Pulmonary Artery Systolic Blood Pressure Research Articles

The role of vitamin D in chronic obstructive pulmonary disease with pulmonary hypertension.

Hypoxia pulmonary hypertension (PH) belongs to the third major category in PH classification. Chronic obstructive pulmonary disease (COPD) is a common cause of hypoxia PH. Low serum vitamin D concentration is considered to be a possible risk factor for chronic lung disease; epidemiological studies have found that vitamin D deficiency increases pulmonary artery pressure. Therefore, this study aimed to explore the role of vitamin D levels in COPD and chronic hypoxic PH. This retrospective study selected three groups of people as research subjects, including: Group N: normal control group (people without any chronic lung disease or PH); Group C: patients with COPD, but without PH; Group C + PH: patients with COPD and PH. Vitamin D levels and pulmonary artery pressure were observed in the three groups. Vitamin D levels of the three groups showed statistical differences in every pairwise comparison; the vitamin D level of Group C (20.27 ng/mL) was lower than Group N (23.48 ng/mL), Group C + PH was the lowest (14.92 ng/mL). The levels of vitamin D in the three groups in this study were generally low. Vitamin D is negatively correlated with pulmonary artery systolic blood pressure. Low vitamin D levels may have a certain relationship with the occurrence and development of COPD. Further reductions in vitamin D levels may influence the development of PH in COPD.

Study of the Relationship between Pulmonary Artery Pressure and Heart Valve Vibration Sound Based on Mock Loop.

The vibration of the heart valves' closure is an important component of the heart sound and contains important information about the mechanical activity of a heart. Stenosis of the distal pulmonary artery can lead to pulmonary hypertension (PH). Therefore, in this paper, the relationship between the vibration sound of heart valves and the pulmonary artery blood pressure was investigated to contribute to the noninvasive detection of PH. In this paper, a lumped parameter circuit platform of pulmonary circulation was first set to guide the establishment of a mock loop of circulation. By adjusting the distal vascular resistance of the pulmonary artery, six different pulmonary arterial pressure states were achieved. In the experiment, pulmonary artery blood pressure, right ventricular blood pressure, and the vibration sound of the pulmonary valve and tricuspid valve were measured synchronously. Features of the time domain and frequency domain of two valves' vibration sound were extracted. By conducting a significance analysis of the inter-group features, it was found that the amplitude, energy and frequency features of vibration sounds changed significantly. Finally, the continuously varied pulmonary arterial blood pressure and valves' vibration sound were obtained by continuously adjusting the resistance of the distal pulmonary artery. A backward propagation neural network and deep learning model were used, respectively, to estimate the features of pulmonary arterial blood pressure, pulmonary artery systolic blood pressure, the maximum rising rate of pulmonary artery blood pressure and the maximum falling rate of pulmonary artery blood pressure by the vibration sound of the pulmonary and tricuspid valves. The results showed that the pulmonary artery pressure parameters can be well estimated by valve vibration sounds.

The impact of pulmonary hypertension on outcomes of transcatheter mitral valve replacement in mitral annular calcification.

To assess the impact of pulmonary hypertension (PH) on outcomes of patients with severe mitral annular calcification (MAC) undergoing transcatheter mitral valve replacement (TMVR). PH is associated with poor outcomes after mitral valve surgery. Whether the presence of PH in patients with MAC undergoing (TMVR) is associated with poor outcomes, is unknown. Retrospective evaluation of 116 patients from 51 centers in 11 countries who underwent TMVR with valve in mitral annular calcification (ViMAC) using balloon-expandable aortic transcatheter valves (THVs) from September 2012 to March 2017. Pulmonary artery systolic blood pressure (PASP) by echocardiogram was available in 90 patients. The subjects were stratified based on PASP: No PH = PASP ≤35 mmHg (n = 11); mild to moderate PH = PASP 36-49 mmHg (n = 21) and severe PH = PASP ≥50 mmHg (n = 58). Clinical, procedural, and echocardiographic outcomes were assessed. Mean age was 72.7 (±12.8) years, 59 (65.6%) were female, Society of Thoracic Surgeons score was 15.8 + 11.8% and 90.0% where in New York Heart Association (NYHA) class III-IV. There was no significant difference in all-cause mortality at 30 days (no PH = 27.3%, mild-moderate PH = 19.0%, severe PH = 31.6%; p = 0.55) or at 1 year (no PH = 54.5%, mild-moderate PH = 38.1%, severe PH = 56.1%; p = 0.36). No difference in adverse events, NYHA class or amount of residual mitral regurgitation at 1 year were observed between the groups. This study suggests that the presence of PH in patients with predominantly mitral stenosis with MAC undergoing TMVR does not impact mortality or adverse events. Further studies are needed to fully understand the effect of PH in this group of patients.

