The ankle-brachial index (ABI) is a simple, inexpensive diagnostic test for peripheral artery disease (PAD). However, it has shown variable accuracy for identification of significant stenosis. The authors performed a structured review of the sensitivity and specificity of ABI ≤ 0.90 for the diagnosis of PAD. MEDLINE, EMBASE, Cochrane databases, Science Citation Index database, and Biological Abstracts database were searched for studies of the sensitivity and specificity of using ABI ≤ 0.90 for the diagnosis of PAD. Eight studies comprising 2043 patients (or limbs) met the inclusion criteria. The result indicated that, although strict inclusion criteria on studies were formulated, different reference standards were found in these studies, and methods of ABI determination and characteristics of populations varied greatly. A high level of specificity (83.3-99.0%) and accuracy (72.1-89.2%) was reported for an ABI ≤ 0.90 in detecting ≥ 50% stenosis, but there were different levels of sensitivity (15-79%). Sensitivity was low, especially in elderly individuals and patients with diabetes. In conclusion, the test of ABI ≤ 0.90 can be a simple and useful tool to identify PAD with serious stenosis, and may be substituted for other non-invasive tests in clinical practice.
Chronic left ventricular failure causes pulmonary congestion with increased lung weight and type-2 pulmonary hypertension. Understanding the molecular mechanisms for type-2 pulmonary hypertension and the development of novel treatments for this condition requires a robust experimental animal model and a good understanding of the nature of the resultant pulmonary remodeling. Here we demonstrate that chronic transverse aortic constriction causes massive pulmonary fibrosis and remodeling, and type-2 pulmonary hypertension in mice. Thus, aortic constriction-induced left ventricular dysfunction and increased left ventricular end-diastolic pressure is associated with up to 5.3-fold increase in lung wet weight and dry weight, pulmonary hypertension and right ventricular hypertrophy. Interestingly, the aortic constriction-induced increase in lung weight was not associated with pulmonary edema, but resulted from profound pulmonary remodeling with a dramatic increase in the percentage of fully muscularized lung vessels, marked vascular and lung fibrosis, myofibroblast proliferation, and leukocyte infiltration. The aortic constriction-induced left ventricular dysfunction was also associated with right ventricular hypertrophy, increased right ventricular end-diastolic pressure and right atrial hypertrophy. The massive lung fibrosis, leukocyte infiltration and pulmonary hypertension in mice after transverse aortic constriction clearly indicate that congestive heart failure also causes severe lung disease. The lung fibrosis and leukocyte infiltration may be important mechanisms in the poor clinical outcome in patients with end-stage heart failure. Thus, the effective treatment of left ventricular failure may require additional efforts to reduce lung fibrosis and the inflammatory response.
Circular RNA (circRNA), a novel type of endogenous noncoding RNA (ncRNA), has become a research hotspot in recent years. CircRNAs are abundant and stably exist in creatures, and they are found with covalently closed loop structures in which they are quite different from linear RNAs. Nowadays, an increasing number of scientists have demonstrated that circRNAs may have played an essential role in the regulation of gene expression, especially acting as miRNA sponges, and have described the potential mechanisms of several circRNAs in diseases, hinting at their clinical therapeutic values. In this review, the authors summarized the current understandings of the biogenesis and properties of circRNAs and their functions and role as biomarkers in cardiovascular diseases.
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