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Biomedical subjects

J Yoshikawa

Publications and source records attributed to J Yoshikawa.

At least 145 records · Page 8Linked to original sources
PubMed1999

Regulation of rat mesangial cell migration by platelet-derived growth factor, angiotensin II, and adrenomedullin.

This study sought to determine whether platelet-derived growth factor (PDGF) and angiotensin II (AngII) stimulate migration of cultured rat glomerular mesangial cells. After finding that this was so, the effects of adrenomedullin (ADM) and cAMP-elevating agents on basal and stimulated mesangial cell migration were examined. Two isoforms of PDGF, AB and BB, stimulated migration in a concentration-dependent manner between 1 and 50 ng/ml, while the AA isoform lacked significant effect. AngII modestly but significantly stimulated migration in a concentration-dependent manner between 10(-7) and 10(-6) mol/L. Rat ADM significantly inhibited the PDGF BB- and AngII-stimulated migration in a concentration-dependent manner between 10(-8) and 10(-7) mol/L. Inhibition by rat ADM was accompanied by an increase in cellular cAMP. cAMP agonists or inducers such as 8-bromo cAMP, forskolin, and prostaglandin I2 also significantly reduced the stimulated migration. H 89, a protein kinase A (PKA) inhibitor, attenuated the inhibitory effect of ADM, and a calcitonin gene-related peptide (CGRP) receptor antagonist, human CGRP (8-37), abolished the inhibitory effects of rat ADM. These results suggest that PDGF AB and BB as well as AngII stimulate rat mesangial cell migration and that ADM can inhibit PDGF BB- and AngII-stimulated migration, at least in part through cAMP-dependent mechanisms likely to involve specific ADM receptors with which CGRP interacts. The adenylate cyclase/cAMP/PKA system may be involved in the migration-inhibitory effect of ADM in these cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

Correlation between the blood supply and grade of malignancy of hepatocellular nodules associated with liver cirrhosis: evaluation by CT during intraarterial injection of contrast medium.

OBJECTIVE: The purpose of this study is to evaluate the correlation between the intranodular blood supply revealed by CT during intraarterial injection of contrast medium, mainly using helical CT, and the grade of malignancy of hepatocellular nodules associated with liver cirrhosis as classified by the International Working Party of the World Congress of Gastroenterology. SUBJECTS AND METHODS: We studied 201 histologically proven nodules (101 resected and 100 biopsied nodules), including 47 low-grade dysplastic nodules (low-DNs), 56 high-grade dysplastic nodules (high-DNs), 24 well-differentiated hepatocellular carcinomas (wd-HCCs), and 74 moderately or poorly differentiated HCCs (mp-HCCs), in 139 cirrhotic patients. Findings on CT during arterial portography (n = 201) and CT during hepatic arteriography (n = 74) were reviewed and compared with the histologic diagnosis. RESULTS: CT findings were classified into four types relative to the surrounding liver: type A (isodense), type B (slightly hypodense), type C (partially hypodense), and type D (markedly hypodense) on CT during arterial portography and type I (isodense), type II (hypodense), type III (partially hyperdense), and type IV (hyperdense) on CT during hepatic arteriography. On CT during arterial portography, the distributions of each type were low-DN (n = 47 [A, n = 36; B, n = 8; C, n = 3]), high-DN (n = 56 [A, n = 18; B, n = 20; C, n = 10; D, n = 8]), wd-HCC (n = 24; [B, n = 4; C, n = 13; D, n = 7]), and mp-HCC (n = 74 [D, n = 74]). On CT during hepatic arteriography, the distributions were low-DN (n = 26 [I, n = 18; II, n = 7; III, n = 1]), high-DN (n = 19 [I, n = 6; II, n = 7; III, n = 4; IV, n = 2]), wd-HCC (n = 15 [I, n = 1; III, n = 8; IV, n = 6]), and mp-HCC (n = 14 [IV, n = 14]). We found a statistically significant correlation between the four types and the grade of malignancy of these nodules. CONCLUSION: Findings on CT during arterial portography and CT during hepatic arteriography correlated positively with histologic grading when overlap in appearance between dysplastic nodules and HCCs occurred. The concept revealed in this study can apply to diagnoses made on the basis of Doppler sonography, dynamic CT, and MR imaging.

