ABSTRACT
BACKGROUND: Determination of mitral valve area (MVA) in patients with mitral stenosis is very important in clinical practice. Therefore, the ability to assess accurately MVA by noninvasive technique is of great meaning to the management of patients with mitral stenosis. Echo-Doppler(ED) method was derived from the study of fluid dynamics that the flow volume is proportional to orifice area, velocity of flow which shows period requird by the flow. It has been proposed recently that measuring the flow convergence region proximal to an orifice by Doppler flow mapping can be used to derive cardiac output or flow rate proximal to stenotic orifices and therefore to calculate their areas by the continuity equation (area=flow rate/velocity). Applying these methods in mitral stenosis would provide a unique way of validating the underlying concept because the predicted areas could be compared with those measured directly by planimetry and pressure half-time method. Valve resistance has been proposed as an alternative hemodynamic indicator, but initially this index was not used because it was unlikely to remain constant at different flow rates. Recently valve resistance provided a better indices of hemodynamic obstruction than mitral valve area, and these indices usually estimated by invasive method, but it is able to calculate from Doppler echocardiography and compared to the results of invasive method. METHODS: The mitral inflow volume can be obtained by estimating the stroke volume (SV) by Teichholz's method from M-mode echocardiogram of the left ventricle, and the mean diastolic velocity(MDV) and diastolic filling period (DFP) by mitral inflow continuous-wave Dopler echocardiogram. Therefore, Echo-Doppler method is MVA=SV/MDV×DFP. Doppler color flow recordings of mitral inflow were obtained from the apex, and the radius of the proximal flow convergence region was measured at its peak diastolic value from the calculated assuming uniform radial flow convergence toward the orifice, modified by a factor that accounted for the inflow funnel angle formed by the mitral leaflets. Mitral valve area was then calculated as peak flow rate divided by peak velocity by continuous-wave Doppler. To Compare the stenotic indices from noninvasive method and invasive method, cardiac catheterization was performed. RESULTS: 1) ED-MVA of these 28 patients with mitral stenosis correlated well at a coeffitient of 0.867 than PHT-MVA(r=0.513) or 2DE(r=0.513) in comparison with Cath-MVA. 2) Excluding 4 patients with mitral regurgitation, the ED-MVA of 24 patients with isolated mitral stenosis showed a better correlation with r=0.944 than with PHT-MVA(r=0.642) or 2DE-MVA(r=0.647) in comparison with Cath-MVA. 3) MVA determined by PISA method were correlated with planimetry method on 2DE(r=0.51, p < 0.001). 4) MVA determined by PISA method were correlated with PTH method(r=0.44, p=0.002). 5) Agreement with planimetrymethod was similar for 26 patients with mitral regurgitation and 24 without it, as well as for 34 in atrial fibrillation. 6) The correlation coefficient of mitral valve area and mitral valve resistance between echocardiography(r=0.87) and cardiac catheterization(r=0.82) showed positive correlation(p < 0.001). 7) Linear regression analysis showed a negative correlation of mitral valve resistance and Gorlin mitral valve area between echocardiography (r=−0.84) and cardiac catheterization(r=−0.84). CONCLUSION: Echocardiographic evaluation of mitral valve stenosis by planimetry, pressur half-time method, Echo-Doppler method, PISA method, and mitral valve resistance were useful noninvasive methods in assessing the severity of mitral stenosis. In mitral stenosis patients with mitral regurgitation and/or aortic regurgitation, PISA and mitral valve resistance methods were also reliable. In conclusion, these results suggested that the echocardiographic methods could be sufficient for assessing the severity of mitral stenosis without the necessity of invasive technique.
