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PubMed2004

Evaluation of right ventricular dysfunction in patients with cardiac amyloidosis using Tei index.

BACKGROUND: Cardiac amyloidosis is an infiltrative disease causing predominant diastolic dysfunction and systolic dysfunction at its advanced stage. Right ventricular (RV) dysfunction is an independent predictor of poor prognosis in congestive heart failure and cardiomyopathies. However, the assessment of RV function is still technically difficult because of the complicated geometry of the RV. The recently proposed Tei index, obtained from the cardiac time interval analysis, allows noninvasive and quantitative estimation of global ventricular function without geometric evaluation. Therefore, this study was designed to assess RV function for patients with cardiac amyloidosis. METHODS: Study patients consisted of 30 consecutive patients with biopsy specimen-proven cardiac amyloidosis and 50 control subjects. Patients were classified as having early or advanced stage of cardiac amyloidosis on the basis of mean left ventricular wall thickness < 15 mm or >/= 15 mm. Tei index, defined as the sum of isovolumetric contraction and relaxation time divided by ejection time, was obtained from tricuspid and pulmonary Doppler flow velocity. RESULTS: RV Tei index was significantly increased for patients with cardiac amyloidosis (0.54 +/- 0.16 vs 0.28 +/- 0.05, amyloidosis vs control, P <.001). The incidences of abnormal RV isovolumetric contraction time, ejection time, isovolumetric relaxation time, and Tei index in all patients with cardiac amyloidosis were 63%, 43%, 73%, and 83%, respectively. The same incidences were 50%, 13%, 63%, and 75% in the early stage and 68%, 54%, 77%, and 86% in the advanced stage, respectively. CONCLUSION: Patients with cardiac amyloidosis frequently have RV dysfunction even in its early stage. Tei index allows simple, noninvasive, and nongeometric estimation of RV dysfunction in patients with cardiac amyloidosis.

Adult↗
PubMed2006

Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy.

The aim this study was to evaluate systolic and diastolic function in volume overload induced myocardial hypertrophy in rats. Volume overload myocardial hypertrophy was induced in thirteen male Wistar rats by creating infrarenal arteriovenous fistula (AVF). The results were compared with a SHAM operated group (n=11). Eight weeks after surgery, tail-cuff blood pressure was recorded, then rats were sacrificed for isolated heart studies using Langendorff's preparation. AVF rats presented increased left and right ventricular weights, compared to controls. The increased normalized ventricular volume (V0/LVW, 0.141+/-0.035 mL/g vs. 0.267+/-0.071 mL/g, P<0.001) in the AVF group indicated chamber dilation. Myocardial hydroxyproline concentration remained unchanged. There was a significant decrease in +dP/dt (3318+/-352 mm Hg s(-1) vs. 2769+/-399 mm Hg s(-1); P=0,002), end-systolic pressure-volume relation (246+/-56 mm Hg mL(-1) vs. 114+/-63 mm Hg mL(-1); P<0,001), and -dP/dt (1746+/-240 mm Hg s(-1) vs. 1361+/-217 mm Hg s(-1), P<0.001) in the AVF group, which presented increased ventricular compliance (DeltaV(25): SHAM=0.172+/-0.05 mL vs. AVF=0.321+/-0.072 mL, P<0.001) with preserved myocardial passive stiffness (Strain(25): SHAM=13.5+/-3.0% vs. AVF=12.3+/-1.9%, P>0.05). We conclude that volume-overload induced hypertrophy causes myocardial systolic and diastolic dysfunction with increased ventricular compliance. These haemodynamic features help to explain the long-term compensatory phase of chronic volume overload before transition to overt congestive heart failure.

Animals↗
PubMed2001

Relation between exercise capacity and left ventricular systolic versus diastolic function during exercise in patients after myocardial infarction.

