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How to Find BIockages without Angiography?

"REALISTIC GEOMETRIC CARTOGRAPHIC IMAGING”

 

Coronary artery blockages, till now, could not be measured by any tests except angiography, which is not only expensive but also exposes the patient to a number of risks and complications. Moreover, angiography needs an admission and now being use by most of the hospitals to compel patients to undertake next procedures like Bypass surgery or Angioplasty.

Good news for heart patients is that in the near future they will be able to find and measure the blockages without angiography, through a Hungarian developed investigation called Realistic Geometric Cartographic Imaging (RGCI).

RGCI can be done at the bedside of the patients, It takes roughly 20 minutes from start to finish. The procedure is done using few disposable electrodes. Complex parameters are obtained using high precision data accusation system. Pressure, volume, time of blood flow are collectively obtained by simultaneously recorded electrocardiography (ECG), phonocardiography (sound of the heart), non-Invasive continuous blood pressure and trans thoracic bio-impedance. The acquired parameters are then mapped against a mathematical model and cartogram is obtained, which is a collective behavioural pattern of the heart and its circulation status. Doctor gets a complete heomodynamic picture of the heart, as well as the location and severity of coronary artery disease and relative oxygen demand of the heart. This can help the doctor in taking appropriate decision regarding management of the patient.

RGC Imaging can detect coronary tube blockages as low as 20%, it is having a sensitivity and specificity of more than 92% which according to the experts is good enough for non-invasive test. This procedure can be used to substitute costly, dangerous and not so accurate procedures for accessing the coronary heart disease (i.e. Angiography). It is also used in the management of critically ill patients since its a bedside procedure.

Scientific papers were presented at the 8th European Congress of Intensive Care Medicines, Athens, Greece 1995; 12th International Congress "The New Frontiers of Arrythmia" Italy 1993; 3rd International Conference on Impedance Cardiography, Domdovan, Hungry 1997; 4th Asia Pacific symposium on Electro-physiology, New Delhi 1997. Recently papers was presented by Manipal Heart FoundaUon, Bangalore during the 50th Scientific Session of Cardiological Society of India, December 1998.

The authenticity of RGCI has been established in the last 10 years. The technique is being studied extensively in many part of Europe and India. The added advantage of RGCI is that people with minimum blockages can also detect their blockages by this procedure, allowing them to prevent heart disease in future.

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Angiograms and Ultrasound Are Not Accurate to Measure Profound Improvement Following Chelation

by Elmer M. Cranton, M.D.

 

It is hard to believe but scientifically proven less than 7 percent increase in the interior diameter of a diseased blood vessel will double the flow of blood. Angiograms and ultrasound imaging are only accurate to within approximately 20 percent and cannot measure such small changes.

 Blood is only about half liquid. The other half is composed of red and white blood cells. These cells rub along blood vessel walls and move much more slowly than more fluid blood in the center of an artery. This makes blood highly viscous and sticky close to the arterial wall. Because the distance relative to blood cells between the outer wall and the center of a vessel is much less in small blood vessels, a small increase in the internal opening will result in a very large increase in the flow of blood. Blood flow past plaques is turbulent, causing even more resistance to flow. In diseased arteries with plaque, an even smaller increase (less than 6 percent) can double the flow of blood and totally relieve symptoms.

 The liquid and cell-free portion of blood is more viscous than water because of its high protein content. Cell-free plasma is about 1-½ times as viscous as water. When blood cells are added, the viscosity increases to more than 3 times that of water.

 The cross sectional area in the opening in a blood vessel decreases exponentially with a decrease in diameter. An artery of half the diameter has only one fourth the cross sectional area.

 Combining all of these factors together, as proven by Poiseuille’ Law, doubling the diameter of the internal channel results in a 16-fold increase in the flow of blood (assuming no change in blood pressure or length). Put another way, a smooth healthy blood vessel will carry twice as much blood if the interior increases less than 7% in diameter. A blood vessel with plaque and has turbulent flow and a mere 5 percent or less increase in diameter of the internal opening will double the flow of blood.

 Angiograms and ultrasound imaging are only accurate to within approximately 20 percent. Even if repeated an hour later on the same patient using the same technique, the reading can vary by as much as 20 percent.  That explains why patients whose symptoms have improved dramatically following chelation therapy often do not show a significant change in reading on followup angiogram. For the same reason, calcium scores on followup ultra-fast, electron-beam, CT scan (EBCT) are also not a reliable way to measure benefit following chelation therapy.

