Experimental & Clinical Cardiology最新文献

Although diabetes due to insulin deficiency or insulin resistance is a major cause of heart disease, the pathogenesis of cardiac dysfunction during the development of diabetic cardiomyopathy is not fully understood. Varying degrees of defects in subcellular organelles, such as sarcolemma, mitochondria, sarcoplasmic reticulum, myofibrils and extracellular matrix have been observed in the diabetic heart. These subcellular abnormalities in chronic diabetes become evident with the occurrence of hormonal imbalance, metabolic defects, oxidative stress and intracellular Ca(2+) overload. During the initial stages of diabetes, hormonal imbalances, including elevated plasma levels of catecholamines and angiotensin II, as well as metabolic defects, appear to favour the development of oxidative stress; these changes lead to subcellular defects in the myocardium. Reductions in sarcoplasmic reticular Ca(2+) pump and Ca(2+) release channel function are associated with cardiac dysfunction, whereas alterations in sarcolemmal Na(+)/Ca(2+) exchanger and Na(+)/K(+) ATPase activities contribute to intracellular Ca(2+) overload at late stages of diabetes. The continued accumulation of Ca(2+) in mitochondria produces Ca(2+) overload in these organelles, and this change induces impairment of energy production and depletion of energy stores as well as further promotion of oxidative stress in chronic diabetes. Generation of oxyradicals due to impaired electron transport results in the opening of mitochondrial pores, leakage of toxic proteins and myocardial cell damage in diabetes. These observations support the view that alterations in sarcoplasmic reticular and mitochondrial functions produce intracellular Ca(2+) overload and depletion of energy stores and, thus, play an important role in the development of cardiac dysfunction in diabetic cardiomyopathy.

Aneurysms of the sinus of Valsalva are rare congenital lesions. Less often, they are encountered secondary to trauma, infective endocarditis or syphilis. The majority of these aneurysms arise from the right coronary sinus. The present report describes a rare case of an aneurysm arising from the noncoronary sinus of Valsalva and rupturing into the right atrium. Patients with unruptured aneurysms often remain asymptomatic. Rupture of the aneurysm usually causes the appearance of a continuous murmur in the left sternal border. Common sites of rupture include the right ventricle, right atrium or left atrium. Surgical repair is usually associated with a favourable outcome.

Objective: To determine the relationship between the number of CD14(+) cells, myocardial infarct (MI) size and left ventricular (LV) volumes in ST segment elevation MI (STEMI) and non-ST segment elevation MI (NSTEMI) patients.

Methods: A total of 62 patients with STEMI (n=34) or NSTEMI (n=28) were enrolled. The number of CD14(+) cells was assessed at admission. Infarct size, left ventricular ejection fraction (LVEF) and LV volumes were measured using magnetic resonance imaging five days after MI and six months after MI.

Results: In STEMI patients, the number of CD14(+) cells was positively and significantly correlated with infarct size at day 5 (r=0.40; P=0.016) and after six months (r=0.34; P=0.047), negatively correlated with LVEF at day 5 (r=-0.50; P=0.002) and after six months (r=-0.46; P=0.005) and positively correlated with end-diastolic (r=0.38; P=0.02) and end-systolic (r=0.49; P=0.002) volumes after six months. In NSTEMI patients, no significant correlation was found between the number of CD14(+) cells and infarct size, LVEF or LV volumes at day 5 or after six months.

Conclusions: The number of CD14(+) cells at admission was associated with infarct size and LV remodelling in STEMI patients with large infarct size, whereas in NSTEMI patients, no relationship was observed between numbers of CD14(+) cells and LV remodelling.

Recent advances in diagnosis, surgery and interventional management have significantly changed the quality of life of patients with congenital heart disease. Historically, congenital heart disease patients with multiple cardiac lesions have been referred for surgery; however, with the advent of newer technologies and expertise, transcatheter treatment has evolved as an alternative option. A series of patients who underwent interventional procedures for multiple congenital heart disease lesions with excellent procedural and medium-term outcomes is reported.

