CLINICAL PATTERNS OF STRUCTURAL AND FUNCTIONAL LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH GOUT ASSOCIATED WITH ARTERIAL HYPERTENSION

The article presents the main pathophysiological mechanisms associated with the development of complications of pregnancy against the background of arterial hypertension in patients without clinical manifestations of left ventricular dysfunction, the possibilities of speckle tracking of echocardiography in revealing latent systolic dysfunction of the left ventricle in pregnant women on the background of preeclampsia not accompanied by proteinuria are shown.Goal. To identify early markers of left ventricular systolic dysfunction in pregnant women with preeclampsia without proteinuria according to speckle tracking echocardiography.Material and methods. 100 pregnant women with hypertension and a gestation period of 29–40 weeks are divided into 2 groups: 1 st group – 50 patients without an arterial hypertension in the anamnesis, 2 nd group – 50 patients with an arterial hypertension in the anamnesis (without the proteinuria during pregnancy). For all patients, echocardiography with evaluation of cardiomyocyte function by speckle-tracking was performed on ultrasonic scanners Aplio ™ 500 and Aplio ™ Artida from Toshiba.Results. Ejection fraction of the left ventricle in the groups was not significantly different, while the longitudinal, radial and circular deformation parameters differed between the groups, with the lowest values characterizing the global longitudinal deformation.Conclusions. In assessing the function of the left ventricle in pregnant women with preeclampsia without diurnal proteinuria, it is not enough to focus on traditional parameters, shifting the emphasis towards derivatives of force, speed and time. Study of myocardium with the help of speckle tracking echocardiography promotes the detection of subclinical left ventricular dysfunction in patients with arterial hypertension without daily proteinuria.

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The functions and geometry of the left ventricle in patients with chronic glomerulonephritis

Kazan medical journal ◽

10.17816/kmj2288 ◽

2012 ◽

Vol 93 (2) ◽

pp. 204-207

Author(s):

O N Sigitova ◽

A G Shcherbakova

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Left Ventricle ◽

Arterial Hypertension ◽

Kidney Function ◽

Left Ventricular Dysfunction ◽

Ventricular Dysfunction ◽

Left Ventricular ◽

Chronic Glomerulonephritis ◽

Stage 1

Aim. To study the functions and the geometry of the left ventricle in patients with chronic glomerulonephritis at different stages of chronic kidney disease, depending on the presence of arterial hypertension and dyslipidemia. Methods. Observed were 156 patients with chronic glomerulonephritis (80 men and 76 women, mean age 40.23±1.1 years), including 91 people with arterial hypertension (observation group), 65 patients without arterial hypertension (comparison group). The observation and comparison groups were divided into subgroups depending on the stage of chronic kidney disease: the first subgroup - stage 1-2, the second subgroup - stage 3-4, the third subgroup - stage 5. The control group consisted of 30 healthy people. Conducted were general clinical, laboratory and instrumental investigations. Results. Left ventricular hypertrophy was formed at stage 1-2 of chronic kidney disease in 52.5% of patients with chronic glomerulonephritis with arterial hypertension, at stage 3-4 - in 69.2%, at stage 5 - in 80.0%. The dominant type of hypertrophy was concentric; with the decrease in kidney function the frequency of eccentric hypertrophy increased. In the early stages of chronic kidney disease the incidence of left ventricular dysfunction was almost similar in arterial hypertension (62.5%) and normal blood pressure (60.0%). With the decline of the kidney function in the presence of arterial hypertension the incidence of left ventricular dysfunction reached up to 84.6% at stage 3-4 and up to 88.0% - at stage 5 of chronic kidney disease. No influence of the lipid profile on the function and the geometry of the left ventricle were found. Conclusion. In patients with chronic glomerulonephritis with arterial hypertension with the decrease in kidney function increases the frequency of left ventricular hypertrophy; in the early stages of chronic kidney disease the incidence of left ventricular dysfunction is the same in patients with and without hypertension, increasing with the decline in renal function in patients with hypertension.

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Myocardial edema, left ventricular function, and pulmonary hypertension

Journal of Applied Physiology ◽

10.1152/jappl.1995.78.1.132 ◽

1995 ◽

Vol 78 (1) ◽

pp. 132-137 ◽

Cited By ~ 52

Author(s):

K. L. Davis ◽

U. Mehlhorn ◽

G. A. Laine ◽

S. J. Allen

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Arterial Hypertension ◽

Pulmonary Artery ◽

Arterial Hypertension ◽

Left Ventricular Dysfunction ◽

Ventricular Dysfunction ◽

Dry Weight ◽

Left Ventricular ◽

Interstitial Edema ◽

Pulmonary Arterial

Left ventricular dysfunction has been reported in both experimentally induced and clinical pulmonary hypertension. However, the mechanism by which pulmonary hypertension causes left ventricular dysfunction is unknown. We hypothesized that acute pulmonary hypertension causes left ventricular myocardial interstitial edema and that it is this edema that causes left ventricular dysfunction. In pulmonary artery-banded or sham-operated dogs, left ventricular diameter (septal-free wall axis) and pressure were measured using sonomicrometry crystals and a micromanometer, respectively. These measurements were used to calculate preload recruitable stroke work (PRSW), an index of contractility, and the rate of active relaxation (tau) to assess systolic and diastolic left ventricular function, respectively. After 3 h of pulmonary arterial hypertension or control, the dogs were killed and the left ventricles were excised to determine wet-to-dry weight ratios. The wet-to-dry weight ratios were significantly higher in the pulmonary artery-banded dogs (3.57 +/- 0.12) than in the sham-operated dogs (3.41 +/- 0.17). PRSW decreased to 56.8 +/- 30.3% of control after 3 h of pulmonary hypertension. tau Slowed significantly from 29.8 +/- 5.8 ms at baseline to 63.6 +/- 30.4 ms after 3 h of pulmonary arterial hypertension. There were no differences in PRSW or tau in the sham-operated dogs. We conclude that pulmonary hypertension causes left ventricular myocardial interstitial edema, which results in both systolic and diastolic left ventricular dysfunction.

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