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Friday, May 22, 2009

Quantum-Biophysical-Semeiotic bedside Detecting Atherosclerosis from initial, asymptomatic Stage. Inherited real Risk.

Endoarteriolar Blocking Devices (EBD), derived from arteriolar medial layer, and ubiquitous in a single point of vascular wall with two (= arterioles) or more (= small arteries) layers of smooth muscle cells, according to Hammersen [1], protruding to the lumen, show very different structure and form, under physiological and pathological conditions: small cushions with wide base, polypoid formations, generally pedunculated [2-5], sphincteric formations, intimal contractile architectures. More precisely speaking, only type II, normal, physiological, EBD, localized in arterioles, are ubiquitous.

EBD are playing a primary role in local microcirculatory flow-motion regulation, as the following clinical evidence demonstrates: when they are abnormal, from both functional and structural quantum-biophysical-semeiotic viewpoint, EBD bring about Functional Microcirculatory Reserve (FMR) impairment, contributing to cause inherited real risk of disorders, like CAD, whose onset will possibly occur after years or decades, as allows me to state a 53-year-long clinical experience with the original physical semeiotics [6-19]. Under such as condition, we observe tissue acidosis, assessed as lowering of gastric aspecific reflex latency time, indicating lowered tissue oxygenation.

Interestingly, the initial stage of whatever disorder, i.e., the inherited real risk, is characterised exclusively by a reflex duration lasting 4 sec. (NN < nn =" 8" style=""> utilizing apnoea test.

In health, the duration of apnoea is inversely correlated with latency time lowering, and directly related to gastric aspecific reflex lasting time (7-9).

Quantum-biophysical Semeiotics allows doctor to find physiological, both type I and type II, EBD, the later exclusively in those biological systems which need temporarily high blood supply, as skeletal muscle, right cerebral hemisphere of individuals CAEMH-positive, and conjunctival mucosa, emphasizing their central role in microcirculatory flow-motion regulation, under physiological as well as pathological conditions,

Beside normal or physiological, either inherited or newborn, type I (= small arteries), and type II (= arterioles), EBD, according to S.B. Curri [4,5], do really exist type I, newborn-pathological EBD, until now unknown by physicians. They are sub-divided in two subtypes: a) subtype, characteristic of oncological real risk, and b) subtype, aspecific, in all other disorder inherited real risks and present in different biological systems, I discovered and described in earlier papers, (See: Physiology, and Pathology,,) [6,7].

These microcirculatory structures play a pivotal role in the patho-physiology of most common and serious human diseases, including diabetes, hypertension, ATS, CVD, cancer, permitting to define the link existing between genetic factor and phenotype, according to Angiobiopathy theory [6-18].

In fact, decade-long clinical study of Endoarteriolar Blocking Devices has allowed me to discover and assess “quantitatively” the genetic abnormalities of all biological systems, preconditioning outcome is based on.

As a consequence of above remarks, EBD clinical evaluation proved to be a paramount tool to bedside recognize individuals at inherited real risk of the more frequent and dangerous human disorders, as well as to comprehend fully the underlying different quantum-biophysical-semeiotic constitutions, I have formerly described, since the birth [9-20].

Due to these reasons, I emphasize the essential value of knowing both anatomy and physiology of such microcirculatory structures, i.e., EBD, both physiological and pathological, at the present time unfortunately either ignored or overlooked by clinicians around the world. EBD are useful to understand the importance of Clinical Microangiology, and particularly its branch, I suggested to term Clinical Microangiology of Endoarteriolar Blocking Devices [6-21].

Furthermore, Quantum-biophysical Semeiotics allows doctor to bed-side detect the persistent opening (technically speaking, hyperstomy) of all artero-venous anastomoses (AVA), ethimologically understood, as clinical and experimental evidence suggests.

In healthy and young inividual, this reflex, that shows an intensity smaller than 2 cm, disappears rapidly if digital pressure becomes “highly intense”. In addition, if the subject hand is raised to 10-15 cm. above the heart level, “mean-intense” digital pressure applied on the finger-pulp does not cause upper ureteral reflex.

On the contrary, in arteriosclerotic patients, from initial stage of its inherited risk, “mean-intense” digital pressure, applied upon the microcirculatory bed, e.g. on the microvessels of a finger pulp, scars, great or little joints, of individuals lying down in the supine position, psycho-physically relaxed with open eyes (= melatonin secretion inhibition) brings about upper ureteral reflex (= upper ureteral tracts dilate about 2,5 cm.), lasting characteristically “stiff” also during “extreme-intense” pressure [6-21].