The level of growth differentiation factor 15 as a predictor of left atrial thrombosis in patients with nonvalvular atrial fibrillation.

Aim To study the role of blood concentration of growth differentiation factor 15 (GDF-15) as a predictor of left atrial/left atrial appendage (LA/LAA) thrombosis in patients with nonvalvular atrial fibrillation (AF).Material and methods 538 patients with nonvalvular AF were admitted to the Tyumen Cardiology Research Center in 2019-2020 for radiofrequency ablation and elective cardioversion. According to findings of transesophageal echocardiography (EcoCG), 42 (7.8%) of these patients had LA/LAA thrombosis and 79 (14.7%) of them had the effect of spontaneous echo contrast (SEC). This comparative, cross-sectional, cohort study included at the initial stage 158 successively hospitalized patients with nonvalvular AF: group 1 (with LA/LAA thrombosis, n=42) and group 2 (without LA/LAA thrombosis and without SEC, n=116). To eliminate significant differences in age between the groups, an additional inclusion criterium was introduced, age from 45 to 75 years. Finally, 144 patients were included into the study: group 1 (with LA/LAA thrombosis, n=42, mean age 60.9±7.2 years) and group 2 (without LA/LAA thrombosis and without SEC, n=116, mean age 59.5±6.0 years). 93 (91%) patients in group 1 and 40 (95%) patients in group 2 had arterial hypertension (p=0.4168); 53 (52%) and 29 (^(%), respectively, had ischemic heart disease (p=0.0611). The groups did not differ in sex, profile of major cardiovascular diseases, or frequency and range of oral anticoagulant treatment. General clinical evaluation, EchoCG, and laboratory tests, including measurements of blood concentrations of GDF-15 and NT-proBNP, were performed.Results In the group with LA/LAA thrombosis, 1) persistent AF prevailed whereas paroxysmal AF was more frequently observed in patients without thrombosis; 2) a tendency toward more pronounced chronic heart failure was observed; 3) tendencies toward a high median CHA2DS2‑VASc score and toward a greater proportion of patients with scores ≥3 were observed. According to EchoCG findings, group 1 had higher values of sizes and volumes of both atria and the right ventricle, left ventricular (LV) end-systolic volume and size, pulmonary artery systolic blood pressure, and LV myocardial mass index. LV ejection fraction (EF) was in the normal range in both groups but it was significantly lower for patients with LA/LAA thrombosis, 59.1±5.1 and 64.0±7.3, respectively (p=0.00006). Concentrations of GDF-15 (p=0.00025) and NT-proBNP were significantly higher in group 1 than in group 2 (p=0.000001). After determining the threshold values for both biomarkers using the ROC analysis, two independent predictors of LA/LAA thrombosis were obtained by the stepwise multiple regression analysis: GDF-15 >935.0 pg/ml (OR=4.132, 95 % CI 1.305-13.084) and LV EF (OR=0.859, 95 % CI 0.776-0.951). The ROC analysis assessed the model quality as good: AUC=0.776 (p<0.001), sensitivity 78.3 %, specificity 78.3 %.Conclusion For patients with nonvalvular AF, both increased GDF-15 (>935.0 pg/ml) and LV EF are independent predictors for LA/LAA thrombosis.

Chronic thromboembolic pulmonary hypertension in patients with persistent chest symptoms after acute pulmonary embolism.

