Normal and shear strains of the left ventricle in healthy human subjects measured by two-dimensional speckle tracking echocardiography.

BACKGROUND: Animal studies have shown that shear deformation of myocardial sheets in transmural planes of left ventricular (LV) wall is an important mechanism for systolic wall thickening, and normal and shear strains of the LV free wall differ from those of the interventricular septum (IVS). We sought to test whether these also hold for human hearts. METHODS: Thirty healthy volunteers (male 23 and female 7, aged 34 ± 6 years) from Outpatient Department of the University of Tokyo Hospital were included. Echocardiographic images were obtained in the left decubitus position using a commercially available system (Aloka SSD-6500, Japan) equipped with a 3.5-MHz transducer. The ECG was recorded simultaneously. The peak systolic radial normal strain (length change), shear strain (angle change) and time to peak systolic radial normal strain were obtained non-invasively by two-dimensional speckle tracking echocardiography. RESULTS: The peak systolic radial normal strain in both IVS and LV posterior wall (LVPW) showed a trend to increase progressively from the apical level to the basal level, especially at short axis views, and the peak systolic radial normal strain of LVPW was significantly greater than that of IVS at all three levels. The time to peak systolic radial normal strain was the shortest at the basal IVS, and increased progressively from the base to the apical IVS. It gradually increased from the apical to the basal LVPW in sequence, especially at short axis views. The peak of radial normal strain of LVPW occurred much later than the peak of IVS at all three levels. For IVS, the shear deformation was clockwise at basal level, and counterclockwise at mid and apical levels in LV long-axis view. For LVPW, the shear deformations were all counterclockwise in LV long-axis view and increased slightly from base to the apex. LVPW showed larger shear strains than IVS at all three levels. Bland-Altman analysis shows very good agreement between measurements taken by the same observer and by two independent observers. CONCLUSION: "Myocardial sheets" theory also holds true for intact human LV. Moreover, dyssynchrony exists even in healthy human subjects, which should be considered when evaluating the diseased hearts.

Volumetric and functional assessment of ventricles in pulmonary hypertension on 3-dimensional echocardiography.

BACKGROUND: Non-invasive assessment of volume and function on the right ventricle (RV) for pulmonary hypertension (PH) is limited. METHODS AND RESULTS: Patients with PH (n=23) underwent 3-dimensional (D) echocardiography (3DECHO), with cardiac magnetic resonance imaging to confirm its precision, and right heart catheterization. On linear regression analysis the RV end-systolic volume index (ESVI) was positively correlated with pulmonary vascular resistance (PVR) and mean pulmonary arterial pressure (mPAP; R=0.42 and 0.46, P=0.03 and 0.03, respectively). The RV end-diastolic volume index (EDVI) was positively correlated with mPAP (R=0.41, P<0.05). The left ventricular (LV) EDVI was inversely correlated with PVR (R=-0.48, P=0.02). The RV ejection fraction was inversely correlated with PVR and mean right atrial pressure (mRAP; R=-0.57, and -0.45, P=0.004, and 0.03, respectively). RVEDVI/LVEDVI and RVESVI/LVESVI (the diastolic and systolic remodeling indices, respectively) had a significantly positive linear relationship with PVR (R=0.67 and 0.55, P=0.0005 and 0.006, respectively), and the former had a significantly positive linear relationship with mRAP (R=0.42, P<0.05). During the recovery process in 1 specific case, the remodeling indices maintained a significant linear relationship with the hemodynamic parameters. CONCLUSIONS: Novel indices provided by 3DECHO may be utilized as alternative indicators of hemodynamic changes in PH patients.

Multiple coronary artery fistulae with biventricular hypertrophy.

Here, we report a case of multiple coronary artery fistulae with biventricular hypertrophy. The initial diagnosis of multiple coronary artery fistulae, draining into the left as well as the right ventricle, was made by standard transthoracic 2-dimensional and Doppler echocardiography. Later, multiple coronary fistulae communicating with the left ventricle through persistent sinusoids were diagnosed by coronary angiography.

Value of live 3D transoesophageal echocardiography in the diagnosis of mitral valve lesions.

We experienced a case in which live 3D transoesophageal echocardiography (TEE) was found much more valuable than 2D TEE in assessing mitral lesions in circumferential direction and making surgical plans for mitral valve prolapse.

