Acute right ventricular dysfunction in severe COVID-19 pneumonia.

To investigate the right heart function in coronavirus disease 2019 (COVID-19) patients with acute respiratory distress syndrome (ARDS), a retrospective analysis of 49 COVID-19 patients with ARDS was performed. Patients were divided into severe group and critically-severe group according to the severity of illness. Age-matched healthy volunteers were recruited as a control group. The cardiac cavity diameters, tricuspid annular plane systolic excursion (TAPSE), tricuspid valve regurgitation pressure gradient biggest (TRPG), pulmonary arterial systolic pressure (PASP), maximum inferior vena cava diameter (IVCmax) and minimum diameter (IVCmin), and inferior vena cava collapse index (ICV-CI) were measured using echocardiography. We found that the TAPSE was significantly decreased in pneumonia patients compared to healthy subjects (P < 0.0001), and it was significantly lower in critically-severe patients (P = 0.0068). The TAPSE was less than 17 mm in three (8.6%) severe and five (35.7%) critically-severe patients. In addition, the TAPSE was significantly decreased in severe ARDS patients than in mild ARDS patients. The IVCmax and IVCmin were significantly increased in critically-severe patients compared to healthy subjects and severe patients (P < 0.01), whereas the ICV-CI was significantly decreased (P < 0.05). COVID-19 patients had significantly larger right atrium and ventricle than healthy controls (P < 0.01). The left ventricular ejection fraction (LVEF) in critically-severe patients was significantly lower than that in severe patients and healthy controls (P < 0.05). Right ventricular function was impaired in critically-severe COVID-19 patients. The assessment and protection of the right heart function in COVID-19 patients should be strengthened.

Presence and function of stress granules in atrial fibrillation.

AIMS: Stress granules (SGs) are transient cytoplasmic mRNA and protein complexes that form in eukaryotic cells under stress. SGs are related to multiple diseases, but there are no reports of the existence of SGs in atrial fibrillation (AF). METHODS AND RESULTS: Cell models of AF were established by field stimulation at 600 times per minute. HL-1 cells, cardiomyocytes and cardiac fibroblasts were transfected with G3BP1-cDNA plasmid by Lipofectamine 2000. The presence of SGs was detected by immunofluorescence analysis against GTPase-activating protein SH3 domain binding protein 1 (G3BP1) and poly(A)-binding protein 1 (PABP-1) and electron microscopy. Stable HL-1 cell lines transfected with lentivirus overexpressing G3BP1were constructed to further induce the formation of SGs in AF. Reactive oxygen species (ROS) and calcium overload in tachypaced HL-1 cells were studied by flow cytometry. The effects of G3BP1 overexpression on cardiac fibroblast proliferation and the protein expression level of collagen I/III and fibronectin-1 were also studied. Additionally, we detected protein synthesis in general and in single cells by puromycin incorporation in paced HL-1 cells. Here, we first showed that SGs are present in both tachypaced mouse cardiomyocytes and HL-1 atrial cells, although the presence is partial and at a low level. G3BP1 overexpression promoted SG formation, inhibited the rapid pacing-induced increase in ROS level, and attenuated calcium overload in HL-1 cells (all P<0.05). Furthermore, G3BP1 overexpression inhibited cardiac fibroblast proliferation (P<0.05) and decreased the protein expression level of collagen I and fibronectin-1 in cardiac fibroblasts stimulated by angiotensin II (all P<0.05). The bulk puromycin incorporation analyzed by Western blot did not show a global reduction in protein synthesis. However, puromycin incorporation in single cells detected by immunofluorescence analysis showed that protein synthesis in SG-containing cells significantly reduced (P<0.01). CONCLUSIONS: SGs are rapidly induced and present partially in AF, and G3BP1 overexpression promotes SG formation and confers cytoprotection against oxidative stress, calcium overload and atrial fibrosis in AF.

Urantide improves the structure and function of right ventricle as determined by echocardiography in monocrotaline-induced pulmonary hypertension rat model.