In other words, in health, under the later condition, AVA are closed, and simultaneously type I and II EBD contract, when evaluated as middle ureteral reflex (See later on), facilitating the blood-flow through nutritional capillaries (= type I, associated, Microcirculatory Functional Reserve activation). Furthermore, since the very early stage of arteriosclerosis, such as reflex persists “stiff” also under the latter conditions, hindering blood supply to local parenchyma.

Interestingly, this quantum-biophysical-semeiotic sign increases suddenly when the patient moves the other, vertically raised hand as waving good-bye – "slightest effort test" – because of the increasing of blood viscosity, bedside detected. Analogously, during the "simulated cold test" (= patient is thinking to dip his hands or a single finger in ice-cold water), arterio-venous anastomoses result slightly opened in healthy subjects.

On the contrary, under identical conditions, AVA opening appears to be particularly increased in patients involved by arteriosclerosis, even initial or asymtomatic: 1,5 cm. vs 2,8 cm., respectively: p<0,001,>

Finally, middle ureteral reflex, different in type, size, duration, nature, induced by digital pressure of different intensity, applied, e.g., on tissue-micro-vascular-units of finger tip, gives useful information about the diverse EBD, type I AVA as well as type II, group I, group II AVA, where present as in the foot-sole (16)

As a consequence, doctor can now-a-days assess the diverse EBDs at the bedside in easiest way, calculating the duration of heart-aspecific gastric and/or -caecal reflex duration: in presence of “normal” EBD alteration and type I newborn-pathological, type I, subtype b), EBD, reflex lasts 4 sec. or more (NN = less than 4 sec.), correlated with the seriousness of underlying disorder. Moreover, the final tonic Gastric Contraction (= intense tissue acidosis) indicates the presence of newborn-pathological, type I, subtype a), “oncological”, EBD, characterized by a large amount of smooth muscle cells.

Certainly, who knows the “direct” evaluation of middle ureteral reflexes can utilize a very refined, exhaustive, and reliable method [6-21].

Finally, knowing the precise location of physiological, type I, EBD (i.e., skeletal muscle, conjunctival mucosa, and right emisphere of individuals CAEMH-positive), doctor recognizes more quickly the type I, subtype a) and b), newborn-pathological EBD.

At this point, reader has to take into account that pathological EBD can transform in physiological type, reducing contemporaneously their number, under efficacious therapy (diet, ethimologically speaking (= BMI about 25, physical exercise, avoiding tobacco smoking, a.s.o.), Melatonin, personalized applications of NIR-LED, a.s.o.), thus ameliorating local microcirculatory blood-flow (= pH), evaluated as duration of latency time and reflex lasting.

It is well known for many years that patients with coronary heart disease may have no symptoms [20, 22], and that the electocardiographic feature of ischaemia may be induced by exercise without accompanying angina [22]. Nevertheless, such "silent ischaemia" has only recently been recognized to be an important feature of ischaemic heart disease [7, 18]. The silent ischaemia prevalence is unknown, although over a quarter of myocardial infarctions are unrecognized and half of them cause no symptoms at all [14]. According to Cohn, there are three categories of people with silent ischaemia, who may be at such risk [5]. People of type 1° have no symptoms and no history of myocardial infarction or angina; those of type 2° are symptomless survivors of myocardial infarction; fìnally, patients of type 3° have angina together with episodes of silent ischaemia, whose mechanisms in most cases are obscure.

My data suggest that quantum-biophysical-semeiotic methods, illustrated above, are reliable, helpful, and then advisable in bed-side detecting individuals, even asymptomatic, who have to undergo, promptly and rationally, whatever stress testing, such as electrocardiographic exercise test, atrial pacing, thallium stress redistribution scintigraphy, exercise radionuclide ventriculography, and spiral CT, a.s.o., during which silent ischaemia usually may be elicited, corroborating bedside diagnosis [1, 2, 21]. Furthermore, the clinical, quantum-biophysical-semeiotic selection of asymptomatic patients is interesting, because it can be applied on very large scale, helping doctors in actively searching for ischemic heart disease, particularly serious when silent, from the clinical viewpoint. As a matter of facts, a lot of data suggest that episodic, silent ischemia carries a poor prognosis in stable coronary artery disease [3, 23].