A larger aortic annulus causes aortic regurgitation and a smaller aortic annulus causes aortic stenosis in bicuspid aortic valve.

A bicuspid aortic valve (BAV) often causes aortic stenosis (AS) or regurgitation (AR). In 54 patients with a BAV (48 +/- 16 years), transthoracic and transesophageal echo were performed to measure aortic annulus diameter (AAD), to evaluate the severity of aortic valve disease (AVD) and to calculate the area eccentricity index (AEI) of a BAV defined as a ratio of the larger aortic cusp area to a smaller aortic cusp area. By multiple linear regression analysis, the severity of AR correlated significantly with the AAD (r = 0.38) and AEI (r = 0.35) (P < 0.05) and that of AS correlated significantly with the AAD (r =-0.40) and AEI (r = 0.34) (P < 0.05). Thirty-six patients showed anteroposteriorly (A-P) located BAVs and 18 patients showed right-left (R-L) located BAVs. The AAD was larger in A-P type than in R-L type (15 +/- 3 vs 13 +/- 2 mm/BSA, P < 0.05) and there was no difference in the age and AEI between the two groups. AR was more severe in A-P type than in R-L type while AS was more severe in R-L type than in A-P type (P < 0.05). Twenty-nine patients showed raphes. The AEI was larger in raphe (+) type than in raphe (-) type (1.83 +/- 0.53 vs 1.51 +/- 0.47, P < 0.05) and there was no difference in the AAD and severity of AVD between the two groups. In conclusion, a BAV with larger aortic annulus or A-P located will tend to cause AR while a BAV with smaller aortic annulus or R-L located will tend to cause AS.

A one-year study of the antiatherosclerotic effect of the angiotensin-II receptor blocker losartan in hypertensive patients. A comparison with angiotension-converting enzyme inhibitors.

Angiotensin receptor blockers (ARB) have been emerging as drugs to treat atherosclerosis. The effectiveness of the ARB losartan at reducing atherosclerosis was compared with that of ACE inhibitors in hypertensive patients. A total of 50 patients with hypertension were divided into 3 groups: a control group receiving neither an ARB nor an ACE inhibitor (n = 14), a losartan group (n = 22) receiving 50 mg/day of losartan, and an ACE inhibitor group (n = 14) receiving either 5 mg/day of enalapril or 5 mg/day of imidapril. Atherosclerosis was evaluated based on the intima-media thickness (IMT) of the common carotid artery measured by B-mode ultrasound at baseline and after approximately 12 months of treatment. After the treatment, IMT significantly decreased with losartan (from 0.87 +/- 0.14 to 0.79 +/- 0.16 mm, P < 0.05) and with ACE inhibitor (from 0.81 +/- 0.14 to 0.74 +/- 0.11 mm, P < 0.05). The reduction was comparable between the two groups, -0.078 +/- 0.136 with losartan and -0.073 +/- 0.109 mm with ACE inhibitor, and the rate of the reduction was similar between the two drugs; -0.098 +/- 0.142 mm/year with losartan and (-0.076 +/- 0.118 mm/year) with ACE inhibitor. On the contrary, IMT did not change in the control group (from 0.90 +/- 0.20 to 0.95 +/- 0.26 mm) during the treatment period. Concomitant medication and coronary risk factors such as hyperlipidemia, diabetes mellitus, and smoking did not differ significantly among the groups. The antiatherosclerotic effect of losartan on the carotid artery was comparable to that of ACE-inhibitors, and less adverse effects, such as coughing that occurs with ACE inhibitors, were observed. Losartan appears to be a better alternative to ACE inhibitors for treating atherosclerosis in Japanese hypertensive patients.

Close physical contact of the heart with diaphragm causes pseudo-asynergy of left ventricular inferior wall in normal subjects.

