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PubMedDate not supplied

[Clinical aspects of the left ventricular diastolic dysfunction at patients with coronary heart disease].

UNLABELLED: Is is known that, besides the systolic disfunction, the presence of diastolic disfunction influences the prognosis of patients with coronary heart disease. The aim of the paper is to study the influence of the presence of diastolic disfunction upon the clinical profile and the functional capacity of the patients with coronary heart disease. METHODS: 189 patients with ischemic heart disease (chronic myocardial infarction, stable angina, ischemic cardiomiopathy) underwent an echocardiographic examination. The diastolic disfunction was assessed at the Doppler examination, by the the ratio of the E and A velocities. Consequently, 138 patients had a E/A ratio under 1 or above 2 and were considered with diastolic disfunction (group A); the other 47 with E/A ratio between 1-2 were included in group B. After the clinical evaluation, 80 patients underwent an exercise testing (47 of group A and 33 of group B). RESULTS: Group A had a greater mean age (62.8 +/- 11.7 vs 51.5 +/- 11.6 years, p = 0.00006) and more females (72.5% vs 46.8%, p = 0.001); dyspnoea was more frequent and severe (NYHA II-IV), the arterial pressure higher (146/85 +/- 25/13 mmHg vs 136/79 +/- 26/15 mmHg, p = 0.004) and cardiac rate higher (82 +/- 18 vs 69 +/- 11/min, p = 0.0003). The echocardiographic assessment revealed a more severe systolic disfunction and a lower ejection fraction (50.3 +/- 10.6% vs 55.7 +/- 10.6%, p = 0.003). At the exercise testing, the maximum level and the duration of exercise were lower at group A than group B (5.41 +/- 2.07 MET vs 7.23 +/- 2.78 MET, p = 0.001 respectively 8.4 +/- 4.5 min vs 11.4 +/- 4.9 min, p = 0.01). CONCLUSIONS: The presence of diastolic disfunction is higher at older patients and at those with associated arterial hypertension. Dyspnoea correlates with the presence and severity of diastolic disfunction and the exercise capacity is lower at these patients.

Aged↗
PubMed1993

Left ventricular diastolic dysfunction late after coarctation repair in childhood: influence of left ventricular hypertrophy.

OBJECTIVES: Left ventricular systolic and diastolic function were evaluated late after successful operation for aortic coarctation in childhood. BACKGROUND: Persistent arterial hypertension and left ventricular hypertrophy after coarctation repair might impair left ventricular function. METHODS: Biplane angiography and simultaneous high fidelity pressure measurements were performed in 12 patients 3 to 12 years postoperatively (residual pressure gradient 4 mm Hg). Eight patients were normotensive and four had borderline hypertension. Data at rest and after nitroprusside infusion (1.7 micrograms/kg per min) were evaluated and compared with data from 12 control subjects. RESULTS: Systolic left ventricular function (ejection fraction-end-systolic wall stress relation) was normal in all patients. However, left ventricular muscle mass (113 vs. 86 g/m2), right atrial pressure (5.2 vs. 1.9 mm Hg) and left ventricular end-diastolic pressure (16 vs. 11 mm Hg) were significantly higher in patients than in control subjects. There was a linear relation between muscle mass and left ventricular end-diastolic (r = 0.66, p < 0.001) or right atrial (r = 0.60, p < 0.01) pressure. Left ventricular relaxation and myocardial stiffness were normal. However, there was an upward shift of the diastolic pressure-volume curve when compared with control values, but this shift was reversed by the administration of nitroprusside. CONCLUSIONS: Systolic function is normal late after coarctation repair. However, diastolic function can be abnormal with an upward shift of the diastolic pressure-volume curve that is reversed by nitroprusside administration and is probably due to residual left ventricular hypertrophy.

Adolescent↗
PubMed1993

Functional and organic components of diastolic dysfunction in hypertensive heart disease: therapeutic implications.

The major structural and functional determinants of impaired left ventricular diastolic function in the hypertensive patient are reviewed, together with the indices normally used to detect this failure. The alteration of functional determinants can be quickly modified, while structural determinants are modified only over the long term. Drug therapy first affects the functional determinants, bringing about their attenuation and initiating the modification of the structural factors, thus accounting for the improvement in diastolic function over the long term.

Cardiomegaly↗
PubMed1998

Contribution of abnormal sarcoplasmic reticulum ATPase activity to systolic and diastolic dysfunction in human heart failure.

