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PubMed1996

Diastolic abnormalities in systemic sclerosis: evidence for associated defective cardiac functional reserve.

OBJECTIVE: To investigate the pattern of diastolic abnormalities in patients with systemic sclerosis (SSc) and the relationship between impaired ventricular filling and systolic function. METHODS: Twenty four patients with SSc underwent M-mode and two dimensional echocardiography using echo-Doppler and gated blood pool cardiac angiography, both at rest and after exercise. RESULTS: An impaired diastolic relaxation of the left ventricle was detected in 10 of the 24 patients with SSc. Left ventricular ejection fraction at rest in these 10 patients with impaired ventricular filling did not differ from that in the remaining 14 patients, but eight of the 10 failed to increase their ejection fraction during exercise, compared with two of the 14 with normal ventricular filling (p = 0.003). CONCLUSION: Impaired relaxation of the left ventricle is a recently described feature of scleroderma heart disease. Diastolic dysfunction in SSc could depend on myocardial fibrosis or myocardial ischaemia, or both. It was found to be associated with a defective cardiac functional reserve. However, its prognostic significance remains to be clarified.

Adult↗
PubMed2004

Value of left ventricular filling parameters to predict mortality and functional class in patients with heart disease from the community.

UNLABELLED: Surprisingly few studies described the value of Doppler parameters in patients from the community. AIM: The aim was to determine the prevalence of prolonged IVRT (>0.105s) or a prolonged EDT (>0.280s) with a reduced E/A (<0.5) in heart patients from the community without valvular, systolic or rhythmic dysfunction. The associations of these parameters to all cause mortality and NYHA functional class were examined as well. METHODS: Seventy-two volunteer stable patients with a history of heart disease were identified from general practice. Patients with LVEF below 0.45, valvular abnormalities, atrial fibrillation, and pacemaker were excluded. Routine blood tests, echocardiography, chest X-ray, physical examination and mortality were evaluated. RESULTS PATIENT FINDINGS: male 33%, mean age of 68 years, hypertension 82%, ischaemic heart disease 43%, and NYHA class I+II+III in 50+39+11%. Abnormal EDT occurred in 4% (95% CI from 0 to 9%), IVRT in 18% (9-27%), E/A in 0%. None had a restrictive pattern. EDT was longer in NYHA III than in NYHA I-II patients (median 0.25 vs. 0.19s, p=0.0006). E/A and IVRT were not associated with NYHA class or mortality. After 7.4 years 16 of 72 patients died. EDT predicted mortality in univariate analysis but not in a multivariate analysis where NYHA class and gender were the only significant predictors. CONCLUSION: Prolonged EDT was weakly associated to NYHA class and mortality while IVRT and E/A were not. Prolonged IVRT was a frequent finding, but a diagnosis of diastolic dysfunction is not supported by mild to moderate abnormal IVRT or E/A.

Aged↗
PubMed1995

Digital subtraction high-frame-rate echocardiography in detecting delayed onset of regional left ventricular relaxation in ischemic heart disease.

BACKGROUND: Because left ventricular (LV) diastolic function is impaired before systolic function in patients with ischemic heart disease and because ischemic heart disease is constituted of regional rather than global abnormalities of the left ventricle, measures of LV regional diastolic dysfunction, if possible, should provide the most sensitive assessment of the coronary involved region. The objectives of this study are to clarify whether high-frame-rate two-dimensional echocardiography, combined with digital subtraction image processing, may be used to visualize regional LV relaxation abnormalities in patients with ischemic heart disease and to clarify whether this technique provides a measure for the noninvasive assessment of the coronary involved region. METHOD AND RESULTS: In 30 normal subjects and 59 patients with ischemic heart disease, two-dimensional echocardiograms obtained at a rate of 60 frames per second were provided on line for digital subtraction analysis, with which digitized images were continuously subtracted on a frame-by-frame basis. The subtracted images were analyzed to determine the onset of the segmental outward motion of the LV wall in early diastole in each of 16 segments per subject. Regional relaxation index, defined as the interval from the second heart sound to the onset of outward wall motion, was significantly prolonged in the coronary involved segments compared with the normal segments (36.3 +/- 18.0 versus 101.2 +/- 34.0 ms, P < .01). The prolongation in the regional relaxation index was observed even in the coronary involved segments without reduction in systolic wall motion. When a cutoff level of 50.0 ms was used, coronary involved segments could be distinguished from normal or border segments with a sensitivity of 92% and a specificity of 81%. CONCLUSIONS: Digital subtraction high-frame-rate echocardiography may be used to visualize regional LV relaxation abnormalities in patients with ischemic heart disease. The time interval from the second heart sound to the onset of the segmental outward motion of the LV wall (regional relaxation index) obtained with this technique provides a noninvasive and accurate measure for assessing coronary involved regions.

