Cardiac dilatation and pump dysfunction without intrinsic myocardial systolic failure following chronic β-adrenoreceptor activation

2007 ◽  
Vol 292 (4) ◽  
pp. H1898-H1905 ◽  
Author(s):  
Oleg E. Osadchii ◽  
Gavin R. Norton ◽  
Richard McKechnie ◽  
Dawn Deftereos ◽  
Angela J. Woodiwiss
Keyword(s):  
Diastolic Pressure ◽  
Systolic Function ◽  
Isolated Heart ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Pump Failure ◽  
Volume Relation ◽  
The Impact ◽  
Fractional Shortening

There is no direct evidence to indicate that pump dysfunction in a dilated chamber reflects the impact of chamber dilatation rather than the degree of intrinsic systolic failure resulting from myocardial damage. In the present study, we explored the relative roles of intrinsic myocardial systolic dysfunction and chamber dilatation as mediators of left ventricular (LV) pump dysfunction. Administration of isoproterenol, a β-adrenoreceptor agonist, for 3 mo to rats (0.1 mg·kg−1·day−1) resulted in LV pump dysfunction as evidenced by a reduced LV endocardial fractional shortening (echocardiography) and a decrease in the slope of the LV systolic pressure-volume relation (isolated heart preparations). Although chronic β-adrenoreceptor activation induced cardiomyocyte damage (deoxynucleotidyl transferase-mediated dUTP nick-end labeling) as well as β1- and β2-adrenoreceptor inotropic downregulation (attenuated contractile responses to dobutamine and salbutamol), these changes failed to translate into alterations in intrinsic myocardial contractility. Indeed, LV midwall fractional shortening (echocardiography) and the slope of the LV systolic stress-strain relation (isolated heart preparations) were unchanged. A normal intrinsic myocardial systolic function, despite the presence of cardiomyocyte damage and β-adrenoreceptor inotropic downregulation, was ascribed to marked increases in myocardial norepinephrine release, to upregulation of α-adrenoreceptor-mediated contractile effects as determined by phenylephrine responsiveness, and to compensatory LV hypertrophy. LV pump failure was attributed to LV dilatation, as evidenced by increased LV internal dimensions (echocardiography), and a right shift and increased volume intercept of the LV diastolic pressure-volume relation. In conclusion, chronic sympathetic stimulation, despite reducing β-adrenoreceptor-mediated inotropic responses and promoting myocyte apoptosis, may nevertheless induce pump dysfunction primarily through LV dilatation, rather than intrinsic myocardial systolic failure.

scholarly journals Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction

2007 ◽  
Vol 292 (4) ◽  
pp. H1847-H1860 ◽  
Author(s):  
Marina R. Bergman ◽  
John R. Teerlink ◽  
Rajeev Mahimkar ◽  
Luyi Li ◽  
Bo-Qing Zhu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Matrix Metalloproteinase ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Membrane Type ◽  
Volume Relation

Although enhanced cardiac matrix metalloproteinase (MMP)-2 synthesis has been associated with ventricular remodeling and failure, whether MMP-2 expression is a direct mediator of this process is unknown. We generated transgenic mice expressing active MMP-2 driven by the α-myosin heavy chain promoter. At 4 mo MMP-2 transgenic hearts demonstrated expression of the MMP-2 transgene, myocyte hypertrophy, breakdown of Z-band registration, lysis of myofilaments, disruption of sarcomere and mitochondrial architecture, and cardiac fibroblast proliferation. Hearts from 8-mo-old transgenic mice displayed extensive myocyte disorganization and dropout with replacement fibrosis and perivascular fibrosis. Older transgenic mice also exhibited a massive increase in cardiac MMP-2 expression, representing recruitment of endogenous MMP-2 synthesis, with associated expression of MMP-9 and membrane type 1 MMP. Increases in diastolic [control (C) 33 ± 3 vs. MMP 51 ± 12 μl; P = 0.003] and systolic (C 7 ± 2 vs. MMP 28 ± 14 μl; P = 0.003) left ventricular (LV) volumes and relatively preserved stroke volume (C 26 ± 4 vs. MMP 23 ± 3 μl; P = 0.16) resulted in markedly decreased LV ejection fraction (C 78 ± 7% vs. MMP 48 ± 16%; P = 0.0006). Markedly impaired systolic function in the MMP transgenic mice was demonstrated in the reduced preload-adjusted maximal power (C 240 ± 84 vs. MMP 78 ± 49 mW/μl2; P = 0.0003) and decreased end-systolic pressure-volume relation (C 7.5 ± 1.5 vs. MMP 4.7 ± 2.0; P = 0.016). Expression of active MMP-2 is sufficient to induce severe ventricular remodeling and systolic dysfunction in the absence of superimposed injury.

