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PubMed1989

Effects of calcium antagonists on hypertension and diastolic function.

Calcium antagonists are known to decrease blood pressure acutely and chronically in hypertensive patients with hypertensive heart disease, and also to improve their systolic function. However, disorders of diastolic function may occur early in hypertensive heart disease. The improvement of diastolic function by nifedipine and diltiazem is described, although it was difficult to exclude systolic unloading as a cause of the improvement. It is emphasised that diastolic dysfunction can exist in hypertensive heart disease, and that the calcium antagonists nifedipine and diltiazem can improve diastolic dysfunction.

Blood Pressure↗
PubMed2005

Diastolic function abnormalities in active rheumatoid arthritis evaluation by conventional Doppler and tissue Doppler: relation with duration of disease.

OBJECTIVE: The aim of this study was to evaluate left ventricular diastolic function in patients with active rheumatoid arthritis (RA), analyzing conventional Doppler and tissue Doppler echocardiographic imaging (TDI) which is a new echocardiographic application, with special regard to disease duration. METHODS: Fifty-two patients with active RA and 47 healthy persons were included in this study. Duration of disease ranged from 3 to 324 months (mean 76+/-85 months). All patients and the control group were evaluated by M-mod, two-dimensional, conventional Doppler echocardiography and TDI. RESULTS: Among conventional Doppler transvalvular mitral flow parameters, late diastolic flow velocity (A) and deceleration time (DT) values were higher in patients with RA than that in the control group (p<0.001). E (early diastolic flow velocity)/A ratio was found to be lower in patients with RA than that in the control group (p<0.001). Mitral annular early diastolic velocity (E (m)), among TDI parameters, was found to be lower in patients with RA than that in the control group (p<0.001). E (m)/A (m) (mitral annular late diastolic velocity) ratio was found to be lower in RA patients compared with that in the control group (p<0.001). The relation was found between A (r=0.43, p=0.001), DT (r=0.30, p=0.03), E/A ratio (r=0.40, p=0.004), E (m) (r=0.32, p=0.02), E (m)/A (m) ratio (r=0.30, p=0.03), and E/E (m) (r=0.32, p=0.02), with disease duration in patients with RA. CONCLUSION: At present, it is concluded that active RA patients, in the absence of clinical evidence of heart disease, show diastolic dysfunction characterized by impaired E/A ratio, E (m)/A (m) ratio, and DT. The relation between diastolic dysfunction and disease duration suggests a subclinical myocardial involvement.

Arthritis, Rheumatoid↗
PubMed2002

Hyperhomocysteinemia leads to adverse cardiac remodeling in hypertensive rats.

Hyperhomocysteinemia (Hhe), linked to cardiovascular disease by epidemiological studies, may be an important factor in adverse cardiac remodeling in hypertension. Specifically, convergence of myocardial and vascular alterations promoted by Hhe and hypertension may exacerbate cardiac remodeling and myocardial dysfunction. We studied male spontaneously hypertensive rats fed one of three diets: control, intermediate Hhe inducing, or severe Hhe inducing. After 10 wk of dietary intervention, cardiac function was assessed in vitro, and cardiac and coronary arteriolar remodeling were monitored by histomorphometric, immunohistochemical, and biochemical techniques. Results showed that Hhe induced diastolic dysfunction, as characterized by the diastolic pressure-volume curve, without significant changes in baseline systolic function. Perivascular collagen levels were increased by Hhe, and there was an increase in left ventricular hydroxyproline levels. Myocyte size was not affected. Coronary arteriolar wall thickness increased with Hhe due to smooth muscle hyperplasia. Mast cells increased in parallel with Hhe and collagen accumulation. In summary, 10 wk of Hhe caused coronary arteriolar remodeling, myocardial collagen deposition, and diastolic dysfunction in hypertensive rats.

Animals↗
PubMed2005

Role of angiotensin II in the evolution of diastolic heart failure.

