123I-BMIPP fatty acid analogue imaging is a novel diagnostic and prognostic approach following acute myocardial infarction.

Fatty acid oxidation is the most efficient mode of myocardial energy production which requires a large amount of oxygen. Thus, alteration of fatty acid oxidation is considered to be a sensitive marker of ischaemia and myocardial damage. (123)I-BMIPP ([123]I-beta-methyl-p-iodophenylpentadecanoic acid) is a newly-investigated single-photon branching free fatty acid radiopharmaceutical with slow metabolism; thus, it is well-suited for single-photon emission computed tomography (SPECT). Assessment of fatty acid metabolism by radionuclide techniques has a potential role for the early detection of myocardial ischaemia and the assessment of the severity of ischaemic heart disease. Although stable patients with a healed myocardial infarction may have a relatively good prognosis, risk stratification in the predischarge period should be valuable for deciding upon appropriate management. In this respect, the presence of discordant BMIPP uptake relative to (201)Tl perfusion appears to be the best predictor of future cardiac events among all other cardiovascular imaging modalities. Since discordant BMIPP uptake correlates well with redistribution on stress (201)Tl imaging and perfusion-metabolism mismatch on positron emission tomography, it is considered that such BMIPP and (201)Tl discordance may identify a high-risk subgroup among patients with acute myocardial infarction. A BMIPP scan may reflect prior severe ischaemia after recovery of perfusion, the so-called "ischaemic memory". Gated BMIPP SPECT has been recently introduced for simultaneous assessment of myocardial metabolism and ventricular function. Such a new technique seems to be valuable for a better understanding of the pathophysiological state of heart failure and cardiomyopathy.

Efficacy of atorvastatin therapy in ischaemic heart disease - effects on oxidized low-density lipoprotein and adiponectin.

The lipid-lowering and anti-atherosclerotic effects of atorvastatin (10 mg/day) were investigated by measuring changes in the levels of oxidized low-density lipoprotein (LDL), serum lipids (total cholesterol [TC], LDL-cholesterol [LDL-C] and triglycerides [TG]), and in the protein adiponectin. This was undertaken in 22 patients with ischaemic heart disease and serum LDL-C levels > 100 mg/dl. After 3 months of therapy, atorvastatin significantly decreased serum lipids, oxidized LDL was reduced from 457.0 +/- 148.6 to 286.9 +/- 88.5 nmol/l, and adiponectin increased from 9.7 +/- 7.4 to 13.9 +/- 9.98 microg/ml. No significant correlation was observed between adiponectin and LDL-C, TG and high-density lipoprotein cholesterol. Atorvastatin therapy was not associated with side-effects, such as myalgia and gastrointestinal disorders, and did not give abnormal laboratory test results. It is concluded that atorvastatin decreases serum lipid and oxidized LDL levels, and increases adiponectin levels in patients with ischaemic heart disease.

The therapeutic effect of lipo PGE1 on diabetic neuropathy-changes in endothelin and various angiopathic factors.

A high blood concentration of endothelin (ET)-1 may participate in the onset and progress of diabetic microangiopathy, resulting in neuropathy. We examined the therapeutic effects of prostaglandin E1 (PGE1), which possesses both a peripheral vasodilating action and inhibition of platelet aggregation, on diabetic microangiopathy. Increases in both skin temperature and peripheral never conduction velocity in diabetic patients were recorded four weeks after Lipo PGE1 administration. A quantitative decrease in urinary albumin concentration was also observed, suggesting its efficacy of action was on diabetic nephropathy. Lipo PGE1 administration reduced the elevated circulating plasma ET-1 levels in the diabetic patients. As an increase in ET-1 concentrations is thought to correlate with the onset and progress of diabetic microangiopathy, the reduction of plasma ET-1 concentration by Lipo PGE1 administration may be one reason for the improvement in diabetic neuropathy and nephropathy.

Risk stratification using serum concentrations of cardiac troponin T in patients with end-stage renal disease on chronic maintenance dialysis.