Ventricular performance, pressure-volume relationships, and O2 consumption during hypothermia

1964 ◽  
Vol 206 (1) ◽  
pp. 67-73 ◽  
Author(s):  
R. G. Monroe ◽  
R. H. Strang ◽  
C. G. LaFarge ◽  
J. Levy
Keyword(s):  
Peak Pressure ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Heart Rates ◽  
Performance Pressure ◽  
Air Chamber ◽  
Lower Temperature

Left ventricular performance in the isolated heart of a dog was observed at normal temperatures (37.7 C) and under hypothermia (32.2 C) at comparable heart rates. The peak pressure of isovolumic contractions at the same ventricular end-diastolic pressures averaged 40% higher at the lower temperature. Diastolic pressure-volume relationships were similar at both temperatures. In studies in which the ventricle ejected fluid and performed work the hypothermic ventricle was capable of performing greater work at comparable heart rates, left ventricular end-diastolic pressures, and loading. When the ventricle was allowed to perform work by compressing air into a chamber of constant volume left ventricular oxygen consumption (Vo2) increased with the peak systolic pressure as the temperature was lowered. If the peak systolic pressure was maintained constant by increasing the volume of the air chamber as the temperature was lowered no consistent relationship could be shown between left ventricular Vo2 and the integral of systolic pressure in time which invariably increased with hypothermia.

Relative systolic dysfunction in female spontaneously hypertensive rat myocardium

2007 ◽  
Vol 103 (1) ◽  
pp. 353-358 ◽  
Author(s):  
Brian F. Renna ◽  
Scott M. MacDonnell ◽  
Patricia O. Reger ◽  
Deborah L. Crabbe ◽  
Steven R. Houser ◽  
...  
Keyword(s):  
Exercise Training ◽  
Spontaneously Hypertensive Rat ◽  
Systolic Function ◽  
Isolated Heart ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Lv Function ◽  
Spontaneously Hypertensive ◽  
Heart Preparation ◽  
Wistar Kyoto

Hypertension and exercise independently induce left ventricular (LV) remodeling and alter LV function. The purpose of this study was to determine systolic and diastolic LV pressure-volume relationships (LV-PV) in spontaneously hypertensive rats (SHR) with and without LV hypertrophy, and to determine whether 6 mo of exercise training modified the LV-PV in SHR. Four-month-old female SHR ( n = 20), were assigned to a sedentary (SHR-SED) or treadmill-trained (SHR-TRD) group (∼60% peak O2 consumption, 5 days/wk, 6 mo), while age-matched female Wistar-Kyoto rats (WKY; n = 13) served as normotensive controls. The LV-PV was determined using a Langendorff isolated heart preparation at 4 (no hypertrophy: WKY, n = 5; SHR, n = 5) and 10 mo of age (hypertrophy: WKY, n = 8; SHR-SED, n = 8; SHR-TRD, n = 7). At 4 mo, the LV-PV in SHR was similar to that observed in WKY controls. However, at 10 mo of age, a rightward shift in the LV-PV occurred in SHR. Exercise training did not alter the extent of the shift in the LV-PV relative to SHR-SED. Relative systolic function, i.e., relative systolic elastance, was ∼50% lower in SHR than WKY at 10 mo of age ( P < 0.05). Doppler-derived LV filling parameters [early wave (E), atrial wave (A), and the E/A ratio] were similar between groups. LV capacitance was increased in SHR at 10 mo ( P < 0.05), whereas LV diastolic chamber stiffness was similar between groups at 10 mo. Hypertrophic remodeling at 10 mo of age in female SHR is manifest with relative systolic decompensation and normal LV diastolic function. Exercise training did not alter the LV-PV in SHR.

