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    Complementary and Alternative Medical Lab Testing Part 4: Vascular
    Complementary and Alternative Medical Lab Testing Part 4: Vascular
    Complementary and Alternative Medical Lab Testing Part 4: Vascular
    Ebook134 pages1 hour

    Complementary and Alternative Medical Lab Testing Part 4: Vascular

    By Ronald Steriti

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    About this ebook

    Complementary and Alternative Medical Lab Testing (CAM Labs) contains summaries of the published research on lab tests, primarily from PubMed trials on humans. Each chapter (disease) begins with a brief summary of conventional lab tests, followed by additional lab tests, including diabetes, insulin resistance, metabolic syndrome, inflammation, etc. There are sections on endocrine hormones (thyroid, adrenal, sex steroids) and environmental medicine (toxic heavy metals). The nutritional assessments section includes minerals, vitamins and amino acids.

    CAM Labs 4 – Vascular

    1. Arterial Stiffness
    2. Arteriosclerosis
    3. Atherosclerosis
    4. Carotid Occlusion
    5. Deep Vein Thrombosis
    6. Intermittent Claudication
    7. Peripheral Arterial Disease
    8. Raynaud's Disease and Syndrome
    9. Thrombophlebitis
    10. Varicose Veins

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 4, 2016
    ISBN9781310870439
    Complementary and Alternative Medical Lab Testing Part 4: Vascular
    Author

    Ronald Steriti

    Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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      Book preview

      Complementary and Alternative Medical Lab Testing Part 4 - Ronald Steriti

      Complementary and Alternative

      Medical Lab Testing

      Part Four: Vascular

      By Ronald Steriti, ND, PhD

      ©

      Complementary and Alternative Medical Lab Testing Clinician’s Guide Part Four: Vascular

      By Ronald Steriti, ND, PhD

      Copyright © 2016

      All rights reserved. No part of this book may be reproduced in any form or by any means, including photocopying, including in a web site, or stored in a retrieval system, or transmitted in any form by any means, without expressed, written permission of the copyright owner.

      The contents of this document are the sole property of the author.

      Disclaimer

      This book has not been evaluated by the FDA and is not intended to diagnose, treat, cure or prevent any disease.

      The information contained in this book is for educational purposes only, and should not be construed as medical advice or instruction. No action should be taken based solely on the contents of this book. Readers should consult appropriate health officials.

      While extensive efforts have been made to ensure the accuracy of the information contained, the possibility of errors, omissions, and misinterpretations cannot be ruled out. The reader is advised to consult the original references for verification and clarification.

      Foreward

      This book is a summary the published research on lab tests, primarily from PubMed. The studies are limited to those with trials on humans. As such, some labs may be excluded due to the lack of published research. That is simply a reflection of the current state of research - much more work is needed!

      Although this book may be useful for differential diagnosis, lab tests are can also be used to identify inderlying causes and associated conditions.

      The sections on conventional lab tests are purposefully brief. These tests are typically used to confirm a diagnosis. There are other more comprehensive sources of information on conventional medical lab testing.

      Table of Contents

      1. Arterial Stiffness

      2. Arteriosclerosis

      3. Atherosclerosis

      4. Carotid Occlusion

      5. Deep Vein Thrombosis

      6. Intermittent Claudication

      7. Peripheral Arterial Disease

      8. Raynaud's Disease and Syndrome

      9. Thrombophlebitis

      10. Varicose Veins

      Chapter 1. Arterial Stiffness

      Physical stiffening of the large arteries is the central paradigm of vascular aging and significantly contributes to cardiovascular diseases in older individuals. It is associated with the leading causes of mortality: systolic hypertension, coronary artery disease, stroke, heart failure and atrial fibrillation. (Shirwany and Zou 2010)

      Arterial stiffness is associated with atherosclerosis (arterial thickening). (van Popele, Grobbee et al. 2001)

      The stiffening or hardening of the vessel wall is associated with age and is a part of other diseases. Complex cellular mechanisms are involved. (Mitchell, Parise et al. 2004)

      Conventional Lab Tests

      Increased pulse pressure (PP): systolic - diastolic BP

      Additional Lab Tests

      Fasting Glucose, Hemoglobin A1C

      A study recruited 697 subjects who visited the health promotion center of a university hospital from May 2007 to August 2008. Fasting plasma glucose (FPG) had an independent, positive association with brachial-ankle pulse wave velocity (ba-PWV) in non-diabetic subjects after correcting for confounding variables. An increase in FPG, even within the normal range, was associated with aggravated arterial stiffness. (Shin et al., 2011)

      The study group consisted of 284 subjects, including 111 subjects with normal fasting glucose (NFG), 61 subjects classed as impaired fasting glucose (IFG) according of the new fasting blood glucose (FBG) cut-off point of 100 mg/dL and 112 patients with diabetes mellitus (DM). Pulse wave velocity, augmentation index and central arterial pressure increased consistently with deterioration of glucose tolerance. PWV was significantly higher in subjects with diabetes than in the normal and IFG groups (p < 0.0001 and p = 0.007, respectively). IFG subjects had marginally higher PWV than normal subjects (p = 0.050). Compared to normal subjects, IFG and diabetes groups were associated with increased AI (p = 0.003 and p < 0.0001, respectively). Arterial stiffness parameters remained significantly higher in both IFG and diabetes groups compared to normal after adjustment for cardiovascular risk factors and concomitant medications. Positive correlations between FBG, HbA1C and arterial stiffness parameters were detected. (Lukich et al., 2010)

