Eutrophic remodeling of small arteries in type 1 diabetes mellitus is enabled by metabolic control: a 10-year follow-up study.

Type 2 diabetes mellitus profoundly changes small artery remodeling in response to hypertension. Abnormal increases of both wall thickness and lumen diameter are associated with an increased mortality. Changes to small artery structure in response to blood pressure (BP) in patients with type 1 diabetes mellitus have never been examined. In 1997, 17 patients with type 1 diabetes mellitus and 9 control subjects underwent in vitro assessment of gluteal-fat small arteries using pressure myography. Patients with BP <140/90 mm Hg (systolic BP: 119+/-3 mm Hg; n=12) had normal-resistance artery structure. However, patients with BP >140/90 mm Hg (systolic BP: 152+/-5 mm Hg; n=5) demonstrated vascular hypertrophic remodeling with a significant increase in the medial cross-sectional area and wall thickness. In 2008, 8 of the original 17 diabetic patients returned for a repeat assessment. All 8 of the patients had significantly improved cholesterol (2008: 154+/-9 mg/dL versus 1997: 191+/-9 mg/dL; P=0.01) and low-density lipoprotein cholesterol (2008: 79+/-8 mg/dL versus 1997: 122+/-9 mg/dL; P=0.003) but higher BPs (systolic BP: 2008: 136+/-3 mm Hg versus 1997: 119+/-6 mm Hg; P=0.03). Glycemia was improved (2008: 7.9+/-0.3% versus 1997: 8.9+/-0.6%; P=0.17), but not significantly so. In the small arteries studied, there were significant increases in medial wall thickness and wall:lumen ratio, but cross-sectional area was unchanged, indicating eutrophic remodeling. Collectively, these findings suggest that, with poor metabolic control, small arteries from patients with type 1 diabetes mellitus show hypertrophic growth in response to elevated BP, similar to that seen in type 2 diabetes mellitus. However, metabolic improvements enable eutrophic remodeling to occur in response to an increase in BP. This has only been observed previously in patients without diabetes mellitus.

Distal myocardial protection with intracoronary beta blocker when added to a Gp IIb/IIIa platelet receptor blocker during percutaneous coronary intervention improves clinical outcome.

OBJECTIVE: The present study tested the hypothesis that intracoronary (IC) propranolol improves clinical outcomes with percutaneous coronary intervention (PCI) when used with background Gp IIb/IIIa receptor blockade. BACKGROUND: We have previously shown that administration of a relatively large weight-based IC dose of the beta blocker propranolol before PCI decreases the incidence of post-PCI myocardial infarction (MI) and improves short- and long-term outcome. It has previously been shown that administration of a Gp IIb/IIIa receptor blocker decreases post-PCI MI and improves short- and long-term clinical outcome. METHODS: Patients undergoing PCI (n = 400) were randomized in a prospective double-blind fashion to IC propranolol (n = 200) or placebo (n = 200) with eptifibatide administered to all the patients. Myocardial isoform of creatine kinase was measured during the first 24 hr and clinical outcomes at 30 days and 1 year. RESULTS: MI after PCI was seen in 21.5% of placebo and 12.5% of propranolol patients (relative risk reduction 0.42; 95%CI 0.09, 0.63; P = 0.016). At 30 days, the composite end point of death, post-procedural MI, urgent target lesion revascularization, or MI after index hospitalization occurred in 22.5% of placebo vs. 13.5% of propranolol patients (risk reduction 0.43; 95%CI 0.08, 0.65; P = 0.018). Similar results were observed at 1 year with adverse outcomes in 21.5% of propranolol and 32.5% of placebo patients (P = 0.01). CONCLUSION: IC propranolol administration with the background Gp IIb/IIIa receptor blockade significantly reduces the incidence of post-PCI MI and improves the short- and long-term clinical outcome when compared with a Gp IIb/IIIa blocker alone.

Regional transient osteoporosis of the foot and vitamin C deficiency.

We describe the clinical presentation and diagnostic tests of a patient with regional transient osteoporosis (RTO) of the foot. This patient presented with a 4-month history of left-foot pain, nonpitting edema, and brownish discolorations of both feet. He had a history of tobacco abuse, alcohol abuse, and malnutrition. Radiological studies revealed severe osteopenia in the feet, and a MRI revealed bone marrow edema. The bone biopsy was consistent with RTO. This patient also had vitamin C deficiency. This case suggests a link between vitamin C deficiency and RTO, a hypothesis supported by our review of relevant literature on osteoporosis and vitamin C.