The inotropic effect of digoxin on an isolated rat heart in hypercapnia and (or) hypoxia

1990 ◽  
Vol 68 (3) ◽  
pp. 455-461
Author(s):  
M. Allam ◽  
C. Saunier ◽  
A. Sautegeau ◽  
D. Hartemann
Keyword(s):  
Rat Heart ◽  
Myocardial Contractility ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Gas Mixture ◽  
Constant Frequency

The explanation for the increased frequency of troubles with digoxin therapy in patients with chronic pulmonary diseases is debated. The reported effects of hypoxia in vivo on myocardial levels of digoxin are contradictory, and there have been few studies on the effects of hypercapnia. In the past, it has been shown in rat myocardial tissue at rest in vitro that hypoxia decreased and hypercapnia acidosis increased the digoxin uptake. We performed a new study in vitro in an isolated beating rat heart perfused at constant flow (37 °C) and stimulated at a constant frequency (6 Hz). The performances were recorded with an intraventricular balloon equipped with a tip-manometer catheter. The action of digoxin was studied by recording systolic pressure (PS) and diastolic pressure (PD), the left ventricular developed pressure (LVDP = PS − PD), the (dP/dt)max, and the ratio (dP/dt)max/PS. First, the heart was perfused for 30 min with a modified Tyrode's solution perfusate aerated with carbogen (pH = 7.40; [Formula: see text]; [Formula: see text]) (1 mmHg = 133.32 Pa). Various parameters of contractions were recorded (initial control values). Then the heart was perfused for 15 min with Tyrode's solution aerated either with a hypoxic gas mixture (pH = 7.41; [Formula: see text]; [Formula: see text]), a hypercapnic gas mixture (pH = 7.08; [Formula: see text]; [Formula: see text]), or a hypoxic–hypercapnic gas mixture (pH = 7.09; [Formula: see text]; [Formula: see text]). Control hearts were continuously perfused with Tyrode's solution aerated with carbogen. During heart perfusion with hypercapnic, hypoxic, or hypoxic–hypercapnic Tyrode's solution, a decrease in LVDP and (dP/dt)max was observed. Finally, the heart was perfused with the same Tyrode's solution plus 1.75 × 10−5 M digoxin. The increase in myocardial contractility produced by digoxin was enhanced by hypercapnia and abolished by hypoxia. The addition of hypercapnia to hypoxia in Tyrode's solution seems to enhance the depressor action of the hypoxia.Key words: isolated heart, digoxin, hypoxia, hypercapnia, myocardial contractility.

scholarly journals A dilated cardiomyopathy mutation blunts adrenergic response and induces contractile dysfunction under chronic angiotensin II stress

2015 ◽  
Vol 309 (11) ◽  
pp. H1936-H1946 ◽  
Author(s):  
Ross Wilkinson ◽  
Weihua Song ◽  
Natalia Smoktunowicz ◽  
Steven Marston
Keyword(s):  
Dilated Cardiomyopathy ◽  
Chronic Stress ◽  
Troponin I ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Relaxation Rates