      A study recruited 33 patients without DM, 53 patients with pre-DM, and 34 subjects with DM. Patients with pre-DM and DM had lower CI (3.8 +/- 2.1 versus 5.2 +/- 3.0 units; P < 0.05 and 3.6 +/- 1.8 versus 5.2 +/- 3.0 units; P < 0.05, respectively) and higher SI (8.0 +/- 2.0 versus 6.7 +/- 1.6 m/s; P < 0.01 and 9.4 +/- 2.3 versus 6.7 +/- 1.6 m/s; P < 0.001, respectively) than patients without DM. The HOMA index was an independent determinant for arterial stiffness. (Chou et al., 2013)

      Insulin Resistance, Metabolic Syndrome

      BMI, systolic blood pressure, fasting plasma glucose, lipid variables, ankle-brachial pressure index and brachial-ankle pulse wave velocity were measured in 2059 subjects from Takasaki city, located approximately 100 km north of Tokyo in Japan. Following a 75-g oral glucose tolerance test, only subjects with normal glucose tolerance were selected. One-hour post-challenge plasma glucose levels were correlated with brachial-ankle pulse wave velocity values (r = 0.340, P < 0.0001). The study found that in normal glucose tolerance, arterial stiffness is advanced in subjects with higher 1-h post-challenge plasma glucose in spite of the normal range for BMI, systolic blood pressure, fasting plasma glucose and lipid variables. Higher 1-h plasma glucose level is a risk factor for arterial stiffness in normal glucose tolerance. (Niijima et al., 2012)

      Four hundred seventy-six subjects were classified at baseline according to their number of cardiovascular (CV) risk factors (from zero to three and more), after adjustment for smoking habits. Subjects were followed for six years. At baseline, BP, HR, plasma creatinine, and PWV were significantly higher (p < 0.001) in the group with three and more CV risk factors than in groups with zero to two risk factors. During the follow-up, the increase in PWV, but not in pulse pressure, was significantly higher (p < 0.01) in the group with three and more risk factors (i.e., metabolic syndrome) than in other groups. Metabolic syndrome is associated with an increased progression of aortic stiffness with age, supporting premature senescence in these patients. (Safar et al., 2006)

      C-Reactive Protein (CRP)

      A case-series study was carried out in 258 hypertensive patients without antecedents of cardiovascular disease or diabetes mellitus. hs-CRP was positively correlated to f carotid intima-media thickness (IMT) (r=0.261), maximum (r=0.290) and to peripheral augmentation index (AIx) (r=0.166) in men, and to PWV in both men (r=0.280) and women (r=0.250). In women, hs-CRP was negatively correlated to central AIx (r= -0.222). For each unit increase in hs-CRP, carotid IMT would increase 0.05 mm in men, and PWV would increase 0.07 m/sec in men and 0.08 m/sec in women, while central AIx would decrease 2.5 units in women. In the multiple linear regression analysis, hs-CRP explained 10.2% and 6.7% of PWV variability in women and men, respectively, 8.4% of carotid IMT variability in men, and 4.9% of central AIx variability in women. (Gomez-Marcos et al., 2012)

      Pulse wave velocity (PWV) and blood pressure were assessed in 427 individuals. In multiple regression models, aortic PWV correlated independently with age, CRP, male gender, and MAP (R2=0.593; P<0.001). CRP was also independently associated with brachial PWV. (Yasmin et al., 2004)

      A study investigated the relation between measures of arterial stiffness and CRP within the framework of the Rotterdam Study, a population-based cohort study including subjects aged 55 years and older. In adjusted models, levels of CRP were linearly associated with pulse wave velocity (regression coefficient 0.088, 95% CI 0.006-0.170). Adjusted mean values of pulse wave velocity were significantly different across tertiles of CRP, being higher in the highest tertile of CRP. (Mattace-Raso et al., 2004)

      Aldosterone

      Aldosterone overproduction increases arterial wall stiffness by accumulation of different types of collagen fibres and growth factors. Forty-nine patients with confirmed primary aldosteronism (PA) and 49 patients with essential hypertension (EH) were matched. Both peripheral and central PWV were significantly higher in PA patients compared to EH patients, while clinical blood pressures were similar. Plasma aldosterone level was the main predictor of peripheral PWV in PA. Our data indicate aldosterone overproduction in PA does not preferentially affect central arterial system. Fibroproliferative effect of higher aldosterone levels lead to alteration of central-elastic as well as peripheral-muscular arteries with subsequent increase in its stiffness. (Rosa et al., 2012)

      Uric Acid

      A total of 5568 participants from

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