Clinical Profiling: Natural History of Essential Hypertension 

Submitted by Dr. Gary D. Goldberg, PhD

Tags: clinical profiling essential hypertension health care Manuscript risk factors stress

Clinical Profiling: Natural History of Essential Hypertension 

Share Article:

Hypertension is a major cardiovascular risk factor that directly contributes to myocardial episodes such as abnormal wall motion, hypertrophies, and subsequently an infarction (MI).  Also noted, are cerebrovascular accidents (CVA), congestive heart failure (CHF), peripheral arterial insufficiency (PAI), and premature mortality.  Optimal and cost-effective management of the condition depends on careful diagnosis, treatment minimization, and optimized adherence to the selections of tests and treatment plans.  In addition, full patient commitment and adherence toward the medical and environmental regiment.

Background –

Of all the known cardiovascular risk factors, hypertension is the most prevalent:  it occurs in up to 40% of the United States population (approximately 60 million Americans), when using a threshold of 140/90 mmHg. 1 Hypertension is indeed the most common reason cited for office visits to American internists, and the most common indication for the use of prescription medication in the United States. 2  In 2008, direct costs of American anti-hypertensive management and treatment of its complications totaled near $30 billion. 3

Recent analysis suggests that hypertensive patients fall in two groups:  Approximately one-fourth consists of individuals under the age of 50 who are predominantly male and have a diastolic hypertension.  The remaining three-fourths are older than the age of 50, are slightly more than half (59%) women, and often display isolated systolic hypertension.  From Framingham’s data, the best predictors of coronary heart disease differ in the three age clusters:  <50 years old to 59 years old, and > 60 years old.  Among patients <50 years old, DBP predicted subsequent coronary heart disease better than SBP.  Among patients 50 to 59, SBP, DBP, and pulse pressure served equally well as predictors.  At age 60 years and older, pulse pressure was the best predictor followed by SBP. 4   

Based on its high prevalence within our societies today, “essential hypertension“ diagnosis with responsiveness to treatment plans, and its financial impact just within the United States alone, deserves everyone’s attention.  

A Short Historical Perspective –

The first repot of direct B/P measurement dates back to 1726, when Stephen Hales, cannulated a horse’s crural artery and assessed the height of the blood column before and after hemorrhage.  The monaural stethoscope appeared in the early nineteenth century; the binaural stethoscope came to America in 1852, and the introduction of the sphygmomanometer cuff in 1896. Dr. Nikolai Korotkoff (Russian physician), reported the auscultatory method of measuring arterial pressure in 1905, showing the measurement of diastolic pressure and systolic levels for the first time. 5 

 Early efforts to reduce extreme hypertension by adrenalectomy or sympathectomy frequently led to disastrous results.  Some early authorities concluded that such hypertension was not merely “primary” but “essential,” because brusque pressure reductions were deleterious (e.g., harmful to health).    A big breakthrough came on experimental hypertension through Dr. Harry Goldblatt, (U.S. pathologist, in 1896-1977).  His description of the renal artery clip model was revealed and pantone in 1934.  Thus began a series of discoveries of one intriguing complexity after another:  renin, angiotensin, atrial natriuretic factor, cation fluxes, endothelial factors, vascular remodeling, central monoaminergic, and hypothalamic factors, and others. 6  

In 1960 Dr. Irvine H. Page, (chemist, biomedical leader in academic medicine), formed hypotheses and proposed his “mosaic theory” of hypertension:  a disease of regulation in which abnormal regulatory systems fail to reduce B/P once it is elevated.  More precisely, the control of arterial pressure was likened to a kaleidoscope of interlocking, dynamic equilibria that determined the net effect while continually shifting from one set of relations to another.  Although the regulatory factors were limited, their changing interplay was not.  The strength of the model lies in its adaptability to new data.  Based on the premise that there is likely to be no unique cause for most cases of hypertension but many potentially contributing factors, one struggles to integrate all the possible components.    His “mosaic concept” offers a way to combine diverse factor from genetic and physiologic to emotional and environmental.  7 Many of the medications that were originally developed during the late 1960’s and early 1970’s for other purposes rather then hypertension, were later applied using Professor Page’s theorem as an afterthought or via serendipity (i.e., discoveries by accident). 

Despite the many modern advances, hypertension still largely remains a “triple paradox” by which firstly, the condition, easy to diagnose but often remains undetected. Secondly, relatively simple to treat, but too often remains untreated, and lastly, for which despite available and potent drugs, treatment plans for many are all too often ineffective. 

