Left Ventricular Mechanics in Asymptomatic Normotensive and Hypertensive Patients with Aortic Regurgitation




Background


The aims of this study were to detect subclinical left ventricular (LV) dysfunction and to determine the impact of arterial hypertension on LV systolic function using speckle-tracking echocardiography in patients with chronic aortic regurgitation (AR).


Methods


Sixty-eight patients with AR and 47 healthy controls were included in the study. LV rotation and longitudinal, radial, and circumferential strain were measured using speckle-tracking imaging.


Results


Longitudinal axis dysfunction was found in patients with moderate AR with hypertension but was not present in patients with moderate AR without hypertension. Radial strain in patients with moderate AR was unchanged, but reduced levels were noted at the apical level in patients with severe AR without hypertension and preserved in those with severe hypertensive AR. LV basal rotation was reduced in patients with severe AR, whereas apical rotation was increased in those with moderate AR. LV torsion was reduced in patients with severe AR.


Conclusions


Patients with asymptomatic AR show subclinical LV longitudinal axis dysfunction, with more attenuation demonstrated in hypertensive than in normotensive patients.


One of the abilities of echocardiography in patients with aortic regurgitation (AR) is the evaluation of left ventricular (LV) function. The recognition of the conversion from normal LV function to systolic dysfunction remains an important target for clinicians in the decision-making process. One of the major goals of surgical intervention is to prevent irreversible LV damage and postoperative heart failure.


Chronic AR represents a condition that exhibits combined volume and pressure overload. According to published data, about 30% of patients with AR have arterial hypertension. Severe chronic LV volume overload increases heart wall stress and may cause subendocardial ischemia and the subsequent deposition of collagen and subendocardial fibrosis and may be the setting for LV dysfunction in AR. In the LV myocardial wall, the myofiber geometry changes from a right-handed helix in the subendocardium to a left-handed helix in the subepicardium. In the midwall of the left ventricle, fibers are aligned circumferentially. Because the subendocardial fibers are aligned more in the longitudinal direction, the long-axis function of the left ventricle may be abnormal in patients with chronic AR but without clinical symptoms. Compensatory LV remodeling that occurs with chronic volume overload is characterized by eccentric hypertrophy, LV chamber dilatation, and initially normal contractile function; therefore, the transition time to heart failure is prolonged.


It has been suggested that Doppler tissue imaging can detect early myocardial dysfunction in asymptomatic patients with severe AR. There are initial data regarding LV global and regional function assessed using speckle-tracking echocardiography in patients with mild AR, but the changes in LV longitudinal, radial, and circumferential function in patients with moderate and severe AR were not analyzed. In each stage of hypertension, from prehypertension to advanced hypertension with heart failure symptoms, different LV strain lesions assessed on speckle-tracking echocardiography have been described.


The aims of our study were to detect subclinical signs of LV dysfunction and to determine the impact of arterial hypertension on LV systolic function using speckle-tracking echocardiography in patients with chronic asymptomatic AR.


Methods


Study Subjects


The study population consisted of 68 patients with AR. They were recruited from the inpatient and outpatient departments of cardiology at the Kaunas University of Medicine Hospital between January 2007 and March 2010. All patients satisfied the following inclusion criteria: adult age, asymptomatic clinical status, greater than mild AR, LV ejection fraction >50% on echocardiography, and optimal echocardiographic image quality. Exclusion criteria included signs of aortic stenosis, evidence of either regional and/or global wall motion abnormalities on echocardiography, greater than mild mitral regurgitation, atrial fibrillation, known ischemic heart disease, heart failure symptoms, and serious noncardiac disease. Thirty-four investigated persons were not included in the study because of the inadequate quality of echocardiographic images, which prevented speckle-tracking analysis.


Patients were divided into two groups: those with moderate AR ( n = 35) and those with severe AR ( n = 33). The severity of AR was estimated according to the recommendations of the American Society of Echocardiography. Moderate and severe AR were differentiated using color flow Doppler (quantitative measurements of vena contracta width [3–6 and >6 mm, respectively] and regurgitant jet width [25%–64% and ≥65% of the LV outflow tract, respectively]), pulsed-wave Doppler (aortic diastolic flow reversal in the upper descending and abdominal aorta [holodiastolic flow reversal in the descending aorta in severe AR]), and continuous-wave Doppler (pressure half-time of diastolic regurgitant jet [500–200 and <200 msec, respectively]).


