Poor Health-Related Quality of Life and Proactive Primary Control Strategy May Act as Risk Factors for Acute Coronary Syndrome

BACKGROUND AND OBJECTIVES: Increasing evidence supports that psychological factors may be related to development of coronary artery disease (CAD). Although psychological well-being, ill-being, and control strategy factors may play a significant role in CAD, rarely have these factors been simultaneously examined previously. We assessed comprehensive psychological factors in patients with acute coronary syndrome (ACS). SUBJECTS AND METHODS: A total of 85 ACS patients (56 unstable angina, 29 acute myocardial infarction; 52.6+/-10.2 years; M/F=68/17) and 63 healthy controls (48.7+/-6.7 years, M/F=43/20) were included. Socio-demographic information, levels of psychological maladjustment, such as anxiety, hostility, and job stress, health-related quality of life (HRQoL), and primary and secondary control strategy use were collected through self-report questionnaires. RESULTS: There was no significant difference between the ACS group and control group in levels of anxiety, hostility, and job stress. However, ACS patients had significantly lower scores on the general health perception and bodily pain subscales of HRQoL than the control group. The ACS group, as compared with the controls, tended to use primary control strategies more, although not reaching statistical significance by univariate analysis. Multivariate logistic regression analysis after adjusting age and gender identified the physical domain of HRQoL {odds ratio (OR)=0.40}, primary control strategy (OR=1.92), and secondary control strategy (OR=0.53) as independent predictors of ACS. CONCLUSION: Poor HRQoL and primary control strategy, proactive behaviors in achieving ones' goal, may act as risk factors for ACS, while secondary control strategy to conform to current situation may act as a protective factor for ACS.

Prognostic Impact of Early ST-Segment Resolution and Biochemical Markers in Patients With ST-Elevation Myocardial Infarction

No abstract available.

Acute pulmonary edema during endovascular stenting of a patient with non-malignant superior vena cava syndrome: A case report / 대한내과학회지

The superior vena cava (SVC) syndrome results from the disturbance of blood flow in superior vena cava caused by the obstruction. The most common etiology of this condition is the external compression by a malignant tumor. Other causes include thrombus from a pacemaker, defibrillator or central venous catheters. The conventional treatment is radiation and chemotherapy. Recently stenting has been used as a first-line therapeutic strategy for non-malignant cases with balloon and self-expanding stents. In our report, a 77 year-old woman had the SVC syndrome without identification of an underlying disease. A percutaneous endovascular intervention was performed. The stent was placed successfully but just after the procedure, the venous return immediately increased and acute pulmonary edema developed. The patient improved after intravenous diuretics and oxygen. Here we report our experience and review the medical literatures for the management of the non-malignant SVC syndrome, with percutaneous endovascular intervention and the rare complication of pulmonary edema.

Stress-Induced Atherosclerosis: Clinical Evidence and Possible Underlying Mechanism

There is increasing recognition in medical fields of the importance of behavioral and psychosocial factors in the development of cardiovascular disease. Although the pathogenesis underlying stress-induced atherosclerosis is not well known, inflammation may play a key role. Activation of stress-induced neuroendocrine pathways, such as the hypothalamo-pituitary-adrenal axis, and the sympathetic nervous and renin angiotensin systems, direct neurogenic inflammation may also contribute to the development of stress-induced atherosclerosis.

Blockade of TGF-beta by Catheter-based Gene Transfer of a Soluble TGF-beta Type II Receptor Inhibits Neointima Formed after Stenting