More than half of all persons with heart failure (HF) have diastolic HF. The prevalence of diastolic HF increases from 46% in persons younger than 45 years to 59% in those 85 years and older. The annual mortality rate associated with diastolic HF is >10%. Diagnosis is based on signs and symptoms of HF, elevated plasma B-type natriuretic peptide, preserved left ventricular systolic function, and evidence of diastolic dysfunction by Doppler examination on two-dimensional echocardiography. Approximately 80% of patients with diastolic HF have increased left ventricular mass and a history of hypertension. Neurohormonal activation is a key aspect of this condition. Studies suggest that activation of the renin-angiotensin-aldosterone system, specifically direct cardiac effects of angiotensin II and aldosterone, contributes to the pathogenesis and progression of diastolic dysfunction. Hence, there is a rationale for use of agents that antagonize the renin-angiotensin-aldosterone system, such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists, in patients with heart failure.

Angiotensin II↗
PubMed2001

Dobutamine-stress magnetic resonance microimaging in mice : acute changes of cardiac geometry and function in normal and failing murine hearts.

The aim of this study was to assess the capability of MRI to characterize systolic and diastolic function in normal and chronically failing mouse hearts in vivo at rest and during inotropic stimulation. Applying an ECG-gated FLASH-cine sequence, MRI at 7 T was performed at rest and after administration of 1.5 microgram/g IP dobutamine. There was a significant increase of heart rate, cardiac output, and ejection fraction and significant decrease of end-diastolic and end-systolic left ventricular (LV) volumes (P<0.01 each) in normal mice during inotropic stimulation. In mice with heart failure due to chronic myocardial infarction (MI), MRI at rest revealed gross LV dilatation. There was a significant decrease of LV ejection fraction in infarcted mice (29%) versus sham mice (58%). Mice with MI showed a significantly reduced maximum LV ejection rate (P<0.001) and LV filling rate (P<0.01) and no increase of LV dynamics during dobutamine action, indicating loss of contractile and relaxation reserve. In 4-month-old transgenic mice with cardiospecific overexpression of the beta(1)-adrenergic receptor, which at this early stage do not show abnormalities of resting cardiac function, LV filling rate failed to increase after dobutamine stress (transgenic, 0.19+/-0.03 microL/ms; wild type, 0.36+/-0.01 microL/ms; P<0.01). Thus, MRI unmasked diastolic dysfunction during dobutamine stress. Dobutamine-stress MRI allows noninvasive assessment of systolic and diastolic components of heart failure. This study shows that MRI can demonstrate loss of inotropic and lusitropic response in mice with MI and can unmask diastolic dysfunction as an early sign of cardiac dysfunction in a transgenic mouse model of heart failure.

Adrenergic beta-Agonists↗
PubMed1999

Optimal control of blood pressure can reverse left ventricular hypertrophy in uremic hypertensive hemodialysis patients.

We investigated the effects of antihypertensive treatment on left ventricular hypertrophy (LVH) of long-term hemodialysis patients. In uremic patients, it is still controversial in antihypertensive effect to the regression of LVH. The left ventricular size and function of 39 uremic hypertensive long-term hemodialysis patients (27 men, 12 women, mean age 58.3) was evaluated with M-mode, 2-dimensional and Doppler echocardiography before, and 12 months after, the start of combined antihypertensive therapy. This therapy included angiotensin II converting enzyme inhibitors, beta-blockers and calcium antagonists. Patients were classified as responders or nonresponders, depending upon whether their systolic blood pressure (SBP) decreased by more than 10 mmHg after antihypertensive treatment for 12 months. Before treatment, 36 (92%) patients had LVH and diastolic dysfunction and three (8%) had systolic dysfunction. At the end of 12 months, only 25 (64%) patients had LVH, 30 (77%) had diastolic dysfunction and 2 (5%) had systolic dysfunction. Left ventricular mass index (LVMI) also decreased from 203.63 +/- 70.47 g/m2 to 178.57 +/- 67.31 g/m2. LVMI correlated with systolic blood pressure (SBP) but did not correlate with diastolic blood pressure (DBP). There were 26 responders and 13 non-responders. Among responders, both the SBP (153.91 +/- 13.24 mmHg vs 134.43 +/- 14.21 mmHg, p < 0.01) and DBP (90.39 +/- 7.89 mmHg vs 79.98 +/- 7.35 mmHg, p < 0.01) decreased significantly after antihypertensive therapy. Responders also exhibited progressive regression of LVH (LVMI decreased significantly from 208.52 +/- 72.03 g/m2 to 168.52 +/- 55.53 g/m2, p < 0.05). However, LVH regression was not found in nonresponders (LVMI showed 194.84 +/- 64.36 g/m2 vs 193.66 +/- 77.67 g/m2). We conclude that good control of blood pressure can reverse LVH in hypertensive hemodialysis patients.