Adult↗
PubMed1999

Left ventricular regional systolic and diastolic function in conscious sheep undergoing ischemic preconditioning.

OBJECTIVE: Late preconditioning diastolic protection and cardiac function optimization by the combined effects of late and early preconditioning have not been studied in conscious animals. This study assessed in fully conscious sheep: (1) whether 24 h after a reversible ischemia, a new ischemic episode results in lesser systo-diastolic dysfunction (late preconditioning protection) and (2) whether the addition of early preconditioning (brief episodes of ischemia-reperfusion before the subsequent sustained ischemia) on the second day of late preconditioning optimized the second window of protection. METHODS: Three protocols were assessed: (a) late preconditioning, 9 min ischemia and 2 h reperfusion was done on two consecutive days; (b) early plus late preconditioning, as in protocol (a) except that on day 2 the heart underwent three periods of 3 min ischemia-6 min reperfusion prior to the sustained 9 min ischemia; (c) early preconditioning, the same protocol as in (b) except that day 2 was separated 1 week from day 1. RESULTS: Late preconditioning decreased regional radial diastolic stiffness from 147 +/- 26% (day 1) to 96 +/- 14% (day 2), at 2 h of reperfusion (mean +/- SEM, p < 0.05), but did not protect against systolic stunning (thickening fraction and regional stroke work). Early plus late preconditioning did not improve late preconditioning findings. Early preconditioning alone did not protect either systolic or diastolic functions. CONCLUSION: In conscious sheep, there is diastolic but not systolic mechanical protection with late preconditioning. Diastolic protection is not enhanced by the addition of early preconditioning.

Animals↗
PubMed1992

Effect of aortic valve stenosis (pressure overload) and regurgitation (volume overload) on left ventricular systolic and diastolic function.

In secondary hypertrophy from chronic pressure or volume overload, or both, systolic as well as diastolic abnormalities of left ventricular (LV) function have been described, but their relation has not been defined. In 58 patients with aortic valve disease (28 with aortic valve stenosis, and 30 with aortic regurgitation) and in 11 control subjects, LV biplane cineangiography was performed simultaneously with LV high-fidelity pressure measurements. LV ejection performance was assessed by ejection fraction, and diastolic function by the time constant of LV pressure decay, the early and late peak filling rates, and the constants of chamber (pressure-volume relation) and myocardial stiffness (stress-strain relation). In the entire cohort (n = 69), ejection fraction was inversely related to the time constant of LV relaxation (r = -0.58, p less than 0.001) and to the constant of myocardial stiffness (r = -0.62, p less than 0.001). Despite preserved systolic contractile function (as evaluated from the ejection fraction-mean systolic stress relation), abnormalities in LV diastolic function were present in 9 of 18 patients with pressure overload and 20 of 22 with volume overload. None of the 58 patients with aortic valve disease had a reduced early peak filling rate, whereas a reduction in late peak filling rate was observed in 3 with aortic stenosis, but in none with aortic regurgitation. This, it appears that abnormalities of relaxation and passive diastolic myocardial stiffness precede alterations in myocardial contractility. Assessment of peak filling rates is not helpful to detect diastolic dysfunction in patients with aortic valve disease.