This study aimed to analyze the role of chronic thromboembolic pulmonary hypertension (CTEPH) in patients with persistent chest symptoms after acute PE. Patients aged between 18 and 80 years who were followed up for acute PE were screened for chest symptoms which persisted after the anticoagulation treatment. Patients suffering other types of pulmonary hypertension (PH) or metastatic malignancies were excluded in this study. Demographic and functional data of patients included this study were collected. The patients underwent transthoracic echocardiography and ventilation/perfusion (VQ) scans. Also, invasive hemodynamic studies were done to patients with intermediate/high probability of VQ scans. Of the 140 patients screen for this study, 29 patients (Female/Male=16/13) with mean age of 56.1±11.2 years and follow-up time of 35.1±17.7 months met the inclusion criteria. The mean systolic pulmonary artery blood pressure (sPAP) on transthoracic echocardiography was 28.9±4.9 mm Hg (range=20-40 mm Hg). Furthermore, intermediate or high probability of VQ scans was detected in 2 patients, who were subsequently diagnosed with CTEPH (6.9%) via right heart catheterization. CTEPH was diagnosed at a low rate in patients with persistent chest symptoms after the anticoagulation treatment for PE. CTEPH is still an elusive entity, which requires a multidisciplinary and invasive approach.

Tricuspid annular displacement measured by 2-dimensional speckle tracking echocardiography for predicting right ventricular function in pulmonary hypertension: A new approach to evaluating right ventricle dysfunction.

This study aimed to determine the ability of tricuspid annular displacement measured by 2-dimensional speckle tracking echocardiography (STE) to predict right ventricular (RV) dysfunction in pulmonary hypertension (PH) patients. Here, we present a new method for assessing RV function that also employs STE and is based on measurement of tricuspid annular displacement.A total of 225 patients were divided into 2 groups according to the pulmonary artery systolic blood pressure (PASP), estimated by echocardiographic measurement of tricuspid regurgitation: group I (PASP ≥50 mm Hg) and group II (36 mm Hg ≤ PASP <50 mm Hg). The tricuspid annular plane systolic excursion (TAPSE), RV index of myocardial performance (RIMP), RV fractional area change (RVFAC), tissue Doppler-derived tricuspid lateral annular systolic velocity (s'), and the tricuspid annular longitudinal displacement (TMAD) parameters were measured. Thirty patients underwent cardiac magnetic resonance (CMR) examination, and right ventricular ejection fraction (RVEF) was calculated.The conventional parameters as well as the TMAD parameters differed significantly between the 2 groups (all P < .01). Good correlation was observed between the TMAD parameters and CMR-derived RVEF (all P < .01). The TMAD parameters had moderate predictive value for predicting RV dysfunction in PH patients (all P < .01). From receiver operating characteristic curves, we determined the optimal cut-off values for TMAD parameters for detecting RV dysfunction with good sensitivity and specificity.The TMAD parameters can predict the decline of RV function in patients with PH and thus provide new diagnostic indices for clinical management of these patients.

Management of a Pregnant Woman with Idiopathic Interstitial Pneumonia Accompanied by Secondary Pulmonary Hypertension: Case Report and Literature Review

Idiopathic interstitial pneumonias (IIPs) typically occur in the fifth and sixth decades, and thus are uncommon in the child-bearing age group. We herein report an extremely rare case of a pregnant woman with IIP accompanied by secondary pulmonary hypertension that had a successful cesarean delivery. A 36-year-old primigravida woman was referred to our Obstetrics department at 6 weeks of gestation. Seven years ago, she had a dry cough and moderate dyspnea, and was diagnosed with non-specific interstitial pneumonia (NSIP), a subtype of IIP. At 11 weeks of gestation, spirometry showed a vital capacity of 1.89 L (60% of predicted). An arterial blood gas analysis showed PaO2 of 77.2 mmHg and oxygen saturation of 95% in breathing room air at rest. An echocardiogram revealed mild pulmonary hypertension; systolic pulmonary artery blood pressure (PABP) of 44 mmHg. Fetal growth and amniotic fluid volume were normal. Our management plan was to maintain oxygen saturation at more than 95% of oxygen saturation and systolic PABP at less than 50 mmHg. Oxygen therapy was initiated at 13 weeks of gestation because of dyspnea at rest. At 28 weeks of gestation, an echocardiogram showed severe pulmonary hypertension with systolic PABP of 64 mmHg. Therefore, we performed cesarean section at 30 weeks of gestation. The newborn was a male weighing 1.452 g with Apgar scores of 6 and 7 at 1 min and 5 min, respectively. Although the patient’s post-operative course was uneventful, she was discharged on a regimen of oxygen therapy. The effects of pregnancy on IIPs remain unclear because of its extreme rarity. In the management of pregnant women with IIPs accompanied by secondary pulmonary hypertension, the maintenance of systolic PABP of less than 50 mmHg on an echocardiogram may be effective.

