Leriche syndrome in a patient with acute pulmonary embolism and acute myocardial infarction: a case report and review of literature.

BACKGROUND:Both acute myocardial infarction and acute pulmonary embolism are distinct medical urgencies while they may conincide. Leriche's syndrome is a relatively rare aortoiliac occlusive disease characterized by claudication, decreased femoral pulses, and impotence. We present the first case of concomitant acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome.CASE PRESENTATION:A 56-year-old male with a history of intermittent claudication was admitted for evaluating the sudden onset of chest pain. Elevated serum troponin level, sustained high D-dimer level, ST-T wave changes on electrocardiogram, and segmental wall motion abnormality of the left ventricle on transthoracic echocardiography were noted. Pulmonary Computed Tomography Angiogram revealed multiple acute emboli. Aortic Computed Tomography Angiogram spotted complete obstructions of the subrenal aorta and bilateral common iliac arteries with collateral circulation, maintaining the vascularization of internal and external iliac arteries. We stated the diagnosis of acute pulmonary embolism and Leriche syndrome and initiated oral anticoagulation. However, Q waves on electrocardiogram and wall motion abnormality on echocardiography persisted after embolus dissolved successfully. Coronary computed tomography angiogram found coronary arterial plaques while myocardial Positron Emission Tomography detected decreased viable myocardium of the left ventricle. We subsequently ratified the diagnosis of concurrent acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome. The patient was discharged and has been followed up at our center.CONCLUSION:We described the first concurrence of acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome.

Inverse relationship of bleeding risk with clot burden during pulmonary embolism treatment with LMW heparin.

INTRODUCTION:Clinically relevant bleeding occurs three times as frequently as recurrent venous thromboembolism in the modern early treatment of pulmonary embolism (PE) with fixed-dose, unmonitored anticoagulants. Unfractionated heparin (UFH) is monitored and adjusted to assure efficacy and minimize bleeding risk, but low molecular weight heparin (LMWH) is not. PE requires more anticoagulant than isolated deep venous thrombosis. Speculating that PE with low clot burden could lead to excess bleeding with unadjusted LMWH treatment but not with UFH, we compared PE patients receiving either UFH or LMWH with high and low clot burden for clinically significant bleeding in an observational study.MATERIALS AND METHODS:Patients with acute PE at multiple Chinese teaching hospitals had been randomized to UFH or LMWH for initial treatment. These treatment cohorts had baseline measurement of pulmonary artery obstruction (PAO) score, which was prospectively separated into quartiles, lowest to highest PAO. All patients were followed for bleeding episodes, which were subsequently analyzed by quartile of PAO.RESULTS:Two hundred seventy-four patients divided between the two groups had similar efficacy and safety outcomes (12 clinically significant bleeds in the UFH group vs 15 in the LMWH group). LMWH recipients with the smallest clot burdens (lowest PAO quartiles) had highest bleeding rates (Cochran-Armitage trend test, P trend = 0.048), but there was no such trend for UFH recipients.CONCLUSIONS:For UFH, excess anticoagulant pro-hemorrhagic potential is down-adjusted via activated partial thromboplastin time monitoring, but for LMWH it is not. For PE patients at high bleeding risk, UFH may be safer if the clot burden is small.

[Clinical features and misdiagnosis of connective tissue disease plus pulmonary embolism].