Urotensin II (UII) has been reported to play a key role in pulmonary arterial hypertension (PAH) development. Doppler echocardiography, a noninvasive and simple tool, is recommended for diagnosing PAH. This study was designed to investigate the effect of urantide, a UII receptor antagonist, on the structure and function of the right ventricle in PAH rat models by Doppler echocardiography. A total of 60 male rats were divided into two groups: early- and late-treatment groups. Rats in the urantide and MCT (monocrotaline) subgroups were injected with 10 µg/kg urantide in the urantide group or an equal amount of normal saline in the MCT group 1 week after PAH model construction in the early-treatment group and 4 weeks after the construction in the late-treatment group. Rats in the control group received an equal volume of normal saline solution. PAH-related indexes were measured by echocardiography. PAH rat models exhibited higher right ventricular diastolic diameter and lower time to peak, ejection time, and peak flow velocity of pulmonary artery than controls (P < 0.05). However, compared with the MCT group, all abovementioned indexes were improved in the urantide group (P < 0.05). No significant differences in pulmonary artery diameter and left ventricular ejection fraction were noted among the groups. Compared with the MCT group, systolic pulmonary arterial pressure (SPAP) and mean pulmonary arterial pressure (mPAP) were significantly lower in the urantide group (P < 0.05). SPAP examined by echocardiography was correlated with mPAP by catheterization (P < 0.05). Urantide treatment improved right heart failure parameters in MCT-induced PAH rats, thus providing a potential new strategy for treating PAH.

High thoracic sympathetic block improves coronary microcirculation disturbance in rats with chronic heart failure.

INTRODUCTION: Coronary microcirculation disturbance plays an important role in chronic heart failure (CHF). High thoracic sympathetic block (HTSB) is effective to treat CHF, but its impact on coronary microcirculation is unclear. METHODS: Forty male Wistar rats were subcutaneously injected with isoproterenol (340 mg/kg) for 2 days. Eight weeks later, 24 surviving rats were randomized to the CHF and HTSB groups and 10 rats were used as the control group. 50 µl of saline and ropivacaine (0.2%) were epidurally infused everyday in the CHF and HTSB group respectively. Four weeks later, echocardiography and pathological and ultrastructural examination, capillary histochemical staining and vascular endothelial growth factor (VEGF) immunohistochemical staining in left ventricular (LV) subendocardial myocardium were performed. RESULTS: Compared with the control group, LV dilation and dysfunction, myocardial focal necrosis, capillary spasm appeared in the CHF group. HTSB ameliorated LV dilation and dysfunction, myocardial necrosis and capillary spasm. Rats in the CHF group had less myocardial capillary density and more VEGF expression than in the control group (1591 ±â€¯99 vs. 1972 ±â€¯118/mm2, 0.62 ±â€¯0.13 vs. 0.33 ±â€¯0.10 optic density, all p < 0.05). Myocardial capillary density (1782 ±â€¯96/mm2) was more and VEGF expression (0.47 ±â€¯0.12 optic density) was less in the HTSB group than in the CHF group (all p < 0.05). CONCLUSION: HTSB improves coronary microcirculation disturbance in CHF, which may contribute to reversing myocardial remodeling and dysfunction. HTSB stimulates myocardial capillary growth independent of VEGF.

Platelet-neutrophil interaction aggravates vascular inflammation and promotes the progression of atherosclerosis by activating the TLR4/NF-κB pathway.

Platelet-neutrophil interaction is well known for its role in inflammatory diseases; however, its biological role in atherosclerosis (AS) progression remains unclear. Human peripheral blood neutrophils were obtained to compare toll-like receptor 4 (TLR4), tumor necrosis factor α (TNF-α), interleukin (IL)-1ß and myeloid-related proteins 8/14 (Mrp8/14) levels in 22 AS patients with those in 18 healthy controls using quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Meanwhile, mouse marrow neutrophils subjected to different treatment were collected for the ELISA assay, cell apoptosis, and Western blot analysis. Normal diet or high-fat diet ApoE-/- mice with or without administration of Mrp8/14 antagonist paquinimod were used for plasma collection to measure total cholesterol, triglycerides, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, TNF-α, IL-1ß, Mrp8/14, TLR4, and nuclear factor (NF)-κB p65 levels. The results showed that Mrp8/14 and TLR4-mediated inflammatory pathway was activated in neutrophils of AS patients. In vitro experiments demonstrated that platelet-neutrophil interaction promoted the Mrp8/14 release and inhibited neutrophil apoptosis via P-selectin. Furthermore, platelet-neutrophil interaction upregulated TLR4/myeloid differentiation factor 88/NF-κB pathway. Conversely, Mrp8/14/TLR4/NF-κB interference alleviated AS progression. In conclusion, Mrp8/14/TLR4/NF-κB activated by platelet-neutrophil interaction is an important inflammatory signaling pathway for AS pathogenesis.