Features of intracardiac hemodynamics disoders in patients with chronic obstructive pulmonary disease complicated by the chronic pulmonary heart disease development and methods for their medical correction

Chronic pulmonary heart disease is a common pathology and has become one of the leading causes of disability and death in recent years [15]. According to the literature, two-thirds of patients with chronic obstructive pulmonary disease die during the period from 15 months to 5 years after the circulatory decompensation onset, which occupies the third place after hypertension and coronary heart disease among causes of death in the age group older than 50 years [14]. Pulmonary hypertension is considered to be the main pathogenetic mechanism of chronic pulmonary heart disease [11]. The mortality rate in patients with chronic pulmonary heart disease is directly related to the level of pulmonary artery systolic blood pressure. Thus, according to literature data, at the pulmonary artery systolic pressure from 30 to 50 mm Hg 4-5-year survival rate is 30%, and at the level of more than 50 mm Hg 5-year survival rate is zero [1]. Thus, pulmonary hypertension is a poor prognostic factor. Furthermore, it is known that the changes identified in the right ventricle amid the pulmonary hypertension are survival predictors in patients with chronic obstructive pulmonary disease [18]. Literature review showed that the hemodynamics feature in patients with chronic pulmonary heart disease is increased pressure in the pulmonary artery, which leads to both ventricles remodeling and in particular to the right heart enlargement, rise of both right and left ventricles diastolic dysfunction, reduced stroke volume and cardiac output. Furthermore, the review describes that such drug classes as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, calcium channel blockers and selective β-blockers are successfully used for the revealed disorders correction in patients with chronic pulmonary heart disease.

The role of heart rate in the left ventricular twist response to increased arterial blood pressure: a 'stiff' challenge?

The role of heart rate in the left ventricular twist response to increased arterial blood pressure: a 'stiff' challenge?

Abstract 11446: Systemic Administration of Mitochondria Alleviates 100% Oxygen-Induced Acute Respiratory Distress Syndrome in Rats

Background: We tested the hypothesis that mitochondria-replacement therapy ameliorated 100% oxygen-induced rat acute respiratory distress syndrome (ARDS). Methods and Results: Adult-Male SD rats (n=24) were equally categorized into group 1 (controls, room air inhalation), group 2 (ARDS: induced by inhalation of 100% oxygen for 48 hrs), and group 3 [ARDS + mitochondrial transfusion (1400 μg/each rat) from intra-venous administration 6 h after ARDS induction]. By 72 h after ARDS induction, the oxygen saturation (O 2 -Sat) was significantly lower in group 3 and more significantly lower in group 2 than in group 1, whereas pulmonary artery systolic-blood pressure showed a reversed pattern of O 2 -Sat among three groups (all p&lt;0.001). H&amp;E stain for lung crowded score showed an identical pattern of O 2 -Sat and number of alveolar sacs and lung weight exhibited an opposite pattern of O 2 -Sat among the three groups. The protein expressions of apoptotic (mitochondrial Bax, cleaved caspase 3 &amp; PARP), fibrotic (Smad5, TGF-β), ROS (NOX-1, NOX-2, NOX-4), oxidative stress (oxidized protein), DNA- &amp; mitochondrial-damaged (γ-H2AX, Ki-67; cytosolic cytochrome-c) and inflammatory (TNF-α, MMP-9, NF-κB) biomarkers, and IHC/IF microscopic findings of inflammatory (CD14+, CD68+), DNA-damaged (γ-H2AX+, Ki-67+) cells exhibited an opposite pattern, whereas the protein expressions of anti-apoptotic (Smad1/3, BMP-2) markers exhibited an identical pattern of O 2 -Sat among three groups (all p&lt;0.001). The anti-oxidant (HO-2, NQO-1), mitochondrial-preserved (mitochondrial cytochrome-c) biomarkers, and cellular levels of anti-oxidants (HO-1, NQO-1, GR, GPx) were significantly higher in group 2 and more significantly higher in group 3 than in group 1 (all p&lt;0.0001). Conclusions: Mitochondria therapy protects against 100% oxygen-induced ARDS. Key words: mitochondrial replacement, acute lung injury, inflammation, oxidative stress, DNA and mitochondrial damage

