Dr. Buhler talks about ProArgi-9 Plus
Dr. Craig Buhler, D.C. shares advice for other physicians on how to use ProArgi-9 Plus in their business and how to expand their opportunity. Dr. Buhler has been the team chiropractor for the NBA Utah Jazz team.
Archive for March, 2010
Dr. Buhler talks about ProArgi-9 Plus
On March - 15 - 2010
BPro (by HealthStats): A Cardio Pulse Wave Analyzer – science and research
On March - 14 - 2010
(You may want to bookmark this page for easy future reference)
BPro (by HealthStats): A Cardio Pulse Wave Analyzer – science and research
Below are a number of scientific research articles on Cardio Pulse Wave analysis technology. Although it is only a sample of the vast amount of research, it will give you some a good idea of what research is available.
Pulse wave analysis: from the basic sciences to clinical applications
Pulse wave analysis and arterial stiffness.
Arterial stiffness and stroke in hypertension: therapeutic implications for stroke prevention.
Antihypertensive therapy and wave reflections
Analyzing the radial pulse waveform: narrowing the gap between blood pressure and outcomes.
Systolic blood pressure, pulse pressure and arterial stiffness as cardiovascular risk factors.
Mechanical principles. Arterial stiffness and wave reflection.
Arterial pressure waveforms in hypertension.
Aortic pulse wave velocity: an independent marker of cardiovascular risk.
Arterial stiffness and cardiovascular outcome.
The indirect assessment of arterial compliance in hypertension patients by tonometric sphygmography
Measurement of pulse wave “augmentation index (AI) “and its clinical application
Pulse wave analysis in the assessment of patients with left ventricular assist device.
Large-artery stiffness, hypertension and cardiovascular risk in older patients.
Mechanisms, pathophysiology, and therapy of arterial stiffness.
Noninvasive assessment of arterial stiffness and risk of atherosclerotic events.
Clinical value of the study of stiffness of arterial wall. Part I
Arterial hemodynamics and pulse wave propagation
Arterial compliance (stiffness) as a marker of subclinical atherosclerosis
Arterial stiffness in diabetes and the metabolic syndrome: a pathway to cardiovascular disease.
Influence of arterial pulse and reflected waves on blood pressure and cardiac function.
Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms.
BPro (by HealthStats): A Cardio Pulse Wave Analyzer – medical device information
On March - 13 - 2010
(You might want to bookmark this page so it is easy for your to find in the future.)
BPro (by HealthStats): A Cardio Pulse Wave Analyzer – medical device information
When you go to the following link below it will take you to the governments FDA site that has the document showing the registration of the BPro (which is the BPro and A-Pulse software (by HealthStats) as found in this document): A Cardio Pulse Wave Analyzer as a class II medical device. Please click on the link below to find this document:
Pulsology Rediscovered (Cardio Pulse Wave)
On March - 12 - 2010
Pulsology Rediscovered
Commentary on the Conduit Artery Function Evaluation (CAFE) Study
(Full original article with notations, references and links found here: http://www.circ.ahajournals.org/cgi/content/full/113/9/1162)
Suzanne Oparil, MD; Joseph L. Izzo, Jr, MD
From the Vascular Biology and Hypertension Program (S.O.), Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, and Erie County Medical Center and the Division of Clinical Pharmacology (J.L.I.), Department of Medicine, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY.
Correspondence to Suzanne Oparil, MD, Vascular Biology and Hypertension Program, University of Alabama at Birmingham, 703 19th St S, ZRB 1034, Birmingham, AL 35294-0007.
Nearly everything that modern practicing clinicians know about hypertension and its treatment is based on simple noninvasive measurement of brachial artery blood pressure. As the study by Williams and colleagues1 illustrates, however, additional knowledge of pulse-wave characteristics may be important in the future to fully assess optimal cardiovascular drug therapy.
The study of pulse-wave characteristics is far older than the study of absolute pressure values, dating back thousands of years to the Chinese masters who used their fingertips and their powers of observation to associate “hardening of the pulse” with adverse outcomes in people who ingested too much salt. These qualitative observations were less well developed in Western medicine, but as early as the 1870s, the sphygmocardiogram was developed as a reproduction of a peripheral pulse wave on a rotating drum via a tonometer attached to a levered stylus.1a Morrell and other early investigators were clearly able to differentiate the effects of nitrovasodilators from digitalis using this early equipment, but interpretations remained largely qualitative. Within a few decades, the development of sphygmomanometry by Korotkovand Riva-Rocci allowed quantitation of brachial cuff blood pressures, and the more descriptive methods largely disappeared.