Plasma microRNAs as potential noninvasive biomarkers for in-stent restenosis.

OBJECTIVE: To investigate whether microRNAs (miRs) can serve as novel biomarkers for in-stent restenosis (ISR). METHODS: This retrospective, observational single-centre study was conducted at the cardiovascular department of a tertiary hospital centre in the north of China. Follow-up coronary angiography at 6 to 12 months was performed in 181 consecutive patients implanted with drug-eluting stents. Fifty-two healthy volunteers served as the control group. The plasma miRs levels were analyzed by quantitative real-time PCR. Receiver-operating characteristic curve (ROC) analysis was performed to investigate the characters of these miRs as potential biomarkers of ISR. RESULTS: MiR-21 levels in ISR patients were significantly higher than those in non-ISR patients and healthy controls (P<0.05), while miR-100 (P<0.05), miR-143 (P<0.001) and miR-145 (P<0.0001) levels were significantly decreased in ISR patients. Further analysis showed that miR-21 levels were remarkably increased (P = 0.045), while miR-100 (P = 0.041), miR-143 (P = 0.029) and miR-145 (P<0.01) levels were dramatically decreased in patients with diffuse ISR compared to those with focal ISR. ROC analysis demonstrated that the area under curve of miR-145, miR-143, miR-100 and miR-21 were 0.880 (95% confidence interval; CI = 0.791-0.987, P<0.001), 0.818 (95% confidence interval; CI = 0.755-0.963, P<0.001), 0.608 (95% confidence interval; CI = 0.372-0.757, P<0.05) and 0.568 (95% confidence interval; CI = 0.372-0.757, P<0.05), with specificity of 83.1%, 80.1%, 68.9% and 68.6%, and sensitivity of 88.7%, 82.1%, 60.2% and 50.1%, respectively. CONCLUSIONS: Circulating miR-143 and miR-145 levels are associated with the occurrence of ISR and can serve as novel noninvasive biomarkers for ISR.

Chronic obstructive sleep apnea causes atrial remodeling in canines: mechanisms and implications.

Obstructive sleep apnea (OSA) is closely related to atrial fibrillation (AF). However, the roles and mechanisms of chronic OSA in atrial remodeling are still unclear. Canine model of chronic OSA was simulated by stopping the ventilator and closing the airway for 4 h per day and lasting for 12 weeks. AF inducibility and duration was increased while atrial effective refractory period (AERP) was shortened after chronic apnea. Meanwhile, upregulation of proteins encoding inward rectifier K(+) current (IK1), delayed rectifier K(+) current (IKr and IKs), acetylcholine activated K(+) current (IKACh), transient outward K(+) current (Ito) and ultra-rapid delayed rectifier potassium current (IKur) as well as downregulation of protein encoding L-type Ca(2+) current (ICa,L) were found after chronic OSA. Besides abnormal electrical activity, chronic OSA induced apoptosis and interstitial fibrosis of atrial myocytes, which was partly mediated by caspase 9, phosphorylation of extracellular-regulated kinase 1/2, and α-smooth muscle actin. In addition, atrial sympathetic and parasympathetic hyperinnervation were found manifesting by enhanced growth-associated protein 43, tyrosine hydroxylase and elevated choline acetyltransferase. Moreover, protein expression of ß1, ß2, and M2 receptor were markedly increased by chronic OSA. In summary, we firstly demonstrated in canine model that chronic OSA could shorten AERP and lead to altered expression of important channel proteins, moreover, induce atrial structure remodeling by increased atrial apoptosis, fibrosis, and autonomic remodeling, eventually promoting the development of a substrate of AF. Our findings suggested that reversing atrial remodeling might be a potential therapeutic strategy for OSA-induced AF.

Microvascular damage after coronary artery bypass surgery: assessment using dobutamine stress myocardial contrast echocardiography.

