Concentric Left Ventricular Hypertrophy Research Articles

A Closer Evaluation for Refractory Atrial Fibrillation with Heart Failure, a Case Report

<h3>Introduction</h3> Atrial fibrillation (AF) is highly prevalent after the age of 55 years. However, it can be associated with infiltrative cardiomyopathy. <h3>Case Report</h3> A 63 years old had new onset of palpitation and shortness of breath. He presented to ED with rapid AF at rate of 140 bpm treated with metoprolol, diltiazem and rivaroxiban. The patient started to develop lower limb swelling, dizziness, shortness of breath with walking short distance. His blood pressure was 110/60 mmHg off antihypertensive medication. He had NYHA class III symptoms and significant peripheral edema. A TTE showed a moderate concentric left ventricle hypertrophy IVS 16 mm with mild global systolic dysfunction LVEF 50% restrictive diastolic function and pericardial effusion. The patient had significant myocardial hypertrophy, HFpEF and AF with intolerance to medical therapy we proceeded with PYP bone scan which was equivocal for TTR amyloidosis. The bone to heart ration was 1.27. Cardiac MRI showed progressive decline in LVEF to 27% with severe RV systolic dysfunction EF 28% . There was a diffused subendocardial delayed enhanced lesion. Given these findings hematology workup sent which showed serum Free Lambda of 147mg/L; Free Kappa 6.71mg/L and Kappa/Lambda ratio of 0.05 (0.26 - 1.65). Bone marrow biopsy showed plasma cell percentage up to 40%. Flowcytometry showed lambda restricted plasma cell population together with positive CD38, CD138, CD56 and negative CD19. Fat Pad biopsy positive for Congo red stain consistent of amyloid deposits. He received chemotherapy CyBorDex 4 cycles followed by reduction in plasma cells to 2% in the bone marrow. He had cardiac function recovery. <h3>Summary</h3> AL cardiac amyloidosis can present with cardiac manifestation. High suspicion of underlying infiltrative disease should be investigated in refractor cases AF and HFpEF.

The Challenges And Rapid Progression Associated With Cardiomyopathy In The Setting Of Danon Disease

In this case a 23 year old female patient was admitted to the intensive care unit (ICU) in January 2020 for veno-arterial extra-corporeal membranous oxygenation (ECMO) to manage cardiogenic shock and recurrent ventricular tachycardia (VT). She had no prior medical history or hospitalisations. Following a positive influenza B swab, elevated troponin I 37,656 ng/L with the clinical presentation, the patient was diagnosed with acute myocarditis. To out rule giant cell myocarditis an endomyocardial biopsy (EMB) was completed. EMB detected ‘vacuoles with cytoplasmic debris and glycogen particles' consistent with Danon Disease (DD). This diagnosis was supported by subsequent genetic screening determining a LAMP2 mutation the causal mutation in DD. The patient's echocardiogram showed severe concentric left ventricular hypertrophy (LVH) consistent with DD and a severely impaired ejection fraction (EF) of 35% (Image 1).The patient was closely monitored as an outpatient and initiated on goal directed heart failure medication. In January 2021 she was readmitted with decompensated heart failure. Troponin I was 12,369ng/L and NTProBNP 10,817ng/l. The admission echo showed a marked deterioration (EF<10%), increasing left ventricular dilatation (Image 1). Mixed venous saturation was 63%. Despite a successful discharge home, the patient was readmitted 6 weeks later with slow VT and cardiogenic shock. A mixed venous saturation was 45% prompting insertion of an intra-aortic balloon pump and the patient was listed on the heart transplant list. The time from index presentation to transplant listing was 425 days (14.2 months). After 3 days on the active list the patient had a successful orthotopic heart transplant (OHT) and discharged from ICU 3 days later. Following a final predischarge mixed venous saturation of 72% the patient was discharged home 28 days post OHT without any adverse complications. Conclusion:This case provides evidence supporting the theory that cardiomyopathies due to genetic abnormalities predispose towards myocarditis as evidenced by this patient. It highlights the importance in investigating potential genetic abnormalities in certain patients within the myocarditis population. Close surveillance of patients with a cardiomyopathy secondary to Danon disease is also paramount as it rapidly progressed to an advanced heart failure stage requiring OHT within 14 months of the patient's initial presentation. Timely listing for heart transplant ultimately contributed towards a successful and timely post-operative clinical recovery.

Intrahepatic Portosystemic Shunt In Cardiac Amyloidosis: Turning Off The Faucet Leads To Resolution Of Hepatic Encephalopathy And Improvement In Heart Failure Symptoms

