The hypertrophic heart rat: a new normotensive model of genetic cardiac and cardiomyocyte hypertrophy

2002 ◽  
Vol 9 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Stephen B. Harrap ◽  
Vennetia R. Danes ◽  
Justine A. Ellis ◽  
Cory D. Griffiths ◽  
Elizabeth F. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Spontaneously Hypertensive ◽  
Fischer 344 ◽  
Lv Mass ◽  
Low Blood Pressure

We describe a new line of rats with inherited cardiomyocyte and ventricular hypertrophy. From a second-generation cross of spontaneously hypertensive and Fischer 344 rats, we selected for low blood pressure and either high or low echocardiographic left ventricular (LV) mass over four generations to establish the hypertrophic heart rat (HHR) and normal heart rat (NHR) lines, respectively. After 13 generations of inbreeding, HHR had significantly greater ( P < 0.0001) LV mass-to-body weight ratio (2.68 g/kg, SE 0.14) than NHR matched for age (1.94 g/kg, SE 0.02) or body weight (2.13 g/kg, SE 0.03). The isolated cardiomyocytes of HHR were significantly ( P < 0.0001) longer and wider (161 μm, SE 0.83; 35.6 μm, SE 2.9) than NHR (132 μm, SE 1.2; 29.5 μm, SE 0.35). Telemetric 24-h recordings of mean arterial pressure revealed no significant differences between HHR and NHR. The HHR offers a new model of primary cardiomyocyte hypertrophy with normal blood pressure in which to examine genotypic causes and pathogenetic mechanisms of hypertrophy and its complications.

Abstract 79: Autophagy Is Necessary in Reversal of Left Ventricular Hypertrophy

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Jota Oyabu ◽  
Osamu Yamaguchi ◽  
Kinya Otsu
Keyword(s):  
Body Weight ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Cross Sectional Area ◽  
Cardiomyocyte Hypertrophy ◽  
Sectional Area ◽  
Cross Sectional ◽  
Lv Mass ◽  
Continuous Injection

Myocardial hypertrophy occurs in response to a variety of stresses as a compensatory mechanism to maintain cardiac output and normalize wall stress. Left ventricular hypertrophy (LVH) in the long term is an independent risk factor for a range of adverse consequences, such as cardiac dysfunction and cardiac mortality. Therefore, prevention or regression of LVH can be a major therapeutic target. Although reversal of LVH occurs after control of etiological factors, the molecular mechanisms remain to be clarified. We have previously reported that inhibition of autophagy, an evolutionarily conserved process for the bulk degradation of cytoplasmic components, induces cardiomyocyte hypertrophy. In the present study, we investigated the role of autophagy in the course of reversal of LVH. Wild-type mice showed left ventricular hypertrophy by continuous injection of angiotensin II (A-II) for 14 days using osmotic mini-pump, and LVH was reversed 7 days after removal of pump. Autophagy was induced after removal of pump, as evidenced by an increase in LC3-II protein levels. Next, we crossed floxed Atg5 mice with transgenic mice expressing Cre recombinase in cardiac specific manner to generate cardiac-specific autophagy-deficient mice (CKO). We subjected CKO and control mice (CTL) to continuous injection of A-II for 14 days. CKO and CTL showed LVH similarly (LV weight/body weight, CKO 4.60±0.16 versus CTL 4.44±0.08, p=n.s., LV mass index, CKO 69.0±5.5 versus CTL 72.1±2.2, p=n.s.) without showing contractile dysfunction 14 days after injection of A-II. Cross-sectional area of cardiomyocytes was similar in CKO and CTL (CKO 281.0±1.0 μm 2 versus CTL 274.0±1.5 μm 2 , p=n.s.). 7days after removal of pump, CKO showed significantly less reversal of LVH compared with CTL (LV weight/body weight, CKO 4.30±0.13 versus CTL 3.65±0.09, p<0.05, LV mass index, CKO 67.8±3.8 versus CTL 56.2±2.6, p<0.05). Cross-sectional area of cardiomyocytes also showed less reversal of LVH in CKO (CKO 270.6.0±7.0 μm 2 versus CTL 220.9±11.4 μm 2 , p<0.05), indicating that reversal of LVH didn’t occur sufficiently in autophagy-deficient heart. Autophagy was suppressed during reversal of LVH in CKO. These results suggest that autophagy is necessary in reversal of LVH.

Catecholamines, Blood Pressure, Renin and Myocardial Function in the Spontaneously Hypertensive Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 455s-459s
Author(s):  
Suzanne Oparil ◽  
Lynda Erinoff ◽  
A. Cutilletta
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Myocardial Function ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Spontaneously Hypertensive ◽  
6 Hydroxydopamine

1. Neither nerve-growth-factor antiserum (NGFAS) administered subcutaneously nor 6-hydroxydopamine administered intraventricularly to immature spontaneously hypertensive rats (SHR) inhibited the development of the hypertensive syndrome. In contrast, NGFAS did not affect blood pressure in normotensive Kyoto/Wistar rats. 2. Peripheral vascular resistance was increased and cardiac index decreased in both NGFAS and 6-hydroxydopamine-treated SHR despite preservation of normal blood pressure. 3. NGFAS treatment did not influence the development of left ventricular hypertrophy in SHR, despite the lowering of blood pressure. In contrast, 6-hydroxydopamine caused an attenuation in the development of left ventricular hypertrophy. 4. Indices of left ventricular contractility were depressed by NGFAS treatment but not by 6-hydroxydopamine. 5. Plasma renin activity was unaffected by NGFAS treatment and increased by 6-hydroxydopamine.