Given the accumulating evidence that ischemia, whether silent or not, carries a poor prognosis in patients with known coronary artery disease, it is justifìed to follow an active policy even in patients who are totally free of symptoms [4, 22]. Essentially, the rationale for the use of histangioprotective drugs (like L-Carnitine, Co Q10, Coniugated-Melatonin, a.s.o.), associated with personalized applications of NIR-LED, in patients with ischemic heart disease clinically silent.

Three necessary premises:

Firstly, the favourable effects of these products on lipid and glucose metabolism, ameliorating mitochondrial respiratory chain, I illustrated previously [14, 20-24].

Secondly, the positive influence of these drugs on angina pectoris as well as on myocardial ischaemic preconditioning, because they improve blood flow in cardiac tissue microcirculatory units [8, 9, 20, 23].

Thirdly, when utilized in early stage, histangio-protective drugs can ameliorate coronary microcirculatory remodelling, e.g., lowering the number of newborn-pathological type I, subtype b) EBD: the intensity of specific middle ureteral reflex significantly decreases under such treatment [23].

Practically, in order to ascertain clinically silent ischaemia it is advisable to assess shape and intensity of low ureteral reflex oscillations, i.e. vasomotion, as illustrated above, which permits doctor to calculate the fractal dimension of myocardial microvessels deterministic chaos (NN > 3 < oscillation =" 3/1">

As far as myocardial ischaemic preconditioning is concerned, it is suffìcient and hence advisable in day-to-day practice to assess the latency time of the second heart-gastric aspecific reflex, i.e., in the second evaluation, performed exactly after 5 sec. interruption, namely soon after 5 sec. from the end of basal evaluation: in health, latency time raises in a significant manner from 8 sec. (basal value) to 16 sec., i. e., to doubly value.

Another difficult, but also refined, elegant method proved to be reliable: the assessment of shortening of left ventricle enlargement duration during the above-described test (NN = from 7 sec. to 5 sec.) and/or conversely the prolonged latency time from 3 sec. to 5 sec. or more, preceding another ventricle dilation, paralleling Ejection Fraction of left ventricle. This latter evaluation, however, is a little more difficult to ascertain by doctors not experienced and skilled in the field of the original semeiotics.

From the practical view-point, both duration (NN <> 3 sec. < class="referencia">[7-10].

Actually, relevant data are easily obtained also by means of the latency time of heart-caecum and/or-aspecific gastric reflex, which informs about myocardial oxygen supply: in health, during “mean” digital pressure upon the skin projection area of heart, basal latency time value is 8 sec. However, doctor must remember that in case of CAD inherited real risk and CAD initial stage, such as parameter value is still normal (NN = 8 sec.), but reflex lasts 4 sec. or more (NN <>

In addition, in health, during "intense" digital pressure upon cutaneous projection area of the heart, as above described, and immediately after about 7 sec. apnea test or Valsalva's manoeuvre, the basal latency time of cardiac-gastric aspecific reflex (basal value = 8 sec.) raises significantly to 16 sec., as well as after preconditioning (i.e., doubly value) (p<0,02),>

In conclusion, in a long, well-established, clinical experience, the above-described quantum-biophysical-semeiotic methods proved to be reliable, easy to perform on very large scale, useful, and suitable for detecting ischemic coronary disease, even clinically silent or really initial, i.e. since CAD “real risk” [23].

Finally, Quantum-biophysical Semeiotics allows doctor to bedside recognize, in only one second, normal heart, as well as arteries [23,24-27]: in health, “intense” digital pressure, applied upon skin projection area of the heart and respectively of a large artery, does not bring about “simultaneously” gastric aspecific reflex.


1. Hammersen F (1968). Zur ultrastruktur der arterio-veno¨sen anastomosen. In: Hammersen F, Gross D (eds). Die Arterio-venoesen Anastomosen Anatomie, Physiologie, Pathologie, Klinik. Verlag Hans Hubert: Bern und Stuttgart. pp 24–37.

2. Bailey I.K.,Griffìth L.S.C., Rouleau J,Strauss H.W., Pitt B., ThalUum201 myocardial perfusion imaging at rest and during exercise. Comparative sensitivity to electrocardiography in coronary artery disease, Circulation, 1977, 55, 79.