Article p 1213
Indeed, brachial cuff blood pressure has become an enduring clinical variable. Actuarial data from the life insurance industry and subsequent prospective observational data have clearly shown that hypertension, or elevated cuff blood pressure, is closely related to many forms of cardiovascular disease.2–4 Most recently, a very large meta-analysis by the Prospective Studies Collaborators that involved almost 1 million persons enrolled in 61 prospective observational studies demonstrated a log-linear relationship between cuff systolic or diastolic blood pressure and mortality due to ischemic heart disease or stroke in middle-aged and elderly adults who did not have overt vascular disease at the beginning of the observation period.5
Abundant clinical trial data indicate that lowering cuff blood pressure with antihypertensive drugs effectively reduces the risk of a variety of cardiovascular outcomes, including cardiovascular death, as well as total mortality.6–10 Regarding the benefits of individual drug classes, a meta-analysis of data by the Blood Pressure Lowering Treatment Trialists’ Collaboration from randomized, controlled trials did not show significant differences in total major cardiovascular events among regimens based on angiotensin-converting enzyme inhibitors, calcium antagonists, diuretics, or ß-blockers, as long as similar cuff blood pressure reductions were achieved, although there were some differences in cause-specific outcomes.10 When specifically tested in randomized trials, however, ß-blockers have fallen short of other therapies in preventing hypertensive complications. The Losartan Intervention For Endpoint reduction (LIFE)11 and the Anglo-Scandinavian Cardiovascular Outcomes (ASCOT)12 trials compared active treatments based on an angiotensin receptor blocker (losartan with or without a diuretic) or a calcium antagonist (amlodipine with or without perindopril) with treatment based on a ß-blocker (atenolol). Brachial cuff blood pressure differences between the treatment arms in LIFE and ASCOT were very small and were judged by the investigators to be insufficient to explain the large treatment-related differences in outcomes, which favored the other drugs over the ß-blocker. However, the editorial accompanying the ASCOT main results publication attributes the benefits of amlodipine-based treatment to superior cuff blood pressure reduction,13 whereas others, including the main investigators of the ASCOT trial, have adduced effects beyond blood pressure lowering to explain the results.14
In this issue, Williams et al1 describe results of the Conduit Artery Function Evaluation (CAFE) study, a substudy of the ASCOT trial, which compared the effects of the ASCOT blood pressure-lowering regimens on central aortic pressure and hemodynamics in more than 2000 patients in 5 ASCOT centers. The CAFE study, using radial applanation tonometry and pulse-wave analysis to calculate derived central blood pressures using the Sphygmacor system, describes a subtle but important difference in arterial pulses in hypertensive patients treated with ß-blockers compared with those taking calcium antagonists. The central finding of the CAFE study is that ß-blockers do not lower central systolic pressure as much as calcium antagonists, an observation that is predictable based on the relative inability of ß-blockers to reduce the magnitude of the reflection (augmentation) wave. This observation is similar to that of Morgan and colleagues,15 who used a 5-way crossover study to determine that only ß-blockers (compared with thiazides, angiotensin-converting enzyme inhibitors, and calcium antagonists) increased the placebo-subtracted magnitude of the reflected wave. Compared with ß-blockers, calcium antagonists and other vasodilators are thus more effective in reducing central systolic pressure, cardiac afterload, and left ventricular mass.16 The results from the CAFE study parallel those of the LIFE trial, in which angiotensin receptor blocker-based therapy was more effective than ß-blocker-based therapy in reducing left ventricular hypertrophy and its consequences.11
The present application of “pulsology” to clinical trials would no doubt please the Chinese masters and the sphygmocardiologists. With ß-blocker-based therapy, as with aging or hypertension in general, the arterial pulse taken at the wrist is more “sustained,” because of a larger reflected wave in late systole. The absence of “pulsology” in Western medical curricula probably contributes to the skepticism of many physicians, along with the ongoing debate over the validity of the techniques currently used.
Although technical questions remain problematic in interpretation of the CAFE results, the overall conclusions drawn by the investigators are reasonably conservative. Radial tonometry, without question, produces a high-fidelity pulse contour that is identical to high-frequency catheter-based data. It easily can be shown that the radial or brachial systolic pulse contour in aging is essentially a “sustained” systolic pulse composed of an increased first peak followed by a secondary shoulder peak (due to wave reflection) that is generally lower.17 In contrast, the central systolic contour in aging or hypertension is composed of a lower first peak followed by a higher second systolic peak (augmentation pressure). It has been proposed that a generalized transfer function can be applied to a radial tonogram to yield a derived central pulse waveform18; this technique has been well validated to estimate peak central systolic blood pressure.19 Although there is ongoing debate over whether the transfer function can be applied to interindividual comparisons,20 in the CAFE study, each individual was compared with his/her own baseline, so the data are probably valid. Other alternative explanations for the differences between treatment arms in CAFE also exist, including differences in 24-hour blood pressure control or other “tissue” mechanisms yet to be described.