BACKGROUND: Although dobutamine stress myocardial contrast echocardiography (DSMCE) has been widely used for the prediction of myocardial functional recovery, dynamic changes that occur at the microcirculatory level during stress have been studied limitedly. The objective of the present study was to use low-dose DSMCE to assess microvascular damage and predict myocardial functional recovery in coronary artery disease (CAD) patients receiving coronary artery bypass grafting. METHODS: Forty-six CAD patients were subjected to low-dose DSMCE, as well as echocardiography and coronary computed tomography angiography before revascularization, 1 year after coronary artery bypass grafting. Dynamic changes occurring at the microcirculatory level during stress were analyzed for the ability to predict functional recovery. Quantitative assessment of functional recovery was determined using myocardial blood flow (MBF) via receiver operating characteristic curve analyses. RESULTS: Patients who failed to recover had fewer changes in MBF (ΔMBF) at rest and with stress compared with the segments showing functional recovery. Semiquantitative changes (enhanced or reduced) of the myocardial perfusion score (ΔMPS) and quantitative changes in ΔMBF of stress myocardial contrast echocardiography enhanced the specificity of resting MPS and the sensitivity of wall motion scores (P < 0.05) for the prediction of functional recovery. CONCLUSIONS: Specific stress ΔMBF more accurately reflected the extent of microvascular damage compared with wall motion scores and resting MPS. ΔMBF and ΔMPS under stress myocardial contrast echocardiography provided higher accuracy than wall motion scores and resting MPS in predicting functional recovery in CAD patients after revascularization.

Effect of graft patency on the prediction of myocardial viability by dobutamine stress and myocardial contrast echocardiography before coronary artery bypass surgery.

BACKGROUND: Myocardial functional recovery after revascularization is considered the "gold standard" for myocardial viability (MV) assessment. However, the patency of the revascularized coronary artery affects myocardial functional recovery in patients subjected to coronary artery bypass grafting (CABG). The influence of graft patency on viability results has not been widely studied. PURPOSE: We evaluated the effect of graft patency on the prediction of MV after CABG by myocardial contrast echocardiography (MCE) and low-dose dobutamine stress echocardiography (LD-DSE). METHODS: Fifty-three subjects with chronic ischemic heart disease scheduled for CABG were divided randomly into groups A (n = 26) and B (n = 27). They underwent MCE and LD-DSE preoperatively. Patients were followed up 12 months after CABG. Group B patients underwent multislice computed tomography angiography to assess CABG patency, and patients with obstructed grafts were excluded. Group A patients were not subjected to multislice CT angiography. The accuracy of MCE and LD-DSE for assessing MV between the two groups was compared. RESULTS: The accuracy and positive predictive values of MCE and LD-DSE for predicting MV were higher in group B than in group A (p < 0.05). CONCLUSIONS: Preoperative LD-DSE and MCE ability to predict MV depends on the patency of CABG.

The effects of high thoracic epidural anesthesia on sympathetic activity and apoptosis in experimentally induced congestive heart failure.

OBJECTIVE: To evaluate the effect of high thoracic epidural analgesia (HTEA) in congestive heart failure (CHF). DESIGN: Rat model of CHF. SETTING: Harbin Medical University, Harbin, Heilongjiang, China. PARTICIPANTS: One hundred thirty-five rats. INTERVENTIONS: HTEA involved 5 times daily injections of 0.1% lidocaine at the T3-T4 level. MEASUREMENTS AND MAIN RESULTS: The authors examined myocardial norepinephrine (NE), angiotensin II (Ang II), endothelin-1 (ET1), and tumor necrosis factor-α (TNF-α) concentrations 2, 4, and 6 weeks after the start of HTEA. They also examined histologic changes in heart tissue and myocardial expression of apoptosis-inducing factor (AIF) and poly (ADP-ribose) polymerase (PARP). Sham rats were used as a control. In the time course, myocardial NE, Ang II, ET1, and TNF-α concentrations were significantly higher in the CHF group compared with the HTEA and sham groups (p< 0.05). Similarly, PARP and AIF protein expression levels were significantly higher in the CHF group compared with the HTEA and sham groups (p< 0.05). Microscopy revealed pronounced damage to myocardial cell structures in the CHF group; this damage clearly was reduced in the HTEA group. In addition, cardiac function evaluation indicated treatment with HTEA resulted in similar heart function as animals that did not have surgically induced CHF. CONCLUSIONS: The findings suggest that HTEA induces changes in sympathetic nervous system, renin-angiotensin system, endothelial, and inflammatory process activity involved in CHF.

