of cardiac damageSurvival analysis according to stage

Presence of myocardial fibrotic or fat change on cardiac CT influences the width of distribution range of J waves in survivors of ventricular fibrillation

Abstract Background The distribution of J waves may correlate with left ventricular (LV) myocardial damage in survivors of ventricular fibrillation (VF). Purpose To determine the relationship of the distribution of J waves with presence of myocardial damage such as fibrotic or fat change on cardiac computed tomography (CT) in survivors of VF. Methods We conducted a retrospective analysis of 21 survivors of VF (17 males; mean age, 61±14 years) that were implanted with a cardioverter defibrillator and underwent cardiac CT. Results On ECG, 4 patients had atrial fibrillation and 15 had J waves. On CT, 13 patients had organized LV myocardial fibrotic and/or fat change in myocardium. The mean corrected QT interval was 453±30 and 429±48 msec in patients with and without myocardial fibrotic and/or fat change, respectively (P=0.182). The distribution of J waves was as follows: 5 had J waves in II, III and aVF leads (one had myocardial fibrotic and/or fat change) and 2 had J waves in III lead (one had myocardial fibrotic and/or fat change). One patient each had J waves in V1 lead; V1,2 leads; II, III, aVF and V1–3 leads; I, III, aVF and V1 leads; II, III, aVF, aVL and V1–6 leads; II, III, aVF and V4,5 leads; II, III, aVF and V2–5 leads; and III and aVF leads. The first one did not have myocardial fibrotic and/or fat change and the remaining 6 had myocardial fibrotic and/or fat change (Figure). If the J waves reached to ≥1 of 3 LV inferior wall leads (II, III, aVF leads) (N=13), 10 (77%) had LV myocardial fibrotic and/or fat change. If not (N=8), 3 (38%) had LV myocardial fibrotic and/or fat change (P=0.071). If the J waves reached ≥2 of 3 LV inferior wall leads (N=11), 9 (82%) had LV myocardial fibrotic and/or fat change. If not (N=10), 4 (40%) had LV myocardial fibrotic and/or fat change (P=0.049). If the J waves reached all three LV inferior wall leads (N=10), 8 (80%) had LV myocardial fibrotic and/or fat change. If not (N=11), 5 (46%) had LV myocardial fibrotic and/or fat change (P=0.104). Conclusions In survivors of VF, organized LV myocardial fibrotic and/or fat changes on cardiac CT correlate with a wider distribution range of J waves (reached to LV inferior wall leads). The distribution of J waves and the presence of myocardial fibrotic and/or fat change on CT may be useful to predict the occurrence of VF. Funding Acknowledgement Type of funding sources: None. CT fibrosis in VF survivorsJ waves and fibrotic and/or fat change

Deficient Myocardial Organization and Pathological Fibrosis in Fetal Aortic Stenosis-Association of Prenatal Ultrasound with Postmortem Histology.

In fetal aortic stenosis (AS), it remains challenging to predict left ventricular development over the course of pregnancy. Myocardial organization, differentiation and fibrosis could be potential biomarkers relevant for biventricular outcome. We present four cases of fetal AS with varying degrees of severity and associate myocardial deformation on fetal ultrasound with postmortem histopathological characteristics. During routine fetal echocardiography, speckle tracking recordings of the cardiac four-chamber view were performed to assess myocardial strain as parameter for myocardial deformation. After pregnancy termination, postmortem cardiac specimens were examined using immunohistochemical labeling (IHC) of key markers for myocardial organization, differentiation and fibrosis and compared to normal fetal hearts. Two cases with critical AS presented extremely decreased left ventricular (LV) strain on fetal ultrasound. IHC showed overt endocardial fibro-elastosis, which correlated with pathological fibrosis patterns in the myocardium and extremely disturbed cardiomyocyte organization. The LV in severe AS showed mildly reduced myocardial strain and less severe disorganization of the cardiomyocytes. In conclusion, the degree of reduction in myocardial deformation corresponded with high extent to the amount of pathological fibrosis patterns and cardiomyocyte disorganization. Myocardial deformation on fetal ultrasound seems to hold promise as a potential biomarker for left ventricular structural damage in AS.