What is the overall value of the CAFE study? At the very least, it opens our eyes to alternative explanations beyond the reach of conventional sphygmomanometry. In the context of clinical trials, radial tonometry adds to our knowledge of the pharmacodynamic effects of vasoactive drugs. Present findings have importance in describing why some classes of antihypertensive agents yield better profiles of target-organ protection than others. For example, the observation that ß-blockers do not reduce central systolic pressure as much as most other antihypertensive drug classes may account for the finding from meta-analyses of antihypertensive trials that ß-blocker-based treatment is no better than placebo for prevention of cardiovascular disease.21,22 This has led many authorities to recommend that ß-blockers not be prescribed as first-line treatment for hypertensive treatment patients in the absence of compelling indications (heart failure, post myocardial infarction, high coronary heart disease risk, angina) for their use. Whether radial tonometry should be performed routinely in individual patients as a diagnostic or therapeutic indicator, however, remains a matter of considerable debate. At present, the technique is probably not quite ready for “prime time” in routine clinical practice.
Full original article with notations, references and links found here: http://www.circ.ahajournals.org/cgi/content/full/113/9/1162
Vitamin D a predictor of health
On March - 11 - 2010
Partial list of scientific studies on L-Arginine
On March - 10 - 2010
Scientific studies on L-Arginine
(Please click “HERE” then you can easily add this page to your favorites so it is simple to find as a resource)
Below are listed a number of scientific studies and article links on L-Arginine research. Please bookmark this page for easy reference in the future.
Anti-hypertensive nutraceuticals and functional foods
Nitric oxide and vascular insulin resistance
The impact of oral L-arginine supplementation on acute smoking-induced endothelial injury and arterial performance
Nitric Oxide, NAD(P)H Oxidase and Atherosclerosis.
Recent Advances on the Roles of NO in Cancer and Chronic Inflammatory Disorders
Oral l-arginine supplementation improves endothelial function and ameliorates insulin sensitivity and inflammation in cardiopathic nondiabetic patients after an aortocoronary bypass
Aged garlic extract supplemented with B vitamins, folic acid and l-arginine retards the progression of subclinical atherosclerosis: A randomized clinical trial
Anorexia nervosa: A role for L-arginine supplementation in cardiovascular risk factors?
Nitric Oxide as an Initiator of Brain Lesions During the Development of Alzheimer Disease.
Effects of neuronal nitric oxide synthase on human coronary artery diameter and blood flow in vivo.
Novel risk factors for cardiovascular disease and tobacco smoke
Participation of nitric oxide in different models of experimental hypertension.
The role of the L-arginine-nitric oxide pathway in preeclampsia.
Variation in L-arginine intake follow demographics and lifestyle factors that may impact cardiovascular disease risk.
Increase in fasting vascular endothelial function after short-term oral L-arginine is effective when baseline flow-mediated dilation is low: a meta-analysis of randomized controlled trials.
Beneficial effects of autologous bone marrow cell infusion and antioxidants/L-arginine in patients with chronic critical limb ischemia.
Arginine metabolism and nutrition in growth, health and disease.
L-arginine analogs–inactive markers or active agents in atherogenesis?
Endogenous nitric oxide synthase inhibitors, arterial hemodynamics, and subclinical vascular disease: the PREVENCION Study.
L-arginine inhibits isoproterenol-induced cardiac hypertrophy through nitric oxide and polyamine pathways.
Effects of nitric oxide and superoxide on relaxation in human artery and vein.
Effect of L-arginine on circulating endothelial progenitor cells in hypercholesterolemic rabbits.
Participation of nitric oxide in different models of experimental hypertension.
Roles of oxidants, nitric oxide, and asymmetric dimethylarginine in endothelial function.
L-arginine analogs–inactive markers or active agents in atherogenesis?
Protective effects of L-arginine against ischemia-reperfusion injury in non-heart beating rat liver graft.
[Endothelium and nitric oxide]
L-Arginine prevents metabolic effects of high glucose in diabetic mice.
Depression and cardiovascular disease: role of nitric oxid.
L-arginine protects from pringle manoeuvere of ischemia-reperfusion induced liver injury
Effect of long term oral administration of L-arginine on experimentally produced myocardial ischemia in rabbits
L-Arginine therapy in cardiovascular pathologies: beneficial or dangerous?
The endothelium as a target in renal diseases.
Pycnogenol, French maritime pine bark extract, augments endothelium-dependent vasodilation in humans
Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals
Inhibitory effects of endogenous L-arginine analogues on nitric oxide synthesis in platelets: role in platelet hyperaggregability in
Endogenous nitric oxide attenuates neutrally mediated cutaneous vasoconstriction.