We investigated cardiac contractility in the ACTC E361G transgenic mouse model of dilated cardiomyopathy (DCM). No differences in cardiac dimensions or systolic function were observed in young mice, whereas young adult mice exhibited only mild diastolic abnormalities. Dobutamine had an inotropic and lusitropic effect on the mouse heart. In papillary muscle at 37°C, dobutamine increased relaxation rates [∼50% increase of peak rate of force decline normalized to force (dF/dtmin/F), 25% reduction of time to 90% relaxation (t90) in nontransgenic (NTG) mice], but in the ACTC E361G mouse, dF/dtmin/F was increased 20–30%, and t90 was only reduced 10% at 10 Hz. Pressure-volume measurements showed increases in maximum rate of pressure decline and decreases in time constant of left ventricular pressure decay in the ACTC E361G mouse that were 25–30% of the changes in the NTG mouse, consistent with blunting of the lusitropic response. The inotropic effect of dobutamine was also blunted in ACTC E361G mice, and the dobutamine-stimulated increase in cardiac output (CO) was reduced from 2,100 to 900 μl/min. Mice were treated with high doses of ANG II for 4 wk. The chronic stress treatment evoked systolic dysfunction in ACTC E361G mice but not in NTG. There was a significant reduction in rates of pressure increase and decrease, as well as reduced end-systolic pressure and increased volume. Ejection fraction and CO were reduced in the ACTC E361G mouse, indicating DCM. In vitro DCM-causing mutations uncouple the relationship between Ca2+ sensitivity and troponin I phosphorylation. We conclude that this leads to the observed, reduced response to β1 agonists and reduced cardiac reserve that predisposes the heart to DCM under conditions of chronic stress.

scholarly journals Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress

2019 ◽  
Vol 142 (2) ◽  
Author(s):  
Ana Cristina Estrada ◽  
Kyoko Yoshida ◽  
Samantha A. Clarke ◽  
Jeffrey W. Holmes
Keyword(s):  
Diastolic Pressure ◽  
Heart Function ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Published Data ◽  
Longitudinal Reinforcement ◽  
Wide Range ◽  
Volume Relationship ◽  
Pressure Volume Relationship

Abstract A wide range of emerging therapies, from surgical restraint to biomaterial injection to tissue engineering, aim to improve heart function and limit adverse remodeling following myocardial infarction (MI). We previously showed that longitudinal surgical reinforcement of large anterior infarcts in dogs could significantly enhance systolic function without restricting diastolic function, but the underlying mechanisms for this improvement are poorly understood. The goal of this study was to construct a finite element model that could match our previously published data on changes in regional strains and left ventricular function following longitudinal surgical reinforcement, then use the model to explore potential mechanisms for the improvement in systolic function we observed. The model presented here, implemented in febio, matches all the key features of our experiments, including diastolic remodeling strains in the ischemic region, small shifts in the end-diastolic pressure–volume relationship (EDPVR), and large changes in the end-systolic pressure–volume relationship (ESPVR) in response to ischemia and to patch application. Detailed examination of model strains and stresses suggests that longitudinal reinforcement reduces peak diastolic fiber stretch and systolic fiber stress in the remote myocardium and shifts those peaks away from the endocardial surface by reshaping the left ventricle (LV). These findings could help to guide the development of novel therapies to improve post-MI function by providing specific design objectives.

Elevated circulating cardiotrophin-1 in heart failure: relationship with parameters of left ventricular systolic dysfunction

2000 ◽  
Vol 99 (1) ◽  
pp. 83-88 ◽  
Author(s):  
S. TALWAR ◽  
I. B. SQUIRE ◽  
P. F. DOWNIE ◽  
R. J. O'BRIEN ◽  
J. E. DAVIES ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stroke Volume ◽  
Wall Motion ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Systolic Dysfunction ◽  
The Relationship ◽  
Fractional Shortening

Cardiotrophin-1 (CT-1) is a cytokine that has been implicated as a factor involved in myocardial remodelling. The objective of the present study was to establish the relationship between circulating levels of CT-1 and measures of left ventricular size and systolic function in patients with heart failure. We recruited 15 normal subjects [six male; median age 60 years (range 30–79 years)] and 15 patients [11 male; median age 66 years (range 43–84 years)] with a clinical diagnosis of heart failure and echocardiographic left ventricular systolic dysfunction (LVSD). Echocardiographic variables (left ventricular wall motion index, end-diastolic and -systolic volumes, stroke volume, fractional shortening) and plasma CT-1 levels were determined. In patients with LVSD [median wall motion index 0.6 (range 0.3–1.4)], CT-1 was elevated [median 110.4 fmol/ml (range 33–516 fmol/ml)] compared with controls [wall motion index 2 in all cases; median CT-1 level 34.2 fmol/ml (range 6.9–54.1 fmol/ml); P < 0.0001]. Log CT-1 was correlated with log wall motion index (r = -0.76, P < 0.0001), log left ventricular end-systolic volume (r = 0.54, P < 0.05), stroke volume (r = -0.60, P = 0.007) and log fractional shortening (r = -0.70, P = 0.001). In a multivariate model of the predictors of log wall motion index, the only significant predictor was log CT-1 (R2 = 56%, P = 0.006). This is the first assessment of the relationship between plasma CT-1 levels and the degree of LVSD in humans, and demonstrates that CT-1 is elevated in heart failure in relation to the severity of LVSD.