BACKGROUND: It has been recently suggested that cardiac troponin T (cTnT) may be more sensitive than troponin I (cTnI) for subclinical myocardial cell injury in patients on chronic dialysis. METHODS: We prospectively compared the predictive value of cTnT with cTnI, atrial (ANP) and brain natriuretic peptide (BNP) in 100 consecutive outpatients on chronic dialysis without acute coronary syndromes over a period of 3 months, and assessed whether the combination of cTnT with clinical information including age, duration of dialysis, and medical histories was useful for risk stratification of these patients. During the 2-year follow-up period, 19 patients died, mostly due to cardiac causes (53%). RESULTS: The area under the receiver operator characteristic (ROC) curve for the cTnT as predictor of both overall and cardiac death was significantly greater than the area under the cTnI curve (p < 0.0001 and p = 0.01), the BNP curve (p < 0.001 and p < 0.01) or the ANP curve (p < 0.0001 and p < 0.005). In a stepwise multivariate Cox regression analysis, only cTnT (p < 0.05 and p < 0.01) and a history of heart failure requiring hospitalization (p < 0.05 and p < 0.005) were independent predictors of both all cause and cardiac mortality. Using parameters of cTnT > or =0.1 microg/l and/or history of heart failure, the overall and cardiac mortality rate for the low risk group (n=66) were 4.5% and 1.5%, respectively, 40% and 16% for the intermediate risk group (n=25), and 67% and 56% for the high risk group (n=9). CONCLUSION: cTnT concentrations offer a higher prognostic accuracy than cTnI, ANP and BNP in patients on chronic dialysis. The combination of elevated cTnT and a history of heart failure may be a highly effective means of risk stratification of these patients.

Transient ventricular wall thickening in acute myocarditis: a serial echocardiographic and histopathologic study.

The present study was designed to determine whether the wall thickening seen in acute myocarditis is caused by interstitial edema. The study group comprised 25 patients (idiopathic myocarditis, 17; eosinophilic myocarditis, 8) in whom acute myocarditis was diagnosed histologically and who underwent echocardiography and endomyocardial biopsy during both the acute and convalescent phases. The following echocardiographic parameters were measured: interventricular septum and left ventricular posterior wall thickness, left ventricular end-diastolic dimension, and left ventricular ejection fraction. Based on the myocardial biopsy specimens, the degree of interstitial edema was classified into 3 grades [(-), 1(+), 2(+)] and the transverse diameter of cardiac myocytes was measured using light microscopy. The thickness of both the interventricular septum and left ventricular wall decreased from 14.3+/-3.7 mm and 13.3+/-2.4 mm in the acute phase to 9.7+/-1.7 mm (p<0.001) and 10.2+/-1.7 mm (p<0.0001), respectively, in the convalescent phase. Edema was present in 22 patients (88.0%) in the acute phase, but in the convalescent phase, edema was present in only 7 patients (28.0%), indicating a significant reduction in the degree of edema (p<0.0001). Cardiac myocyte diameter did not differ significantly between the acute (13.6+/-1.1 microm) and convalescent (13.8+/-1.8 microm) phases.

Histopathologic evaluation of coronary artery thrombi obtained by directional coronary atherectomy in patients with restenosis-induced unstable angina pectoris.

The pathogenesis of unstable angina pectoris (UAP) following percutaneous transluminal coronary angioplasty (PTCA) or directional coronary atherectomy (DCA) has not been adequately investigated, so the present study aimed to determine whether thrombi are present in restenotic lesions. The study group comprised 14 patients (16 arterial branches) with angina pectoris in whom either PTCA or DCA was performed and who had developed UAP associated with restenosis, and who then underwent DCA of the restenosed lesion (R-UAP group). The control groups comprised individuals with UAP undergoing DCA with no prior history of PTCA or DCA (P-UAP group; n=29, 29 branches), patients with acute myocardial infarction (AMI group; n=34, 34 branches), and patients with stable angina pectoris (SAP group; n=31, 33 branches). The presence of thrombi was determined by light microscopy of histologic specimens. Thrombus was present in only 1 of the 16 (6.3%) branches in the R-UAP group. 21 of the 29 (72.4%) branches in the P-UAP group, and in 25 of the 34 (73.5%) in the AMI group. In the SAP group, it was detected in only 2 of the 33 (7.1%) branches. The incidence of thrombus was significantly lower in the R-UAP group than in the P-UAP group. In conclusion, the role of thrombus is limited in causing post-interventional UAP at restenosed sites.

Endomyocardial biopsy findings in 50 patients with idiopathic atrioventricular block: presence of myocarditis.