BACKGROUND: Enhanced extracellular matrix (ECM) accumulation is an important finding in coronary stent restenotic tissue, in which TGF-beta, implicated in ECM formation, is expressed abundantly. We assessed the hypothesis that blockade of TGF-beta by the local delivery of an adenovirus expressing a soluble form of the TGF-beta type II receptor (AdT beta-ExR), inhibits stent-induced neointima in porcine coronary arteries. METHODS: Two remote coronary arterial segments (n=20) per pig randomly received 1x10(9) pfu of either AdT beta-ExR or adenovirus expressing beta-galactosidase (AdLacZ)/PBS, using an Infiltrator(TM). Stents (n=20) were deployed, after gene transfer, in each segment of 10 pigs. Localized transgene expression was confirmed by both reverse transcription-PCR and immunohistochemistry. Computer-based morphometric assessment was performed in the stented arteries 4 weeks after the gene transfer. RESULTS: There was significantly less intimal area (1.57+/-0.49 vs. 2.13+/-0.34 mm2), area ratio of intima/media (0.84+/-0.44 vs. 1.32+/-0.48) and higher neointimal cell density (3121+/-330 vs. 2812+/-183 cells/mm2) in the arteries treated with AdT beta-ExR compared to the controls (all, p<0.05). Neither the cell proliferation rate, assessed by PCNA immunohistochemistry, nor the injury score were significantly different between the two groups. The distribution of hyaluronan in the intima was less in 4 of the 6 AdT beta-ExR treated arteries compared to the controls. CONCLUSION: Blockade of TGF-beta, by a local in vivo gene transfer of a soluble TGF-beta receptor, inhibits stent-induced neointima, probably by inhibiting the ECM accumulation in porcine coronary arteries, which may have therapeutic potential in the inhibition of restenosis after stenting.

Inhibition of TGF-beta by Gene Delivery does not Alter the Neointima Area, but Enhances Inflammation in In-Stent Stenosis of Pig Coronary Arteries

BACKGROUND: We have shown that extracellular matrix (ECM) rather than cell proliferation contributes to in-stent restenosis. Transforming growth factor-beta (TGF-beta), a positive regulator of ECM deposition by vascular cells, may be implicated in in-stent restenosis. We assessed if the blockade of TGF-beta by catheter-based local delivery of an adenovirus expressing a soluble form of TGF-beta type II receptor (AdTbeta-ExR) can inhibit stent-induced neointima. METHODS: AdTbeta-ExR was applied onto a coronary arterial segment of a pig using an Infiltrator(TM), and either of adenovirus expressing beta-galactosidase (AdLacZ) or PBS was applied onto other remote segment of the same pig (n=10). Then, stents (n=20) were deployed in the treated arterial segment. RESULTS: Computer-based morphometric analysis 4 weeks after stenting showed no significant difference in neointima area between the AdTbeta-ExR-infected and control groups (AdLacZ and PBS). However cell density of neointima was significantly increased in the AdTbeta-ExR group compared with control group (3121+/-331 vs 2812+/-183 cells/mm2, p<0.05). Notably, the AdTbeta-ExR group had more extensive CD3 positive T cell infiltration. In addition matrix metalloproteinase (MMP)1 expression and accumulation of hyaluronan was greater in the AdTbeta-ExR group. Cell proliferation rate was significantly increased in the media of the AdTbeta-ExR group compared with control group (2.04+/-1.21% vs 1.18+/-1.06%, p<0.05). CONCLUSION: Blockade of TGF-beta by use of catheter-based local in vivo gene delivery did not alter neointima formation significantly in our porcine coronary artery stent model, however it increased inflammation and pathological changes that could promote lesion formation.

A case of prostacyclin responsive pulmonary hypertension complicated in a patient with systemic lupus erythematosus / 대한내과학회지

A 36-year-old woman was admitted due to dyspnea and generalized edema, and was diagnosed as systemic lupus erythematosus and right ventricular heart failure due to accompanied pulmonary hypertension. The patient had been treated with diuretics, digoxin, high dose steroid and high dose nifedipine to treat right ventricular heart failure and pulmonary hypertension. Although the symptom and pulmonary hypertension responded transiently by these treatment, dyspnea was aggravated again and pulmonary arterial pressure was elevated in 1 week after high dose nifedipine treatment. The combination therapy of oral prostacyclin analogue (Beraprost), high dose steroid, azathioprine, hydrochloroquine sulfate was tried subsequently and decrease of pulmonary hypertension and improvement of clinical symptoms was noted in 45 days after beraprost treatment.

