Objective: The age at which arteriosclerosis begins to contribute to events is uncertain. We determined, across the adult lifespan, the extent to which arteriosclerosis-related changes in arterial function occur in those with precipitous arterial events (stroke and critical limb ischemia). Approaches and Results: In 1082 black South Africans (356 with either critical limb ischemia [n=238] or stroke [n=118; 35.4% premature], and 726 age, sex, and ethnicity-matched randomly selected controls), arterial function was evaluated from applanation tonometry and velocity and diameter measurements in the outflow tract. Compared with age- and sex-matched controls, over 10-year increments in age from 20 to 60years, multivariate-adjusted (including steady-state pressures) aortic pulse wave velocity, characteristic impedance (Zc), forward wave pressures (Pf), and early systolic pulse pressure amplification were consistently altered in those with arterial events. Increases in Zc were accounted for by aortic stiffness (no differences in aortic diameter) and Pf by changes in Zc and not aortic flow or wave re-reflection. Multivariate-adjusted pulse wave velocity (7.48±0.30 versus 5.82±0.15 m/s, P <0.0001), Zc ( P <0.0005), and Pf ( P <0.0001) were higher and early systolic pulse pressure amplification lower ( P <0.0001) in those with precipitous events than in controls. In comparison to age- and sex-matched controls, independent of risk factors, pulse wave velocity, and Zc ( P <0.005 and <0.05) were more closely associated with premature events than events in older persons and Pf and early systolic pulse pressure amplification were at least as closely associated with premature events as events in older persons. Conclusions: Arteriosclerosis-related changes in arterial function are consistently associated with arterial events beyond risk factors from as early as 20 years of age.

Introduction: The aim of this study was to determine if any patterns of infection or bacterial resistance existed in critically ill polytrauma patients admitted to the intensive care unit (ICU) at the CM Johannesburg Academic Hospital (CMJAH). Methods: This was a prospective, single-center study of patient laboratory records of 73 critically injured polytrauma patients admitted to an ICU. The data collected from each patient, beginning with admission and extending until discharge from the ICU, included age, gender, admission hemoglobin levels, injury severity score, length of ICU stay, microbiological cultures and sensitivity (MCS), and types and numbers of surgical procedures. Results: Upon admission to the ICU, the injury severity score (ISS) was 40.86 (± 15.64). In total, 73.98% of the patients required the use of a ventilator during their ICU stay. The most prevalent organisms isolated from specimens were Pseudomonas aeruginosa (30.1%), Klebsiella species (25.7%), Acinetobacterbaumanni (16.4%), and Staphylococcus aureus (5.8%). Multi-drug resistance (MDR) was identified in 63% of patients, with Klebsiella (73.91%) and Pseudomonas (65.21%) occurring most frequently. Multivariate analysis showed MDR to be the only significant predictor associated with a higher risk for hospital mortality when age, gender, ventilation, duration of ICU stay, ISS score, and the number of surgeries undergone was taken into account. Conclusion: Critically ill polytrauma patients are at particularly high risk for Gram-negative sepsis.

Aim: We aimed to determine whether the impact of aortic stiffness on atherosclerotic or small vessel end organ damage beyond brachial blood pressure depends in-part on stiffness-induced increases in central arterial pressures produced by an enhanced resistance to flow (characteristic impedance, Zc). Methods: We studied 1021 participants, 287 with stroke or critical limb ischaemia, and 734 from a community sample with atherosclerotic or small vessel end organ measures. Central arterial haemodynamics were determined from arterial pressure (SphygmoCor) and velocity and diameter assessments in the outflow tract (echocardiography). Results: Although Zc and carotid–femoral pulse wave velocity (PWV) were correlated (P < 0.0001), these relations were not independent of confounders (P = 0.90). Both Zc and hence central arterial pressures generated by the product of Zc and aortic flow (Q) (PQxZc), as well as PWV were independently associated with carotid intima–media thickness, estimated glomerular filtration rate (eGFR), endothelial activation markers [vascular cell adhesion molecule-1 (V-CAM-1)] and events. With further adjustments for brachial pulse pressure (PP) or SBP, PWV and PQxZc were both associated with eGFR and V-CAM-1. Relationships between PWV and eGFR or V-CAM-1 were independent of PQxZc (P < 0.05) and relationships between PQxZc and eGFR and V-CAM-1 were independent of PWV (P < 0.005). Similarly, with adjustments for confounders and brachial PP or SBP, across the full adult lifespan, both aortic PWV and PQxZc were increased in those with arterial events (P < 0.005). Relationships between PWV and events were again independent of PQxZc (P < 0.005) and between PQxZc and events were independent of PWV (P < 0.0001). Conclusion: Beyond brachial blood pressure, the impact of aortic stiffness on arterial damage involves effects that are both dependent (proximal aortic Zc and hence PQxZc) and independent (full aortic length indexed by PWV) of central arterial pulsatile load. Hence, PWV and brachial PP may be insufficient to account for all of the damage mediated by increases in aortic stiffness.

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