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Biomedical subjects

Junichi Yoshida

Publications and source records attributed to Junichi Yoshida.

At least 19 recordsLinked to original sources

Therapeutic effects of angiotensin II type 1 receptor blocker at an advanced stage of hypertensive diastolic heart failure.

OBJECTIVE: Angiotensin II type 1 receptor blocker (ARB) is increasingly prescribed for the treatment of systolic heart failure with a growing body of clinical evidence. The roles of ARB, however, remain to be clarified in the treatment of diastolic heart failure (DHF), particularly at its advanced stage. This experimental study investigated the effects of ARB administered at an advanced stage of hypertensive DHF. METHODS: Dahl salt-sensitive rats fed an 8% NaCl diet from age 7 weeks represent overt DHF at age 20 weeks, as noted in previous studies (hypertensive DHF model). The DHF model rats were randomly divided into two groups at age 17 weeks when left ventricular diastolic dysfunction, hypertrophy, fibrosis, macrophage infiltration and reactive oxygen species generation were already augmented; six rats treated for 3 weeks with a subdepressor dose of ARB (olmesartan 0.6 mg/kg per day), and six untreated rats. RESULTS: The 3-week administration of ARB significantly decreased the left ventricular end-diastolic pressure in association with attenuation of left ventricular hypertrophy, fibrosis and diastolic dysfunction. Macrophage infiltration was attenuated with decreased gene expression of transforming growth factor-beta1 and monocyte chemoattractant protein-1 in the left ventricular myocardium of the ARB-treated rats. The production of reactive oxygen species also decreased with NADPH oxidase activity. CONCLUSIONS: ARB provides beneficial effects in hypertensive DHF independent of its antihypertensive effects even if initiated at an advanced stage. The beneficial effects are at least partly attributed to the attenuation of inflammatory changes and oxidative stress through the suppression of cytokine and chemokine production and of NADPH oxidase activity.

Angiotensin II Type 1 Receptor Blockers↗

Elevated cardiac tissue level of aldosterone and mineralocorticoid receptor in diastolic heart failure: Beneficial effects of mineralocorticoid receptor blocker.

Cardiac aldosterone levels have not been evaluated in diastolic heart failure (DHF), and its roles in this type of heart failure remain unclear. This study aimed to detect cardiac aldosterone by use of a liquid chromatographic-mass spectrometric method and to assess the effects of mineralocorticoid receptor blockade on hypertensive DHF. Dahl salt-sensitive rats fed 8% NaCl diet from 7 wk (hypertensive DHF model) were divided at 13 wk into three groups: those treated with subdepressor doses of eplerenone (12.5 or 40 mg x kg(-1) x day(-1)) and an untreated group. Dahl salt-sensitive rats fed 0.3% NaCl diet served as controls. Cardiac aldosterone was detected in the DHF rats but not in the control rats, with increased ventricular levels of mineralocorticoid receptor. Cardiac levels of 11-deoxycorticosterone, corticosterone, and 11-dehydrocorticosterone were not different between the control and DHF rats, but the tissue level of corticosterone that has an affinity to mineralocorticoid receptor was 1,000 times as high as that of aldosterone. Aldosterone synthase activity and CYP11B2 mRNA were undetectable in the ventricular tissue of the DHF rats. Administration of eplerenone attenuated ventricular hypertrophy, ventricular fibrosis, myocardial stiffening, and relaxation abnormality, leading to the prevention of overt DHF. In summary, the myocardial aldosterone level increased in the DHF rats. However, its value was extremely low compared with corticosterone, and no evidence for enhancement of intrinsic myocardial aldosterone production was found. The upregulation of mineralocorticoid receptor may play a central role in the pathogenesis of DHF, and blockade of mineralocorticoid receptor is likely an effective therapeutic regimen of DHF.

Aldosterone↗

SFTG international collaborative study on in vitro micronucleus test IV. Using CHL cells.