Aged↗
PubMed1999

[Evaluation of mitral valve lesions in patients with infective endocarditis by three-dimensional echocardiography].

Recognition of the involved lesions is extremely important in mitral valve repair for infective endocarditis. Transesophageal echocardiography (TEE) is more sensitive for the detection of lesions than transthoracic echocardiography, but localization of the lesions is sometimes difficult by TEE. Three-dimensional (3D) TEE provides images of the mitral valve similar to the view from the left atrium. This study evaluated the value of 3D echocardiography for the diagnosis of involved lesions in 12 patients who underwent surgery for mitral regurgitation due to infective endocarditis. The location of the lesion in the mitral valve was classified as the medial, central and lateral portions of the anterior leaflet, and the medial, middle and lateral scallops of the posterior leaflet, respectively. In all patients, the involved sites were confirmed at operation. The sensitivities of 3D TEE for detecting the lesions at the medial, central and lateral portions of the anterior leaflet, and the medial, middle and lateral scallops of the posterior leaflet were 100%, 78% and 67%, and 100%, 100% and 100%, respectively. The specificities were 90%, 100% and 78%, and 100%, 100% and 100%, respectively. The lesions diagnosed by 3D TEE coincided with lesions confirmed at operation in 23 (92%) of 25 lesions. 3D TEE is useful for the assessment of the involved lesion of the mitral valve in patients with infective endocarditis.

Echocardiography, Three-Dimensional↗
PubMed1999

[Effects of imaging parameters on automated cardiac flow measurement using color Doppler echocardiography].

The color Doppler echocardiographic technique has been developed for automated cardiac flow measurement (ACM). This study evaluated the effect of imaging parameters on stroke volume measurement. Cardiac output derived from the ACM method was compared with that obtained from pulsed wave Doppler in 36 patients (26 men and 10 women, mean age 54 +/- 8 years) in whom clear two-dimensional and color Doppler images of the left ventricular outflow tract were obtained. The effects of frame rate, color gain and moving target indicator (MTI) filter on cardiac output were evaluated in 13 patients (8 men and 5 women, mean age 49 +/- 6 years). Using ACM at a frame rate of 30 Hz, optimal color gain setting and high-frequency MTI filter (cutoff frequency: 915 Hz), there was an excellent correlation in cardiac output between the ACM and pulsed wave Doppler methods (stroke volume: r = 0.91, SEE = 0.32 l/min). Using ACM at a frame rate of 30, 22 and 15 Hz, the differences in stroke volume were 4.4%, 5.2% and 8.6%, respectively. When color gain was reduced, left ventricular stroke volume reduction was 12.1% (-2 dB), 18.9% (-4 dB). In contrast, there was no significant change in stroke volume measurement when color gain was increased. There was a significant decrease in stroke volume using the low-frequency MTI filter [cutoff frequency: 467 Hz (-35.6%)] and medium-frequency MTI filter [cutoff frequency: 703 Hz (-13.4%)]. Color Doppler imaging parameters are extremely important for automated assessment of cardiac output.

Automation↗
PubMed1999

Anti-atherosclerotic action of vascular D1 receptors.

1. Vascular smooth muscle cell (VSMC) migration and proliferation are believed to play key roles in atherosclerosis. To elucidate the role of vascular dopamine D1-like (D1 and D5) receptors in atherosclerosis, the effects of dopamine and the specific D1-like receptor agonists SKF 38393 and YM 435 on platelet-derived growth factor (PDGF)-BB-mediated VSMC migration, proliferation and hypertrophy were investigated. 2. We observed that cell stimulated by 5 ng/mL PDGF-BB showed increased migration, proliferation and hypertrophy. These effects were prevented by co-incubation with dopamine, SKF 38393 or YM 435 at 1-10 mumol/L and this prevention was reversed by Sch 23390 (1-10 mumol/L), a specific D1-like receptor antagonist. These actions of D1-like receptor agonists were mimicked by 1-10 mumol/L forskolin, a direct activator of adenylate cyclase, and 0.1-1 mmol/L 8-bromo-cAMP. The actions were blocked by the specific protein kinase A (PKA) inhibitor N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinoline-sulphonamide (H 89), but were not blocked by its negative control N-[2-(N-formyl-p-chlorocinnamylamino) ethyl]-5-isoquinoline sulphonamide (H 85). Platelet-derived growth factor-BB (5 ng/mL)-mediated activation of phospholipase D (PLD), protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activity was significantly suppressed by co-incubation with dopamine. 3. These results suggest that vascular D1-like receptor agonists inhibit migration, proliferation and hypertrophy of VSMC, possibly through the activation of PKA and the suppression of activated PLD, PKC and MAPK activity.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

[Pathophysiology of vascular complications in diabetes].

