Cardiac Impairment Evaluated by Transesophageal Echocardiography and Invasive Measurements in Rats Undergoing Sinoaortic Denervation

Background: Sympathetic hyperactivity may be related to left ventricular (LV) dysfunction and baro- and chemoreflex impairment in hypertension. However, cardiac function, regarding the association of hypertension and baroreflex dysfunction, has not been previously evaluated by transesophageal echocardiography (TEE) using intracardiac echocardiographic catheter.Methods and Results: We evaluated exercise tests, baroreflex sensitivity and cardiovascular autonomic control, cardiac function, and biventricular invasive pressures in rats 10 weeks after sinoaortic denervation (SAD). the rats (n = 32) were divided into 4 groups: 16 Wistar (W) with (n = 8) or without SAD (n = 8) and 16 spontaneously hypertensive rats (SHR) with (n = 8) or without SAD (SHRSAD) (n = 8). Blood pressure (BP) and heart rate (HR) did not change between the groups with or without SAD; however, compared to W, SHR groups had higher BP levels and BP variability was increased. Exercise testing showed that SHR had better functional capacity compared to SAD and SHRSAD. Echocardiography showed left ventricular (LV) concentric hypertrophy; segmental systolic and diastolic biventricular dysfunction; indirect signals of pulmonary arterial hypertension, mostly evident in SHRSAD. the end-diastolic right ventricular (RV) pressure increased in all groups compared to W, and the end-diastolic LV pressure increased in SHR and SHRSAD groups compared to W, and in SHRSAD compared to SAD.Conclusions: Our results suggest that baroreflex dysfunction impairs cardiac function, and increases pulmonary artery pressure, supporting a role for baroreflex dysfunction in the pathogenesis of hypertensive cardiac disease. Moreover, TEE is a useful and feasible noninvasive technique that allows the assessment of cardiac function, particularly RV indices in this model of cardiac disease.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Fac Med, Cardiomyopathy Unit, Heart Inst InCor,Hosp Clin, São Paulo, BrazilUniv São Paulo, Fac Med, Hypertens Unit, Heart Inst InCor,Hosp Clin, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, São Paulo, BrazilWeb of Scienc

Does Quantitative Left Ventricular Regional Wall Motion Change after Fibrous Tissue Resection in Endomyocardial Fibrosis?

OBJECTIVES: We compared left ventricular regional wall motion, the global left ventricular ejection fraction, and the New York Heart Association functional class pre- and postoperatively. INTRODUCTION: Endomyocardial fibrosis is characterized by fibrous tissue deposition in the endomyocardium of the apex and/or inflow tract of one or both ventricles. Although left ventricular global systolic function is preserved, patients exhibit wall motion abnormalities in the apical and inferoapical regions. Fibrous tissue resection in New York Heart Association FC III and IV endomyocardial fibrosis patients has been shown to decrease morbidity and mortality. METHODS: We prospectively studied 30 patients (20 female, 30&plusmn;10 years) before and 5&plusmn;8 months after surgery. The left ventricular ejection fraction was determined using the area-length method. Regional left ventricular motion was measured by the centerline method. Five left ventricular segments were analyzed pre- and postoperatively. Abnormality was expressed in units of standard deviation from the mean motion in a normal reference population. RESULTS: Left ventricular wall motion in the five regions did not differ between pre- and postoperative measurements. Additionally, the left ventricular ejection fraction did not change after surgery (0.45&plusmn;0.13% x 0.43&plusmn;0.12% pre- and postoperatively, respectively). The New York Heart Association functional class improved to class I in 40% and class II in 43% of patients postoperatively (p<0.05). CONCLUSIONS: Although endomyocardial fibrosis patients have improved clinical symptoms after surgery, the global left ventricular ejection fraction and regional wall motion in these patients do not change. This finding suggests that other explanations, such as improvements in diastolic function, may be operational

Tissue Doppler imaging data of mitral and tricuspid annulus data obtained by transesophageal echocardiography.