Clinical manifestations of hepatopulmonary syndrome

Objective: Hepatopulmonary syndrome (HPS) occurs in one third of patients with decompensated cirrhosis and is defined by perturbed gas exchanges, arterial hypoxemia, and vasodilatation in the lungs, in the absence of primary cardiopulmonary disease. Respiratory symptoms are severe when Pa O2 levels are <60 mm Hg: centrally-induced cyanosis, dyspnea, hippocratic fingers, platypnea, and orthodeoxia. Portopulmonary hypertension (PPH) occurs in 2% of cirrhotic patients and it is suspected in hypoxemic patients presenting no pulmonary vasodilatation. It is clinically manifested by stress dyspnea, orthopnea, thoracic pain, fatigue, and dizziness. Systolic blood pressure in pulmonary artery is over 25 mm Hg and pulmonary capillary blood pressure is blocked below 15 mm Hg. Methods: A five-year (2008–2012) retrospective evaluation of pulmonary pathology occurring with hepatic cirrhosis showed 50 patients presenting dyspnea, a symptom suggesting pulmonary involvement. Echocardiography monitored the following parameters: pulmonary artery acceleration time, measured in the parsternal window; pulmonary artery systolic blood pressure was measured by means of tricuspid regurgitation method and right-atrium blood pressure was evaluated according to inferior vena cava collapse with inspiration. Results: The 50 patients in the study group presented dyspnea as a symptom suggestive of pulmonary involvement. Platypnea and orthodeoxia were present in 12% of the cases. In 88% of the cases, dyspnea did not display particular characteristics; it became stronger under stress conditions and in dorsal decubitus position, according to the pathology associated with hepatic cirrhosis. Patients’ average age was 52. There was no constant correlation between hepatic dysfunction biochemical markers and degree of dyspnea. Severe hypoxemia (SaO2 < 80%) was present in 12% of the cases. Pulmonary artery systolic blood pressure was higher in patients with portal hypertension, with measurements exceeding 35 mm Hg in 60% of the cases. Right-atrium blood pressure, evaluated according to IVC collapse with inspiration, was high (11 ± 4 mm Hg) in 62% of the cases and normal (5 mm Hg) in 36%. We considered that pulmonary hypertension associated with portal hypertension in the study group was caused by hyperdynamic status and it was not portopulmonary hypertension proper. Conclusions: Hepatopulmonary syndrome should be used among the diagnostic variants for a patient with hepatic involvement and/or portal hypertension, in whom significant hypoxemia is observed, which has no restrictive basis and is not justified by any co-occurring cardiopulmonary condition. Platypnea and orthodeoxia in a hepatic condition developing with portal hypertension increase the possibility of HPS suspicion. The only definitive and efficient treatment in hepatopulmonary syndrome is liver transplantation.