In patients with primary atrioventricular (AV) conduction disturbances, lesions are commonly believed to be limited to the conduction system. In the present study, myocardial lesions were analyzed histologically in patients with AV conduction disturbances to determine the presence of myocarditis. We studied 50 patients with second or third degree AV block in whom the cause was not clear (AVB group). Endomyocardial biopsy was performed from the right ventricle and examined by light microscopy. Tissue specimens also were obtained from 12 normal hearts at autopsy as a control group (N group). The diagnosis of myocarditis was based on the Dallas criteria. The myocyte transverse diameter was 15.4+/-4.1 microm in the AVB group and 11.7+/-3.1 microm in the N group (P<0.01). The fibrosis area ratio also was significantly higher in the AVB group than in the N group (10.1+/-6.7% vs 5.1+/-2.0%). The mean number of lymphocytes per 400-fold magnified field was significantly greater in the AVB group than in the N group (1.9+/-1.6 vs 1.3+/-0.4). In addition, disorganization of the cardiac myocytes was noted in 8 patients in the AVB group (16%), myocyte disarrangement in 39 patients (78%), myocytolysis in 23 patients (46%), and nuclear deformity in 21 patients (42%). Myocarditis was diagnosed in 3 of the 50 patients (6%). The present study demonstrates that myocardial lesions can be detected in a large proportion of patients with AV conduction disturbances. Furthermore, myocarditis is present in 6% of the cases.

Relationship between thrombolytic therapy and perfusion defect detected by Gd-DTPA-enhanced fast magnetic resonance imaging in acute myocardial infarction.

To study whether thrombolytic therapy affects Gd-DTPA-enhanced pattern and whether its pattern indicates myocardial viability, Gd-DTPA-enhanced magnetic resonance imaging (MRI) was performed in 43 patients with reperfused acute myocardial infarction 14.8+/-5.0 days after onset with breathhold scanning on a 1.5-T whole body system. The hypoenhanced area at 90 sec after contrast injection was defined as a perfusion defect (PD). Patients were divided into PD(+) and PD(-) groups. The PD was detected in 77.8% of patients treated with direct percutaneous transluminal coronary angioplasty (PTCA) and in 28.6% of patients treated by thrombolytic therapy with or without PTCA in the thrombolysis in myocardial infarction grade 3 group (p < 0.05). The myocardial wall was divided into seven segments based on the American Heart Association committee report. Wall motion of each segment was classified by one of six patterns (wall motion score [WMS]: dyskinesis, -1; akinesis, 0; severe hypokinesis, 1; hypokinesis, 2; slight hypokinesis, 3; normal, 4). By echocardiography, the average WMS and ejection fraction were similar between the PD(+) group and the PD(-) group on admission. Those parameters were significantly worse in the PD(+) group than in PD(-) group 1 month after onset. The change in WMS was significantly lower in the PD(+) group than in the PD(-) group. The number of patients and segments with more than two grades of improvement of WMS in the PD(+) group was significantly lower than that in the PD(-) group. Angiographically, left ventricular ejection fraction and WMS of the PD(+) group were significantly lower than those of the PD(-) group 3 months later. PDs were detected significantly less frequently in patients treated with thrombolytic therapy, suggesting that microvascular embolization related to formation of the no-reflow phenomenon.

Plasma concentration of brain natriuretic peptide as a biochemical marker for the evaluation of right ventricular overload and mortality in chronic respiratory disease.

The purpose of this study was to evaluate whether the plasma brain natriuretic peptide (BNP) concentration is a useful marker of right ventricular (RV) overload and whether it has prognostic value as a predictor of death in patients with chronic respiratory disease (CRD). We measured the plasma BNP and atrial natriuretic peptide (ANP) concentrations in 31 consecutive patients with CRD who underwent right-heart catheterization to evaluate pulmonary hypertension. All patients were followed for >12 months. The plasma BNP concentration closely correlated with the mean pulmonary artery pressure and pulmonary vascular resistance (r=0.62, P<0.0005 and r=0. 85, P<0.0001), and showed a weak linear correlation with cardiac output (r=-0.36, P<0.05). During the follow-up period, 5 (16%) end-stage CRD deaths (4 RV heart failure and 1 respiratory infection) and 2 non-end-stage CRD deaths occurred. In a stepwise multivariate Cox proportional-hazards regression analysis including age, sex, BNP, ANP, hemodynamic variables and the ratio of PaO(2) to fraction of inspired oxygen, only BNP (P<0.05) was an independent predictor of end-stage CRD death. The upward and leftward shift in the receiver operating characteristic curve between patients with end-stage CRD death and those without was greater for BNP than for ANP. Our findings suggest that the plasma BNP concentration may be an inexpensive, simple and useful marker of RV overload and end-stage CRD death in CRD patients. These preliminary results need to be confirmed in a large series of CRD patients.

