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PubMed2001

[Diastolic dysfunction in human immunodeficiency virus infection].

AIMS: We sought to determine the prevalence and characteristics of echocardiographic abnormalities (systolic and/or diastolic dysfunction, pericardial effusion) in patients with human immunodeficiency virus infection (HIV) with no symptoms or previous history of cardiac disease, and compare them with a healthy control group. PATIENTS AND METHOD: Transthoracic echocardiography was performed in 125 patients (73% male, mean age 33.2 +/- 6.6 years) with HIV infection without cardiac involvement and 47 age and sex-matched healthy volunteers (78% male, 31.6 +/- 7.3 years). The immunologic situation was determined by CD4 lymphocyte counts. RESULTS: Abnormal left ventricular relaxation and filling patterns (E/A relation 1.31 +/- 0.35 in HIV group, 1.66 +/- 0.38 in control group, p < 0.001; pressure half-time 57.5 +/- 13 in HIV group, 50.6 +/- 6.6 in control group, p < 0.001), segmental wall-motion abnormalities (15%) and pericardial effusion (7.2%) were found in patients with HIV infection. Systolic function (EF 64.8 +/- 8.3) and left ventricular dimension (diastolic diameter 4.94 +/- 0.55, systolic diameter 3.17 +/- 0.51) showed normal patterns and did not significantly differ from those of the control group. CONCLUSIONS: Silent echocardiographic abnormalities in patients with HIV infection are frequent suggesting a direct myocardial effect of the virus. The development of diastolic dysfunction is directly related to a worse immunologic situation. Prospective studies are needed to clarify the clinical prognosis of these asymptomatic abnormalities.

Adult↗
PubMed1993

Reversal of diastolic dysfunction by intravenous magnesium chloride.

OBJECTIVE: To treat diastolic dysfunction in patients with coronary artery disease (CAD). DESIGN: Open study of the intravenous injection of 5 mL of a solution containing 17% magnesium chloride (equal to 100 mg of elemental magnesium) during routine coronary angiography in patients with a raised left ventricular end-diastolic pressure (LVEDP). SETTING: A hospital department of cardiac hemodynamics. SUBJECTS: Ten patients with angiographically documented CAD. RESULTS: After magnesium chloride injection, the LVEDP was significantly reduced in all patients, from a mean of 24 +/- 3 to 16 +/- 3 mmHg (P < 0.001). CONCLUSIONS: Under the short term conditions of the study, the injection of magnesium chloride effectively improved left ventricular diastolic function. Further study of the long term effect is required.

Aged↗
PubMed2004

Diastolic dysfunction: can it be diagnosed by Doppler echocardiography?

Heart failure with a normal ejection fraction (HFNEF) predominantly afflicts older, female individuals and is considered to be a consequence of diastolic dysfunction. Doppler echocardiography has become the standard method for identifying and characterizing diastolic function. However, the important distinction between Doppler measures of filling dynamics and true indexes of intrinsic ventricular diastolic chamber properties is not widely appreciated. Herein, we delineate physiologic measures of intrinsic ventricular diastolic function, as determined by pressure volume analysis, and compare and contrast these measures with those derived from Doppler echocardiography. Doppler-derived indexes of ventricular filling do not provide specific information on intrinsic passive diastolic properties, and thus, abnormal filling dynamics do not necessarily equate with intrinsic myocardial diastolic dysfunction. This raises a fundamental question as to whether delayed relaxation and/or stiffened passive properties are the unifying pathophysiologic mechanisms in all patients who present with HFNEF.

Aged↗
PubMed2003

The assessment of mitral inflow propagation velocity in the diagnosis of advanced left ventricular diastolic dysfunction.

