Contribution of the pericardium to left ventricular torsion and regional myocardial function in patients with total absence of the left pericardium.

OBJECTIVE: The relationship between left ventricular (LV) torsional deformation and myocardial function has recently been recognized. However, little is known about whether the pericardium affects this relationship. Our aim was to identify the contribution of the pericardium to LV torsion and regional myocardial function in the clinical setting. METHODS: We examined LV torsion in basal and apical LV short-axis views, and regional LV myocardial function, such as longitudinal strain in apical 4-chamber view, and circumferential and radial strains in parasternal LV short-axis views using 2-dimensional speckle-tracking imaging method in 5 patients with congenital total absence of the left pericardium and systolic paradoxical ventricular septal motion on M-mode echocardiogram and in 10 control subjects. Diagnosis of the pericardial defect was based on chest radiograph, computed tomography, jugular phlebogram, and M-mode and 2-dimensional echocardiogram. LV torsion was defined as the net difference in LV rotation in the basal and apical planes. RESULTS: There was no significant difference in LV ejection fraction determined by 2-dimensional echocardiography between the pericardial defect and control groups. LV torsion was markedly decreased in the pericardial defect group compared with the control group. There were no significant differences in longitudinal, radial, and circumferential systolic strains and systolic and early diastolic strain rates in the LV walls and in longitudinal systolic strains and systolic and early diastolic strain rates in the left atrial walls between the two groups. CONCLUSIONS: Pericardial defects cause a lack of LV torsion while maintaining LV regional myocardial function in patients with systolic paradoxical ventricular septal motion. Therefore, pericardium plays an important role in LV torsion.

Arterial stiffness is associated with left ventricular diastolic function in patients with cardiovascular risk factors: early detection with the use of cardio-ankle vascular index and ultrasonic strain imaging.

BACKGROUND: It is well known that left ventricular (LV) diastolic function declines in the elderly, especially in patients with cardiovascular risk factors. However, few data are available on the early detection of relationship between arterial stiffness and LV diastolic dysfunction. METHODS AND RESULTS: The common carotid artery intima-media thickness (IMT) and cardio-ankle vascular index (CAVI) were measured to determine the presence of subclinical atherosclerosis in 30 patients (13 men and 17 women; mean age 59 +/- 5.7 years) with 1 or more cardiovascular risk factors. LV systolic and diastolic function also were determined by measuring transmitral flow velocity, mitral annular motion velocity, and myocardial strain and strain rate profiles using pulsed Doppler, tissue velocity, and ultrasonic strain imaging. The CAVI correlated with the peak early diastolic velocity of transmitral flow velocity (r = -0.50, P < .01), the ratio of peak early to late diastolic transmitral flow velocity (r = -0.37, P < .05), the deceleration time from peak to baseline of the early diastolic transmitral flow velocity (r = 0.57, P < .01), the peak early diastolic mitral annular motion velocity (r = -0.41, P < .05), and the peak early diastolic strain rates at the endocardial sites of the LV posterior and inferior walls (r = 0.61, P < .001; r = 0.56, P < .001, respectively). There were no relationships between CAVI and LV ejection fraction, peak systolic mitral annular motion velocity, or peak systolic strain rates of the LV walls. Multiple regression analysis revealed that the early diastolic strain rates at the endocardial sites of the LV walls are strongly correlated with CAVI. There were no relationships between the IMT and the LV systolic and diastolic parameters. CONCLUSION: These results suggest that cardiovascular risk factors interact to affect arterial stiffness and LV relaxation, and therefore support the importance of screening using CAVI and ultrasonic strain imaging and early intervention in this patient population.

Predictive value of associations between carotid arterial sclerosis and left ventricular diastolic dysfunction in patients with cardiovascular risk factors.