[On angiotensin II receptor distribution after myocardial infarction in dogs].

OBJECTIVE: To investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI). METHODS: Canines were divided into sham-operated control group (n=7), infarction group (n=7) and Valsartan group (10 mg x kg(-1) x day(-1) for 4 weeks after MI operation, n=7). Four weeks after operation, Doppler tissue imaging (DTI) was used to evaluate regional ventricular function in the noninfarcted myocardium (apical and basal near to the infarction region). The mRNA and protein expressions of angiotensin II type 1 receptor (AT1-R) and angiotensin II type 2 receptor (AT2-R) on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively. Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group (P < 0.05) which could be downregulated by valsartan (P < 0.05). AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas (P < 0.05). Myocardial peak systolic velocity (Sm), myocardial peak early diastolic velocity (Em) and myocardial peak late diastolic velocity (Am) at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan. CONCLUSION: Both mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI, valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.

Effects of spironolactone on electrical and structural remodeling of atrium in congestive heart failure dogs.

BACKGROUND: Renin-angiotensin-aldosterone system has been demonstrated to be associated with both congestive heart failure (CHF) and atrial fibrillation (AF). This study investigated the effects of spironolactone, a kind of aldosterone antagonist, on atrial electrical remodeling and fibrosis in CHF dogs induced by chronic rapid ventricular pacing. METHODS: Twenty one dogs were randomly divided into sham-operated group, control group, and spironolactone group. In control group and spironolactone group, dogs were ventricular paced at 220 beats per minute for 6 weeks. Additionally, spironolactone at 15 mg x kg(-1) x d(-1) was given to dogs 1 week before rapid ventricular pacing until pacing stopped. Transthoracic and transoesophageal echocardiographic examinations were performed to detect structural and functional changes of the atrium. Swan2 Ganz floating catheters were used to measure hemadynamics variances. Atrial effective refractory period (AERP), AERP dispersion (AERPd), intra- and inter-atrium conduction time (CT) and intra-atrium conduction velocity (CV) were determined. The inducibility and duration of AF were also measured in all groups. Finally, atrial fibrosis was quantified with Masson staining. RESULTS: AERP did not change significantly after dogs were ventricular paced for 6 weeks. However, AERPd, intra- and inter-atrium CT increased significantly, and CV decreased apparently, which was negatively correlated to the atrial fibrosis (r = -0.74, P < 0.05). Simultaneously, left atriums were enlarged and cardiac hemadynamics worsened in pacing dogs. Although spironolactone could not affect cardiac hemadynamics effectively, it can obviously improve left atrial ejection fraction (P < 0.05). Spironolactone treatment did not alter AERP duration, but this medicine dramatically decreased AERPd (P < 0.05), shortened intra- and inter-atrium conduction time (P < 0.05), and increased atrium CV. Moreover, spironolactone decreased the inducibility and duration of AF (P < 0.05), as well as atrial fibrosis (P < 0.01) induced by chronic rapid ventricular pacing. CONCLUSION: Spironolactone contributes to AF prevention in congestive heart failure dogs induced by chronic rapid ventricular pacing, which is related to atrial fibrosis reduction and independent of hemadynamics.

[The effects of combined beta(1) adrenergic receptor antagonist and beta(2) adrenergic receptor agonist therapy on cardiac function and myocardial apoptosis in heart failure rats].

