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Systolic Pressure (systolic + pressure)
Kinds of Systolic Pressure Selected AbstractsEffects of Formaldehyde on Cardiovascular System in In Situ Rat HeartsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2009Daisuke Takeshita After 20,30 min. of intravenous infusion of 3.7% formaldehyde solution (FA) at 10 ,l (3.7 mg)/kg/min, normal and hypertrophic hearts showed significant decreases in left ventricle end-systolic pressure (ESP), heart rate and cardiac output per minute, indicating an acute pumping failure. Hypertrophic hearts showed significantly smaller ESP, stroke volumes and cardiac output than those in normal hearts. Systolic pressure,volume area at midrange left ventricular volume (PVAmLVV: a mechanical work capability index) was significantly smaller than that in normal hearts and per cent of mean PVAmLVVversus pre-infusion mean value in hypertrophic hearts was significantly decreased compared to normal hearts 30 min. after FA infusion. The marked decrease in pH, base excess and no changes in PaO2 and PaCO2 suggest metabolic acidosis. The correction of metabolic acidosis with 9% NaHCO3 did not influence on the acute pumping failure, indicating that metabolic acidosis did not cause it. Ultrastructural observations revealed marked dilation of the sarcoplasmic reticulum with intact sarcolemmal membranes and no disintegration of muscle myofibrils. Ryanodine receptors and calcium (Ca2+) pumps (SERCA2A) located in the sarcoplasmic reticulum have major roles in the cytosolic Ca2+ handling. Taken together, acute pumping failure by FA may derive from the impairment of Ca2+ handling in the cardiac excitation,contraction coupling. [source] Evaluation of Right Ventricular Fibrosis in Adult Congenital Heart Disease Using Gadolinium-enhanced Magnetic Resonance Imaging: Initial Experience in Patients with Right Ventricular Loading ConditionsCONGENITAL HEART DISEASE, Issue 5 2006Lopa P. Hartke MD ABSTRACT Objective., Gadolinium-enhanced cardiac magnetic resonance imaging has been used to show myocardial fibrosis, a finding that appears as late gadolinium enhancement. Its role in the evaluation of right ventricular fibrosis in congenital heart disease is unclear. The purpose of this study was to demonstrate late gadolinium enhancement of the right ventricle in adult and adolescent congenital heart disease and to investigate the relationship between this enhancement and clinical and pathophysiological data. Design., In total, 24 patients, 16 patients with congenital heart disease and right ventricular loading conditions and 8 controls, underwent gadolinium-enhanced viability imaging. Diagnoses varied and included repaired, palliated, and unrepaired lesions. The presence and extent of right ventricular late gadolinium enhancement was compared with patient clinical and hemodynamic data. Exact Wilcoxon tests, Fisher's exact tests, and Spearman's rank correlation were used to compare variables. Results., Nine of 16 patients (56%) were found to have right ventricular late gadolinium enhancement, ranging from 5% to 80% of right ventricular myocardium affected (mean 36.1%, SD 29.7). The combination of right ventricular systolic pressure ,98 mm Hg and systemic oxygen saturation ,93% strongly suggested the presence of right ventricular late gadolinium enhancement (positive predictive value 100%), but no single variable or combination of variables could reliably predict its absence (negative predictive values ,75%). Extent of right ventricular late gadolinium enhancement did not correlate with degree of either hypoxia or right ventricular hypertension. Conclusions., Gadolinium-enhanced cardiac magnetic resonance demonstrates right ventricular late gadolinium enhancement in some patients with congenital heart disease and right ventricular loading conditions. Clinical variables were associated with the presence of fibrosis but did not reliably predict severity. Myocardial preservation is likely a multifactorial process that may affect the right and left ventricles differently. [source] Glutathione deficiency intensifies ischaemia-reperfusion induced cardiac dysfunction and oxidative stressACTA PHYSIOLOGICA, Issue 1 2001S. Leichtweis The efficacy of glutathione (GSH) in protecting ischaemia-reperfusion (I-R) induced cardiac dysfunction and myocardial oxidative stress was studied in open-chest, stunned rat heart model. Female Sprague,Dawley rats were randomly divided into three experimental groups: (1) GSH-depletion, by injection of buthionine sulphoxamine (BSO, 4 mmol kg,1, i.p.) 24 h prior to I-R, (2) BSO injection (4 mmol kg,1, i.p.) in conjunction with acivicin (AT125, 0.05 mmol kg,1, i.v.) infusion 1 h prior to I-R, and (3) control (C), receiving saline treatment. Each group was further divided into I-R, with surgical occlusion of the main left coronary artery (LCA) for 30 min followed by 20 min reperfusion, and sham. Myocardial GSH content and GSH : glutathione disulphide (GSSG) ratio were decreased by ,50% (P < 0.01) in both BSO and BSO + AT125 vs. C. Ischaemia-reperfusion suppressed GSH in both left and right ventricles of C (P < 0.01) and left ventricles of BSO and BSO + AT125 (P < 0.05). Contractility (+dP/dt and ,dP/dt) in C heart decreased 55% (P < 0.01) after I and recovered 90% after I-R, whereas ±dP/dt in BSO decreased 57% (P < 0.01) with ischaemia and recovered 76 and 84% (P < 0.05), respectively, after I-R. For BSO + AT125, ±dP/dt were 64 and 76% (P < 0.01) lower after ischaemia, and recovered only 67 and 61% (P < 0.01) after I-R. Left ventricular systolic pressure in C, BSO and BSO + AT125 reached 95 (P > 0.05) 87 and 82% (P < 0.05) of their respective sham values after I-R. Rate-pressure double product was 11% (P > 0.05) and 25% (P < 0.05) lower in BSO and BSO + AT125, compared with Saline, respectively. BSO and BSO + AT125 rats demonstrated significantly lower liver GSH and heart Mn superoxide dismutase activity than C rats after I-R. These data indicate that GSH depletion by inhibition of its synthesis and transport can exacerbate cardiac dysfunction inflicted by in vivo I-R. Part of the aetiology may involve impaired myocardial antioxidant defenses and whole-body GSH homeostasis. [source] Association of Coronary Sinus Diameter with Pulmonary HypertensionECHOCARDIOGRAPHY, Issue 9 2008Yilmaz Gunes M.D. Background: Impaired venous drainage secondary to increased right atrial pressure (RAP) may result in coronary sinus (CS) dilatation.,Methods: Two hundred fifteen patients referred for transthoracic echocardiography were included in the study. CS diameters were measured from apical four-chamber view with the transducer being slightly tilted posteriorly to the level of the dorsum of the heart. Pulmonary artery systolic pressure (PASP) is estimated by measurement of tricuspid regurgitation velocity (v) and estimate RAP based on size and collapsibility of inferior vena cava (VCI) with the formula PASP: 4v2+RAP. Patients with PASP >35 mmHg were considered to have pulmonary