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Objectives: Acute cardiomyopathy is a health problem worldwide. Few studies have shown an association between acute cardiomyopathy and low vitamin D status. Paricalcitol, a vitamin D receptor activator, clinically benefits patients with advanced kidney disease. The effect of paricalcitol supplement on cardiac remodeling in cardiomyopathic rats is unknown. This experimental study investigated the effect of paricalcitol in rats with cardiomyopathy induced by isoproterenol.Design: Prospective, randomized, controlled experimental study.Setting: Hospital-affiliated animal research institution.Subjects: Eight-week-old male Wistar-Kyoto rats.Interventions: Male Wistar-Kyoto rats were first injected intraperitoneally with isoproterenol to create a rat model of acute cardiomyopathy. Then paricalcitol was administered intraperitoneally to isoproterenol-injected rats at a dosage of 200 ng three times a week for 3 weeks. Relevant cardiomyopathy-related variables were measured regularly in three groups of rats, controls, isoproterenol, and isoproterenol plus paricalcitol. Rat hearts were obtained for evaluation of cardiac fibrosis using Masson trichrome staining and commercially available software, and evaluation of cell transition using immunofluorescence staining analysis.Measurements and Main Results: Isoproterenol infusions generated significant cardiac fibrosis (p < 0.001). Subsequent paricalcitol treatment attenuated the isoproterenol-induced cardiac fibrosis (p = 0.006). Fluorescence showed colocalization of endothelial and fibroblast cell markers (cluster differentiation 31 and α-smooth muscle actin, respectively) in the isoproterenol-treated hearts. Paricalcitol injections attenuated the isoproterenol-induced fluorescence intensity of two cell markers (p < 0.01).Conclusions: Paricalcitol injections may ameliorate isoproterenol-induced cardiac fibrosis possibly through regulating cell transition. [ABSTRACT FROM AUTHOR]

The cold temperature reduces the immunity and re-production activities of the poultry. This study aimed to investigate the effects of acute and chronic cold exposure on the regulation of nuclear factor-kappa B (NF-jB) and tumor necrosis factor-a (TNF-a) expression in the duodenum, jejunum, and ileum of quails. In this study, 96 15-d-old male quails were randomly allocated into 12 groups (eight each group) for exposure to acute (up to 12 h) and chronic (up to 20 days) cold stress (12 ± 1 °C). Antioxidative function was examined by superoxide dismutase (SOD) and oxidative damage was examined by malondialdehyde (MDA) detection. qRT-PCR was performed to analyze expression of NF-jB and TNF-a, and DNA sequencing was performed to analyze PCR products. The data showed that under cold stress, the SOD level decreased, and the MDA level had the tendency to increase in duodenum, jejunum and ileum of quails, while the mRNA expression of NF-jB increased and TNF-a decreased in duodenum, jejunum and ileum of quails. The data from the current study indicated that both acute and chronic cold stresses were able to induce inflammatory responses in the duodenum, jejunum and ileum, which might be due to the colddamaged intestinal oxidative stress. [ABSTRACT FROM AUTHOR]