OBJECTIVE:To evaluate the clinical features and reasons of misdiagnosis of connective tissue disease plus pulmonary embolism (PE).METHODS:The clinical data were reviewed retrospectively for 22 hospitalized patients with connective tissue disease and PE from February 2006 to March 2014. And the features of onset, clinical and laboratory characteristics, imaging tests and causes of misdiagnosis were analyzed.RESULTS:There were 12 males and 10 females with an average age of (36.2 ± 14.2) years. And 12 (54.5%) PE patients had concurrent deep venous thrombosis. Antiphospholipid syndrome and Behcet's disease were the major causes of connective tissue disease. Chest distress, palpitation and extremity swelling were initial symptoms. There were elevated erythrocyte sedimentation rate (n = 11, 50.0%), elevated C-reactive protein (n = 8, 36.4%) and abnormal autoantibody (n = 15, 68.2%) respectively. Computed tomography showed pulmonary arteries stenosis, occlusion and aneurismal dilation. Eighteen (81.8%) patients had pulmonary hypertension with a systolic pulmonary pressure of (72 ± 20) mmHg (1 mmHg = 0.133 kPa). And 3 of them presented severity of pulmonary pressure non-matched to the degree of pulmonary vascular involvement. And 18 (81.8%) patients with connective tissue disease were missed due to a lack of typical symptoms and physician understanding of disease before admission. Three (13.6%) patients had a misdiagnosis of idiopathic pulmonary arterial hypertension. The median time of diagnosis was 12 months.CONCLUSIONS:Connective tissue disease may develop PE as the initial symptom. And some patients lack typical clinical manifestations of connective tissue disease. It should raise an alert with the physicians.

Rare case of multiple pulmonary artery aneurysms with mural thrombus and right ventricle capillary hemangioma.

[Relationship between serum uric acid levels and patient conditions and prognosis in idiopathic pulmonary arterial hypertension].

OBJECTIVE:To explore the relationship between serum uric acid levels and patient conditions and prognosis in idiopathic pulmonary arterial hypertension (IPAH).METHODS:A total of 76 IPAH patients confirmed by right heart catheterization were enrolled consecutively and followed up until the endpoint of all-cause death. Their baseline data were recorded and analyzed by Spearman's rank test and independent t-test. And the follow-up outcomes were analyzed with Kaplan-Meier plots.RESULTS:There were 27 males and 49 females with a mean age of 29.7 ± 9.7 years. They were classified into World Health Organization functional class (WHO-FC)II (n = 28), class III (n = 45) and class IV (n = 3). Their baseline mean pulmonary artery pressure was (65 ± 16) mm Hg, pulmonary vascular resistance (1677 ± 669) dyn×s(-1)×cm(-5), pulmonary capillary wedge pressure (9.6 ± 5.0) mm Hg, mean right atrial pressure (9.8 ± 6.1) mm Hg, cardiac index (2.07 ± 0.57) L ×min(-1)× m(-2) and serum uric acid (391 ± 103) µmol/L. The correlation analysis indicated that the serum level of uric acid correlated positively with right ventricular diameter (r = 0.28, P = 0.018) and negatively with CI (r = -0.34, P = 0.003). Independent t-test results indicated that the patients with a higher level of uric acid were apt to have a worse WHO-FC, and the higher level uric acid group (serum uric acid > 416.5 µmol/L) had a relative higher level of WHO-FC, NT-proBNP and endothelin-1. A lower level of CI denoted more severe conditions and prognosis. Survival analysis indicated that the serum level of uric acid could strongly predict survival in IPAH patients with over time and those with a high level of uric acid had a worse prognosis.CONCLUSION:The serum level of uric acid correlates significantly with patient conditions and prognosis in IPAH. And a higher serum level of uric acid predicts worse conditions and prognosis.

[Multicenter study of disease attributes in adult patients with pulmonary hypertension].