BACKGROUND: It is known that left ventricular systolic function at rest does not correlate well with exercise capacity of patients with heart failure. However, the contribution of left ventricular diastolic dysfunction, especially during exercise, to exercise capacity of cardiac patients remains to be determined. OBJECTIVE: To determine the impact of left ventricular systolic and diastolic function during exercise on exercise capacity of patients with left ventricular dysfunction after myocardial infarction. METHODS: A symptom-limited exercise test was performed with measurements for hemodynamics and uptake of oxygen (Vo2) of 26 men who had previously suffered myocardial infarction. These patients were divided into two groups according to their peak Vo2 (group 1 with peak Vo2 > or = 16 ml/kg per min, n= 13; and group 2 with peak Vo2 < 16 ml/kg per min, n= 13). Pulmonary arterial pressure, left ventricular and systemic arterial pressure, and cardiac output were measured at rest and during exercise. RESULTS: At rest, there was no difference between the two groups in terms of hemodynamic parameters except for minimal dP/dt, minimal left ventricular pressure (LVP) and time constant for decay of left ventricular pressure (tau). During peak exercise, cardiac output, left ventricular end-diastolic pressure (EDP), minimal dP/dt, minimal LVP, and tau for the two groups were significantly different. Furthermore, peak Vo2 was significantly correlated with T, minimal LVP, minimal dP/dt, EDP, and maximal dP/dt during peak exercise for the whole group of patients. CONCLUSION: Left ventricular diastolic function during exercise, i.e. diastolic reserve, may be an important determinant of exercise capacity of patients with left ventricular dysfunction after myocardial infarction.

Adult↗
PubMed2001

Gender and aging in a transgenic mouse model of hypertrophic cardiomyopathy.

Mutations in the cardiac myosin heavy chain (MHC) can cause familial hypertrophic cardiomyopathy (FHC). A transgenic mouse model has been developed in which a missense (R403Q) allele and an actin-binding deletion in the alpha-MHC are expressed in the heart. We used an isovolumic left heart preparation to study the contractile characteristics of hearts from transgenic (TG) mice and their wild-type (WT) littermates. Both male and female TG mice developed left ventricular (LV) hypertrophy at 4 mo of age. LV hypertrophy was accompanied by LV diastolic dysfunction, but LV systolic function was normal and supranormal in the young TG females and males, respectively. At 10 mo of age, the females continued to present with LV concentric hypertrophy, whereas the males began to display LV dilation. In female TG mice at 10 mo of age, impaired LV diastolic function persisted without evidence of systolic dysfunction. In contrast, in 10-mo-old male TG mice, LV diastolic function worsened and systolic performance was impaired. Diminished coronary flow was observed in both 10-mo-old TG groups. These types of changes may contribute to the functional decompensation typically seen in hypertrophic cardiomyopathy. Collectively, these results further underscore the potential utility of this transgenic mouse model in elucidating pathogenesis of FHC.

Aging↗
PubMed2000

Use of an age-adjusted Doppler E/A ratio in patients with moderate to severe hypertension.

OBJECTIVE: To assess the ratio of early (E) to late atrial (A) mitral Doppler peak flow velocity (Doppler E/A ratio) before and after adjustment for age in patients with moderate to severe hypertension, in whom left ventricular diastolic dysfunction is an early finding. Mitral flow patterns can be used to assess diastolic filling characteristics, and the Doppler E/A ratio is the parameter most commonly used, although it is known to be strongly age dependent. There are no established normal values for this ratio. DESIGN: Retrospective data analysis. SETTING: A 2000-bed tertiary-care teaching hospital. PATIENTS: We studied 190 patients (99 women and 91 men; ages 55 +/- 13 years) with moderate to severe hypertension. INTERVENTIONS: The ratio of early (E) to late atrial (A) mitral Doppler peak flow velocity was measured. As this ratio depends on age, a Z score was calculated to control for this influence. The Z score is the standardized normal deviation of the mean, with a normal value of 0 +/- 2. MAIN OUTCOME MEASURES: Sensitivities and specificities for detecting an age-dependent reduction in Doppler E/A score (Z score less than -2) with a non-age-dependent Doppler E/A ratio (less than 1) were calculated. RESULTS: In 106 of the patients (56%) the Doppler E/A ratio was less than 1.0. Only nine patients (4.7%) had a Z score less than -2. The sensitivity of the Doppler E/A ratio threshold of 1.0 for detecting a Z score less than -2 was 0.89 and the specificity was 0.46. A Z score less than -2 was found only in patients younger than 45 years. CONCLUSIONS: The Doppler E/A ratio was reduced in a large proportion of our patients. However, after correction for age it was decreased in only 4.7% of these patients. The use of a single Doppler E/A ratio threshold value has a weak diagnostic power to detect age-independent changes in mitral flow patterns.

Adult↗
PubMed1999

Myocardial diastolic function and exercise.