hypertension (PH).,Results: CS diameter was measured in 80.3% of the patients with normal PASP (8.1 ± 2.4 mm) and 93.1% of the patients having PH (12.3 ± 2.5 mm). PASP was significantly correlated with CS diameter (r = 0.647, P < 0.001), RA volume index (r = 0.631, P < 0.001), RV volume index (r = 0.475, P < 0.001), VCI diameter (r = 0.365, P < 0.001), and left ventricular ejection fraction (LVEF) (r =,0.270, P < 0.001). CS diameter was also correlated significantly with estimated RAP (r = 0.557, P < 0.001), RA volume index (r = 0.520, P < 0.001), RV volume index (r = 0.386, P < 0.001), LVEF (r =,0.327, P < 0.001), and VCI diameter (r = 0.313, P < 0.001). Multivariate analyses, testing for independent predictive information of CS size, VCI diameter, RA and RV volume indexes, and estimated RAP for the presence of PH revealed that estimated RAP (beta = 0.465, P < 0.001) and CS size (beta = 0.402, P = 0.003) were the significant predictors.,Conclusions: Coronary sinus is dilated in patients with pulmonary hypertension. Coronary sinus diameter significantly correlates with PASP, RAP, right heart chamber volumes, LVEF, and VCI diameter. [source] Incorporation of Pulmonary Vascular Resistance Measurement into Standard Echocardiography: Implications for Assessment of Pulmonary HypertensionECHOCARDIOGRAPHY, Issue 10 2007Kimberly B. Ulett B.S Doppler estimation of pulmonary artery systolic pressure (PASP) from tricuspid regurgitation velocity is a simple approach to the detection of pulmonary hypertension but may be influenced by right ventricular stroke volume. We sought the clinical utility of incorporating Doppler calculation of pulmonary vascular resistance (PVR) into determination of pulmonary hypertension in 578 consecutive patients with tricuspid regurgitation. Right atrial pressure was estimated from vena caval dimensions and collapsibility. Pulmonary hypertension was classified on the basis of a) PASP >35mmHg, b) age-/gender normalized PASP, c) PVR >2 Wood units. The mean PASP was 40 ± 13 mmHg and PVR was 1.9 ± 0.8 Wood units. Standard PASP identified pulmonary hypertension in 58%, compared with 36% by age-/gender normalized PASP (P < 0.0001), and 31% by PVR (P < 0.0001). Of patients who had pulmonary hypertension by PASP, 33% were reclassified as normal on the basis of PVR and 6% were reclassified from normal to pulmonary hypertension. PVR is easy to incorporate into a standard echo exam, and identifies a small group with normal PASP as having PAH, and a larger group of apparently increased PASP as normal. [source] Right Heart Function and Scleroderma: Insights from Tricuspid Annular Plane Systolic ExcursionECHOCARDIOGRAPHY, Issue 2 2007Chiu-Yen Lee M.D. Objective: The purpose of this study was to evaluate the use of echocardiographic parameters as predictors of rehospitalization in scleroderma patients. Methods: Echocardiographic studies were conducted in 38 patients with systolic scleroderma (SSc) to assess cardiopulmonary function. Forty-five age-matched volunteers without any sign of heart failure served as the control group. Transmitral flow pattern, tricuspid annular plane systolic excursion (TAPSE), left ventricular ejection fraction (LVEF), and right ventricular ejection fraction (RVEF) were evaluated. All patients were subsequently followed for one year. Results: Peak transmitral early-diastolic velocity (mitral E) and TAPSE measurements were significantly different between SSc and control patients (mitral E: 74.1 ± 16.3 vs. 83.5 ± 17.0 cm/s with P = 0.012; TAPSE: 2.4 ± 0.43 vs. 1.9 ± 0.39 cm with P < 0.0001). LVEF was similar, but RVEF was lower in the SSc group (LVEF: 61.7 ± 9.7 vs. 61.7 ± 5.8% with P = 0.962; RVEF: 49.6 ± 6.8 vs. 39.2 ± 6.7% with P < 0.0001). A strong correlation was found between TAPSE and RVEF. A TAPSE less than 1.96 cm indicted a RVEF less than 40% with a sensitivity of 81% and specificity of 78%. Contrary to expectation, pulmonary artery systolic pressure (PASP) did not correlate well with RV function (r = 0.261, r2= 0.068, P = 0.016). Finally, the frequency of rehospitalization was inversely correlated with RVEF and TAPSE in SSc patients. Conclusions: We can predict the rehospitalization rate of SSc patients by TAPSE and RVEF, suggesting the involvement of heart, skin, lung, and other organs in scleroderma patients. [source] Correlation between Right Ventricular Indices and Clinical Improvement in Epoprostenol Treated Pulmonary Hypertension PatientsECHOCARDIOGRAPHY, Issue 5 2005Jayant Nath M.D. The aim of this study was to evaluate which parameter of right ventricular (RV) echocardiographic best mirrors the clinical status of patients with pulmonary arterial hypertension. Patients with pulmonary arterial hypertension on epoprostenol therapy were identified via hospital registry. Twenty patients, (16 females, 4 males) were included in the study, 9 with primary pulmonary hypertension and 11 with other diseases. Echocardiograms before therapy and at 22.7 (±9.3) months into therapy were compared. The right ventricular myocardial performance index (RVMPI) was measured as the sum of the isometric contraction time and the isometric relaxation time divided by right ventricular ejection time. Other measures included peak tricuspid regurgitation jet velocity (TRV), pulmonary artery systolic pressure (PASP), pulmonary valve velocity time integral (PVVTI), PASP/PVVTI (as an index of total pulmonary resistance) and symptoms by New York Heart Association (NYHA) functional class. Echo parameters of right ventricular function were analyzed in patients, before and during therapy. There was significant improvement of NYHA class in patients following epoprostenol therapy (P < 0.0001). Peak tricuspid regurgitant jet velocity (pre 4.2 ± 0.6 m/sec, post 3.8 ± 0.7 m/sec, P = 0.02) and PASP/PVVTI (pre 6.7 ± 3.3 mmHg/m per second, post 4.8 ± 2.2 mmHg/m per second, P < 0.0001) were significantly improved during treatment. RVMPI did not improve (pre 0.6 ± 0.3, post 0.6 ± 0.3, P = 0.54). Changes in NYHA class did not correlate with changes in RVMPI (P = 0.33) or changes in PASP/PVVTI (P = 0.58). Despite significant improvements in TRV, PASP/PVVTI, and NYHA class, there was no significant change in RVMPI on epoprostenol therapy. Changes in right ventricular indices were not correlated with changes in NYHA class. [source] Impact of Body Mass Index on Markers of Left Ventricular Thickness and Mass Calculation: Results of a Pilot AnalysisECHOCARDIOGRAPHY, Issue 3 2005Ranjini Krishnan M.D. Specific correlations between body mass index (BMI) and left ventricular (LV) thickness have been conflicting. Accordingly, we investigated if a particular correlation exists between BMI and echocardiographic markers of ventricular function. Methods: A total of 122 patients, referred for routine transthoracic echocardiography, were included in this prospective pilot study using a 3:1 randomization approach. Patient demographics were obtained using a questionnaire. Results: Group I consisted of 80 obese (BMI was >30 kg/m2), Group II of 