Pathogenic variants in plakophilin-2 gene (PKP2) are associated with better survival in arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is mainly caused by mutations in genes encoding desmosomal proteins. Variants in plakophilin-2 gene (PKP2) are the most common cause of the disease, associated with conventional ARVC phenotype. The study aims to evaluate the prevalence of PKP2 variants and examine genotype–phenotype correlation in Polish ARVC cohort. All 56 ARVC patients fulfilling the current criteria were screened for genetic variants in PKP2 using denaturing high-performance liquid chromatography or next-generation sequencing. The clinical evaluation involved medical history, electrocardiogram, echocardiography, and follow-up. Ten variants (5 frameshift, 2 nonsense, 2 splicing, and 1 missense) in PKP2 were found in 28 (50%) cases. All truncating variants are classified as pathogenic/likely pathogenic, while the missense variant is classified as variant of uncertain significance. Patients carrying a PKP2 mutation were younger at diagnosis (p = 0.003), more often had negative T waves in V1–V3 (p = 0.01), had higher left ventricular ejection fraction (p = 0.04), and were less likely to present symptoms of heart failure (p = 0.01) and left ventricular damage progression (p = 0.04). Combined endpoint of death or heart transplant was more frequent in subgroup without PKP2 mutation (p = 0.03). Pathogenic variants in PKP2 are responsible for 50% of ARVC cases in the Polish population and are associated with a better prognosis. ARVC patients with PKP2 mutation are less likely to present left ventricular involvement and heart failure symptoms. Combined endpoint of death or heart transplant was less frequent in this group.

Comparison of Clinical Features between Primary Aldosteronism and Essential Hypertension in Chinese Patients: A Case-Control Study.

Primary aldosteronism (PA) is one of the most common forms of secondary hypertension. Recent studies suggest that, compared with essential hypertension (EH), PA presents more severe disorders of glycolipid metabolism and organ damages. This case-control retrospective study aimed to ascertain clinical features and metabolic parameters between Chinese patients of PA and EH. 174 PA patients and 174 matched EH patients were recruited. Their clinical features, biochemistry parameters, the ventricular septal thickness, and left ventricular mass index (LVMI) were compared. HOMA-β% and HOMA-IR were calculated to evaluate glucose metabolism. The results showed that there was no significant difference regarding BMI, waist-to-hip ratio, and blood pressure between the two groups. The blood potassium level was significantly lower in PA patients than those in EH patients. The abnormal glucose tolerance and the incidence of diabetes in the PA group were not significantly different from those in EH group, but the insulin secretion levels at 0 min and 30 min were significantly weaker than those in the EH group, and the HOMA-β% was also lower in the PA group than those in the EH group. Left ventricular structural abnormalities in PA patients were more severe than those in EH patients. Subtype analysis indicated that patient with aldosterone-producing adenoma (APA) has more serious hypokalemia and lower levels of HOMA-β% and HOMA-IR comparing to those in the idiopathic adrenal hyperplasia (IHA) patient. These findings demonstrated that PA patients showed more impaired insulin secretion function and more severe left ventricular structural damage compared with EH patients.

Refined staging classification of cardiac damage associated with aortic stenosis and outcomes after transcatheter aortic valve implantation.

A new staging classification of aortic stenosis (AS) characterizing the extent of cardiac damage was established and validated in patients undergoing transcatheter aortic valve implantation (TAVI). We aimed to validate an updated classification system in patients undergoing TAVI. In a prospective TAVI registry, AS patients were categorized into the following stages: no cardiac damage (Stage 0), left ventricular damage (Stage 1), left atrial or mitral valve damage (Stage 2), pulmonary vasculature or tricuspid valve damage (Stage 3), or right ventricular (RV) damage or low-flow state (Stage 4). Stage 3 was sub-divided into Stage 3a (≤moderate pulmonary hypertension) and Stage 3b (severe pulmonary hypertension). Stage 4 was sub-divided into Stage 4a (low-flow without RV dysfunction), Stage 4b (RV dysfunction without low-flow), and Stage 4c (RV dysfunction with low-flow). The primary endpoint was all-cause death at 1 year. Among 1156 eligible patients, 14 were classified as Stage 0, 38 as Stage 1, 105 as Stage 2278 as Stage 3, and 721 as Stage 4. There was a stepwise increase in mortality according to advancing stages of cardiac damage: 3.9% (Stage 0-1), 9.6% (Stage 2), 14.1% (Stage 3), and 17.4% (Stage 4) (P = 0.002). After multivariable adjustment, only Stage 3b, Stage 4b, and Stage 4c conferred a significantly increased risk of mortality compared to Stage 0-1. More than one-third of patients had advanced cardiac damage (severe pulmonary hypertension or RV dysfunction) before TAVI, associating with a five- to seven-fold increased risk of mortality at 1 year. https://www.clinicaltrials.gov. NCT01368250.