Adolescent↗
PubMed2005

Vasopeptidase inhibition has beneficial cardiac effects in spontaneously diabetic Goto-Kakizaki rats.

In this study we examined diabetes- and hypertension-induced changes in cardiac structure and function in an animal model of type 2 diabetes, the Goto-Kakizaki (GK) rat. We hypothesized that treatment with omapatrilat, a vasopeptidase inhibitor, which causes simultaneous inhibition of angiotensin converting enzyme and neutral endopeptidase, provides additional cardioprotective effects, during normal- as well as high sodium intake, compared to treatment with enalapril, a selective inhibitor of angiotensin converting enzyme. Fifty-two GK rats were randomized into 6 groups to receive either normal-sodium (NaCl 0.8%) or high-sodium (NaCl 6%) diet and enalapril, omapatrilat or vehicle for 12 weeks. The GK rats developed hypertension, cardiac hypertrophy and overexpression of cardiac natriuretic peptides and profibrotic connective tissue growth factor compared to nondiabetic Wistar rats. The high dietary sodium further increased the systolic blood pressure, and changed the mitral inflow pattern measured by echocardiography towards diastolic dysfunction. Enalapril and omapatrilat equally decreased the systolic blood pressure compared to the control group during normal- as well as high-sodium diet. Both drugs had beneficial cardioprotective effects, which were blunted by the high dietary sodium. Compared to enalapril, omapatrilat reduced the echocardiographically measured left ventricular mass during normal-sodium diet and improved the diastolic function during high-sodium diet in GK rats. Furthermore, omapatrilat reduced relative cardiac weight more effectively than enalapril during high sodium intake. Our results suggest that both the renin-angiotensin and the neutral endopeptidase system are involved in the pathogenesis of diabetic cardiomyopathy since vasopeptidase inhibition was shown to provide additional benefits in comparison with selective angiotensin converting enzyme inhibition alone.

Aldosterone↗
PubMed2004

Impaired up-regulation of CD25 on CD4+ T cells in IFN-gamma knockout mice is associated with progression of myocarditis to heart failure.

Inflammation has been recognized increasingly as a critical pathologic component of a number of heart diseases. A mouse model of autoimmune myocarditis was developed to study the role of immune mediators in the development of cardiac dysfunction. We have found previously that IFN-gamma deficiency promotes inflammation in murine myocarditis. It has been unclear, however, how IFN-gamma deficiency in myocarditis affects cardiac function and what underlying immune mechanisms are responsible for these effects. In this work, we show that IFN-gamma knockout (KO) mice have more pronounced systolic and diastolic dysfunction and greater frequency of progression to dilated cardiomyopathy and heart failure compared with WT mice. Cardiac dysfunction in the KO mice is associated with the expansion of activated (CD44(high)) CD3+ T cells due to reduced apoptosis of CD4+, but not CD8+, T cells. CD4+ T cells in the KO mice show impaired up-regulation of CD25 upon activation, resulting in the expansion of CD4+CD44+CD25- T cells and their infiltration into the heart. CD4+CD25- T cells are less apoptosis-prone compared with the CD25+ population, and their infiltration into the heart is associated with greater severity of myocarditis. We conclude that IFN-gamma deficiency in autoimmune myocarditis is associated with preferential expansion of CD4+CD44+CD25- T cells resulting in increased cardiac inflammation. An exaggerated inflammatory response in IFN-gamma KO mice causes cardiac dysfunction, leading to dilated cardiomyopathy and heart failure.

Animals↗
PubMed1997

Left ventricular function after repeated episodes of ventricular fibrillation and defibrillation assessed by transoesophageal echocardiography.