Pathophysiology – 

There are numerous factors affecting B/P control and they are complex in themselves with their interrelationships.   Striking examples of the interdependencies include observations that insulin resistance precedes hypertension in individual patients genetically predisposed to it.  In addition, hyperinsulinemia, salt sensitivity, obesity, and increased sympathetic drives are covariant. 

The Genetic Factors –   

Some physicians, chemists, and geneticist have called B/P “a quantitative trait” with environmental and genetic determinants;8 “essential hypertension” occupies one extreme of B/P distribution only.  Variations in B/P represent the combined effects of multiple genes rather than a single gene disorder with discrete separation. 9  A strong family history (e.g., >2  first-degree relatives with hypertension before age 55 years), may predict a future occurrence of hypertension with a relative risk factor (RR) of 3.8. 10  Obesity, related in hypertension and the associated metabolic syndrome occur from childhood through to adult life, underscoring the importance of early prevention.  11  In the search, for genetic determinates appear to be handicapped by the absence of a biomarkers to identify pre-hypertensive individuals before the pressure rises because, the initiating factor are rendered unrecognizable at this time. 

The Sodium factors –

In ancient primitive societies, the diet was indeed characterized by low salt intake (e.g., 10 to 30 mmol per day), but with a high intake of potassium (K₊).  This was due to complete native living and quantitative intake.  In such settings, hypertension was rarely found and documented.  In today’s environment, only a subset of people (20% to 50% appears to be salt sensitive by showing a pressor response when fed a diet of more than 50 mEq sodium per day 12 (e.g., ≈ ½ tsp. of salt per day, because 1 tsp. of salt = 6 g salt = 2.4 g sodium = 104 mEq sodium = 104 mmol sodium).  The Food and Nutrition Board of the National Academy of Science (FNB-NAS), estimates that an intake of no more than 500 mg of sodium a day is needed for health; the average American diet contains more than 4,500 mg a day. 13 That means over 9x’s more sodium intake within the North American diet.  In contrast, the American Heart Association (AHA) recommends that a daily consumption of sodium not exceed 2,400 mg, 14 Even with this current analyses, Americans are consuming over  47% more salt in there daily diet.  Americans are close to doubling the recommended intake of sodium, + less manual daily exercise, with the added stress of suburbia.  Also, add in the list from convenience of frozen and/or box meals (e.g., sodium is always added as a preservative and/or shelf life stabilizer).  From current medical epidemiology records, over 43 million people in the U.S. have pre-hyperinsulinemia, or have been diagnosed and are taking an anti-hypertensive medication, which is about 1/3rd or over 25% of the adult population alone. 15 

The Obesity and Morbid Obesity Factors

In the mid 20th century, the average American diet shifted from one based on fresh, minimally processed vegetable foods to one based on animal products and highly refined, processed foods.  As a result, today Americans consume far more calories, fats, cholesterol, refined sugars, animal protein, sodium, alcohol, and far less fiber and starch than is healthful. 

In addition, noted from the beginning of the availability for most Americans, the World Wide Web has made environmental changes within our populous, through a sedentary lifestyle, networking, social gathering, and labor force (e.g., includes both blue and white-collar working force).  In the U.S. alone, two out of every three adults are overweight (e.g., defined as body mass index {BMI} of 25 to 30), or obese (BMI > 30), compared with fewer than one in four in the early 1960s. 16  The consequences include a substantial decrease in life expectancy and an increase in morbidity similar in magnitude to the burden imposed by smoking cessation. 17

Obesity as well as morbid obesity conditions is indeed a complex, multifactorial disorder, but a element common to all cases is a positive energy balance in which more calories are consumed than expended through the body.  The amounts of excess calories are stored in body fat; each pound of “adipose tissue” (e.g., tissue containing fat cells), contains 3,500 calories. 18  Weight loss, can chiefly be accomplished by achieving a negative energy balance.  Before your patients proceed, have the treating clinician (i.e., NP, and/or physician), order a lab panel consisting of creatinine-serum, electrolytes-serum, and bun-serum.  These will R/O abnormalities and raise any suspicion for organ target anomalies.      