THE СLINICAL IMPACT OF PULMONARY ARTERY DISTENSIBILITY INDEX IN PATIENTS WITH PULMONARY HYPERTENSION

Objective.Vascular remodeling in patients with pulmonary artery hypertension (PAH) may be assessed by measurement of contrast magnetic-resonance imaging (CMRI) derived pulmonary artery distensibility (PAD) index. The objective of our study was to investigate whether PAD index could be used as a marker for the evaluation of PAH severity.Design and methods.Forty four patients with PAH (mean age — 42,8 ± 14,5 years, males:females = 11:33) were enrolled: 29 patients with idiopathic pulmonary arterial hypertension, 4 subjects with corrected congenital heart disease, 3 subjects with scleroderma PAH and 8 patients with inoperable chronic thromboembolic pulmonary hypertension. All patients underwent 6-minute walk test, right heart catheterization (RHC), heart ultrasound (ECHO), CMRI, cardiopulmonary exercise testing, and serum N-terminal-pro-brain natriuretic peptide (NT-proBNP) level was defined.Results.PAD index was decreased in PAH patients 11,9 % (9,3-19,7). Patients with decreased PAD index &lt; 20 % had higher NT-proBNP level, lower tricuspid annular systolic velocity and right ventricle/left ventricle ratio by ECHO. Patients with PAD index &lt; 20 % had higher pulmonary artery systolic blood pressure (96,5 ± 22,4 versus 77,9 ± 19,4 mmHg; p &lt; 0,05), and reduced cardiac output which were determined by RHC (3,98 ± 1,1 versus 4,95 ± 1,21 l/min; p &lt; 0,05). Decreased VO2peak was found in patients with PAD index &lt; 20 % (14,8 versus 18,8 ml/min/kg; p = 0,05).Conclusions.PA distensibility index may be used for noninvasive assessment of PAH severity and progression.

Pregnancy outcome in women with pulmonary arterial hypertension: single-center experience from India

A retrospective analysis of the records of all the patients of pulmonary arterial hypertension with pregnancy at AIIMS, New Delhi, India, to study maternal and perinatal outcome and to compare outcome between severe and mild pulmonary arterial hypertension. A retrospective analysis was carried out of 30 pregnancies in women with pulmonary arterial hypertension (PAH) who delivered at ≥ 28 weeks of gestation from July 2006 through July 2012 at a tertiary care center in India. Pulmonary artery blood pressure (PABP) during the first trimester of pregnancy or before pregnancy was considered to define PABP as severe or mild, with severe cases having systolic PABP >50 mmHg on echocardiography. Out of 30 patients, 14 patients had severe PAH and 16 patients had mild PAH. Women with severe PAH had a significantly higher incidence of preterm delivery (11 vs. 3, P < 0.05), small for gestational age infants (10 vs. 2, P < 0.05) and cardiac complications (6 vs. 1, P < 0.05) compared to women with mild PAH. There was maternal mortality in a patient with Eisenmenger syndrome. In women with severe PAH and mild PAH, PABP increased in later pregnancy from 63.14 ± 7.6 to 71.57 ± 7.9 mmHg (P < 0.05) and from 40.37 ± 3.6 to 41.69 ± 4.1 mmHg (P < 0.05), respectively. Pregnancy in women with severe PAH is associated with higher maternal morbidity and adverse fetal outcome compared to pregnancy in women with mild PAH.

Maternal Outcome in Pregnancy Complicated With Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH), including Eisenmenger syndrome, has a risk of mortality in pregnancy of 10-40%. The aim of this study was to investigate whether pulmonary artery blood pressure (PABP) is a prognostic factor for pregnancy outcome in patients with PAH. The subjects were 42 patients with PAH during pregnancy. Severe and mild cases were defined by PABP before and during the first 14 weeks of pregnancy, with severe cases having mean PABP >40 mmHg by catheterization or systolic PABP >50 mmHg on echocardiography. Eighteen women chose termination of pregnancy before 14 weeks, leaving 24 women (10 mild, 14 severe) for analysis. The women with severe PAH delivered earlier (35.4 vs. 31.5 weeks, P<0.05) and had higher rates of small-for-gestational-age infants (0/10 vs. 7/14, P<0.01). Among the women with severe PAH, the New York Heart Association class dropped by 1 in 9 cases, by 2 in 3 cases, and remained the same in 2 cases as pregnancy progressed, whereas among the women with mild PAH, the class dropped by 1 in 1 case and 9 women remained in the same class. Among the severe cases, 1 woman died and there was 1 fetal death; PABP markedly increased in later pregnancy from 54 to 74 mmHg (catheter measurement) and from 78 to 93 mmHg (echocardiography) (P<0.05). The level of PABP before or in the early stage of pregnancy is an important predictor of pregnancy outcome.