Adult↗
PubMed2003

Diastolic mitral annular velocity during the development of heart failure.

OBJECTIVES: We sought to investigate the mechanism of reduced diastolic mitral annular velocity with diastolic dysfunction, despite elevated left atrial (LA) pressure. BACKGROUND: The peak rate of left ventricular (LV) early diastolic filling (E) and velocity of the mitral annulus due to long-axis lengthening (E(M)) are reduced in mild diastolic dysfunction. With more severe dysfunction, E increases in response to increased LA pressures. In contrast, E(M) decreases, despite increased LA pressure. METHODS: We studied eight dogs instrumented to measure LA pressure, LV pressure, and internal dimensions during the progressive development of heart failure (HF) produced by rapid pacing. RESULTS: Early diastolic filling decreased after four days of pacing from 114 +/- 32 to 88 +/- 22 ml/s (p < 0.05), but with more severe HF, it progressively increased to 155 +/- 32 ml/s (p < 0.05). In contrast, E(M) progressively decreased from 44 +/- 12 mm/s during the control period to 24 +/- 8 mm/s after four weeks (p < 0.05). Although E(M) was related to the time constant of LV relaxation (tau) (R(2) = 0.85), E was not. The latter occurred coincident with termination of the early diastolic LA to LV pressure gradient during all conditions. In contrast, with increasing HF, E(M) was progressively delayed after LA to LV pressure crossover by 37 +/- 12 ms (p < 0.05). The time from E to E(M) was related to tau (R(2) = 0.97). CONCLUSIONS: With slowed relaxation during the development of HF, E(M) is reduced and delayed so that it occurs after early, rapid filling. Thus, with slowed relaxation, E(M) does not respond to the early diastolic LA to LV pressure gradient, because it occurs when LV pressure is greater than or equal to LA pressure.

Animals↗
PubMed2000

Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease.

BACKGROUND: In arterial hypertension, left ventricular hypertrophy (LVH) includes myocyte hypertrophy and fibrosis, which leads to LV diastolic dysfunction and, finally, heart failure. In spontaneously hypertensive rats, myocardial fibrosis was regressed and LV diastolic function was improved by treatment with the angiotensin-converting enzyme inhibitor lisinopril. Whether this holds true for patients with hypertensive heart disease was addressed in this prospective, randomized, double-blind trial. METHODS AND RESULTS: A total of 35 patients with primary hypertension, LVH, and LV diastolic dysfunction were treated with either lisinopril (n=18) or hydrochlorothiazide (HCTZ; n=17). At baseline and after 6 months, LV catheterization with endomyocardial biopsy, Doppler echocardiography with measurements of LV peak flow velocities during early filling and atrial contraction and isovolumic relaxation time, and 24-hour blood pressure monitoring were performed. Myocardial fibrosis was measured by LV collagen volume fraction and myocardial hydroxyproline concentration. With lisinopril, collagen volume fraction decreased from 6.9+/-0.6% to 6. 3+/-0.6% (P:<0.05 versus HCTZ) and myocardial hydroxyproline concentration from 9.9+/-0.3 to 8.3+/-0.4 microg/mg of LV dry weight (P:<0.00001 versus HCTZ); this was associated with an increase in the early filling and atrial contraction LV peak flow velocity ratio from 0.72+/-0.04 to 0.91+/-0.06 (P:<0.05 versus HCTZ) and a decrease in isovolumic relaxation time from 123+/-9 to 81+/-5 ms (P:<0.00002 versus HCTZ). Normalized blood pressure did not significantly change in either group. No LVH regression occurred in lisinopril-treated patients, whereas with HCTZ, myocyte diameter was reduced from 22. 1+/-0.6 to 20.7+/-0.7 microm (P:<0.01 versus lisinopril). CONCLUSIONS: In patients with hypertensive heart disease, angiotensin-converting enzyme inhibition with lisinopril can regress myocardial fibrosis, irrespective of LVH regression, and it is accompanied by improved LV diastolic function.