Both AR groups were subdivided into hypertensive and nonhypertensive AR patient subgroups. Arterial hypertension was defined by the international guidelines for the management of arterial hypertension using records in the medical files from the outpatient department. Hypertension was diagnosed when patients who had been followed up for ≥12 months had recorded systolic blood pressures ≥140 mm Hg and/or diastolic blood pressures ≥90 mm Hg recorded at repeated visits obtained over that time period. All patients with histories of arterial hypertension were on antihypertensive treatment.


The control group consisted of 47 age-matched and gender-matched healthy subjects without any known cardiac disease, who were normotensive, were without ischemic signs on resting electrocardiography, had no histories of serious noncardiac disease, and were without signs of cardiac disease on echocardiography.


Among the analyzed patients, 38.2% had bicuspid aortic valves, 29.4% had aortic root dilatation, 5.9% had aortic valve cusp prolapse, 10.3% had degenerative impairment, and 16.2% had mixed-etiology AR.


All patients provided written informed consent to participate in the study. Procedures were performed according to approval by the local ethics committee.


Echocardiography


Both conventional and speckle-tracking echocardiography were performed using a Vivid 7 (GE Vingmed Ultrasound AS, Horten, Norway) with an M3S transducer. All images were acquired by a single cardiologist with the subject lying in the left lateral decubitus position. Standard transthoracic echocardiographic measurements were performed according to the guidelines of the American Society of Echocardiography. LV mass was calculated by the Devereux-modified cube formula. Transmitral and aortic flows were recorded using pulsed Doppler echocardiography. The sample volume with a fixed length of 2.0 mm was placed between the tips of the mitral leaflets to record the transmitral flow and at the level of the LV outflow tract to record the aortic flow. Pulsed-wave spectral tissue Doppler recordings of the septal, anterior, lateral, and inferior parts of the mitral annulus were used for the assessment of peak systolic mitral annular velocity (S′).


After adjusting for a frame rate of 50 to 90 frames/sec, the cine loop of three consecutive beats was stored for offline speckle-tracking analysis (EchoPAC PC; GE Vingmed Ultrasound AS). The images were stored during end-expiratory apnea. Apical four-chamber and two-chamber views were used for the assessment of longitudinal strain in septal, lateral, anterior, and inferior walls, whereas parasternal short-axis views at the base (at the tips of the mitral valve leaflets), at the level of papillary muscles, and at the apex (with the minimal circular LV cavity at end-systole) were used for radial strain, circumferential strain, and rotation analyses.


Before speckle-tracking analysis, the timing of aortic and mitral valve opening and closing was assessed using pulsed-wave Doppler recordings of aortic and transmitral flows. The interval between two subsequent closures of the mitral valve was used for the regional strain and rotation analysis.


LV endocardium was traced at end-systole. Then, a software-generated region of interest was adjusted to an optimal width of the myocardial wall. In each echocardiographic view, the myocardium was automatically divided into six segments. The apical short-axis view was manually corrected to four myocardial segments. Software-generated tracking results that were acceptable were manually approved ( Figure 1 ). Deformation and rotation values for each segment were collected from the results window. Global longitudinal strain was calculated as a longitudinal strain average of the septal, lateral, anterior, and inferior LV walls. Radial and circumferential strain and rotation were calculated arithmetically as a strain average of six basal segments (radial and circumferential strain and rotation at the basal level), six segments at the papillary level (radial and circumferential strain at the papillary level), and four apical segments (radial and circumferential strain and rotation at the apical level). Global radial and circumferential strain were calculated as a strain average at the basal, papillary, and apical levels.




Figure 1


LV speckle-tracking echocardiography for the assessment of strain and rotational values. (A) LV septal and lateral wall longitudinal strain assessed from the apical four-chamber view. (B) Inferior and anterior wall longitudinal strain assessed from the apical two-chamber view. (C) Radial strain, (D) circumferential strain, (E) apical rotation, and (F) basal rotation assessed from short-axis views. White dots show peak systolic values of strain and rotation, collected for analysis.


LV twist was calculated as an absolute apex-to-base difference in LV rotation. LV torsion was calculated as LV twist normalized with respect to the ventricular diastolic longitudinal distance between the LV apex and the mitral plane ([apical LV rotation − basal LV rotation]/LV diastolic longitudinal length).


Statistical Analysis


Data were analyzed using SPSS version 15.0 for Windows (SPSS, Inc., Chicago, IL). Continuous variables are presented as mean ± SD. Continuous variables were compared using one-way analysis of variance, and Fisher’s exact test was applied for post hoc comparisons. The χ 2 test was used to determine differences between categorical variables. Significance was assessed at the P < .05 level.