In this report, are presented the results of an international collaborative study on the in vitro micronucleus assay, using CHL cells. Fourteen laboratories participated in this study which was coordinated by an organizing committee supported by the SFTG (the French branch of the European Environmental Mutagen Society). Nine coded substances, having different modes of action and at different levels were assessed in the in vitro micronucleus test, using a common protocol. Mitomycin C was used as a positive control. In order to help to define a standard protocol on CHL cells, short and long treatment periods followed by various recovery times, with or without cytochalasin B, were compared. After an evaluation of the acceptability of the assays, the tested chemicals were classified as negative, positive or equivocal. Mannitol and clofibrate were judged as negative in all treatment schedules. Bleomycin was positive in all the treatment schedules, with an increase in the number of micronucleated cells in both mononucleate and binucleate cells when using cytochalasin B. This was also shown for the aneugens colchicine, diethylstilboestrol and griseofulvin, as expected. Urethane was judged as equivocal only after long treatment with cytochalasin B, and negative in all other treatment schedules. In any case, no genotoxic compound would have been missed with schedules including a short and a long treatment time, whether the treatment was followed by a recovery period or not and whether cytochalasin B was used or not. Thus, these results show that CHL cells were suitable for accurately detecting clastogenic and aneugenic compounds of various types in the in vitro micronucleus test.

Aneugens↗

Surgical site infection in general and thoracic surgery: surveillance of 2 663 cases in a Japanese teaching hospital.

PURPOSE: We conducted a prospective survey of 2 663 surgical patients in a Japanese teaching hospital to look for any risk factors predisposing to surgical site infection (SSI) other than the National Nosocomial Infection Surveillance (NNIS) System risk indices; namely, performance status, operative time, wound classification, and endoscopic use. METHODS: Our Infection Control Team recorded data for 5 years using the Japanese SSI surveillance system. We divided the incidence of SSI for each risk index category by the NNIS reference data to produce the standardized infection ratio (SIR). RESULTS: The representative procedure, SSI rate, and SIR in the 2663 patients were as follows: colectomy, 6.0%, 0.917; esophagectomy, 19.4%, 6.020; mastectomy, 0.5%, 0.401; rectal surgery, 8.7%, 1.136; thoracic surgery, 1.5%, 1.137; and biliary surgery, 13.4%, 1.937. We also found age to be a significant risk factor. CONCLUSIONS: The NNIS system risk indices should separate rectal surgery from colorectal surgery, and separate esophagectomy from other gastrointestinal surgery. Age should also be included as an SSI risk index.

Data Collection↗

Different effects of long- and short-acting loop diuretics on survival rate in Dahl high-salt heart failure model rats.

OBJECTIVES: We compared therapeutic effects of furosemide, a short-acting loop diuretic, and azosemide, a long-acting one, in hypertensive heart failure rats to test the hypothesis that long-acting diuretics are superior to short-acting types in heart failure. METHODS: Dahl salt-sensitive rats fed an 8% NaCl diet from age 8 weeks were divided at age 21 weeks (compensated hypertrophic stage) into three groups: rats treated with furosemide (40 mg/kg/day), those treated with azosemide (80 mg/kg/day) and untreated rats. Rats fed a 0.3% NaCl diet served as controls. RESULTS: Both medications prevented left ventricular systolic dysfunction and enlargement at age 31 weeks, and attenuated macrophage infiltration, reactive oxygen species generation, and gelatinolytic activity to the same degree. Azosemide suppressed left ventricular fibrosis to the control level, but furosemide did not. Azosemide ameliorated myocardial catecholamine depletion and improved survival rate. Furosemide increased plasma norepinephrine levels and did not exert such beneficial effects. CONCLUSIONS: Azosemide provided better prognosis in heart failure rats compared with furosemide, partly through attenuation of the reflex increase in cardiac sympathetic neuronal activity caused by the development of heart failure. The current findings suggest a need for clinical trials examining whether long- and short-acting diuretics provide a different prognosis in patients with heart failure.

Animals↗

Evaluation of liver and peripheral blood micronucleus assays with 9 chemicals using young rats. A study by the Collaborative Study Group for the Micronucleus Test (CSGMT)/Japanese Environmental Mutagen Society (JEMS)-Mammalian Mutagenicity Study Group (MMS).

We conducted simultaneous liver and peripheral blood micronucleus assays in young rats with seven rodent hepatocarcinogens-4,4'-methylenedianiline (MDA), quinoline, o-toluidine, 4-chloro-o-phenylenediamine (CPDA), dimethylnitrosamine (DMN), p-dimethylaminoazobenzene (DAB), and di(2-ethylhexyl)phthalate (DEHP)-and two mutagenic chemicals-kojic acid and methylmethanesulfonate (MMS). Quinoline, DMN, and DAB were positive in the liver assay, while o-toluidine, kojic acid, DAB, and MMS were positive in the peripheral blood assay. o-Toluidine, kojic acid, and DAB are reportedly negative in mouse bone marrow micronucleus assays, indicating a species difference. Our results revealed a correlation between micronucleus induction in hepatocytes and hepatocarcinogenicity. This technique can be useful for the detection of micronucleus-inducing chemicals that require metabolic activation, and it enables simultaneous comparison of the micronucleus-inducing potential of chemicals in the liver and peripheral blood in the same individual.

