scholarly journals P1253 A case report of acromegalic cardiomyopathy with severe left ventricular hypertrophy

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
M D Kuklina ◽  
K V Melkozerov ◽  
V Y Kalashnikov
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Pituitary Tumor ◽  
Ventricular Hypertrophy ◽  
Systolic Function ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Lv Function ◽  
Acromegalic Cardiomyopathy

Abstract Introduction Acromegaly is a rare disease, mostly caused by a growth hormone (GH)-secreting benign pituitary tumor, with an increased production of GH and insulin-like growth factor 1 (IGF-1). One hallmark feature of the disease is acromegalic cardiomyopathy, a syndrome of progressive cardiac dysfunction characterized by left ventricular hypertrophy, diastolic dysfunction, and combined systolic and diastolic dysfunction in the very advanced stage. Clinical case A 54-year-old male with history of arterial hypertension and abnormal electrocardiogram (ECG) for more than 10 years was diagnosed with active stage of acromegaly (IGF-1-1711ng/ml, cardiac magnetic resonance (CMR) – pituitary tumor). Surgical treatment was recommended. He was referred for preoperative cardiac evaluation preceding transsphenoidal resection of a pituitary adenoma. He denied syncope or any chest pain. The standard 12-lead ECG demonstrated sinus rhythm, left atrial enlargement and left ventricular (LV) hypertrophy with deep negative T waves in V3-V6 leads. Holter monitor demonstrated episodes of non-sustained ventricular tachycardia. Transthoracic echocardiography revealed severe asymmetric LV hypertrophy without LVOT obstruction at rest and maneuver Valsalva (max. grad. – 19mm. Hg) with mildly abnormal LV ejection fraction (48%, range ≥52%), severe reduced global longitudinal strain (-8,2%, range <-18%) and grade II diastolic dysfunction. CMR imaging was performed. According to CMR suggested hypertrophic cardiomyopathy (HCM) demonstrating area of myocardial fibrosis on extensive late gadolinium enhancement, maximal LV wall thickness of 40 mm, increased myocardial mass (index 277g/m2, range 68–103g/m2) and mildly reduced systolic LV function (LVEF - 54%, range 57-74%). Coronary angiography did not show significant stenosis. After cardiac examination, transsphenoidal adenomectomy was done. There are currently no algorithms sudden cardiac death (SCD) for patients with acromegalic cardiomyopathy, but he was recommended implantation of cardioverter defibrillator devices on a scale for HCM (Risc SCD – 4,17%). Acromegaly-induced cardiomyopathy can mimic HCM. He was also recommended genetic typing for HCM, considering the results of MRI. Conclusion/Discussion: Reduction GLS might be expected to result in a fall in LVEF, however this is often not the case in hypertrophic LV diseases. It is important to note that measures of regional function such as myocardial strain may actually reflect global systolic function better than the ejection fraction. The results may improve our ability to provide a more accurate prognosis and better assessment of actual systolic function. Because cardiomyopathy is an important cause of mortality in acromegaly, diagnosis and appropriate management are critical to improve survival. Abstract P1253 Figure.

P4134Impaired left ventricular systolic function in alcohol abusers expressed by both 3D calculated ejection fraction and longitudinal strain by AFI

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
P Hamala ◽  
J D Kasprzak ◽  
P Lipiec ◽  
K Wierzbowska-Drabik
Keyword(s):  
Alcohol Abuse ◽  
Ejection Fraction ◽  
Longitudinal Strain ◽  
Systolic Function ◽  
Global Longitudinal Strain ◽  
Harmful Effect ◽  
Left Ventricular ◽  
Control Group ◽  
Lv Function ◽  
Alcohol Abusers

