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Vascular Hypertrophy – 

     At the cellular level, hyperinsulinemia and insulin resistance commonly co-exist with “essential hypertension,” augmenting the overall cardiovascular risk profile.  In contrast, “secondary hypertension” does not lead to insulin resistance.  Patient follow-up (e.g., about every 4 to 6 weeks, including lab panels), with elevated fasting insulin usually demonstrates a higher correlation with subsequent development of hypertension at two-to threefold higher rate than control.  22  The association is not perfect; individual patients from ethnic groups with high prevalence of diabetes mellitus do not display higher incidences of hypertension.  Course, complex interactions among genetic, environmental, and other factors determine the clinical outcomes, because insulin’s ability to mediate (i.e., Latin-atus, to divide or sub-divide in the middle), glucose disposal can differ by as much as tenfold among individuals subjects, with normal range glucose tolerance.  

     Among the obese and morbid obese individuals tested, the degree of insulin resistance does not increase if hypertension is present.  This lack of additive effect suggests that hypertension, exogenous obesity, and diabetes mellitus may act independently, but along a final common pathway. 23

     Note:  Along with this important finding, a review of 25 prospective studies correlating plasma insulin levels with heart disease (CAD) did not support hyperinsulinemia by itself as a major cardiovascular risk factor.  In contrast, insulin resistance correlates closely with atherosclerosis, thrombogenesis, hypertension, obesity, and diabetes mellitus. 24

     Note:  Not surprising, given the several overlapping effects, hypertension may be “clustered” with obesity, dys-lipidemia, glucose intolerance, and type ll diabetes mellitus.  Sometimes, these conditions are lumped together as “metabolic X” or “insulin resistance syndrome.”

 

Risk Profiling - 

     Just by single B/P determinations alone, nearly one in every four adult Americans shows early signs of hypertension.  Each year, approximately 2 million new hypertensive patients are diagnosed and added to the pool of Americans who may benefit from antihypertensive intervention.  25 

     When assessing the hypertensive patient, the nurse practitioner, and/or clinician should seek and clearly articulate with the patient (or family members), the findings by:

  1. Confirm the existence and magnitude of hypertension,
  2. Assess the extent of possible organ damage,
  3. Evaluate for contributing comorbidities and risk factors,
  4. Screen for secondary causes of hypertension,
  5. Understand any special circumstances that may impact treatment over time and,
  6. Help create professional trust and the patient’s commitment for reducing cardiovascular risk issues over time. 

Note:  The most important components of the initial and follow-up visits in regards to the ambulatory settings should be the act of enumerating the importance.  

 

     In the National Health and Nutrition Examination Survey ll, the prevalence of hypertension (B/P > 160/95) was 2.9 times higher among patients who were overweight compared to those who were not.  Obesity brings a two-to six fold increase in the probability of developing hypertension 26 and may account for 65% to 78% of its attributing risk factors.  Also, upper-body or android fat patterns (e.g., apple-like), are more dangerous cardiovascular than lower-body or gynoid (e.g., pear-like), patterns. 27

 

     Smoking and alcohol daily use also raises the risk factors, and has been documented for contributing toward hypertension.  The jury has deliberated and return to the court with evidence-based-research through decades of clinical trials stating that “cigarette smoking directly and indirectly leads to endothelial (i.e., smooth layer of cells that forms the interior lining of the heart, and lymphatic vessels plus the cavities of the body), damage and accelerated atherosclerosis.” 28 According to the Institute findings:  epidemiologically, smoking was found negatively associated with B/P reading, relative body weight and physical activity during leisure; smoking was found positively associated with total cholesterol, psychological stress, and alcohol abuse. 29 Consuming three or more alcoholic drinks a day (≈40 g ethanol per day), increases B/P, even when controlling body mass index, cigarette smoking, and age factor, contribute toward the onset of “essential hypertension.“

 

Looking at Refractory Hypertension – 

 

     “Resistant” or refractory hypertension can be defined:  as failure to lower B/P to <140/90 mm Hg despite a regimen of >3 anti-hypertensive agents.  These phenomena may indeed occur from factors related to the prescribing clinician, or the patient, who may not be taking their anti-hypertension medications prescribed by the treating clinician.  The possibility of progression of the disease, and that it has not shown up through evidenced –based signs and/or symptoms.  Also, the possibility of all three factors working in combination, causing a “resistant’s.” 

    

      The differential diagnosis of refractory hypertension heavily depends on selective factors of primary care versus referral practice.  Whereas, partial compliance with prescribed regimens may figure prominently in primary care, most common cause of “resistant” hypertension is usually inappropriate or inadequate drug regimens in a referral practice. 30 

        

     A patient’s failure to adhere to prescribed medications are sometimes termed “partial compliance” or adherence; frequently reflects suboptimal knowledge of the regimen or of the importance of consistent medication taking. 31 When queried non-confrontationally, many patients acknowledge that a variety of “hassle” factors interfere, such as complex regimens, disruption of daily schedules, side effects, and cost issues.

 

     Strategies for the treating practitioner and/or clinician include: 

    

  1. Watching for non-attendees and non-responders. 
  2. Inquiring non-confrontationally about compliance barriers.
  3. Encouraging the development and use of the patient’s own medication-taking system. 
  4. Providing simple and clear instructions.
  5. Simplifying the regimen as much as possible.
  6. Guiding behavioral changes in small packets.
  7. Monitoring progress to goal, both in B/P and in compliance.
  8. Reinforcing desirable behaviors and outcomes whenever possible.
  9. Emphasizing the importance of “dose-timing” when appropriate, and customizing the regimen to the patient’s needs. 
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