The Clinical Outcome of Pulmonary Thromboendarterectomy for the Treatment of Chronic Pulmonary Thromboembolism

Background: Diagnosing chronic pulmonary embolism at an early stage is difficult because of the patient’s nonspecific symptoms. This condition is not prevalent in Korea, and in fact, there have been only a few case reports on this in the Korean medical literature. We analyzed the surgical outcome of performing pulmonary thromboendarterectomy in patients with chronic pulmonary embolism. Material and Method: The study subjects included those patients who underwent surgery for chronic pulmonary embolism from 1996 to 2008. For making the diagnosis, echocardiography, chest CT and a pulmonary perfusion scan were performed on the patients who complained of chronic dyspnea. Result: Pulmonary endarterectomy was performed as follows: by incision via a mid-sternal approach (7 patients); by incision via a left posterolateral approach (1 patient); using the deep hypothermic circulatory arrest technique (4 patients); under ventricular fibrillation (3 patients); and under cardioplegic arrest (1 patient). The postoperative systolic pulmonary artery blood pressure significantly decreased from a preoperative value of 78.9±14.5 ㎜Hg to 45.6±17.6 ㎜Hg postoperatively (p=0.000). The degree of tricuspid regurgitation was less than grade Ⅱ after surgery. Two patients died early on, including one patient who had persistent pulmonary hypertension without improvement and right heart failure. Conclusion: Patients who have chronic pulmonary embolism are known to have a poor prognosis. However, we think that early surgical treatment along with making the proper diagnosis before the aggravation of right heart failure can help improve the quality of a patient’s life.

Echocardiographic findings in patients with sickle cell disease

Pulmonary hypertension is a complication of sickle cell disease that is associated with increased mortality. Whether this complication is associated with hemolysis has been questioned. Systolic pulmonary artery blood pressure can be estimated from echocardiography-determined tricuspid regurgitation velocity (TRV). A velocity of 2.5 m/s or higher suggests possible pulmonary hypertension. A retrospective review of hospital records from adult patients with sickle cell disease undergoing echocardiography in 2006 and 2007 was performed at a tertiary level hospital. Echocardiographic, demographic, and clinical laboratory data were collected. Echocardiographic results were available for 105 adult sickle cell patients. Of these, 62 (59%) had a TRV ≥2.5 m/s and 24 (22.8%) had a TRV ≥3.0 m/s. Mitral valve regurgitation was observed in 44% and left ventricular abnormalities (defined by either hypertrophy or dilation) in 28% of cases. Elevated TRV had independent and significant associations with greater age, higher serum lactate dehydrogenase (LDH) concentration, and lower hemoglobin concentration. We confirmed that elevated TRV is common among hospital-based adults with sickle cell disease. Significant, independent associations were found with both elevated LDH concentration and degree of anemia, suggesting that hemolytic and other mechanisms contribute to pulmonary hypertension in patients with sickle cell disease.

Pulmonary Artery Pressure Changes during Ethanol Embolization Procedures to Treat Vascular Malformations: Can Cardiovascular Collapse be Predicted?

Ethanol has been used for embolization of vascular malformations. Cardiovascular collapse, although rare, has been reported, occurring immediately to a few hours after ethanol embolization. The pathophysiology has been theoretically attributed to direct toxicity to the cardiac conduction system or pulmonary artery (PA) vasospasm leading to cardiovascular collapse. Because of cardiovascular collapse in one patient at the authors' institution, it was standard of care at the time of this study to monitor the pulmonary artery pressures during ethanol embolization. This study was conducted to clarify the effect of ethanol on the PA pressure during these procedures. Data from 92 ethanol embolization procedures performed on 56 patients with vascular malformations between May 2001 and May 2003 are reported. PA and noninvasive cuff systemic pressures were recorded before and after each injection and also before and after the entire procedure. Upper limit for volume of ethanol used during these procedures was drawn at 1 mL/kg. Simple and multiple linear regression analyses were done to study factors affecting changes in PA and systemic blood pressure. For each injection, ethanol volume averaged 3.1 mL per injection. The systolic systemic and PA systolic pressures increased by 2.3 and 1.0 mm Hg, respectively. Amount of ethanol injected and systemic blood pressure changes were predictive of change in PA blood pressure. During the entire procedure, systemic systolic blood pressure increased by an average of 11.6 mm Hg, and PA systolic blood pressure by 5 mm Hg. Change in systemic blood pressure was a strong predictor of, and volume of ethanol was a weak predictor of, change in PA blood pressure. The mild rise in PA blood pressure in the patients during ethanol embolization correlated strongly with minor elevation in systemic blood pressure throughout the procedure, which the authors believe is related to pain from the ethanol injection causing sympathetic stimulation, even when patients are under general anesthesia. The minimal rise in PA blood pressure during these procedures does not elucidate the cause of the rare complication of cardiovascular collapse during ethanol embolization.

