Total arterial coronary artery bypass grafting in patients with diabetes: an 8-year experience.

OBJECTIVE: Coronary artery bypass grafting using arterial conduits may improve survival and minimise harvest site complications. However, in diabetes, the outcomes of coronary artery bypass grafting performed exclusively using arterial conduits are uncertain. We reviewed our experience with this approach. METHODS: From 1996 to 2008, 400 patients with diabetes (managed with oral hypoglycaemics, insulin or both) underwent primary isolated coronary artery bypass grafting for triple vessel coronary disease. In 246 (61.5%), total arterial revascularisation was achieved using single or bilateral internal thoracic arteries supplemented by one or more radial arteries (arterial group), while in the remaining 154 (38.5%), at least one venous conduit was used (mixed conduits group: mean 1.5 veins per patient). Propensity-score matching was used to adjust for bias. RESULTS: Total arterial revascularisation patients were more likely to be younger (arterial: 63 ± 10 years vs mixed: 67 ± 10 years, P < 0.0001), of elective priority (85% vs 75%, P = 0.018) and less likely to have moderate-severe left ventricular dysfunction (23% vs 36%, P = 0.024). Use of bilateral internal thoracic arteries was similar between groups (16% vs 11%, P = 0.19). There was a comparable in-hospital mortality (1.9% vs 2.0%, P > 0.99) and major morbidities, except the arterial group who experienced less stroke (0.4% vs 3.2% vs P = 0.04) and harvest site infections (0.4% vs 4%, P = 0.016). Mean follow was 7.8 ± 3.7 years. Estimated survival at 12-year survival in the arterial group was 80% ± 3.2% vs 54% ± 5.5% (P < 0.0001). Subsequently, 103 propensity-score-matched patient pairs were created between the two groups. After matching, in-hospital mortality (1% vs 2%, P > 0.99) and major morbidities were similar, as was an estimated 12-year survival (69% ± 6.1% vs 59% ± 6.5%, P > 0.99). CONCLUSIONS: The use of veins to supplement arterial conduits did not deleteriously affect survival. However, the significant number of patients receiving arterial grafts in both groups may have masked any potential difference. Greater numbers and longer follow-up will reveal the potential of this approach.

Effects of age and coronary artery disease on cerebrovascular reactivity to carbon dioxide in humans.

Alterations in cerebrovascular reactivity to CO2, an index of cerebrovascular function, have been associated with increased risk of stroke. We hypothesised that cerebrovascular reactivity is impaired with increasing age and in patients with symptomatic coronary artery disease (CAD). Cerebrovascular and cardiovascular reactivity to CO2 was assessed at rest and during hypercapnia (5% CO2) and hypocapnia (hyperventilation) in subjects with symptomatic CAD (n=13) and age-matched old (n=9) and young (n=20) controls without CAD. Independent of CAD, reductions in middle cerebral artery blood velocity (transcranial Doppler) and cerebral oxygenation (near-infrared spectroscopy) were correlated with increasing age (r = -0.68, r = -0.51, respectively, P < 0.01). In CAD patients, at rest and during hypercapnia, cerebral oxygenation was lower (P < 0.05 vs. young). Although middle cerebral artery blood velocity reactivity was unaltered in the hypercapnic range, middle cerebral artery blood velocity reactivity to hypocapnia was elevated in the CAD and age-matched controls (P < 0.01 vs. young), and was associated with age (r = 0.62, P < 0.01). Transient drops in arterial PCO2 occur in a range of physiological and pathophysiological situations, therefore, the elevated middle cerebral artery blood velocity reactivity to hypocapnia combined with reductions in middle cerebral artery blood velocity may be important mechanisms underlying neurological risk with aging. In CAD patients, additional reductions in cerebral oxygenation may place them at additional risk of cerebral ischaemia.

Identical pattern of cerebral hypoperfusion during different types of syncope.

Syncope is caused by insufficient oxygen supply to the brain. There have been attempts to classify syncope on the basis of defects in the venous system, arterial system (that is impaired systemic vascular resistance) or a combination of the two (that is mixed). We examined the hypothesis that a comparable decrease in cerebral perfusion would be evident at pre-syncope irrespective of the category of dysfunction. Young healthy volunteers (N=37) participated. The protocol consisted of 15 min supine rest, followed by 60 degrees head-up tilt and lower body suction in increments of -10 mm Hg for 5 min each until pre-syncope. Beat-to-beat blood pressure (BP) (Finometer or intra-arterial), cardiac output (Finometer), middle cerebral artery blood velocity (MCAv), end-tidal CO(2) and cerebral oxygenation were monitored continuously. At pre-syncope, mixed dysfunction was common (21 out of 37 participants), followed by venular dysfunction (15 out of 37 participants). In the venular and mixed groups, comparable orthostatic tolerance and declines in BP (-37 vs -43% from baseline, respectively), end-tidal PCO(2), MCAv (-35 vs -38%) and cerebral oxygenation (-5 vs -7%) were evident despite distinct mechanisms purportedly being responsible for the hypotension. Although different determinants of hypotension do exist, cerebral hypoperfusion occurs to a similar extent.