BACKGROUND: The echocardiographic assessment of left ventricular diastolic function is usually based on mitral inflow parameters. The main limitation of this method is caused by pseudonormalisation of mitral inflow profile in advanced stages of diastolic dysfunction. AIM: To evaluate the value of propagation velocity (Vp) of early and atrial mitral inflow wave in the diagnosis of pseudonormalisation. METHODS: We examined 180 subjects (104 males, mean age 58+/-11) by transthoracic echocardiography with the assessment of propagation velocity in colour-M-mode. The studied group consisted of 120 patients with coronary artery disease and 60 healthy controls. The values of E/A (ratio of early to atrial mitral inflow peak velocity) were calculated and subjects with normal (early wave deceleration time, Edt > or =150 ms) and pseudonormal (Edt <150 ms) mitral inflow patterns were identified. Propagation velocities were compared between groups with normal and pseudonormal mitral inflow profiles and optimal cut-off values were estimated. RESULTS: In the pseudonormal group, velocities of early and atrial propagation were significantly lower than those in the normal group: 25+/-11 vs 46+/-8 cm/s (p<0.001) and 33+/-10 vs 43+/-11 cm/s, (p<0.01), respectively. Both parameters showed the same optimal cut-off value for the diagnosis of pseudonormalisation which was < or =31 cm/s. Sensitivity, specificity and accuracy for the detection of pseudonormal mitral inflow pattern for early wave propagation were 87, 96 and 94%, and for atrial wave propagation - 60, 83 and 78%, respectively. CONCLUSIONS: Decreased value of mitral inflow early wave propagation velocity offers high sensitivity and specificity for the diagnosis of mitral inflow pseudonormalisation. Atrial wave propagation velocity has also potential value for advanced quantitative assessment of diastolic function.

Aged↗
PubMed1985

Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia.

Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1996

Diastolic dysfunction and natriuretic peptides in systolic heart failure. Higher ANP and BNP levels are associated with the restrictive filling pattern.

BACKGROUND: Left ventricular diastolic dysfunction is common in patients with systolic heart failure and the restrictive type of filling pattern appears to be associated with increased cardiac mortality. Both artrial and brain (or ventricular) natriuretic peptides are also proven markers of the severity of heart failure. The aim of this study was to determine in a large cohort of patients with systolic heart failure whether diastolic abnormalities, and in particular the restrictive filling pattern of transmitral flow velocity, correlate with plasma atrial and brain natriuretic peptide levels. METHODS: Sixty-eight consecutive patients with symptomatic systolic heart failure (ejection fraction < 0.5) underwent two-dimensional Doppler echocardiography of left ventricular systolic and diastolic function, together with measurement of atrial and brain natriuretic peptides. RESULTS: The restrictive filling pattern was present in 62%, the abnormal relaxation pattern in 31% and only 7% were normal. Atrial and brain natriuretic peptide (ANP/BNP) levels were significantly higher in the restrictive compared to the abnormal relaxation group (ANP: 202.2 +/- 31.7 vs 102.5 +/- 22.1 pg.ml-1, P = 0.012; BNP: 277.8 +/- 27.7 vs 162.4 +/- 21.9 pg.ml-1, P = 0.002). In addition, a restrictive filling pattern was associated with lower ejection fractions (P = 0.026), higher pulmonary artery systolic pressure (P < 0.001), larger left atrial size (P = 0.044), and were more likely to be in New York Heart Association class III or IV than those with an abnormal relaxation pattern (P = 0.007). Both atrial and brain natriuretic peptides correlated inversely with ejection fraction (P < 0.001), fractional shortening (P < 0.001), and positively with pulmonary artery pressure (P = 0.004 and 0.001 respectively). There were no significant correlations between single diastolic parameters and atrial or brain natriuretic peptide levels for the total patient group except between mitral peak A wave velocity and brain natriuretic peptides (r = -0.3, P = 0.01). For those with abnormal relaxation pattern mitral, valve E-wave deceleration time correlated significantly with both atrial and brain natriuretic peptide levels (P < 0.01). CONCLUSIONS: This study confirms that the restrictive filling pattern of transmitral flow velocity is a marker of more severe heart failure, as indicated by its association with higher atrial and brain natriuretic peptide levels, lower ejection fraction and higher pulmonary artery pressure. Thus, this easily obtained Doppler-derived marker of diastolic dysfunction is useful for identifying those patients with more severe heart failure.

Aged↗
PubMed2002

Left ventricular diastolic dysfunction as a predictor of the first diagnosed nonvalvular atrial fibrillation in 840 elderly men and women.