It is well known that arterial stiffness affects the morbidity and mortality associated with cardiovascular disease. However, there are limited data addressing the relationship between arterial stiffness and left ventricular (LV) diastolic function in patients with cardiovascular risk factors. Subclinical atherosclerosis was determined by measuring the intima-media thickness and stiffness (beta) of the left and right common carotid arteries using B- and M-mode ultrasonography in 30 patients with one or more cardiovascular risk factors. LV systolic and diastolic function were also determined by measuring transmitral flow velocity, mitral annular motion velocity, and myocardial strain and strain rate profiles using pulsed Doppler, tissue velocity, and ultrasonic strain imaging. The carotid stiffness beta was greater and the peak early diastolic strain rates of the LV posterior and inferior walls were lower in these patients than in the age-matched control group. The carotid intima-media thickness correlated only with body mass index and LV wall thickness. The carotid stiffness beta correlated with age, peak early diastolic velocity and deceleration time of the transmitral flow, peak early diastolic mitral annular motion velocity, and peak early diastolic strain rates of the LV walls. Multiple linear regression analysis revealed that early diastolic strain rates of the LV walls are strongly related to carotid stiffness beta. In conclusion, LV relaxation is significantly associated with carotid arterial atherosclerosis, particularly sclerosis, in patients with cardiovascular risk factors. These results support the importance of screening using ultrasonic strain imaging and early intervention in this patient population.

Three-dimensional evaluation of dobutamine-induced changes in regional myocardial deformation in ischemic myocardium using ultrasonic strain measurements: the role of circumferential myocardial shortening.

Early identification of myocardial ischemia during high-dose dobutamine stress (DOB) has important clinical implications. Myocardial strain imaging can evaluate regional myocardial contractility in the radial, longitudinal, and circumferential directions. The aim of this study was to assess precisely the differences in deterioration of myocardial deformation among the 3 directions in patients with newly developed myocardial ischemia during high-dose (40 microg/kg/min) DOB infusion. Color Doppler tissue 2-dimensional images were recorded during DOB infusion in 20 patients without myocardial ischemia and 25 patients with scintigraphically diagnosed myocardial ischemia caused by left anterior descending coronary artery stenosis. In the offline analysis, systolic radial strain (Sr), longitudinal strain (Sl), and circumferential strain (Sc) were determined in the anteroseptal and anterolateral left ventricular walls. In 20 patients without myocardial ischemia, the peak systolic strains significantly increased in all 3 directions during DOB infusion at rates between 5 and 10 microg/kg/min (Sr 50%-69%, Sl 27%-36%, Sc 29%-38%, all P < .01) with a greater rate of change in the Sr (1.8 and 1.9 times, respectively, P < .001) than in the Sl and Sc. However, the peak systolic strains decreased significantly during DOB infusion at rates between 5 and 10 microg/kg/min in all 3 directions (Sr 56%-35%, Sl 27%-13%, both P < .01; Sc 29%-7%, P < .001) with the greatest rate of change in the Sc in 25 patients with newly developed myocardial ischemia. In conclusion, circumferential myocardial shortening deteriorated to a greater extent during DOB infusion in patients with coronary artery stenosis, and its measurement is a promising tool for detecting newly developed myocardial ischemia.

Losartan improves regional left ventricular systolic and diastolic function in patients with hypertension: accurate evaluation using a newly developed color-coded tissue doppler imaging technique.