16 overweight (BMI between 26 and 29 kg/m2), and Group III of 26 normal BMI (BMI < 25 kg/m2) individuals. No difference was found in left ventricular wall thickness, LV end-systolic cavity dimension, fractional shortening (FS), or pulmonary artery systolic pressure (PASP) among the groups. However, mean LV end-diastolic cavity dimension was greater in Group I (5.0 ± 0.9 cm) than Group II (4.6 ± 0.8 cm) or Group III (4.4 ± 0.9 cm; P < 0.006). LV mass indexed to height2.7 was also significantly larger in Group I (61 ± 21) when compared to Group III (48 ± 19; P < 0.001). Finally, left atrial diameter (4.3 ± 0.7 cm) was also larger (3.8 ± 0.6 and 3.6 ± 0.7, respectively; P < 0.00001).Discussion: We found no correlation between BMI and LV wall thickness, FS, or PASP despite the high prevalence of diabetes and hypertension in obese individuals. However, obese individuals had an increased LV end-diastolic cavity dimension, LV mass/height2.7, and left atrial diameter. These findings could represent early markers in the sequence of cardiac events occurring with obesity. A larger prospective study is needed to further define the sequence of cardiac abnormalities occurring with increasing BMI. [source] Endothelin receptors blockade blunts hypoxia-induced increase in PAP in humansEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2010I. Pham Eur J Clin Invest 2010; 40 (3): 195,202 Abstract Background, Activation of the endothelin-1 (ET-1) pathway may be involved in hypoxia-induced pulmonary vasoconstriction, increase in pulmonary pressure and high altitude pulmonary oedema. Thus, we investigated the effect of the ETA/ETB receptor antagonist, bosentan, on pulmonary artery systolic pressure (PASP) in healthy subjects (n = 10). Design, We used a double-blind, placebo-controlled, randomized, cross-over design to study the effects of a single oral dose of bosentan (250 mg) on PASP after 90-min-exposure to normobaric hypoxia (FiO2 = 0·12). We measured PASP and cardiac output by echocardiography, systolic arterial blood pressure, arterial O2 saturation (SaO2), and blood gases at rest and during a sub-maximal exercise. Results, PASP in normoxia at rest was 23·5 ± 2·7 and during exercise 39·8 ± 11·6 mmHg (P < 0·0001). During the placebo period, hypoxia induced a significant decrease in SaO2, PaO2 and PCO2 and increase in pH. PASP at rest increased significantly: 32·1 ± 3·5 mmHg (P < 0·001 vs. normoxia). Bosentan significantly blunted the hypoxia-induced increase in PASP: bosentan: 27·0 ± 3·3 mmHg, P = 0·002 vs. placebo at rest, but not during exercise: bosentan 39·8 ± 11·6 vs. placebo 43·0 ± 8·5 mmHg, ns. Bosentan had no effect on the hypoxia-induced changes in blood gases, or on cardiac output and systolic arterial blood pressure, which were not modified by hypoxia. Conclusion, A single oral dose of bosentan blunted an acute hypoxia-induced increase in PASP in healthy subjects, without altering cardiac output or systemic blood pressure. [source] Evaluation of the one-minute exercise test to detect peripheral arterial diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2008E. K. Hoogeveen ABSTRACT Background,, Asymptomatic peripheral arterial disease (PAD) is common amongst the elderly and is a risk factor for cardiovascular morbidity and mortality. PAD can be assessed by non-invasive tests such as the ankle/brachial pressure index (ABPI) at rest and Doppler flow velocity (DFV) scanning, but these tests may underestimate the prevalence of PAD. The aim of this study was to estimate the added value, for the detection of PAD, of the one-minute exercise test, defined as positive if the drop of the ankle systolic pressure was more than 30 mmHg. We also investigated whether the combination of the ABPI at rest and the one-minute exercise test could replace DFV scanning. Materials and methods,, We studied this in a random sample (n = 631) of a 50- to 75-year-old population. Results,, Of these subjects 11% (66/631) had an abnormal ABPI (< 0·9) and 16% (102/631) had an abnormal DFV curve. Of this sample 72% of the subjects performed a one-minute exercise test. Of all subjects 6% (27/451) had an abnormal ABPI (< 0·9) and 12% (54/451) had an abnormal DFV curve. The one-minute exercise test revealed seven cases of PAD (beyond the 67 already identified) which were not detected by an abnormal ABPI at rest and/or DFV scanning. As a result the prevalence of PAD increased by 2%. All patients with an aortoiliac or femoropopliteal obstruction had an ABPI at rest < 0·9. The sensitivity of the combination of the ABPI at rest and the one-minute exercise test to detect abnormal DFV curves was low for crural obstructions. Conclusion,, The one-minute exercise test slightly improves the detection of peripheral arterial disease in the general population. [source] Urinary albumin excretion is associated with pulmonary hypertension in sickle cell disease: potential role of soluble fms-like tyrosine kinase-1EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2010Kenneth I. Ataga Abstract Background:, Pulmonary hypertension (PHT) is reported to be associated with measures of renal function in patients with sickle cell disease (SCD). The purpose of this exploratory study was to determine the relationship between albuminuria and both clinical and laboratory variables in SCD. Design and methods:, This cross-sectional study was performed using a cohort of adult patients with SCD and control subjects without SCD. Spot urine for microalbumin/creatinine ratio, measures of hemolysis, inflammation and other laboratory studies were obtained. Pulmonary artery systolic pressure was determined by Doppler echocardiography, and the diagnosis of PHT was defined using age-, sex- and body mass index-adjusted reference ranges. Results:, Seventy-three patients with SCD and 21 healthy, race-matched control subjects were evaluated. In patients with SCD, normoalbuminuria was observed in 34 patients (46.6%), microalbuminuria in 24 patients (32.9%) and macroalbuminuria in 15 patients (20.5%). There was a significant correlation between urine albumin excretion and age. In patients with HbSS and S,0 thalassemia, the levels of sFLT-1, soluble VCAM and NT pro-BNP were significantly higher in those with macroalbuminuria, compared to patients with microalbuminuria and normoalbuminura, but no significant differences were observed in the levels of laboratory measures of hemolysis. Urine albumin excretion was associated with PHT and a history of stroke. Conclusions:, Our study confirms the high prevalence of albuminuria in SCD. The association of urine albumin excretion with sFLT-1 suggests that this vascular endothelial growth factor receptor family member may contribute to the development of albuminuria in SCD. By inducing endothelial activation and endothelial dysfunction, sFLT-1 appears to be a link between glomerulopathy and PHT in SCD. [source] Correlation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in ratsEXPERIMENTAL PHYSIOLOGY, Issue 3 2006Donatella Stilli