Hyperglycemia is an important causative factor in the development of micro- and macrovascular complications in diabetes. It activates polyol pathway and protein kinase C, which result in the increase in insulin resistance and oxidative stress in vascular tissues, leading to the accelerated atherosclerosis. Increased hematocrit and blood viscosity are observed in diabetes, which contribute to an increased risk of thrombosis and accelerated vasculopathy. Blood glucose control as well as blood pressure control are important in the prevention of diabetic vascular complications as evidenced by large-scale interventional studies.

Diabetic Angiopathies↗
PubMed1999

A reverse flow-metabolism mismatch pattern on PET is related to multivessel disease in patients with acute myocardial infarction.

UNLABELLED: Hypoperfused myocardium with increased uptake of 18F-fluorodeoxyglucose (FDG) is considered to be ischemic but viable myocardium. However, the significance of a more severe defect of FDG than of 13N ammonia (NH3) (i.e., reverse flow-metabolism mismatch) is not well understood. METHODS: To study a reverse flow-metabolism mismatch pattern, PET with NH3 and FDG under glucose loading was performed in 35 patients within 2 wk after onset of first acute myocardial infarction (AMI) and in 29 patients with old myocardial infarction (OMI). The left ventricle was divided into nine segments on a bull's eye polar map, and the mean counts of NH3 (%NH3) and FDG (%FDG) were compared for the segment with the least %NH3. RESULTS: Ten patients in the AMI group demonstrated a marked reverse flow-metabolism mismatch pattern (greater than 10% difference between %NH3 and %FDG), whereas only 2 patients in the OMI group demonstrated the mismatch pattern (P < 0.05). Sixteen patients with AMI demonstrated %FDG > %NH3 (group 1), and 19 patients with AMI demonstrated %FDG < %NH3 (group 2). There were no significant differences in age, sex, location of infarction, diameter of stenosis of infarct-related artery or left ventricular ejection fraction between groups 1 and 2. Eleven patients in group 2 and only 3 in group 1 had multivessel disease (P < 0.02). There was no significant relationship between the number of diseased vessels and the flow-metabolism pattern in patients with OMI. CONCLUSION: The finding of a reverse flow-metabolism mismatch on PET in the subacute phase of myocardial infarction was closely related to multivessel disease.

Adult↗
PubMed1999

[Measurement of left ventricular filling by automated contour tracking method in echocardiography: comparison with radionuclide ventriculography].

Recent development of an automated contour tracking (ACT) method using the energy minimization principle provides automated edge detection and tracking of the endocardial boundary of the left ventricle, without tracing a region of interest. This study determined whether left ventricular filling indexes obtained from the ACT method provide a reliable estimate of left ventricular diastolic filling. Fourteen patients were examined by the ACT method and equilibrium radionuclide ventriculography. The volume-time wave form for ACT measurements was obtained from the 4-chamber views. Peak filling rate and time to peak filling rate measured by the ACT method were compared with those determined by radionuclide ventriculography. Peak filling rate and time to peak filling rate by the ACT method were closely correlated with those determined by radionuclide ventriculography (peak filling rate: r = 0.88, y = 0.71x + 0.36, SEE = 0.54 ml/end-diastolic volume/sec, time to peak filling rate: r = 0.89, y = 0.72x + 30.0, SEE = 0.02 msec, respectively) The ACT method is useful for the assessment of left ventricular diastolic filling.

Aged↗
PubMed1998

Induction by lysophosphatidylcholine, a major phospholipid component of atherogenic lipoproteins, of human coronary artery smooth muscle cell migration.