P282 Elevated serum uric acid associated with both electrocardiographic and echocardiographic left ventricular hypertrophy independent of blood pressure in healthy individuals

2020 ◽  
Vol 41 (Supplement_1) ◽  
Author(s):  
C W Liu ◽  
W C Chang ◽  
R H Pan
Keyword(s):  
Blood Pressure ◽  
Uric Acid ◽  
Left Ventricular Hypertrophy ◽  
Serum Uric Acid ◽  
Ventricular Hypertrophy ◽  
Cardiac Fibrosis ◽  
Elevated Serum ◽  
Left Ventricular ◽  
Healthy Individuals ◽  
Lv Mass

Abstract Funding Acknowledgements TSGH 108-11 Background Elevated serum uric acid (SUA) is associated with cardiac fibrosis and hypertrophy. A growing body of evidence showed the positive correlation between hyperuricemia (HUA) and left ventricular hypertrophy (LVH), but most studies defined LVH by a single method such as electrocardiogram or echocardiogram; the former is generally used in massive screen but the latter take advantage of the accuracy of LVH. Purpose We conducted this study to concomitantly investigate the association between SUA and electrocardiographic and echocardiographic LVH. Methods We initially enrolled 17,913 healthy individuals, who routinely underwent an annual health exam at our hospital between 2016/1/1∼2016/12/31. Of them, 347 individuals received transthoracic echocardiography because of abnormal results in their electrocardiogram. Amplitudes of 12-lead electrocardiogram were artificially measured by a study assistant under the supervision and by artificial intelligence. HUA is defined as an SUA level of ≥7 mg/dl in men and ≥6 mg/dl in women. Electrocardiographic LVH is defined by the criteria of Cornel voltage and product and Sokolow-Lyon and the Minnesota Code ECG classification. Echocardiographic LVH is defined by LV mass index ≥115g/m² in men or ≥95g/m² in women. Results The HUA group (n = 233) vs. normouricemic group (n = 114) was older and predominant male with greater values of body mass index, systolic and diastolic blood pressure and laboratory biomarkers, including non-high density total cholesterol, fasting glucose impairment, creatinine clearance, and haemoglobin. The two groups had comparable lifestyle choices, including tobacco use, alcohol intake, and physical activities per week. The HUA group compared with the normouricemic group had greater values of S amplitude of V1 plus R amplitude of V5 (3031 ± 2055 uV vs. 2566 ± 1021 uV, P = 0.005), R amplitude in lead I plus S amplitude in lead III (842 ± 443 uV vs. 696 ± 386 uV, P = 0.002) and LV mass index (95 ± 23 g/m² vs. 85 ± 30 g/m², P = 0.001). The prevalence of electrocardiographic and echocardiographic LVH was greater in the HUA group than the normouricemic group (7.0% vs. 2.1%, P = 0.034 for electrocardiographic LVH and 15.8% vs. 7.7%, P = 0.025 for echocardiographic LVH). In multivariate logistic regression analyses, elevated SUA was associated with LVH after the confounders were fully adjusted (OR: 1.38, 95% CI: 1.07-1.77, P = 0.012 for electrocardiographic LVH and OR: 1.58, 95% CI 1.15-2.17, P = 0.004 for echocardiographic LVH). Conclusion Elevated SUA is independently associated with the prevalence of both electrocardiographic and echocardiographic LVH in healthy individuals from Taiwan. Future studies might evaluate urate-lowering effects on the regression of LVH.

scholarly journals Left ventricular hypertrophy in a contemporary cohort of autosomal dominant polycystic kidney disease patients

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Huanwen Chen ◽  
Terry Watnick ◽  
Susie N. Hong ◽  
Barry Daly ◽  
Yongfang Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Linear Regression ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Autosomal Dominant ◽  
Left Ventricular ◽  
Polycystic Kidney ◽  
Lv Mass ◽  
Autosomal Dominant Polycystic Kidney