We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source] The Effect of Progesterone on Coronary Blood Flow in Anaesthetized PigsEXPERIMENTAL PHYSIOLOGY, Issue 1 2001C. Molinari The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h,1 of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h,1. The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of N, -nitro-L-arginine methyl ester (L-NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L-NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide. [source] Comprehensive geriatric assessment for community-dwelling elderly in Asia compared with those in Japan: VI.GERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2005Maubin in Myanmar Background: The objective of the present study is to compare the findings of comprehensive geriatric assessments of community-dwelling elderly in Maubin township, Myanmar with those in Japan. Methods: A cross-sectional, study was undertaken of community-dwelling people aged 60 years and over who were living in downtown Maubin and two rural villages near Maubin city, and 411 people aged 65 years and over who were living in Sonobe, Kyoto, Japan. They were examined using a common comprehensive geriatric assessment tool, which included interviews regarding activities of daily living (ADL), medical and social history, quality of life (QOL) and the 15-item Geriatric Depression Scale. Anthropometric, neurobehavioral and blood chemical examinations were also conducted. Using anova and Post Hoc Scheffe's F -test, findings from the three groups were compared. Results: Scores of basic ADL, instrumental self-maintenance, intellectual activities, social roles, QOL, Tokyo Metropolitan Institute of Gerontology Index of Competence, body mass index, total cholesterol levels, blood hemoglobin levels and HDL levels were lower in Myanmar's elderly subjects than in Japanese ones. There was no significant difference in prevalence of depression. Mean blood pressure measurements and rates of subjects with systolic pressure > 140 mmHg or diastolic pressure > 90 mmHg and prevalence of stroke were higher in downtown Maubin than in Japan. The atherogenic index was higher in Myanmar's elderly than in Japanese. Conclusion: In Myanmar subjects had lower ADL and QOL scores than Japanese elderly. Of particular note is the higher prevalence of anemia and subjects with history of stroke in Myanmar than in Japan. Further study is needed to detect the cause of high prevalence of stroke in Myanmar. [source] Clinical risk factors for portopulmonary hypertension,HEPATOLOGY, Issue 1 2008Steven M. Kawut Portopulmonary hypertension affects up to 6% of patients with advanced liver disease, but the predictors and biologic mechanism for the development of this complication are unknown. We sought to determine the clinical risk factors for portopulmonary hypertension in patients with advanced liver disease. We performed a multicenter case-control study nested within a prospective cohort of patients with portal hypertension recruited from tertiary care centers. Cases had a mean pulmonary artery pressure > 25 mm Hg, pulmonary vascular resistance > 240 dynes · second · cm,5, and pulmonary capillary wedge pressure , 15 mm Hg. Controls had a right ventricular systolic pressure < 40 mm Hg (if estimable) and normal right-sided cardiac morphology by transthoracic echocardiography. The study sample included 34 cases and 141 controls. Female sex was associated with a higher risk of portopulmonary hypertension than male sex (adjusted odds ratio = 2.90, 95% confidence interval 1.20-7.01, P = 0.018). Autoimmune hepatitis was associated with an increased risk (adjusted odds ratio = 4.02, 95% confidence interval 1.14-14.23, P = 0.031), and hepatitis C infection was associated with a decreased risk (adjusted odds ratio = 0.24, 95% confidence interval 0.09-0.65, P = 0.005) of portopulmonary hypertension. The severity of liver disease was not related to the risk of portopulmonary hypertension. Conclusion: Female sex and autoimmune hepatitis were associated with an increased risk of portopulmonary hypertension, whereas hepatitis C infection was associated with a decreased risk in patients with advanced liver disease. Hormonal and immunologic factors may therefore be integral to the development of portopulmonary hypertension. (HEPATOLOGY 2008.) [source] Scintigraphic evaluation of intrapulmonary shunt in normoxemic cirrhotic patients and effects of terlipressinHEPATOLOGY RESEARCH, Issue 10 2010George Kalambokis Aim:, The magnitude of intrapulmonary shunt (IPS) in cirrhotic patients without hypoxemia remains undefined. We evaluated the severity and clinical correlations of IPS in normoxemic cirrhotics, and possible IPS alterations after terlipressin treatment. Methods:, Fifteen patients with alcoholic cirrhosis without hypoxemia were studied at baseline and after the administration of 2 mg of terlipressin. The IPS fraction was evaluated by lung perfusion scan after the i.v. injection of technetium-99m -labeled macroaggregated albumin (99mTc-MAA) and calculation of brain uptake (positive value ,6%). Cardiac output (CO), pulmonary artery systolic pressure (PASP) and pulmonary vascular resistance (PVR) were evaluated by Doppler echocardiography. Mean arterial pressure (MAP) was measured and the ratio MAP/CO was calculated as an index of systemic vascular resistance (SVR). Portal vein velocity (PVV) and portal venous flow (PVF) were also assessed by Doppler ultrasonography. Results:, Three patients (20%) had an IPS fraction of more than 6%. A significant inverse correlation with platelet count (P = 0.001) and a direct correlation with Child,Pugh score (P = 0.06), PVV (P = 0.07) and PVF (P = 0.07) were noted. IPS fractions decreased significantly after terlipressin administration (P = 0.00001); the IPS fraction fell below 6% in all three patients with positive baseline values. Terlipressin treatment induced a significant decrease in CO (P = 0.003) and significant increases in MAP (P = 0.0003), SVR (P = 0.0003), SPAP (P = 0.001) and PVR (P = 0.01). Conclusion:, IPS fractions detected by 99mTc-MAA lung scan were inversely correlated with platelet count and directly with liver disease severity, and found abnormal in 20% of normoxemic cirrhotic patients. Terlipressin reduced significantly the magnitude of the shunt. [source] Influence of hypertension on lower urinary tract symptoms in benign prostatic hyperplasiaINTERNATIONAL JOURNAL OF UROLOGY, Issue 11 2003KIMIO SUGAYA Abstract Aim:, To clarify the influence of hypertension on lower urinary tract symptoms (LUTS) we examined the relationship between blood pressure, LUTS, and the effect of terazosin on LUTS in patients with benign prostatic hyperplasia (BPH). Methods:, The subjects were patients who had LUTS and BPH. They were treated with terazosin (1 mg, twice-a-day) for 12 weeks. Calculation of the International Prostate Symptom Score (IPSS), measurement of blood pressure, and uroflowmetry were performed before and after 12 weeks of therapy. Patients were divided into a