Adolescent↗
PubMed2000

[Usefulness of Doppler echocardiography in patients with ischemic cerebrovascular disease].

We carried out transthoracic Doppler echocardiography on 213 patients with ischemic cerebrovascular disease to examine cardiac functions. The prevalence of valvular regurgitation, left ventricular diastolic function (E/A ratio), and ejection fraction (EF) of each patient were studied by transthoracic Doppler echocardiography. In patients with embolic strokes, the prevalence of valvular regurgitation of the left ventricular system such as mitral regurgitation was significantly higher than that of normal controls. In contrast, there was no significant difference in the prevalence of valvular regurgitation in the right ventricular system. Although there was no significant difference in the ejection fraction between groups, the E/A ratio in patients with ischemic cerebrovascular disease showed a significantly lower value than that in normal controls. Patients with ischemic cerebrovascular disease showed a tendency to have an atherosclerotic change in the systemic arteries including cerebral and coronary arteries, reflecting an aggravation of cardiac wall compliance and diastolic dysfunction resulting in lowering of the E/A ratio. Thus, transthoracic Doppler echocardiography was useful to evaluate cardiac diastolic dysfunction and valvular regurgitation in patients with ischemic cerebrovascular disease.

Acute Disease↗
PubMed2004

Norepinephrine-induced acute heart failure in transgenic mice overexpressing erythropoietin.

OBJECTIVE: Overexpression of erythropoietin (Epo) in mice (Epo-tg6) leads to an increase in hematocrit and blood volume, and strongly reduces endurance upon exercise. It was the aim of this study to characterize the mechanisms underlying the reduced cardiac performance. METHODS: Left (LV) and right (RV) ventricular function was measured with and without norepinephrine (NE) stimulation in 12 anaesthetized Epo-tg6 and in 13 wild-type (WT) control mice. RESULTS: There were no differences in heart function under baseline resting conditions. Stimulation with NE (10 microl bolus injections of 1-100 ng per mouse) in WT mice led to a dose-dependent increase in heart rate (HR), LV developed pressure (LVDP) and rate of rise in LV pressure (LV dP/dt(max)), while LV end-diastolic pressure (LVEDP) was unchanged. Except for HR, these parameters increased to a lesser extent in EPO-tg6 mice. Strikingly, LVEDP strongly increased in Epo-tg6 mice after NE (up to >20 mmHg). Eleven out of 13 Epo-tg6, but none of the WT mice died or required resuscitation after high-doses of NE. In these cases severe diastolic dysfunction became overt since the relative myocardial relaxation time was significantly prolonged and the duration of diastole was shortened. Moreover, the ECG showed a marked ST segment depression as well as deep negative T-waves. The NE-induced reduction in myocardial adenosin-triphosphate (ATP) content was more pronounced in Epo-tg6 mice after 10 min of continuous NE infusion (50 ng/min per mouse). CONCLUSION: NE-induced stress in Epo-tg6 mice led to acute heart failure associated with diastolic dysfunction and myocardial ischemia.

Acute Disease↗
PubMed1994

Increased left ventricular diastolic chamber stiffness immediately after coronary artery bypass surgery.