Hyperhomocysteinemia as a Risk Factor for Coronary Artery Disease / 대한진단검사의학회지

BACKGROUND: Hyperhomocysteinemia is considered as a risk factor for coronary artery disease (CAD). In this study, we investigated the relationship between plasma homocysteine concentration and coronary artery disease. METHODS: We measured plasma homocysteine concentration by fluorescent polarization immunoas-say (IMx, Abbott) in 58 healthy controls (39-72 years) and in 37 patients (42-84 years) who were diagnosed with stable angina (11), unstable angina (14), acute myocardial infarction (8), old myocardial infarction (1) and silent myocardial ischemia (3). RESULTS: The risk of CAD was independently associated with old age, decreased HDL cholesterol and hyperhomocysteinemia (P >or=12.8 nmol/L) and adjusted odds ratios were 2.8, 3.4, and 6.0, respec-tively. The risk for CAD in the upper two homocysteine quartiles (P >or=10.8 nmol/L and 8.1- 10.7 nmol/L) was 11.1 (95% CI, 2.5- 49.4) times and 6.3 (95% CI, 1.4- 27.7) times higher than in the lowest quar-tile (<6.9 nmol/L) (P=0.002 and 0.014, respectively). The mean plasma homocysteine values (M +/- SD) were higher in CAD patients (11.8 +/- 7.4 nmol/L) than in the control group (8.0 +/- 2.4 mol/L) (P=0.0006). In the control group, the mean plasma homocysteine concentration in men was signifi-cantly igher than in women (9.1 vs. 7.2 mol/L, P=0.002). Age and logarithmically transformed plasma homocysteine levels exhibited significant positive correlation in controls (r=0.43, P=0.001), ut no significant correlation in CAD patients (r=-0.024, P=0.9). Plasma homocysteine levels were significantly higher in the elderly, male subjects and smokers in the univariate analysis. CONCLUSIONS: Hyperhomocysteinemia is one of the independent risk factors for CAD.

Catheter-based adenovirus-mediated local intravascular gene delivery of a soluble TGF-beta type II receptor using an Infiltrator in porcine coronary arteries: efficacy and complications

Enhanced extracellular matrix (ECM) accumulation is an important finding in human restenotic arterial neointima after angioplasty. Transforming growth factor b1(TGF-beta1) is known to regulate the synthesis and turnover of a variety of ECM components, and may play an important role in restenosis. Recombinant adenoviral vector expressing an ectodomain of the TGF-beta type II receptor fused to the human immunoglobulin Fc portion (AdT beta-ExR) inhibits the action of TGF-beta probably either by adsorbing TGF-beta or by acting as a dominant negative receptor. We carried out a catheter-based local adenovirus mediated gene delivery using an Infiltrator in porcine coronary arteries to know the pattern of gene expression, efficacy and procedural complications. Twenty four coronary arteries in 13 pigs were used for intravascular gene delivery by intramural injection with either AdT beta-ExR or adenovirus expressing b-galactosidase (AdCALacZ). Direct immunofluorescent staining and reverse transcription polymerase chain reaction (RTPCR) were used for detection of type II TGF-beta receptor and its mRNA respectively. X-Gal histochemistry was performed to identify b-galactosidase. Both soluble TGF-beta receptor and b-galactosidase were expressed locally in the media and adventita at injected arterial segments without any significant dissemination to remote area. Intravascular gene transfection performed with various titer of each adenoviral vector showed that AdT beta-ExR of 5x10(8) pfu and AdCALacZ of 2.5 x 10(8) pfu were the minimum titer for the expression of each transgene. Infiltration of CD3 positive T cells was detected by immunohistochemical staining in the area of each transgene expression, and tends to decrease over time after gene delivery. Pathological study of 24 treated arteries showed complications such as disruption of external elastic lamina with hemorrhage (n = 4), minimal disruption of internal elastic lamina and endothelial layer, and medial thickening. In conclusion, catheter-based local intravascular gene delivery of adenoviral vector is feasible and effective in a selected artery, but must be undertaken with caution due to possible lethal complications. Local delivery of soluble TGF-beta type II receptor in this way may provide an effective intravascular gene therapy to inhibit TGF-beta signal pathway without any significant systemic side effect.