Abstract Aim Despite knowledge regarding the existence of alcohol cardiomyopathy the exact impact of alcohol abuse in consecutive subject is poorly examined. We aimed to evaluate the left ventricle (LV) function in chronic abusers group and compared classical and novel echocardiography parameters in alcohol abusers (ALC) and control group (C). Methods We compared 75 adults (mean age 48±12, 60 male) without other overt heart disease, coronary artery disease excluded, but with alcohol abuse history: average alcohol intake 32 alcohol unit per week (AUW) with control group consisted of 40 subjects without history of excessive drinking, abstinents or drinking ≤8 AUW (mean age 50±4, 16 men). One unit was defined as 10 grams of pure etanol. All patients underwent TTE examination including ejection fraction (EF) calculation with 3D and longitudinal strain assessment by AFI method. Results ALC group showed LV systolic dysfunction expressed as EF 48±14 vs 60±9%, global longitudinal strain (AFI GLS) −15.6±6.6 vs −18.7±3.4; p<0.0001 and p 0.0064, respectively. On the other hand the LV and left atrial diameters as well as diastolic function were similar in both groups, indicating on relatively low advancement of heart remodeling. ALC vs Control group comparison ALC N75 C N40 p value Age 48±12 50±4 ns BMI 24±6 28±6 0.0009 LVd 48±13 47±4 ns LVs 34±15 32±4 ns LA 38±9 38±3 ns EF 48±14 60±9 <0.0001 E/A 1.1±0.6 1.1±0.3 ns E' lateral 10.6±3.9 10.6±2.9 ns AFI 2ch −15.9±6.9 −18.8±4.8 0.0143 AFI 3ch −15.9±6.9 −18.9±3.6 0.0116 AFI 4ch −15.2±7.1 −18.6±3.5 0.0053 AFI GLS −15.6±6.6 −18.7±3.4 0.0064 Conclusions Chronic alcohol abuse revealed harmful effect on LV systolic function which can be assessed quantitatively by both decreased EF and absolute values of myocardial longitudinal strain. This systolic function impairment seems to anticipate the overt remodelling of the heart.

scholarly journals Curcumin, an Inhibitor of p300-HAT Activity, Suppresses the Development of Hypertension-Induced Left Ventricular Hypertrophy with Preserved Ejection Fraction in Dahl Rats

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2608
Author(s):  
Yoichi Sunagawa ◽  
Masafumi Funamoto ◽  
Kana Shimizu ◽  
Satoshi Shimizu ◽  
Nurmila Sari ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ejection Fraction ◽  
Ventricular Hypertrophy ◽  
Systolic Function ◽  
Left Ventricular ◽  
High Salt ◽  
Preserved Ejection Fraction ◽  
High Salt Diet ◽  
Salt Diet ◽  
Hat Inhibitor

We found that curcumin, a p300 histone acetyltransferase (HAT) inhibitor, prevents cardiac hypertrophy and systolic dysfunction at the stage of chronic heart failure in Dahl salt-sensitive rats (DS). It is unclear whether curcumin suppresses the development of hypertension-induced left ventricular hypertrophy (LVH) with a preserved ejection fraction. Therefore, in this study, we randomized DS (n = 16) and Dahl salt-resistant (DR) rats (n = 10) at 6 weeks of age to either curcumin or vehicle groups. These rats were fed a high-salt diet and orally administrated with 50 mg/kg/d curcumin or its vehicle for 6 weeks. Both curcumin and vehicle treatment groups exhibited similar degrees of high-salt diet-induced hypertension in DS rats. Curcumin significantly decreased hypertension-induced increase in posterior wall thickness and LV mass index, without affecting the systolic function. It also significantly reduced hypertension-induced increases in myocardial cell diameter, perivascular fibrosis and transcriptions of the hypertrophy-response gene. Moreover, it significantly attenuated the acetylation levels of GATA4 in the hearts of DS rats. A p300 HAT inhibitor, curcumin, suppresses the development of hypertension-induced LVH, without affecting blood pressure and systolic function. Therefore, curcumin may be used for the prevention of development of LVH in patients with hypertension.