P6 Characterisation of right heart dysfunction in left ventricular systolic failure

2020 ◽  
Vol 41 (Supplement_1) ◽  
Author(s):  
H H L Chen ◽  
C H Gan ◽  
D Makarious ◽  
C H Ng ◽  
A Bhat ◽  
...  
Keyword(s):  
Systolic Function ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Disease Process ◽  
Left Ventricular ◽  
Pulmonary Artery Systolic Pressure ◽  
P Value ◽  
Basal Diameter ◽  
Lv Dysfunction ◽  
Rv Function

Abstract Funding Acknowledgements Nil Background Left and right ventricular (RV) function is proposed to be intimately linked. Reduced systolic ventricular interaction in patients with reduced global left ventricular (LV) performance is hypothesised to result in a reduction in RV contractile performance, even if the RV is not directly involved in the disease process. Concurrent RV and LV dysfunction is known to carry a poorer prognosis. However, the incidence of RV structural change and systolic dysfunction in patients with LV dysfunction in patients in a clinical setting is not well characterised. Purpose To determine the prevalence of RV systolic impairment in patients with LV systolic impairment from non-ischaemic cardiomyopathy (NICM); and to characterise the relationship between LV and RV systolic function using echocardiographic parameters. Methods 86 consecutive patients with stable heart failure with reduced ejection fraction secondary to NICM without valvular, congenital, and pulmonary disease were recruited. All patients underwent a comprehensive transthoracic echocardiogram and were stratified into tertiles based on LVEF (mild: 40-49%, moderate: 30-39%, severe: &lt;30%). RV function was characterised using standard and novel measures. 2D RV free wall peak systolic strain (RV FWS) was measured using vendor independent software (TomTec Image Arena, Germany v4.6).  Results Of the mild, moderate and severe groups (mean age 58 ± 34, 36% men): mean LVEF (%) was 46 ± 6, 35 ± 6, 22 ± 10 ; mean pulmonary artery systolic pressure (mmHg) was 28 ± 24, 34 ± 31, 38 ± 24; 26%, 79%, 74% had mild or moderate pulmonary hypertension respectively. 33% had RV impairment based on TAPSE of &lt;1.6cm; 48% had RV impairment based on RVS’ of &lt;10cm/s; and 65% had RV impairment based on a FAC of &lt;35%.  Conclusion Whilst there is a concurrent increase in the prevalence of RV impairment with severity of LV systolic impairment, interestingly not all patients with LV dysfunction had RV dysfunction. The presence of RV dysfunction is greatest when measured using FAC and RV FWS. Routine screening of RV dysfunction in patients with HFrEF secondary to NICM may help identify patients with poorer prognosis, who could benefit with more intensive follow up and treatment. LVEF 40-49% (n = 31) LVEF 30-39% (n = 28) LVEF &lt; 30% (n = 27) ONE WAY ANOVA Significance (P value) Mean RV Basal Diameter (cm) 4.1 ± 1.3 3.7 ± 1.6 3.6 ± 1.5 0.51 Mean TAPSE (cm) 2.1 ± 0.8 1.9 ± 1.0 1.7 ± 1.1 0.49 Mean RVS" (cm/s) 11 ± 5 11 ± 6 9 ± 6 0.24 Mean FAC (%) 44 ± 20 29 ± 21 17 ± 13 0.000 Mean RV FWS (%) -27.4 ± 14.4 -17.2 ± 11.6 -7.9 ± 6 0.000