OBJECTIVES: The objective of this study was to determine whether diastolic dysfunction is associated with increased risk of nonvalvular atrial fibrillation (NVAF) in older adults with no history of atrial arrhythmia. BACKGROUND: Few data exist regarding the relationship between diastolic function and NVAF. METHODS: The clinical and echocardiographic characteristics of patients age > or =65 years who had an echocardiogram performed between 1990 and 1998 were reviewed. Exclusion criteria were history of atrial arrhythmia, stroke, valvular or congenital heart disease, or pacemaker implantation. Patients were followed up in their medical records to the last clinical visit or death for documentation of first AF. RESULTS: Of 840 patients (39% men; mean [+/- SD] age, 75 +/- 7 years), 80 (9.5%) developed NVAF over a mean (+/- SD) follow-up of 4.1 +/- 2.7 years. Abnormal relaxation, pseudonormal, and restrictive left ventricular diastolic filling were associated with hazard ratios of 3.33 (95% confidence interval [CI], 1.5 to 7.4; p = 0.003), 4.84 (95% CI, 2.05 to 11.4; p < 0.001), and 5.26 (95% CI, 2.3 to 12.03; p < 0.001), respectively, when compared with normal diastolic function. After a number of adjustments, diastolic function profile remained incremental to history of congestive heart failure and previous myocardial infarction for prediction of NVAF. Age-adjusted Kaplan-Meier five-year risks of NVAF were 1%, 12%, 14%, and 21% for normal, abnormal relaxation, pseudonormal, and restrictive diastolic filling, respectively. CONCLUSIONS; The presence and severity of diastolic dysfunction are independently predictive of first documented NVAF in the elderly.

Age Factors↗
PubMed1999

Losartan improves diastolic ventricular filling of hypertensive patients with diastolic dysfunction.

To evaluate the role of losartan on left ventricular (LV) function of hypertensive patients. Hypertensive patients (n = 19) underwent evaluation of systolic and diastolic LV function, using radionuclide ventriculography (RVG), before and at 3 mo into the treatment with the angiotensin II antagonist losartan. All patients underwent a baseline 12 lead ECG and an echocardiogram (ECHO), which was also repeated at 3 mo into treatment. Results are expressed as mean +/- SEM and statistics were performed using paired t-test. A p value < or = 0.05 was considered significant. Treatment with losartan for 3 mo had no effect on LV mass measured by echo (141+/-5 vs. 139+/-6 g/m2). The LV ejection fraction, measured by RVG, was unchanged by treatment when compared to the baseline study (58+/-2% vs. 57+/-2%, respectivelly, p = 0.49). Considering all patients involved in the study (n = 19), the LV "Peak Filling Rate" (PFR), a parameter of diastolic function measured by RVG, was also unchanged by treatment when compared to baseline (2.5+/-0.2 EDV/s vs. 2.5+/-0.3 EDV/s, respectively, p = 0.9). However the analysis of those patients with evidence of diastolic dysfunction (n = 12) on the baseline RVG (PFR < 2.5 EVD/s), demonstrated significant improvement of LV filling after therapy with losartan (PFR = 1.8+/-0.1 EDV/s vs. 2.3 +/-0.2 EDV/s, respectively, p = 0.05). This change was associated with improvement of symptoms. Our results demonstrated that hypertensive patients with diastolic dysfunction on radionuclide ventriculography have significant improvement of ventricular filling at 3 mo into treatment with losartan.

Adult↗
PubMed1996

Effect of sublingual nifedipine on left ventricular diastolic dysfunction in hypertensives: echo-Doppler study at rest and during handgrip.

Using digitized M-mode echocardiography, we evaluated the acute effect of nifedipine on left ventricular (LV) diastolic dysfunction in 30 untreated hypertensives, evaluated at rest and during handgrip, both before and 30' after nifedipine (20 mg sublingually). At rest, after nifedipine blood pressure and end-systolic wall stress significantly decreased and peak lengthening rate of LV diameter, peak thinning rate of LV posterior wall and Doppler E/A ratio increased. Before and after nifedipine handgrip induced significant increases of blood pressure, heart rate and end-systolic wall stress; diastolic parameters significantly decreased during basal handgrip and did not change during handgrip after nifedipine. Nifedipine induced an acute improvement of LV diastolic dysfunction, that persisted when afterload increased during handgrip. Therefore nifedipine seems to improve LV diastolic function not only by reducing afterload, but also through a direct action on the myocardium. Besides, these results demonstrate that LV diastolic abnormalities in hypertension are partly dynamic and reversible.

Administration, Sublingual↗
PubMed1999

[Hypertensive heart disease with left ventricular diastolic dysfunction demonstrating restrictive hemodynamics: a case report].