Catheter-based adenovirus-mediated local intravascular gene delivery of a soluble TGF-beta type II receptor using an Infiltrator in porcine coronary arteries: efficacy and complications

Enhanced extracellular matrix (ECM) accumulation is an important finding in human restenotic arterial neointima after angioplasty. Transforming growth factor b1(TGF-beta1) is known to regulate the synthesis and turnover of a variety of ECM components, and may play an important role in restenosis. Recombinant adenoviral vector expressing an ectodomain of the TGF-beta type II receptor fused to the human immunoglobulin Fc portion (AdT beta-ExR) inhibits the action of TGF-beta probably either by adsorbing TGF-beta or by acting as a dominant negative receptor. We carried out a catheter-based local adenovirus mediated gene delivery using an Infiltrator in porcine coronary arteries to know the pattern of gene expression, efficacy and procedural complications. Twenty four coronary arteries in 13 pigs were used for intravascular gene delivery by intramural injection with either AdT beta-ExR or adenovirus expressing b-galactosidase (AdCALacZ). Direct immunofluorescent staining and reverse transcription polymerase chain reaction (RTPCR) were used for detection of type II TGF-beta receptor and its mRNA respectively. X-Gal histochemistry was performed to identify b-galactosidase. Both soluble TGF-beta receptor and b-galactosidase were expressed locally in the media and adventita at injected arterial segments without any significant dissemination to remote area. Intravascular gene transfection performed with various titer of each adenoviral vector showed that AdT beta-ExR of 5x10(8) pfu and AdCALacZ of 2.5 x 10(8) pfu were the minimum titer for the expression of each transgene. Infiltration of CD3 positive T cells was detected by immunohistochemical staining in the area of each transgene expression, and tends to decrease over time after gene delivery. Pathological study of 24 treated arteries showed complications such as disruption of external elastic lamina with hemorrhage (n = 4), minimal disruption of internal elastic lamina and endothelial layer, and medial thickening. In conclusion, catheter-based local intravascular gene delivery of adenoviral vector is feasible and effective in a selected artery, but must be undertaken with caution due to possible lethal complications. Local delivery of soluble TGF-beta type II receptor in this way may provide an effective intravascular gene therapy to inhibit TGF-beta signal pathway without any significant systemic side effect.

Safety of transradial coronary intervention with early discharge in selected patients

BACKGROUND AND OBJECT: Transradial percutaneous coronary intervention enables early ambulation and caused less complications at the puncture site. This study was performed to evaluate the safety of transradial coronary intervention with early discharge in selected patients. MATERIALS AND METHOD: Thirty patients were studied retrospectively. Twenty five patients had transradial percutaneous coronary intervention with next morning discharge and 5 patients had transradial percutaneous coronary intervention on an outpatient basis. Each patient was checked for cardiovascular complication and any other problems at the puncture site immediately after, 2 weeks after and 1 month after the procedure. RESULTS: This study group consisted of 30 patients with a mean age of 60+/-10 years. The indication for intervention were unstable angina (63.3%), stable angina (20.0%), and restenosis at 6-month follow-up after intervention. A total of 21 stents were implanted at 40 lesions. No major cardiovascular complication nor puncture site complication was reported at 1 month follow-up. CONCLUSION: Early discharge is supposed to be safe for those with optimal angiographic results and no clinical problems for at least 5 hours after intervention.