<h3>Introduction</h3> Spontaneous portosystemic shunts (SPSS) are extremely rare and usually extrahepatic due to portal hypertension in the setting of cirrhosis. Current knowledge regarding SPSS in adults in the absence of cirrhosis is limited. The implications of SPSS in patients with transthyretin amyloid cardiomyopathy (ATTR-CM) are unknown. <h3>Case</h3> A 76-year-old man with a history of HTN, CAD and systolic dysfunction (EF 45%) presented to the hospital with symptoms of HF exacerbation and cognitive dysfunction. Initial cardiac labs were notable for a borderline elevated troponin and high natriuretic peptic level. Hepatic labs were notable for mild elevation in transaminases, thrombocytopenia and an elevated ammonia level. Transthoracic echocardiogram (TTE) revealed that the EF was stable at 45%, but there was biatrial enlargement and progression of concentric LVH to 1.8cm and resultant small LV cavity (EDV index 39ml/m²), suspicious for infiltrative cardiomyopathy (Fig A). SPEP/UPEP with immunofixation and serum free light chains were normal and Tc-99m PYP study was consistent with ATTR-CM (Fig B). Abdominal US revealed a large intrahepatic venous shunt from the right portal vein to the right hepatic vein. Right heart catheterization, portal venogram and liver biopsy revealed a right atrial pressure of 14mmHg, cardiac output of 6.2L/min, normal pulmonary vascular resistance, hepatic vein pressure of 14mmHg, portal vein pressure of 15mmHg, confirmation of the large SPSS (Fig C) and no evidence of cirrhosis. The patient underwent embolization of the SPSS with a 22mm vascular plug (Fig D). Following closure, the patient's HF symptoms and HE improved dramatically and his abnormal hepatic labs normalized. He was started on a stabilizer for the treatment of his ATTR-CM. At one year, he has not had recurrent symptoms of HE, nor repeat hospitalization for HF exacerbation. <h3>Discussion</h3> This patient most likely had a SPSS that only manifested clinically in the setting of elevated right atrial and hepatic pressures due to the development of ATTR-CM. Ultimately, the decision was made to close the SPSS for two reasons. The first was to treat HE—in the same way that transjugular intrahepatic portosystemic shunt (TIPS) procedure can cause HE and subsequent TIPS closure can be an effective treatment for refractory HE. The second was to improve HF symptoms. Although this patient's cardiac output was "normal", it was likely actually high in the context of the severe LVH and small LV cavity due to ATTR-CM and the increased venous return was poorly tolerated given the underlying restrictive cardiomyopathy.

Remodeling of heart in patients with stable ischemic heart disease combined with chronic obstructive pulmonary disease as a basis for development of heart failure

The aim of this study was to determine phenotypes of remodeling of heart and the status of systolic and diastolic function in patients with ischemic heart disease (IHD) combined with chronic obstructive pulmonary disease (COPD) with early symptoms and signs of heart failure (HF). We enrolled 108 males with stable IHD and spirometrically confirmed COPD which preceded the manifestations of IHD – the main group (group 1). As comparison groups 30 males with stable IHD (group 2) and 30 males with COPD (group 3) were examined. Control group included 30 males without IHD and respiratory diseases. All groups were comparable in age, groups 1 and 2 – in the duration of IHD, groups 1 and 3 – in the duration of COPD. The patients of the group 1 were divided into 3 subgroups: subgroup 1 – 45 patients with stable angina, subgroup 2 – 27 patients with postinfarction cardiosclerosis, subgroup 3 –36 patients with combination of stable IHD and arterial hypertension (AH) without history of myocardial infarction. The patients of group 1 had different phenotypes of heart remodeling, which depended on the clinical forms of IHD, the presence of concomitant AH, the severity of bronchial obstruction. The patients of subgroup 1 in 60.0% cases had concentric remodeling and concentric left ventricular hypertrophy (LVH), in 26.7% – normal LV geometry, in all these cases ejection fraction (EF) was preserved. Only in 13.3% of cases eccentric LVH with mildly reduced EF was found. 59.3% of patients in subgroup 2 had eccentric LVH, left atrium dilatation and 55.6% had reduced EF. All patients of subgroup 3 had concentric direction of LV remodeling. The phenotypes of HF with reduced and mildly reduced EF were accompanied by impaired LV diastolic function. In assessing the likelihood of HF with preserved EF the HFA-PEFF score showed better accuracy. Pulmonary hypertension had a mixed cause with predominance of postcapillar component.

Cardiac Phenotypes of Pregnant Women with Hypertensive Disorders in Different Ethnic Groups

