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Biomedical subjects

Timothy S Roush

Publications and source records attributed to Timothy S Roush.

3 recordsLinked to original sources

Arteriopathy in the high-performance athlete.

Pain occurs frequently in high-performance athletes and is most often due to musculoskeletal injury or strain. However, athletes who participate in sports that require highly frequent, repetitive limb motion can also experience pain from an underlying arteriopathy, which causes exercise-induced ischemia. We reviewed the clinical records and follow-up care of 3 high-performance athletes (mean age, 29.3 yr; range, 16-47 yr) who were admitted consecutively to our institution from January 2002 through May 2003, each with a diagnosis of limb ischemia due to arteriopathy. The study group comprised 3 males: 2 active in competitive baseball (ages, 16 and 19 yr) and a cyclist (age, 47 yr). Provocative testing and radiologic evaluation established the diagnoses. Treatment goals included targeted resection of compressive structures, arterial reconstruction to eliminate stenosis and possible emboli, and improvement of distal perfusion. Our successful reconstructive techniques included thoracic outlet decompression and interpositional bypass of the subclavian artery in the 16-year-old patient, pectoralis muscle and tendon decompression to relieve compression of the axillary artery in the 19-year-old, and patch angioplasty for endofibrosis affecting the external iliac artery in the 47-year-old. Each patient was asymptomatic on follow-up and had resumed participation in competitive athletics. The recognition and anatomic definition of an arteriopathy that produces exercise-induced ischemia enables the application of precise therapy that can produce a symptom-free outcome and the ability to resume competitive athletics.

Adolescent↗

Does post-stenotic dilatation enhance collateral flow?

Our goal was to investigate whether post-stenotic dilatation (PSD) enhances collateral blood flow. In vitro experiments and computer modeling analysis were used to study the flow through stenotic segments and through collateral channels in the presence and absence of PSD. Pulsatile blood flow was provided by a left heart simulator primed with glycerol or normal saline. Pressure gradients across the stenosis were measured at different "cardiac" outputs. Computer models were constructed to simulate the experiments. Flow patterns and pressure drop across the stenosis were determined for a steady flow of 3 L/min. We observed that PSD was associated with a larger pressure drop across the stenosis than the absence of PSD when the flow was occurring through the stenosis only. There was, however, no difference in the pressure drop between the two geometries when the flow was occurring through both the stenotic orifice and the collateral channels when saline solution was used, but a small pressure difference prevailed for glycerol. At all different geometries there was considerable turbulence at PSD, and PSD geometry was found to be either at a disadvantage or at no advantage when compared to the tapered geometry for the total flow past the stenosis. The PSD geometry, however, enhanced the flow through the collateral while the flow through the orifice decreased concomitantly, resulting in no net increase in the total flow. This was true for any proportion of the total flow going through the collateral channels. For the total flow past the stenosis, PSD does not offer a benefit over tapered geometry.

Blood Circulation↗

Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial.

CONTEXT: Contrast-induced nephropathy remains a common complication of radiographic procedures. Pretreatment with sodium bicarbonate is more protective than sodium chloride in animal models of acute ischemic renal failure. Acute renal failure from both ischemia and contrast are postulated to occur from free-radical injury. However, no studies in humans or animals have evaluated the efficacy of sodium bicarbonate for prophylaxis against contrast-induced nephropathy. OBJECTIVE: To examine the efficacy of sodium bicarbonate compared with sodium chloride for preventive hydration before and after radiographic contrast. DESIGN, SETTING, AND PATIENTS: A prospective, single-center, randomized trial conducted from September 16, 2002, to June 17, 2003, of 119 patients with stable serum creatinine levels of at least 1.1 mg/dL (> or =97.2 micromol/L) who were randomized to receive a 154-mEq/L infusion of either sodium chloride (n = 59) or sodium bicarbonate (n = 60) before and after iopamidol administration (370 mg iodine/mL). Serum creatinine levels were measured at baseline and 1 and 2 days after contrast. INTERVENTIONS: Patients received 154 mEq/L of either sodium chloride or sodium bicarbonate, as a bolus of 3 mL/kg per hour for 1 hour before iopamidol contrast, followed by an infusion of 1 mL/kg per hour for 6 hours after the procedure. MAIN OUTCOME MEASURE: Contrast-induced nephropathy, defined as an increase of 25% or more in serum creatinine within 2 days of contrast. RESULTS: There were no significant group differences in age, sex, incidence of diabetes mellitus, ethnicity, or contrast volume. Baseline serum creatinine was slightly higher but not statistically different in patients receiving sodium bicarbonate treatment (mean [SD], 1.71 [0.42] mg/dL [151.2 [37.1] micromol/L] for sodium chloride and 1.89 [0.69] mg/dL [167.1 [61.0] micromol/L] for sodium bicarbonate; P =.09). The primary end point of contrast-induced nephropathy occurred in 8 patients (13.6%) infused with sodium chloride but in only 1 (1.7%) of those receiving sodium bicarbonate (mean difference, 11.9%; 95% confidence interval [CI], 2.6%-21.2%; P =.02). A follow-up registry of 191 consecutive patients receiving prophylactic sodium bicarbonate and meeting the same inclusion criteria as the study resulted in 3 cases of contrast-induced nephropathy (1.6%; 95% CI, 0%-3.4%). CONCLUSION: Hydration with sodium bicarbonate before contrast exposure is more effective than hydration with sodium chloride for prophylaxis of contrast-induced renal failure.

Adult↗