Abstract 2180: Relationship of Left Ventricular Systolic Function to Persistence or Development of Electrocardiographic Left Ventricular Hypertrophy in Hypertensive Patients: Implications for the Development of New Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Peter M Okin ◽  
Kristian Wachtell ◽  
Eva Gerdts ◽  
Kurt Boman ◽  
Markku S Nieminen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Increased Risk ◽  
Cornell Product

Background : We have previously demonstrated that persistence or development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria are associated with an increased risk of developing heart failure (HF) compared with regression or continued absence of LVH. We postulated that this relationship might be in part mediated via worse LV systolic function in patients with new and persistent LVH. Methods : Baseline and year-3 ECG LVH and LV midwall shortening (MWS) were examined in 725 patients in the LIFE echocardiographic substudy. MWS was measured and considered abnormal if <14.2%; stress-corrected MWS (scMWS) was considered abnormal if 2440 mm-msec. Results : Between baseline and 3 years follow-up, there was continued absence (n=260) or regression (n=167) of LVH in 427 patients and persistence (n=259) or development (n=39) of ECG LVH in 298 patients. Although there was no difference in baseline prevalence of abnormal MWS (23.4 vs 26.5%, p=0.389) or abnormal scMWS (24.6 vs 26.4%, p=0.663) between groups, after 3 years follow-up persistence or development of new LVH was associated with significantly lower mean MWS and scMWS and with higher prevalence and odds of abnormal MWS and scMWS than continued absence or regression of LVH (Table ). After controlling for differences in age, gender, race, treatment group, baseline and change from baseline to year-3 of heart rate, Sokolow-Lyon voltage, systolic and diastolic pressure and baseline severity of LVH by Cornell product, persistent or new ECG LVH remained associated with a >2-fold increased risk of abnormal MWS or scMWS at year 3. Conclusions : Persistence or development of new ECG LVH during antihypertensive therapy is associated with an increased risk of LV systolic dysfunction after 3 years of follow-up. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with changing risk of developing HF. < Midwall LV Function in Relation to Persistence or Development of ECG LVH Between Baseline and Year-3

Abstract 258: Progressive Diastolic Dysfunction, Perivascular Fibrosis and Left Ventricular Hypertrophy in LDL-Receptor Deficient Mice

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Walid Nachar ◽  
Candace Lee ◽  
Foued Maafi ◽  
Yanfen Shi ◽  
Téodora Mihalache-Avram ◽  
...  
Keyword(s):  
Vitamin D ◽  
Left Ventricular Hypertrophy ◽  
Diastolic Dysfunction ◽  
Ventricular Hypertrophy ◽  
Systolic Function ◽  
Mrna Level ◽  
Left Ventricular ◽  
Normal Diet ◽  
Control Group ◽  
Type I

Background and Aim: Left ventricular diastolic dysfunction (LVDD) refers to abnormal filling of the left ventricle (LV) due to its impaired relaxation or increased stiffness. Animal models of LVDD are limited and underlying mechanisms remain largely unknown. We aimed to assess LVDD in Ldlr -/- mice using imaging and gene expression measurements. Methods: Sixty-nine Ldlr -/- mice were fed with a western-type diet supplemented with vitamin D 2 (30 U/g/day) for 20 weeks to induce LVDD. Eight normal mice were fed with a normal diet and used as control group. Serial echocardiograms were used to assess cardiac structure and function, histological analyses were done on LV sections, and RT-PCR was performed on LV samples. Results: Echocardiographic results show the development of LVDD over time (P values <0.05), with a modest increase in LV mass/BW and preserved systolic function. There was an increase of perivascular fibrosis (14.9%±1.0% (14.9 to 100) vs 9.0%±1.6%; (9 to 100), respectively, P<0.01) in Ldlr -/- mice compared to controls as detected by Masson’s trichrome staining, which was correlated with increased mRNA expression for TGFß1 and Smad2 and 3 (P<0.05 for all). This was accompanied by numerical increases in Type I and III collagen mRNAs ( Col I : 1.33 (1.03; 1.97) vs 1.03 (0.90; 1.11), P=0.06; Col III : 1.49±0.30 vs 1.00±0.10, P=0.14). The angiotensin II precursor Agt mRNA level was also higher (1.07±0.08 vs 0.72±0.05; P<0.01) in Ldlr -/- mice compared to controls. Conclusion: Taken together, Ldlr -/- mice fed with a western diet supplemented with vitamin D 2 develop progressive LVDD, perivascular fibrosis and mild left ventricular hypertrophy, which represents a new model of lipid-mediated diastolic dysfunction that may be used in future studies for the evaluation of novel treatments.

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