Aniline Compounds↗

Long-term histological outcomes of injected autologous fat into human vocal folds after secondary laryngectomy.

OBJECTIVE: To histologically evaluate the long-term outcomes of autologous fat grafts after injection laryngoplasty in the human larynx. STUDY DESIGN AND SETTING: We injected liposuctioned fat for vocal fold augmentation in patients with vocal fold paralysis. We suctioned autologous fat from the low abdomen with an 18-G disposable needle and a 20-mL disposable syringe under negative pressure. This is different from the conventional liposuction technique and avoids the use of special equipment. In this article, we report the histological evaluation of 2 patients (patient 1: 12 months, patient 2: 41 months) who required total laryngectomy after autologous fat injection into the vocal folds. RESULTS: Histological examination revealed normal-appearing viable adipocytes with minimal inflammatory response in both patients. CONCLUSIONS: Our liposuctioned autologous fat injection histologically offered long-term improvement in patients with impaired glottal closure from vocal fold paralysis.

Adipocytes↗

ACE inhibitor and angiotensin II type 1 receptor blocker differently regulate ventricular fibrosis in hypertensive diastolic heart failure.

BACKGROUND: Promoted myocardial stiffening has a crucial role in the transition to overt diastolic heart failure (DHF) in hypertensive hearts and is attributed to progressive ventricular fibrosis. Previous studies revealed the effects of an angiotensin II type 1 receptor blocker (ARB) and an angiotensin-converting enzyme inhibitor (ACEI) on the synthesis and degradation of collagens in the other phenotype of heart failure, systolic heart failure, which has a different pathophysiology; however, little is known about their effects in DHF. OBJECTIVE: To investigate effects of an ACEI and an ARB on the regulatory system of ventricular fibrosis in hypertensive DHF. DESIGN AND METHODS: Dahl salt-sensitive rats fed a diet containing 8% NaCl from age 7 weeks (DHF model) were divided into three groups: six untreated rats, six rats treated with a subdepressor dose of an ARB, candesartan cilexetil (1 mg/kg per day), from age 8 weeks, and six rats treated with a subdepress or dose of an ACEI, temocapril hydrochloride (0.2 mg/kg per day), from age 8 weeks. Six Dahl salt-sensitive rats fed on normal chow served as controls. Data were collected when animals were aged 20 weeks. RESULTS: The administration of an ARB or an ACEI inhibited ventricular fibrosis to the same degree. The ACEI decreased the level of type I collagen mRNA, but the decrease was less than that induced by the ARB. The difference in collagen synthesis was probably cancelled out by that in degradation: both in-vitro and in-situ zymography showed that gelatinase activity was greater in the rats treated with the ACEI than in those treated with the ARB. CONCLUSIONS: An ARB and an ACEI inhibited ventricular fibrosis through different mechanisms in hypertensive DHF.

Angiotensin II Type 1 Receptor Blockers↗

Long-term effect of spironolactone on cardiac structure as assessed by analysis of ultrasonic radio-frequency signals in patients with ventricular hypertrophy.

BACKGROUND: An effect of aldosterone on ventricular fibrosis has been demonstrated in animals, but remains unclear in human patients. This study aimed to investigate (1) the relationship between left ventricular (LV) fibrosis and myocardial ultrasonic texture as assessed with myocardial radio-frequency (RF) signals analyzed from the viewpoint of their waveform with chaos theory in animals and (2) serial changes in myocardial ultrasonic texture following long-term aldosterone blockade in patients with LV hypertrophy. METHODS AND RESULTS: In an animal study, Sprague-Dawley rats were divided into 2 groups with and without adriamycin administration, and the relationship between the RF signals and LV fibrosis was assessed. In a clinical study, effects of 12-month-administration of spironolactone were assessed in patients with LV hypertrophy. The animal study revealed that the correlation dimension (CD) calculated from the RF signals inversely correlated with the area of fibrosis. The clinical study demonstrated an increase in CD following 6-month administration of spironolactone. The changes in CD positively correlated with those in the serum carboxy-terminal telopeptide of collagen type I. CONCLUSION: Myocardial RF signals analyzed with chaos theory reflect the severity of LV fibrosis. Aldosterone blockade may alter myocardial ultrasonic texture with regression of LV fibrosis, at least partly through enhanced collagen degradation.