Abstract Background Patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) often develop hypertension in childhood or early adulthood. Although this could result in left ventricular hypertrophy (LVH), a major risk factor for cardiovascular morbidity and mortality, prior studies of LVH in ADPKD have yielded conflicting results. We estimated the prevalence of LVH using consensus echocardiography criteria and examined the independent association of ADPKD severity with LV mass in a contemporary cohort of ADPKD patients. Methods Adults with ADPKD and eGFR> 15 ml/min/1.73m2 were enrolled in a single-center study. Left Ventricular Mass (LVM) was quantified using 2D echocardiography, and LVH was defined using gender-specific cut-points of LVM and LVM indexed to body surface area (LVMI) from consensus guidelines. Total Kidney Volume (TKV) was quantified using Magnetic Resonance Imaging, and GFR was estimated from serum creatinine using the CKD-Epi equation. Multiple linear regression was used to estimate the association of TKV and eGFR with LVM and LVMI, adjusting for potential confounders. Results Among 126 participants (78% with hypertension), median age was 46 years, median eGFR 63 ml/min/1.73 m2, and median [IQR] systolic blood pressure was 125 [116–133] mmHg. Prevalence of LVH was 21.4% as defined by LVMI and was not significantly different (p = 0.8) between those with and without HTN, and was similar (21.4%) after excluding those (N = 21) with known cardiac disease. Greater TKV and lower eGFR were directly correlated with greater LVMI (p = .016 and p < .001, respectively). In multiple linear regression models accounting for potential confounders including blood pressure, greater TKV was positively associated with LVM ($$ \hat{\beta} $$ β ̂ =0.19, p = 0.04). Conclusions In a contemporary cohort of ADPKD patients with well-controlled blood pressure, the prevalence of LVH is high, and ADPKD severity as reflected by TKV is independently associated with greater LV mass. These results may suggest a relationship between ADPKD pathophysiology and increased LV mass.

Age-related changes in cardiac structure and function in Fischer 344 × Brown Norway hybrid rats

2006 ◽  
Vol 290 (1) ◽  
pp. H304-H311 ◽  
Author(s):  
Timothy A. Hacker ◽  
Susan H. McKiernan ◽  
Pamela S. Douglas ◽  
Jonathan Wanagat ◽  
Judd M. Aiken
Keyword(s):  
Heart Function ◽  
Weight Ratio ◽  
Volume Density ◽  
Left Ventricular ◽  
Male Rats ◽  
Brown Norway ◽  
Cardiac Structure ◽  
F1 Hybrid ◽  
Fischer 344 ◽  
Lv Mass

The effects of aging on cardiovascular function and cardiac structure were determined in a rat model recommended for gerontological studies. A cross-sectional analysis assessed cardiac changes in male Fischer 344 × Brown Norway F1 hybrid rats (FBN) from adulthood to the very aged ( n = 6 per 12-, 18-, 21-, 24-, 27-, 30-, 33-, 36-, and 39-mo-old group). Rats underwent echocardiographic and hemodynamic analyses to determine standard values for left ventricular (LV) mass, LV wall thickness, LV chamber diameter, heart rate, LV fractional shortening, mitral inflow velocity, LV relaxation time, and aortic/LV pressures. Histological analyses were used to assess LV fibrotic infiltration and cardiomyocyte volume density over time. Aged rats had an increased LV mass-to-body weight ratio and deteriorated systolic function. LV systolic pressure declined with age. Histological analysis demonstrated a gradual increase in fibrosis and a decrease in cardiomyocyte volume density with age. We conclude that, although significant physiological and morphological changes occurred in heart function and structure between 12 and 39 mo of age, these changes did not likely contribute to mortality. We report reference values for cardiac function and structure in adult FBN male rats through very old age at 3-mo intervals.

Basal and maximal inotropic state in renal hypertensive dogs with cardiac hypertrophy

1983 ◽  
Vol 245 (1) ◽  
pp. H33-H41 ◽  
Author(s):  
A. Broughton ◽  
P. I. Korner
Keyword(s):  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Body Weight Ratio ◽  
Absolute Value ◽  
Inotropic State ◽  
Lv Mass ◽  
Autonomic Blockade ◽  
Mean Aortic Pressure

We studied three isovolumic indexes of contractility, i.e., dP/dtmax, dP/dtDP40, and (dP/dt)/TPmax, in normal dogs and in a matched group of chronically hypertensive dogs with left ventricular hypertrophy (LVH) [DP40, developed LV pressure of 40 mmHg; TP, total LV pressure above atmospheric]. The LVH was moderate in degree with the LV-to-body weight ratio 50% greater than in normal dogs. The experiments were performed under pentobarbital with open chest, autonomic blockade, and independent control of mean left atrial pressure (LAP) and mean aortic pressure (MAP). We found that dP/dtmax provided the most consistent comparison of inotropic state in the two groups under both basal conditions and with norepinephrine (NE). The other indexes occurred too early in systole to reflect complete LV activation, particularly during the infusion with NE. Under controlled conditions basal dP/dtmax of LVH dogs was 1.28 times the value of normal dogs, with the increase accounted for by the amplifier effect of the increase in LV mass. But with moderate lowering of aortic pressure, inotropic state was more easily compromised in LVH than in normal dogs. With steady-state stimulation by infusing increasing amounts of NE, dP/dtmax rose by 10 times basal in both LVH and normal dogs at maximum stimulation. The absolute value of the index was 1.31 times higher in the LVH group, with the amplifier effect thus the same as under basal conditions. The results suggest that basal and maximal inotropic states are normal in LVH under optimum loading conditions.

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