Prognostic implications of cardiac damage classification based on computed tomography in severe aortic stenosis.

An echocardiographic staging system of severe aortic stenosis (AS) based on additional extra-valvular cardiac damage has been associated with prognosis after transcatheter aortic valve implantation (TAVI). Multidetector row computed tomography (MDCT) is key in the evaluation of AS patients undergoing TAVI and can potentially detect extra-valvular cardiac damage. This study aimed at evaluating the prognostic implications of an MDCT staging system of severe AS in patients undergoing TAVI. A total of 405 patients (80 ± 7 years, 52% men) who underwent full-beat MDCT prior to TAVI were included. The extent of cardiac damage was assessed by MDCT and classified in five categories; Stage 0 (no cardiac damage), Stage 1 (left ventricular damage), Stage 2 (left atrium and mitral valve damage), Stage 3 (right atrial damage), and Stage 4 (right ventricular damage). Twenty-seven (7%) patients were stratified as Stage 0, 96 (24%) as Stage 1, 152 (38%) as Stage 2, 78 (19%) as Stage 3, and 52 (13%) as Stage 4. During a median follow-up of 3.7 (IQR 1.7-5.5) years, 150 (37%) died. On multivariable Cox regression analysis, cardiac damage Stage 3 (HR vs. Stage 0: 4.496, P = 0.039) and Stage 4 (HR vs. Stage 0: 5.565, P = 0.020) were independently associated with all-cause mortality. The MDCT-based staging system of cardiac damage in severe AS effectively identifies the patients who are at higher risk of death after TAVI.

Staging cardiac damage associated with aortic stenosis in patients undergoing transcatheter aortic valve implantation.

A new staging classification of aortic stenosis (AS) characterizing the extent of cardiac damage was established and validated in patients undergoing transcatheter aortic valve implantation (TAVI). The present study was aimed to refine the staging system by integrating a quantitative evaluation of right ventricular (RV) dysfunction defined by current echocardiographic guideline recommendations. In a prospective TAVI registry, patients were categorized into the stages: no cardiac damage (Stage 0), left ventricular damage (Stage 1), left atrial or mitral valve damage (Stage 2), pulmonary vasculature or tricuspid valve damage (Stage 3), or RV damage (Stage 4) based on baseline echocardiography. Among 1133 eligible patients undergoing TAVI, 8 (3.4%) patients were categorized as Stage 0, 113 (10.0%) as Stage 1, 397 (35.0%) as Stage 2, 239 (21.1%) as Stage 3, and 346 (30.5%) as Stage 4. There was a stepwise increase in all-cause and cardiovascular mortality rates at 1year according to increasing stages of secondary cardiac damage: 5.4% and 0% in Stage 0, 5.3% and 1.8% in Stage 1, 8.9% and 5.9% in Stage 2, 17.7% and 12.9% in Stage 3, and 25.8% and 19.9% in Stage 4, respectively. After multivariable adjustment, increasing stages of cardiac damage gradually correlated with all-cause and cardiovascular mortality. A significant number of patients with AS underwent TAVI only once cardiac damage has already occurred. Integrating a guideline-based definition of RV dysfunction increased the sensitivity of the staging system to identify patients at increased risk of death after TAVI.

Nuclear imaging of chemotherapy-induced cardiotoxicity

The high efficiency of modern chemotherapy has made it possible to achieve great success in the treatment of cancer. Cardiovascular adverse effects are a major disadvantage of anticancer therapy, often requiring low and less effective doses or even drug withdrawal. Nuclear imaging techniques are the most sensitive in early detection of left ventricular damage and dysfunction during chemotherapy. This review presents modern data on the potential of nuclear imaging of cardiotoxicity.

Outcome of aortic stenosis according to invasive cardiac damage staging after transcatheter aortic valve replacement.