normotensive (NT) group and a hypertensive (HT) group at the time of first examination. Results:, The IPSS for urinary frequency and nocturia in BPH-HT patients (n = 21; mean age, 71 years) were significantly higher than those in the BPH-NT patients (n = 21; mean age, 69 years) before the administration of terazosin. The total IPSS the BPH-HT patients was also significantly higher than that of the BPH-NT patients. There were no differences of uroflowmetric parameters between the two groups. After 12 weeks of therapy, systolic and diastolic blood pressure decreased in the BPH-HT patients, but not in the BPH-NT patients. However, the systolic pressure of the BPH-HT patients was still significantly higher than that of the BPH-NT patients. The score for each IPSS parameter decreased in both groups, but the difference of the score between the two groups increased. Conclusion:, Hypertension may worsen LUTS and may decrease the improvement of symptoms by terazosin. [source] Response to Cardiac Resynchronization Therapy Predicts Survival in Heart Failure: A Single-Center ExperienceJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2007YONG-MEI CHA M.D. Objective: To determine whether survival after cardiac resynchronization therapy (CRT) is related to improvement in clinical or echocardiographic parameters. Background: In clinical trials, CRT improved symptoms, left ventricular (LV) structure, function, and survival. In clinical practice, response to CRT is highly variable and whether survival benefit is confined to those patients who experience improvement in clinical status or cardiac structure and function is unclear. Methods: This is a single-center study of patients receiving clinically indicated CRT between January 2002 and December 2004. Results: Of 309 patients (age 68 ± 11 years, 83% male) receiving CRT at our institution during the study period, 174 returned for follow-up and 127 had repeat echocardiography. Baseline clinical characteristics and survival were similar among those who did or did not return for follow-up. In paired analyses, New York Heart Association (NYHA) class (,0.56 ± 0.07, p < 0.0001), ejection fraction (EF, 6.3 ± 0.7%, P < 0.0001), LV dimension (,2.7 ± 0.6 mm, P < 0.0001), pulmonary artery systolic pressure (PASP, ,4.6 ± 1.3 mm Hg, P = 0.0007), and MR severity grade (,0.20 ± 0.05, P = 0.0002) improved after CRT. Survival after CRT was associated with decrease in NYHA class (risk ratio [RR]= 0.43, P = 0.0004), increase in EF (RR = 0.94, P = 0.02), and decrease in PASP (RR = 0.96, P = 0.03). Change in EF and NYHA class were correlated (r =,0.46, P < 0.0001) and, adjusting for this covariance, change in NYHA (P = 0.04) but not EF (P = 0.12) was associated with improved survival. Conclusion: Patients who experience improved symptoms, ventricular function, and/or hemodynamics have better survival after CRT. These data enhance understanding of the relationship between CRT clinical response and survival benefit in clinical practice. [source] Timing of Depolarization and Contraction in the Paced Canine Left Ventricle:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003Experiment, Model Introduction: For efficient pump function, contraction of the heart should be as synchronous as possible. Ventricular pacing induces asynchrony of depolarization and contraction. The degree of asynchrony depends on the position of the pacing electrode. The aim of this study was to extend an existing numerical model of electromechanics in the left ventricle (LV) to the application of ventricular pacing. With the model, the relation between pacing site and patterns of depolarization and contraction was investigated. Methods and Results: The LV was approximated by a thick-walled ellipsoid with a realistic myofiber orientation. Propagation of the depolarization wave was described by the eikonal-diffusion equation, in which five parameters play a role: myocardial and subendocardial velocity of wave propagation along the myofiber cm and ce; myocardial and subendocardial anisotropy am and ae; and parameter k, describing the influence of wave curvature on wave velocity. Parameters cm, ae, and k were taken from literature. Parameters am and ce were estimated by fitting the model to experimental data, obtained by pacing the canine left ventricular free wall (LVFW). The best fit was found with cm= 0.75 m/s, ce= 1.3 m/s, am= 2.5, ae= 1.5, and k= 2.1 × 10,4 m2/s. With these parameter settings, for right ventricular apex (RVA) pacing, the depolarization times were realistically simulated as also shown by the wavefronts and the time needed to activate the LVFW. The moment of depolarization was used to initiate myofiber contraction in a model of LV mechanics. For both pacing situations, mid-wall circumferential strains and onset of myofiber shortening were obtained. Conclusion: With a relatively simple model setup, simulated depolarization timing patterns agreed with measurements for pacing at the LVFW and RVA in an LV. Myocardial cross-fiber wave velocity is estimated to be 0.40 times the velocity along the myofiber direction (0.75 m/s). Subendocardial wave velocity is about 1.7 times faster than in the rest of the myocardium, but about 3 times slower than as found in Purkinje fibers. Furthermore, model and experiment agreed in the following respects. (1) Ventricular pacing decreased both systolic pressure and ejection fraction relative to natural sinus rhythm. (2) In early depolarized regions, early shortening was observed in the isovolumic contraction phase; in late depolarized regions, myofibers were stretched in this phase. Maps showing timing of onset of shortening were similar to previously measured maps in which wave velocity of contraction appeared similar to that of depolarization. (J Cardiovasc Electrophysiol, Vol. 14, pp. S188-S195, October 2003, Suppl.) [source] Serum Cardiac Troponin I Concentration in Dogs with Precapillary and Postcapillary Pulmonary HypertensionJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010C. Guglielmini Background: Pulmonary hypertension (PH) is a disease condition leading to right-sided cardiac hypertrophy and, eventually, right-sided heart failure. Cardiac troponin I (cTnI) is a circulating biomarker of cardiac damage. Hypothesis: Myocardial damage can occur in dogs with precapillary and postcapillary PH. Animals: One hundred and thirty-three dogs were examined: 26 healthy controls, 42 dogs with mitral valve disease (MVD) without PH, 48 dogs with pulmonary hypertension associated with mitral valve disease (PH-MVD), and 17 dogs with precapillary PH. Methods: Prospective, observational study. Serum cTnI concentration was measured with a commercially available immunoassay and results were compared between groups. Results: Median cTnI was 0.10 ng/mL (range 0.10,0.17 ng/mL) in healthy dogs. Compared with the healthy population, median serum cTnI concentration was increased in dogs with precapillary PH (0.25 ng/mL; range 0.10,1.9 ng/mL; P < .001) and in dogs with PH-MVD (0.21 ng/mL; range 0.10,2.10 