OBJECTIVE: To observe the effects of combined beta(1) adrenergic receptor (AR) antagonist with beta(2)AR agonist therapy on cardiac function and cardiomyocyte apoptosis in heart failure rats. METHODS: Heart failure was induced by isoproterenol and rats were randomly divided into metoprolol group (50 mg/kg twice daily/gavage, n = 11), combined treatment group (fenoterol 125 microg/kg and metoprolol 50 mg/kg twice daily/gavage, n = 11) and placebo group (saline, n = 10), another normal 9 male Wistar rats served as control group. After 8 weeks' treatment, cardiac function, apoptosis index (AI), Caspase-3 activity, expression levels of bcl-2 and bax protein, organ weight/body weight and collagen volume fraction (CVF) were evaluated. RESULTS: (1) Left ventricular end diastolic dimension, left ventricular end systolic dimension and E/A ratio were significantly increased and fractional shortening, ejection fraction significantly reduced post isoproterenol (all P < 0.05 vs. control) and these changes were significantly attenuated by metoprolol alone (all P < 0.05 vs. placebo) and further attenuated by the metoprolol and fenoterol combination therapy (all P < 0.05 vs. placebo and metoprolol). (2) Left ventricular weight to body weight ratio, lung weight to body weight ratio and CVF were also significantly reduced in metoprolol and combined treatment group than those in placebo group (all P < 0.01). (3) Compared with placebo group, AI and Caspase-3 activity were significantly lower in metoprolol group (all P < 0.01 vs. placebo) and further reduced in combined treatment group (all P < 0.01 vs. metoprolol). (4) The expression level of bax protein was significantly lower in metoprolol group while bcl-2/bax significantly higher than those in placebo group. These changes were more significant in combined treatment group (all P < 0.01 vs. metoprolol). CONCLUSIONS: beta(1)AR antagonist in combination with beta(2)AR agonist further improved the cardiac function and prevented cardiac remodeling compared with using beta(1)AR antagonist alone in heart failure rats. Downregulated bax and upregulated bcl-2/bax expressions might contribute to the observed beneficial therapy effects by reducing cardiomyocyte apoptosis in these animals.

Chronic blocking of beta 3-adrenoceptor ameliorates cardiac function in rat model of heart failure.

BACKGROUND: Stimulation of the heart beta 3-adrenoceptor (AR) may result in a negative inotropic effect. Being up-regulated, beta 3-AR plays a more important role in the regulation of cardiac function during heart failure. However, the effect of chronic blocking of beta 3-AR on heart failure has not been fully elucidated. In this study, we used a selective beta 3-AR antagonist SR59230A to treat a well defined heart failure rat model chronically, then evaluated its effect on cardiac function and investigated the mechanism. METHODS: Male Wistar rats were chosen randomly as controls (n = 8). Isoproterenol induced heart failure rats were randomly divided into ISO group (n = 10) and SR group (n = 10). The ISO group received intraperitoneal injection of 1 ml saline twice a day; the SR group received intraperitoneal injection of SR59230A 85 nmol in 1 ml saline twice a day; and the control group received no treatment. The treatment was started 24 hours after the last isoproterenol injection and continued for 7 weeks. Then we measured the following indexes: the ratio of heart weight to body weight (HW/BW) and the ratio of left ventricular weight to body weight (LVW/BW), collagen volume fraction (CVF), left ventricular end diastolic dimension (LVEDd), left ventricular end systolic dimension (LVESd), ejection fraction (EF), fractional shortening (FS) and the ratio of E wave to A wave (E/A), the mRNA and protein expression of beta 3-AR and eNOS, and cGMP level in the heart. RESULTS: The ratios HW/BW and LVW/BW were significantly increased in the ISO group compared with the control group (P < 0.01), but they were limited in the SR group (P < 0.05 compared with the ISO group). CVF increased in the ISO group and the SR group (P < 0.01), but it was significantly attenuated in the SR group (P < 0.01). LVEDd, LVESd and E/A ratio were significantly increased in the ISO group compared with the control group (P < 0.01), while EF and FS were significantly decreased (P < 0.01). Compared with the ISO group, the SR group showed that LVEDd, LVESd and E/A ratio were significantly decreased (P < 0.01), whereas EF and FS were significantly increased (P < 0.01). beta(3)-AR and eNOS mRNA and protein in the ISO group were significantly increased when compared with the control group (P < 0.01). These increases were all attenuated in the SR group compared with the ISO group (P < 0.01). The level of cGMP in myocardial tissue was significantly increased in the ISO group compared with the control group (P < 0.01), whereas SR59230A treatment normalized this increment (P < 0.01). CONCLUSIONS: Chronic blocking of beta 3-AR could ameliorate cardiac function in heart failure rats and its mechanism involves inhibition of the negative inotropic effect and attenuation of cardiac remodeling.

[Effects of cardiac sympathetic blockade on left ventricular diastolic function in patients with dilated cardiomyopathy and severe heart failure].