BACKGROUND: Investigators studying the effects of cardioverter-defibrillators on left ventricular systolic function have given only minor attention to the diastolic effects. OBJECTIVES: The purpose of this study was to investigate the impact of repeated episodes of ventricular fibrillation and defibrillation on systolic function and diastolic filling of the left ventricle during non-thoracotomy implantation of a cardioverter-defibrillator. METHODS: Systolic function and diastolic filling of the left ventricle were assessed peri-operatively on a beat-by-beat basis using a transoesophageal echo-Doppler technique in 12 patients during > or = 4 episodes of ventricular fibrillation and defibrillation. Systolic function was assessed from the fractional area change and diastolic filling from the E/A ratio. Arterial blood pressure and the ECG were recorded continuously. RESULTS: Blood pressure and heart rate did not change significantly throughout the procedure. The systolic function, similarly, was not significantly affected; the only changes were seen in the first two beats after defibrillation when the mean fractional area increased from 0.2 +/- 0.01 to 0.4 +/- 0.02 and 0.3 +/- 0.02, respectively (P < 0.001). Diastolic filling was, however, impaired as reflected by a decrease in the E/A ratio from 2.6 +/- 0.5 before to 1.6 +/- 0.4 (P < 0.01) after repeated threshold tests. CONCLUSIONS: While the combined ischaemic and electrical trauma caused by repeated episodes of ventricular fibrillation and defibrillation during the implantation of a cardioverter-defibrillator did not cause any systolic dysfunction, diastolic filling was significantly impaired.

Adult↗
PubMed2003

Cardiac dysfunction in the Goto-Kakizaki rat. A model of type II diabetes mellitus.

METHODS: Both isolated perfused hearts and isolated ventricular myocytes from GK and matched control Wistar rat hearts were studied. Percent myocyte twitch shortening (%TS) and corresponding intracellular calcium transients (indo-1 fluorescence ratio, R) were measured over a range of stimulation frequencies (0.5-2.5 Hz; 32 degrees C, n = 16-24 cells). In isolated Langendorff-perfused hearts, we measured systolic LV pressure (LVP(max)), left ventricular end diastolic pressure (LVEDP), maximal rate of LV pressure rise (LV dP/dt(max)) and fall (LV dP/dt(min)) and isovolumic LV relaxation (exponential time constant, T) both at baseline and during brief (10 minutes) hypoxia. RESULTS: The %TS and corresponding indo-1 R were similar between GK and control myocytes at all stimulation frequencies (e.g. at 2.5 Hz: % TS = 8.6 +/- 0.77 and 8.2 +/- 0.19; R = 0.19 +/- 0.009 and 0.18 +/- 0.018, GK and control respectively, P = NS). Similarly, there were no significant differences in baseline LVP(max) (129 +/- 6.2 and 135 +/- 9.6 mmHg; GK and control respectively, P = NS), LV dP/dt(max) (3169.5 +/- 165.80 and 3390.6 +/- 232.60 mmHg/s; GK and control respectively, P = NS), LV dP/dt(min) or T (24 +/- 0.7 and 25 +/- 0.6 ms, GK and control respectively, P = NS). During 10 min hypoxia, LV dP/dt(max) decreased significantly more, and LVEDP and T increased significantly more, in GK compared to control hearts (LV dP/dt(max): 668.90 +/- 32.8 versus 1027.10 +/- 84.0 mmHg/s; LVEDP: 21.4 +/- 4.3 versus 11.6 +/- 0.6 mmHg; T: 102 +/- 13.8 versus 56 +/- 3.0 ms; GK versus control respectively; all P < 0.05). These abnormalities in GK hearts were reversed with acute addition of insulin (0.01 i. u./ml) to the perfusion buffer. CONCLUSION: The GK model of Type II diabetes displays a mild cardiomyopathy evident as exaggerated diastolic dysfunction during hypoxia. The mechanism is likely to involve substrate deficiency. Experimental study of cardiac function in the diabetic heart has focussed mostly on models of Type I diabetes. We studied cardiac function in the Goto-Kakizaki (GK) rat, an inbred model of spontaneous non-obese, Type II diabetes.

Animals↗
PubMed1985

Left ventricular filling is usually normal in uncomplicated coronary disease.