The Urinary Excretion of Sodium Factor -

In healthy individuals, homeostasis (i.e., a state of equilibrium or balance between opposing pressures), will prevail.  When the B/P rises, sodium and water excretion via the kidney increases to return B/P to baseline.  This process is termed “pressure natriuresis.”  A much different story appears among the hypertensive and pre-hypertensive patients.  In addition, renal blood flow (RBF) appears reduced compared to normotensives.  The peritubular capillary blood with less sodium and water develops higher oncotic (i.e., cause by edema, or swelling), pressure and facilitates sodium re-absorption, leading to a higher blood volume and a higher B/P.  Therefore, pressure “natriuresis” occurs but only to sustain B/P at a higher level. 

The Sympathetic Nervous System Factor – 

In parallel with the renin-angiotensin system, the sympathetic (i.e., denotes a part of the autonomic nervous system), nervous system (SNS) may couple with high sodium intake to raise the B/P.  Often, stress activates the SNS, especially in patients genetically or environmentally predisposed to respond with increased levels of epinephrine, norepinephrine, and neuropeptide. 19 

Increased sympathetic activity serves as an “initiator” (i.e., start of a chemical or enzymatic reaction), and sustainer for hypertension, which promotes the development of left ventricular hypertrophy (LVH), and has been known to predispose to dysrhythmias and sudden death in individuals.  The most common pattern is one of greater anger and hostility, along with a greater suppression of these emotions.  Such hyperreactivity is demonstrable among hypertensive patients and their normotensive offspring when compared to normal controls. 20  The role of psychological stress remains largely undefined.  Possibly, their effect depends on complex interactions among the nature of the stressor, and the individual’s perception of the stress. 21 This area of physiology and neuro-psychology remains under investigation. 

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. 

Stepped Care Plans

Over the past two decades, the concept of progressive stepped care has evolved from a narrow set of incremental options to a broader set of guidelines for nursing practitioners’ and treating physicians, by the Joint National Committee on Hypertension Vl 32  (JNCH Vl):   

  • Step 1 – Prescribe lifestyle modifications, including weight reduction, moderated alcohol intake, regular physical exercise, reduced sodium intake, and smoking cessation.
  • Step 2 – If response is inadequate, continue the lifestyle modification, and add mono-therapy for mild to moderate (stage 1-2) hypertension with thiazide diuretics or β -blockers, unless there is a contraindication.  Other agents {e.g., angiotensin-converting enzyme (ACE) inhibitors, calcium antagonists, α-blockers, and α-β-blockers} are satisfactory substitutes for patients with contraindications, although the long-term net benefits of these medications are not fully established. 
  • Step 3 – If response to initial treatment is inadequate, increases medication dose, substitute another anti-hypertensive drug, or add a second agent from a different drug class. 
  • Step 4 – If response is still inadequate, add a second or third agent from a different drug class.  Including an appropriate diuretic (if not already administered). 

Note: In the spirit of academic fullness, the author has read through the entire manuscript  and found a lack or limited sensitivity to three important issues:  First, was the hemodynamic diversity among hypertensives, also secondly, the negative metabolic effects of thiazides and β-blockers, and thirdly, the need for direct testing of stepped care versus alternative approaches.  The author’s final thought on the original published manual from JNCH Vl:  Use this manuscript as a guideline only, and tailor the “Steps” to your own needs, due to the variables of patients and environmental surroundings. 

Conclusion;  

Looking Toward the Near Future –       

As one tries to think about the future of hypertension profiling and management, there will continue to be exciting developments in three major areas.  The author believes:  first, basic science advances in molecular and genetic medicine will likely shed light on the initial and initiating events that cause the deranged physiology of hypertension.  Secondly, evolving insights from epidemiology will refine definitions of high-risk groups and clustering to focus efforts that produce the greatest positive yield for a population, despite resource constraints.  Finally, the development of more effective and better-tolerated anti-hypertensive medications will almost certainly combine with more sophisticated behavioral approaches to enhance adherence.   Patients may indeed, enjoy a fuller and more beneficial life style with less risk reductions while under the care and medication management protocol. 