Subject(s)
Humans , Aortic Valve Insufficiency , Atrial Fibrillation , Cardiac Catheterization , Cardiac Catheters , Cardiac Output , Clothing , Constriction, Pathologic , Echocardiography , Echocardiography, Doppler , Heart Ventricles , Hemodynamics , Hydrodynamics , Linear Models , Methods , Mitral Valve , Mitral Valve Insufficiency , Mitral Valve Stenosis , Radius , Stroke VolumeABSTRACT
BACKGROUND: Flail mitral valve due to ruptured chordae tendinae usually result in actue, severe mitral regurgitation. Because transesophageal echocardiography with color Doppler flow mapping permits high resolution imaging of mitral valve anatomy and mitral regurgitation, we compared this procedure with transthoracic echocardiography in the diagnosis and evaluation of flail mitral valve. METHODS: From 1990 to 1992 years, fourteen patients (7 males, 7 females ; age range 30-81years)with flail mitral valve admitted to Kyung Hee University was evaluated by transesophageal echocardiography and transthoracic echocardiography. RESULTS: 1) Transthoracic echocardiography revealed 11 cases of abnormal coaptation, I case of ruptured chordae tendinae and 2 cases not defined. Compared with transthoracic imaging, transesophageal echocardiography revealed 13 cases of abnormal coaptation and I case of ruptured chordae tendinae. 2) The site of flail leaflet was 6 cases in anterior, 7 cases in posterior and one case was not defined with transthoracic echocardiography. With transesophageal echocardiography, the site was 5 cases in anterior, 5 cases in posterior and 4 cases in both leaflets. 3) By color flow mapping, MR jet directed toward anterior in 5, posterior in 7 and both in 2 with transthoracic echocardiography. With transesophageal echocardiography,MR jet directed toward anterior in 5, posterior in 7 and both in 4. 4) In a flail anterior leaflet, transesophageal echocardiography showed abnormal leaflet coaptation in systole, displacement of the unsupported anterior leaflet into the left atrium and formation of a regurgitant channel between the mitral leaflets. By Doppler color flow pattern, mitral regurgitation associated with a flail anterior leaflet moved in a counter-clockwise direction around the left atrium in the standard 4 chamber view, whereas regurgitation associated with a flail posterior leaflet moved in a clockwise direction. Regurgitation associated with flail anterior and posterior leaflets moved in both directions. CONCLUSION: Transesophageal echocardiography with color Doppler flow mapping of mitral regurgitation were complementary to transthoracic echocardiography in the diagnosis and localization of flail mitral valve.
Subject(s)
Female , Humans , Male , Diagnosis , Echocardiography , Echocardiography, Doppler, Color , Echocardiography, Transesophageal , Heart Atria , Mitral Valve Insufficiency , Mitral Valve , SystoleABSTRACT
BACKGROUND: The association between the levels of serum lipids and lipoproteins and coronary artery disease(CAD) was well established. This study examines to assess the relation of the concentrations of serum lipids and lipoproteins to the severity of coronary atherosclerosis quantified by angiography. METHODS: We studied 72 patients(men 47, women 25 and mean age 55.6 years) who underwent coronary arteriography for suspected coronary artery disease. Coronary lesion scores were represented by estimates of stenosis in four major coronary vessels. We determined the levels of serum total cholesterol, triglyceride and HDL-cholesterol by biochemical methods. Serum apolipoprotein A-I, apolipoprotein B and lipoprotein(a) were quantified by radioimmunoassay. RESULTS: The distribution of Lp(a)levels among the subject population was highly skewed, with a mean Lp(a) level of 20.0mg/dL and a median of 15.2mg/dL. Coronary lesion scores significantly correlated with Lp(a), HDL-cholesterol levels and the age of patient by univariate statistical analysis. By multivariate analysis, levels of Lp(a) were associated significantly and independently with lesion scores and tend to correlate with the presence of CAD. In men, overall lesion severity of coronary atherosclerosis was related to Lp(a) levels, whereas in women it was related to apolipoprotein B levels by multiple regression anaylsis. CONCLUSION: The serum Lp(a) may be considerably more reliable index of advanced coronary artery disease than other lipids and lipoproteins, especially in men.
Subject(s)
Female , Humans , Male , Angiography , Apolipoprotein A-I , Apolipoproteins , Cholesterol , Constriction, Pathologic , Coronary Artery Disease , Coronary Vessels , Lipoprotein(a) , Lipoproteins , Multivariate Analysis , Radioimmunoassay , TriglyceridesABSTRACT
BACKGROUND: Hyperlipidemia is the one of the major risk factors causing the atherosclerosis of coronary arteries. Treatment of hyperlipidemia with drugs has been confirmed the effcts of therapy showing a decreased incidence of coronary artery disease. Pravastation is one of the new HMG-CoA reductase inhibitors and we studied the long-term hypolipidemic effects and safety of pravastatin in patients with hyperlipidemia and lipid profile after cessation of pravastatin therapy. METHODS: We studied 27 patients(6 males and 21 females, range of age : 36~67 years) for 14.7 months whose plasma levels of total cholesterol were higher than 250mg% after one month period of diet therapy. Pravastatin was administered 10mg/day and measured lipid profile at 4 weeks interval, and at 2~3 months after cessation of therapy. RESULTS: 1) Pravastatin significantly reduced the plasma total cholesterol, LDL-cholesterol and triglyceride, but HDL-cholesterol was increased significantly after 12 months pravastatin therapy(p<0.05). 2) Two to three months after the cessation of pravastatin therapy, plasma total cholesterol, LDL-cholesterol and triglyceride were significantly increased(p<0.05), but no significant difference was observed for HDL-cholesterol. 3) The clinical and laboratory examinations before and after pravastatin treatment showed no particular abnormal findings. CONCLUSION: These results suggested that long-term pravastatin therapy in patients with hyperlipidemia seems to be very effective and safe. But hyperlipidemia developed again two to three months after the cessation of pravastatin therapy.