OBJECTIVE:To understand the demographic, hemodynamic and clinical features of adult patients with pulmonary hypertension (PH) in China.METHODS:Between May 2007 and October 2010, a total of 551 adult PH patients were recruited from 31 clinical centers all over China. All fulfilled the traditional hemodynamic criteria diagnosed through right heart catheterization (RHC). The relevant data of demographic, clinical and hemodynamic features of all patients, analyzed the similarities and differences of demographic characteristics between different subtypes. They were divided into 2 groups: WHO functional class I/II and III/IV. And their hemodynamic and clinical features were compared.RESULTS:There were 165 males and 386 females with a mean age of (35 ± 12) years. The mean body mass index (BMI) was (21 ± 4) kg/m(2). There were pulmonary arterial hypertension (PAH, n = 487) and chronic thromboembolic pulmonary hypertension (CTEPH, n = 64). Fatigue (421, 76.4%) and dyspnea (398, 72.2%) were the most common symptoms; Physical examination revealed such a common sign as an accentuated pulmonic second sound (P(2)) in 510 patients (92.6%). Over half (325, 59.0%) of them were of WHO functional class II and 213 (38.6%) patients functional class III. The 6-minute walking distance (6MWD) and Borg dyspnea score were (352 ± 91) m and 3.0 (2.0 - 4.0) respectively. ECG of 497 (90.2%) patients showed right ventricular hypertrophy. Mean right atrial pressure was (9 ± 6) mm Hg (1 mm Hg = 0.133 kPa), pulmonary arterial pressure (67 ± 20) mm Hg, cardiac index (2.7 ± 1.2) Lmin(-1)m(-2) and pulmonary vascular resistance (1496 ± 783) dyn.sec.cm(-5).CONCLUSIONS:Young females with a low BMI are predominantly affected by PH. Severe functional and hemodynamic compromises often appear on presentation. And hemodynamic impairment is correlated with 6MWD and WHO functional class.

Mechanisms of pulmonary hypertension related to ventricular septal defect in congenital heart disease.

BACKGROUND:The aim of this study was to investigate differences in molecular mechanisms of pulmonary hypertension between patients with complete transposition of the great arteries (TGA) combined with ventricular septal defect (VSD) and those with VSD alone.METHODS:Twenty-four consecutive patients with pulmonary hypertension (mean pulmonary artery pressure > 30 mm Hg) underwent surgical correction of TGA + VSD (n = 10) or VSD alone (n = 14). Lung specimens were taken from the right middle lobe before cardiopulmonary bypass (CPB). Extent of pulmonary hypertension was graded according to the Heath-Edwards pathologic classification. Enzyme-linked immunosorbent assay (ELISA) was used to determine expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), endothelin-1 (ET-1), endothelin A and B receptors (ET-AR, ET-BR), matrix metalloproteinases 2 and 9 (MMP-2, MMP-9), and tissue inhibitor of metalloproteinase (TIMP).RESULTS:There were no statistically significant differences in age, height, weight, VSD diameter, or preoperative pulmonary artery pressure between groups. Hemoglobin level, pulmonary artery oxygen saturation, and reduction in postoperative pulmonary artery pressure were significantly higher in patients undergoing correction of TGA + VSD (p < 0.05). All patients had grade 0 to II Heath-Edwards morphologic changes in lung biopsy samples. Expression of eNOS and MMP-2 was significantly lower in the TGA + VSD group than in the VSD-alone group (eNOS, 280.13 ± 101.92 ng/mg versus 488.41 ± 249.60 ng/mg; p < 0.05; MMP-2, 31.68 ± 15.36 ng/mg versus 69.28 ± 49.12 ng/mg; p < 0.05). There were no statistically significant differences between groups in expression of iNOS, ET-1, ET-AR, ET-BR, MMP-9, or TIMP.CONCLUSIONS:In patients with TGA + VSD, high oxygenation in the pulmonary circulation decreases expression of MMP-2 and eNOS, which may affect the progress and reversibility of pulmonary hypertension.

[Analysis on inpatient pulmonary hypertension surveillance in Fuwai Cardiovascular Hospital from 1996 to 2005].

OBJECTIVE:To investigate the inpatient pulmonary hypertension (PH) surveillance in a single center of cardiovascular hospital during last ten years.METHODS:In this retrospective analysis, data from patients with discharge diagnosis as PH from Jan. 1996 to Dec. 2005 were collected.RESULTS:A total of 7085 out of 106 640 patients (6.63%) were documented as PH during the survey period and 3.77% PH was idiopathic, 65.93% PH originated from congenital heart diseases, 22.61% from left heart diseases, 5.66% from thrombotic diseases, 0.89% from respiratory diseases, 0.61% from connective tissue diseases, 0.51% from pulmonary vasculitis and 0.03% from portal hypertensive diseases. Both total inpatient number and patients with PH increased year by year during the last 10 years in our hospital. The number of in-hospital patients with PH was significantly higher in 2004 - 2005 than that in 1996 - 2003 (P < 0.0001) and more PH was originated from cardiomyopathy and valvular heart diseases. Idiopathic pulmonary hypertension also tended to increase and PH due to congenital heart diseases was significantly reduced during 2004 - 2005.CONCLUSION:The data from a single center of cardiovascular hospital shows a tendency for increased in-hospital prevalence of pulmonary hypertension during the last ten years.

