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Diastolic dysfunction in post-cardiac surgical management.

Although an appropriate definition of primary diastolic failure is still not at hand, primary diastolic failure is a distinct pathophysiologic syndrome. It is due to an increased resistance to ventricular filling and results in an inappropriate upward shift of the diastolic P-V relationship, especially during exercise. This leads to exercise intolerance with symptoms of congestion. The causes are known, ie, impaired systolic relaxation, decreased diastolic compliance, and inappropriate tachycardia. Pathophysiologically impaired (incomplete or slowed) systolic relaxation must be distinguished from physiologic, compensatory prolonged contraction (delayed or retarded relaxation). Treatment of diastolic failure is feasible, but necessitates a clear understanding of the etiology, pathogenesis, and pathophysiology of the underlying cardiac disease. Optimal therapy will depend on the type of disease, on the phase during the pathophysiologic evolution of a given disease, and on the coexistence and relative contribution of various compensatory or decompensatory mechanisms. This often requires a comprehensive analysis of hemodynamics, for example, with echo-doppler, completed, whenever necessary, by catheterization.

Cardiac Output, Low↗

Right ventricular diastolic dysfunction in the postoperative period of tetralogy of Fallot.

OBJECTIVE: To assess right ventricular diastolic function in the intermediate postoperative period of repair of tetralogy of Fallot. METHODS: We carried out a case-control study with 60 patients divided into 2 groups as follows: 1) group I - 30 patients who had undergone repair of tetralogy of Fallot and 2) group II - 30 healthy children. The 2 groups were paired for age, sex, and body surface. The flows in the pulmonary and tricuspid valves were analyzed with Doppler echocardiography. The presence of anterograde flow at the end of diastole in the pulmonary artery defined restrictive right ventricular physiology. Surgical, radiological, electrocardiographic, and echocardiographic variables were analized in the group I. RESULTS: The velocity of the A wave and the E/A ratio for the tricuspid valve showed significant differences between the groups. Cases with E/A < 1.30 predominated in inspiration (group I - 19/30, and group II - 5/30). The duration of the QRS complex on the electrocardiogram was significantly increased in patients with E/A <1.30. Nineteen (63.3%) patients had restrictive right ventricular physiology, which had a longer postoperative period, longer duration of the QRS complex, and a lower E/A ratio in inspiration. The surgical and radiological variables showed no statistical difference. CONCLUSION: Restrictive right ventricular physiology was detected on the intermediate follow-up of most patients undergoing repair of tetralogy of Fallot. The postoperative period and QRS duration were increased in patients with impairment in diastolic function.

Adolescent↗

"Isolated" diastolic dysfunction in left ventricular outflow tract obstruction.

We sought to investigate the prescence of "isolated" diastolic disease, defined as reduced long-axis early diastolic velocity with normal systolic velocity, in 21 young patients with left outflow tract obstruction. Most patients had depressed systolic velocities despite normal ejection fractions. The close relations amond long-axis velocities suggest isolated diastolic disease is unlikely.

Adult↗

The relative efficiency of beta adrenoceptor coupling to myocardial inotropy and diastolic relaxation: organ-selective treatment for diastolic dysfunction.

The relative effects of drugs which elevate cytosolic cyclic AMP on inotropy and diastolic relaxation (lusitropy) of guinea pig atria were quantified in vitro. There was a temporal difference between these responses in that inotropy reached peak response considerably faster than lusitropy. Also, although the relaxation response was sustained to an elevated steady state, the inotropic responses to beta adrenoceptor agonists were transient and returned to base line over 90 min. However, the inotropic responses to forskolin and dibutyryl cyclic AMP (cAMP) were sustained. For all of the drugs tested, the lusitropic response was at least 4 times more sensitive than the inotropic response (i.e., the concentration response curve for relaxation was shifted to the left of the curve for inotropy). In the case of beta adrenoceptor agonists, these differences were greater, presumably because of the fading inotropic response over 90 min. It was found that although high efficacy beta adrenoceptor agonists such as isoproterenol (and the direct activator of adenylate cyclase forskolin) produced both inotropy and lusitropy, lower efficacy agonists produced predominant lusitropy. The low efficacy agonist prenalterol produced insignificant inotropy but 60% maximal lusitropy. These data were modeled mathematically by a "differential coupling model" which assumed that a uniform cytosolic level of elevated cAMP activated two biochemical processes of differing sensitivity. Thus, the lusitropic response (phosphorylation of phospholamban) was coupled more efficiently to the cAMP response than the inotropic response (phosphorylation of calcium channels). A second model ("differential messenger concentration model") which calculated the effects of a compartmentalization of cAMP concentration within the cardiac cell by restricted diffusion and/or selective degradation by phosphodiesterases also was used.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

Left ventricular hypertrophy and diastolic dysfunction in alcohol-associated hypertension.

In order to assess left ventricular structure and diastolic function, 50 hypertensive male subjects, 25 with and 25 without a history of alcohol abuse, and 20 normotensive male controls underwent Doppler echocardiographic examination followed by ambulatory blood pressure monitoring for 24 hours. Left ventricular mass was significantly higher in alcoholic hypertensives in relation to non-alcoholic hypertensives (p < 0.05) and normotensive controls (p < 0.001). Moreover, Doppler parameters expressing left ventricular filling pattern were significantly worse in alcoholic than in non-alcoholic hypertensives (p < 0.01). Clinic and ambulatory blood pressure were similar in alcoholic and non-alcoholic hypertensives, while mean day-time heart rate was significantly higher in alcoholics (p < 0.01). Collected data suggest that non-hemodynamic factors are probably involved in the development of cardiovascular abnormalities in hypertensive alcoholics, and that echocardiography should be employed for risk-profile definition in alcohol-associated hypertension.

Alcoholism↗

Effects of nifedipine on left ventricular diastolic dysfunction after myocardial infarction.

In order to assess the effects of nifedipine on left ventricular diastolic abnormalities, 26 patients (mean age 52 year, range 42-66) were studied 10 days after a first myocardial infarction, at rest and during handgrip by Doppler examination. The time-velocity integral for the rapid (E) and atrial (A) filling phases and the E/A ration were used; stroke volume was calculated as the aortic time-velocity integral times the cross-sectional valvular area. Twenty age-matched normal subjects constituted the controls. Twenty-one patients had a reversal of the early to late diastolic filling pattern; five patients had a restrictive pattern. Nifedipine normalized left ventricular filling in patients with a reverse pattern, both at rest and during handgrip. Moreover, these patients showed a descending left ventricular function curve by relating at rest and handgrip values of cardiac index and the E/A ratio. After nifedipine, these study patients showed an ascending left ventricular curve, similar to that of normal subjects, with an increase in cardiac index and a slight decrease in the E/R ratio. No beneficial effects were detectable in patients with a restrictive pattern of left ventricular filling.

Adult↗