Clinical usefulness of intravenous albunex for the Doppler assessment of aortic stenosis.

Optimal Doppler recordings of stenotic aortic flow are not always easy to obtain. Therefore, the present study investigated how useful intravenous Albunex injections were for improving the Doppler assessment of pressure gradients for aortic stenosis in 20 consecutive patients who underwent Doppler and left-heart catheterization studies within a 1-week period. Continuous-wave Doppler echocardiography was performed using both a 2.5 MHz duplex and a 1.9MHz independent transducer before and after Albunex injections. The maximum and mean pressure gradients were calculated from the highest Doppler velocity tracings using the simplified Bernoulli equation. Pullback catheterization pressure tracings from the left ventricle to the ascending aorta were superimposed for determination of the maximum instantaneous and mean pressure gradients. The Doppler-derived peak and mean pressure gradients showed significant underestimation compared with the catheterization gradients (23+/-17 mmHg and 11+/-7 mmHg, respectively). However, this underestimation disappeared with Albunex injection (-2+/-7 mmHg and -1+/-4mmHg, respectively). Although the Doppler-derived instantaneous and mean pressure gradients correlated well with the catheterization gradients (r=0.909 and r=0.879, respectively), they became much closer with Albunex (r=0.987 and r=0.963, respectively). The improvements in the Doppler-derived peak pressure gradients were significant from an apical window (n=12, 84-120mmHg, p<0.001). but less so from non-apical windows (n=8, 84-91 mmHg, p=0.0146). Accordingly, Albunex is most useful for Doppler recordings of stenotic aortic flow available from the apical window, but not less so from other acoustic windows.

Contribution of cardiac muscle cell disorganization to the clinical features of hypertrophic cardiomyopathy.

Heart failure rarely develops in the setting of hypertrophic cardiomyopathy (HCM). Because of this, cardiac muscle cell disorganization (CD), which is a histologic characteristic of HCM, is not believed to be responsible for the development of systolic dysfunction. The aim of the present study was to clarify whether CD can cause systolic dysfunction and ventricular dilation in patients with HCM. Sixteen hearts from patients with HCM obtained at autopsy were divided into two groups: group A (n = 11), without biventricular dilation, and group B (n = 5), with dilation. Specimens consisting of transverse and longitudinal tissue sections of the ventricles were prepared, and the extent of CD and interstitial fibrosis was quantified, using light microscopy. None of the patients in group A had had chronic congestive heart failure, while all of the patients in group B had died of congestive heart failure. In group B, CD was not limited to the interventricular septum. Rather, diffuse CD was observed in both ventricular free walls. The extent of CD was significantly greater in group B than in group A, while the degree of interstitial fibrosis was similar in the two groups (13.6% in group A vs 14.6% in group B). These results suggest that CD may be responsible for systolic dysfunction and ventricular dilation.

Can beta-blocker therapy be withdrawn from patients with dilated cardiomyopathy?

BACKGROUND: It has yet to be determined whether withdrawing beta-blocker therapy from patients with dilated cardiomyopathy (DCM) is safe. METHODS: The influence of tapering and then stopping metoprolol was clarified in 13 patients with DCM who had been receiving this agent for >/=30 months. RESULTS: Seven of the 13 patients deteriorated, including 4 who died suddenly or of congestive heart failure during the 4-month period after metoprolol cessation. CONCLUSION: In patients with DCM in whom beta-blocker therapy is effective, withdrawal of these agents may lead to death. We conclude that beta-blockers should not be stopped in this patient group.

Histologic diagnostic rate of cardiac sarcoidosis: evaluation of endomyocardial biopsies.