[Relationship between myocyte proliferation and cardiac function in adult rats with heart failure].

OBJECTIVE:To confirm whether there is myocytes proliferation in the adult rat with heart failure or not, and to investigate the relationship between myocyte proliferation and heart function.METHODS:Descending anterior branch of left coronary artery was ligated in 20 adult male SD rats so as to establish an heart failure models. Eight rats were used as controls. Hemodynamic parameters, blood pressure (BP), left ventricle end systolic pressure (LVESP), left ventricle end diastolic pressure (LVEDP), +LVdp/dt(max), and -LVdp/dt(max), were measured 30 days after the coronary occlusion. Based on the results of heart function examination, the heart infarct rats were divided into 2 subgroups: cardiac functional compensation subgroup (8 rats), and cardiac functional decompensation subgroup (6 rats). Then the rats were killed and their hearts were taken out and stained with propidium iodide (PI) and antibody to alpha-sarcomeric actin. Immunohistochemistry was used to detect the proliferation cell nuclear antigen (PCNA). Confocal microscopy was used to observe the mitotic image. Light microscopy was used to observe the PCNA positive rate in the myocardium.RESULTS:(1) Mitotic images of myocytes could be identified by confocal microscopy in the left ventricle of all rats. (2) PCNA expression was detected in the nuclei of both infarct and normal hearts. The PCNA positive rate of the cardiac functional compensation subgroup was 7.2% +/- 1.4%, significantly higher than that of the control group (2.2% +/- 0.8%, P = 0.648). However, the PCNA positive rate of the cardiac functional decompensation subgroup was 3.0% +/- 1.3%, not significantly different from that of the control group (P = 0.648). (3) The correlation coefficient between PCNA-positivity of cardiomyocytes and +LVdp/dt(max) in the infarct rats were 0.80 (P < 0.01) and the correlation coefficient between PCNA-positivity of cardiomyocytes and -LVdp/dt(max) was -0.76 (P = 0.01).CONCLUSION:(1) There is myocyte proliferation in the adult rat heart. (2) Myocyte proliferation is positively correlated with heart systolic function, and negatively correlated with heart diastolic function in chronic heart failure.

Changes of the proportion and mortality of pulmonary thromboembolism in hospitalized patients from 1974 to 2005.

BACKGROUND:Pulmonary thromboembolism (PTE) has become a common disease that severely endangers people's health. This study analysed the changes in proportion and mortality of PTE in hospitalized patients to provide data for prevention and management of the disease.METHODS:The data of 763 hospitalized patients with PTE from 1974 to 2005 in Fuwai Hospital were analysed.RESULTS:During the 1970s, 0.27% of patients in a cardiovascular hospital had PTE (< 5 cases per year); while so far this century the proportion is 0.94% (48 to 113 per year). The mortality of hospitalized PTE patients fell from 20.00% in the 1970s to 4.10% this century. Prior to 1990, the mortality of hospitalized PTE patients was 12.50%, and in the years after 1990 only 3.40%. The difference was statistically significant (P < 0.005). People with this disease were mostly between the ages of 30 and 69 years. Men were most susceptible between the ages of 30 and 69 years, while women between the ages of 40 and 69 years. Men contracted PTE 10 years earlier than women. The mortality of male PTE patients was 4.70%, not significantly different from female patients, 5.06% (0.50 < P < 0.75). There were not any significant differences between the mortality of patients in the different age groups overall (< or = 39, 40 - 49, 50 - 59, and > or = 60 years, P > 0.1). More people contracted the disease in winter than in other seasons (P < 0.05). There was no obvious difference between the mortality in different seasons overall (0.75 < P < 0.90).CONCLUSION:PTE is an increasingly significant disease and deserves adequate attention.