Abnormalities in left ventricular filling have been described as an early finding in coronary artery disease (CAD) and more recently, in hypertension (HTN). The present study was undertaken to compare the prevalence and pattern of diastolic dysfunction in these two entities. Three groups of patients were studied: 10 normal volunteers (NLS), 39 HTN patients, and 30 CAD patients. The CAD patients were divided into two subgroups--one with normal ejection fraction (mean 0.60 +/- 0.06) and the second with either a depressed ejection fraction (EF) or a history of HTN (mean EF 0.44 +/- 0.15). The diastolic indices examined were peak filling rate (PFR, in end-diastolic volume [EDV]/sec), time to peak filling rate (TPFR, in msec), and first-third filling fraction (FF 1/3, in sec-1). The PFR in CAD and HTN was significantly reduced (1.86 +/- 0.63 and 2.29 +/- 0.49 vs 2.70 +/- 0.35 EDV/sec in NLS, p less than 0.025 and p less than 0.001, respectively), with the CAD group also being significantly lower than the HTN group (p less than 0.005). TPFR was prolonged in HTN, but not in CAD. FF 1/3 was reduced in both HTN and CAD (0.38 +/- 0.11 and 0.50 +/- 0.14 vs 0.61 +/- 0.06 sec-1 in NLS, p less than 0.001 and p less than 0.025, respectively), but it was significantly lower in HTN than in CAD (p less than 0.001). However, when the subgroup of CAD patients with normal global systolic function was examined separately, diastolic indices were only slightly depressed. More importantly, only one, two, and five patients had PFR, TPFR, and FF 1/3, respectively, which were below the normal values of our laboratory.

Adult↗
PubMedDate not supplied

Acute ventricular reduction with the acorn cardiac support device: effect on progressive left ventricular dysfunction and dilation in dogs with chronic heart failure.

BACKGROUND AND AIM: Surgical resection of myocardium that acutely reduces left ventricular (LV) volume in patients with advanced heart failure (HF), the so-called "Batista Operation," remains controversial. We examined the effects of acute LV reduction with the Acorn Cardiac Support Device (CSD) in dogs with HF (LV ejection fraction < 30%). METHODS: HF was produced in 15 dogs by intracoronary microembolization. In nine dogs, intravenous dobutamine was administered to reduce LV end-diastolic dimension (LVEDD) by 10%-25%. While on dobutamine infusion, the CSD, a preformed knitted polyester device, was surgically placed around the ventricles, anchored to the arteriovenous (AV) groove, and tailored anteriorly to fit snugly over the ventricles. Dogs were then weaned off dobutamine. RESULTS: On average, the procedure reduced LVEDD by 7 +/- 1 mm (range 5-12 mm). Of the nine dogs, two died before completion of the study and seven survived for the entire period. Six dogs did not undergo device placement and served as controls. All were followed for 3 months prior to sacrifice. In controls, LV end-diastolic volume increased after 3 months (66 +/- 5 mL vs 77 +/- 6 mL; p = 0.007), while in CSD-treated dogs (n = 7), it decreased (80 +/- 5 mL vs 60 +/- 3 mL; p = 0.002). In controls, LV ejection fraction (EF) decreased after 3 months (27 +/- 1% vs 23 +/- 1%; p = 0.001) but was unchanged in CSD-treated dogs (25 +/- 1% vs 26 +/- 1%; p = 0.66). Compared to controls, CSD-treated dogs showed improved LV diastolic dysfunction and chamber sphericity, decreased wall stress, and no functional mitral regurgitation (MR). CONCLUSION: In dogs with advanced HF, acute LV reduction with the Acorn CSD prevents progressive global LV dilatation and ameliorates functional MR.

Acute Disease↗
PubMed2003

Biochemical, histological and echocardiographic changes during experimental cardiomyopathy in STZ-induced diabetic rats.

