Gender-specific differences of cardiac remodeling in subjects with left ventricular dysfunction: a population-based study

Luchner, Andreas; Bröckel, Ulrich; Muscholl, M.; Hense, Hans‐Werner; Döring, Angela; Riegger, Günter A.J.; Schunkert, Heribert

doi:10.1016/s0008-6363(01)00510-7

Cited by 105 publications

(88 citation statements)

References 32 publications

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“…Results from our study indicate that myocytes from female FVB mice were characterized by a significantly reduced peak shortening and maximum rate of shortening= relengthening, and a longer duration of relengthening as compared to male counterparts. This was consistent with some studies that showed a weaker contractile function in female hearts (10). Furthermore, the gender difference was significantly augmented in older FVB mice.…”

Section: Discussionsupporting

confidence: 93%

“…Recent clinical, epidemiological and experimental evidence has convincingly suggested that there is a gender bias in the progression of diabetic cardiomyopathy. In general, while difference in cardiac rhythm and arrhyathmia exists between genders, premenopausal women are much less susceptible to heart failure, and display much more favorable myocardial adaptation to hemodynamic overload both in contractile function and hypertrophic reserve (8)(9)(10)(11)(12)(13)(14). However, this ''gender-bias'' or ''female advantage'' may be significantly dampened with the onset of diabetes in pre-menopausal women (15).…”

Section: Introductionmentioning

confidence: 99%

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Influence of Gender on Intrinsic Contractile Properties of Isolated Ventricular Myocytes from Calmodulin‐Induced Diabetic Transgenic Mice

Zhang

Duan

et al. 2003

Endocrine Research

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Diabetes mellitus impairs ventricular function, which itself may be disparately influenced by gender. This study compared the impact of gender on cardiac contractile response in ventricular myocytes from wild-type FVB and calmodulin-induced diabetic transgenic (OVE26) mice at young (2 month) and older (11 month) age. Mechanical and intracellular Ca 2þ properties of cardiac myocytes were evaluated using an IonOptix MyoCam 1 system. Diabetic mice of both genders exhibited significantly elevated blood glucose regardless of age. OVE26 myocytes displayed reduced peak shortening (PS) and maximal velocity of shortening=relengthening (AEdL=dt), and prolonged time-to-PS (TPS) and time-to-90% relengthening (TR 90 ), associated with higher resting intracellular Ca 2þ levels and attenuated Ca 2þ -induced intracellular Ca 2þ release compared with the FVB myocytes. Peak shortening and AEdL=dt were smaller in female FVB groups when compared to the age-matched male counterparts. However, these gender differences were ablated by the diabetic state. No significant gender-related differences in intracellular Ca 2þ handling were noted in either FVB or OVE26 myocytes, with the exception of overt gender differences in OVE26 mice when age was taken into account. Young female OVE26 mice exhibited better-preserved mechanical function while older female OVE26 mice displayed the worst mechanical function among all four OVE26 groups. In conclusion, our data confirmed impaired cardiac contractile function in diabetes, partially due to altered intracellular Ca 2þ handling, in both genders. Mechanical differences existed between genders but were ''cancelled off'' by diabetic state. Nevertheless, a ''female advantage'' in ventricular function may still persist in young female diabetic subjects.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Influence of Gender on Intrinsic Contractile Properties of Isolated Ventricular Myocytes from Calmodulin‐Induced Diabetic Transgenic Mice

Zhang

Duan

et al. 2003

Endocrine Research

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“…extracellular matrix remodeling; ovariectomy; gender; hypertrophy; hormone; collagen; MT1-MMP; ventricle THE RISKS AND BENEFITS ASSOCIATED with estrogen replacement therapy remain uncertain. Conflicting results regarding the effect of estrogen replacement on the outcome of cardiovascular disease have been obtained from population studies, animal models, and clinical trials (2,16,20,21,32,33,61). The inconsistency of these findings demonstrates the lack of understanding of the mechanisms by which estrogen exerts its beneficial effects on the cardiovascular system.…”

mentioning

confidence: 99%

Estrogen improves TIMP-MMP balance and collagen distribution in volume-overloaded hearts of ovariectomized females