A 57-year-old woman with a history of hypertension, hyperlipidemia and stable angina is described. A coronary angiogram revealed the presence of a single coronary artery arising from the right sinus of Valsalva that was providing the left anterior descending (LAD), left circumflex and right coronary artery branches, with noncritical occlusive atherosclerotic plaques at the proximal circumflex artery. A small hypoplastic LAD tapering proximally was found, but no LAD and compensatory collateral circulatory vessels were observed distally. In the present report, the authors discuss this extremely rare combination of congenital coronary anomalies and their clinical implications.

Objective: To compare the effects of a 12-week treatment course of a rosiglitazone-based versus a metformin- or glyburide-based strategy on inflammatory biomarkers and adipokine levels in hypertensive, type 2 diabetes patients.

Methods: One hundred three treatment-naive patients or patients on monotherapy with either metformin or glyburide, and a hemoglobin A1C (A1C) ≥7.5%, were randomly assigned to either rosiglitazone add-on (4 mg/day ± titration to 8 mg/day) or a combination of metformin (250 mg twice per day [BID] titrated to 500 BID if A1C ≥7.5% and ≤8.0%; 500 mg BID titrated to 1 g BID if A1C >8.0%) and glyburide (2.5 mg BID titrated to 5 mg BID if A1C ≥7.5% and ≤8.0%; 5 mg BID titrated to 10 mg BID if A1C >8.0%).

Results: Rosiglitazone add-on produced significantly greater reductions in high-sensitivity C-reactive protein (2.1 mg/L to 0.9 mg/L) and increases in adiponectin (8.7 mg/mL to 14.8 mg/mL) levels compared with metformin/glyburide (both P<0.005). At close-out, all patients had improved fasting plasma glucose and A1C levels (8.5% to 7.4% and 8.8% to 7.1% for rosiglitazone add-on and metformin-glyburide, respectively [P<0.001 for both arms]) relative to the corresponding baseline values.

Conclusions: The present study demonstrated that in hypertensive, diabetic subjects, a rosiglitazone-based treatment strategy results in favourable changes in inflammatory biomarkers compared with metformin/glyburide.

In vivo data have been unable to provide conclusive results with regard to the relative impact of circumferential and longitudinal shortening on stroke volume. The objective of the present study was to assess the relative contribution of circumferential and longitudinal myocardial shortening to left ventricular stroke volume and ejection fraction, and to evaluate the effect of left ventricular hypertrophy. A two-shell, three-dimensional mathematical model was used to assess the individual contributions of longitudinal and midwall circumferential shortening (or strain) to stroke volume and ejection fraction. Reducing either circumferential or longitudinal shortening resulted in a reduced ejection fraction and stroke volume. The stroke volume fell by 43% when circumferential strain was reduced from -20% to -5%, but only by 19% when longitudinal strain was similarly reduced. The sole contribution of circumferential and longitudinal shortening to stroke volume was 67% and 33%, respectively. These proportions were independent of wall thickness. The present study demonstrated that both longitudinal and midwall circumferential shortening contribute to different extents depending on the degree of abnormality of myocardial shortening. Contrary to most previous studies, the present study shows that circumferential shortening has a relatively greater contribution to stroke volume (ie, two-thirds) and ejection fraction than longitudinal shortening. These observations have important clinical and research implications in the assessment of left ventricular function.

Cardiac angiosarcomas are rare, rapidly progressive tumours that often present as diagnostic dilemmas resulting in delayed diagnosis. They should be considered in patients with recurrent pericardial effusions.A 33-year-old man presented for evaluation of a recurrent pericardial effusion. Infectious and rheumatological workups were negative. Pericardial fluid cytology and pericardial biopsy were unremarkable. Imaging, including echocardiogram and magnetic resonance imaging, were nondiagnostic.While awaiting surgical intervention, the patient developed respiratory failure requiring urgent intubation. Intraoperatively, he experienced significant hemorrhage from the myocardium. Hemostasis could not be achieved and the patient expired. Pathology reports revealed metastatic angiosarcoma.The present case illustrates a rare case of primary cardiac angiosarcoma posing a diagnostic dilemma in a young man. The authors present the challenges in diagnosis, and review the most current diagnostic and therapeutic strategies in the care of patients with this condition.