Diabetes mellitus is associated with an increased susceptibility to cardiovascular disease and it has been suggested that alterations in myocardial function may contribute to the development of diabetic cardiovascular complications. The objective of the present study is to examine the left ventricular (LV) function in streptozotocin (STZ)-induced diabetic rats in a definite course of time by non-invasive methods, i.e. M-mode and Doppler echocardiography. From the results, it was found that treatment of animals with STZ resulted in increase in blood glucose, triglycerides, cholesterol, low density lipoproteins (LDL) and decrease in serum total protein levels. Echocardiographic studies revealed that LV internal dimension (mm) during systole was significantly increased after 12 weeks of diabetes when compared to base line data of the same animals and with control animals 6.50+/-0.13 versus 4.25+/-0.17, versus 4.34+/-0.25 (P<0.05), however there was no significant change after 4-8 weeks of diabetes. Also LV internal dimension (mm) during end diastole increased significantly only after 12 weeks of diabetes than to base line data of the same animals and with control animals 7.71+/-0.34 versus 6.18+/-0.25, versus 6.25+/-0.18 (P<0.05). Fractional shortening (%), 15.69+/-5.1 versus 31.22+/-1.7, versus 30.56+/-2.1 (P<0.05), and ejection fraction (%) 37+/-2.31 versus 68.18+/-2.8, versus 60.32+/-3.5 (P<0.05), differ significantly after 12 weeks of diabetes when compared to base line data of the same animals and with control animals. E-wave (cm/s) was significantly decreased after 12 weeks of diabetes 21.11+/-1.5 versus 35.19+/-4.5, versus 32.75+/-3.0 (P<0.05), and A-wave (cm/s) was significantly increased after 12 weeks of diabetes 34.88+/-4.2 versus 19.21+/-2.8, versus 20.59+/-2.1 (P<0.05); thus, diabetic animals after 12 weeks had an inversed E/A ratio. Histological studies revealed that after 8 weeks of diabetes, necrosis was minimal, but after 12 weeks of diabetes extensive focal endomyocardial necrosis was observed. From this study, we conclude that overt LV systolic and diastolic dysfunction was fully visible at 12 weeks of diabetes on echocardiography and this non-invasive technique of echocardiography is useful in diagnosing LV dysfunction in diabetic rats without the need of invasive histopathological procedures.

Animals↗
PubMed2001

Brain natriuretic peptide blood levels in the differential diagnosis of dyspnea.

STUDY OBJECTIVES: In dyspneic patients without left ventricular enlargement, it may be difficult to differentiate between obstructive lung disease and diastolic heart failure. Determination of plasma brain natriuretic peptide (BNP) levels, known to increase with ventricular stretch, may be of clinical relevance in this situation. We compared the discriminant power of BNP blood levels and of echocardiography in patients with either chronic obstructive lung disease or diastolic heart failure. PATIENTS: Twenty-six New York Heart Association class III dyspneic patients with normal left ventricular systolic function were enrolled: 17 patients with chronic obstructive lung disease and 9 patients with unequivocal diastolic heart failure. RESULTS: Echocardiographic data were unable to accurately differentiate between the two groups, whereas BNP levels were significantly and markedly higher in patients with diastolic heart failure when compared to those with obstructive lung disease (224 +/- 240 pg/mL vs 14 +/- 12 pg/mL, p < 0.0001). CONCLUSIONS: These preliminary results warrant a prospective, large-scale evaluation of the value of BNP assay for determining diastolic dysfunction, a common cause of dyspnea in elderly patients, and differentiating it from other diagnoses such as obstructive lung disease.

Aged↗
PubMed2005

Pioglitazone improves left ventricular diastolic function in patients with essential hypertension.