3. Bonow R.O., Bacharach S.L., Gren M.V., La Fremere R.L., Ehstein S.E., Prognostic implicaiions of symptomatic versus asymtomatic (silent) myocardial ischemia induced by exercise in mild symptomatic and in asymptomatic patients with angiographically dociimented coronary artery diseas, Am. J. Cardio!., 1987, 60, 77.

4. Curri S.B. Le Microangiopatie. Inverni della Beffa, Milano, 1986.

5. Curri S.B. Pannicolopatia Mammaria da Stasi, Parte seconda. Inverni della Beffa, Milano, 1984

6. Stagnaro Sergio. Newborn-pathological Endoarteriolar Blocking Devices in Diabetic and Dislipidaemic Constitution and Diabetes Primary Prevention. The Lancet. March 06 2007. and especially:,

7. Stagnaro-Neri M., Stagnaro S. Introduzione alla Semeiotica Biofisica. Il Terreno Oncologico. Travel Factory, Roma, 2004.

8. Stagnaro Sergio. Teoria Patogenetica Unificata, 2006, Ed. Travel Factory, Roma.

9. Stagnaro Sergio. Role of Coronary Endoarterial Blocking Devices in Myocardial Preconditioning -c007i. Lecture, V Virtual International Congress of Cardiology.
Stagnaro S., Stagnaro-Neri M., Single Patient Based Medicine.La Medicina Basata sul Singolo Paziente: Nuove Indicazioni della Melatonina. Ed. Travel Factory, Roma, 2005.
11. Stagnaro Sergio. New bedside way in Reducing mortality in diabetic men and women. Ann. Int. Med.
12. Stagnaro Sergio. Newborn-pathological Endoarteriolar Blocking Devices in Diabetic and Dislipidaemic Constitution and Diabetes Primary Prevention. The Lancet. March 06 2007.

13. 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]

14. Stagnaro-Neri M, Stagnaro S., Deterministic chaotic biological system: the microcirculatory bed, Gazz. Med. It.-Arch. Sci. Med., 1994, 153, 99.

15. Stagnaro S., Moscatelli G., Biophysical Semeiotics, Deterministic Chaos and Biological System, Gazz. Med. It. Arch. Sci . Med. 1996, 155, 125.

16. Stagnaro-Neri M., Stagnaro S., Auscultatory percussion evaluation of arteriovenous anastomoses dysfunction in early arteriosclerosis, Acta Medica Mediterranea, 1989, 5, 141.

17. Stagnaro-Neri M., Stagnaro S., Deterministic Chaos, Preconditioning and Myocardial Oxygenation evaluated clinically with the aid of Biophysical Semeiotics in the Diagnosis of ischaemic Heart Disease even silent. Acta Med. Medit. 13, 109, 1997.

18. Stagnaro-Neri M., Stagnare S., La manovra di Ferrero-Marigo nella diagnosi clinica di Iperinsulinemia - Insulinoresistenza, Acta Med. Medit., 1997, 13, 15.

19. Stagnaro Sergio. Role of Coronary Endoarterial Blocking Devices in Myocardial Preconditioning - c007i. Lecture, V Virtual International Congress of Cardiology, 2007.

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

21. Stagnaro S., Stagnaro-Neri M., Le Costituzioni Semeiotico-Biofisiche.Strumento clinico fondamentale per la prevenzione primaria e la definizione della Single Patient Based Medicine. Ed. Travel Factory, Roma, 2004.

22. Wood P., Me Gregor M., Magidson O., Writteker W. The effort test in angina pectoris, Br. Heart J., 1950, 12, 363.

23. Stagnaro Sergio. Il “Reale Rischio” Semeiotico-Biofisico. Ruolo diagnostico e fisiopatologico dei Dispositivi Endoarteriolari di Blocco, neoformati patologici tipo I, sottotipo a) e b). Ed. Travelfactory, Roma, in press.

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

25. Stagnaro Sergio. Diagnosi clinica di cuore sano in un secondo! 7 Aprile 2008.

26. Stagnaro Sergio. Bedside Biophysical-Semeiotic Osteocalcin Test in Diagnosing and Monitoring Diabetes. The Lancet, January 28, 2008.; See especially,

27. Stagnaro Sergio. Semeiotica Biofisica Quantistica: Diagnosi Clinica di Melanoma a partire dal suo Reale Rischio Congenito., 23 luglio 2008,

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