الفهرس 
PATHOPHYSIOLOGY OF HYPERTENSION IN RELATION TO SYSTOLIC AND DIASTOLIC FUNCTION
Statistical analysisOnly 14 pages are availabe for public view
 |  | from | 214 |  |  |
| | | from | 214 | | |
Abstract
A
subset of hypertensive patients with no signs and/or symptoms of HF have impaired systolic longitudinal function when assessed using mitral annular velocities by the assessment of LV longitudinal function by TDI which plays an important role in identifying not only diastolic dysfunction, but also subclinical LV systolic dysfunction.
Radial shortening is predominantly dependent on contraction of circumferential myocardial fibrers in mid wall .whereas longitudinal shortening is governed by both longitudinal subendocardial and subepicardial fibers because subendocardium is more vulnerable to ischemia and interstitial fibrosis, a decrease in longitudinal function might be a sensitive marker for Subclinical alterations in LV systolic function (Ballo, 2007).
The aim of this study was to assess left ventricular longitudinal systolic and diastolic function in hypertensive patients without symptoms of heart failure This study included 90 patients divided into 3 groups, group A: included 30 hypertensive patients with heart failure symptoms, group B: included 30 hypertensive patients with no evidence of heart failure, Group C: included 30 normal control groups. (Normotensive and not on any medication or cardiovascular symptoms with no history of hypertension or diabetes) age and sex matched.
Inclusion criteria: Recently discovered Hyper-tensive patients without treatment who will be defined as patients with systolic blood pressure (more or equal to 140mmHg and/or more or equal to 90mmhg diastolic pressure on two consecutive visits. With or without symptoms suggestive of heart failure (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, lower limb odema) with Ejection fraction >50.
Exclusion criteria were Impaired systolic function (EF <50%), Patient with atrial fibrillation, significant valvular heart disease, congenital heart disease, myocardial disease, dyspnea due to other causes: (decompensated liver disease, renal failure, respiratory disease), poorly echogenic patients, Diabetes mellitus and Body mass index >30.
All patients in the study were subjected to Full history taking Complete general and local exami-nation: Bl/pressure and heart rate measurement, signs of heart failure, laboratory investigation (liver functions-renal function), 12 leads Electrocardio-graphy, body surface area calculated by the given height and weight: from the formula of DuBois and DuBois, Echocardiographic examination performed to all patients for assessment of:
1. LV dimensions and volumes, wall thickness (LVDd, LVSd, LVEDVI, LVESVI) where (LVDd, LVSd are the left ventricular dimensions in diastole and systole respectively and LVEDVI and LVESVI are end ventricular diastolic and systolic volume index respectively).
2. EF using modified Simpson’s method.
3. Left atrial area calculated in the apical 4 chamber and left atrial volume index calculated by area length formula.
4. LV mass index: calculated based on the area-length formula left ventricular mass index (LVMI) is calculated by dividing LVM by body surface area, then further classification of group A and group B of our study into 2 sub groups: increased LVMI and normal LVMI.
5. Pulsed wave Doppler of transmitral flow to assess global diastolic function, measure E-wave velocity (E), A wave velocity, E-wave deceleration time, E/A ratio, isovolumic relaxation time.
6. Assessment of long axis function by TDI: in the septal and lateral corners of mitral annulus in apical 4 chamber view and anterior ,inferior corners in apical 2 chamber view to record mitral peak systolic annuluar velocity (Sّ ) and peak diastolic annuluar velocities during early diastolic filling (E`) and atrial contraction (A`).
7. E/E` calculated
Using the average values obtained in our control group to determine the cut off points for each wave separately by using (mean 2 SD)
Results of our study:
1. Range of age was from 56.97.44 in group A, 538.54 in group B, 53.36.68 in group C.
2. 48 patients were female and 42 were males,
3. In group A 18 patients had normal LVMI and 12 patients had Increased LVMI but in group B 16 patients had normal LVMI and 14 patients had Increased LVMI.
4. LAVI was high in Increased LVMI group.
• Using the average values obtained in our control group to determine the cut off points for each wave separately by using (mean 2SD) impaired longitudinal systolic function was defined in our study as Average of peak systolic annuluar velocity (Sّ) 6.7cm/sec, we demonstrated that 30% (9 patients) of asymp-tomatic hypertensive patients (group B) had impaired longitudinal systolic function, and 44% (13 patients) of diastolic heart failure group (group A) had impaired longitudinal systolic function.
• The late (p<0.0001) diastolic annular velocities A´, LV mass index, LA volume index and the peak early (p<0.0001) E´, E/E´ ratio were found to be independent predictors of peak systolic annular velocities (impaired longitudinal systolic function).
from all these mentioned results Systolic long-axis LV function was impaired in a subset of hypertensive patients without DHF by the assessment of LV longitudinal function by TDI which plays an important role in identifying not only diastolic dysfunction, but also subclinical LV systolic dysfunction and should be routine part of echocardio-graphic study of our hypertensive patients whether symptomatic or not in order to identify asymptomatic LVSD (LV systolic dysfunction) which is a preclinical phase of CHF that warrants early treatment.