OBJECTIVE: To investigate the effects of cardiac sympathetic blockade on left ventricular diastolic function in patients with dilated cardiomyopathy and severe heart failure (HF). METHODS: Thirty-nine consecutive patients with dilated cardiomyopathy and severe HF with a left ventricular ejection fraction < 35% were randomly divided into 2 groups: control group (n = 16, 12 males and 4 females, aged 56 +/- 16, undergoing routine anti-HF treatment), and cardiac sympathetic blockade (TEB) group (n = 23, 18 males and 5 females, aged 51 +/- 13, undergoing sympathectomy at the interspinal space T3 - 4 or T4 - 5 in addition to the routine anti-HF treatment). Transthoracic echocardiography was conducted before the treatment and 1 month after the treatment to measure the left atrial diameter (Lad), left ventricular diastolic end diameter (LVDEd), ejection fraction (EF), peak early and late diastolic mitral inflow velocity (Em and Am) at 6 mitral annular sites, and the mean values of Em and Am (MEm and MAm). RESULTS: The Lad of the TEB group was 40.4 +/- 5.3 mm, significantly shorter than that of the control group (45.2 mm +/- 7.3 mm. P < 0.05). The LEDEd of the TEB group was 66 mm +/- 6 mm, significantly shorter than that of the control group (71 mm +/- 6 mm, P < 0.05). The EF of the TEB group was 35% +/- 7%, significantly higher than that of the control group (23% +/- 6%, P < 0.05). The MEm of the TEB group was 5.7 cm/s +/- 1.5 cm/s, significantly faster than that of the control group (7.1 cm/s +/- 1.7 cm/s, P < 0.05); and the MAm of the TEB group was 7.1 cm/s +/- 2.1 cm/s, significantly faster than that of the control group (5.4 cm/s +/- 1.8 cm/s, P < 0.05). In the control group the values of Lad, LVDEd, EF, Am, MEm, and MAm did not change significantly, and the Em values significantly increased only at 2 mitral annular sites after the treatment. CONCLUSION: Sympathetic blockade reduces the left ventricular cavity and boosts up the ejection performance, thus improving the left ventricular diastolic function.

[Evaluation of right ventricular function by tissue Doppler echocardiography and Tei index in right ventricular myocardial infarction].

OBJECTIVE: With tissue Doppler imaging and right ventricular Tei index, right ventricular function in patients with right ventricular myocardial infarction (RVMI) was assessed. METHOD: 51 patients admitted to coronary care units and diagnosed as acute inferior myocardial infarction were further studied with the ECG criterion of ST segment elevation >or= 1mm in V(4R) to establish the diagnosis of RVMI. 23 patients were thus diagnosed as RVMI and 28 patients not. 20 healthy subjects served as controls. Clinical and echocardiography index were recorded. Peak systolic and peak early and late diastolic velocities (Sm, Em, Am) and Em/Am were acquired from the apical four-chamber view at the lateralside of tricuspid annulus, the septal side of the tricuspid annulus and the RV free mid-wall using DTI. Interval between tricuspid closing and reopening and ejection time (ET) from parasternal short-axis view were recorded by pulse-wave Doppler. RV Tei index was calculated. RESULTS: Sm and Em at the lateral side of tricuspid annulus and the RV free mid-wall reduced significantly in patients with RVMI as compared with those without RVMI and healthy individuals (Sm at the lateral (7.0 +/- 2.0) cm/s vs (8.7 +/- 1.9) cm/s and (10.6 +/- 2.1) cm/s, P < 0.01; Em at the lateral (6.3 +/- 1.9) cm/s vs (7.9 +/- 1.8) cm/s and (9.6 +/- 1.9) cm/s, P < 0.01; Sm at the RV free mid-wall (6.4 +/- 1.9) cm/s vs (8.0 +/- 1.9) cm/s and (9.4 +/- 2.0) cm/s, P < 0.05; Em at the RV free mid-wall (6.1 +/- 2.0) cm/s vs (7.6 +/- 2.0) cm/s and (9.2 +/- 2.3) cm/s, P < 0.05). RV Tei index in patients with RVMI also increased as compared with that in the other two groups (0.65 +/- 0.19 vs 0.40 +/- 0.15 and 0.26 +/- 0.10; P < 0.01). CONCLUSIONS: The evaluation of velocities at the lateral side of tricuspid annulus and the RV free mid-wall using DTI and RV Tei index provides a noninvasive and rapid method for assessing right ventricular function in patients with RVMI.