ng/mL; P < .001). Median serum cTnI concentration of dogs with MVD (0.12 ng/mL; range 0.10,1.00 ng/mL) was not significantly different compared with control group and dogs with PH-MVD. In dogs with MVD and PH-MVD, only the subgroup with decompensated PH-MVD had significantly higher cTnI concentration compared with dogs with compensated MVD and PH-MVD. Serum cTnI concentration showed significant modest positive correlations with the calculated pulmonary artery systolic pressure in dogs with PH and some echocardiographic indices in dogs with MVD and PH-MVD. Conclusions and Clinical Importance: Serum cTnI is high in dogs with either precapillary and postcapillary PH. Myocardial damage in dogs with postcapillary PH is likely the consequence of increased severity of MVD. [source] Interpretation of radial pulse contour during fentanyl/nitrous oxide anesthesia and mechanical ventilationACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2002S. Söderström Background: Peripheral arterial blood pressure is not a reliable substitute for proximal aortic pressure. Recognition of this phenomenon is important for correct appreciation of cardiac afterload. Our aim was to evaluate the utility of the radial pulse wave to better understand ventriculo-vascular coupling during anesthesia. Methods: We observed the differences between aortic systolic pressure (AoSAP, tipmanometry) and radial systolic pressure in 15 patients, (including two women) aged 53,78 years, before coronary artery bypass surgery. We studied the induction of anesthesia with fentanyl (20 µg kg,1), moderate volume loading, and thereafter the addition of 70% nitrous oxide. The circulatory effects of mechanical ventilation were studied by doubling the tidal volumes. Pulse wave contours were assessed by calculation of radical and aortic augmentation indices (AI), which measure the second systolic pressure peak. Results: Radial systolic pressure was higher than AoSAP in the control situation (8±2 mmHg), and this SAP gradient increased further with fentanyl (12±2 mmHg). The gradient persisted throughout the study, but was partially reduced by volume loading and nitrous oxide, respectively. Radial augmentation index was the only parameter remaining in a stepwise multivariate model to explain the variance in the SAP gradient (r2=0.48). Radial augmentation index also correlated with aortic pulse pressure (r2=0.71). Mechanical ventilation had significant and similar effects on pulse wave augmentation both in the aorta and in the radial artery, and did not affect the radial to aortic SAP gradient. Conclusion: These elderly coronary patients had stiff vasculature (high aortic AI) and considerable pulse wave reflection, which was beneficially delayed by fentanyl. Changes in the radial pulse wave augmentation during mechanical ventilation were mainly a result of cyclic changes in the stroke volume, and were seldom associated with an increased systolic pressure gradient from the aorta to the radial artery. [source] Alleviation of Pulmonary Hypertension by Cardiac Resynchronization Therapy is Associated with Improvement in Central Sleep ApneaPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2008KAI-HANG YIU M.B.B.S. Background: Recent studies have demonstrated that cardiac resynchronization therapy (CRT) reduces sleep apnea in heart failure (HF); however, the mechanism of benefit remains unclear. Methods: Overnight polysomnography (PSG) was performed in consecutive HF patients who were scheduled for CRT implant. Patients with sleep apnea defined by an apnea-hypopnea index (AHI) of >10/hour were recruited and underwent echocardiogram examination at baseline and 3 months after CRT. Results: Among 37 HF patients screened, 20 patients (54%) had sleep apnea and 15 of them consented for the study. After 3 months of CRT, there was a significant improvement in New York Heart Association functional class (3.1 ± 0.1 vs 2.1 ± 0.1, P < 0.01), quality-of-life (QoL) score (62.9 ± 3.3 vs 56.1 ± 4.5, P = 0.02), left ventricular ejection fraction (LVEF, 28.8 ± 2.5% vs 38.1 ± 2.3%, P < 0.01), and reduction in pulmonary artery systolic pressure (PASP, 41.0 ± 2.7 vs 28.6 ± 2.2 mmHg; P < 0.01) compared with baseline. Repeated PSG after CRT demonstrated a reduction in the duration of arterial oxygen desaturation ,95% (251.2 ± 36.7 vs 141.0 ± 37.1 minutes), AHI (27.5 ± 4.7 vs 18.1 ± 3.0, P = 0.05), and number of central sleep apnea (CSA) (7.8 ± 2.6 vs 3.0 ± 1.3/hour, P = 0.03), but not number of obstructive sleep apnea (OSA, 8.6 ± 3.3 vs 7.2 ± 2.3/hour, P = 0.65) compared to baseline. Percentage change in PASP was significantly correlated with percentage changes in LVEF (r=,0.57, P = 0.04), AHI (r = 0.5, P = 0.05), and number of CSA episodes (r = 0.55, P = 0.02). Conclusions: The results demonstrated that CRT significantly reduces CSA in patients with HF. Importantly, we have noted a decrement of PASP correlated to drop in CSA which maybe one of the mechanisms explaining this observation. Future studies are required to confirm our finding and elucidate other possible mechanisms in this regard. [source] Clinical significance of reduced systemic Windkessel size in severe ventricular septal defect patientsPEDIATRICS INTERNATIONAL, Issue 3 2008Keiko Kamisaka Abstract Background: Large-shunt ventricular septal defect (VSD) infants manifest varied serious symptoms resulting from peripheral arterial constriction to compensate for increased pulmonary blood flow (Qp) and concomitantly decreased systemic blood flow (Qs). The aim of the present paper was therefore to estimate the whole arterial space proximal to arterioles as the systemic Windkessel size (WS) in these infants and compare it with aortic volume (AV) estimated angiographically. Method: Subjects were divided into three groups. Group 1a consisted of the so-called balanced-pressure VSD infants; group 1b consisted of those with normal or moderately increased pulmonary artery pressure (PAP) and highly augmented Qp; and group 2 consisted of those with a history of mucocutaneous lymph node syndrome as controls for Qp and pulmonary artery pressure. WS was computed from the Windkessel model, while the AV was calculated from the angiogram. Maximal systolic (WSs), mean (WSm), and minimum diastolic (WSd) WS were defined, computed, and compared. Result: All WS were significantly smaller in group 1a; those of group 1b were between group 1a and group 2, with Qs-dependent reduction of WS throughout all these three groups. WSs, WSm, and WSd had negative correlations with right ventricular systolic pressure/left ventricular systolic pressure in group 1a and group 1b. WSm, or the time averaged size, proved to be larger than the corresponding AV in all patients. The ratio of WSm/AV was significantly reduced in group 1a compared to group 1b and group 2, indicating that systemic arterial Windkessel space in severe VSD infants is significantly small, especially so in terms of space distal to aortic valve and proximal to arterioles. Conclusion: In severe VSD infants the whole