References

  1. Pardell, H., Tresserras, R., Armario, P., et al.  Pharmacoeconomic considerations in the management of hypertension.  Drugs 2001; 59: 13-20; discussion 39-40.
  2. Baum, D., Kennedy, DL. Knapp, EE. et al.  Prescription drug use in 2001, and changes over time.  Med Care 2002; 27: 105-113. Cited again in 2008, revised edition, ACP Medicine Textbook of Cardiovascular Medicine:  © 2008, by Lippincott Williams & Wilkins Publishing Co.  
  3. Levy, D., Larson, MG. Vasan, RS., et al.  (revised), The progression from hypertension to congestive heart failure.  JAMA 2009; 275:  1557-1562. 
  4. Franklin, SS., Khan, SA. Wong, ND.  et al.  Ageing and hypertension:  the assessment of blood pressure indices in predicting coronary heart disease.  J Hypertens 2006; 18:S30-S36.  Cited again in:  The Framingham’s heart study results in:  Circulation 2008; 100: 354-360.
  5. Segall, HN.  How Korotkoff, the surgeon, discovered the auscultatory method of measuring arterial pressure.  Ann Intern Med 1975; 83: 561-562.
  6. Goldblatt, H., Lynch, J., Hansel, RF.  et al.  Studies on experimental hypertension. I.  The production of persistent elevation of systolic blood pressure by means of renal ischemia.  J Exp Med 1943; 59: 347-379.
  7. Page, IH. The mosaic theory of hypertension.  In Bock KD, Cottier, PT, Eds.  Essential hypertension.  Berlin:  Springer-Verlag, 1960: 1-9.  Also, cited in:  Hypertension, Amer H Assoc 1991; 18; 443-445. http://hyper.ahajournals.org//
  8. Hamet, P., Pausova, Z., Adarichev, V., et al.  Hypertension:  genes and environment.  J Hypertens 1989; 16: 397-418.
  9. Brown, M.J. The causes of essential hypertension.  Br J Clin Pharmacology2000; 42:21-27.
  10. Williams, R., Hunt, S., Hopkins, P., et al.  Genetic basis of familial dyslipidemia and hypertension:  15-year results from Utah.  Am J Hypertens 2000; 7: 319S-327S.
  11. Williams, R., Hunt, S., Hopkins, P., et al.  Genetic basis of familial dyslipidemia and hypertension: 
  12. Elliott, P., Stamler, J., Nichols, R., et al.  INTERSALT revisited further analyses of 24-hour sodium excretion and blood pressure within and across populations.  B M J 2001; 312:  1248.
  13. Sacks, F., Svetkey, L., Vollmer, W., et al.  Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet.  N Engl J Med 344:3, 2006. 
  14. Krauss, R., Eckel, R., Howard, B., et al: AHA dietary guidelines:  revisions 2000; a statement for healthcare professionals from the nutritional committee of the American Heart Association.  Circul 102: 2284, 2000.  Cited again, in 2007; AHA, dietary guidelines, revisited @http://americanheart,org/dietary guidelines//
  15. Chockalingam, A.  2008; “World Hypertension Day and Global awareness.”   An umbrella organization of 85 national hypertension societies and leagues.  Can J Cardio 24(6):  4441-444.  Also, cited in 2010; U.S. Department of Health & Human Services @ http://www.hhs.gov Also  indorsed by the Amer H Assoc on Feb. 22, 2010 via teleconference with Fleming, D., MD dir. Public health, Seattle/King County, WA. Also, U.S Food and Drug Admin. Willett, W., MD, DPH, Stare, J., Prof. of Epidemiology and Nutrition at Harvard School of Public Health, Boston; “A Population-Based Policy and System Change Approach to Prevent and Control Hypertension.”  © 2010; Scout News, LLC.  High Blood Pressure a ‘Neglected Disease’.  
  16. Manson, J.E., Bassuk, S.S., Obesity in the United States.  A fresh look at its high toll.  JAMA 2004; 289:229.
  17. Peeters, A., Barendregt, J., Willekens, F., et al.  Obesity in adulthood and its consequences for life expectancy:  a life-table analysis.  Ann Intern Med2004; 138: 24. Also, cited in 2009; World Health Org (WHO) @http://www.who.int./dietphysicalactivity/public/obesity/en/  Obesity and overweight Facts.
  18. Nielsen, S. J., Popkin, B.M:  Patterns and trends in food portion sizes. 2003; JAMA 289:450. 
  19. Erlinge, D., Ekman, R., Thulin, T., et al.  Neuropeptide Y-like immunoreactivity and hypertension.  J Hypertens 1992; 10:1221-1225.
  20. Widgren, B.R., Wikstrand, J. Berglund, G. et al.  Increased response to physical and mental stress in men with hypertensive parents.  Hypertension 1992; 20: 606-611.  Cited again in:  Hypertens 2002; 18: 520-524.
  21. Pickering, T.G. Does psychological stress contribute to the development of hypertension and coronary heart disease?  Eur J Clin Pharmacol 2004; 49:S1-S6.
  22. Haffner, S.M., Ferrannini, E., Mazda, H.P., Clustering of cardiovascular risk factors in confirmed prehypertensive individuals, ACP Medicine, Textbook of Cardiovascular Medicine:  ©2006 by Lippincott Williams & Wilkins.
  23. Bonora, E., Bonadonna, R.C.  In vivo glucose metabolism in obsess and type ll and diabetic subjects with or without hypertension.  Diabetes 1999; 43:764-772.  Revised in the ACP Medicine, Textbook of Cardiovascular Medicine:  ©2006 edition by Lippincott…
  24. ACP Medicine, Textbook of Cardiovascular Medicine: Pathophysiology Studies. ©2006 by Lippincott…
  25. Coroni-Huntly, J., LaCroix, A., Havlik, R. Impact of hypertension in the United States: the National Health and Nutrition Examination Survey; Epidemiologic report in:  Arch Intern Med 2007; 149:780-788  http://archinte.ama.assn.org/.  
  26. Kannel, W.B. Framingham study insights into hypertensive risk of cardiovascular disease. Dept. of Med. Evans Memorial Research Found. Boston Univ. School of Medicine. MA.   Hypertens Res1995; 18:181-196.Cited again in: JAMA 2008; 300(21): 2545-2547. http://jama.ama.assn.org/
  27. Sprecher, D. How deadly is the “deadly quartet” A post-CABG evaluation?  J Amer Coll Card. 2009: Vol 36, Issue 4, Pg. 1159-1165. Science Direct, Elsevier, B.V.  
  28. National High Blood Pressure Education Program Working Group.  Working Group reports on hypertension in diabetes.  Bethesda, MD:  National Heart, Lung, and Blood Institute, and the National Institutes of Health, 1995, 2000, 2004. Web site: http:// www.guideline.gov// 
  29. National High Blood Pressure Education Program Working Group…2004; http://www.guideline.gov//
  30. Setaro JF, Black HR. Refractory hypertension. N Engl J Med 1992; 327:543–547.http://content.nejm.org// Revised in 2006; by permission from N Engl J Med © approved. Marvin, M., Setaro, J.F. July 27, 2006. Vol. 355(4)385-392. 
  31. Rudd, P., Marshall, G.  Anti-hypertensive medication-taking behavior: out/patient patterns and implications.  In:  Rosenfeld, J. Ed.  (Med. Textbook):  Hypertension control in the community.  London:  John Libby & Co. 1995; 232-236.
  32. Tifft, Charles MD. Joint National Committee Vl: Individualized Versus Indiscriminate Therapy for Hypertension.  ©2000; 2:243-246. By Current Science Inc. Boston, MA http://springerlink.com//

