> In designing and development of such a CV, one should make sure that each modeled concept is represented by a unique preferred term and that synonyms are included as references to that term.
Furthermore, despite a large cumulative patient exposure to linagliptin, individual patient exposure was for a maximum of 2.2 years, so the time available for the development of CV events, or modulation of CV risk, was limited.
Renal dysfunction has been shown an independent risk factor for the development of cardiovascular (CV) diseases [ 1, 2] and is associated with worsened outcome in patients with hypertension [ 3], post myocardial infarction (MI) [ 4, 5], and a broad spectrum of patients with left ventricular dysfunction [ 6, 7].
Risk factors in childhood create a life-long burden important in the development of cardiovascular (CV) disease in adulthood.
CRP may therefore facilitate the development of diverse CV diseases via its influence on the events mediated by NO, prostacyclin, and endothelin-1.
The progressive development of cardiovascular (CV) disease (CVD) resulting from pathophysiological changes mediated by angiotensin II in the presence of risk factors is well established [ 2] and local activation of RAS in the vascular walls is thought to contribute to atherosclerosis [ 5].
The FDA guidelines outline the scope of evidence/data that would be considered appropriate to determine CV safety during the development of a T2DM medication.
Of relevance, compared with awake or 24-h BP means, nocturnal BP levels have been shown to be superior in predicting CV morbidity and mortality (24– 28, 28, 46, 47), the development of CV events (24, 25, 40– 42), and overall mortality (24– 26, 41, 44, 45).
Since CV disease is the most common cause of premature mortality in RA, an important step forward might be to identify high-CV risk RA patients who would benefit from active therapy to prevent the development of CV complications.
A limitation of the cross-sectional design is a lack of information on the sequence of the disease and CVD events, and hence a causal relationship between the advent of inflammatory arthritis and development of CV disease can not be proven.
Where the stress inversion observed in the calcite vein sample CV-2 (338-C0002F-258-SMW) ofcurs during development of (a) folds and (b) seismic cycles.
