Experimental & Clinical Cardiology最新文献

Background: The calcium sensitizer levosimendan has been used in cardiac surgery for the treatment of postoperative low cardiac output syndrome (LCOS) and difficult weaning from cardiopulmonary bypass (CPB).

Objectives: To evaluate the effects of preoperative treatment with levosimendan on 30-day mortality, the risk of developing LCOS and the requirement for inotropes, vasopressors and intra-aortic balloon pumps in patients with severe left ventricular dysfunction.

Methods: Patient with severe left ventricular dysfunction and an ejection fraction <25% undergoing coronary artery bypass grafting with CPB were admitted 24 h before surgery and were randomly assigned to receive levosimendan (loading dose 10 μg/kg followed by a 23 h continuous infusion of 0.1μg/kg/min) or a placebo.

Results: From December 1, 2002 to June 1, 2008, a total of 252 patients were enrolled (127 in the levosimendan group and 125 in the control group). Individuals treated with levosimendan exhibited a lower incidence of complicated weaning from CPB (2.4% versus 9.6%; P<0.05), decreased mortality (3.9% versus 12.8%; P<0.05) and a lower incidence of LCOS (7.1% versus 20.8%; P<0.05) compared with the control group. The levosimendan group also had a lower requirement for inotropes (7.9% versus 58.4%; P<0.05), vasopressors (14.2% versus 45.6%; P<0.05) and intra-aortic balloon pumps (6.3% versus 30.4%; P<0.05).

Conclusion: Patients with severe left ventricle dysfunction (ejection fraction <25%) undergoing coronary artery bypass grafting with CPB who were pretreated with levosimendan exhibited lower mortality, a decreased risk for developing LCOS and a reduced requirement for inotropes, vasopressors and intra-aortic balloon pumps. Studies with a larger number of patients are required to confirm whether these findings represent a new strategy to reduce the operative risk in this high-risk patient population.

Background: There is a comprehensive body of experimental and clinical evidence suggesting that exogenous supplementation of natural antioxidants or augmentation of endogenous antioxidants attenuates the damage caused by myocardial infarction.

Objective: To evaluate the cardioprotective effects of Cl-chalcone and F-chalcone against ischemia/reperfusion (I/R)-induced myocardial infarction in rats.

Methods: Myocardial infarct size was measured using the staining agent 2,3,5-triphenyltetrazolium chloride. Malondialdehyde was measured in serum and heart tissue, and superoxide dismutase and catalase in heart tissue were measured spectrophotometrically.

Results: I/R resulted in significant cardiac necrosis, indicated by a rise in the end products of myocardial lipid peroxidation (malondialdehydes). A loss of antioxidative enzymes (superoxide dismutase and catalase) in heart tissue was also observed in animals subjected to in vivo myocardial I/R injury.

Discussion: The present study demonstrated that treatment with Cl-chalcone and F-chalcone significantly limited infarct size, partially but significantly attenuated the level of lipid peroxidation and moderated the loss of antioxidant reserves in rats subjected to 30 min coronary artery occlusion followed by a 4 h reperfusion in comparison with I/R groups.

Conclusions: The results of the present study suggest that chalcones have cardioprotective activity against I/R-induced myocardial infarction in rats.

Despite the potential benefit of granulocyte colony-stimulating factor (G-CSF) therapy in patients with acute myocardial infarction (MI), the efficacy of G-CSF in regenerating the heart after MI remains controversial. The authors hypothesize that the limited efficacy of G-CSF is related to its inhibitory effect on recruitment of bone marrow-derived cells (BMCs) to the infarcted tissue. MI was induced in rats with intrabone marrow-bone marrow transplantation from syngenic rats expressing green fluorescence protein to track BMCs. G-CSF was administered for five days after the onset of MI. G-CSF increased the number of CD45(+) cells in the peripheral circulation but did not increase their recruitment to the heart. G-CSF had no effect on myocardial stromal-derived factor-1 alpha and chemokine (C-X-C motif) receptor 4 (CXCR4) expression in mononuclear cells in the peripheral blood and CXCR4(+) cells in the heart. G-CSF had no effect on angiogenesis, myocardial fibrosis or left ventricular function four weeks after MI. These results suggest that G-CSF mobilizes BMCs to the peripheral circulation but does not increase recruitment to the infarcted myocardium despite preservation of the stromal-derived factor-1 alpha/CXCR4 axis.