There are several important links between aerobic exercise performance and the diastolic phase of the cardiac cycle. During acute exercise, diastolic function must be augmented in order for left ventricular filling to match increased left ventricular output, i.e., cardiac output. This challenges the myocardium because the shortened duration of diastole during exercise may compromise left ventricular filling, thereby limiting the stroke volume. Additionally, left ventricular filling must be accomplished at relatively low filling pressures, otherwise pulmonary vascular congestion may occur. Left ventricular diastolic function may be impaired in the elderly and/or in individuals with ischemic coronary syndromes. Regular aerobic exercise training appears to enhance left ventricular diastolic function and may benefit patients with clinically relevant "diastolic dysfunction." The purpose of this paper is to discuss the relative importance between diastole and exercise and to review some of the involved putative mechanisms.

Diastole↗
PubMed1989

Influence of alteration in preload on the pattern of left ventricular diastolic filling as assessed by Doppler echocardiography in humans.

We examined the influence of alterations in preload on pulsed Doppler indexes of left ventricular diastolic function in 50 patients including 12 without cardiovascular disease, 29 with coronary artery disease, and nine with critical aortic stenosis. Micromanometer left ventricular pressure was recorded simultaneously with pulsed Doppler echocardiography of left ventricular inflow and M-mode echocardiography of left ventricular diameter. Chamber stiffness constants, kd and kv, were obtained from the diastolic pressure-diameter and pressure-volume relations, respectively. Relaxation was measured by the isovolumic relaxation time constants, TL and TD, derived from the exponential left ventricular pressure decay and maximum negative dP/dt. In 41 patients after nitroglycerin treatment, left ventricular end-diastolic pressure decreased from 18 +/- 5 to 13 +/- 4 mm Hg (p less than 0.001). The ratio of peak early to peak atrial filling velocities and time-velocity integral ratios decreased from 1.08 +/- 0.57 to 0.90 +/- 0.42 (p less than 0.001) and from 1.77 +/- 0.95 to 1.41 +/- 0.71 (p less than 0.001), respectively. The peak early filling velocity and time-velocity integral decreased from 56.1 +/- 15.7 to 49.9 +/- 14.5 cm/sec (p less than 0.001) and from 7.9 +/- 2.7 to 6.8 +/- 2.8 cm (p less than 0.001), respectively. Relaxation (TL, TD, and maximum negative dP/dt) and chamber stiffness (kd and kv) were not impaired after nitroglycerin administration. In 48 patients after ventriculography, left ventricular end-diastolic pressure increased from 18 +/- 6 to 22 +/- 8 mm Hg (p less than 0.001). The peak early and peak atrial filling velocities increased from 57.4 +/- 15.2 to 68.3 +/- 19.7 cm/sec (p less than 0.001) and from 61.0 +/- 22.7 to 69.4 +/- 23.2 cm/sec (p less than 0.01), respectively. As a result, the ratio of peak early to peak atrial filling velocity was unchanged. However, in the aortic stenosis group, the ratio of peak early to peak atrial filling velocity increased from 0.95 +/- 0.64 to 1.10 +/- 0.72 (p less than 0.02). Relaxation and chamber stiffness were unchanged. Thus, a reduction or increase in preload may induce a diastolic filling pattern that mimics or masks diastolic dysfunction, respectively. Preload conditions need to be accounted for when the status of diastolic function is extrapolated from the pulsed Doppler mitral inflow velocity profile.

Aortic Valve Stenosis↗
PubMed1999

[Congestive heart failure in the aged. Diagnosis].

THREE DIAGNOSTIC PITFALLS: The difficulty in diagnosing congestive heart failure in the elderly subject is basically caused by three factors. First, clinical expression is often atypical. Secondly, severity is often underestimated as the prevalence of asymptomatic systolic dysfunction increases with age. Half of all cases of left ventricular systolic dysfunction go unrecognized if clinical signs alone are considered. Finally, the pathophysiology of diastolic dysfunction, which predominates in the over 75 population, is still poorly understood. COMPLEMENTARY EXPLORATIONS: As the clinical signs are the same whatever the mechanism of the ventricular dysfunction, echocardiography is the key exploration for diagnosis and for guiding management. Comorbidity is often a confounding factor preventing precise diagnosis and risk stratification.

Aged↗
PubMed1987

[Left ventricular diastolic function in PTCA: a Doppler echocardiographic study].