In recent studies, a 5-stage cardiac damage classification in severe aortic stenosis (AS) based on echocardiographic parameters has shown to provide predictive value regarding clinical outcome. The objective of this study was to investigate the prognostic impact of a cardiac damage classification based on invasive hemodynamics in patients with AS undergoing transcatheter aortic valve replacement (TAVR). A total of 1400 patients with symptomatic AS and full invasive hemodynamic assessment before TAVR were included. Patients were categorized according to their cardiac damage stage into five groups that are defined as: stage 0, no cardiac damage; stage 1, left ventricular damage; stage 2, left atrial and/or mitral valve damage; stage 3, pulmonary vasculature and/or tricuspid valve damage; stage 4, right ventricular damage. 9.9% patients were classified as stage 0, 23.6% as stage 1, the majority of patients as stage 2 (33.5%), 23.1% as stage 3 and 10% as stage 4. One- and 4-year mortality were 10.1%/29.5% in stage 0, 16.1%/60.6% in stage 1, 17.3%/39.4% in stage 2, 22%/54.6% in stage 3, 27.1%/62.2% in stage 4 (p = 0.001/p < 0.001). The extent of cardiac damage was independently associated with increased mortality after TAVR (HR 1.16 per each increment in stage, 95% confidence interval 1.03-1.18; p = 0.018). Cardiac damage staging in severe AS patients based on invasive hemodynamics appears to show strong association between the extent of cardiac damage and post-TAVR mortality. This staging classification provides predictive value and may improve risk stratification, therapy management and decision-making in patients with AS. Invasive Staging Classification of Cardiac Damage in Severe Symptomatic Aortic Stenosis has an Impact on Outcome after TAVR. (Top) Invasive staging criteria for cardiac damage in five stages using left ventricular end-diastolic pressure (LVEDP) for stage 1 (red), post-capillary wedge pressure (PCWP) for stage 2 (green), systolic pulmonary artery pressure (SPAP) for stage 3 (purple) and right atrial pressure (RAP) for stage 4 (yellow). The cake chart shows the distribution of the different stage in the whole cohort. (Bottom) Survival Analyses According to Stage of Cardiac Damage after Transcatheter Aortic Valve Replacement using Invasive Criteria. Kaplan-Meier plots comparing overall (left) and cardiovascular (right) 4-year survival showing with the more advancing stage a higher mortality rate.

Right Ventricular Damage in COVID-19: Association Between Myocardial Injury and COVID-19.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2, is a global pandemic. It has resulted in considerable morbidity and mortality around the world. The respiratory system is the main system invaded by the virus involved in COVID-19. In addition to typical respiratory manifestations, a certain proportion of severe COVID-19 cases present with evidence of myocardial injury, which is associated with excessive mortality. With availability of an increasing amount of imaging data, right ventricular (RV) damage is prevalent in patients with COVID-19 and myocardial injury, while left ventricular damage is relatively rare and lacks specificity. The mechanisms of RV damage may be due to increased RV afterload and decreased RV contractility caused by various factors, such as acute respiratory distress syndrome, pulmonary thrombosis, direct viral injury, hypoxia, inflammatory response and autoimmune injury. RV dysfunction usually indicates a poor clinical outcome in patients with COVID-19. Timely and effective treatment is of vital importance to save patients' lives as well as improve prognosis. By use of echocardiography or cardiovascular magnetic resonance, doctors can find RV dilatation and dysfunction early. By illustrating the phenomenon of RV damage and its potential pathophysiological mechanisms, we will guide doctors to give timely medical treatments (e.g., anticoagulants, diuretics, cardiotonic), and device-assisted therapy (e.g., mechanical ventilation, extracorporeal membrane oxygenation) when necessary for these patients. In the paper, we examined the latest relevant studies to investigate the imaging features, potential mechanisms, and treatments of myocardial damage caused by COVID-19. RV damage may be an association between myocardial damage and lung injury in COVID-19. Early assessment of RV geometry and function will be helpful in aetiological determination and adjustment of treatment options.

