Download CAD Inherited Real Risk: Nosography and

CAD Inherited Real Risk: Nosography and Therapy.
The Concept of Angiobiopathy
(by Sergio Stagnaro*)
Introduction.
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 www.semeioticabiofisica.it/microangiologia).
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 “meanintense” 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 newbornpathological, 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
(www.semeioticabiofisica.it/microangiologia).
Discussion.
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 http://www.semeioticabiofisica.it and
http://www.semeioticabiofisica.it/microangiologia.it). 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 -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,
Coniugated–Melatonine, 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).
*Dott. Sergio Stagnaro
Founder of Quantum Biophysical Semeiotics.
16037 Riva Trigoso (Genova)
www.semeioticabiofisica.it
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