The objective of this study was to conduct a comparative analysis of the features of LV myocardial remodeling in pregnant women with chronic arterial hypertension (CAH) and preeclampsia (PE) on the background of CAH. Methods and Results: The study cohort included pregnant women (n=547) with hypertensive disorders. All women were divided into two groups: Group 1 included 376 Caucasian patients living in the Republic of Dagestan; Group 2 included 171 patients living in the Republic of Sakha (Yakutia) (indigenous residents [Yakuts and Evenks). Later on, all patients were divided into the following subgroups: Sub1A (n=134), and Sub2A (n=69) – pregnant women with CAH; Sub1B (n=242) and Sub2B (n=102) – pregnant women with PE on the background of CAH. The diagnosis of pregnant women with CAH was made on the basis of existing national and foreign recommendations that an increase in SBP ≥140 mmHg and/or DBP ≥90 mmHg indicates CAH. Different patterns of left ventricular (LV) geometry were defined based on left ventricular mass index (LVMI) and relative wall thickness (RWT), as recommended by the American Society of Echocardiography. The observed/predicted LVM ratio was calculated as 100×(oLVM/pLVM). Participants with an oLVM/pLVM ratio of &gt;128% were categorized as having “inappropriate” LVM (iLVM). iLVM was found in Subgroups 1B and 2B in the third trimester. The frequency of LV remodeling in pregnant women of Subgroups 1 A and 2A in the second and third trimesters did not differ significantly. In Subgroup 1B, the frequency of concentric left ventricular hypertrophy (cLVH) was higher in the third trimester (42.6%) than in the second trimester (26.9%) (P=0.000). Moreover, in the third trimester, the frequency of cLVH was significantly higher in Subgroup 1B than in Subgroup 2B (42.6% and 29.4%, respectively, P=0.022). At the same time, in the third trimester, the frequency of left ventricular concentric remodeling (LVCR) was significantly higher in Subgroup 2B than in Subgroup 1B (56.9% and 44.2%, respectively, P=0.032). In the second trimester in Subgroup 1B, the frequency of LVCR was higher than in Subgroup 1A: 50% and 38.1%, respectively, P=0.026). By the third trimester, the severity of LV remodeling has increased significantly in Subgroup 1B. Thus, in Subgroup 1B, the frequency of c LVH reached 42.6% compared to 31.3% in Subgroup 1A (P=0.03). In Subgroup 2B, in the third trimester, the frequency of LVCR was slightly higher than in Subgroup 2A (56.9% and 43.5%. respectively, P=0.08). Conclusion: Living conditions predetermine the prevalence of iLVM and LVCR in pregnant northerners with CAH. A more common type of LV remodeling in pregnant women with CAH in conditions of high-altitude hypoxia is also LVCR, which transforms into cLVH by the third trimester in pregnant women with PE on the background of CAH. The study of the type of LV geometry and the appropriateness of LVM allows us to clarify the degree of LV damage in hypertension-related pregnancy. iLVM in pregnant women with CAH appears to be a predictor of the development of PE. The revealed changes in the LV structure—LVCR and cLVH—are more significant in PE on the background of CAH.

CONSTITUTIONAL FEATURES IN MEN WITH DIFFERENT TYPES OF LEFT VENTRICULAR REMODELING AND HAVE CORONARY HEART DISEASE

Purpose. The study of constitutional features in men with various types of left ventricular remodeling, having a comorbid association of arterial hypertension with coronary heart disease.&#x0D; Materials and methods. We examined 57 men with isolated arterial hypertension and 115 men with arterial hypertension combined with coronary artery disease. The standard method of anthropometric research used, followed by the determination of constitutional types, as well as the determination of types of geometric LV remodeling according to ultrasound examination of the heart.&#x0D; Results. The constitutional features of the frequency of unfavorable types of remodeling in men of the examined groups revealed. The largest group among the examined men, both with isolated arterial hypertension and with arterial hypertension in combination with coronary artery disease, consisted of representatives of the muscular and abdominal type of constitution. The presence of left ventricular remodeling detected in 91.2% of the examined men with isolated hypertension and in 89.6% of men with hypertension in combination with coronary artery disease. At the same time, both among men with isolated hypertension and men with hypertension in combination with coronary heart disease, the most common type of geometry was concentric left ventricular hypertrophy. It found that in all constitutional types, patients with concentric left ventricular hypertrophy were more common.&#x0D; Conclusion. Left ventricular hypertrophy was more common in all constitutional types in men of both groups. Normal geometry of the left ventricle more often observed in men with isolated arterial hypertension of the thoracic constitutional type, and among men with arterial hypertension in combination with coronary artery disease - of the muscular type.

Cardio-omentopexy requires a cardioprotective innate immune response to promote myocardial angiogenesis in mice

ObjectiveThe pedicled greater omentum, when applied onto stressed hearts using omentopexy, has been shown to be protective in humans and animals. The mechanisms underlying cardioprotection using omentopexy remain elusive. This study examined whether macrophage-mediated angiogenesis accounts for the cardioprotective effect of omentopexy in mice. MethodsC57BL/6 mice were subjected to minimally invasive transverse aortic constriction for 6 weeks and subsequent cardio-omentopexy for 8 weeks. Control mice underwent the same surgical procedures without aortic constriction or cardio-omentopexy. ResultsTransverse aortic constriction led to left ventricular concentric hypertrophy, reduced mitral E/A ratio, increased cardiomyocyte size, and myocardial fibrosis in the mice that underwent sham cardio-omentopexy surgery. The negative effects of transverse aortic constriction were prevented by cardio-omentopexy. Myocardial microvessel density was elevated in the mice that underwent aortic constriction and sham cardio-omentopexy surgery, and cardio-omentopexy further enhanced angiogenesis. Nanostring gene array analysis uncovered the activation of angiogenesis gene networks by cardio-omentopexy. Flow cytometric analysis revealed that cardio-omentopexy triggered the accumulation of cardiac MHCIIloLyve1+TimD4+ (Major histocompatibility complex class IIlow lymphatic vessel endothelial hyaluronan receptor 1+ T cell immunoglobulin and mucin domain conataining 4+) resident macrophages at the omental–cardiac interface. Intriguingly, the depletion of macrophages with clodronate-liposome resulted in the failure of cardio-omentopexy to protect the heart and promote angiogenesis. ConclusionsCardio-omentopexy protects the heart from pressure overload-elicited left ventricular hypertrophy and dysfunction by promoting myocardial angiogenesis. Cardiac MHCIIloLyve1+TimD4+ resident macrophages play a critical role in the cardioprotective effect and angiogenesis of cardio-omentopexy. Video Abstract [Display omitted]

Anomalous branching of the aortic arch in a dog.