Pathophysiologic risk stratification of chronic heart failure: coexisting left atrial and right ventricular damage and the role of pulmonary circulation

Abstract Funding Acknowledgements Type of funding sources: None. Background in heart failure with reduced ejection fraction (HFrEF) the chronic increase of filling pressures progressively involves left atrium (LA), pulmonary circulation (PC) and right ventricle (RV), leading to worse outcome. Purpose we investigated the prognostic impact of either isolate LA impairment, RV dysfunction combined with pulmonary hypertension, or both, in HFrEF, using basic and advanced echocardiography. Methods 106 outpatients with HFrEF were enrolled. Exclusion criteria were primary lung disease, non-sinus rhythm, previous cardiac surgery, poor acoustic window. Clinical examination and basic echocardiography were performed. Speckle tracking analysis was used to measure peak atrial longitudinal strain (PALS) and a new marker of interaction between RV and PC: absolute free wall RV longitudinal strain(fwRVLS)/systolic pulmonary artery pressure(sPAP). Patients were followed for all-cause or cardiovascular death and heart failure (HF) hospitalization. Results of 84 eligible patients [mean age: 60.1 ± 11.5; 82% male, mean left ventricular ejection fraction (LV EF) 28 ± 5%], 48 reached the combined endpoint. Population was divided into 3 groups: Group 1 [PALS≥15 and fwRVLS/sPAP ≤ 0.5]; Group 2 [PALS ≤ 15 and fwRVLS/sPAP ≤ 0.5 or PALS≥15 and fwRVLS/sPAP≥0.5]; Group 3 [PALS ≤ 15 and fwRVLS/sPAP≥0.5]. Mean follow-up was 3.5 ± 0.3years. The increasing severity groups were associated with higher LA volume index (LAVI), New York Heart Association (NYHA) class, mitral regurgitation (MR) and tricuspid regurgitation (TR) grades, lower LV EF, LV global longitudinal strain (GLS), PALS, tricuspid annular plane systolic excursion (TAPSE), sPAP, fwRVLS and global RVLS(p &amp;lt; 0.0001). Reduced PALS and fwRVLS/sPAP were independent predictors of NYHA &amp;gt; 2 at univariate and multivariate analysis adjusted for age, sex, LV EF, and of any events with adjusted Cox models (Table 1). Kaplan-Meier curves showed a clear divergence between the groups for the prediction of the combined endpoint (Fig.1), cardiovascular death and HF hospitalization. Conclusions the combination of LA and RV damage could represent the transition point to end-stage HF, with considerably worse prognosis. Its assessment with PALS and fwRVLS/sPAP could help risk stratification of HFrEF patients in order to provide early treatment. Table 1 Unadjusted hazard ratio [95% CI] Adjusted for GLS hazard ratio [95% CI] Adjusted for GLS, LAVi, TR, RVFAC hazard ratio [95% CI] Group 3 vs 1 10.61 [4.16-27.06], p &amp;lt; 0.0001 10.24 [3.49-30.02], p &amp;lt; 0.0001 9.54 [2.95-30.92], p = 0.0002 Group 3 vs 2 3.90 [1.92-7.93], p = 0.0002 3.82 [1.74-8.36], p = 0.0008 3.78 [1.66-8.61], p = 0.002 Group 2 vs 1 2.72 [1.03-7.20], p = 0.04 2.69 [0.99-7.25], p = 0.05 2.53 [0.84-7.58], p = 0.1 CI, confidence interval; EF, ejection fraction; GLS, global longitudinal strain;LAVI, left atrial volume index; MR, mitral regurgitation, TR, tricuspid regurgitation Abstract Figure. Fig.1

The inflammation link between periodontal disease and coronary atherosclerosis in patients with acute coronary syndromes: case\u2013control study