Leriche syndrome in a patient with acute pulmonary embolism and acute myocardial infarction: a case report and review of literature.

BACKGROUND:Both acute myocardial infarction and acute pulmonary embolism are distinct medical urgencies while they may conincide. Leriche's syndrome is a relatively rare aortoiliac occlusive disease characterized by claudication, decreased femoral pulses, and impotence. We present the first case of concomitant acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome.CASE PRESENTATION:A 56-year-old male with a history of intermittent claudication was admitted for evaluating the sudden onset of chest pain. Elevated serum troponin level, sustained high D-dimer level, ST-T wave changes on electrocardiogram, and segmental wall motion abnormality of the left ventricle on transthoracic echocardiography were noted. Pulmonary Computed Tomography Angiogram revealed multiple acute emboli. Aortic Computed Tomography Angiogram spotted complete obstructions of the subrenal aorta and bilateral common iliac arteries with collateral circulation, maintaining the vascularization of internal and external iliac arteries. We stated the diagnosis of acute pulmonary embolism and Leriche syndrome and initiated oral anticoagulation. However, Q waves on electrocardiogram and wall motion abnormality on echocardiography persisted after embolus dissolved successfully. Coronary computed tomography angiogram found coronary arterial plaques while myocardial Positron Emission Tomography detected decreased viable myocardium of the left ventricle. We subsequently ratified the diagnosis of concurrent acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome. The patient was discharged and has been followed up at our center.CONCLUSION:We described the first concurrence of acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome.

Inverse relationship of bleeding risk with clot burden during pulmonary embolism treatment with LMW heparin.

INTRODUCTION:Clinically relevant bleeding occurs three times as frequently as recurrent venous thromboembolism in the modern early treatment of pulmonary embolism (PE) with fixed-dose, unmonitored anticoagulants. Unfractionated heparin (UFH) is monitored and adjusted to assure efficacy and minimize bleeding risk, but low molecular weight heparin (LMWH) is not. PE requires more anticoagulant than isolated deep venous thrombosis. Speculating that PE with low clot burden could lead to excess bleeding with unadjusted LMWH treatment but not with UFH, we compared PE patients receiving either UFH or LMWH with high and low clot burden for clinically significant bleeding in an observational study.MATERIALS AND METHODS:Patients with acute PE at multiple Chinese teaching hospitals had been randomized to UFH or LMWH for initial treatment. These treatment cohorts had baseline measurement of pulmonary artery obstruction (PAO) score, which was prospectively separated into quartiles, lowest to highest PAO. All patients were followed for bleeding episodes, which were subsequently analyzed by quartile of PAO.RESULTS:Two hundred seventy-four patients divided between the two groups had similar efficacy and safety outcomes (12 clinically significant bleeds in the UFH group vs 15 in the LMWH group). LMWH recipients with the smallest clot burdens (lowest PAO quartiles) had highest bleeding rates (Cochran-Armitage trend test, P trend = 0.048), but there was no such trend for UFH recipients.CONCLUSIONS:For UFH, excess anticoagulant pro-hemorrhagic potential is down-adjusted via activated partial thromboplastin time monitoring, but for LMWH it is not. For PE patients at high bleeding risk, UFH may be safer if the clot burden is small.

[Clinical features and misdiagnosis of connective tissue disease plus pulmonary embolism].