OBJECTIVES: The aim of this study was to assess the incidence and severity of left ventricular diastolic dysfunction immediately after coronary artery bypass surgery by utilizing simultaneous transesophageal echocardiographic and hemodynamic monitoring. BACKGROUND: Left ventricular diastolic dysfunction has been documented after coronary bypass surgery, but its measurement has been technically difficult to acquire and limited by dependence on loading conditions. METHODS: End-diastolic pressure-area curves were constructed before and immediately after coronary bypass surgery in 20 patients. Transesophageal echocardiographic images at the midpapillary level of the left ventricle and hemodynamic data were recorded. Volume status was manipulated to alter loading conditions, and multiple measurements were taken at each loading condition. RESULTS: Diastolic function worsened in all patients, as manifested by a postoperative leftward shift of the end-diastolic pressure-area curve. At a comparable preload, mean end-diastolic area +/- SEM decreased by 15% from 17.6 +/- 0.8 to 14.9 +/- 0.8 cm2 postoperatively (p = 0.0001). CONCLUSIONS: Left ventricular diastolic chamber stiffness frequently increases immediately after coronary artery bypass surgery. Simultaneous hemodynamic and transesophageal echocardiographic monitoring, through the construction of end-diastolic pressure-area curves, is a useful method to evaluate diastolic function and guide management after cardiac surgery.

Aged↗
PubMed2004

Effect of a cardiac rehabilitation program on left ventricular diastolic function and its relationship to exercise capacity in patients with coronary heart disease: experience from a randomized, controlled study.

BACKGROUND: A cardiac rehabilitation and prevention program (CRPP) is a recognized nonpharmacological modality in the management of coronary heart disease (CHD). However, the effect of a CRPP on systolic function of the heart is controversial, and no data exists on diastolic function in CHD. A randomized, controlled study was conducted to address these issues. METHODS: Patients (n = 269) with recent acute myocardial infarction (n = 193) or after percutaneous coronary intervention (PCI) (n = 76) were randomized to either CRPP (2-hour twice-weekly exercise program for 8 weeks) or conventional therapy (control group). Serial treadmill exercise testing and at-rest echocardiography were performed during phases 1 (baseline), 2 (post-exercise training), and 3 (8-month follow up). RESULTS: The prevalence of left ventricular (LV) abnormal relaxation pattern (ARP) of diastolic dysfunction was increased in the control group only in phase 3 (65% vs 88%, chi2 = 7.6, P <.01). Significant improvement of individual LV diastolic parameters towards less severe delayed relaxation was also observed in the CRPP group, especially in those with recent acute myocardial infarction or ARP. The gain in exercise capacity was faster and more substantial in the CRPP than the control group (P <.001 for phase 2, P <.05 for phase 3), and was significantly correlated with LV diastolic indices in those with ARP. Exercise training had neutral effects on LV systolic function and rate-pressure product. CONCLUSIONS: In patients with CHD, CRPP prevented the progression of resting LV diastolic dysfunction, without affecting systolic function. In those with ARP, the improvement of diastolic function predicted the gain in exercise capacity.

Adult↗
PubMedDate not supplied

B-type natriuretic peptide testing for detection of heart failure.

The incidence of heart failure (HF) is on the increase with the aging population. Heart failure can manifest as either systolic or diastolic dysfunction. Systolic dysfunction causes impaired ventricular contractility with an ejection fraction of less than 45%. In contrast, diastolic dysfunction is evidenced by impaired ventricular relaxation and an ejection fraction greater than 45%. The diagnosis of HF is challenging with patients who present with acute dyspnea and a history of chronic obstructive pulmonary disease or pneumonia. The pathophysiology of HF and the resulting compensatory mechanisms involve a complex neuroendocrine response that includes a release of natriuretic peptides including B-type natriuretic peptides (BNPs). Elevation of BNP is in response to ventricular wall stress and volume overload from HF. BNP promotes natriuresis, diuresis, and vasodilitation and therefore counteracts some of the deleterious effects of the neuroendocrine response in HF Recently, a new laboratory test for BNP has been developed to assist in rapid identification of patients with HF. Research studies have shown that BNP testing assists in differentiating between cardiac and pulmonary causes of acute dyspnea and could be used to evaluate effectiveness of therapy and as a predictor for length of stay and readmission.