Two of the most significant characteristics of failing human myocardium are an increased diastolic [Ca2+]i and a prolonged diastolic relaxation. These abnormalities are more pronounced at higher frequencies of stimulation and may be caused by an altered Ca2+ resequestration into the sarcoplasmic reticulum (SR). The force-frequency relationship was determined in multicellular preparations obtained from non-failing (n=6) and failing human myocardium (n=11). The active force in non-failing tissue increased as a function of the frequency of stimulation. In failing myocardium, an increase in frequency of stimulation (>1 Hz) was accompanied by a decrease in active force. Changes in the frequency of stimulation and active force were also associated with changes in intracellular calcium concentrations. The diastolic force in failing myocardium was augmented following an increase in frequency of stimulation, whereas in non-failing tissue, no increase in diastolic force was observed. Associated with the increase in diastolic force was an increase in intracellular diastolic calcium concentrations. The SR Ca2+ ATPase activity was reduced in failing compared to non-failing myocardium. SR Ca2+ ATPase was positively correlated with diastolic force in non-failing myocardium. The relationship between Ca2+ ATPase activity at 1 micromol/l [Ca2+] and active force between 0.5 and 2.0 Hz was different between failing and non-failing myocardium. The diastolic force demonstrate an inverse relationship with the SR Ca2+ ATPase activity in failing myocardium. These data suggest that a reduction in SR Ca2+ ATPase activity contributes to the impairment in both systolic and diastolic function of failing human hearts.

Adenosine Triphosphatases↗
PubMed1994

Post-ischemic diastolic dysfunction.

Though a sustained post-ischemic decrease in contractile function has been clearly established, post-ischemic diastolic function has not been thoroughly investigated. Accordingly, 11 anesthetized (isoflurane 1%) open-chest beagles were instrumented to measure left ventricular pressure and dimensions (circumferential length and wall thickness) in an apicoanterior area supplied by the left anterior descending coronary artery (LAD). Pressure-dimension relations were modified by stepwise infusion and withdrawal of 200 mL of the animals' own blood during baseline, 45 minutes partial occlusion of the LAD (systolic bulging), and 60 minutes after the onset of reperfusion. Stiffness constants were derived from the end-diastolic pressure-length and stress-strain relations, respectively. Myocardial ischemia was associated with significant (P < 0.05) alterations of the following parameters of diastolic function: (1) 47% increase in end-diastolic pressure; (2) 22% decrease in peak negative dP/dt; (3) 9% increase in the time constant of isovolumic relaxation (tau); (4) postcystolic contraction; (5) 6% increase in end-diastolic length and 10% decrease in end-diastolic thickness; (6) 12% increase in unstressed length (creep) and 13% decrease in unstressed thickness; (7) 51% increase in chamber stiffness and a 63% increase in myocardial stiffness; and (8) 40% decrease in the peak lengthening rate. After 60 minutes of reperfusion, only end-diastolic pressure and tau had returned to baseline values whereas systolic shortening fraction, postsystolic contraction, and end-diastolic and unstressed dimensions had only partially recovered. No recovery occurred in peak negative dP/dt, chamber stiffness, myocardial stiffness, and peak lengthening rate. Thus, both myocardial ischemia and reperfusion are associated with complex changes in global and regional left ventricular diastolic function.

Anesthesia, Inhalation↗
PubMed1994

Dopamine-dependent diastolic dysfunction in moderate hypothermia.

We designed an experimental animal study to study the effects of dopamine (DA) on diastolic function in hypothermia. DA was applied at five incremental infusion rates in 6 sheep during normothermia and moderate hypothermia (29 degrees C). Left ventricular end-diastolic pressure (LVEDP) was increased during hypothermia as compared with normothermia at all doses of DA. Contraction and relaxation velocity were changed only slightly during hypothermia; during normothermia, both velocities were markedly increased. The pronounced hemodynamic effect observed during hypothermia was further intensified by occurrence of aftercontractions, which disappeared at very high DA doses. These paradoxic results were considered the result of hypothermia-induced reduction in active transport mechanisms responsible for regulation of the cytoplasmic CA2+ concentration. The generally reduced inotropic effect of DA, the risk of paradoxic reactions, and the occurrence of aftercontractions must be taken into account when emergency drugs are administered clinically during hypothermia.

Animals↗
PubMed1998

Effects of Metformin on Collagen Glycation and Diastolic Dysfunction in Diabetic Myocardium.