BACKGROUND: The objectives of the present study were (1) to determine whether lysophosphatidylcholine (lyso-PC), a prominent component of oxidatively modified LDL, induces migration of human coronary artery smooth muscle cells (SMCs) and, if so, to clarify the mechanism, and (2) to investigate the possible interactions of lyso-PC and platelet-derived growth factor (PDGF)-BB, endothelin- (ET-1), adrenomedullin (AM), or vitamin E on SMC migration by the Boyden's chamber method. METHODS AND RESULTS: Lyso-PC induced SMC migration in a concentration-dependent manner between 10(-6) and 5 x 10(-5) mol/L. By contrast, phosphatidylcholine was without significant activity, and lysophosphatidylinositol and lysophosphatidylserine were much less effective than lyso-PC. Lyso-PC increased basic fibroblast growth factor (bFGF) production in a concentration-dependent manner between 10(-6) and 5 x 10(-5) mol/L in these cells. Furthermore, lyso-PC-induced SMC migration was inhibited by neutralizing antibody to bFGF but not by neutralizing antibody to transforming growth factor-beta1. Lyso-PC-induced migration was significantly enhanced by PDGF-BB or ET-1 but was clearly inhibited by human AM and vitamin E. CONCLUSIONS: These results indicate that (1) lyso-PC induces human coronary artery SMC migration at least in part through release of endogenous bFGF and (2) this lyso-PC-induced migration can be further induced by PDGF-BB and ET-1 and can be inhibited by human AM and vitamin E. Lyso-PC may recruit medial SMCs during the process of coronary atherosclerosis in part by releasing bFGF in concert with PDGF-BB or ET-1 in vascular tissues. This lyso-PC-induced SMC migration may be suppressed by AM and vitamin E under certain pathological conditions.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

Efficacy and safety of early coronary stenting for unstable angina.

To determine the efficacy and safety of early coronary stenting for unstable angina, we studied 91 consecutive patients with unstable angina. Thirty-one patients underwent stenting 72 h or more after admission, and another 60 patients underwent stenting within 72 h of admission. The clinical and angiographic follow-up had been done for 6 mo. There were no differences between the baseline clinical and angiographic characteristics of both groups. The maximum balloon pressure was higher (14.1 +/- 1.2 vs. 12.6 +/- 0.9, P < 0.01) and the hospital stay was shorter (9.7 +/- 2.7 vs. 18.7 +/- 5.8 d, P < 0.0001) in the early stenting group. These two groups were similar in the clinical success rate (90.0% vs. 93.5%), without any abrupt closure, subacute thrombosis, death, myocardial infarction, or coronary bypass surgery. These findings indicate that early stenting can be useful in patients with unstable angina.

Aged↗
PubMed1998

Long acting calcium antagonist amlodipine prevents left ventricular remodeling after myocardial infarction in rats.

OBJECTIVE: The purpose of this study was to examine the effect of amlodipine, a long-acting calcium antagonist, on the left ventricular remodeling, including systolic and diastolic dysfunction, the change of cardiac gene expression in the myocardial infarcted rats (MI). METHODS: On the first day after myocardial infarction, the animals were randomly assigned to amlodipine treatment (n = 8) or untreated groups (MI; n = 9). We then performed Doppler-echocardiographic examinations and measured the hemodynamics at four weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. RESULTS: Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 22 +/- 1 mmHg and 5 +/- 1 mmHg. Amlodipine reduced LVEDP and CVP to 15 +/- 1 mmHg (P < 0.01) and 3 +/- 0 mmHg (P < 0.01). The weight of right ventricle in MI was significantly larger than in the control rats (Control; 0.48 +/- 0.01 g/kg, MI; 0.79 +/- 0.04 g/kg, P < 0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3 +/- 0.3 mm (P < 0.01) (Control; 6.2 +/- 0.3 mm). Amlodipine prevented an increase of the weight of right ventricle (0.62 +/- 0.03 g/kg, P < 0.01) and LVDd (7.9 +/- 0.2 mm, P < 0.01 to MI). The rats in MI showed systolic dysfunction shown by the decreased fractional shortening (Control; 31 +/- 2% versus MI; 15 +/- 1%, P < 0.01), and diastolic dysfunction shown by E wave deceleration rate (Control; 18.1 +/- 2.0 m/s2, MI; 32.6 +/- 2.1 m/s2, P < 0.01). Amlodipine significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, alpha-skeletal actin, and ANP mRNAs in the non-infarcted left ventricle and right ventricle at four weeks after the myocardial infarction were all significantly suppressed by the treatment with amlodipine. On the other hand, depressed alpha-MHC was restored to normal levels by amlodipine in both regions. CONCLUSIONS: Amlodipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction.