BACKGROUND: An early diagnosis of cardiac sarcoidosis is important, particularly when considering the need for administering corticosteroid therapy. However, no reports are available on the success rate of diagnosis on the basis of biopsy findings in patients with cardiac sarcoidosis. This study investigated the diagnostic success rate of histologic evaluation of endomyocardial biopsy specimens in patients with this disease. METHODS AND RESULTS: Right ventricular endomyocardial biopsy was performed in 26 patients in whom cardiac sarcoidosis was strongly suspected according to the Diagnostic Criteria of Sarcoidosis, plus abnormalities on the electrocardiogram, cardiac radionuclide images, or in left ventricular wall motion. A mean of 4.0 sites were sampled per patient. In each case we determined whether a definitive diagnosis of cardiac sarcoidosis could be made histologically. Noncaseating granulomas were found in only 5 (19.2%) of the 26 cases, thus permitting a histologic diagnosis of cardiac sarcoidosis. A histologic diagnosis was made in 4 (36.4%) of 11 patients who exhibited a dilated cardiomyopathy-like clinical picture, in contrast to only 1 (6.7%) of 15 patients in whom conduction disturbances were the major clinical feature and whose left ventricular ejection fraction was within normal limits. CONCLUSIONS: The diagnostic rate achieved with biopsy in cardiac sarcoidosis is low; the patients with sarcoidosis and evidence of significant cardiac involvement should be treated for cardiac sarcoidosis despite negative myocardial biopsies for this disease.

[The role of angioscopy and intravascular ultrasound imaging in acute coronary syndrome].

Evaluation of the severity of coronary atherosclerosis by intracoronary imaging may be closely relevant with the prevention and treatment of acute coronary syndromes. Coronary angioscopy as one of the innovative methods of imaging and intravascular ultrasound makes the insight visualization of coronary vessel wall and histological recognition possible recently. Yellow plaques rich in lipid materials and covered by thin membrane are more often ruptured than white ones to cause acute coronary syndromes. In patients with unstable angina and acute myocardial infarction, the yellow plaques with intimal flaps and irregularities are frequently observed by angioscopy. Angioscopy is also the most powerful tool to detect intracoronary thrombus. In patients with acute myocardial infarction, thrombosis occludes vessel lumen totally, but it does not in the unstable angina cases. After thrombolytic therapy, the white thrombus is more often observed than the red one. Although angioscopy is superior to any other examination in diagnosing thrombosis, some complicated plaques are difficult to distinguish from thrombus. In addition to measurements of vascular dimension and plaque volume, histological diagnosis of plaque is being made by intravascular ultrasound. More precise evaluation of plaque histology may be a clue to predict the occurrence of acute coronary syndrome. Intravascular ultrasound is not so useful enough to diagnose thrombosis. In conclusion, the applications of intravascular imaging technologies, such as angioscopy and intravascular ultrasound, may play a critical role in the diagnosis and treatment of acute coronary syndromes.

Use of percutaneous cardiopulmonary support of patients with fulminant myocarditis and cardiogenic shock for improving prognosis.

Percutaneous cardiopulmonary support was used in 9 patients with fulminant myocarditis and cardiogenic shock. Although 2 of the patients died, 7 improved and were able to resume social activities. Percutaneous cardiopulmonary support should be administered routinely to patients with fulminant myocarditis developing into cardiogenic shock.

[Clinical evaluation of acute and chronic pulmonary thromboembolism using intravascular ultrasound and angioscopy].

Pulmonary artery thrombi and parietal lesions were observed in 13 patients (mean age 58 +/- 18 years) with acute pulmonary thromboembolism (n = 4) and chronic pulmonary thromboembolism (n = 9) using intravascular ultrasound and angioscopy at the time of right heart catheterization. Patients with acute pulmonary thromboembolism without underlying disease mainly had non-echogenic intraluminal mass, and good pulsatile vessel without intimal thickening. Angioscopy directly showed red thrombi with white fibrin coating, and no parietal lesions. Patients with chronic pulmonary thromboembolism could be classified into 3 groups: 1) Poor extensibility of the vessel wall and intimal thickening with non-echogenic thrombi on intravascular ultrasound, and relatively fresh parietal thrombi consisting of a mixture of red blood cell and fibrin, and spider web-like fibrin net on angioscopy (6 patients). 2) Crescent parietal thrombi and wall irregularity on intravascular ultrasound, and probably organized thrombi with a mixture of red and white surface on angioscopy (one patient). 3) Marked and echogenic intimal thickening and poor extensibility on intravascular ultrasound, and intimal surface irregularities and yellowish changes on angioscopy (one patient). All patients suffering acute deterioration in the chronic phase belonged to groups 1) or 2). Intravascular ultrasound and angioscopy are useful for characterizing the thrombi and related pulmonary artery lesions in patients with pulmonary thromboembolism. The pulmonary artery intima and thrombus differ between acute and chronic pulmonary thromboembolism.