BACKGROUND: Collagen accumulation in the myocardial interstitium of diabetic animals is considered to promote diastolic stiffness through advanced glycosylation. Because in vitro data suggest that metformin can modify glycosylation, this study was undertaken in a canine diabetic model 4 months in duration. METHODS AND RESULTS: Untreated diabetics (group II) and diabetics treated with metformin alone (group III) or with insulin (group IV) were compared in the basal state and during volume infusion. Basal hemoglobin A(1c), heart rate, aortic pressure, and ejection fraction were comparable. Left ventricular end-diastolic pressure was significantly increased in the untreated diabetics of group II, associated with a reduced end-diastolic volume. By contrast these parameters in the metformin-treated diabetics of group III were comparable with those in the normals of group I. Similarly in group IV end-diastolic volume was higher than that in group II, but filling pressure, although lower, was not significantly so. Calculation of left ventricular chamber stiffness in the basal state indicated a higher level for group II compared with controls and the treatment groups. During the systemic infusion of dextran, the untreated diabetics of group II had the largest end-diastolic pressure increase and the smallest rise of end-diastolic volume of the treatment groups, consistent with a significantly greater chamber stiffness. Myocardial collagen concentration was increased in group II with an interstitial distribution on morphological exam. Levels of collagen-linked advanced glycosylation end products isolated from the left ventricular were significantly greater in group II than in group I. Treatment with metformin prevented the increment observed in the untreated diabetic but had no effect on the elevated collagen concentration. CONCLUSIONS: Untreated diabetics exhibited increased diastolic chamber stiffness associated with collagen-linked glycation in myocardium compared with control animals. Chronic metformin use prevented the abnormalities of function and composition.

Journal Article↗
PubMed1999

[Efficacy of diltiazem in uremic hemodialyzed patients with isolated diastolic dysfunction and dialysis hypotensive crisis].

The aim of our study was to assess the effects of diltiazem on diastolic function, left ventricular mass and intradialytic hypotension, in uremic patients on maintenance hemodialysis. Forty-eight uremic patients on maintenance hemodialysis (mean age 46 +/- 5 years) with diastolic heart failure and normal systolic function (ejection fraction > 40%), although hemodialysis had been correctly performed, were included in the study. All patients had left ventricular hypertrophy. Diltiazem was given at the dosage of 60 mg, twice a day, for 3 months. At the end of this period, significant improvement of Doppler echocardiographic filling pattern and clinical symptomatology were observed, but left ventricular mass index was unchanged. Episodes of intradialytic hypotension were significantly reduced. We conclude that diltiazem improves symptoms and left ventricular diastolic filling in uremic patients with diastolic heart failure, without modifying left ventricular mass index; impaired diastolic function has an important role in recurrent dialysis hypotension.

Adult↗
PubMedDate not supplied

Left ventricular diastolic function assessment by tissue Doppler echocardiography in relation to hormonal replacement therapy in postmenopausal women with diastolic dysfunction.

The objective of this study was to evaluate the effect of hormone replacement therapy (HRT) regimens on left ventricular diastolic function by using mitral pulsed wave Doppler (MPWD) and tissue Doppler velocities (TDE). Seventy-eight postmenopausal women with normotensive and impaired diastolic left ventricular filling were included in the study. All the patients began a six-cycle HRT course. This formulation consisted of E2 valerate plus Medroxy progesterone acetate (MPA). Left ventricular diastolic function at rest was evaluated by M-mode, two-dimensional, MPWD and TDE in 78 postmenopausal women with normal blood pressure before the treatment for 6 months of HRT. The M-mode, two-dimensional, and MPWD parameters assessed were heart rate, systolic blood pressure, diastolic blood pressure, left ventricular mass index, ejection fraction of the left ventricle (EF), septal (IVS) and posterior wall (PW) thickness, left ventricular end-systolic (LVESD) and end-diastolic (LVEDD) diameter, left atrial diameter, peak early diastolic velocity (E), peak atrial velocity (A), E/A ratio, E acceleration time, E deceleration time, diastolic filling period, and isovolumic relaxation time (IVRT). The TDE parameters assessed were peak early diastolic velocity (E'), peak late diastolic velocity (A'), peak systolic velocity, E'/A' ratio, E' acceleration time, E' deceleration time, IVRT', and E/E' ratio. Quantitative data were analyzed using Student t test. Among the MPWD parameters, peak A velocity, E deceleration time, and IVRT significantly decreased, while peak E velocity and E/A ratio increased after a 6-month treatment. From the point of TDE parameters, E' velocity and E'/A' ratio increased, while A' velocity, E' deceleration time, E/E' ratio and IVRT' decreased. Some MPWD and TDE parameters were partially reversed after HRT. TDE velocities and especially E/E' ratio may provide better and true information of the diastolic function. TDE parameters were independent from the preload and did not produce pseudonormal pattern. HRT may cause increase in the blood volume and produce pseudonormal pattern in transmitral flow. In that case, TDE may be a beneficial method for evaluation of diastolic function.

Diastole↗