A 47-year-old man with hypertensive heart disease and left heart failure due to left ventricular diastolic dysfunction was admitted to our hospital because of emergent hypertension. Chest radiography on admission showed slight cardiomegaly and mild pulmonary congestion with right pleural effusion Echocardiography showed concentric hypertrophy and normal contraction of the left ventricular wall Pulsed Doppler left ventricular inflow velocity wave and pulmonary venous flow velocity wave disclosed restrictive filling patterns. After Ca antagonist, nitrate, and diuretics were administered, blood pressure was normalized, and left ventricular inflow velocity wave showed the relaxation abnormality pattern and pulmonary venous flow velocity wave showed the normal pattern. Radioiodinated iodine-123 metaiodobenzyl guanidine (123I-MIBG) imaging in the state of normalized blood pressure showed decreased heart to mediastinum ratio and increased washout rate. Left heart catheterization and angiography revealed normal end-diastolic pressure and coronary arteries, but coronary flow reserve evaluated with Doppler flow wire and intracoronary adenosine triphosphate administration was impaired: Plasma level of atrial and brain natriuretic peptides, which were markedly elevated on admission, decreased with the improvement of heart failure. Doppler flow velocity patterns, plasma levels of atrial natriuretic peptide and brain natriuretic peptide, cardiac sympathetic nerve activity, and coronary flow reserve might be useful for evaluating the severity of left ventricular diastolic dysfunction in patients with hypertensive heart disease.

Atrial Natriuretic Factor↗
PubMed2001

Mitral regurgitation and left ventricular diastolic dysfunction similarly affect mitral and pulmonary vein flow Doppler parameters: the advantage of end-diastolic markers.

Enhanced early mitral flow and reduced systolic pulmonary vein flow may be caused both by increased left ventricular pressure as the result of diastolic dysfunction and by increased transmitral flow as the result of mitral regurgitation. Nevertheless, Doppler parameters are widely used to predict left ventricular filling pressure. We aimed to analyze the interference of mitral regurgitation with Doppler parameters usually used to estimate left ventricular filling pressure and to identify markers independent of mitral regurgitation, which could reliably estimate increased left ventricular filling pressure. Eighty-four patients (age, 62 +/- 9 years; 82% men) had a complete echocardiographic Doppler examination. Transmitral E- and A-wave velocity, E deceleration time and A duration, pulmonary vein systolic and diastolic velocities, and reversal flow duration and maximal and minimal left atrial volumes were measured. The difference between the duration of pulmonary vein and mitral A waves was calculated (A'-A). Mitral regurgitant volume was quantitatively assessed by echocardiography. Left ventricular end-diastolic pressure was measured invasively. Patients had a wide range of left ventricular ejection fraction (14% to 70%), mitral regurgitant volume (0 to 94 mL), and left ventricular end-diastolic pressure (3 to 37 mm Hg). E velocity, E/A, pulmonary vein systolic and diastolic, and systo-diastolic ratios were significantly and independently correlated with both left ventricular end-diastolic pressure and mitral regurgitant volume. A'-A showed a strong correlation with left ventricular end-diastolic pressure (r = 0.70; P <.0001), but the relation with mitral regurgitant volume was not significant (r = 0.19; P =.08). Mitral regurgitation affects the majority of Doppler parameters widely used to predict filling pressure but does not influence Ad'-Ad, which proved to be the strongest predictor of left ventricular end-diastolic pressure.

Aged↗
PubMed2000

Diastolic dysfunction as a cause of exercise intolerance.

Tachycardia accompanying exercise shortens the duration of diastole, reducing the time available for the left ventricular (LV) filling. Thus, the LV must fill more rapidly for the stroke volume to increase (or even be maintained) during exercise. Normally, this is accomplished without requiring an excessive increase in left atrial (LA) pressure by an acceleration of LV relaxation and a fall in LV early diastolic pressure during exercise. This response is lost following the development of heart failure due to systolic dysfunction, both in experimental animals and in patients. In fact, in such situations, LV relaxation slows and LV early diastolic pressure increases due to exercise. Thus, any diastolic dysfunction present at rest in CHF during systolic dysfunction is exacerbated during exercise. Similarly, patients with primary diastolic dysfunction heart failure with preserved systolic function may not be able to augment LV filling rates without an abnormal increase in LA pressure. Thus, diastolic dysfunction may contribute to exercise intolerance, both in systolic dysfunction and primary diastolic dysfunction. Acute studies suggest that treatment with angiotensin II receptor blockers or verapamil may improve exercise tolerance in some patients with primary diastolic dysfunction.