<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>S’ = peak velocity of systolic velocity obtained by tissue Doppler imaging; E’ = peak velocity of early diastolic velocity obtained by tissue Doppler imaging; A’ = peak velocity of late diastolic velocity obtained by tissue Doppler imaging.</p>a<p>p<0.05 vs. W, ^bp<0.05 vs. SAD, and ^cp<0.05 vs. SHR.</p

Blood pressure, heart rate, baroreflex sensitivity and cardiovascular autonomic modulation of normotensive and hypertensive groups.

<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>HR = heart rate; PI = pulse interval; SD PI = standard deviation of pulse interval; SBP = systolic blood pressure; SD SBP = standard deviation of systolic blood pressure; PIV = pulse interval variance; LF (ms²) = low-frequency band of heart rate variability; HF (ms²) = high-frequency band of heart rate variability; LF band (%) = low-frequency band of heart rate variability; HF band (%) = high-frequency band of heart rate variability; SBPV = SBP variability; LF SBP (mmHg²) = low frequency band of SBPV; BRI = bradycardic response index; TRI = tachycardic response index;</p>a<p>p<0.05 vs. W, ^bp<0.05 vs. SAD, and ^cp<0.05 vs. SHR.</p

Transesophageal echocardiography of spontaneously hypertensive rats showing right ventricle (RV) (A), tricuspid inflow (B) and tissue Doppler imaging of the tricuspid annulus (C).

<p>Transesophageal echocardiography of spontaneously hypertensive rats showing right ventricle (RV) (A), tricuspid inflow (B) and tissue Doppler imaging of the tricuspid annulus (C).</p

Volumes and ejection fraction of the right ventricle, and biventricular diastolic function data obtained by transesophageal echocardiography.

<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>FE VD = right ventricular ejection fraction; E/A = ratio of peak velocity of E and A waves of mitral or tricuspid inflow; DT = deceleration time of E wave; IVRT = isovolumic relaxation time of LV; AFF = atrial filling fraction.</p>a<p>p<0.05 vs. W, ^bp<0.05 vs. SAD and ^cp<0.05 vs. SHR.</p

Correlations between invasive and noninvasive data in all animals.

<p>Values are mean ± SD.</p><p>AFF = atrial filling fraction; LV = left ventricle; AcT TTE = aceleration time of right ventricular outflow (transthoracic echocardiography); AcT TEE = aceleration time of right ventricular outflow (transesophageal echocardiography); TT = time from the beginning to the end of right ventricular outflow; CI = cardiac index; LVMass = left ventricular mass; MPI = myocardial performance index; EF = ejection fraction; E/E’ =  ratio of peak velocity of E wave of mitral inflow and peak velocity of early diastolic velocity obtained by tissue Doppler imaging; EDP = end-diastolic pressure.</p

Myocardial performance index, right ventricular outflow by transesophageal, transthoracic echocardiography and invasive data.

<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>MPI = myocardial performance index; LV = left ventricle; RV = right ventricle; AcT = aceleration time of right ventricular outflow; TT = time from the beginning to the end of right ventricular outflow; EDPRV = end-diastolic pressure of right ventricle; EDPLV = end-diastolic pressure of left ventricle; ESPRV = end-systolic pressure of the right ventricle.</p>a<p>p<0.05 vs. W, ^bp<0.05 vs. SAD, and ^cp<0.05 vs. SHR.</p

Cardiac morphology obtained by M-mode transthoracic echocardiography.

<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; GSHR = spontaneously hypertensive rats; GSHRDSA = spontaneously hypertensive rats with denervation;</p><p>LVd = left ventricular end-diastolic dimension; LVd = left ventricular end-systolic dimension; IVSd = interventricular septum thickness in diastole; PWd = posterior wall thickness in diastole; FS = fractional shortening; CI = cardiac index; LVMass = left ventricular mass; RWT = relative wall thickness; Ao = aortic dimension; LA = left atrium thickness in diastole.</p>a<p>p<0.05 vs. W and ^bp<0.05 vs. SAD.</p