BACKGROUND: Left ventricular (LV) hypertrophy and diastolic dysfunction, which are common cardiac consequences of hypertension, are modified by insulin resistance. The present study assessed the hypothesis that primary treatment of insulin resistance may reverse such cardiac changes in hypertensive patients. METHODS: A total of 30 patients with essential hypertension were enrolled in this study. In echocardiographic examinations, LV mass index, the peak velocity ratio of early diastolic to atrial filling (E/A), and the E-wave deceleration time (DcT) were determined. Insulin sensitivity test with steady-state plasma glucose (SSPG) method, oral glucose tolerance test, and blood samplings for measurement of adiponectin and matrix metalloproteinase (MMP)-2 were also performed. Six months after treatment with pioglitazone (30 mg/day), an insulin sensitizer, these examinations were repeated. RESULTS: Pioglitazone significantly increased E/A and decreased DcT, without a change in LV mass index. These improvements in diastolic properties were much greater in subjects with a marked (>or==3.3 mmol/L) decrease in SSPG (n=11) than the others (n=19), although the decrease in glucose levels did not differ between the two groups. In addition, the changes in E/A and DcT were closely correlated with the decrease in SSPG. Pioglitazone treatment significantly elevated plasma adiponectin and MMP-2 levels, and the increase in MMP-2 was positively correlated with the increase in adiponectin. CONCLUSIONS: The present findings demonstrate that pioglitazone improves LV diastolic function without LV mass regression in hypertensive patients in proportion to the amelioration of insulin resistance. These findings suggest that increased adiponectin and MMP may be involved in the beneficial effect of pioglitazone on diastolic function.

Adiponectin↗
PubMed2003

Angiotensin II type 1 receptor blockade prevents diastolic heart failure through modulation of Ca(2+) regulatory proteins and extracellular matrix.

BACKGROUND: Angiotensin II type 1 receptor (AT(1)R) blockade attenuates left ventricular relaxation abnormality and myocardial stiffening in a model of hypertensive diastolic heart failure, but the mechanisms remain unclear. OBJECTIVE: To test the hypothesis that such benefits are provided by modulation of the quantitative or qualitative changes, or both, in Ca2+ regulatory proteins and extracellular matrix. DESIGN AND METHODS: Dahl salt-sensitive rats fed a diet containing 8% sodium chloride from 7 weeks of age present pulmonary congestion as a result of diastolic dysfunction with preserved systolic function, around 20 weeks of age. In this study, animals of this model were divided into groups that received (n = 7) or did not receive (n = 6) a subdepressor dose of an AT(1)R antagonist (candesartan cilexetil) from 8 weeks of age. RESULTS: Long-term AT(1)R blockade prevented the development of diastolic heart failure through attenuation of left ventricular relaxation abnormality and myocardial stiffening without a reduction in blood pressure. Left ventricular relaxation abnormality was not associated with any change in the ratio of abundance of phospholamban to that of sarcoplasmic reticulum Ca2+-ATPase 2a protein, but was accompanied by a decrease in Ser16-phosphorylated phospholamban. The AT(1)R blockade inhibited this decrease. Attenuation in myocardial stiffening was associated with reduced tissue collagen content, attenuated collagen cross-linking, and suppressed gene expression of collagen type I rather than type III. CONCLUSIONS: AT(1)R blockade prevented abnormal relaxation at least partly through functional alterations in Ca2+-handling proteins in a hypertensive model of diastolic heart failure. It attenuated myocardial stiffening through preventing a shift in the phenotype of collagen synthesized and the accumulation of cross-linked collagen. These beneficial effects of AT(1)R blockade in diastolic heart failure are achieved without a reduction in blood pressure.

Angiotensin Receptor Antagonists↗
PubMed1998

Optimizing the hemodynamic performance of the DDD pacemaker: impact of the atrioventricular delay on the pulmonary venous flow pattern.