Adult↗

Activation of matrix metalloproteinases precedes left ventricular remodeling in hypertensive heart failure rats: its inhibition as a primary effect of Angiotensin-converting enzyme inhibitor.

BACKGROUND: Matrix metalloproteinases (MMPs) are activated in dilated failing hearts, and angiotensin-converting enzyme (ACE) inhibition prevents left ventricular (LV) dilatation. However, it remains unclear whether activation of MMPs precedes or is secondary to LV remodeling, and an effect of ACE inhibition on MMPs is unknown. METHODS AND RESULTS: Dahl salt-sensitive rats fed a high-salt diet from 8 weeks served as the hypertensive heart failure (HF) model. LV echo, histological study, measurement of mRNA levels, and gelatin zymography were performed before (at 23 weeks) and after (at 26 weeks) the development of LV dilatation and pulmonary edema. The same procedures were conducted in the HF model rats treated with a subdepressor dose of ACE inhibitor (enalapril 5 mg x kg(-1) x d(-1)) from 9 weeks. Rats fed on normal chow served as age-matched controls. In the untreated HF model rats, gene expression of MMP-2 and MMP-9 and tissue gelatinase activity were elevated at 23 weeks without LV dilatation. LV dilatation, LV systolic dysfunction, and pulmonary edema occurred at 26 weeks, with further enhancement of the expression and activity of MMPs. ACE inhibition prevented such geometrical and functional deterioration. The gene expression and activity of MMPs were suppressed by ACE inhibition at 23 weeks without a decrease in blood pressure, and the suppressive effects continued at 26 weeks. CONCLUSIONS: MMPs are likely to trigger and promote LV remodeling, and ACE inhibition directly exerts inhibitory effect on MMPs, leading to the prevention of LV remodeling and dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗

AT1 receptor blocker added to ACE inhibitor provides benefits at advanced stage of hypertensive diastolic heart failure.

Diastolic heart failure (DHF) has become a social burden; however, evidences leading to its therapeutic strategy are lacking. This study investigated effects of addition of angiotensin II type 1 receptor blocker (ARB) to angiotensin-converting enzyme inhibitor (ACEI) at advanced stage of DHF in hypertensive rats. Dahl salt-sensitive rats fed 8% NaCl diet from age 7 weeks served as DHF model, and those fed a normal chow served as control. The DHF model rats were arbitrarily assigned to 3 treatment regimens at age 17 weeks: ACEI (temocapril 0.4 mg/kg per day), combination of ACEI (temocapril 0.2 mg/kg per day) with ARB (olmesartan 0.3 mg/kg per day), or placebo. At age 17 weeks, this model represents progressive ventricular hypertrophy and fibrosis, relaxation abnormality, and myocardial stiffening. Data were collected at age 20 weeks. As compared with the monotherapy with ACEI, the addition of ARB induced more prominent suppression of ventricular hypertrophy and fibrosis, leading to suppression of myocardial stiffening, improvement of relaxation, and inhibition of hemodynamic deterioration. Such benefits were associated with greater decreases in reactive oxygen species (ROS) generation, macrophage infiltration, and gene expression of transforming growth factor (TGF)-beta(1) and interleukin (IL)-1beta, but not with changes in gene expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-alpha. Thus, ARB added to ACEI provides more benefits as compared with ACEI alone in DHF when initiated at an advanced stage. The additive effects are likely provided through more prominent suppression of ROS generation and inflammatory changes without effects on expression of MCP-1 and TNF-alpha.

Angiotensin II Type 1 Receptor Blockers↗

Elevation of plasma brain natriuretic peptide is a hallmark of diastolic heart failure independent of ventricular hypertrophy.