The Evaluation of the Clinical Significance and the Normal Reference Range of the Plasma Homocysteine / 대한임상병리학회지

BACKGROUND: The cardiovascular diseases are a major cause of the mortality in Korean. The homocysteine(HCY) was accepted as a risk factor of the cardiovascular disease, recently. We estimate the normal reference range of the plasma HCY according to the age and sex, and the clinical significance in the cardiovascular disease. METHODS: Blood from the 57 healthy people who are 34 women and 23 men(39-72 years old) and 26 patients(25-75 years old) who are diagnosed 8 stable angina, 10 unstable angina, 7 acute myocardial infarction and 1 old myocardial infarction was drawn into EDTA vacutainer tube. The HCY concentration was measured by the automated fluorescence polarizing immunoassay(FPIA, IMx, Abbott, USA). RESULTS: Inter- and intra-assay coefficient of variations(CVs) ranged from 0.7% to 2.8% and from 1.1% to 1.6%, respectively. Low detection limits showed 0.05+/-0.08 micromol/L. The recovery rates were 98.6-99.9%. The mean plasma HCY concentration(M+/-SD) of the healthy people was 7.9+/-2.11 micromol/L and was increased with aging. The mean plasma HCY concentration in men was significantly higher than that in women(7.2 vs. 8.8 micromol/L, P=0.008). In the coronary artery disease group(CAD), the mean values were 13.1+/-13.18 micromol/L and the median value 8.0micromol/L. After excluding 3SD outliers, the mean values were 9.0+/-2.83 micromol/L(P=0.08 to the healthy group). In CAD, the ratio over the cut-off value of total cholesterol, HDL-cholesterol and triglyceride were 42.3%, 34.6%, and 26.9%, respectively, the ratio above the HCY 15 micromol/L was 15.4% which was the same positivity in LDL-cholesterol. CONCLUSIONS: The plasma HCY in the normal control group was significantly increased with aging and was shown higher in men than in women. In CAD, the value was also increased more than normal control. Now multicenter study is needed in order to get the normal range of Korean to diagnosis, treatment and management of the cardiovascular disease.

Histopathological Characteristics of Human Coronary Stent Restenosis

BACKGROUND AND OBJECTIVES: Neointimal ingrowth rather than stent recoil is thought to be important for coronary in-stent restenosis. However only limited pathologic data are available to adress the mechanisms of in-stent restenosis. With the specific aim of measuring cell replication and of assessing cellularity and extracellular matrix (ECM) composition, we analyzed atherectomized coronary arterial in-stent restenotic specimens. METHODS AND RESULTS: In the present study, we analyzed 29 atherectomized coronary arterial in-stent restenotic tissue samples (14 LAD, 10 RCA, and 5 LCX) retrieved from 25 patients (m/f:18/7: age 59+/-13 yr) at 0.5-23 (mean 5.7) months after deployment of Palmaz-Schatz stent. Histopathological analysis of cellular components and ECM was performed using H & E, modified Movat pentachrome, and immunocytochemical staining. Cellular proliferation rate, as estimated by use of antibodies to Ki-67 nuclear antigen showed low proliferation rate with the range of 0-4%, and no positive cells were found in 62% of cases. Myxoid tissue having ECM enriched with versican and hyaluronan was found in 69% of cases, and decreased over time after stenting. Foci of cell poor area were found in 57% of cases, and could be classified into as: (1) containing collagen-rich ECM and (2) containing a proteoglycan-rich ECM. Versican, biglycan, perlecan, and hyaluronan were identified with varying individual distributions in the proteoglycan rich area. Specimens with foci of cell poor area tended to increase over time after stenting (31% in & 4 mo vs. 81% in > or =4 mo after stenting, p<0.01). alpha-smooth muscle actin staining identified the majority of cells as smooth muscle cells (SMC) and occasional macrophages (< or =12 cells per section) were detected by CD68 antibody. CONCLUSIONS: These data suggest that enhanced ECM accumulation rather than cell proliferation may be important mechanisms for stent restenosis. Angioplasty of stent restenosis may therefore fail due to transient compression of this hygroscopic matrix.