The measurement of left ventricular inflow by Doppler echocardiography provides a continuous, non-invasive assessment of parameters of diastolic function. We studied changes in left ventricular diastolic function during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending coronary artery (LAD). In ten patients, the diastolic flow velocity profile across the mitral valve was measured by Doppler echocardiography, before and 60 s after inflation and 60 s after deflation of the balloon. The peak velocity of early diastolic filling (VE) significantly decreased during angioplasty, from 68 +/- 12 to 56 +/- 10 cm/s (p less than 0.001), while the peak velocity of late diastolic filling caused by atrial contraction (VA) showed no change. This resulted in a significant decline in the diastolic velocity ratio (VE/VA) from 1.11 +/- 0.47 to 0.92 +/- 0.35 (p less than 0.01). The total area under the diastolic flow velocity profile representing the total filling volume fell from 14.3 +/- 4.1 to 10.9 +/- 3.6 cm (p less than 0.001). The early diastolic filling fraction decreased from 68 +/- 5% to 64 +/- 7%, in favor of the filling fraction due to atrial contraction, which increased from 32 +/- 5%, to 36 +/- 7% (p less than 0.01). 60 s after deflation of the balloon, the parameters of diastolic filling returned to baseline values. We conclude from our results that diastolic dysfunction caused by angioplasty of the LAD results in a decrease in early diastolic left ventricular filling, which is completely reversible after 60 s.

Adult↗
PubMed1988

Left ventricular diastolic function in diabetics.

Left ventricular diastolic function was studied in 29 young diabetic patients (aged from 14 to 44 years) without any clinical sign of heart disease. The metabolic state, the presence and the degree of microvascular and neuropathic complications have been established. Age and sex matched 32 healthy subjects served as controls. The parameters of left ventricular diastolic function were determined by means of phonomechanocardiography. By this method in diabetic patients impaired diastolic function of the left ventricle was found. This alteration could be best characterized by the values of normalized relaxation index referring to the isovolumetric relaxation of the left ventricle. A close correlation was found between the microvascular and neuropathic complications and the left ventricular diastolic dysfunction, while no correlation could be demonstrated between the metabolic state and the diastolic cardiac disorder.

Adult↗
PubMed1990

Doppler assessment of left ventricular filling pattern in silent ischemia in patients with Prinzmetal's angina.

Spontaneous angina is an ideal condition in which to study left ventricular (LV) dysfunction induced by acute myocardial ischemia. In 6 patients with Prinzmetal's angina, LV diastolic function during 16 episodes of spontaneous angina was studied by simultaneous recordings of electrocardiographic (ECG), echocardiographic and hemodynamic parameters. In particular, pulsed Doppler echocardiography measured peak velocity of early (E) and late (A) transmitral flow and E/A ratio, as indexes of relative early versus late LV filling. During the ischemic attacks, the time sequence of pulsed Doppler echocardiographic and ECG changes showed 3 distinct phases: (1) "waxing phase: transmitral flow changes with minimal ECG modifications (E/A = 0.85 +/- 0.1); (2) "steady" phase: maximal ECG changes (E/A = 0.9 +/- 0.1); and (3) "waning" phase: regression of the ECG changes (E/A = 1.26 +/- 0.15). In each phase, E/A ratio showed a significant difference from the baseline value (E/A = 1.17 +/- 0.2) as a result of changes in E, suggesting that myocardial ischemia affects mainly the early phase of diastole. In the waxing phase, LV diastolic dysfunction preceded systolic abnormalities, as documented by a significant reduction of E/A ratio in the absence of alterations in LV ejection fraction, as well as in systemic arterial and pulmonary wedge pressures. Finally, all the recorded parameters were consistent with LV "contractile rebound" occurring in the waning phase and affecting both diastole and systole.

Angina Pectoris, Variant↗
PubMed2000

Iron-overload cardiomyopathy: evidence for a free radical--mediated mechanism of injury and dysfunction in a murine model.

Iron-overload cardiomyopathy is a restrictive cardiomyopathy that manifests itself as systolic or diastolic dysfunction secondary to increased deposition of iron in the heart and occurs with common genetic disorders such as primary hemochromatosis and beta-thalassemia major. Although the exact mechanism of iron-induced heart failure remains to be elucidated, the toxicity of iron in biological systems is believed to be attributed to its ability to catalyze the generation of oxygen-free radicals. In the current investigation, the dose-dependent effects of chronic iron-loading on heart tissue concentrations of iron, glutathione peroxidase (GPx) activity, free-radical production, and cardiac dysfunction were investigated in a murine model of iron-overload cardiomyopathy. It was shown that chronic iron-overload results in dose-dependent (a) increases in myocardial iron burden, (b) decreases in the protective antioxidant enzyme GPx activity, (c) increased free-radical production, and (d) increased mortality. These findings show that the mechanism of iron-induced heart dysfunction involves in part free radical-mediated processes.