Anomalies in the subclavian and common carotid arteries can be of interest in cases of cranial mediastinal surgeries, as well as to diagnose the cause of oesophageal constrictions leading to clinical signs of dysphagia (dysphagia lusoria). The development and regression of the aortic arches are of key importance in understanding the origin of these type of vascular anomalies. This report describes the congenital anomalous aortic origin of the common carotid and the subclavian arteries in a 14-year-old dog and the plausible developmental pattern failure. Academic dissection revealed a common bicarotid trunk and bisubclavian trunk arising from the most cranial aspect of the aortic arch. Despite the abnormal origin, these vessels displayed a predominantly standard anatomical course. All the anticipated branches were identified and described. Cardiac abnormalities were also noted including right atrial dilation, coronary sinus enlargement, right and left valvular endocardiosis, a patent foramen ovale and marked concentric left ventricular hypertrophy with compensatoryleft atrial dilation. Additionally, the right recurrent laryngeal nerve demonstrated an aberrant course consistent with a 'non-recurrent laryngeal nerve' (non-RLN). Awareness of the anatomical variations of the aortic arch is important for surgical interventions of the cranial mediastinum as well as radiological interpretation. Although infrequent, the variants similar to the one described here have been reported in different species.

Geometrical changes of the left ventricle and cognitive impairment in hypertensive patients

Abstract Funding Acknowledgements Type of funding sources: None. Introduction From the view of the heart-brain axis, several biomarkers have been suggested for the assessment, eventually for the prevention of cognitive impairment. Remodeling of the left ventricular (LV) structure could be such a marker. Purpose: This study aimed to investigate the relationship between cognitive functions and left ventricular geometrical structure. Methods: We enrolled 512 consecutive hypertensive patients (mean age 68 ±9.5 years, females: 51%, males 49%), the mean blood pressure was 135/81 mmHg (±19/11 mmHg). Cognitive abilities were measured with two questionnaires the Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA), considering cognitive impairment under 24 and 26 points respectively. Measures of the left ventricular structure were performed with transthoracic echocardiography using left ventricular mass indexed to body surface area (LVMI) and relative wall thickness (RWT). Cut off value for LV geometrical changes were: LVMI 115 g/m2 in males and 95 g/m2 in females and RWT 0.42 mm. IBM SPSS v20. was used for statistical analyses. Results: Normal geometry of LV was present in 7.4% and remodeling of LV in the studied group was: concentric remodeling in 16.8%, concentric hypertrophy in 61.9% and eccentric hypertrophy in 13.9%. Lower MoCA scores were observed in LV hypertrophy (22.6 vs. 23.4, p = 0.08). Patients with LV concentric hypertrophy had significantly lower cognitive scores compared to eccentric hypertrophy (mean MoCA 22.4 vs. 23.8 p = 0.02; mean MMSE 26.1 vs. 27.0 p = 0.02). Increased RWT alone were associated with poorer cognition (mean MoCA 22.58 vs. 23.89 p = 0.009; mean MMSE 26.17 vs. 26.99 p = 0.02). Higher LVMI negatively correlated with MoCA scores (p = 0.018, r=-0.105), but not with MMSE scores (p = 0.216, r=-0.006). Conclusions: Left ventricular hypertrophy and even changes in relative wall thickness may cause cognitive impairment. Preventing LV geometrical changes may prevent the deterioration of cognitive abilities.

Segmental analysis of microvascular dysfunction and tissue characterization in hypertrophic cardiomyopathy by magnetic resonance imaging

Abstract Funding Acknowledgements Type of funding sources: None. Background While left ventricular hypertrophy (LVH) and myocardial fibrosis are frequently evaluated in hypertrophic cardiomyopathy (HCM), microvascular dysfunction is often overlooked. The aim of this study was to assess the association between wall thickness, microvascular dysfunction and tissue characteristics in HCM patients (P), comparing individual myocardial segments. Methods Prospective evaluation of adult P with HCM (P with "end-stage" HCM, prior septal reduction therapy or epicardial coronary artery disease were excluded). All underwent a cardiac magnetic resonance (CMR) protocol (1.5-T), from which the following parameters were analysed: maximal LV wall thickness (MLVWT), T1 and T2 mapping, extracellular volume (ECV), late gadolinium enhancement (LGE) and stress perfusion. Results were stratified according to the 16 American Heart Association segments. Multivariate regression analyses for perfusion defects and tissue characteristics were performed. Results 75 P (total of 1200 myocardial segments analysed), 63% male, mean age 55 ± 15 years, MLVWT of 20 ± 4.5mm (61% asymmetric septal LVH, 29% apical LVH and 8% concentric LVH). 28% presented LV outflow tract obstruction. MLVWT was greater in the basal and mid septum (table 1). Among the 424 segments (35.3%) with a perfusion defect, 286 (23.8%) had a defect only in the endocardial layer and 138 (11.5%) in both endocardial and epicardial layers with defects more often detected in hypertrophied segments. This association was verified in segments with MLVWT 12-14mm and MLVWT ≥15mm (OR 7.83, 95% CI 5.75-10.67, p &amp;lt; 0.001) (table 2). Among the 660 segments with normal MLVWT (≤11mm), 123 (19%) presented perfusion defects. A perfusion defect was more frequent in segments of obstructive HCM P (OR 1.48, 95% CI 1.13-1.92, p = 0.004). Microvascular dysfunction was associated with changes in tissue characteristics. For the same thickness, segments with perfusion defects had a higher T1 mapping (β-estimate 20.91, 95% CI 16.87-24.96, p &amp;lt; 0.001) and T2 mapping mean values than those without. Furthermore, regardless of MLVWT, segments with perfusion defects had LGE more often (OR 4.16, 95% CI 3.19-5.41, p &amp;lt; 0.001) and a higher ECV. On the other hand, among the 424 segments with a perfusion defect, 115 (27%) did not present LGE. MLVWT was associated with tissue characteristics. Comparing to non-hypertrophied segments, T1 mapping mean value was higher in segments with MLVWT 12-14mm and with ≥15mm (β-estimate 37.71, 95% CI 31.2-44.21, p &amp;lt; 0.001). Segments with MLVWT ≥15mm showed a significantly superior ECV mean value comparing to non-hypertrophied segments. LGE was more frequent in the more hypertrophied segments: MLVWT 12-14mm and ≥15mm (OR 9.02, 95% CI 6.42-12.67, p &amp;lt; 0.001) (Table 2). Conclusion Microvascular dysfunction is more prevalent in obstructive HCM, particularly in the more hypertrophied segments. The presence of microvascular dysfunction is associated with diffuse tissue abnormalities and replacement fibrosis. Abstract Table 1: Characteristics of AHA segments Abstract Table 2: Multivariable analyses