Paradoxical outward movement of left ventricular (LV) inferior wall in systole is occasionally recognized in normal subjects and clinically important in terms of the differential diagnosis between physiological pseudo-asynergy and pathological asynergy. In this study, the potential mechanisms by which pseudo-asynergy of LV inferior wall (PLI) is observed in normal subjects were investigated. PLI was defined as the outward movement of LV inferior wall observed during more than 50% of systole. The incidence of PLI was evaluated in 7843 consecutive subjects in routine echocardiography. The effects of body position and artificial gravity on the manifestation of PLI were also examined. PLI was observed in 0.11% (9/7842) of subjects on left lateral position. Measurement of the angle formed by LV long-axis and the long-axis of the body on frontal plane revealed that hearts in subjects with PLI were in relatively horizontal position. PLI was observed on sitting position in 43% (40/92) of subjects without PLI on left lateral position. The subjects with sitting position-induced PLI exhibited significantly higher obesity index. PLI was also induced by artificial gravity in 67% (14/21) of healthy volunteers on supine position, and the degree of PLI correlated with the intensity of gravity. Although the incidence of PLI in routine echocardiography is relatively low, PLI can be induced in normal subjects by any condition that causes close contact of LV inferior wall to diaphragm. Thus, PLI should be taken into consideration in the differential diagnosis of abnormal LV inferior wall motion, especially when performing exercise echocardiography.

Carvedilol therapy improved left ventricular function in a patient with arrhythmogenic right ventricular cardiomyopathy.

An asymptomatic 35 year-old man was referred to our hospital because of abnormal ECG findings. The ECG showed complete right bundle branch block and left anterior hemiblock. Echocardiography revealed a moderately enlarged right ventricle (RV) and an apical aneurysm. RV wall motion showed diffusely moderate impairment, while the systolic function of the left ventricle (LV) was slightly decreased. The ejection fractions (EF) of the RV and LV were calculated as 28.1% and 41.9% by Simpson's method using multiple cardiac computed tomography (CT) scans. A 24 hour ambulatory ECG showed only 372 single premature ventricular contractions (PVC). Cardiac catheterizaion revealed that the RV was enlarged with prominent trabeculation and decreased motion. In an electrophysiologic study, neither electrical stimulation of the RV nor electrical stimulation plus isoproterenol infusion could induce ventricular tachycardia. Pathological examination of a biopsy from the interventricular septum of the RV revealed fibrofatty change in the myocardium. Based on these results, we made a diagnosis of arrhythmogenic right ventriclular cardiomyopathy (ARVC) and administered 5 mg of carvedilol. Sixty days after the initiation of carvedilol therapy, we performed repeat cardiac CT. The EF of the LV was markedly improved from 41.9% to 62.0%, although the EF of the RV was not changed. The number of PVCs showed no change. This case suggests that carvedilol is not only useful for controlling arrhythmia but also for improving left ventriclular function in some patients with ARVC. Sympathetic overactivity is reported to cause sudden death, so carvedilol may be a first-line drug for some patients with ARVC.

Common carotid intima-media thickness is correlated with myocardial flow reserve in patients with coronary artery disease: a useful non-invasive indicator of coronary atherosclerosis.

BACKGROUND: The common carotid intima-media thickness (IMT) is correlated with the angiographically determined coronary artery stenosis. However, their correlation is weak, which limits the clinical application of the IMT as a predictor of coronary artery stenosis. The IMT reflects diffuse early-phase atherosclerosis, whereas the angiographically determined coronary artery stenosis is a late-phase phenomenon. The latter is localized and rapidly progressive with plaque rupture and acute thrombosis. Instead of the angiographically determined coronary artery stenosis, we employed myocardial flow reserve (MFR) that reflects diffuse early-phase coronary atherosclerosis and impaired coronary vasodilatation function. We evaluated the relationship between the IMT and the MFR. METHODS: Twenty-three patients with angiographically diagnosed coronary artery disease (CAD) underwent B-mode ultrasound examination to measure their common carotid IMT and positron emission tomography (PET) with dipyridamole intervention to obtain their MFR. We also performed B-mode ultrasound examination in 21 patients with hypertension without CAD and in 15 control subjects. RESULTS: The common carotid IMT in patients with CAD was thickened (0.92+/-0.15 vs. 0.81+/-0.14 mm in patients with hypertension (P<0.05) and 0.69+/-0.13 mm in control subjects (P<0.01)). The IMT was inversely correlated with the MFR (r=0.51, P<0.01). The correlations between the MFR and most of the coronary risk factors (age, blood pressure, serum cholesterol level and triglyceride level, HbA1c level, smoking index) did not reach statistical significance. CONCLUSIONS: Thickened common carotid IMT is also an indicator of reduced MFR or early-phase coronary atherosclerosis.

Sodium calcium exchanger plays a key role in alteration of cardiac function in response to pressure overload.