Actins↗
PubMed1998

Activation of mitogen-activated protein kinases and activator protein-1 in myocardial infarction in rats.

OBJECTIVE: The purpose of this study was to examine the activation of mitogen-activated protein kinases (MAPK) plus activator protein-1 (AP-1) and nuclear factor-kB (NF-kB) DNA binding activities, all of which seem to be important in a signal transduction cascade upstream of the increased level of mRNA expression observed after myocardial infarction. METHODS: Myocardial infarction was produced in Wistar rats. The activities of MAPKs in the ischemic region were measured using an in-gel kinase method or an in vitro kinase method. AP-1 and NF-kB binding was determined using an electrophoretic mobility shift assay. Levels of transforming growth factor beta-1(TGF-beta-1) and collagen I and III mRNAs were analyzed by Northern blot hybridization. RESULTS: p42 Extracellular signal-regulated kinase (ERK), p44ERK and p38MAPK activities increased 5.2-fold, 4.3-fold and 1.9-fold (P < 0.01), respectively, at 5 min after coronary artery ligation but returned to normal levels by 30 min. p55c-Jun NH2-terminal kinase (JNK) and p46JNK activities increased 4.0-fold and 3.2-fold (P < 0.01), respectively, at 15 min and returned to normal levels by 24 h after ligation. AP-1 DNA and NF-kB binding activities increased 8.7-fold and 7.1-fold (P < 0.01), respectively, at 3 days but returned to normal levels by 7 days after ligation. Interestingly, analyses of the levels of TGF-beta-1, collagen I and III mRNAs revealed increases of 6.3-fold, 15.2-fold and 12.0-fold (P < 0.01), respectively, at 1 week after myocardial infarction. CONCLUSIONS: Myocardial ischemia increased MAPK activities, which were followed by enhancement of AP-1 and NF-kB DNA binding activity in areas of myocardial infarction in rats. These signal transduction mechanisms may contribute to the myocardial ischemia and injury associated with myocardial infarction by causing an increased expression of TGF-beta-1 mRNA, collagen I and III in the area.

Animals↗
PubMed1998

Heparin inhibits human coronary artery smooth muscle cell migration.

Heparin, an anticoagulant, has been shown to reduce neointimal proliferation and restenosis following vascular injury in experimental studies, but the clinical trials of heparin in coronary balloon angioplasty have been negative. The current study, therefore, examined the effect of heparin on basal or stimulated migration by serum and platelet-derived growth factor (PDGF)-BB in cultured human coronary artery smooth muscle cells (SMCs) by Boyden's chamber method. In addition, the reversibility of the heparin effect on human coronary artery SMC migration was examined. Fetal calf serum (FCS) and PDGF-BB stimulated SMC migration in a concentration-dependent manner. Heparin in moderate to high concentration (10 to 100 U/mL) exhibited concentration-related inhibition of FCS- and PDGF-BB-stimulated SMC migration; however, a low concentration (1 U/mL) of heparin had no inhibitory effects. Heparin also had weak inhibitory effects on nonstimulated SMC migration. The SMCs that were exposed to a high concentration (100 U/mL) of heparin for 6 hours were capable of migrating after a short lag period of removal of heparin from the culture medium. These SMCs also showed recovery of responses to FCS and PDGF-BB by migrating significantly greater than the nonstimulated level. Furthermore, heparin-containing medium did not contain detached cells. These results indicate that heparin inhibits human coronary artery SMC migration, especially when stimulated by FCS or PDGF-BB, and that this inhibitory effect of heparin is reversible and not simply a function of killing cells.

Anticoagulants↗
PubMed1998

Flow dynamics of angiographically no-flow patent internal mammary artery grafts.