BackgroundCoronary atherosclerosis and periodontal disease, due to their prevalence, are a serious epidemiological problem. Pathophysiological evidence points to their possible common inflammatory etiopathological background. The aim of the study was to analyze the relationship between the presence and severity of periodontitis, systemic inflammation and selected parameters of myocardial injury and heart function in patients with acute myocardial infarction.MethodsThe study group consisted of 71 patients 54.22 (7.05)-year-old hospitalized due to acute myocardial infarction. The patients underwent a coronary angiographic examination and echocardiography. The following laboratory parameters were determined: blood morphology, high sensitivity C-reactive protein (hsCRP), erythrocyte sedimentation rate (ESR), fibrinogen, troponin I, creatine kinase myocardial band (CK-MB), brain natriuretic peptide (BNP), lipidogram, glucose, creatinine, glomerular filtration rate (GFR), thyroid stymulating hormone (TSH), glycated hemoglobin (HbA1c). Dental assessment of the patients was performed and the following indicators were included: the number of teeth preserved, approximal plaque index (API), bleeding on probing (BoP), pocket depth (PD), the number of bleeding periodontal pockets ≥ 4 mm in depth (NoPD ≥ 4 mm), the percentage of bleeding periodontal pockets ≥ 4 mm in depth (%PD ≥ 4 mm), clinical attachment loss (CAL). The control consisted of 40 patients 52 (± 8.43)-year-old without a history of coronary heart disease. These patients were subjected to a periodontal examination using the above parameters and classification methods. The following statistical tests were implemented: Shapiro–Wilk test, Levene's test, Mann Whitney's U analysis, Univariate Analysis of Variance (ANOVA); the post-hoc analysis was performed with the use of Tukey's honest significant difference test (HSD), Kruskal–Wallis's non-parametric test, Spearman's rank correlation, logistic regression analysis, linear regression analysis and ROC analysis.ResultsThe BoP (bleeding on probing) significantly correlated with fibrynogen (R-0.36; p-0.006). All indices regarding the pocket depth correlated significantly with the number of leukocytes: PD (R-0.27; p-0.02), NoPD ≥ 4 mm (R-0.28, p-0.02), %PD ≥ 4 mm (R-0.27; p-0.02). PD (R-0.28; p-0.01) and NoPD ≥ 4 mm (R-0.24; p-0.04) were also associated significantly with the level of hsCRP. The BoP is correlated closely with the levels of BNP (R-0.29, p-0.02). The multifactorial analysis showed that significant predictors of myocardial infarction are API and BoP. The analysis showed that API and BoP are important predictors of troponin levels. Linear regression analysis showed that only CAL is a significant predictor of BNP.ConclusionsPatients with acute myocardial infarction have worse periodontal status compared to people without coronary heart disease. Greater severity of periodontitis, plaque accumulation and bleeding on probing are associated with acute myocardial infarction. Periodontitis is a risk factor for myocardial infarction and also affects the degree of post-infarction left ventricular damage, which means that there is an inflammatory link between these two diseases.

Cardiac hemodynamic disorders in patients with active chronic viral hepatitis and the effectiveness of antiviral therapy

Aim. To study cardiac hemodynamic disorders in patients with chronic viral hepatitis (CVH) and evaluate the effectiveness of antiviral therapy (AVT).Material and methods. Seventy-nine patients with CVH (mean age, 38,6 years, disease duration, 4,7 years) were examined. The patients were divided into two groups: group 1 (n=42) — normal level of alanine aminotransferase (ALT), group 2 — ALT 3-10 times higher than normal (n=37). Fourteen patients with CVH underwent AVT. Control group consisted of 23 people. Doppler echocardiography was performed. Statistical processing was carried out using Statistica 10.0.Results. In patients with active hepatitis, atrial volume, end diastolic volume, left ventricular (LV) mass index, LV stroke volume increased, and the tricuspid (TC) annular systolic velocity decreased in comparison with the control and 1st groups. In patients with normal ALT levels, the left atrial volume index increased by 8% in comparison with control group. Concentric remodeling was the predominant variant of LV remodeling in patients with active hepatitis. In patients with active hepatitis, LV lateral wall, interventricular septal (IVS), and TC Em/Am ratio decreased. LV diastolic dysfunction was reported in 12 patients with active and 3 patients with inactive CVH. After AVT, left atrium (LA) volume, IVS thickness, LV mass decreased, while TC and mitral annular systolic velocity increased. The viral load has a relationship with mitral annular systolic velocity (r=0,91, p=0,001) and LV mass (r=0,64, p=0,05).Conclusion. In patients with active hepatitis, along with LV and LA dilatation and hypertrophy, a relative right atrial increase, a decrease in the right ventricular longitudinal systolic velocity, and the formation of biventricular diastolic dysfunction develop. In patients with inactive hepatitis, only the left atrial volume increased. The established correlations indicate possible LV damage. Antiviral therapy has a beneficial effect on the main structural and functional cardiac parameters.