UNLABELLED: This study evaluated the impact of the atrioventricular delay (AVD) on the pulmonary venous flow pattern (PVFP). METHODS: Transthoracic Doppler PVFP were obtained during atrial and ventricular pacing at a fixed rate of 70 beats/min in 20 patients equipped with a DDD pacemaker, diastolic dysfunction linked to an impaired relaxation, a mean ejection fraction of 49%, and AV block. Two subgroups were analyzed equally: group I: seven patients with a normal ejection fraction and group II: 13 patients with decreased ejection fraction. Three different AVDs were studied: short (50 ms), intermediate (150 ms), and long (250 ms). RESULTS: As the AVD increased, the diastolic filling time and the peak atrial reverse flow wave decreased (P < 0.001). There was a decreasing D wave and no significant change in the peak velocity of the S wave. The S wave became biphasic in all patients at the longest AVD of 250 ms. The systolic (S) velocity time integral (VTI) of the pulmonary wave and the systolic/total PVF-VTI ratio increased significantly (P < 0.001). A similar response was seen in both group of patients. CONCLUSIONS: These data correlated the AVD with PVFP, supplying critical systolic information completing the diastolic data obtained from mitral Doppler patterns. These systolic measurements were especially useful for patients with heart failure and a DDD pacemaker, in order to obtain the longest diastolic filling time at the lowest atrial pressure.

Aged↗
PubMed2005

[Assessment of left ventricular systolic and diastolic function by Doppler tissue imaging in patients with chronic heart failure].

OBJECTIVE: To investigate the application of pulsed-wave Doppler tissue imaging ( PW-DTI) in evaluating left ventricular systolic and diastolic function in patients with chronic heart failure (CHF). METHODS: Mitral annular velocities (MAV) were measured by PW-DTI in 35 patients with CHF and 25 healthy subjects. Traditional indices for evaluating the global left ventricular function by conventional echocardiography were also studied as a comparison. RESULTS: Peak systolic, peak early diastolic, peak late diastolic mitral annular velocities ( Sa, Ea, Aa), and Ea/Aa ratio progressively decreased in CHF patients compared with the healthy subjects (P <0.01 ). Sa of the mitral annulus correlated linearly with the left ventricle ejection fraction (LVEF) (r =0.890, P < 0.01). Compared with the healthy subjects, Ea in all 3 subgroups of diastolic dysfunction in the CHF group significantly decreased (P <0.01). Aa in 2 subgroups (pseudonormal filling and restrictive filling) decreased (P < 0.01 ) and the decreased Ea/Aa was found in the delayed relaxation and pseudonormal filling subgroups compared with the healthy subjects (P<0.001). CONCLUSION: MAV measured by PW-DTI can be used for assessing the left ventricular systolic and diastolic function in CHF patients.

Diastole↗
PubMed1996

Antihypertensive treatment in hypertensive patients with normal left ventricular mass is associated with left ventricular remodeling and improved diastolic function.

Antihypertensive therapy in hypertensive patients with left ventricular (LV) hypertrophy causes hypertrophy regression and improved diastolic filling. Whether similar changes occur in hypertensive patients with diastolic dysfunction and no hypertrophy is unknown. We determined the effect of antihypertensive therapy of LV geometry and function in hypertensive patients without hypertrophy. In 18 mild to moderate hypertensive patients without significant hypertrophy, baseline echocardiograms and rest and exercise and radionuclide angiograms were performed. Subjects were treated for 8 to 12 months with the calcium channel blocker felodipine and then restudied 2 weeks after treatment withdrawal. Blood pressure normalized with treatment (165 +/- 22/98 +/- 9 to 128 +/- 12/80 +/- 5 mm Hg, p <0.001) and returned to pretreatment levels after therapy withdrawal. Rest ejection fraction and peak oxygen consumption and cardiac outputs were unchanged after treatment, but rest peak filling rate increased (2.63 +/- 0.57 to 3.11 +/- 0.95 end-diastolic volume/second, p <0.05). Ejection fraction increased with exercise only after treatment (64 +/- 5% at rest to 71 +/- 8% at peak exercise, p <0.05). LV mass index was unchanged (97 +/- 18 to 101 +/- 23 g/m2), but relative wall thickness declined (0.41 +/- 0.05 to 0.37 +/- 0.05) and LV end-diastolic dimension increased (4.9 +/- 0.4 to 5.2 +/- 0.4, p = 0.01). Blood pressures control in hypertensive patients without hypertrophy leads to improved peak filling rates and remodeling with decreased relative wall thickness. Improved diastolic function can occur without alterations in LV mass.

Antihypertensive Agents↗