Microvascular dysfunction and myocardial fibrosis impact on left ventricular myocardial deformation in hypertrophic cardiomyopathy: per segment analysis by magnetic resonance imaging

Abstract Funding Acknowledgements Type of funding sources: None. Background Left ventricular hypertrophy (LVH) and microvascular dysfunction are hallmarks of hypertrophic cardiomyopathy (HCM). We hypothesized that microvascular dysfunction contributes to LV myocardial deformation impairment. Methods Prospective evaluation of adult patients with HCM (patients with "end-stage" HCM, prior septal reduction therapy or epicardial coronary artery disease were excluded). All underwent a cardiac magnetic resonance (CMR) protocol (1.5-T), from which the following parameters were analysed: maximal LV wall thickness (MLVWT), T1 and T2 mapping, extracellular volume, late gadolinium enhancement (LGE) and stress perfusion. Three-dimensional strain analysis was obtained by using feature-tracking from cine images. Results were stratified according to the 16 American Heart Association segments. Multivariate regression analyses for longitudinal, circumferential and radial strain were performed. Results A total of 1200 myocardial segments were analysed (Table 1) (75 patients, 63% male, age 54.6 ± 14.7 years) including 61% with asymmetric septal LVH, 29% with apical LVH, 8% with concentric LVH, 28% exhibiting LV outflow tract obstruction. The mean MLVWT was 20 ± 4.5mm. Higher values of longitudinal strain (lower deformation) were found in segments with MLVWT ≥15mm (β-estimate: 2.31, 95% CI 0.91-3.70, p &amp;lt; 0.001) and in patients with obstructive HCM (β-estimate: 2.44, 95% CI 1.15-3.72, p &amp;lt; 0.001]) (Table 2). No association was found between perfusion defects, LGE and longitudinal strain. Higher values of circumferential strain (lower deformation) were found in segments with MLVWT 12-14mm (β-estimate: 2.31, 95% CI 1.36-3.25, p &amp;lt; 0.001), MLVWT ≥15mm (β-estimate: 5.29, 95% CI 4.47-6.12, p &amp;lt; 0.001), with perfusion defects (β-estimate: 2.75, 95% CI 2.0-3.5, p &amp;lt; 0.001), with LGE (β-estimate: 2.49, 95% CI 1.77-3.22, p &amp;lt; 0.001) and in patients with obstructive HCM (β-estimate: 1.25, 95% CI 0.44-2.06, p = 0.003). Lower radial strain values were found in segments with MLVWT 12-14mm (β-estimate: -10.64, 95% CI -13.95 to -7.33, p &amp;lt; 0.001), with MLVWT ≥15mm (β-estimate: -20.67, 95% CI -23.36 to -17.97, p &amp;lt; 0.001), with perfusion defects (β-estimate: -10.60, 95% CI -13.08 to -8.13, p &amp;lt; 0.001), and with LGE (β-estimate: -10.49, 95% CI -12.86 to -8.11) (table 2). Diabetes, hypertension and BMI &amp;gt; 25 kg/m2 were also associated with impaired myocardial deformation. Male gender correlated with worse radial and circumferential strain values. No association was found between parametric mapping values and LV myocardial deformation. Conclusion In patients with HCM, three-dimensional speckle tracking parameters for LV systolic function were particularly impaired in segments with LVH, microvascular dysfunction or fibrosis. LVH was associated with abnormal longitudinal, circumferential and radial strain while perfusion defects and LGE correlated with impaired circumferential strain and radial strain. Abstract Table 1: Characteristics of AHA segments Abstract Table 2: Multivariate analysis

Left ventricle structure and function relations with the levels of plasma markers of fibrosis in hypertensive patients with NonSTEMI

