Experimental & Clinical Cardiology最新文献

Background: Unstable plaque is believed to be responsible for major adverse cardiac events (MACE).

Objective: To determine whether coronary computed tomography angiography (CCTA) could be used to predict future MACE.

Methods: Patients undergoing CCTA between January 2008 and February 2010 were consecutively enrolled in the study. The hospital database was screened for patients who later developed acute ST segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI) or cardiac death. Plaque scores were calculated and analyzed using one-way ANOVA to examine the relationship between plaque scores and MACE.

Results: Of the 8557 patients who underwent CCTA, 1055 had hospital records available for follow-up. During follow-up, 25 patients experienced MACE including death (six patients), heart failure (two patients), STEMI (11 patients) and NSTEMI (six patients). The plaque scores were significantly increased in patients who later died, developed heart failure or experienced STEMI (P<0.05). Calcification, erosion and severe stenosis were responsible for the events (P<0.05). Mild and moderate lesions, positive remodelling, drug-eluting stent placement, occlusion and diffuse lesions were not predictive of MACE (P>0.05).

Conclusion: Severe calcification, erosion and severe stenosis predict death, heart failure and STEMI.

Pulmonary embolism is an important clinical entity with considerable mortality despite advances in diagnosis and treatment. In the present article, the authors offer a comprehensive review focused mainly on epidemiology, risk factors, risk stratification, pathophysiological considerations and clinical presentation. Diagnosis based on assessment of clinical likelihood, electrocardiography, chest x-ray, D-dimer levels, markers of myocardial injury and overload, and blood gases is discussed in detail. Special attention is devoted to the clinical use of computed tomography, pulmonary angiography and echocardiography in the setting of pulmonary embolism.

Early and accurate diagnosis and a prompt initiation of treatment are critical for the prognosis of light-chain amyloidosis. The present article describes a case involving a 62-year-old patient who experienced unexplained, chronic diarrhea with negative duodenal and rectal biopsies. Serum immunofixation, a free light-chain assay, electrocardiography and echocardiography were performed after the patient developed syncope. The results of these diagnostic investigations showed characteristic signs of systemic amyloidosis. Cardiac and bone marrow biopsies confirmed the diagnosis of systemic light-chain amyloidosis. The chronic diarrhea was found to be due to an autonomic neuropathy of the enteric nervous system.

Objective: To investigate the effect of ischemic postconditioning on the expression of matrix metalloproteinase (MMP)-2 during ischemia-reperfusion of myocardium in a rabbit model.

Methods: Thirty-six male New Zealand white rabbits were randomly divided into sham, ischemia-reperfusion and ischemic postconditioning groups. Myocardial ischemia-reperfusion was created by ligating the left anterior descending coronary artery for 30 min followed by 3 h of reperfusion. Myocardial infarction sizes were determined by dual staining with triphenyltetrazolium chloride and trypan blue. Plasma levels of MMP-2 were measured using ELISA. Myocardial MMP-2 messenger RNA was analyzed by reverse transcription polymerase chain reaction.

Results: The mean (± SD) infarct size in the ischemic postconditioning group was significantly smaller compared with the ischemia-reperfusion group (37.1±3.8% versus 57.5±1.9%; P=0.02). The incidence of ventricular tachycardia in the ischemic postconditioning group was also lower than in the ischemia-reperfusion group (8.5% versus 75%; P=0.003). MMP-2 messenger RNA expression in the ischemic postconditioning group was significantly lower compared with the ischemia-reperfusion group (0.4944±0.0476 versus 0.6989±0.0694; P=0.02).

Conclusion: Ischemic postconditioning reduces myocardial ischemia-reperfusion injury, possibly by inhibiting the expression of MMP-2.

The role of oxidative stress in cardiovascular disease processes, such as atherogenesis, ischemic-reperfusion injury and cardiac remodelling, has been increasingly recognized in the past few decades. Currently, an increasing number of studies suggest that levels of oxidative stress markers in body fluids correlate with atherosclerotic disease activity. This finding may lead to novel clinical approaches in patients with coronary artery disease. Assessment of oxidative stress markers could modify risk stratification and treatment of patients with suspected coronary artery disease or myocardial infarction.