The Na+-Ca2+ exchanger (NCX) on the plasma membrane is thought to be the main calcium extrusion system from the cytosol to the extracellular space in many mammalian excitable cells, including cardiac myocytes. However, the pathophysiological role of NCX in the heart is still unclear because of the lack of known specific inhibitors of NCX. To determine the role of NCX in cardiac contraction and the development of cardiac hypertrophy, we imposed pressure overload on the heart of heterozygous NCX knockout (KO) mice by constricting transverse aorta, and examined cardiac function and morphology 3 wk after operation. Although there was no difference in cardiac function between sham-operated KO mice and sham-operated wild-type (WT) mice, KO mice showed higher left ventricular pressure and better systolic function than WT mice in response to pressure overload. Northern blot analysis revealed that mRNA levels of sarcoplasmic reticulum Ca2+-ATPase were reduced by pressure overload in left ventricles of WT but not of KO mice. However, hypertrophic changes with interstitial fibrosis were more prominent in KO mice than WT mice. These results suggest that reduction of NCX results in supernormalized cardiac function and causes marked cardiac hypertrophy in response to pressure overload.

Effusive constrictive pericarditis due to rheumatoid arthritis revealed by pericardiocentesis with simultaneous pressure recording--a case report.

A 59-year-old man had a history of rheumatoid arthritis. He presented with incurable pericardial effusion. He was repeatedly treated with pericardiocentesis with only transient attenuation of his symptoms because the underlying pericardial constriction had been overlooked. This time the authors diagnosed effusive constrictive pericarditis due to rheumatoid arthritis using the hemodynamic findings observed before and after pericardiocentesis.

Effects of rapid saline infusion on orthostatic intolerance and autonomic tone after 20 days bed rest.

To test whether acute volume expansion can normalize orthostatic intolerance and autonomic tone after prolonged bed rest (BR), 23 men were subjected to 20 days BR. Left ventricular (LV) echocardiography was performed during the lower body negative pressure (LBNP) test before and after BR with and without preceding rapid infusion of saline (1,500 ml/30 min). Saline infusion restored heart rate, LV dimension, and stroke volume during LBNP, increased cardiac output (from 4.1 +/- 1 to 5.3 +/- 1 L/min), and normalized LBNP tolerance time (from 11 +/- 4 to 23 +/- 6 minutes). In 9 men, a Holter electrocardiogram was recorded on the day before BR, the fourth and twentieth days of BR, and the day after BR. The high-frequency component of heart rate variability during sleep gradually decreased and reached the lowest level on the day after BR (100%, 66 +/- 16%, 39 +/- 18%, 10 +/- 8%). Thus, restoring decreased blood volume is an effective countermeasure for orthostatic intolerance after BR. However, decreased vagal tone persisted, suggesting reset autonomic tone.

Effects of Dobutamine Infusion on Mitral Regurgitation.

Both intensity of mitral regurgitant murmur and color-coded Doppler regurgitant signal area have been reported to correlate with the degree of regurgitation. To evaluate the relationship between the intensity of regurgitant murmur and severity of mitral regurgitation, phonocardiography, echocardiography, and Doppler ultrasound were performed in 18 patients with mitral regurgitation before and during dobutamine infusion. Mitral regurgitation was due to mitral valve prolapse with ruptured chordae tendineae in 8 patients, rheumatic change in 5 patients, and dilated cardiomyopathy in 5 patients. With intravenous dobutamine infusion, heart rate (77-103 beats/min), systolic blood pressure (119-144 mmHg), peak mitral regurgitant jet velocity (4.5-5.4 m/sec), intensity of mitral regurgitant murmur (to 201% of that before infusion in early systole) increased, while left ventricular end-diastolic volume (124-102 mm), left ventricular end-systolic volume (57-42 mm), mitral anular diameter (33-28 mm), and color Doppler mitral regurgitant signal area (704-416 mm(2)) decreased (P < 0.05). Total (forward + backward) left ventricular stroke volume (66-61 mL/beat) showed no change. Dobutamine decreased mitral regurgitant flow/beat, regardless of etiology of mitral regurgitation, which was probably due to the decrease of left ventricular size and mitral annular diameter. Although total (forward + backward) left ventricular stroke volume was unchanged, dobutamine effectively increased forward left ventricular stroke volume by decreasing backward regurgitation. Mitral regurgitant murmur became louder despite the decrease of mitral regurgation, indicating the uselessness of auscultation in the grading of the severity of mitral regurgitation.