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. The myocardial fibrosis lies in the basis of left ventricle remodelling in patients with hypertension. Cardiomyocites hypertrophy, fibroblasts proliferation, enlargement of interstitial collagen volume and their ratio disorders may increase severity of stroke and myocardial infarction. Purpose. The purpose of the study is to evaluate relations between the plasma levels of myocardium fibrosis markers and left ventricle remodelling, systolic and diastolic function in hypertensive patients with NonSTEMI. Methods. Were examined 138 hypertensive patients (both men and women) with NonSTEMI. The mean age of patients was 51.2 (11.2) years. Patients with arrhythmias and conduction abnormalities, diabetes mellitus and autoimmune diseases were excluded form the study. In all patients was performed ECG in 12 standard leads; EchoCG (according to ASE/EACVI 2015 recommendations); evaluation plasma levels of tissue inhibitor of metalloproteinases-1 (TIMP-1) and insulin-like growth factor 1 (IGF-1). HF NYHA functional class was determined by performing 6MWT. Statistical significance was defined at the level of methods for p &amp;lt; 0,05. Results. The averaged levels for plasma markers of myocardium fibrosis were: TIMP-1 - 322.0 (250.0; 483.5) ng/mL; IGF-1 - 160.0 (141.0; 175.0) ng/mL. Results of correlative analysis revealed relations between IGF-1 and ILV mass (R=-0.59; p &amp;lt; 0.001), and weak correlation between IGF-1 and E/e" averaged (R=-0.19; p = 0.027) (Picture 1). These negative correlations may be explained by the growth in both fibroblasts and collagen production in myocardium. Also there were positive correlations between TIMP-1 and ILV mass (R = 0.63; p &amp;lt; 0.001) and TIMP-1 and E/e" average (R = 0.37; p &amp;lt; 0.001) (Picture 1) which may be due to an increase of myocardial stiffness as the result of fibrosis activity. The results of the comparison of TIMP-1 and ICF-1 plasma levels, structural and functional parameters of the LV in groups of patients with different types of LV geometry can be seen in Table 1. Conclusion. Thus, the results of the study show that plasma markers of fibrosis was significantly higher in patients with concentric and eccentric LV hypertrophy which may reflects the higher levels of myocardium stiffness. Abstract Table 1. Abstract Figure. Picture 1.

Predictors of Peripheral Artery Disease Progression. Is there Any Role for Vascular Age?

Predictors of Peripheral Artery Disease Progression. Is there Any Role for Vascular Age?

The interleukin-1 receptor type I promotes the development of aging-associated cardiomyopathy in mice

BackgroundAging is associated with metabolic and structural changes causing heart failure with preserved ejection fraction (HFpEF). Interleukin-1 (IL-1) is a pro-inflammatory cytokine involved in aging-related inflammation. ObjectiveWe sought to determine whether IL-1 mediates aging-related changes in the heart, as seen in HFpEF. MethodsWe studied age-matched young (4-month-old), middle-aged (14-month-old), and old (23-month-old) wild-type (WT) C57BL/6J and IL-1 receptor type I deficient (IL1RI-KO) male mice. Echocardiography was used to evaluate left ventricular (LV) dimensions and systolic/diastolic function, and a pressure transducer was used to measure the LV end-diastolic pressure. Picrosirius red stain was used to assess for myocardial interstitial fibrosis (MIF) at pathology. ResultsWT and IL-1RIKO mice showed a normal cardiac phenotype at young age, without any differences between the two groups. With aging, the WT mice developed LV concentric hypertrophy (as measured by a significant increase in LV mass [+42%, P < 0.01] and relative wall thickness [+34%, P < 0.01]), whereas the aging IL-1RI-KO mice did not. With aging, the WT mice also developed diastolic dysfunction (as measured by a significant increase in isovolumetric relaxation time [+148%, P < 0.01] and a significantly higher LV end-diastolic pressure [+174%, P < 0.01]), whereas the aging IL1RI-KO did not. Aged WT mice showed a significant increase in MIF (+124%, P < 0.01) at cardiac pathology, whereas the aging IL-1RI-KO did not. ConclusionsGenetically-modified mice lacking the IL-1RI receptor, not responsive to IL-1, are protected from aging-related LV hypertrophy, fibrosis, and diastolic dysfunction. These data support a central role of IL-1 in the pathophysiology of aging-related HFpEF.

A Preclinical Rat Model of Heart Failure With Preserved Ejection Fraction With Multiple Comorbidities.

Heart failure with preserved ejection fraction (HFpEF) is a common complex clinical syndrome for which there are currently few evidence-based therapies. As patients with HFpEF very often present with comorbidities comprising the metabolic syndrome, we hypothesized, that metabolic syndrome could lead over time to the development of diastolic dysfunction and HFpEF. Obesity-prone rats were exposed to high-fat diet and compared to obesity-resistant rats fed with standard chow. Phenotyping of metabolic syndrome, associated with echocardiographic and cardiac hemodynamic measurements, was performed after 4 and 12 months. Blood and myocardial tissue sampling were performed for pathobiological evaluation. High-fat diet in obesity-prone rats elicited metabolic syndrome, characterized by increased body and abdominal fat weights, glucose intolerance and hyperlipidemia, as well as increased left ventricular (LV) systolic pressure (after 12 months). This was associated with LV diastolic dysfunction (assessed by increased LV end-diastolic pressure) and pulmonary hypertension (assessed by increased right ventricular systolic pressure). Echocardiography revealed significant concentric LV hypertrophy, while LV ejection fraction was preserved. LV remodeling was associated with cardiomyocyte hypertrophy, as well as myocardial and perivascular fibrosis. Circulating levels of soluble ST2 (the interleukin-1 receptor-like) markedly increased in rats with HFpEF, while plasma NT-proBNP levels decreased. RNA-sequencing analysis identified clusters of genes implicated in fatty acid metabolism and calcium-dependent contraction as upregulated pathways in the myocardium of rats with HFpEF. High-fat diet during 12 months in obesity-prone rats led to the development of a relevant preclinical model of HFpEF with multiple comorbidities, suitable for investigating novel therapeutic interventions.

