giovedì 11 marzo 2010

CAD Inherited Real Risk: Nosography and Therapy. The Concept of Angiobiopathy


Mutations in parenchimal cell n-DNA and mit-DNA are the the conditio sine qua non of the most common human disorders, like diabetes and cancer, today’s epidaemics (1-17). In fact, all these diseases are based on a particular congenital, functional, mithocondrial cytopathy, transmitted through mother, I termed Congenital Acidosic Enzyme-Metabolic Histangiopathy, CAEMH (1, 13, 14). In addition, parenchymal gene mutations cause local microcirculatory remodelling, doctor can evaluate at the bedside in a reliable manner, gathering indirect information on relative parenchymal cell inherited modifications, since biological system functional modifications parallel gene mutation , according to Angiobiopathy theory (1,18, 19).

Nosography of CAD Inherited Real Risk.

In presence of intense CAEMH in a well-defined myokardial area, involved by gene mutations in both n-DNA and mit-DNA, can brings about CAD Real Risk, charcaterized by microcirculatory remodelling from biophysical-semeiotic viewpoint, especially intense under environmental risk factors (1, 6, 7, 16). Such as congenital microvascular remodelling, including also vasa vasorum of large coronary arteries, show since birth interesting structures, i.e., newborn-pathological, type I, subtype b), Endoarteriolar Blocking Devices, EBD, localized in small arteries, according to Hammersen, I discovered (See also

Interestingly, CAD Inherited Real Risk is associated to endothelial dysfunction (there are mitochondria also in endothels, although in small amount), doctor can bedside assess in easy and reliable way, at rest as well as under stress tests (1-10, 18, 19).

As a consequence of above, briefly referred remaks, physicians are able nowadays to demonstrate the presence of typical pathological EBDs in coronary microvessel, which play a central role in CAD Inherited Real Risk.

First of all, in health, due to the non local realm, present in all biological systems beside the local realm (20, 21), as I demonstrated earlier (2-25), “intense” digital pressure on cutaneous projection area of the hearth (precordium) (= activation of the local microcirculatory blood-flow, according to type I) do not provoke “simultaneously” aspecific gastric reflex, which occurs exactly after 16 sec. of latency time (1-5, 20, 21).

On the contrary, in case of CAD Real Risk, under the indentical experimental condition, referred above, doctor observes a gastric aspecific reflex “simoultaneous to intense digital pressure”, whose intensity parallels the seriousness of underlying disorder.

Fig. 1

Aspecific Gastric Reflex:in the stomach, both body and fundus are dileted,

whereas antel-pyloric regions contracts.

As a matter of facts, the hearth-aspecific reflex, reliable and easy to apply, brought about by “mean-intense” digital stimulation of cardiac trigger-points (precordium), appears after 8 sec. physiological latency time, but lasting 4 sec. (NN = less tha 4 sec.): this is an important parameter value, corresponding to Microcirculatory Functional Reserve (MFR) activity of related coronary microvessel, thus correlated with the function and anathomy of the microcirculatory bed, or more precisely speaking, microvascular tissular-unit.

In fact, hearth-aspecific gastric reflex, when pathologically lasting 4 sec. or more (NN less than 4 sec.), indicates local microcirculatory remodelling, and thus MFR impairment due to newborn-pathological, type I, subtype b), aspecific, EBD, which reduce tissue oxygenation, through lowering microcirculatory blood-flow.

Reliable and precise information is provided by hearth preconditioning in both its Inherited Real Risk and in very initial stage of CAD (6, 11), not to speak of clinical microcirculatory analysis, which needs a thorough knowledge of the original methods (


From the above remarks, Angiobiopathy theory results once again corroborated. As a matter of fact, according to this theory, which carries out Tischendorf’s Angiobiotopy, every inherited pathological condition of every parenchyma associates since birth with a subsequent modification of related microcirculatory bed, so that microcirculatory remodelling give reliable information on related parenchymal cells.