systemic arterial space proximal to arterioles (WS) is reduced in size according to severity. [source] Echocardiographic abnormalities in sickle cell diseaseAMERICAN JOURNAL OF HEMATOLOGY, Issue 3 2004Shahid Ahmed Abstract Echocardiographic abnormalities in patients with sickle cell disease (SCD) were determined, and pulmonary arterial systolic pressure (PASP) was estimated. Clinical data and echocardiograms of 38 adult hospitalized patients with SCD at two tertiary care hospitals were reviewed. Fisher's exact test was performed to determine correlation between pulmonary hypertension and various clinical variables. Pulmonary hypertension was the most common abnormality identified in 22 (58%) patients. The estimated mean PASP was 37.5 ± 10.9 mmHg. Older age and prior history of acute chest syndrome were significantly correlated with an increased prevalence of pulmonary hypertension (P < 0.05). Patients with hemoglobin levels <8 g/dL had PASP 43.2 ± 0.5 compared to a mean PASP of 33.3 ± 6.0 in patients with hemoglobin ,8 g/dL (P = 0.01). Eight (21%) patients had evidence of a hyperdynamic left ventricle. Left heart abnormalities included dilated atrium in 14 (37%), dilated ventricle in 5 (13%), ventricle hypertrophy in 5 (13%), and ventricle dysfunction in 3 (9%) patients. Right heart abnormalities included dilated atrium in 9 (24%), dilated ventricle in 6 (16%), and ventricle dysfunction in 3 (9%) patients. Despite an increased incidence of abnormal flow across the valves on Doppler analysis, no patient had structurally abnormal valves. A majority of patients with SCD had evidence of pulmonary hypertension, which correlated with older age and history of acute chest syndrome. Other structural and functional echocardiographic abnormalities were less common. Am. J. Hematol. 76:195,198, 2004. © 2004 Wiley-Liss, Inc. [source] A case of pulmonary arteritis with stenosis of the main pulmonary arteries with positive myeloperoxidase-antineutrophil cytoplasmic autoantibodiesRESPIROLOGY, Issue 4 2000Hiroyuki Nakayama A 53-year-old woman was referred to our hospital with the main symptoms of productive cough, fever and exertional dyspnoea. Chest X-ray revealed enlargement of the left hilar shadow and cavitary infiltration in the right upper lobe. 99mTechnetium-macroaggregated albumin (99mTc-MAA) perfusion scintigram showed complete hypoperfusion through the entire right lung. A pulmonary angiogram revealed stenotic lesions in the right and left main pulmonary arteries. Right cardiac catheterization showed an elevated right ventricular systolic pressure. There was no evidence of systemic arterial lesions nor vasculitis. The patient was positive for myeloperoxidase (MPO)antineutrophil cytoplasmic autoantibodies (ANCA) (168 EU). The Mycobacterium avium complex sputum culture was positive. The pulmonary stenotic lesions were surgically resected. The resected pulmonary arterial lesions were pathologically diagnosed as non-specific vasculitis. The cavitary lesion disappeared 6 months after the surgery. Two years after the surgery, although the MPO-ANCA level had decreased to 12 EU, stenosis of the pulmonary arteries reappeared. It is suggested that the patient became positive for MPO-ANCA in association with the Mycobacterium avium complex infection, and that the presence of MPO-ANCA may not be related to the development of pulmonary stenosis of the main pulmonary arteries. [source] Independent association of rheumatoid arthritis with increased left ventricular mass but not with reduced ejection fractionARTHRITIS & RHEUMATISM, Issue 1 2009Rebecca L. Rudominer Objective Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with premature atherosclerosis, vascular stiffening, and heart failure. This study was undertaken to investigate whether RA is associated with underlying structural and functional abnormalities of the left ventricle (LV). Methods Eighty-nine RA patients without clinical cardiovascular disease and 89 healthy matched controls underwent echocardiography, carotid ultrasonography, and radial tonometry to measure arterial stiffness. RA patients and controls were similar in body size, hypertension and diabetes status, and cholesterol level. Results LV diastolic diameter (4.92 cm versus 4.64 cm; P < 0.001), mass (136.9 gm versus 121.7 gm; P = 0.004 or 36.5 versus 32.9 gm/m2.7; P = 0.01), ejection fraction (71% versus 67%; P < 0.001), and prevalence of LV hypertrophy (18% versus 6.7%; P = 0.023) were all higher among RA patients versus controls. In multivariate analysis, presence of RA was an independent correlate of LV mass (P = 0.004). Furthermore, RA was independently associated with presence of LV hypertrophy (odds ratio 4.14 [95% confidence interval 1.24, 13.80], P = 0.021). Among RA patients, age at diagnosis and disease duration were independently related to LV mass. RA patients with LV hypertrophy were older and had higher systolic pressure, damage index scores, C-reactive protein levels, homocysteine levels, and arterial stiffness compared with those without LV hypertrophy. Conclusion The present results demonstrate that RA is associated with increased LV mass. Disease duration is independently related to increased LV mass, suggesting a pathophysiologic link between chronic inflammation and LV hypertrophy. In contrast, LV systolic function is preserved in RA patients, indicating that systolic dysfunction is not an intrinsic feature of RA. [source] Diabetes-induced Alterations in Latissimus Dorsi Muscle Properties Impair Effectiveness of Dynamic Cardiomyoplasty in RatsARTIFICIAL ORGANS, Issue 4 2004Kįtia De Angelis Abstract:, Short-term diabetes was induced in male Wistar rats with streptozotocin injection. The effects of diabetes on latissimus dorsi (LD) muscle contractile and biochemical properties and acute cardiomyoplasty (CDM) were assessed and compared with data from 16 control rats. Isometric force, contractile properties, and fatigue were measured in electrically stimulated muscles (0.3 ms, 1,256 Hz), and Na+K+ and Ca2+ATPase activities were quantified in muscle membrane preparations. Systolic arterial pressure and aortic blood flow were recorded at rest and during LD muscle stimulation. Compared with control muscle, diabetic muscle showed smaller maximum specific tetanic tension and lower rates of rise and fall in force. Diabetic LD muscle also showed lower muscle enzyme activities. Twitch tension and fatigue did not differ between groups. Smaller increases in aortic flow and systolic pressure after CDM were found in diabetic rats compared to controls. The marked decrease in CDM effectiveness in diabetic rats likely reflected the alterations in muscle properties associated with diabetes. [source] Better Correction of Metabolic Acidosis, Blood Pressure Control, and Phagocytosis with Bicarbonate Compared to Lactate Solution in Acute Peritoneal DialysisARTIFICIAL ORGANS, Issue 2 2001Visith Thongboonkerd Abstract: Lactate solution has been the standard dialysate fluid for a long time. However, it tends to convert back