Intraobserver variability was assessed for the measurement of systolic longitudinal strain in the septal and lateral walls, systolic radial strain at the basal and apical levels, and systolic rotation at the basal and apical levels in 15 randomly selected subjects using intraclass correlation coefficients (ICCs) and a Bland-Altman plot.




Results


Demographic and Conventional Echocardiographic Parameters


Demographic, clinical, and conventional echocardiographic characteristics for all patients with AR and healthy controls are shown in Table 1 . The groups did not differ in age, gender, or mean heart rate during the investigation. Systolic blood pressure was higher in the severe AR patient group and in patients with hypertension. Diastolic blood pressure was lower in nonhypertensive moderate and severe AR patients but higher in hypertensive severe AR patients.



Table 1

Demographic, clinical, and conventional echocardiographic data

















































































































































































Controls Moderate AR Moderate AR without AH Moderate AR with AH Severe AR Severe AR without AH Severe AR with AH
Variable ( n = 47) ( n = 35) ( n = 19) ( n = 16) ( n = 33) ( n = 15) ( n = 18)
Demographic data
Age (years) 43.5 ± 12.5 43.0 ± 14.5 37.8 ± 15.1 46.5 ± 10.5 48.8 ± 11.6 43.7 ± 12.4 51.4 ± 11.1
Women/men 12/35 9/26 4/15 5/11 7/26 3/12 4/14
Heart rate (beats/min) 67.2 ± 9.7 67.2 ± 10.4 67.2 ± 9.3 68.6 ± 11.9 66.5 ± 11.7 69.4 ± 13.0 68.1 ± 11.2
Systolic BP (mm Hg) 127.2 ± 9.6 132.5 ± 12.3 126.5 ± 5.7 136.5 ± 12.6 138.9 ± 15.5 § 128.2 ± 10.4 146.6 ± 11.3
Diastolic BP (mm Hg) 75.4 ± 7.2 75.1 ± 9.0 70.5 ± 4.3 79.2 ± 9.7 78.4 ± 13.3 66.4 ± 12.6 82.0 ± 8.3
Conventional echocardiographic data
Mild mitral regurgitation 21/47 17/35 8/19 6/16 29/33 11/15 11/18
Left atrial diameter (mm) 36.6 ± 3.8 38.2 ± 6.0 35.8 ± 3.6 39.8 ± 6.6 41.4 ± 4.8 § 39.7 ± 4.0 43.8 ± 5.8
LV diastolic diameter (mm) 47.4 ± 4.2 53.3 ± 5.3 54.1 ± 3.1 53.0 ± 7.7 59.2 ± 6.6 § 59.1 ± 6.3 59.0 ± 7.0
LV systolic diameter (mm) 31.2 ± 4.2 37.0 ± 5.9 37.7 ± 4.7 36.9 ± 7.6 40.8 ± 6.6 § 40.8 ± 6.1 39.4 ± 6.8
LV diastolic length (mm) 82.7 ± 7.1 88.3 ± 7.7 88.0 ± 7.0 89.3 ± 9.7 95.4 ± 7.5 § 94.1 ± 7.3 97.8 ± 6.3
LV systolic length (mm) 68.0 ± 6.9 76.6 ± 7.9 76.3 ± 7.2 77.5 ± 9.8 83.0 ± 7.6 § 81.6 ± 8.7 84.2 ± 6.6
LV diastolic volume (mL) 83.4 ± 19.8 109.8 ± 30.8 108.6 ± 22.3 115.2 ± 41.5 157.0 ± 46.5 § 154.5 ± 41.9 160.0 ± 50.2
LV systolic volume (mL) 33.5 ± 8.6 46.8 ± 15.7 45.6 ± 10.0 51.0 ± 21.5 68.6 ± 24.6 § 66.4 ± 22.8 70.2 ± 25.5
LV myocardial mass (g) 150,7 ± 31,4 235,0 ± 43,0 224,0 ± 37,8 249,1 ± 46,4 293,9 ± 79,1 § 279,8 ± 71,3 304,9 ± 85,0
LV ejection fraction (%) 59.9 ± 3.8 57.6 ± 4.1 57.7 ± 3.7 56.3 ± 4.0 56.8 ± 4.7 57.3 ± 4.7 56.6 ± 4.5
S′ (cm/s) 9.3 ± 1.5 8.0 ± 1.4 8.3 ± 1.5 7.6 ± 1.2 7.7 ± 1.0 8.1 ± 1.1 7.3 ± 0.8

Data are expressed as mean ± SD.

AH , Arterial hypertension.

P < .05 vs normal subjects.