Background Door-to-balloon (D2B) time is an important factor in the outcome of ST segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention. We aimed to use failure mode and effect analysis to reduce the D2B time for patients with STEMI and to improve clinical outcomes. Methods There were three stages in this study. In Stage 0, data collected from 2005-2006 was used to identify failures in the process, and during Stage 2 (2007) and Stage 3 (2008) the efficacy of intrahospital and interhospital strategies to reduce the D2B time were evaluated. This study enrolled 385 patients; 86 from 2005-2006; 80 in 2007; and 219 in 2008. Results By making improvements in these steps, the median D2B time was reduced from 146 min to 32 min for all patients. The proportion of patients with a D2B time of <90 min significantly increased from Stage 0 to Stage 1 and from Stage 1 to Stage 2, for all patients as well as for the non-transferred and transferred subgroups of patients (all p values <0.0001). For non-transferred patients, only reinfarction-free survival showed significant difference among the three stages (p=0.0225), and for transferred patients, only overall survival showed significant difference among the three stages (p=0.0322). Cox's proportional hazards regression analysis showed Stage 2 was associated with a lower risk of reinfarction and mortality compared with Stage 0. Conclusions This study found that failure mode and effect analysis is a powerful method for identifying weaknesses in D2B processes and evaluating strategies to reduce the D2B time. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to investigate the changes of regional tissue Doppler velocity after volume removal following regular hemodialysis (HD) in uremic patients. Is tissue Doppler velocity really preload-independent? Background: Diastolic dysfunction was divided into four stages: normal pattern, abnormal relaxation pattern, pseudonormalization pattern, and restrictive pattern. Pulse wave Doppler and color Doppler echocardiography were important diagnostic tools for these forms of diastolic dysfunction. However, they were preload-dependent and sometimes there was confusion between the normal pattern and the pseudonormalization pattern. Tissue Doppler echocardiography was promising for problems in diastolic dysfunction and appeared to be preload-independent. However, there are still some disputes over this point. Methods: Ninety-three uremic patients receiving regular HD were included in the study. There were 45 males and 48 females aged 59 ± 14 years. The mean volume removed after HD was 2.3 ± 0.9 kg. The mean heart rates before and after HD were 77 ± 11 and 76 ± 12 beats per minute, respectively (p = 0.73). All patients received complete transthoracic echocardiography examinations before and after HD. The studies included cardiac chamber size, left ventricular systolic performance, pulse wave Doppler echocardiographic data of mitral inflow and the right upper pulmonary vein including peak velocity of early diastolic E wave, E wave time velocity integral (TVI-E), peak velocity of late diastolic A wave, A wave TVI, systolic phase of pulmonary vein (S wave TVI), early diastolic phase of pulmonary vein (D wave TVI) and atrial contraction phase of pulmonary vein (Ar wave TVI). Pulsed tissue Doppler echocardiography (TDE) was performed and a 4-mm sample volume was placed at the 6 corners of the mitral annulus including septal, lateral, anterior, inferior, anteroseptal and posterior corners. Five to ten cardiac cycles were recorded and the data were averaged. Measurements performed included peak velocity of systolic phase (Sa), early diastolic phase (Ea), late diastolic phase (Aa), Ea/Aa ratio and time from the beginning of electrocardiogram Q wave to the beginning of Sa (Q-Sa time). The same measurements were repeated after HD. Results: After HD, left atrium diameter and left ventricular internal dimensions at end diastole became smaller. There were significant reductions for mitral peak E wave velocity, TVI-E, peak A wave velocity and E/A ratio. As for the pulmonary vein, systolic phase of pulmonary vein and early diastolic phase of pulmonary vein decreased significantly. Peak Ar wave did not change significantly. For TDE, Sa and Aa did not change but Ea did decrease. Conclusion: After HD, there is a significant reduction of intravascular effective volume. No significant change is found for myocardial peak systolic velocity and peak late diastolic velocity. However, there is a significant reduction of myocardial early diastolic phase peak velocity. This suggests that TDE is not completely preload-independent; at least, it is phase-dependent within each cardiac cycle. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Real-time myocardial contrast echocardiography (MCE) has the potential to evaluate myocardial perfusion and wall motion (WM) simultaneously. The purposes of this study were to correlate the diagnostic value of MCE with radionuclide single-photon emission computed tomography (SPECT), and to assess the sensitivity and specificity of real-time MCE in detecting coronary artery disease (CAD). Seventy patients with clinically suspected CAD underwent MCE and SPECT at baseline and after dipyridamole infusion. Segmental perfusion with MCE using low mechanical index after 0.3–0.4-ml bolus injections of perfluorocarbon exposed sonicated dextrose albumin solution was performed. All patients had a dual-isotope (rest thallium-201, stress sestamibi) study performed both at baseline and after dipyridamole infusion, and 40 patients had subsequent quantitative coronary angiography. Abnormalities were noted in 27 patients (38.6%) by MCE, in 29 patients (41.4%) by WM analysis, and in 30 patients (42.9%) by SPECT imaging. When MCE and WM analysis were combined, the agreement with SPECT imaging improved from 75.7% (Kappa = 0.50) to 82.0% (Kappa = 0.62). In 40 patients (120 territories) who underwent coronary angiography, good perfusion concordance was achieved for the left anterior descending and left circumflex arteries, and was fair for the right coronary arteries. Compared with quantitative angiography, there was no difference in sensitivity, specificity, and accuracy in detecting significant CAD among the three modalities. The combination of MCE and WM had a better sensitivity (84%), specificity (93.3%), and accuracy (87.5%) than the MCE and WM analysis alone. However, the difference did not reach statistical significance. Real-time MCE has a good agreement with SPECT imaging for detecting CAD. The combination of MCE and WM appears to have higher sensitivity, specificity, and accuracy in detecting CAD than either technique alone. [ABSTRACT FROM AUTHOR]