First of all, analogously to all other biological systems, appears the finctional alteration of the mitochondrial respiratory chain, i.e., CAEMH), after that, come congenital gene mutations (n-DNA and mit-DNA) in myocardial cells, which cause biological alterations, and thus local microcirculatory remodelling, associated with endothelial dysfunction.

Notoriously, negative environmental risk factors can worsen already present dangerous effects of such as gene inherited modifications (inherited real risk), but cannot independently bring about them directly.

Undoubtadly, metabolic syndrome (MS) is major target in Primary Prevention of today’s epidaemias: diabetes, dyslipidaemias, hypertension, a.s.o. However, we have firstly to remember beside "classic" form of MS also the "variant" one, I described earlier with a clinical method, conditio sine qua non of lithyasis (1-8) (See and In addition, I described the Pre-Metabolic Syndrome (classic and "variant", of course) that follows biophysical-semeiotic constitutions, and comes for the MS, years or decades long: "Pre-Metabolic Stage" represents the LOCUS of primary prevention (1-6).

Finally, the above remarks account for the reason that only in some cases of MS, but not in ALL, there is diabetes, which is absent in a second subgroup of individuals with MS. Notoriously, patients with MS can be subdivided in two subgroups, as regards glucose metabolism impairment (25).

In fact, besides individuals showing IIR and/or high FPG and/or PPG levels, IGT, and finally diabetes, we observe patients with IIR, who will never suffer from diabetes. My 52 year-long clinical experience allows me to state that “biophysical-semeiotic dyslipidaemic AND diabetic” constitutions account for the reason of such as different outcome. Really, only patients with inherited pancreatic islet b-cell insufficiency, can be involved – in life-span – by insulin secretion failure, due to the exhaustion of hormone production (25).

As a consequence, cigarette smoking, diabetes, dyslipidaemias, hypertension, a.s.o., do not contribute to provoke CAD in ALL individuals, but exclusively in individuals among those involved by inherited CAD real risk (1, 11-13). Therefore, in all researches, aiming to recognize risk factors of human diseases, like cigarette smoking, inappropriate diet, hypertension, diabetes, a.s.o., especially individuals with the congenital real risk have to be enrolled. From the therapeutic viewpoint, in my long well-established clinical experience, diet ethimologically speaking, ConiugatedMelatonine, and NIR-LED application in pesonalized way, proved to be really efficacious against every inherited real risk form, including cancer real risk, due to their positive influence on mitochondrial respiratory function, which results normalized or even increased (26).

* Sergio Stagnaro MD

Via Erasmo Piaggio 23/8,

16039 Riva Trigoso (Genoa) Italy

Founder of Quantum Biophysical Semeiotics

Who's Who in the World (and America)

since 1996 to 2009

Ph 0039-0185-42315

Cell. 3338631439


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14.Stagnaro S., Stagnaro-Neri M. Istangiopatia Congenita Acidosica Enzimo Metabolica. Gazz. Med. It.- Arch. Sci. Med. 144, 423, 1985.

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19.Sergio Stagnaro. Mitochondrial Genome of the Mastodon highlights Human Constitutions. PLOS Biology, (01 August 2007)

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23.Stagnaro Sergio e Paolo Manzelli. L’Esperimento di Lory. Scienza e Conoscenza, 23, 13 Marzo 2008.

24.Stagnaro Sergio e Paolo Manzelli, 09-1-2008, Semeiotica Biofisica Quantistica: la manovra di attivazione surrenalica jatrogenetica.

25. Stagnaro Sergio. Epidemiological evidence for the non-random clustering of the components of the metabolic syndrome: multicentre study of the Mediterranean Group for the Study of Diabetes. Eur J Clin Nutr. 2007 Sep;61(9):1143-4. Epub 2007 Feb 7. [MEDLINE]

26. Stagnaro S., Stagnaro-Neri M., La Melatonina nella Terapia del Terreno Oncologico e del “Reale Rischio” Oncologico. Travel Factory, Roma, 2004.

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