Association of Dietary Factors with Progression of AA in Stroke/TIA Patients
- *Corresponding Author:
- Souvik Sen
Professor and Chairman
Department of Neurology
University of South Carolina, School of Medicine
8 Medical Park, Suite 420,
Columbia, SC 29203, USA
Tel: (803) 545-6073
E-mail: [email protected]
Received date: April 28, 2016; Accepted date: June 27, 2016; Published date: June 30, 2016
Citation: Kodumuri N, Giamberardino L, Hinderliter A, Sen S (2016) Association of Dietary Factors with Progression of AA in Stroke/TIA Patients . J Neurol Disord 4: 270. doi:10.4172/2329-6895.1000270
Copyright: © 2016 Sen S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: To investigate the effect of dietary factors such as calorie intake and dietary fats on the progression of aortic arch atheroma (AA). Background: In stroke/TIA patients, progression of AA is associated with recurrent vascular events. Design/Methods: Consecutive patients with measurable (>1 mm) AA atheroma on baseline transesophageal echocardiogram (TEE) evaluation consented to a protocol mandated follow-up TEE at 12 months. Patients that had adequate paired AA images were assessed for progression, defined as Δ ≥ 1 grade worsening (based on plaque thickness over 12 months). Stroke risk factors and fasting lipid profile were assessed at baseline. The patient’s nutritional intake was measured at baseline using the Gladys Block Food Frequency Questionnaire. Results: One-hundred-nine patients (70 strokes, 33 TIAs) had sequential TEEs, of whom 27% (N=30) progressed and 73% (N=79) did not. Patients with progression had higher daily calorie (1778 ± 623 vs. 1378 ± 406 Calories, p=0.008), fat (76 ± 33 vs. 52 ± 23 grams, p=0.0002), carbohydrate (208 ± 78 vs. 169 ± 57 grams, p=0.01) and protein (73 ± 26 vs. 57 ± 21 grams, p=0.005) intake. On Further analysis among different fats showed a higher consumption of saturated fats (25 ± 12 vs. 17 ±8 grams, p=0.00051) as well as unsaturated fats (44 ± 20 vs. 30 ± 13 grams, p=0.002). These differences remained significant after we adjusted for the medication use. However the significance of these differences was attenuated after adjusting for the calorie intake. Cholesterol consumption did not differ between the progression and no-progression group (262 ± 125 vs. 213 ± 149 mg, p=0.2). Conclusions/Relevance: Calorie intake plays a significant role in the progression of AA. Further studies are needed to confirm these findings and determine the specific dietary modifications that may prevent AA progression and associated recurrent vascular events.