Microalbuminuria as an Independent Risk Factor for Developing Concentric Left Ventricular Hypertrophy in Primary Hypertension: A Single-Center Observational Study From South India.

IntroductionMicroalbuminuria and concentric left ventricular hypertrophy (LVH) are both associated with primary hypertension. We aimed to study the correlation between these two parameters in a cohort of patients with primary hypertension.MethodsWe conducted a single-center observational comparative study involving patients suffering from primary hypertension in a tertiary care hospital in the southern state of Kerala in India. Patients aged more than 18 years who were diagnosed to have primary hypertension were enrolled in the study irrespective of duration of illness or treatment status. The primary objective of the study was to assess whether microalbuminuria was an independent risk factor for concentric LVH in patients with primary hypertension. The secondary objective of the study was to study the relationship between various other studied biomarkers with concentric LVH in patients with primary hypertension.ResultsMicroalbuminuria was found to be associated with concentric LVH in patients with primary hypertension (p=0.003). Multivariate regression analysis showed that serum creatinine, high diastolic blood pressure, and microalbuminuria appeared to be independent risk factors for concentric LVH (p<0.001, 0.016, and 0.016 respectively).ConclusionsMicroalbuminuria is a reliable marker for predicting the prevalence of concentric LVH in patients with primary hypertension. A high serum creatinine and high diastolic blood pressure are also independent risk factors for having concentric LVH.

Difference in Antihypertensive Medication Pattern in the First Year Compared to More than a Year of Maintenance Hemodialysis: A Northern India Tertiary Care Experience

Introduction There is a high prevalence of hypertension in maintenance hemodialysis patients. Information regarding prevalent pattern of antihypertensive medications will help modify it to prevent future cardiovascular morbidity and mortality. Materials and Methods In this cross-sectional study, patients on maintenance hemodialysis, aged ≥18 years visiting Nephrology outpatient department (OPD) from April 2019 to May 2020 were included. The patients were divided into two groups based on their dialysis vintage, ≤12 months and &gt;12 months. Their antihypertensive medication patterns and two-dimensional (2D) echocardiography (ECHO) findings were compared. Independent t-test was used to compare continuous variables. One-way analysis of variance was used to study the antihypertensive drug-dosing pattern in both the groups. Results Out of 250 patients, 131 had a dialysis vintage of ≤12 months, whereas 119 had a vintage of &gt;12 months. There was no significant difference in the number of antihypertensive agents used in either of the vintage groups. Calcium channel blockers (87.02 and 89.07%, respectively, in ≤12 and &gt;12 months' vintage groups) and β blockers (64.12 and 65.54%, respectively, in ≤12 and &gt;12 months' vintage groups) were the commonly used antihypertensive agents. Metoprolol use was higher in ≤12 months' group, whereas carvedilol usage was higher in &gt;12 months' group (p = 0.028). Mean pill burden was more than five in both the groups. Concentric left ventricular hypertrophy was significantly more common in &gt;12 months' group. Renin–angiotensin system (RAS) blocking agent use was limited to 3% of patients. Conclusion This study shows a high antihypertensive pill burden in dialysis patients likely due to underlying chronic volume overload in addition to the perceived efficacy of certain class of drug in a frequent dosing pattern. Low use of RAS blocking agent was also underlined. This study highlights the need to bring about changes in the antihypertensive prescription pattern in line with the existing evidence.

HISTOMORPHOLOGICAL SPECTRUM OF VARIOUS CARDIAC CHANGES IN SUDDEN DEATH: AN AUTOPSYSTUDY

INTRODUCTION : Cardiovascular disease (including coronary artery disease, stroke and peripheral vascular disease) is no.1 cause of worldwide mortality, with about 80% of burden occurring in developing countries. Sudden cardiac death is dened as unexpected death from cardiac causes either without symptoms or within 1-24 hours of onset of symptoms(1). The common cause of sudden cardiac death is ischaemic heart disease. Non ischaemic sudden cardiac death occurs in hypertrophic obstructive cardiomyopathy and in severe left ventricular hypertrophy(2). The purpose of this study will be to determine the causes of sudden death and observe the spectrum of morphological and histopathological changes in heart after sudden death. MATERIALS AND METHODS: This autopsy study was conducted on 121 cases of sudden death over a period extending from January 2019 to August 2020 in autopsy section of Pathology department of BJGMC, Pune. In this autopsy study hearts of patients with a history of sudden death were evaluated for histological and morphological changes. Each heart was grossed adopting the inow outow method and short axis method. Staining solutions used were Solution A: Alum Hematoxylin and Solution B: 1% Eosin Y. OBSERVATIONS : 50 (41.32%) cases out of 121 cases had coronary artery disease along with myocardial infarction of which 43 cases were males and 7 cases were females. No cardiac aetiology was found in 23.96% cases. Coronary artery disease was independently seen in 14.87% cases. Left ventricular concentric hypertrophy was noted in 4.13% cases. Myocardial infarction independently was noted in 3.30%cases, Myocarditis in 2.47% cases, myocarditis with pericarditis in 1.65% cases, HOCM, lipoma, mitral stenosis, pericarditis, septic infarct, secondaries of adenocarcinoma, early vegetation and small vessel disease in 0.82% cases. Calcic aortic stenosis was demonstrated in 1 case. Brown atrophy was demonstrated in 1 case. DISCUSSION : Out of 69 cases of coronary artery disease calcication was commonly seen in 34(49.27%) cases. 47(82.45%) (M-39,l F-8) out of 57 cases of myocardial infarction demonstrated chronic or old infarct. Single vessel involvement was most common in which left anterior descending coronary artery was signicantly involved in 68.75 % cases. Posterior wall was most commonly involved by myocardial infarction which included posterior, posteroseptal, and posterolateral infarcts.