OBJECTIVE:To evaluate the clinical features and reasons of misdiagnosis of connective tissue disease plus pulmonary embolism (PE).METHODS:The clinical data were reviewed retrospectively for 22 hospitalized patients with connective tissue disease and PE from February 2006 to March 2014. And the features of onset, clinical and laboratory characteristics, imaging tests and causes of misdiagnosis were analyzed.RESULTS:There were 12 males and 10 females with an average age of (36.2 ± 14.2) years. And 12 (54.5%) PE patients had concurrent deep venous thrombosis. Antiphospholipid syndrome and Behcet's disease were the major causes of connective tissue disease. Chest distress, palpitation and extremity swelling were initial symptoms. There were elevated erythrocyte sedimentation rate (n = 11, 50.0%), elevated C-reactive protein (n = 8, 36.4%) and abnormal autoantibody (n = 15, 68.2%) respectively. Computed tomography showed pulmonary arteries stenosis, occlusion and aneurismal dilation. Eighteen (81.8%) patients had pulmonary hypertension with a systolic pulmonary pressure of (72 ± 20) mmHg (1 mmHg = 0.133 kPa). And 3 of them presented severity of pulmonary pressure non-matched to the degree of pulmonary vascular involvement. And 18 (81.8%) patients with connective tissue disease were missed due to a lack of typical symptoms and physician understanding of disease before admission. Three (13.6%) patients had a misdiagnosis of idiopathic pulmonary arterial hypertension. The median time of diagnosis was 12 months.CONCLUSIONS:Connective tissue disease may develop PE as the initial symptom. And some patients lack typical clinical manifestations of connective tissue disease. It should raise an alert with the physicians.

Rare case of multiple pulmonary artery aneurysms with mural thrombus and right ventricle capillary hemangioma.

[Relationship between serum uric acid levels and patient conditions and prognosis in idiopathic pulmonary arterial hypertension].

OBJECTIVE:To explore the relationship between serum uric acid levels and patient conditions and prognosis in idiopathic pulmonary arterial hypertension (IPAH).METHODS:A total of 76 IPAH patients confirmed by right heart catheterization were enrolled consecutively and followed up until the endpoint of all-cause death. Their baseline data were recorded and analyzed by Spearman's rank test and independent t-test. And the follow-up outcomes were analyzed with Kaplan-Meier plots.RESULTS:There were 27 males and 49 females with a mean age of 29.7 ± 9.7 years. They were classified into World Health Organization functional class (WHO-FC)II (n = 28), class III (n = 45) and class IV (n = 3). Their baseline mean pulmonary artery pressure was (65 ± 16) mm Hg, pulmonary vascular resistance (1677 ± 669) dyn×s(-1)×cm(-5), pulmonary capillary wedge pressure (9.6 ± 5.0) mm Hg, mean right atrial pressure (9.8 ± 6.1) mm Hg, cardiac index (2.07 ± 0.57) L ×min(-1)× m(-2) and serum uric acid (391 ± 103) µmol/L. The correlation analysis indicated that the serum level of uric acid correlated positively with right ventricular diameter (r = 0.28, P = 0.018) and negatively with CI (r = -0.34, P = 0.003). Independent t-test results indicated that the patients with a higher level of uric acid were apt to have a worse WHO-FC, and the higher level uric acid group (serum uric acid > 416.5 µmol/L) had a relative higher level of WHO-FC, NT-proBNP and endothelin-1. A lower level of CI denoted more severe conditions and prognosis. Survival analysis indicated that the serum level of uric acid could strongly predict survival in IPAH patients with over time and those with a high level of uric acid had a worse prognosis.CONCLUSION:The serum level of uric acid correlates significantly with patient conditions and prognosis in IPAH. And a higher serum level of uric acid predicts worse conditions and prognosis.

[Multicenter study of disease attributes in adult patients with pulmonary hypertension].