Information of the effect of statin on lipoproteins such as apolipoprotein (apo) A-I, lipoprotein (a) [Lp (a)], or apolipoprotein B levels is limited. This investigation was a crossover study designed to evaluate the efficacy and safety of atorvastatin and simvastatin in patients with hyperlipidemia. Sixty-six patients were involved in the study. Group I consisted of 32 patients, who were first treated with atorvastatin (10 mg) then switched to simvastatin (10 mg). Group II consisted of 34 patients, who were first treated with simvastatin then switched to atorvastatin. Each regimen was used for 3 months (phase I), stopped for 2 months, and then restarted for another 3 months (phase II). Both statins effectively reduced total cholesterol, low-density lipoprotein cholesterol (LDL-C), apo B, and Lp (a) ( P < 0.001 in all comparisons). A significant increase in the high-density lipoprotein cholesterol (HDL-C) was noted after both statin treatments ( P < 0.05 in all comparisons). Both statins caused an increase in the apo A-I levels, and the extent of changes in apo A-I revealed no difference between the two drugs. Compared to the simvastatin group, there were more patients in the atorvastatin group achieving the National Cholesterol Education Program ATP-III LDL-C goal ( P < 0.05) and European LDL-C goal ( P < 0.001). Both treatments were well tolerated; no patient was withdrawn from the study. This study demonstrates that both statins can effectively improve lipid profiles in patients with hyperlipidemia. Atorvastatin is more effective in helping patients reach the ATP-III and European LDL-C goals than simvastatin at the same dosage. [ABSTRACT FROM AUTHOR]

Carvedilol is a useful cardiovascular drug for treating heart failure, however, thein vitroeffect on many cell types is unclear. In human MG63 osteosarcoma cells, the effect of carvedilol on intracellular Ca2+ concentrations ([Ca2+]i) and cytotoxicity was explored by using fura-2 and tetrazolium, respectively. Carvedilol at concentrations greater than 1μM caused a rapid rise in[Ca2+]i in a concentration-dependent manner (EC50=15μM). Carvedilol-induced[Ca2+]i rise was reduced by 60% by removal of extracellular Ca2+. Carvedilol-induced Mn2+-associated quench of intracellular fura-2 fluorescence also suggests that carvedilol induced extracellular Ca2+ influx. In Ca2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, caused a monophasic[Ca2+]i rise, after which the increasing effect of carvedilol on[Ca2+]i was inhibited by 50%. Conversely, pretreatment with carvedilol to deplete intracellular Ca2+ stores totally prevented thapsigargin from releasing more Ca2+. U73122, an inhibitor of phospholipase C, abolished histamine (an inositol 1,4,5-trisphosphate-dependent Ca2+ mobilizer)-induced, but not carvedilol-induced,[Ca2+]i rise. Pretreatment with phorbol 12-myristate 13-acetate and forskolin to activate protein kinase C and adenylate cyclase, respectively, did not alter carvedilol-induced[Ca2+]i rise. Separately, overnight treatment with 0.1–30μM carvedilol inhibited cell proliferation in a concentration-dependent manner. These findings suggest that in human MG63 osteosarcoma cells, carvedilol increases[Ca2+]i by stimulating extracellular Ca2+ influx and also by causing intracellular Ca2+ release from the endoplasmic reticulum and other stores via a phospholipase C-independent manner. Carvedilol may be cytotoxic to osteoblasts. [ABSTRACT FROM AUTHOR]