Right ventricle myocardial infarctions (RVMIs) accompany inferior wall ischemia in up to one-half of cases. The clinical sequelae of RVMIs vary from no hemodynamic compromise to severe hypotension and cardiogenic shock. Diagnosis is based on physical examination, electrocardiography, echocardiography and coronary angiography. Because the standard 12-lead electrocardiogram is insufficient for the assessment of RV involvement, right-sided precordial leads should always be included. Adequate fluid administration in combination with positive inotropic agents and early coronary reperfusion are crucial components of treatment, while diuretics and nitrates should be avoided. Intra-aortic balloon counterpulsation and right ventricle assist devices may be used with success in RVMIs associated with medically refractory heart failure. Right ventricular involvement appears to be an independent prognostic factor that dramatically increases in-hospital mortality, due, in part, to a significantly higher risk of hemodynamically compromising arrhythmias. Thus, using right-sided precordial leads and early RVMI identification to trigger an appropriately aggressive treatment protocol may improve patients' prognosis.

The ductus arteriosus originates from the persistence of the distal portion of the left sixth aortic arch. It connects the descending aorta (immediately distal to the left subclavian artery) to the roof of the main pulmonary artery, near the origin of the left pulmonary artery. Persistence of the duct beyond 48 h after birth is abnormal and results in patent ductus arteriosus (PDA). PDA is rare in adults because it is usually discovered and treated in childhood. Mechanical closure remains the definitive therapy because the patency of ductus arteriosus may lead to multiple complications, depending on the size and flow through the ductus. PDA closure is indicated in patients with symptoms and evidence of left heart enlargement, and in patients with elevated pulmonary pressures when reversal is possible. Transcatheter closure is the preferred technique in adults because it avoids sternotomy, reduces the length of hospital stay and is associated with fewer complications compared with surgery. First demonstrated in 1967, both the technique and the occluder devices used have since evolved. However, designing an ideal PDA occluder has been a challenge due to the variability in size, shape and orientation of PDAs. The present article describes a case involving a 35-year-old woman who presented to the Center for Advanced Heart Failure (Houston, USA) with congestive heart failure due to a large PDA, which was successfully occluded using an Amplatzer (St Jude Medical, USA) muscular ventricular septal defect closure device. The wider waist and dual-retention discs of these ventricular septal defect closure devices may be important factors to consider in the future development of devices for the occlusion of large PDAs.

Cocaine is the most commonly abused drug in patients presenting to emergency rooms. Compliance with medical instructions and medications is poor in patients who use cocaine. A case involving a 41-year-old cocaine user who developed subacute stent thrombosis is described. The patient underwent bare metal stent implantation three days before presentation and had confirmed compliance with dual antiplatelet therapy. The stent thrombosis was treated with a manual and mechanical thrombectomy, in addition to percutaneous transluminal coronary angioplasty. Given the issue of compliance and the increased evidence of cocaine-induced thrombosis in native vessels and stents, it is recommended that balloon angioplasty alone should be the treatment of choice when intervention is required.

Background: Low-dose hydroxychloroquine (HCQ) and ataxia-telangiectasia-mutated (ATM) protein kinase have recently been postulated to be beneficial for the prevention of the age-associated metabolic syndrome including hypertension, hypercholesterolemia and glucose intolerance; however, the effects of low-dose HCQ on the expression of ATM downstream phosphorylated Akt (protein kinase B) and p53 proteins and cardiomyocyte apoptosis in the peri-infarct myocardium remain unclear.

Objective: To explore the effects of low-dose HCQ on the expression of phosphorylated Akt and p53 proteins and cardiomyocyte apoptosis in the peri-infarct myocardium in a rat model.

Methods: Myocardial infarction (MI) was induced experimentally in a subset of rats, while others underwent sham operation (sham). Three days after operation, surviving Sprague-Dawley male rats were divided into MI+HCQ, MI, sham+HCQ and sham groups. MI+HCQ and sham + HCQ groups were treated with HCQ (3.4 mg/kg); and MI and sham groups were treated with phosphate buffered (ie, physiological) saline (10 mL/kg) by gavage every day for 12 weeks. The expression of phosphorylated Akt and p53 proteins and cardiomyocyte apoptosis in the peri-infarct myocardium was detected by Western blot and terminal deoxynucleotidyl transferase dUTP nick end labelling, respectively.

Results: Twelve weeks after treatment, the expression of phosphorylated Akt protein was significantly increased (P<0.05). Expression of phosphorylated p53 protein was not significantly different (P>0.05) in the peri-infarct myocardium of the MI+HCQ group from that in the MI group. The cardiomyocyte apoptosis rate in the peri-infarct myocardium was significantly decreased in the MI+HCQ group compared with the MI group (P<0.05).

Conclusion: Low-dose HCQ can significantly increase the expression of phosphorylated Akt protein without significantly impacting expression of phosphorylated p53 protein in the peri-infarct myocardium. Accordingly, it can inhibit cardiomyocyte apoptosis in the peri-infarct myocardium.