Atrial Natriuretic Factor↗
PubMed2006

Metalloproteinase inhibitor counters high-energy phosphate depletion and AMP deaminase activity enhancing ventricular diastolic compliance in subacute heart failure.

Cardiac matrix metalloproteinases (MMPs) stimulated by the sympathomimetic action of angiotensin II (AII) exacerbate chamber diastolic stiffening in models of subacute heart failure. Here we tested the hypothesis that MMP inhibition prevents such stiffening by favorably modulating high-energy phosphate (HEP) stores more than by effects on matrix remodeling. Dogs were administered AII i.v. for 1 week with tachypacing superimposed in the last two days (AII+P; n = 8). A second group (n = 9) underwent the same AII+P protocol but was preceded by oral treatment with an MMP inhibitor PD166793 [(S)-2-(4-bromo-biphenyl-4-sulfonylamino-3-methyl butyric acid] 1 week before and during the AII+P period. Pressure-volume analysis was performed in conscious animals, and myocardial tissue was subjected to in vitro and in situ zymography, collagen content, and HEP analysis (high-performance liquid chromatography). As reported previously, AII+P activated MMP9 and MMP2 and specifically exacerbated diastolic stiffening (+130% in chamber stiffness). PD166793 cotreatment prevented these changes, although myocardial collagen content, subtype, and cross-linking were unaltered. AII+P also reduced ATP, free energy of ATP hydrolysis (DeltaG(ATP)), and phosphocreatine while increasing free [ADP], AMP catabolites (nucleoside-total purines), and lactate. PD166793 reversed most of these changes, in part due to its inhibition of AMP deaminase. MMP activation may influence cardiac diastolic function by mechanisms beyond modulation of extracellular matrix. Interaction between MMP activation and HEP metabolism may play an important role in mediating diastolic dysfunction. Furthermore, these data highlight a potential major role for increased AMP deaminase activity in diastolic dysfunction.

AMP Deaminase↗
PubMed1996

The Effects of Amlodipine on Left Ventricular Mass and Diastolic Function in Concentric and Eccentric Left Ventricular Hypertrophy.

BACKGROUND: The effects of the antihypertensive therapy with amlodipine (5-10 mg/day) on left ventricular mass and diastolic function were examined in 30 mild to moderate essential hypertensive patients who have left ventricular hypertrophy (LVH) and diastolic dysfunction. METHODS AND RESULTS: Each patient's left ventricular mass was measured, and left ventricular diastolic function was assessed by echocardiographic Doppler examination at entry, and at 3 and 6 months after the initiation of the treatment. Amlodipine reduced both blood pressure (from 164 +/- 14/104 +/- 6 mmHg to 134 +/- 9/83 +/- 4 mmHg) and left ventricular mass index (from 160 +/- 30 g/m(2) to 137 +/- 26 g/m(2)) significantly at 3 months and both parameters maintained at these levels for 6 months. When the patients were classified according to the type of the LVH, a significant regression in left ventricular mass index was seen only in the patients who had concentric LVH was a relative wall thickness >/=0.44 (n = 16), but not in the eccentric LVH group (n = 14), although both groups were not significantly different from each other regarding the basal hemodynamic parameters, baseline left ventricular mass index and the decrease in blood pressure in response to amlodipine treatment. The mitral inflow E/A ratio did not show any significant change in either group. CONCLUSIONS: Amlodipine produced significant regression in LVH only in the patients with concentric LVH, but not those with eccentric LVH, while it did not change the diastolic dysfunction. Therefore, the type of LVH seems to be an important feature in determining the effects of antihypertensive treatment on left ventricular mass index.