OBJECTIVES: We tested a hypothesis that elevation of the plasma level of brain natriuretic peptide (BNP) is one of the characteristics of patients with diastolic heart failure (DHF) independent of left ventricular (LV) hypertrophy. BACKGROUND: The clinical characteristics of DHF are not well acknowledged, although DHF has become a great social burden. Such a lack of clinical information leads to inaccuracy in the diagnosis of DHF. We have demonstrated enhancement of ventricular production of BNP with progression of maladaptive ventricular hypertrophy, but not with development of compensatory hypertrophy in an animal DHF model. METHODS: Of 372 patients who presented to the emergency department because of acute pulmonary congestion without acute coronary syndrome between January 1996 and May 2002, those with an ejection fraction > or =45% upon admission, who were stably controlled at least for a year in our outpatient clinics, comprised the DHF group (n = 19). A control group consisted of 22 hypertensive patients with a LV mass index greater than or equal to its minimum value of the DHF group and an ejection fraction > or =45%, in whom cardiac symptoms had not occurred. RESULTS: Despite a similar distribution of LV mass index, the BNP level was higher in the DHF group than in the control group (149 +/- 38 vs. 31 +/- 5 pg/ml, p < 0.01). There was no difference in LV cavity size or parameters derived from pulsed Doppler transmitral flow velocity curves. CONCLUSIONS: An elevation of BNP may be a hallmark of patients with or at risk of DHF among subjects with preserved systolic function independent of LV hypertrophy.

Aged↗

N-methylethanolamine attenuates cardiac fibrosis and improves diastolic function: inhibition of phospholipase D as a possible mechanism.

AIM: Ventricular fibrosis is promoted by many effectors that chronically activate phospholipase D (PLD), and induces cardiac dysfunction and heart failure in cardiovascular diseases. Since ethanolamine is a product of PLD, we hypothesised that an administration of an analogue of ethanolamine, N-methylethanolamine (MEA), decreases PLD activity through a negative feedback mechanism, suppresses collagen accumulation, and thus prevents organ dysfunction. METHODS AND RESULTS: In human fibroblasts 1-butanol inhibited collagen synthesis and enhanced collagenase production, but iso-butanol did not. These indicate crucial roles of PLD in collagen synthesis and degradation. In fibroblasts, MEA dose-dependently decreased PLD activity, inhibited collagen synthesis and enhanced collagenase production. In a hypertensive heart failure model using Dahl-Iwai salt-sensitive rats, PLD activity increased with progressive ventricular fibrosis, leading to myocardial stiffening and overt heart failure. Long-term administration of MEA did not significantly decrease blood pressure, however, but decreased PLD activity and collagen content with inhibited gene expression of collagens, leading to the prevention of myocardial stiffening and haemodynamic deterioration. MEA also attenuated ventricular hypertrophy, another detrimental structural alteration. CONCLUSION: MEA may exert therapeutic effects on cardiac disorders due to ventricular fibrosis through suppression of PLD activity and modulation of the fibrosis pathway even without relief from mechanical stress.

Animals↗

Prolonged oral treatment with an essential amino acid L-leucine does not affect female reproductive function and embryo-fetal development in rats.

L-leucine, an essential amino acid, is one of the most popular ingredients in dietary supplements. To investigate a possibility of its embryo-fetal toxicity in rats, 11- to 12-week old dams were orally administered an aqueous solution of L-leucine at doses of 300 or 1000 mg/kg body weight on gestational days 7-17. Body weight and feed intake was evaluated throughout the whole course of pregnancy (days 0-20). L-Leucine did not influence body weight, but at a dose of 1000 mg/kg, slightly enhanced feed intake on days 14 and 18 of pregnancy. Caesarean section (day 20) revealed no influences on the litter size and weight of live-born fetuses, the number of corpora lutea, implantation index or the quality of placenta, and the minor increase in feed intake was considered irrelevant to the pregnancy outcomes. Fetuses were evaluated in a battery of external, visceral and skeletal examinations. No effects of L-leucine on gender ratio and external abnormalities, and no significant treatment-related variations in visceral and skeletal pathologies were observed. These results suggested that L-leucine, administered orally during organogenesis at doses up to 1000 mg/kg body weight, did not affect the outcome of pregnancy and did not cause fetotoxicity in rats.

Administration, Oral↗

Temocapril prevents transition to diastolic heart failure in rats even if initiated after appearance of LV hypertrophy and diastolic dysfunction.