We prospectively evaluated the antihypertensive effect and tolerability of three different antihypertensive agents, losartan (angiotensin II receptor blocker), amlodipine (calcium channel blocker), and lisinopril (angiotensin-coverting enzyme inhibitor), in patients with mild-to-moderate hypertension. After a 2-week washout period, 121 patients were randomly allocated to three different groups for 12 weeks. Medications were titrated upward as necessary to achieve the goal office-recorded sitting diastolic blood pressure (SiDBP) (defined as SiDBP «90?mmHg or SiDBP ?900?mmHg but with a ?10?mmHg drop from baseline). Efficacy and tolerability were assessed after 4, 8, and 12 weeks of therapy with each regimen. At 12 weeks, significant differences in SiDBP compared with data of baseline were noted in all three groups ( P « 0.001 in all comparisons). Similarly, significant differences in the sitting systolic blood pressure compared with baseline data were also seen for all three groups ( P « 0.001 in all comparisons). The number of patients reaching goal SiDBP were comparable for the three groups: 25 patients (62.5%) in the losartan group, 27 patients (67.5%) in the amlodipine group, and 22 patients (59.5%) in the lisinopril group (not significant). Amlodipine produced a more pronounced reduction in SiDBP than the other two medications, although without statistical significance. Patients receiving lisinopril showed a high incidence of coughing (31.7%). Low leg edema was noted only in the amlodipine group (7.5%). Compared with the amlodipine and lisinopril groups, the losartan group seemed to have relatively fewer episodes (7.5%), and fewer patients (three cases) experienced adverse effects. In conclusion, this study demonstrates that losartan has the same antihypertensive effect, but has superior tolerability compared with the other two drugs. Coughing was a common side effect of lisinopril therapy in our population. [ABSTRACT FROM AUTHOR]

Evaluation of the severity of valvular mitral stenosis and measurements of the effective rheumatic mitral valve area by noninvasive echocardiography has been well accepted. The area is measured by the two-dimensional planimetry (PLM) method and the Doppler pressure half-time (PHT) method. Recently, the proximal isovelocity surface area (PISA) by color Doppler technique has been used as a quantitaive measurement for valvular heart disease. However, this method needs more validation. The aim of this study was therefore to investigate the clinical applicability of the PISA method in the measurements of effective mitral valve area in patients with rheumatic valvular heart disease. Forty-seven patients aged from 23 to 71 years, with a mean age of 53 ± 13 (25 male and 22 female, 15 with sinus rhythm, mean heart rate of 83 ± 14 beats per minute, with rheumatic valvular mitral stenosis without hemodynamically significant mitral regurgitation) were included in the study. Effective mitral valve area (MVA) derived by the PISA method was calculated as follows: 2 ×Π× (proximal aliasing color zone radius)2× aliasing velocity/peak velocity across mitral orifice. Effective mitral valve areas measured by three different methods (PLM, PHT, and PISA) were compared and correlated with those calculated by the “gold standard” invasive Gorlin's formula. The MVA derived from PHT, PLM, PISA and Gorlin's formula were 1.00 ± 0.31cm2, 0.99 ± 0.30 cm2, 0.95 ± 0.30 cm2 and 0.91 ± 0.29 cm2, respectively. The correlation coefficients (r value) between PHT, PLM, PISA, and Gorlin's formula, respectively, were 0.66 (P = 0.032, SEE = 0.64), 0.67 (P = 0.25, SEE = 0.72) and 0.80 (P = 0.002, SEE = 0.53). In conclusion, the PISA method is useful clinically in the measurement of effective mitral valve area in patients with rheumatic mitral valve stenosis. The technique is relatively simple, highly feasible and accurate when compared with the PHT, PLM, and Gorlin's formula. Therefore, this method could be a promising supplement to methods already in use. (ECHOCARDIOGRAPHY, Volume 21, January 2004) [ABSTRACT FROM AUTHOR]