It is a waste of time, a waste of money, and can involve unnecessary risk to do follow-up angiograms merely to document improvement from EDTA chelation therapy. The proof of the pudding is in the eating. If symptoms improve it is logical to assume that blood flow has increased. If that benefit can be retained by periodic maintenance chelation treatments with the most effective nutritional supplements, much can be achieved without surgery, stents or other potentially dangerous procedures. 

 

References

 http://www.answers.com/topic/poiseuille-s-law

 http://hyperphysics.phy-astr.gsu.edu/hbase/ppois.html

 http://www.cvphysiology.com/Hemodynamics/H003.htm

 

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Bangalore team's invention gets FDA approval

Our Bureau

Bangalore, July 21, A MEDICAL diagnostic device invented by a Bangalore research team has become the first such hi-tech Indian tool to win the US FDA approval for its clinical use in the US and certification from the EU.The device, called Haemotron, is non-invasive and uses 3D mapping technology or 3D cardiovascular cartography (3D-CCG) to measure the heart's functions and blood flow. The painless 3D-CCG technique takes barely 20 minutes and gives a comprehensive picture of the heart and any of its abnormalities in early stages, according to its inventors.

The Haemotron, developed over six years and in use for two years, has been invented by Dr Rajah Vijaykumar, Chief Scientific Officer, and his biomedical engineering team at the Centre for Advanced Research & Development (CARD) in Bangalore. Costing around Rs 35 lakh, it is manufactured by Scalene Cybernetics in India and Austin Systems, Inc, US, and ASKIT kft in Europe.

According to a panel of doctors at a press conference, the 3D CCG way costs Rs 3,500 each and can detect cardiovascular blocks very early at even 10 per cent of the blocks, compared to angiograms that are effective in cases with more than 40 per cent of blocks and are three to four times costlier. Prevention of heart attacks could begin five years earlier than with other tests.

 

Source: The Hindu Business Line

(http://www.blonnet.com/2003/07/22/stories/2003072201051700.htm)

 

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Cardiovascular Cartography: The Message Is The Medium
Cardiovascular Cartography [CCG], a new non-invasive tool with a systemic approach for interpreting haemodynamics, is based on modelling and simulation techniques. Its clinical application is keyed to diagnoses, estimation of prognosis, and modification of therapeutic modalities — especially in coronary artery disease [CAD].

Dr G N Shirbur, Dr S S Sibia, Dr N T Murlimohan & Dr Rajasimha

Measure what is measurable, and make measurable what is not so. -- Galileo

The prevalence of CAD in India is of the highest magnitude. It has been confirmed by several studies.¹ It is also a construct that requires mass screening not only to detect anomalies, but also follow-up and strategy for cost-effective treatment.

The technique, which is simple, easy-to-perform, and painless, can be repeated as many times as may be required. Its sensitivity and specificity have no less been assessed and validated in a blind study with angiographic findings in confirmed CAD patients.² Our experience with about 1,900 patients screened contemplatively, so far, with angiograms, echocardiography, stress ECG and clinical assessment, has shown detection of CAD, with a mean accuracy of well over 90%.

There has been a great deal of misunderstanding or balderdash in the popular media about this technique. This explains why we need to set the record straight. We are the actual users. Inaddition, our [benefited] patients and we stand by its capabilities. More so, because the technique which was studied by a group of researchers with utmost scientific diligence and fidelity, not to speak of painstaking precision, has been acquiesced to with the stamp of authority, what with results presented in scientific forums in Europe and India.

We wish to briefly elaborate the functional theory behind cardiovascular cartography. In simple terms, the technique makes scientific sense and uses a very advanced method of modelling and simulation with a 24 parameter kinetic model.

Historically, kinetic models were built to assess continuously changing non-linear dynamics of large scale data in the field of electronic warfare, weather prediction, and nuclear physics. Its application in the cardiovascular domain was, in the first place, discovered by Kumar and co-workers.

Basic Theory — Get it Right
The cardiovascular system functions as a closed loop dynamic fluid mechanics system based on pressure, volume, time and flow principles which occur independently and simultaneously. In other words, it is non-linear. The efficacy, or any deviation, in its functions for assessment purposes requires measurement of various haemodynamic parameters responsible for a dynamic event of the heart. This is called the cardiac cycle — a product of non-linear physiological activity occurring in unit time.

The measurement of pressure, and volume, can be executed by methods like Doppler or radio nuclear studies, but flow measurement is possible only by way of Transthoracic Bio-Impedance [TBI]. The clinical use of TBI has been in vogue for more than 30 years. It was first formulated by Kubicek³ and only recently by Gomory.⁴

The usage of pulsatile changes that occur due to flow of blood is a function of TBI. TBI produces signals [curves] that are precisely time-related to other physiological curves like ECG, PCG etc., The signals produced are due to the electromechanical activity of the blood flow. The CCG integrates the measured and derived parameters from these curves, and the first derivative⁵, [dz/dt, which is similar to dp/dt curve] of the modulated curves. The numerical values of the individual beat, or cycle, of systolic time interval and diastolic filling phase are derived from this specific.