Journal Article↗
PubMed1988

Noninvasive follow-up study in hypertrophic obstructive cardiomyopathy.

The clinical course of hypertrophic cardiomyopathy with left ventricular outflow obstruction showed a symptomatic progression in 25% of patients, independent of the of degree of left ventricular obstruction. Echocardiographic and mechanocardiographic examinations showed a close relationship between severity of asymmetric ventricular hypertrophy and diastolic failure. During the follow-up septal hypertrophy became more severe without left ventricular dilatation. Global diastolic function deteriorated and the left atrium dilated. The probability of survival was 67.2%. Our data suggest that septum hypertrophy and diastolic dysfunction are progressive in HOCM. The mortality is independent of the severity of hypertrophy and diastolic dysfunction, and shows a close correlation with arrhythmias.

Adult↗
PubMedDate not supplied

Transthoracic Doppler assessment of pattern of left ventricular dysfunction in hypertensive heart disease: combined analysis of mitral and pulmonary venous flow velocity patterns.

Although mitral flow velocity pattern changes with the progression of left ventricular (LV) diastolic dysfunction, it lacks predictive value in individual patients because of pseudonormalization in the presence of congestive heart failure and many physiologic and pathologic contributors to the mitral flow velocity pattern. To determine whether analysis of pulmonary venous flow velocity patterns complements the information obtainable from the mitral flow velocity patterns in the evaluation of patterns of LV dysfunction of hypertensive heart disease in individual patients, the ratio of the peak early diastolic filling velocity/peak filling velocity at atrial contraction (E/A ratio) in the mitral flow velocity pattern and the ratio of the peak systolic forward flow velocity (S)/peak diastolic forward flow velocity (D) (S/D ratio) in the pulmonary venous flow velocity pattern by the transthoracic approach were determined in 107 hypertensive patients with and without congestive heart failure. Age-related normal values of the E/A and S/D ratios were determined in 61 normal subjects and used to judge the normality or abnormality of the patterns. Results of the study indicate that (1) although an increased mitral E/A ratio is strongly indicative of heart failure with normal LV systolic function, the mitral E/A ratio is frequently within the normal range in hypertensive patients with heart failure; (2) association of decreased pulmonary venous S/D ratios with a normal mitral flow velocity pattern indicates the presence of heart failure as a result of LV systolic dysfunction that is usually observed at the most advanced pattern of LV dysfunction; (3) mild LV diastolic dysfunction is likely to exist in patients with normal E/A ratios if the pulmonary venous S/D ratio is higher than normal value; (4) predictive accuracy in the detection of LV systolic and diastolic dysfunction would be improved if both mitral and pulmonary venous flow velocity patterns rather than the mitral flow velocity pattern alone were analyzed. In conclusion, analysis of pulmonary venous flow velocity recordings improves accuracy and reliability of the Doppler assessment of LV systolic and diastolic dysfunction, particularly in individual hypertensive patients with normal mitral flow velocity patterns.

Adult↗
PubMed2005

[Experiences with serum BNP (B type natriuretic peptide) in patients with systolic and diastolic heart failure].

Current study confirms and extends recent observations concerning the diagnostic usefulness of B type natriuretic peptide. It discriminates well between dyspnea of cardiac and non-cardiac origin in the unselected population. Echocardiography represents useful diagnostic tool for assessment of systolic and diastolic ventricular function. In diastolic heart failure the elasticity of left chamber decreases due to the increase of the filling pressure. B type natriuretic peptide predominantly derived from the atrial tissue in patients with chronic heart failure. In the literature contradictory data has been found about serum B type natriuretic peptide level and diastolic dysfunction in cases with good left ventricular function. Authors reviewed 35-34 unselected patients with chronic systolic and isolated diastolic dysfunction. The serum B type natriuretic peptide level increased significantly in all the systolic heart failure patients, while, in patients with isolated diastolic heart failure the values were increased only cases with increased atrial value (calculated to the body surface).

Adult↗