BACKGROUND: Angiotensin II receptor antagonists have recently been accepted as antihypertensive therapy. Tissue Doppler imaging (TDI) has been developed as a noninvasive tool to assess quantitatively regional myocardial motion abnormalities. This study was designed to determine whether our newly developed technique of color-coded TDI may be a useful means of quantifying the improvement in regional left ventricular (LV) myocardial contractility and relaxation after treatment with losartan in patients with hypertension. METHODS AND RESULTS: Losartan (50 to 100 mg) was administered for 6 months to 37 previously untreated patients with essential hypertension. Averaged myocardial velocity profiles (MVPs) for color-coded TDI were recorded in the ventricular septum and LV posterior wall before and after treatment. Peak myocardial velocities and peak myocardial velocity gradients (MVGs) in the LV walls were determined during systole and early diastole. The plasma concentration of transforming growth factor (TGF)-beta1 also was measured in all patients. Blood pressure and plasma TGF-beta1 level decreased after initiation of losartan therapy. The LV mass index and LV meridional end-systolic wall stress also decreased after treatment with losartan. LV geometry changed from a pattern consistent with concentric hypertrophy to normal geometry in 10 patients and to a pattern consistent with concentric remodeling in 5 patients, and from concentric remodeling to normal geometry in 5 patients after treatment with losartan. The ratio of early to late diastolic filling for the transmitral flow velocity increased after losartan treatment. The peak systolic and early diastolic myocardial velocities and MVGs in the ventricular septum and LV posterior wall increased after treatment with losartan, although the values 6 months after treatment with losartan were still lower than those in normal individuals. There were good correlations between changes in plasma TGF-beta1 level and changes in systolic and early diastolic MVGs 6 months after losartan. However, there were no significant correlations between changes in the systolic blood pressure and LV end-systolic wall stress and changes in the TDI parameters. CONCLUSION: Losartan improves regional LV function in patients with hypertension. Our newly developed averaged MVP and MVG measurements may be useful for accurately evaluating regional LV myocardial contractility and relaxation in these patients.

Diagnosis of cardiac amyloidosis based on the myocardial velocity profile in the hypertrophied left ventricular wall.

The myocardial velocity profile (MVP), derived from color-coded tissue Doppler imaging (TDI), can identify transmural heterogeneity based on the physiology and pathology of the myocardium. This study sought to clarify whether the MVP can differentiate cardiac amyloidosis from other causes of left ventricular hypertrophy. We recorded the MVP and determined its myocardial velocity gradient (MVG) in the ventricular septum and left ventricular posterior wall using color-coded TDI in 10 patients with cardiac amyloidosis, in 25 patients with hypertensive hypertrophied left ventricular wall, in 25 patients with asymmetric septal hypertrophy of hypertrophic cardiomyopathy, and in 20 clinically normal controls. End-diastolic ventricular septal thickness was similar among the cardiac amyloidosis, hypertension, and hypertrophic cardiomyopathy groups. Percent systolic thickening of the ventricular septum and left ventricular posterior wall calculated from M-mode left ventricular echocardiograms was lower in the cardiac amyloidosis group than in the hypertension, hypertrophic cardiomyopathy, or control group. Peak MVGs during systole and early diastole were lowest in the cardiac amyloidosis group, followed, in order, by the control, hypertension, and hypertrophic cardiomyopathy groups. The systolic and early diastolic MVPs in the ventricular septum and left ventricular posterior wall showed a characteristic serrated pattern in all patients with cardiac amyloidosis, but not in any other patient groups. In conclusion, MVPs in the ventricular septum and left ventricular posterior wall show a distinctive serrated pattern that may be related to amyloid deposition in the myocardium. Myocardial tissue characterization using color-coded TDI provides diagnostic information in patients with cardiac amyloidosis.

Syncope upon swallowing caused by an esophageal hiatal hernia compressing the left atrium: a case report.

We describe a patient with syncope associated with swallowing. This syncope was caused by transient compression of the left atrium (LA) by an esophageal hiatal hernia. Two-dimensional echocardiography demonstrated a hyperechoic mass compressing the LA from the posterior. With air insufflation of the esophagus, compression of the LA by this hernia sac was seen to increase. Pulsed and color Doppler echocardiography revealed greatly decreased velocity of blood flowing into the LA and left ventricle (LV). Thus, marked compression of the LA by an esophageal hiatal hernia can cause syncope by impeding blood flow from the LA to the LV. Echocardiography proved highly useful in diagnosis.

A patient responding to combined therapy with pirmenol and midodrine for refractory neurally mediated syncope complicated by prostatic hypertrophy.

