Cardiac Chamber Hypertrophy Research Articles

Effect of long-term glucocorticoid therapy on cardiac functions in children with congenital adrenal hyperplasia.

Glucocorticoids play an important role in cardiac physiology. Chronic exposure and higher doses may cause adverse effects on the myocardium, especially in young patients receiving long-term therapy. To assess cardiac function in children with congenital adrenal hyperplasia (CAH) and its relation to glucocorticoid dose and therapy duration. Forty-seven patients with CAH due to 21-hydroxylase deficiency were compared to 47 controls. Patients were subdivided according to treatment duration (Group A: less than 6years, Group B: more than 6years). Mean daily glucocorticoid and cumulative glucocorticoid doses were calculated. Echocardiography was performed for patients and controls to evaluate cardiac functions, chamber dimensions and tissue Doppler valvular status. Compared to controls, patients had cardiac chamber hypertrophy reflected by higher M-mode dimensions. Patients had lower fractional shortening, defective ventricular relaxation, lower average mitral and tricuspid e´/a´ ratios (e´ early diastolic, a´ late diastolic) as well as s´ (systolic) velocities, higher average mitral E/e ratio and higher left ventricle TDI Tei index (P<.05). Group B had lower average mitral e´/a´ and tricuspid s´ velocities, and higher average mitral E/e ratio (P<.05). Cumulative glucocorticoid dose significantly correlated with different echocardiographic parameters. Long-term glucocorticoid therapy even within the recommended therapeutic range adversely affects cardiac functions in children with 21-hydroxylase deficiency.

42. A study of cardiovascular dysfunction in cirrhosis of liver & its correlation with the severity of cirrhosis in Eastern India

Background and Aims: Cirrhosis of liver is associated with subclinical cardiovascular (CVS) dysfunction characterized by diminished systolic responsiveness to stress stimuli, impaired diastolic relaxation, electrophysiological abnormalities, and enlargement and hypertrophy of cardiac chambers, all in the absence of known cardiac disease. However, evidence suggests that patients with cirrhosis display primarily left ventricular diastolic dysfunction (LVDD) with normal systolic function at rest. We aim to evaluate cardiovascular dysfunction in patients of cirrhosis and its correlation with severity of liver cirrhosis as by Child pugh turcotte (CPT) and MELD scoring system and circulatory function. Methods: Prospective observational study, where CVS evaluation of 60 patients (20 patients each in CHILD A, B and C) was done by both conventional 2D and tissue Doppler echocardiography. Statistical analysis was done using SPSS 20 software and p < 0.05 considered significant. Results: GR1, GR2 And GR3 LVDD were present in 23.33%, 43.33% and 20% of the patients respectively. Patients with LVDD had significantly higher (p < 0.05) left atrial diameter (LAD), E wave transmitral /early diastolic mitral annular velocity (E/e ratio), pulmonary arterial systolic pressure (PASP), natriuretic peptide level, CTP and MELD score. GR2 and GR3 LVDD were associated with ascites and increased plasma renin activity compared to GR 1 LVDD and without LVDD suggestive of direct correlation between LVDD and circulatory dysfunction. Heart rate and systolic function were normal in all cases. Survival was not different according to the degree of LVDD (p = 0.739) in 3 groups of patients. Conclusions: LVDD occurs simultaneously with other changes in cardiac structure and function in cirrhosis and is associated with circulatory dysfunction. Both conventional 2D Echocardiography and tissue Doppler imaging (TDI) are non-invasive, real-time, rapid imaging technology with a high accuracy for diagnosing CVS abnormalities, such as those indicative of cirrhotic cardiomyopathy. The authors have none to declare.

Cirrhotic cardiomyopathy: Implications for liver transplantation.

The majority of patients on a waiting list for liver transplantation have end-stage liver disease. Because of the marked peripheral vasodilatation of end-stage cirrhosis that masks a latent myocardial dysfunction, cardiac abnormalities in the resting state are usually subclinical and escape the attention of physicians. However, when challenged, the systolic and diastolic contractile responses are attenuated. In addition to these contractile abnormalities, morphological changes, such as enlargement or hypertrophy of cardiac chambers, and electrophysiological repolarization changes, including a prolonged QT interval, can be observed. The constellation of these cardiac abnormalities is termed cirrhotic cardiomyopathy. Liver transplantation induces significant cardiovascular stress. Clamping of the inferior vena cava and portal vein, hemorrhage and blood/volume infusion, and ischemia/reperfusion all cause hemodynamic fluctuation. The changing cardiac preload and afterload status increases the cardiac workload, and thus, the previously subclinical ventricular dysfunction may manifest as overt heart failure during the operative and perioperative periods. Cardiac dysfunction contributes to morbidity and mortality associated with liver transplantation. Cardiovascular events are the third leading cause of death in liver recipients. However, because liver transplantation is the only definitive treatment for end-stage liver failure and also appears to reverse cardiac abnormalities, it is important to understand the challenges of the heart in liver transplantation. This review focuses on cardiac status before, during, and after liver transplantation. Liver Transplantation 23 826-835 2017 AASLD.

AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram

The detection and assessment of cardiac chamber hypertrophy has long been an important objective of clinical electrocardiography. Its importance has increased in recent years with the recognition that hypertrophy can be reversed with therapy, and that by doing so, adverse clinical outcomes can be

Cardiac Chamber Hypertrophy following Hematopoietic Stem Cell Transplantation for Primary Immunodeficiency

Children with primary immune deficiency (PID) who receive hematopoietic stem cell transplantation (HSCT) often suffer from graft-versus-host disease (GVHD), which is commonly treated with corticosteroids (CS). CS may cause hypertension, development of cardiac chamber hypertrophy (CCH), and left ventricular outflow tract obstruction (LVOTO). We followed the development of CCH and LVOTO by serial echocardiograms in 10 children with PID before and 6 to 12 weeks after HSCT, and correlated their development with age of transplant, GVHD, use of CS and hypertension. CCH developed in all 4 children transplanted before 1 year of age who received high dose CS treatment for grade III or IV acute GVHD (aGVHD), but not in the 6 children who were transplanted at later ages or who had not received high-dose CS ( P = .07). Significant correlation ( P < .002) was found between CCH and blood pressure measurements that deviated above the 99th percentile. One child also suffered from severe LVOTO. CCH and LVOTO improved when CS treatment was discontinued and blood pressure normalized. We conclude that following HSCT, young children who suffer from aGVHD, treated with high CS doses, and have excessive hypertension are at risk of developing CCH.

Therapy Insight: cirrhotic cardiomyopathy

Liver cirrhosis is associated with several cardiovascular disturbances. These disturbances include hyperdynamic systemic circulation, manifested by an increased cardiac output and decreased peripheral vascular resistance and arterial pressure. Despite the baseline increase in cardiac output, cardiac function in patients with cirrhosis is abnormal in several respects. Patients show attenuated systolic and diastolic contractile responses to stress stimuli, electrophysiological repolarization changes, including prolonged QT interval, and enlargement or hypertrophy of cardiac chambers. This constellation of cardiac abnormalities is termed cirrhotic cardiomyopathy. It has been suggested that cirrhotic cardiomyopathy has a role in the pathogenesis of cardiac dysfunction and even overt heart failure after transjugular intrahepatic portosystemic shunt placement, major surgery and liver transplantation. Cardiac dysfunction contributes to morbidity and mortality after liver transplantation, even in many patients who have no prior history of cardiac disease. Depressed cardiac contractility contributes to the pathogenesis of hepatorenal syndrome, especially in patients with spontaneous bacterial peritonitis. Pathogenic mechanisms underlying cirrhotic cardiomyopathy include cardiomyocyte-membrane biophysical changes, attenuation of the stimulatory beta-adrenergic system and overactivity of negative inotropic systems mediated via cyclic GMP. The clinical features, general diagnostic criteria, pathogenesis and treatment of cirrhotic cardiomyopathy are discussed in this review.

ELECTROCARDIOGRAPHIC CRITERIA OF LEFT VENTRICULAR HYPERTROPHY

Soon after the advent of clinical electrocardiography it was recognized by Einthoven and others that characteristic deviations occur in association with hypertrophy of the cardiac chambers. Important contributions were made by several early investigators,1but for a long time interest in electrocardiography was focused chiefly on differentiation of the arrhythmias and the diagnosis of myocardial disease, with little emphasis on the clinical value of the electrocardiogram as a means of detecting cardiac hypertrophy. While the association of characteristic electrocardiographic patterns with hypertrophy of the various cardiac chambers is well recognized, the mechanism of these changes remains a subject of some controversy, and specific criteria for the electrocardiographic diagnosis of hypertrophy have not been established. The present investigation was actuated by the necessity of establishing specific electrocardiographic criteria of left ventricular hypertrophy in connection with a study on prognosis of hypertension.2It was felt, and the belief was subsequently