In like manner, the vertical lines plotted are used to compute the pre-ejection [PEP], ventricular ejection time [VET], and QS2 intervals [electromechanical systole/See Fig. 1]. With the amplitude modulations of TBI synchronous with pumping of blood in the heart and proportional to the amount of blood pumped out, the modulations are practically equivalent to stroke volume — an absolute value proportionate to the duration of systole, flow velocity and the resistance of blood, that depends on haematocrit^6,7

Thus, the value of stroke volume can be calculated from the measurable, modulated curve as well as its proportions related to the amount of fluid in the thorax and the volume of the connective tissues of the thoracic cavity with Kubicek formula², and corrected to body habitus. From the measurable data of these four recorded signals, the heart rate and the amount of blood pushed out by the heart per beat can be calculated, along with the cardiac output.^6,7,8 Furthermore, with the knowledge of the various systolic time intervals and the pressure values measured, the remaining/ derived haemodynamic parameters can be obtained for every beat.

 Principles of Cardiovascular Cartography
The 3-D mathematical modelling and simulation using high-speed computation enables non-linear haemodynamic parameters of a patient to be mapped against the mathematical model of the cardiovascular system. Using neural network computing, a predictive model of the patient is created. The measured haemodynamic behaviour is superimposed on the predictive model. The resultant dynamic deviation is represented in a form called cardiovascular cartogram. The resultant deviation difference is distributed as pressure zone, volume zone, time zone and flow zone, in a clockwise direction on the cartogram [Fig. 2]. The K-Scale on the cartogram is an independent scale. It has positivity and negativity elements and indicates the deviation difference, aside from reflecting a physiological, pathological or compensatory phenomenon to assessing the efficacy and function/s of the cardiovascular system.

The pattern of change that occurs in the flow zone of the cartogram [contractility, acceleration, after-load, ventricular depolarisation to peak ejection delays] is obviously related to the anterioseptal regions of the myocardium. The pattern of change in the volume zone [rate pressure product, stroke volume, cardiac output, and pre-load] is, thus, related to inferioseptal regions of the myocardium and the time zone; intracycle timings, and LV ejection rate are related to the lateral regions of the myocardium. In an ICU setting, it is these factors that we try to correct — especially in situations where there is myocardial infarction in the respective regions...

The Vertical Acceleration Detector [VAD] is a special device that picks up subsonic waves that are transmitted from the heart to the chest wall. It is similar to the seismic waves that get transmitted from deep inside the earth to the surface during a quake. The VAD picks up subsonic signals throughout the cardiac cycle. This includes every component of the first and second heart sounds, just as much as specialised spectrum analysis and digital signal processing enable us to detect and extract micro variations in the subsonic activity during early-, mid- and late-diastolic [passive] filling phase.

The second component of the second heart sound is of prime importance in cardiovascular cartography because it signifies the onset of diastole. The turbulence in flow is differentiated and extracted during a period when there is maximal coronary flow: a parameter that is used to detect primary presence of coronary obstruction. The power and frequency signifies the regions from which these signals originated. It is correlated with zonal [pressure, volume, time and flow] behaviour to obtain a three-dimensional array of information that is suitable for image reconstruction.

The first part of reconstruction is to identify the ischaemic zones and reconstruct the regions on the short axis slices of the LV muscle mass [Fig. 3]. This enables one to identify the major vessel supplying the region. The appropriate site of the lesions embedded on the realistic geometry coronary model also helps us to get the realistic geometric reconstruction of the most probable location of coronary occlusion.^9,10 [Fig. 4]. {Note: These are microsecond events that have been studied. There are no parallel methods available, at present, for detecting non-invasively CAD [positive/negative], with this aggregate}.

The vast amount of data acquired during a cardiovascular cartography study enables us in computing other vital information. Some of the important information that will have diagnostic, management and prognostic value are: regional myocardial blood flow, coronary flow reserve, global cardiac efficiency, arterial compliance [specially in diabetics], ANS predominance, besides pre-load, contractility, and after-load.

CCG Test Protocols and Procedure for CAD Detection
Following strict protocol, in our opinion, will ensure best results. Unlike many other test procedures for CAD detection, where linear changes in unilateral function like electrical conduction pattern in stress ECG or material uptake in stress thallium are ratified, CCG is based on non-linear dynamics of blood flow. Drugs, for example, alter cardiac haemodynamics and maintain a forced balance.