Animals↗
PubMed1992

Effects of progressive myocardial ischaemia on systolic function, diastolic dysfunction, and load dependent relaxation.

OBJECTIVE: The aims were to determine (1) the relationship between changes in contractile function (systolic shortening) and the appearance of diastolic dysfunction (postsystolic shortening) during progressive regional left ventricular ischaemia; (2) the effects of increased afterload (acute constriction of the descending thoracic aorta) on ischaemic contractile dysfunction; and (3) the effects of loading during ischaemia on load dependent relaxation. METHODS: Regional myocardial function, using sonomicrometry, was measured in the short and long axes of the apex of the left ventricle of eight open chest anaesthetised dogs (16-20 kg). Progressive apical ischaemia was induced by graded reductions in left anterior descending coronary artery flow (critical constriction, ischaemia 1, ischaemia 2, total coronary occlusion, and postocclusive maximum reactive hyperaemia). Acute afterloading was induced by a snare placed around the descending aorta. RESULTS: Consistent decreases in systolic shortening and increases in postsystolic shortening relative to the total segmental shortening in the short axis of the apical region were seen with worsening ischaemia. Aortic constriction increased the magnitude of apical postsystolic shortening and decreased apical systolic shortening in the short axis during critical constriction, ischaemia 1, and ischaemia 2. Long axis function changed in a qualitatively similar but quantitatively different manner. There was a significant decrease in the load dependency of relaxation with total coronary occlusion. CONCLUSIONS: (1) Changes in systolic and diastolic function occurred concomitantly as mild regional myocardial ischaemia developed and intensified; (2) afterloading significantly worsened regional systolic and diastolic dysfunction during mild ischaemia; and (3) progression of regional ischaemia resulted in loss of load dependent relaxation.

Animals↗
PubMed2005

Intravenous milrinone infusion improves congestive heart failure caused by diastolic dysfunction: a brief case series.

Although there have been significant advances in the medical treatment of heart failure patients with impaired systolic function, very little is known about the diagnosis and treatment of diastolic dysfunction. We report the cases of 3 patients in New York Heart Association functional class IV who had echocardiographically documented diastolic dysfunction as the main cause of heart failure. All 3 patients received medical therapy with long-term milrinone infusion.

Adult↗
PubMed2002

Elevated serum uric acid levels are associated with diastolic dysfunction in patients with dilated cardiomyopathy.

OBJECTIVE: To assess whether serum uric acid, which is a marker of impaired oxidative metabolism, might correlate with left ventricular systolic and diastolic dysfunction in patients with chronic heart failure (CHF). BACKGROUND: Uric acid levels, which are frequently elevated in patients with CHF, correlate with leg vascular resistance. The effects of elevated levels of uric acid on cardiac function in patients with CHF have never been evaluated. METHODS: We studied 150 outpatients with CHF who came to our heart failure clinic. Patients underwent a complete echo-Doppler examination, with measurement of mitral E wave and mitral A wave velocities, E/A ratio, E wave deceleration time (DtE), left ventricular volumes, ejection fraction, and stroke volume. A restrictive mitral filling pattern (RMFP) was defined as either E/A ratio >2 or E/A >1 and DtE <140 milliseconds. RESULTS: Mean age was 62.2 +/- 7.8 years (86% male); 24 patients (16%) had an RMFP. Patients with an RMFP had significantly higher uric acid levels compared with patients without RMFP (0.48 +/- 0.14 mmol/L vs 0.38 +/- 0.08 mmol/L, respectively, P <.001). Uric acid levels correlated significantly with mitral E wave velocity (r =.22, P <.01), E/A ratio (r =.21, P <.05), DtE (r =.26, P <.01), and RMFP (P =.0001). There was no correlation between uric acid and left ventricular volumes, ejection fraction, or stroke volume. In a multivariate model, uric acid predicted DtE independently of renal function, diuretic dose, and left ventricular volumes. CONCLUSION: Elevated uric acid levels are associated with diastolic dysfunction in CHF. Xanthine oxydase inhibition in patients with CHF might theoretically result in an improvement of diastolic function.