Animals↗
PubMed1989

Recently diagnosed idiopathic dilated cardiomyopathy: incidence of myocarditis and efficacy of prednisone therapy.

Fifty-two patients with recently diagnosed idiopathic dilated cardiomyopathy were studied to determine the incidence of myocarditis; patients were randomly assigned to receive either conventional therapy alone or conventional therapy plus prednisone to assess possible therapeutic efficacy with regard to survival. Inflammatory criteria were present in 23% of the population studied with 13% having overt myocarditis according to the Dallas criteria. The addition of prednisone to conventional therapy did not improve survival in a homogeneous population with new-onset dilated cardiomyopathy. Furthermore, the diagnosis of myocarditis by endomyocardial biopsy did not influence 2-year survival once dilated cardiomyopathy had developed. Biopsy-documented myocarditis resolved in all patients, according to results of 3-month follow-up endomyocardial biopsies, regardless of treatment group. There was a trend for patients with a left ventricular ejection fraction less than 20% to show reduced survival at 2 years compared to the group with a higher ejection fraction (p = 0.07). Right ventricular dysfunction determined at catheterization was present in 20 of 52 patients and was the most significant predictor of survival. Patients with preserved right ventricular function had a 95% 24-month survival rate compared to 47% for patients with right ventricular diastolic dysfunction (right ventricular end-diastolic pressure greater than or equal to 11 mm Hg) (p = 0.005).

Adult↗
PubMed2006

Assessment of stress-induced pulmonary interstitial edema by chest ultrasound during exercise echocardiography and its correlation with left ventricular function.

Ultrasound lung comet images (ULC) are useful for the noninvasive assessment of extravascular lung water (EVLW). We investigated the modification of EVLW, its relation to indices of left ventricular systolic and diastolic function, and noninvasively determined pulmonary capillary wedge pressure (PCWP) (PCWP = 1.24 ratio of early diastolic mitral inflow velocity to early diastolic velocity of the mitral annulus [E/Em] + 1.9) at rest and its variation during exercise echocardiography. A total of 72 patients (mean age 66.4 +/- 8.4 years) with mean ejection fraction of 41.2 +/- 14.4% underwent symptoms-limited exercise echocardiography. The sum of the ULC yielded a score of EVLW. The ULC increased significantly from baseline to postexercise (5.9 +/- 14.9 vs 11 +/- 20.7, P = .0001). Positive linear correlations were found between baseline ULC score and baseline ejection fraction (r = -0.37, P = .002), systolic pulmonary artery pressure (r = 0.69, P = .0001), E/Em (r = 0.70, P = .0001), and estimated PCWP (r = 0.69, P = .0001). The variation between postexercise and baseline ULC score correlated significantly with the variation between peak stress and rest PCWP (r = 0.62, P = .0001), systolic pulmonary artery pressure (r = 0.44, P = .0001), wall-motion score index (r = 0.30, P = .01), and peak stress E/Em (r = 0.71, P = .0001), whereas no significant correlations were found between variations of ULC score and ejection fraction. This study shows that ULC represents a simple way to assess the presence of excess EVLW. Increased EVLW is associated with estimated PCWP and indices of left ventricular systolic and diastolic dysfunction. The additional exercise-induced increase of PCWP, the worsening of left ventricular diastolic function, and extensive wall-motion abnormalities correlate with variations of EVLW.

Aged↗
PubMed2004

Plasma B-type natriuretic peptide reflects left ventricular hypertrophy and diastolic function in hypertension.