Angiographic Differences Analysis of Coronary Artery Lesions in Patients with Stable and Unstable Angina Pectoris

BACKGROUND AND OBJECTIVES: As previously reported, unstable angina is usually related to characteristic coronary artery lesion's morphology analyzed by coronary angiogram. This takes the form of an eccentrically placed convex stenosis with a narrow neck due to one or more overhanging edges or irregular, scalloped borders, or both. Although most studies were done for lesions with high degree stenosis(>50%), recent studies emphasized the role of vulnerability of plaque in acute coronary syndrome and even mild degree stenotic lesions may progress rapidly to evoke acute coronary syndrome. Therefore in this study, we analyzed the morphological characteristics of coronary artery lesions with mild degree stenosis as well as severe stenosis. MATERIALS AND METHODS: We conducted a retrospective study of 96 patients with angina pectoris (42 of stable patients and 54 of unstable patients) who underwent coronary angiography. Each lesions with 25% or greater diameter stenosis were categorized into simple and complex lesion(convex intraluminal obstruction with a narrow neck or irregular borders, diffuse irregularities, ulceration, thrombus). Calcification of coronary artery, extents of lesions were analyzed and stenosis grade and location were categorized by AHA classification. RESULTS: There were no significant differences between the stable angina and unstable angina in risk factors and vessel involvement, numbers of lesions, calcification and total obstruction. In morphologic analysis, complex lesions were more frequent in unstable angina than stable angina (49% vs 33%, p<0.05). The mean of percent diameter stenosis was not signigicantly different between two groups, but severe stenotic lesions with 90% or more stenosis were more frequent in unstable angina (34% vs 22%, p<0.05). Locations of involved vessels were similar between the angina groups. Complex lesions were distributed more frequent in RCA and simple lesions were more in LAD and LCX (p<0.05). CONCLUSIONS: The lesions with both complex morphology and severe degree stenosis are closely implicated in unstable angina.

A Histopathologic Analysis of Atherectomized Human Coronary Stent Restenosis :Potential Role of Cell Migration and Extracellular Matrix Formation

BACKGROUND: Neointimal ingrowth rather than stent recoil has thought to be important for coronary arterial in-stent restenosis. Intuitively cell migration and extracellular matrix (ECM) formation seems to be important in the pathogenesis of stent restenosis. Therefore, with specific aim of identifying molecules implicated in cell migration and extracellular matrix formation, histopathologic analysis on atherectomized coronary arterial in-stent restenotic tissue was performed. METHODS: In the present study we analyzed 29 atherectomized coronary arterial in-stent restenotic tissue specimens (LAD 14, LCX 5, RCA 10) retrieved (5.7+/-5.4 months after stent deployment) from 25 patients (age 59+/-13, M/F:18/70) in whom restenosis complicated previous revascularization with Palmaz-Schatz stent. Histopathologic analysis was performed after immunostaining. Antibodies against TGF- 1, hyaluronan synthase (HAS) 1, MMP1, MMP9, urokinase type plasminogen activator, PDGF receptor were used for immunostaining. RESULTS: Myxoid tissue characterized by stellate-shaped cells embedded in a loose ECM was present in 20 out of 29 specimens, and tends to decrease over time after stenting. Foci of cell poor area (48-320 cells/mm2) in a microscopic field was present in 17 out of 29 specimens, and tends to increase over time after stenting (13/16 in or =4 mo, p<0.01). Various proportions of specimens show positive stained cells with respect to each antibodies: TGF 1 in 16 out of 20:HAS1 in 10 out of 13:MMP1 in 8 out of 16:MMP9 in 4 out of 13:PDGF receptor in 12 out of 17 specimens. Abundant cells labled with certain antibodies (TGF 1, uPA, PDGF receptor) were frequently found in myxoid tissue. CONCLUSIONS: Myxoid tissue, frequently found in stent restenotic tissue, may be a biologically active tissue in terms of cell migration and of ECM formation. ECM accumulation tends to increase over time after stenting and may be important in pathogenesis of coronary arterial stent restenosis.