Temporal evaluation of left ventricular remodeling and function in rats with chronic volume overload

1996 ◽  
Vol 271 (5) ◽  
pp. H2071-H2078 ◽  
Author(s):  
G. L. Brower ◽  
J. R. Henegar ◽  
J. S. Janicki
Keyword(s):  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular Remodeling ◽  
Isolated Heart ◽  
Volume Overload ◽  
Left Ventricular ◽  
Control Value ◽  
Chronic Volume Overload ◽  
And Function

The left ventricle (LV) significantly dilates and hypertrophies in response to chronic volume overload. However, the temporal responses in LV mass, volume, and systolic/diastolic function secondary to chronic volume overload induced by an infrarenal arteriovenous (A-V) fistula in rats have not been well characterized. To this end, LV end-diastolic pressure, size, and function (i.e., isovolumetric pressure-volume relationships in the blood-perfused isolated heart) were assessed at 1, 2, 3, 5, and 8 wk post-A-V fistula and compared with age-matched control animals. Progressive hypertrophy (192% at 8 wk), ventricular dilatation (172% at 8 wk), and a decrease in ventricular stiffness (257% at 8 wk) occurred in the fistula groups. LV end-diastolic pressure increased from a control value of 4.2 +/- 3.1 mmHg to a peak value of 15.7 +/- 3.6 mmHg after 3 wk of volume overload. A subsequent decline in LVEDP to 11.0 +/- 6.0 mmHg together with further LV dilation (169%) corresponded to a significant decrease in LV stiffness (222%) at 5 wk post-A-V fistula. Myocardial contractility, as assessed by the isovolumetric pressure-volume relationship, was significantly reduced in all A-V fistula groups; however, the compensatory remodeling induced by 8 wk of chronic biventricular volume overload tended to preserve systolic function.

scholarly journals AGE, SEX, AND FRAILTY INFLUENCE AGE-DEPENDENT CHANGES IN VENTRICULAR STRUCTURE AND FUNCTION IN C57BL/6 MICE

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S88-S88
Author(s):  
Susan E Howlett ◽  
Alice Kane ◽  
Elise Bisset ◽  
Kaitlyn Keller
Keyword(s):  
Cardiovascular Diseases ◽  
Ejection Fraction ◽  
Diastolic Function ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiac Aging ◽  
Lv Mass ◽  
Age Dependent ◽  
The Impact ◽  
Fractional Shortening

Abstract The heart undergoes maladaptive changes during aging that set the stage for cardiovascular diseases, but frail older individuals are most likely to develop such diseases. We investigated the impact of frailty on left ventricular (LV) remodeling in male and female mice (aged 9-23 mos). Ventricular function/structure and frailty were assessed with echocardiography (Vevo 2100) and a frailty index (FI) tool. Fractional shortening (systolic function) increased with age (9 vs 23 mos) in males (27.7±2.6 vs 38.4±1.6%; p&lt;0.05) and females (26.9±1.4 vs 32.5±1.8%; p&lt;0.05); similar results were seen with ejection fraction. Conversely, E/A ratios (diastolic function) declined with age in males (1.9±0.1 vs 1.3±0.1; p&lt;0.05) and females (2.1±0.3 vs 1.6±0.1; p&lt;0.05). LV mass and LV internal diameter (diastole) increased with age in females but not in males, while intraventricular septum (diastole) increased in males only. As age-dependent changes were heterogeneous, we stratified the data by FI scores. Interestingly, fractional shortening (r=0.52; p=0.006) and ejection fraction (r=0.52; p&lt;0.0001) were graded by FI score, but only in males. By contrast, LV mass was graded by frailty, but only in females (r=0.55; p&lt;0.0001). Thus, diastolic function declines with age in both sexes while systolic function actually increases. Aging females display increased LV mass and LV dilation whereas older males exhibit septal thickening. These maladaptive changes are graded by frailty, suggesting that cardiac aging is prominent in those with poor overall health. Age, sex and frailty influence cardiac aging, which may predispose frail older men and women to develop different cardiovascular diseases as they age.

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