BACKGROUND: Hypertension is associated with changes in concentrations of vasoactive peptides and procollagen propeptides, but their relationships with left ventricular hypertrophy and cardiac function are unclear. METHODS: We measured plasma levels of atrial natriuretic peptide (ANP), its amino terminal propeptide (NT-proANP), B-type natriuretic peptide (BNP), endothelin-1 (ET-1), and serum levels of the aminoterminal propeptide of type I procollagen (PINP) and the aminoterminal propeptide of type III procollagen (PIIINP) and echocardiographic parameters in 97 patients with hypertension in the Anglo-Scandinavian Cardiac Outcomes Trial. RESULTS: Median values (reference values) of the peptides were: ANP 11.2 (6.9-14.9) pmol/l, NT-proANP 351 (143-311) pmol/l, BNP 1.1 (0.4-7.2) pmol/l, ET-1 8.7 (1.2-5.0) pmol/l, PIIINP 2.8 (1.7-4.2) microg/l and PINP 29 (19-84) microg/l. Plasma BNP levels in patients with left ventricular hypertrophy (1.2 pmol/l) and patients with echocardiographic signs of diastolic dysfunction (1.5 pmol/l) were greater than those in patients without hypertrophy (0.7 pmol/l) and normal diastolic parameters (0.9 pmol/l) (p<0.05). BNP was the only biochemical parameter that independently predicted interventricular septal diastolic diameter (p<0.05), left ventricular mass index (p<0.01) and ratio of the velocity-time integrals of the E and A waves of the mitral inflow in a stepwise logistic regression analysis (p<0.05). CONCLUSIONS: The results show that BNP reflects the remodelling process in hypertension.

Adult↗
PubMed2001

The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: a cine MRI study.

Cardiac remodeling in case of hypertension induces hypertrophy of myocytes and elevated collagen content and, subsequently, impaired diastolic filling of the left ventricle. The purpose of this prospective study was to evaluate changes of left ventricular (LV) myocardial mass, as well as diastolic filling properties, in hypertensive patients treated with the ACE inhibitor fosinopril. Sixteen hypertensive patients with echocardiographically documented LV hypertrophy and diastolic dysfunction received fosinopril (10-20 mg daily). Measurements of LV myocardial mass and properties of diastolic filling (peak filling fraction (PFF); peak filling rate (PFR)) were performed prior to medication, as well as after 3 and 6 months of therapy using cine magnetic resonance imaging (MRI). Ten healthy subjects served as a control group. LV myocardial mass (g/m2) decreased continuously within 3-6 months of follow-up by 32% (148 +/- 40 vs. 120 +/- 26 vs. 101 +/- 22 g/m2; P < 0.0001/0.005). The extent of regression correlated to the severity of LV hypertrophy at baseline (r = 0.77; P < 0.004). Early diastolic filling increased significantly within 6 months of therapy (PFF (%): 36 +/- 6 vs. 61 +/- 7, P < 0.0001; PFR (mL/second): 211 +/- 48 vs. 282 +/- 48, P < 0.001). Cine MRI can be used to assess the time course of pharmacological effects on cardiac remodeling in the course of hypertension. ACE inhibitor therapy results in a significant reduction of LV mass within 3 months and is accompanied by a normalization of diastolic filling that is completed after 6 months.

Adult↗
PubMed2006

Severe impairment of ventricular compliance accounts for advanced age-associated hemodynamic dysfunction in rats.

Advanced aging is associated with hemodynamic dysfunction in rats as in humans. The aim of this study was to assess the mechanisms of development of left ventricular (LV) dysfunction in the rat model of aging. In vivo hemodynamics and ex vivo LV papillary muscle mechanics, myofilaments sensitivity to calcium in skinned fibers and pressure/volume curves in isolated perfused hearts were performed in 3, 24 and 28 month old (mo) male Wistar rats. Hemodynamic dysfunction occurs in 28 mo rats and is characterized by both a systolic and diastolic dysfunction and a LV hypertrophy (+34.7% of LV weight). In papillary muscle, normalized active developed force and myofilament sensitivity to calcium were unchanged between 24 and 28 months of age. In contrast, both resting force/total force ratio in papillary muscle and the slope of the pressure/volume curves in isolated heart are increased between 3 and 24 mo but also between 24 and 28 mo, indicating a progression of the impairment of both papillary muscle stiffness and LV compliance in advanced aging. Hemodynamic dysfunction occurring at advanced age, i.e. 28 mo in rats mainly results from impairment of ventricular compliance resulting from fibrosis.

Actin Cytoskeleton↗
PubMed1998

Isolated diastolic heart failure--what is it?

Epidemiological evidence suggests that 20 to 40% of all patients with heart failure have normal systolic function. Isolated diastolic dysfunction may be the principle pathophysiological mechanism in these patients. The diagnosis of isolated diastolic heart failure is problematic and not merely based on demonstrating normal systolic function. The prognosis in isolated diastolic heart failure is more favourable than in systolic heart failure. At the present time, there is no licensed treatment for isolated diastolic heart failure and treatment is largely empirical.

Diastole↗