OBJECTIVE:To understand the demographic, hemodynamic and clinical features of adult patients with pulmonary hypertension (PH) in China.METHODS:Between May 2007 and October 2010, a total of 551 adult PH patients were recruited from 31 clinical centers all over China. All fulfilled the traditional hemodynamic criteria diagnosed through right heart catheterization (RHC). The relevant data of demographic, clinical and hemodynamic features of all patients, analyzed the similarities and differences of demographic characteristics between different subtypes. They were divided into 2 groups: WHO functional class I/II and III/IV. And their hemodynamic and clinical features were compared.RESULTS:There were 165 males and 386 females with a mean age of (35 ± 12) years. The mean body mass index (BMI) was (21 ± 4) kg/m(2). There were pulmonary arterial hypertension (PAH, n = 487) and chronic thromboembolic pulmonary hypertension (CTEPH, n = 64). Fatigue (421, 76.4%) and dyspnea (398, 72.2%) were the most common symptoms; Physical examination revealed such a common sign as an accentuated pulmonic second sound (P(2)) in 510 patients (92.6%). Over half (325, 59.0%) of them were of WHO functional class II and 213 (38.6%) patients functional class III. The 6-minute walking distance (6MWD) and Borg dyspnea score were (352 ± 91) m and 3.0 (2.0 - 4.0) respectively. ECG of 497 (90.2%) patients showed right ventricular hypertrophy. Mean right atrial pressure was (9 ± 6) mm Hg (1 mm Hg = 0.133 kPa), pulmonary arterial pressure (67 ± 20) mm Hg, cardiac index (2.7 ± 1.2) Lmin(-1)m(-2) and pulmonary vascular resistance (1496 ± 783) dyn.sec.cm(-5).CONCLUSIONS:Young females with a low BMI are predominantly affected by PH. Severe functional and hemodynamic compromises often appear on presentation. And hemodynamic impairment is correlated with 6MWD and WHO functional class.

Mechanisms of pulmonary hypertension related to ventricular septal defect in congenital heart disease.

BACKGROUND:The aim of this study was to investigate differences in molecular mechanisms of pulmonary hypertension between patients with complete transposition of the great arteries (TGA) combined with ventricular septal defect (VSD) and those with VSD alone.METHODS:Twenty-four consecutive patients with pulmonary hypertension (mean pulmonary artery pressure > 30 mm Hg) underwent surgical correction of TGA + VSD (n = 10) or VSD alone (n = 14). Lung specimens were taken from the right middle lobe before cardiopulmonary bypass (CPB). Extent of pulmonary hypertension was graded according to the Heath-Edwards pathologic classification. Enzyme-linked immunosorbent assay (ELISA) was used to determine expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), endothelin-1 (ET-1), endothelin A and B receptors (ET-AR, ET-BR), matrix metalloproteinases 2 and 9 (MMP-2, MMP-9), and tissue inhibitor of metalloproteinase (TIMP).RESULTS:There were no statistically significant differences in age, height, weight, VSD diameter, or preoperative pulmonary artery pressure between groups. Hemoglobin level, pulmonary artery oxygen saturation, and reduction in postoperative pulmonary artery pressure were significantly higher in patients undergoing correction of TGA + VSD (p < 0.05). All patients had grade 0 to II Heath-Edwards morphologic changes in lung biopsy samples. Expression of eNOS and MMP-2 was significantly lower in the TGA + VSD group than in the VSD-alone group (eNOS, 280.13 ± 101.92 ng/mg versus 488.41 ± 249.60 ng/mg; p < 0.05; MMP-2, 31.68 ± 15.36 ng/mg versus 69.28 ± 49.12 ng/mg; p < 0.05). There were no statistically significant differences between groups in expression of iNOS, ET-1, ET-AR, ET-BR, MMP-9, or TIMP.CONCLUSIONS:In patients with TGA + VSD, high oxygenation in the pulmonary circulation decreases expression of MMP-2 and eNOS, which may affect the progress and reversibility of pulmonary hypertension.

[Analysis on inpatient pulmonary hypertension surveillance in Fuwai Cardiovascular Hospital from 1996 to 2005].

OBJECTIVE:To investigate the inpatient pulmonary hypertension (PH) surveillance in a single center of cardiovascular hospital during last ten years.METHODS:In this retrospective analysis, data from patients with discharge diagnosis as PH from Jan. 1996 to Dec. 2005 were collected.RESULTS:A total of 7085 out of 106 640 patients (6.63%) were documented as PH during the survey period and 3.77% PH was idiopathic, 65.93% PH originated from congenital heart diseases, 22.61% from left heart diseases, 5.66% from thrombotic diseases, 0.89% from respiratory diseases, 0.61% from connective tissue diseases, 0.51% from pulmonary vasculitis and 0.03% from portal hypertensive diseases. Both total inpatient number and patients with PH increased year by year during the last 10 years in our hospital. The number of in-hospital patients with PH was significantly higher in 2004 - 2005 than that in 1996 - 2003 (P < 0.0001) and more PH was originated from cardiomyopathy and valvular heart diseases. Idiopathic pulmonary hypertension also tended to increase and PH due to congenital heart diseases was significantly reduced during 2004 - 2005.CONCLUSION:The data from a single center of cardiovascular hospital shows a tendency for increased in-hospital prevalence of pulmonary hypertension during the last ten years.