A 67-year-old man with neurally mediated syncope (NMS) complicated by prostatic hypertrophy responded well to combined therapy with pirmenol and midodrine. In 2003, syncope occurred while the patient was driving a car. Results of head-up tilt-table testing (HUT) suggested a mixed type of NMS. Oral administration of disopyramide provided severe urinary obstruction. Pirmenol treatment was not associated with syncope during ordinary HUT, but nausea, sweating, and syncope occurred during HUT with provocative administration of isosorbide dinitrate. Combined therapy with pirmenol and midodrine avoided syncope during HUT, and has prevented attacks since discharge from the hospital.

Novel approach to the quantitation of regional left ventricular systolic and diastolic function using tissue Doppler imaging to create a myocardial velocity profile and gradient.

The myocardial velocity profile (MVP) and gradient (MVG) between the endocardium and epicardium of the left ventricular (LV) wall measured by color-coded tissue Doppler imaging (TDI) are new indices for evaluating regional LV myocardial function. However, accurate recording and measurement of the MVP is difficult using conventional methodology because of the stochastic nature of the ultrasound signal; that is, the effect of speckled noise. The aim of this study was to validate the accuracy and establish the validity of a newly developed method for measuring the MVP and MVG using 10 clinically normal controls and 10 patients with a hypertensive hypertrophied LV posterior wall. A non-isotropic, averaging algorithm was developed that was capable of obtaining a stable MVP (averaged MVP). Averaged MVP was recorded using parasternal, LV short-axis, color-coded TDI, placing regions of interest along the LV posterior wall with the reference point for angle-correction being at the center of LV contraction. The velocity from epicardium to endocardium within the region of interest was automatically angle-corrected to calculate the velocity component radially relative to the LV cavity and was spatially averaged along the circumference within the region of interest. Inter- and intraobserber variabilities of measurements were lower in the averaged MVP and MVG than in the conventional MVP and MVG. The correlation coefficients of the linear regression lines of systolic and early diastolic MVPs in the LV posterior wall were higher in all controls and hypertensive patients with the averaged method than with the conventional TDI procedures. The mean peak systolic and early diastolic MVGs were lower in the hypertensive group than in the controls. In conclusion, the newly developed averaged MVP provides a stable and reproducible index for the quantitative assessment of regional LV myocardial function.

Prognostic value of the atrial systolic mitral annular motion velocity in patients with left ventricular systolic dysfunction.

BACKGROUND: Transmitral flow velocity variables are powerful predictors of poor prognosis in patients with left ventricular (LV) systolic dysfunction. However, these variables may not accurately reflect the severity of pulmonary congestion. This study was designed to determine whether the peak atrial systolic mitral annular motion velocity (MA-Aw) measured by pulsed Doppler tissue imaging can predict cardiac death or hospitalization for worsening heart failure in patients with LV systolic dysfunction. METHODS: MA-Aw was recorded in 96 patients with LV systolic dysfunction who were followed up for 29 +/- 10 months. All patients underwent Doppler echocardiography on entry into the study, and cardiac catheterization was performed in 45 patients. Patients were divided into 3 groups on the basis of the ratio of early (E) to late (A) diastolic filling (E/A) of the transmitral flow velocity: group 1 (n=31; E/A < 1); group 2 (n=37; 1 < or = E/A < 2); and group 3 (n=28; E/A > or = 2). RESULTS: During follow-up, 36 patients (38%) died of cardiac causes and 34 (35%) were hospitalized for worsening heart failure. There were 2 cardiac deaths (6%) in group 1, 14 (39%) in group 2, and 20 (56%) in group 3. The MA-Aw correlated closely with the mean pulmonary capillary wedge pressure. Univariate Cox model analysis showed that MA-Aw < or = 5 cm/s was the most powerful predictor of cardiac death or hospitalization for worsening heart failure compared with clinical, hemodynamic, and the other echocardiographic variables. Furthermore, MA-Aw < or = 5 cm/s was clearly discernible as a good predictor of cardiac mortality on multivariate Cox model and as assessed by Kaplan-Meier method. CONCLUSION: The MA-Aw obtained by pulsed Doppler tissue imaging is a sensitive index of pulmonary congestion in patients with LV systolic dysfunction. It is a simple and noninvasive outcome measure and can be used to monitor treatment.