Left ventricular dysfunction, pulmonary hypertension, obesity, and sleep apnea.

The purpose of this study was to determine the frequency of central and obstructive sleep apnea in adult patients who have echocardiographic evidence of left ventricular dysfunction and pulmonary hypertension. Subjects with left ventricular dysfunction, pulmonary hypertension (pulmonary artery systolic pressure >30 mm Hg) and no lung disease were evaluated for risk factors associated with pulmonary hypertension. Of eight eligible adults, six completed the study. Subjects were from suburban and inner city family practices. Spirometric assessment, pulse oximetry on room air, rheumatologic evaluation, polysomnography, and additional history were taken. All six subjects had sleep apnea (apnea-plus-hypopnea index, or AHI, > or = 20): obstructive, central, or mixed. All were obese, and almost all the subjects had a restrictive pattern on spirometry, which is consistent with obesity. All had a pulmonary artery systolic blood pressure of 35 mm Hg or greater. None had daytime hypoxemia or collagen vascular disease, and none had ever used appetite suppressants. This study found a strong association between pulmonary hypertension and obstructive or central sleep apnea in obese patients with congestive heart failure (CHF). We propose that a pulmonary artery systolic pressure of 35 mm Hg or greater in ambulatory patients with CHF may signify an increased risk of sleep apnea.

Pleural effusion as a cause of right ventricular diastolic collapse.

We hypothesized, after seeing several suggestive clinical examples, that a process leading to a large bilateral pleural effusion in the presence of an otherwise insignificant pericardial effusion could result in right ventricular diastolic collapse (RVDC) as seen by two-dimensional echocardiography. This noninvasive marker for hemodynamically significant cardiac tamponade occurs when pericardial fluid is under pressure. Therefore, RVDC resulting from a large pleural effusion would represent a false-positive indication of cardiac tamponade caused by excessive pericardial fluid. Seven spontaneously breathing dogs were chronically instrumented to measure ascending aortic, right atrial, intrapericardial, intrapleural, left atrial, and pulmonary artery pressures and cardiac output. Intravascular volume was adjusted before each experiment to the euvolemic range with saline solution. The onset of RVDC was observed in each animal by two-dimensional echocardiography during seven paired episodes of tamponade induced by infusions of warm saline into the pericardial space alone and, after drainage of the pericardial fluid and complete recovery, into the pleural space in the presence of a small pericardial effusion. The onset of RVDC occurred at the same intrapericardial (8.17 versus 9.47 mm Hg) and right atrial (7.41 versus 7.46 mm Hg) blood pressures regardless of whether it was produced by an intrapericardial or an intrapleural effusion but began in expiration during the former and in inspiration during the latter. Intrapericardial pressure increased in the same manner as intrapleural pressure during intrapleural saline infusion. Nevertheless, cardiac output and aortic blood pressure were better preserved, and at the onset of RVDC, the pulmonary artery systolic blood pressure was higher (p less than 0.0001) and the degree of pulsus paradoxus lower (p less than 0.01) with intrapleural infusion. These results indicate that a large bilateral pleural effusion can elevate intrapericardial pressure sufficiently to cause RVDC and, perhaps, lead to misdirected therapy of an otherwise insignificant pericardial effusion.