[Relationship between myocyte proliferation and cardiac function in adult rats with heart failure].

OBJECTIVE:To confirm whether there is myocytes proliferation in the adult rat with heart failure or not, and to investigate the relationship between myocyte proliferation and heart function.METHODS:Descending anterior branch of left coronary artery was ligated in 20 adult male SD rats so as to establish an heart failure models. Eight rats were used as controls. Hemodynamic parameters, blood pressure (BP), left ventricle end systolic pressure (LVESP), left ventricle end diastolic pressure (LVEDP), +LVdp/dt(max), and -LVdp/dt(max), were measured 30 days after the coronary occlusion. Based on the results of heart function examination, the heart infarct rats were divided into 2 subgroups: cardiac functional compensation subgroup (8 rats), and cardiac functional decompensation subgroup (6 rats). Then the rats were killed and their hearts were taken out and stained with propidium iodide (PI) and antibody to alpha-sarcomeric actin. Immunohistochemistry was used to detect the proliferation cell nuclear antigen (PCNA). Confocal microscopy was used to observe the mitotic image. Light microscopy was used to observe the PCNA positive rate in the myocardium.RESULTS:(1) Mitotic images of myocytes could be identified by confocal microscopy in the left ventricle of all rats. (2) PCNA expression was detected in the nuclei of both infarct and normal hearts. The PCNA positive rate of the cardiac functional compensation subgroup was 7.2% +/- 1.4%, significantly higher than that of the control group (2.2% +/- 0.8%, P = 0.648). However, the PCNA positive rate of the cardiac functional decompensation subgroup was 3.0% +/- 1.3%, not significantly different from that of the control group (P = 0.648). (3) The correlation coefficient between PCNA-positivity of cardiomyocytes and +LVdp/dt(max) in the infarct rats were 0.80 (P < 0.01) and the correlation coefficient between PCNA-positivity of cardiomyocytes and -LVdp/dt(max) was -0.76 (P = 0.01).CONCLUSION:(1) There is myocyte proliferation in the adult rat heart. (2) Myocyte proliferation is positively correlated with heart systolic function, and negatively correlated with heart diastolic function in chronic heart failure.

Changes of the proportion and mortality of pulmonary thromboembolism in hospitalized patients from 1974 to 2005.

BACKGROUND:Pulmonary thromboembolism (PTE) has become a common disease that severely endangers people's health. This study analysed the changes in proportion and mortality of PTE in hospitalized patients to provide data for prevention and management of the disease.METHODS:The data of 763 hospitalized patients with PTE from 1974 to 2005 in Fuwai Hospital were analysed.RESULTS:During the 1970s, 0.27% of patients in a cardiovascular hospital had PTE (< 5 cases per year); while so far this century the proportion is 0.94% (48 to 113 per year). The mortality of hospitalized PTE patients fell from 20.00% in the 1970s to 4.10% this century. Prior to 1990, the mortality of hospitalized PTE patients was 12.50%, and in the years after 1990 only 3.40%. The difference was statistically significant (P < 0.005). People with this disease were mostly between the ages of 30 and 69 years. Men were most susceptible between the ages of 30 and 69 years, while women between the ages of 40 and 69 years. Men contracted PTE 10 years earlier than women. The mortality of male PTE patients was 4.70%, not significantly different from female patients, 5.06% (0.50 < P < 0.75). There were not any significant differences between the mortality of patients in the different age groups overall (< or = 39, 40 - 49, 50 - 59, and > or = 60 years, P > 0.1). More people contracted the disease in winter than in other seasons (P < 0.05). There was no obvious difference between the mortality in different seasons overall (0.75 < P < 0.90).CONCLUSION:PTE is an increasingly significant disease and deserves adequate attention.