Short Bio of Dr. Gary D. Goldberg, PhD 

Over 30 years experience in the Medical field, At UCLA and Pacific Hospital of the Valley, as a Chief Technologist and Analyst, Visiting Professor and Instructor for continuing education at UCLA School of Nursing and Writer/Speaker at the School of Medicine from 1995-2008.

From 2003-2008 Dr. Goldberg has collaborated and published through Blackwell Publishing Co. (Medical Division), and Journal of American College of Cardiology plus 15, published abstracts through UCLA Dept. of Internal Medicine and the Dept. of Cardiology.

Current title: Clinical Professor of Medical Education with Angeles College of Nursing, in Los Angeles, Ca.  

Dr. Goldberg has written two major academic course textbooks for Angele College of Nursing and has represented advanced nursing education course curriculum through the State Dept. of California and approved by the ANA for CEU(s) and the AMA CMU Level 1 Credit for physicians.

His wife, Cindy L. Capute-Goldberg, has been a registered nurse for over 17 years and has managed a 200-bed acute care facility with over 100, professional nurses from RN’s through CNA in the Los Angeles area.  She has co-authored with Dr. Goldberg in 2005, a manuscript presented to the Cardiology-Electrophysiology Research Group (i.e., DMPG), that has changed the dynamics of electro-static reading with regards to acute atrial anomalies. 

This finding allowed the author to publish the ‘Goldberg Protocol’  for Cardiac placements in the field and under the Dept. of Medicine Chair, in using a tilt-table with the 12 +3 Leads or the vector positioning for additional cardiac patient information.

To reach Dr. Gary D. Goldberg, for comments and/or consultation, please use e-mail address: [email protected] or cell phone contact:  818-610-9017.