Coronary Fistula Anastomosing between Right Coronary Artery and Left Bronchial Artery Accompanied with Cystic Lung Disease

We report a case of 86-year-old woman with coronary artery fistula connecting the right coronary artery and left bronchial artery accompanied with cystic lung disease presenting with dyspnea and chest pain. Coronary angiography revealed that right coronary artery was anastomosed with the collaterals of left bronchial artery at the right hilum and tortuously ascended along the aortic arch and descended connecting with left pulmonary lobar artery at a certain site which is faintly opcified showing to and pro phasic movement. Chest CT scan shows the multicystic changes of the left lower lobe of the lung and hypertrophied bronchial artery of left lobar bronchus. Under the diagnosis of coronary artery fistula, hypertensive heart disease and multicystic lung disease, patient's symptoms and signs were improved by conservative treatment without surgical intervention.

Giant Aneurysm of a Congenital Coronary Arteriovenous Fistula Arising from the Left Coronary Artery

Congenital coronary arteriovenous fistula is a rare condition which is an abnormal communication of the coronary artery with the right ventricle, right atrium, left atrium or left ventricle. Coronary artery aneurysm is an uncommon disease which is defined as coronary dilatation which exceeds the diameter of normal adjacent segments or the diameter of the patient's largest coronary vessel by 1.5 times. In young ages, symptoms are unusual, but significant symptoms and complications such as congestive heart failure, subacute bacterial endocarditis, coronary steal syndrome, aneurysm formation, rupture, and pulmonary hypertension may appear among the older age group. We report a case of giant aneurysm of a congenital coronary arteriovenous fistula between left co-ronary artery and right ventricular outflow tract with significant left to right shunt confirmed in a 84-year old female with a brief review of literature.

Risk of Coronary Artery Disease Homocyst (e)in, Low HDL Cholesterol, Fibrinogen

No abstract available.

A Case of Left Ventricular Outflow Obstruction Caused by Mitral Valve Replacement

The pathophysiology, clinical presentation and prognosis of left ventricular obstruction present an important cardiological problem. Various anatomical and functional abnormality can cause this phenomenon. Rarely, left ventricular outflow obstruction can result after mitral valve surgery. We experienced a case of left ventricular outflow obdtruction 13 years after mitral valve replavement. The diagnosis was made using two-dimensinal Doppler echocardiography and confirmed by cardiac catheterization. The pressure gradient across the left ventricular outflow obstruction was 96mmHg. A second mitral valve replacement was performed. Because severe fibrosis, pannis around the prosthetic mitral valve and a subaortic web were detected during the operation, the subaortic web was removes.

Changes in LV Mass, LV Morphology and Diastolic Function of LV in Response to Antihypertensive Treatment

BACKGROUND: Left ventricular hypertrophy is major cardiovascular risk factor for sudden death, acute myocardial infarction and congestive heart failure. Antihypertensive treatment able to normalize blood pressure and regression of left ventricular mass would also favorabley affect coronary flow reserve and cardiovascular mortality. OBJECT: This study was designed to explore changes of left venrtricular mass, echocardiographic datas such as interventricular septal thickness in diastole, posterior wall thickness in diastole, left ventricular end diastolic dimension, relative wall thickness, mainmorphologic change of LV, and diastolic function after antihypertensive treatment. METHODS: From May 1988 to Agust 1997, in 41 patients(14 men, 27 women) with estaiblished essential hypertension aged 35 to 78(mean 56+/-13) year were studied. We obtained the basal echocardiography and follow up echocardiography after treatment. RESULT: The results were as followings: 1) Baseline blood pressure was 157/92mmHg and fell to 137/81mmHg(p<0.001), and LV mass were reduced from 133.9g/mg2 to 132.9g/m2 without statistical significance. 2) Most of the patients(48.8%) were remained increased LV mass and only 12% of the patients were revert to normal LV mass. 3) Most of the patients remained same LV morphology after antihypertensive treatment. 4) Normalization of LV diastolic dysfunction was not observed after antihypertensive treatment. CONCLUSION: Most of the patients were remained increased LV mass, same morphology, and relaxation abnormality of LV after antihypertensive treatments. For analysis of our result, follow up studies are needed about regression of LV mass, remodeling of LV, diastolic function after antihypertensive treatment.