OBJECTIVES: This study sought to assess the flow dynamics of internal mammary artery grafts (IMAGs) in no-flow situations by use of a Doppler guide wire. BACKGROUND: Functionally no-flow and anatomically patent IMAGs have been reported by angiography in patients with a patent recipient coronary artery. METHODS: The study included 12 patients with an IMAG to the left anterior descending coronary artery (LAD) in whom no-flow patency of the graft was suspected angiographically. Thirteen patients with a normally functioning IMAG whose LAD was occluded in the proximal portion and was supplied only from the graft served as control patients. Phasic flow velocities were recorded in the distal portion of the graft and the recipient LAD using a 0.014-in., 15-MHz Doppler guide wire at rest and during hyperemia (0.14-mg/kg body weight per min intravenous adenosine infusion). RESULTS: There were no significant differences in systolic (15+/-3 vs. 19+/-6 cm/s, p = NS), diastolic (35+/-11 vs. 37+/-7 cm/s, p = NS) and time-averaged peak velocities at rest (20+/-5 vs. 21+/-5 cm/s, p = NS), during hyperemia (51+/-12 vs. 54+/-8 cm/s, p = NS) and in coronary flow velocity reserve (2.8+/-0.9 vs. 2.7+/-0.3, NS) in the native LAD in patients with a no-flow patent graft versus control patients. Within the graft, to and fro signals with systolic reversal and diastolic anterograde flow were seen in the no-flow patent grafts, although anterograde flow signals were recorded in systole and diastole in control patients. Systolic (-28+/-19 vs. 22+/-9 cm/s, p < 0.01), diastolic (18+/-17 vs. 44+/-14 cm/s, p < 0.01) and time-averaged (-2+/-6 vs. 26+/-9 cm/s, p < 0.01) peak velocities at rest were significantly smaller in the no-flow patent grafts than in control grafts. During hyperemia, anterograde flow became predominant, with a reduction in retrograde systolic flow signal and an increase in diastolic flow velocity and time-averaged peak velocity in the no-flow patent grafts, and no-flow situations disappeared temporarily. CONCLUSIONS: Functionally no-flow situations of IMAGs manifesting to and fro signals with systolic flow reversal and diastolic antegrade low flow velocity are temporary conditions in certain hemodynamic circumstances, and these grafts function as conduits during hyperemic states.

Adolescent↗
PubMed1998

Restricted coronary flow reserve in patients with mitral regurgitation improves after mitral reconstructive surgery.

OBJECTIVES: The purpose of this study was to assess coronary flow characteristics in patients with chronic mitral regurgitation (MR). BACKGROUND: Coronary flow reserve (CFR) has been reported to be restricted in cases with left ventricular (LV) volume overload caused by aortic regurgitation and increased LV preload. METHODS: The study populations consisted of 31 patients with nonrheumatic chronic MR. Eleven with chest pain and normal coronary arteries served as control subjects. Phasic coronary flow velocities were obtained in the proximal segment of the angiographically normal left anterior descending coronary artery at rest and during hyperemia (0.14 mg/kg/min adenosine infusion intravenously) using a 0.014-in. (0.036 cm), 15-MHz Doppler guide wire. Coronary flow reserve was obtained from the ratio of hyperemic/baseline time-averaged peak velocity (APV). Thirteen cases who underwent mitral valve reconstructive surgery were also studied 1 month after surgery. RESULTS: Compared with control subjects, CFR was significantly reduced in cases with MR (2.1+/-0.5 vs. 33+/-0.6, respectively, p < 0.01) because baseline APV was significantly greater (28+/-8 vs. 19+/-6 cm/s, respectively, p < 0.01), although maximal hyperemic APV was not significantly different (56+/-14 vs. 61+/-16 cm/s, respectively, p = NS). Significant correlations were obtained between CFR and LV end-diastolic pressure (LVEDP) (r = 0.70, p < 0.01), LV mass index (r = 0.42, p < 0.01), LV end-diastolic volume (r = 038, p = 0.04) and MR volume (r = 0.39, p = 0.03), and stepwise regression analysis showed LVEDP was the most important determinant of CFR in MR (r2 = 0.49, p < 0.0001). This restricted CFR improved significantly after mitral valve reconstructive surgery (2.1+/-0.5 vs. 3.1+/-0.6, respectively, p < 0.01) because of reduction of baseline APV (28+/-8 vs. 21+/-8 cm/s, respectively, p < 0.01). CONCLUSIONS: Coronary flow reserve is limited in cases with MR because of elevation of baseline resting flow velocity. This reduction of CFR correlates well with increase in LV preload, mass and volume overload, especially with increase in LV preload, and this restricted CFR improves after mitral valve surgery.

Adult↗