Previous reports have found that amiodarone is effective for conversion of atrial fibrillation and maintenance of sinus rhythm. The potential of amiodarone-associated proarrhythmia, especially torsades de pointes, may be under-recognized. We present the case of a patient who had a history of atrial fibrillation that was converted to sinus rhythm by amiodarone. However, the patient developed torsades de pointes during maintenance treatment. Salient features of this case history and relevant brief review of the literature on this topic are presented. [ABSTRACT FROM AUTHOR]

The effects of five lignans (epi-aschantin, epi-magnolin, epi-yangambin, deoxypodophyllotoxin, yatein) isolated from Hernandia nymphaeifolia (Presl.) Kubitzki (Hernandiaceae) on intracellular Ca2+ levels ([Ca2+]i) in human neutrophils were investigated by using fura-2 as a fluorescent probe. In both Ca2+-containing and Ca2+-free media, the lignans (50–100 µM) did not alter basal [Ca2+]i but inhibited the [Ca2+]i increase induced by platelet activating factor (PAF, 10 µM), leukotriene B4 (LTB4, 0.2 µM), and thapsigargin (1 µM) to different extents. In Ca2+-free medium, after depleting stores of Ca2+ with PAF, LTB4 or thapsigargin, addition of 3 mM Ca2+ induced Ca2+ influx. Each of the lignans (50–100 µM) caused 39–89% inhibition of PAF-induced Ca2+ influx; whereas only epi-aschantin was able to inhibit LTB4- and thapsigargin-induced Ca2+ influx by 54–79%. Together, the results suggest that in human neutrophils, these lignans did not alter basal [Ca2+]i but inhibited Ca2+ movement induced by Ca2+ mobilizing agents. [ABSTRACT FROM AUTHOR]

Previous reports did not encourage balloon mitral commissurotomy (BMC) when left atrial (LA) thrombi were located beyond LA appendage. We hypothesize that LA thrombi may be resolved in some patients after anticoagulant therapy, and BMC can be performed subsequently. In the present study, we used transesophageal echocardiography (TEE) to evaluate the effects of anticoagulant on LA thrombi in patients with mitral stenosis, to compare the clinical differences between patients with (group A) and without (group B) resolution of LA thrombi, and to evaluate the safety of subsequent BMC in these patients. TEE was performed on 190 consecutive patients with mitral stenosis; 14 (7.4%) of them were found with LA thrombi. Serial TEE was performed and optimal anticoagulant therapy was achieved in all 14 patients. The thrombi were located within the LA appendage in 6 cases, attached to the LA posterior wall in 5, posterior wall and interatrial septum in 1, and LA appendage and posterior wall in 2. Based on the 6-month TEE follow-up, we found that the LA thrombi disappeared in 8 (57.2%) patients (group A) and persisted in 6 patients (group B). LA thrombi resolved within 3 months in 7 group A patients (87.5%). Furthermore, the resolution of LA thrombi was more frequently observed in patients either with a smaller LA dimension (51.9 ± 3.4 vs. 57.8 ± 4.8 mm, p = 0.02) or with their thrombi located inside their LA appendage (p = 0.03). No differences in other clinical and echocardiographic variables were noted between these two groups. Subsequently, group A patients underwent BMC without complications of systemic embolization. In conclusion, LA thrombi can be resolved after optimal anticoagulant therapy in a considerable proportion of patients with mitral stenosis. Serial TEE studies are helpful to observe LA thrombus resolution; they may also be useful in planning the treatment strategy. [ABSTRACT FROM AUTHOR]