Vectorcardiographic evaluation of myocardial infarct size: comparisons with thallium myocardial scintigraphy.

OBJECTIVE: To determine the usefulness of vectorcardiography (VCG) in assessing myocardial infarct size. METHODS: The correlation of spatial and scalar parameters of VCG with the percent defect volume (%DV) of thallium myocardial single photon emission computed tomography (SPECT) was investigated in 63 patients with first-onset myocardial infarction (MI). VCG parameters included: (1) spatial parameters: magnitude, azimuth and elevation of the maximal vector, vectors at 20 ms and 30 ms, and (2) scalar parameters: amplitudes of 20 ms and 30 ms vectors at X, Y, and Z scalar leads abbreviated as X20, Y20, Z20, X30, Y30 and Z30, respectively. RESULTS: For anteroseptal MI, the azimuth of 30 ms vector and Z20 showed a significant correlation with %DV (r = 0.572, P < 0.05 and r = 0.832, P < 0.001) while in anteroseptal MI with involvement of lateral wall, the azimuth of 30 ms vector and X30 were correlated with %DV significantly (r = 0.775, and r = 0.780, P < 0.01). For inferior and inferoposterior MI, the elevation of 30 ms vector and Y30 were correlated well with %DV (r = 0.871, P < 0.01, r = 0.928, P < 0.001 for inferior MI and r = 0.678, P < 0.01, r = 0.760, P < 0.001 for inferoposterior MI). CONCLUSION: VCG parameters, especially scalar parameters, can be used to evaluate myocardial infarct size easily and non-invasively with remarkable accuracy.

Vectorcardiographic evaluation of myocardial infarct size: departure parameters are superior to conventional spatial parameters.

To determine whether the departure parameters derived from a "departure loop" of a vectorcardiogram are more accurate than conventional spatial parameters in evaluating myocardial infarct size, 74 patients with first-onset myocardial infarction (MI) were studied. The correlation between the departure parameters (amplitudes in scalar leads of the departure loop) and the percent defect volume of thallium myocardial scintigrams (%DV) was compared with that of the spatial parameters (magnitude, azimuth, and elevation of the original QRS loop). In anteroseptal MI, the amplitude of a 20-msec vector in the z-axis and the azimuth of a 30-msec vector (H30) were significantly correlated with %DV (r=0.783, p<0.001 and r=0.572, p<0.05). In anteroseptal MI with involvement of the lateral wall, the amplitude of a 30-msec vector in the x-axis and H30 showed significant correlation with %DV (r=0.802, p<0.001 and r=0.772, p<0.01). In inferior and inferoposterior MI, the amplitude of a 30-msec vector in the y-axis and the elevation of a 30-msec vector were significantly correlated with %DV (r=0.920, 0.891, p<0.001 and r=0.871, 0.678, p<0.01, respectively). In conclusion, the departure parameters are more accurate than the spatial parameters for evaluation of myocardial infarct size.

[Relationship between mitral valve echo score and hemodynamic variables in patients with mitral stenosis].

Mitral valve echo score has been proposed as a predictor or of the outcome of balloon mitral valvotomy in patients with mitral stenosis. The relationship between mitral echo score and the hemodynamic variables was evaluated. In 41 patients with pure mitral stenosis (nine men and 32 women, aged 57.9 +/- 9.4 years), mitral echo score was estimated from two-dimensional echocardiographic findings, and mitral valve area was measured by planimetry on the two-dimensional short-axis view. Apex phonocardiography and continuous-wave Doppler echocardiographic recording of transmittral flow were simultaneously performed to measure left atrial/left ventricular mean transmittral pressure gradient, pressure half-time and (Q-1)-(2-OS) interval. Linear regression analysis revealed that both mitral echo score and mitral valve area were significantly correlated with mean transmittral gradient (r = 0.522, p = 0.0005 and r = -0.651, p < 0.0001, respectively), pressure half-time (r = 0.491, p < 0.005 and r = -0.757, p < 0.0001) and (Q-1)-(2-OS) interval (r = 0.551, p < 0.0005 and r = -0.487, p < 0.005, respectively). Mitral echo score has a significant correlation with hemodynamic variables, which were comparable to but slightly different from mitral valve area, in patients with mitral stenosis.