into lactic acid in poor tissue-perfusion states. The aim of this study was to evaluate the efficacy of magnesium (Mg)- and calcium (Ca)-free bicarbonate solution compared with lactate solution in acute peritoneal dialysis (PD). Renal failure patients who were indicated for dialysis and needed acute PD were classified as shock and nonshock groups, and then were randomized to receive either bicarbonate or lactate solution. Twenty patients were enrolled in this study (5 in each subgroup). In the shock group, there were more rapid improvements and significantly higher levels of blood pH (7.40 ± 0.04 versus 7.28 ± 0.05, p < 0.05), serum bicarbonate (23.30 ± 1.46 versus 18.37 ± 1.25 mmol/L, p < 0.05), systolic pressure (106.80 ± 3.68 versus 97.44 ± 3.94 mm Hg, p < 0.05), mean arterial pressure (80.72 ± 2.01 versus 73.28 ± 2.41 mm Hg, p < 0.05), percentages of phagocytosis of circulating leukocytes (65.85%± 2.22 versus 52.12%± 2.71, p < 0.05), and percentages of positive nitroblue tetrazolium (NBT) reduction test without and with stimulation (14.43 ± 1.93 versus 9.43 ± 2.12, p < 0.05 and 65.08 ± 6.80 versus 50.23 ± 4.21, p < 0.05, respectively) in the bicarbonate subgroup compared with the lactate subgroup. In the nonshock group, blood pH, serum bicarbonate, and phagocytosis assays in both subgroups were comparable. Lactic acidosis was more rapidly recovered and was significantly lower with bicarbonate solution for both shock and nonshock groups (3.63 ± 0.37 versus 5.21 ± 0.30 mmol/L, p < 0.05 and 2.92 ± 0.40 versus 3.44 ± 0.34 mmol/L, p < 0.05, respectively). Peritoneal urea and creatinine clearances in both subgroups were comparable for both shock and nonshock groups. There was no peritonitis observed during the study. Serum Mg and Ca levels in the bicarbonate subgroup were significantly lower, but no clinical and electrocardiographic abnormality were observed. We concluded that Mg- and Ca-free bicarbonate solution could be safely used and had better outcomes in correction of metabolic acidosis, blood pressure control, and nonspecific systemic host defense with comparable efficacy when compared to lactate solution. It should be the dialysate of choice for acute PD especially in the poor tissue-perfusion states such as shock, lactic acidosis, and multiple organ failure. [source] Catheter-based ventricle-coronary vein bypassCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 3 2005Motoya Hayase MD Abstract The goal of this study was to investigate the feasibility of a catheter-based ventricle-to-coronary vein bypass (VPASS) in order to achieve retrograde myocardial perfusion by a conduit (VSTENT) from the left ventricle (LV) to the anterior interventricular vein (AIV). Percutaneous coronary venous arterialization has been proposed as a potential treatment strategy for otherwise untreatable coronary artery disease. In an acute setting, the VSTENT implant was deployed percutaneously using the VPASS procedure in five swine. Coronary venous flow and pressure patterns were measured before and after VSTENT implant deployment with and without AIV and left anterior descending artery (LAD) occlusion. In a separate chronic pilot study, the VPASS procedure was completed on two animals that had a mid-LAD occlusion or LAD stenosis. At day 30 post-VPASS procedure, left ventriculography and magnetic resonance imaging (MRI) were performed to assess the patency and myocardial viability of the VSTENT implants. Pre-VSTENT implantation, the mid-AIV systolic wedge pressure was significantly lower than LV systolic pressure during AIV blockage (46 ± 19 vs. 90 ± 16 mm Hg; P < 0.01). The VSTENT implant deployment was performed without complication and achieved equalization of the AIV and LV systolic pressures and creation of retrograde flow in the distal AIV (maximal flow velocity: 37 ± 7 cm/sec). At day 30 post-VPASS procedure, left ventriculography showed VSTENT implant patency. MRI perfusion images demonstrated myocardial viability even with an LAD occlusion. Coronary retrograde perfusion using the VPASS procedure is feasible and may represent a potential technique for end-stage myocardial ischemia. Catheter Cardiovasc Interv 2005. © 2005 Wiley-Liss, Inc. [source] Acute effect of antidiabetic 1,4-dihydropyridine compound cerebrocrast on cardiac function and glucose metabolism in the isolated, perfused normal rat heartCELL BIOCHEMISTRY AND FUNCTION, Issue 2 2008Janina Briede Abstract Diabetes mellitus (DM) is an important cardiovascular risk factor and is associated with abnormalities in endothelial and vascular smooth muscle cell function, evoked by chronic hyperglycemia and hyperlipidemia. Chronic insulin deficiency or resistance is marked by decreases in the intensity of glucose transport, glucose phosphorylation, and glucose oxidation, plus decreases in ATP levels in cardiac myocytes. It is important to search for new agents that promote glucose consumption in the heart and partially inhibit extensive fatty acid beta-oxidation observed in diabetic, ischemia. When the oxygen supply for myocardium is decreased, the heart accumulates potentially toxic intermediates of fatty acid beta-oxidation, that is, long-chain acylcarnitine and long-chain acyl-CoA metabolites. Exogenous glucose and heart glycogen become an important compensatory source of energy. Therefore we studied the effect of the antidiabetic 1,4-dihydropyridine compound cerebrocrast at concentrations from 10,10,M to 10,7,M on isolated rat hearts using the method of Langendorff, on physiological parameters and energy metabolism. Cerebrocrast at concentrations from 10,10,M to 10,7,M has a negative inotropic effect on the rat heart. It inhibits L -type Ca2+channels thereby diminishing the cellular Ca2+ supply, reducing contractile activity, and oxygen consumption, that normally favors enhanced glucose uptake, metabolism, and production of high-energy phosphates (ATP content) in myocardium. Cerebrocrast decreases heart rate and left ventricular (LV) systolic pressure; at concentrations of 10,10,M and 10,9,M it evokes short-term vasodilatation of coronary arteries. Increase of ATP content in the myocytes induced by cerebrocrast has a ubiquitous role. It can preserve the integrity of the cell plasma membranes, maintain normal cellular function, and inhibit release of lactate dehydrogenase (LDH) from cells that is associated with diabetes and heart ischemia. Administration of cerebrocrast together with insulin shows that both compounds only slightly enhance glucose uptake in myocardium, but significantly normalize the rate of contraction and relaxation (,±,dp/dt). The effect of insulin on coronary flow is more pronounced by administration of insulin together with cerebrocrast at a concentration of 10,7,M. Cerebrocrast may promote a shift of glucose consumption from aerobic to anerobic conditions (through the negative inotropic properties), and may be very significant in prevention of cardiac ischemic episodes. Copyright © 2007 John Wiley & Sons, Ltd. [source] | |||||||||||||||||||||||||||||||