Indicators and predictors of in-hospital mortality and survival in patients with ventricular septal rupture

BackgroundVentricular septal rupture (VSR), a mechanical complication of myocardial infarction (MI), usually presents with rapid clinical deterioration with acute heart failure or cardiogenic shock. VSR may occur within 24 h to several days after MI and can occur in both anterior and inferior wall MI. Although guidelines recommend emergent surgery, this is associated with a high mortality rate of up to 40%. Intra-aortic balloon pump (IABP) and extracorporeal membrane oxygenation (ECMO) stabilize patients in preparation for angiography and surgery. Delayed surgery allows better septal repair in scarring tissue but also carries the risk of rupture extension and death while waiting. Percutaneous closure of the defect with appropriately designed devices results in better survival in the subacute phase. AimsTo study the indicators and predictors of VSR in the current era of primary percutaneous coronary interventions and mechanical circulatory support. MethodsOf total of 34,681 patients presenting with MI, the incidence of VSR was 0.45%. We sought to evaluate the predictors of survival and death in VSR. Coronary angiography (CAG) was performed, hemodynamic support provided to unstable patients, and consenting patients were referred to definitive therapy, either surgery or percutaneous device closure. The previously postulated hypotheses of triple vessel disease (TVD), diabetes mellitus (DM), and concentric left ventricular hypertrophy (LVH) due to Hypertension (HTN) being protective against VSR were explored. ResultsOf the 169 patients with VSR, we found that the group that survived was mostly men and the mean age was 61.5 years; this was in contrast to the non-survivors, who were mainly women, and the mean age was 65.2 years (p = 0.025); higher Killip Class was 111-1V (p = 0.001), lower LVEF (p = 0.010), apical VSR and LV aneurysm (p = 0.015 and p = 0.002, respectively) were predictors of death. 48 patients underwent CAG, with single vessel disease (SVD) with lower-grade Rentrop collateral flow being most common in the death group. 25 patients were subjected to definitive therapy with surgical patch closure or percutaneous device closure. The patients who died were older by approximately 7 years. The risk factors for coronary artery disease, such as HTN, diabetes, and smoking, were not statistically different between the two groups. ConclusionPrevention of myocardial infarction is more important than managing a VSR, which carries a high mortality despite advanced mechanical support and definitive interventional therapy such as emergent surgery and percutaneous device closure.

Left Ventricular Mass and Functions in Egyptian Children with Chronic Kidney Disease in Comparison to Normal Subjects.

Left ventricular hypertrophy (LVH) and cardiac fibrosis are common accompaniments of chronic kidney disease (CKD). They can be rather easily assessed by conventional cardiac imaging modalities, most practically by M-mode or two-dimensional (2D) echocardiography, with adequate recognition of pitfalls. This study uncovers the impact of impaired renal function on left ventricular mass (LVM) and LVM index (LVMI) in children with CKD on regular hemodialysis (HD) attending the Zagazig University Hospital for Children. A total of 80 Egyptian children, out of which 40 subjects having a mean age of 11.2 ± 3.12 years were cases with CKD in stage 5 on regular HD and the other 40 healthy subjects as controls, with a mean age of 12.2 ± 2.54 years, were included in the study and assessed for LVH and LVMI by 2D echocardiography. HD children had a significantly higher mean LVMI (102.3 ± 19.1 vs. 49.6 ± 4.11 g/m2, P <0.001) than controls. Relative wall thickness was significantly higher in the patients with CKD patients on HD compared with controls (P <0.001) with a mean value of 0.46 indicating concentric LVH in renal patients. Comparing mitral inflow velocities between both the groups revealed that the patient group had a significant decrease in mitral E-wave velocity (0.88 ± 0.2 vs. 1.1 ± 0.1 m/sec, P <0.001) and E/A velocity ratio (1.3 ± 0.3 vs. 1.7 ± 0.3, P <0.001) in comparison with the control group, but there was no statistically significant difference in A-wave velocity. This indicates early diastolic dysfunction in CKD patients. LV mass changes in CKD children were strongly related to hypocalcemia and Vitamin D deficiency. Children with CKD are prone to the development of cardiac diastolic dysfunction and LVH, so early and regular echocardiographic studies of all children with CKD are recommended to detect early cardiac changes and institute interventions.