P < .05 vs moderate nonhypertensive AR.


P < .05 vs moderate hypertensive AR.


§ P < .05 vs moderate AR.


P < .05 vs severe nonhypertensive AR.



LV end-diastolic and systolic diameters, end-diastolic and systolic lengths, end-diastolic and systolic volumes, and LV myocardial mass were significantly higher in the AR groups and subgroups than in controls, but these parameters in the nonhypertensive subgroup did not differ from the parameters in the hypertensive subgroup for moderate and severe AR. The LV ejection fraction was lower in patients with AR, but still exceeded 50% in all AR groups. The systolic velocity of the mitral annulus was lower in patients with AR.


LV Global Mechanics


Global longitudinal strain was lower in the AR groups than in controls. However, in the subgroup analysis, these differences were noted only in those patients with systemic hypertension ( Figure 2 , Table 2 ).




Figure 2


LV global longitudinal, radial, and circumferential strain, basal and apical rotation, and torsion. P < .05 vs controls.


Table 2

LV systolic longitudinal and radial strain and rotation





























































































































































Controls Moderate AR Moderate AR without AH Moderate AR with AH Severe AR Severe AR without AH Severe AR with AH
Variable ( n = 47) ( n = 35) ( n = 19) ( n = 16) ( n = 33) ( n = 15) ( n = 18)
LV global mechanics
Global longitudinal strain (%) −20.3 ± 2.3 −18.6 ± 2.3 −19.2 ± 1.8 −17.9 ± 2.8 −18.4 ± 3.0 −18.9 ± 3.4 −17.8 ± 2.8
Global radial strain (%) 47.0 ± 11.1 46.9 ± 11.1 46.3 ± 12.1 47.2 ± 10.8 41.6 ± 9.5 37.7 ± 6.0 46.2 ± 13.0
Global circumferential strain (%) −20.9 ± 3.1 −20.8 ± 2.4 −20.9 ± 2.1 −20.6 ± 2.8 −20.5 ± 2.9 −20.7 ± 3.3 −20.3 ± 2.7
LV twist (°) 16.9 ± 5.3 18.7 ± 6.8 19.1 ± 6.1 17.5 ± 8.5 16.6 ± 4.7 15.5 ± 4.1 16.9 ± 5.0
LV torsion (°/cm) 2.0 ± 0.7 2.1 ± 0.8 2.2 ± 0.7 2.0 ± 1.0 1.7 ± 0.5 § 1.6 ± 0.4 1.7 ± 0.5
LV regional mechanics
Radial strain at basal level (%) 47.4 ± 16.9 41.8 ± 16.4 43.1 ± 18.3 39.9 ± 16.1 46.8 ± 14.6 40.9 ± 13.3 52.0 ± 16.3
Radial strain at papillary level (%) 59.7 ± 16.8 58.3 ± 18.9 59.7 ± 19.1 55.3 ± 20.7 52.9 ± 15.9 58.0 ± 12.9 47.4 ± 16.4
Radial strain at apical level (%) 34.3 ± 17.3 36.3 ± 21.1 31.9 ± 20.4 40.9 ± 21.6 28.3 ± 18.5 20.1 ± 10.9 38.8 ± 23.4
Circumferential strain at basal level (%) −18.3 ± 3.3 −17.4 ± 3.03 −17.7 ± 3.2 −16.1 ± 2.5 −18.8 ± 3.3 −18.9 ± 2.7 −18.4 ± 3.2
Circumferential strain at papillary level (%) −19.6 ± 2.9 −20.2 ± 2.9 −20.0 ± 2.7 −19.6 ± 2.9 −19.5 ± 2.9 −19.8 ± 3.2 −19.8 ± 2.7
Circumferential strain at apical level (%) −25.1 ± 5.2 −24.3 ± 3.7 −24.8 ± 3.6 −22.9 ± 3.7 −22.6 ± 5.6 −22.5 ± 6.3 −23.8 ± 5.3
Basal rotation (°) −7.47 ± 2.4 −6.7 ± 3.0 −6.3 ± 3.3 −7.2 ± 2.7 −5.7 ± 1.7 −6.2 ± 1.7 −5.1 ± 1.3
Apical rotation (°) 9.3 ± 4.5 11.7 ± 5.0 12.6 ± 4.2 10.2 ± 6.0 10.9 ± 4.5 9.4 ± 4.0 11.6 ± 4.7

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Jun 15, 2018 | Posted by in CARDIOLOGY | Comments Off on Left Ventricular Mechanics in Asymptomatic Normotensive and Hypertensive Patients with Aortic Regurgitation

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