Induction of insulin secretion in engineered liver cells by nitric oxide
Nitric oxide deficiency in chronic kidney disease
Plasma asymmetric dimethylarginine and L-arginine levels in patients with cardiac syndrome X.
Intracarotid L-arginine reverses motor evoked potential changes in experimental cerebral vasospasm.
L-arginine transporters in cardiovascular disease: a novel therapeutic target
Effect of inhibition of neuronal nitric oxide synthase and L-arginine supplementation on renal ischaemia-reperfusion injury and the renal nitric oxide system
Concomitant treatment with oral L-arginine improves the efficacy of surgical angiogenesis in patients with severe diffuse coronary artery disease: the Endothelial Modulation in Angiogenic Therapy randomized controlled trial
Role of nitric oxide in inflammatory diseases
Obesity reduces the bioavailability of nitric oxide in juveniles
Clinical use of nitric oxide donors and L-arginine in obstetrics
Whole body nitric oxide production is not decreased in patients with coronary atherosclerosis but is inversely related to plasma homocysteine
L-arginine infusion decreases plasma total homocysteine concentrations through increased nitric oxide production and decreased oxidative status in Type II diabetic patients
Decreased whole body endogenous nitric oxide production in patients with primary pulmonary hypertension.
Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: implications for nitric oxide production
Nitric oxide in health and disease of the nervous system
Endogenous nitric oxide synthesis: biological functions and pathophysiology
Vascular endothelium and nitric oxide in childhood hypertension
Clinical significance of nitric oxide in hypertension]
Nitric oxide, L-arginine and the kidney. Experimental studies of new therapy approaches]
The role of nitric oxide in hypertension and renal disease progression
Nitric oxide, L-arginine and the kidney. Experimental studies of new therapy approaches]
Therapeutic potential of nitric oxide donors in the prevention and treatment of atherosclerosis
Coronary endothelial vasodilator dysfunction: clinical relevance and therapeutic implications
Cutaneous neuronal nitric oxide is specifically decreased in postural tachycardia syndrome
The prophylactic effect of L-arginine in acute ischaemic colitis in a rat model of ischaemia/reperfusion injury
The L-arginine paradox: Importance of the L-arginine/asymmetrical dimethylarginine ratio
Mechanisms of disease: L-arginine in coronary atherosclerosis–a clinical perspective.
L-Arginine in coronary atherosclerosis
Effects of L-arginine on the endogenous angiogenic response in a model of hypercholesterolemia
L-arginine in cardiovascular disease: dream or reality?
L-Arginine, the substrate for NO synthesis: an alternative treatment for premature atherosclerosis?
Dan Higginson endorsed training – notes for countries outside the USA
On March - 9 - 2010
I have recieved a couple of questions regarding the Dan Higginson endorsed founders training site www.dhfounderstraining.com and the challenge of signing up if you do not live in the USA. Below are the instructions for you to be able to register for the training when you do not live in the USA.
So what are you waiting for? Follow these instructions below and sign up now. (To listen to the original introduction to this training go to http://ericglenn.com/2010/03/dan-higginson-ceo-training-endorsement/)
There are two different ways for someone outside the United States to enroll in our training. They are:
1. When filling out the information page about the student (name address phone number) if the student who lives outside the US will simply enter their address and then when it asks for State they can enter Utah. This will allow them to enroll. All other information needs to be correct so we have a way of contacting them.
2. The second way is for the student to call 801-769-8323. This is the telephone number for technical support. They can enroll manually over the phone this way. Everything works the same.
The reason for this is each country has a code for credit card processing and we are in the process of adding each country code but it will take some time to get this done. In the meantime the above two methods will allow them to enroll if they are outside the US.
L Arginine After a Heart Attack
On March - 9 - 2010
L Arginine After a Heart Attack
Dr. Joe Prendergast addresses the question of using L-Arginine after heart attacks and with heart conditions. Great information for those that might have this question. It is very instructive and fortunate that we can have an individual that is so highly regarded as Dr. Prendergast help us understand the why of ProArgi9 Plus.
Eric Glenn, Communication Importance
On March - 8 - 2010
Eric Glenn, Communication Importance
I was asked by Synergy to come be filmed on a few short cuts about communication in business. Here is one of the three videos that was recorded. Communication to family, friends, business associates and to the public in general are all important and each are better served with their own best form of communication. (You know I listen to mysef and wonder at times why I try to cover and say to much at once…the message gets lost when you do that…so learn from my mistakes!!)
Diabetic Neuropathy and L-Arginine
On March - 7 - 2010
Diabetic Neuropathy and L-Arginine
This is a short video by Dr. Joe Prendergast that addresses diabetic neuropathy and the impact of L-Arginine, antioxidants and vitamins. He explains how he has had success using the Synergy products being ProAri9 Plus and Mistica. A super vitamin mix is the NutriMor.