Aged↗
PubMed1998

Treatment of diastolic dysfunction in hypertensive patients without left ventricular hypertrophy.

The aim of this study was to evaluate the influence of verapamil SR 240 mg (V) and the combination amiloride 5 mg + hydrochlorothiazide 50 mg (AH) on diastolic dysfunction of hypertensive patients without left ventricular hypertrophy (LVH). Twenty-six hypertensive patients with diastolic dysfunction, normal systolic function and without LVH were included into a 2-week washout period and then randomised to a 6-month V or AH treatment. One blinded-to-treatment echocardiographist at baseline and at weeks 4, 12 and 24 assessed Doppler-echocardiography. Both V and AH, satisfactorily controlled blood pressure, but only V improved diastolic function shown by a tendency to reduce peak A and to increase peak E/A ratio, and by a significant reduction in deceleration time. After 24 weeks, V significantly reduced wall thickness in comparison with AH. These results need to be confirmed in a larger scale study.

Adult↗
PubMed2003

[Effect of manshuailing oral liquid on left ventricular diastolic dysfunction in patients with heart disease of Xin-Shen Yang deficiency type].

OBJECTIVE: To investigate the effect of Manshuailing Oral Liquid (MSL) on left ventricular diastolic dysfunction (LVDD) in patients with heart disease. METHODS: Ninety patients with LVDD were randomly divided into the conventional treated group (Group A, treated by conventional treatment with western drugs of cardiotonic, diuretic, coronary dilator, etc.) and the Chinese drug treated group (Group B, treated by conventional treatment plus MSL 2 times a day, 100 ml each time), 45 in each group. After 4 months treatment, the total heart failure coefficient (HFC) and cardiac functions were re-determined. RESULTS: After treatment, in both groups, the HFC lowered significantly (P < 0.05 or P < 0.01), the left ventricular peak velocity of early diastolic rapid filling (Emas) quickened, the left atrial systolic peak velocity (Amas) slowed down and Emas/Amas (E/A) enhanced, the isovolumetric relaxation time shortened. However, comparison between the two groups showed significant difference (P < 0.05) in either item, Group B was superior to Group A (P < 0.05). In the 62 patients with mixed heart failure, i.e. both systolic and diastolic dysfunction of left ventricle, Group B was superior to Group A in increasing ejection fraction, cardiac output and thickening rate of left ventricular posterior wall (P < 0.05). CONCLUSION: MSL could improve the heart function of patients with LVDD, and alleviate their clinical symptoms.

Aged↗
PubMed2006

Effect of losartan and hydrochlorothiazide on exercise tolerance in exertional hypertension and left ventricular diastolic dysfunction.

A randomized, double-blind study of 6 months of losartan 50 mg or hydrochlorothiazide (HCTZ) 12.5 mg was performed in 40 subjects with left ventricular diastolic dysfunction (mitral flow velocity E/A ratio < 1), exercise systolic blood pressure (BP) > 200 mm Hg, systolic BP at rest < 150 mm Hg, ejection fraction > 50%, and no ischemia. Before treatment, exercise systolic BP was 213 +/- 13 mm Hg (mean +/- SD) in the 19 patients randomized to losartan and 209 +/- 11 mm Hg in the 21 patients who received HCTZ. After 6 months, exercise systolic BP was similarly reduced in patients who received losartan (197 +/- 23 mm Hg, p < 0.01) and HCTZ (191 +/- 11 mm Hg, p < 0.01). With losartan, treadmill exercise time increased from 894 +/- 216 to 951 +/- 225 seconds (p = 0.011), and quality of life improved from 15 +/- 12 to 7 +/- 10 (p = 0.015) without a change in oxygen consumption (1,895 +/- 470 to 1,954 +/- 539 ml/min, p = 0.30). With HCTZ, exercise time (842 +/- 225 to 872 +/- 239 seconds, p = 0.32) and quality of life (19 +/- 21 vs 19 +/- 24, p = 0.43) did not change, whereas oxygen consumption decreased from 2,144 +/- 788 to 1,960 +/- 706 ml/min (p = 0.022). In conclusion, in patients with diastolic dysfunction and hypertensive responses to exercise, 6 months of losartan and HCTZ blunted systolic BP during exercise. Only losartan increased exercise tolerance and improved quality of life.

Antihypertensive Agents↗