OBJECTIVE: Congestive heart failure with left ventricular (LV) diastolic dysfunction and preserved systolic function, i.e. diastolic heart failure (DHF), is often observed in hypertensive patients. Although angiotensin converting enzyme (ACE) inhibitors are widely used as antihypertensive therapy, there is a continued controversy about long-term effect of ACE inhibition on diastolic function. The current study was designed to elucidate a therapeutic effect of ACE inhibitor, temocapril, administration initiated after LV hypertrophy (LVH) and diastolic dysfunction are evident. METHODS: Dahl salt sensitive rats fed on 8% NaCl diet from 7 weeks (hypertensive DHF model) were studied at 13 weeks (n=6) or at 19 weeks following chronic administration of a subdepressor dose of temocapril (0.2 mg/kg/day, TEM(+), n=6) or placebo (TEM(-), n=7) from 13 weeks. RESULTS: Compensatory LVH was associated with prolonged time constant of LV relaxation (Tau) at 13 weeks. In TEM(-), progression of LVH and fibrosis and elevation of LV end diastolic pressure were observed at 19 weeks. Administration of temocapril from 13 weeks prevented the further progression of LVH and fibrosis, attenuated increases in myocardial stiffness constant and Tau, and prevented the development of DHF. These effects were accompanied with the attenuation of decreases in sarcoplasmic reticulum calcium(2+)-ATPase 2a and phosphorylated phospholamban and of hypertrophic signalings' upregulation. CONCLUSIONS: This study demonstrated that chronic administration of temocapril exerts a therapeutic effect on diastolic dysfunction and prevents the transition to DHF even if initiated after appearance of LVH and diastolic dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗

Differential activation of matrix metalloproteinases in heart failure with and without ventricular dilatation.

OBJECTIVE: Remodeling of extracellular matrix (ECM) is considered to contribute to progression of left ventricular (LV) remodeling and matrix metalloproteinases (MMPs) play crucial roles in regulation of ECM. Activation of MMPs is observed in systolic heart failure (SHF) and is suggested to be responsible for LV dilatation in SHF. Diastolic heart failure (DHF) that is not associated with LV dilatation is also accompanied with collagen accumulation; however, differences in ECM regulatory system, especially activation of MMPs, between SHF and DHF remain to be clarified. This study was conducted to clarify whether MMPs are activated even in DHF, and if so, to characterize the difference in activation of MMPs between SHF and DHF for identification of a target for the prevention of LV remodeling in SHF. METHODS: To exclude effects of differences in underling cardiovascular diseases and genetic background on the comparison between DHF and SHF, we used Dahl salt-sensitive rats fed on high salt diet starting at 7 weeks of age as DHF model and at 8 weeks as SHF model, both of which our laboratory recently developed. RESULTS: LV fibrosis progressed in the DHF and SHF model rats. MMP-2 was activated to the same degree in both rats. Activation of MMP-9 was enhanced in the DHF model rats, but the activity was more enhanced in the SHF rats. Film in situ zymography showed that enhanced gelatinolytic activity appeared only in the mid layer of the LV wall in the DHF rats and throughout the wall in the SHF rats. The distribution of gelatinolytic activity was consistent with that of expression of MMP-9 as assessed in immunohistochemical study. CONCLUSIONS: MMP-9 rather than MMP-2 may be involved in LV dilatation in SHF and be a specific target for the prevention of LV remodeling.

Animals↗

Instantaneous assessment of left ventricular midwall mechanics with tissue Doppler tracking technique.

BACKGROUND: Left ventricular (LV) systolic function is better characterized by midwall mechanics in patients with LV hypertrophy than by endocardial LV function, and the midwall mechanics is an independent predictor of prognosis. However, a complex calculation is currently required to assess it, and it is not routinely assessable in clinical practice. Tissue Doppler imaging enables tracking of a point within the LV wall though a cardiac cycle; we tested our hypothesis that the tissue Doppler tracking technique provides an instantaneous and reliable evaluation of midwall mechanics. METHODS: LV M-mode echocardiogram was recorded in 18 subjects with conventional echocardiography and with tissue Doppler imaging. The midwall shortening was calculated from the data obtained with conventional echocardiography for the comparison with that measured with the tissue Doppler tracking technique. The tissue Doppler-determined midwall shortening correlated well with conventionally calculated value (r=.84, P<.0001), and their difference was small irrespective of absolute value of the midwall shortening. CONCLUSIONS: The midwall mechanics can be instantaneously and accurately evaluated with the tissue Doppler tracking technique.

Adult↗