Shear stress stimulates nitric oxide (NO) release in endothelial cells. Stretch-activated ion channels (SACs) and the transient receptor potential vanilloid type 1 (TRPV1) receptor respond to mechanical stimulus and are permeable to Na(+), Ca(2+) and K(+). The influence of SACs and the TRPV1 receptor on NO release on the heart and on the vascular reactivity of the thoracic aorta (TA) was studied. Experiments were performed in isolated perfused heart, cultured endothelial cells and TA rings from Wistar rats. Capsaicin (10 μM, 30 μM) was used as a NO release stimulator, capsazepine (6 μM, 10 μM) was used as a capsaicin antagonist and gadolinium (3 μM, 5 μM) was used as an inhibitor of SACs. NO was measured by the Kelm and Tenorio methods. Left ventricular pressure was recorded and coronary vascular resistance was calculated. Capsaicin increased NO release in the heart by 58% (395±8 pmol/mL to 627±23 pmol/mL). Capsazepine and gadolinium inhibited NO release by 74% and 82%, respectively. This tendency was similar in all experimental models. Capsaicin attenuated the effects of norepinephrine (10 M to 7 M) on TA and had no effect in the presence of N (ω)-nitro-L-arginine methyl ester. Therefore, the authors conclude that SACs and the TRPV1 receptor are both present in the coronary endothelium and that both participate in Ca(2+)-dependent NO release.

Percutaneous and surgical left atrial ablation has been widely used to treat paroxysmal and persistent atrial fibrillation. However, left atrial ablation may result in left atrial tachycardia due to an iatrogenic substrate created by the ablation lesion sets. Ablation of these iatrogenic arrhythmias can be technically challenging, requiring prolonged procedures and the use of three-dimensional electroanatomical mapping systems. In some cases, the atrial tachycardia may terminate during mapping, or may degenerate into atrial fibrillation during the procedure before adequate mapping. Some patients also have several arrhythmia circuits, each requiring separate mapping, which may be time consuming. The present article reports the cases of three patients in whom a large cryoballoon was used to empirically ablate the pulmonary vein antral region, which is important for the initiation and maintenance of these arrhythmias.

Doxorubicin (DOXO) is an efficient and low-cost chemotherapeutic agent. The use of DOXO is limited by its side effects, including cardiotoxicity, that may progress to cardiac failure as a result of multifactorial events that have not yet been fully elucidated. In the present study, the effects of DOXO at two different doses were analyzed to identify early functional and molecular markers of cardiac distress. One group of rats received 7.5 mg/kg of DOXO (low-dose group) and was followed for 20 weeks. A subset of these animals was then subjected to an additional cycle of DOXO treatment, generating a cumulative dose of 20 mg/kg (high-dose group). Physiological and biochemical parameters were assessed in both treatment groups and in a control group that received saline. Systolic dysfunction was observed only in the high-dose group. Mitochondrial function analysis showed a clear reduction in oxidative cellular respiration for animals in both DOXO treatment groups, with evidence of complex I damage being observed. Transcriptional analysis by quantitative polymerase chain reaction revealed an increase in atrial natriuretic peptide transcript in the high-dose group, which is consistent with cardiac failure. Analysis of transcription levels of key components of the cardiac ubiquitin-proteasome system found that the ubiquitin E3 ligase muscle ring finger 1 (MuRF1) was upregulated in both the low- and high-dose DOXO groups. MuRF2 and MuRF3 were also upregulated in the high-dose group but not in the low-dose group. This molecular profile may be useful as an early physiological and energetic cardiac failure indicator for testing therapeutic interventions in animal models.

A high-grade stenosis to viable myocardium typically produces a positive fractional flow reserve. In the present report, a case of subtotal occlusion of a saphenous vein graft to a viable myocardial territory with normal fractional flow reserve is described, and a possible explanation for this observation is discussed.

Embolic myocardial infarction is an uncommon but increasingly recognised complication of infective endocarditis. This complication has a high mortality rate and is deemed a relative contraindication to thrombolytic therapy. The present article describes an episode of acute myocardial infarction associated with infective endocarditis. Systemic thrombolytic therapy was administered, which resulted in resolution of cardiac ischemia but was complicated by a fatal intracerebral bleed. There are a number of published cases describing the use of systemic thrombolysis, primary percutaneous intervention and early valvular surgery in this circumstance, but the optimal course of treatment for myocardial infarction in the context of infective endocarditis remains to be elucidated. Additional guidance for those who are likely to encounter this condition in clinical practice would be welcomed.

Ruptured sinus of Valsalva aneurysm is an uncommon condition with variable manifestation that results in aortocardiac shunt. The presentation may range from an asymptomatic murmur to cardiogenic shock. The initial diagnosis is established or suspected by two-dimensional echocardiography and colour flow Doppler. Transesophageal echocardiography is especially helpful in delineating the anatomy of the aneurysm and its connections to other chambers. The gold standard diagnostic method for ruptured sinus of Valsalva aneurysm is cardiac catheterization and aortography. Recent reports have suggested a potential role of cardiac computed tomography in establishing diagnosis in such cases. The high spatial resolution of cardiac computed tomography provides anatomical details of the ruptured aneurysm by depicting a jet of contrast materials extending from the aneurysm and adjacent cardiac chamber. In addition, cardiac computed tomography provides a comprehensive cardiac evaluation including coronary artery anatomy, and the presence of other associated cardiac or vascular anomalies.