Voloshenyuk

Gardner

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Our previous studies demonstrate that 17␤-estradiol limits chronic volume overload-induced hypertrophy and improves heart function in ovariectomized rats. One possible cardioprotective mechanism involves the interaction between estrogen, estrogen receptors, and proteins of the extracellular matrix (ECM). The impact of estrogen deficiency and replacement on left ventricular (LV) hypertrophy and ECM protein expression was studied using five female rat groups: intact sham-operated, ovariectomized sham-operated, intact with volume overload, ovariectomized with volume overload, and ovariectomized with volume overload treated with estrogen. After 8 wk, LV protein extracts were evaluated by Western blot analysis for matrix metalloproteinase-2 (MMP-2) and MMP-9, MT1-MMP, tissue inhibitors of MMPs (TIMP)-1, TIMP-2, TIMP-3 and TIMP-4, collagens type I and III, and estrogen receptor ␣ and ␤ expression. MMP proteolytic activity was assessed by zymography. All volume-overloaded groups exhibited LV hypertrophy, which was associated with a loss of interstitial collagen and perivascular fibrosis. After 8 wk of volume overload, 70% of ovariectomized rats developed heart failure, in contrast to only one intact rat. A downregulation of MMP-2, estrogen receptor-␣ (ER␣), and ER␤, and upregulation of MMP-9 and MT1-MMP were found in the volume-overloaded hearts of ovariectomized rats. Estrogen treatment improved TIMP-2/MMP-2 and TIMP-1/MMP-9 protein balance, restored ER␣ expression, and prevented MMP-9 activation, perivascular collagen accumulation and development of heart failure. However, estrogen did not fully restore ER␤ expression and did not prevent the increase of MMP-9 expression or loss of interstitial collagen. These results support that estrogen limits undesirable ECM remodeling and LV dilation, in part, through modulation of ECM protein expression in volume-overloaded hearts of ovariectomized rats. extracellular matrix remodeling; ovariectomy; gender; hypertrophy; hormone; collagen; MT1-MMP; ventricle THE RISKS AND BENEFITS ASSOCIATED with estrogen replacement therapy remain uncertain. Conflicting results regarding the effect of estrogen replacement on the outcome of cardiovascular disease have been obtained from population studies, animal models, and clinical trials (2,16,20,21,32,33,61). The inconsistency of these findings demonstrates the lack of understanding of the mechanisms by which estrogen exerts its beneficial effects on the cardiovascular system. Using a rodent model, we demonstrated that hearts of intact female rats are resistant to chronic volume overload-induced adverse cardiac remodeling and dysfunction (12). This apparent cardioprotection is lost following ovariectomy (6). Estrogen replacement delays the development of left ventricular (LV) hypertrophy and dilation, and it prevents the onset of congestive heart failure (CHF) in ovariectomized rats with volume overload (13). However, the mechanisms of estrogen's protective effects in prevention of adverse myocardial remodeling remain unclear.Changes in extra...

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“…However, it is of note that in the general population, elevated plasma BNP was associated with a greater likelihood of future blood pressure increase only in men. 14 In addition, Luchner et al 15 showed that plasma BNP concentrations are much better correlated to left ventricular mass and function in men as compared with women. …”

Section: Hocher Et Al Relaxin Predicts Death In Men 2267mentioning

confidence: 99%

Relaxin Is an Independent Risk Factor Predicting Death in Male Patients With End-Stage Kidney Disease

et al. 2004

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Background-Patients with end-stage kidney disease (ESKD) have a reduced life expectancy mainly as the result of cardiovascular diseases. Relaxin has been implicated in the pathogenesis of cardiovascular diseases. We analyzed the impact of relaxin on death in patients with ESKD. Methods and Results-Patients (n ϭ245; 122 women, 123 men) on long-term hemodialysis were followed for 1140 days for death. Blood samples for analysis of relaxin, C-reactive protein, Troponin T, cholesterol, HDL, brain natriuretic peptide, and albumin were taken at study entry. Survival was compared by the Kaplan-Meier method and Cox regression analysis. One hundred seven patients died during the observation period; 66 died of cardiovascular diseases and 28 died of infectious diseases. Elevated serum relaxin concentrations (greater than median) predicted death in male but not in female patients with ESKD: All-cause death (men: relative risk, 2.63; 95% CI, njections of serum from pregnant rabbits induced relaxation of the interpubic ligament of guinea pigs. 1 The hormone responsible for this action was named relaxin. Corpus luteum, decidua, and placenta secrete this hormone during pregnancy. Relaxin has many important roles in pregnancy, including softening effects on connective tissue, reducing uterine contractility, and control of mammary gland growth and differentiation. 1 Recently, however, it was recognized that relaxin also plays a role in the cardiovascular system. Patients with chronic heart failure have increased myocardial relaxin gene expression and elevated plasma relaxin concentrations. 2 Relaxin stimulates cardiac ANP secretion 3 and increases coronary blood flow through a nitric oxide-mediated mechanism. 3 It was furthermore shown that relaxin is a vasodilator of small systemic resistance arteries. 4 Relaxin is also involved in the regulation of cardiac 5 and renal 6 collagen synthesis.We analyzed whether relaxin is a mortality risk factor in patients with end-stage kidney disease (ESKD). Patients with ESKD have a substantially reduced life expectancy. The mortality risk is about 50% higher in elderly patients with ESKD and even much more in younger patients with ESDK as compared with age-matched persons without renal disease. 7,8 MethodsThe 245 patients (122 women, 123 men) were recruited from two dialysis centers (KfH Dialysezentrum-Neukölln, Berlin, and KfH Dialysezentrum-Moabit, Berlin). The patients are dialyzed at least 3 times weekly in 4-to 6-hour sessions, sufficient to provide an urea kinetic on dialysis (KT/V) of at least 1.3. The included patients represent all patients being on stable hemodialysis in these centers without actual health problems. All patients were included in the study in March 2000 and followed for 1140 days. The following patients characteristics were documented: age, gender, body mass index, cause of ESKD, time on dialysis, diabetes, hypertension, and coronary heart disease (patients with a history of myocardial infarction, coronary heart disease confirmed by heart catheterization, or typical ...

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Gender-specific differences of cardiac remodeling in subjects with left ventricular dysfunction: a population-based study

Cited by 105 publications

References 32 publications

Influence of Gender on Intrinsic Contractile Properties of Isolated Ventricular Myocytes from Calmodulin‐Induced Diabetic Transgenic Mice

Influence of Gender on Intrinsic Contractile Properties of Isolated Ventricular Myocytes from Calmodulin‐Induced Diabetic Transgenic Mice

Estrogen improves TIMP-MMP balance and collagen distribution in volume-overloaded hearts of ovariectomized females

Relaxin Is an Independent Risk Factor Predicting Death in Male Patients With End-Stage Kidney Disease

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