The Protocol We Use and Recommend

·      The patient should abstain from all drugs that alter cardiac haemodynamics for a period of 12 hours prior to the test. We have found that there is no significant change in the test results between a 12-hour avoidance or a longer period. [Note: CCG is based on relative beat to beat changes, and not on absolute values. If drugs do not interfere with the relative changes, this is sufficient]

·     Alcohol plays an important role, mainly as a diuretic. The patient should abstain from alcohol for a period of 24 hours prior to the test

·     Patients should abstain from all types of stimulants like coffee, tea and other soft drinks for a period of 12 hours prior to the test

·     The patient should generally be fasting [A light breakfast, or a glass of milk and some biscuits, two to three hours prior to the test do not alter test results]

·      It is important that the patient should empty his/her bladder and be relaxed during the entire test procedure. Test results will be inconclusive in non-co-operative patients

The patient is wired to the CCG system with meticulous care. Generating electrodes should not be interchanged with measuring [or, pick-up] electrodes. VAD should be placed at a site where the second heart sound is of maximum amplitude [this will need some practice]. The bed used should be at 180 degrees; any inclination will alter the pre-load and result in an error.

The test is performed in two phases: the first phase in supine position following the above protocol, and the second phase during the same sitting by creating a vasodilator response and altering the coronary flow reserve [CFR] that is severely decompensated at rest in case of certain types and severity of coronary occlusion [NYHA Class III-IV]. In certain cases, where there is a large by-lane flow [collateral flow], the CFR will be near-normal [4~5:1], but will start to get effected after induction of reactive hyperaemia, usually by the administration of a coronary vasodilator, where a steal phenomena is induced secondary to pre-stenotic vasodilatation.

To exactly understand the second phase of the cardiovascular cartography study, one has to have adequate knowledge of coronary circulation, factors governing coronary flow, dominion of auto-regulation, resistance, large and small vessel pathophysiology, type of stenosis [rigid, dynamic etc.,] and coronary artery steal. It is, however, beyond the scope of this article to discuss all these factors. For the purpose of understanding, we will only discuss a few of the important ones.

Dynamic Coronary Artery Stenosis

If coronary lesions were hard and geometrically fixed, physical activity would be proportional to the maximal luminal area reduction or coronary blood flow. It would also explain most of the signs and symptoms of coronary artery disease. Yet, anatomical studies indicate that most human coronary stenosis contain at least some normal wall segment.^11,12

A normal epicardial coronary artery vasoconstriction will decrease the luminal area, but this will have no significant effect on either flow or pressure across the vessel.¹³ On the other hand, for a truly circumferential stenosis, liable to change its size and shape, vasoconstriction will have no influence on its cross-sectional area or stenotic haemodynamic severity. For diffuse smooth muscle stenosis and eccentric stenosis, alteration in smooth muscle tone will have significant, physiologically important effects on the cross-sectional area, possibly causing rest or exertional angina.

Large vs Small Vessels
The large and the small coronary arteries respond differently to the same vasoactive substances. Table 1 shows the physiological and biochemical characteristics of small and large coronary arteries.¹⁴

For example, in whole_animal and isolated_heart preparations, the small vessel vasodilatation with nitroglycerine was found to last only 20 to 30 seconds, whereas the larger coronary arteries remained dilated for up to 10 minutes.¹⁵ The differences in response to vasoconstrictors between the large and the small coronary arteries have not been extensively studied.

Stenotic Modulation
Rigid stenosis is where there is a geometrically fixed stenosis, the arterial wall is rigid, and the luminal area cannot change. Regardless of the degree of stenosis, decreasing distal resistance always increases flow, while increasing distal resistance always decreases it. With mild underlying rigid stenosis, decreasing distal resistance leads to a large flow increase, while with a severe rigid stenosis decreasing distal resistance results in a greatly attenuated flow increase. Thus, a patient with mild rigid stenosis can perform substantial physical exercise such as running etc., whereas a patient with severe rigid stenosis can only perform light work such as climbing stairs.

In case of a dynamic stenosis, where vasoconstriction, perfusion pressure and distal resistance, can each alter luminal areas, interaction[s] among vasoconstriction, perfusion pressure and distal resistance can occur. Correspondingly, altering distal resistance changes the luminal area; decreasing distal resistance decreases the luminal area; and, increasing distal resistance increases the luminal area. Also, proximal coronary artery vasoconstriction can decrease the vessel size. For example, in mild underlying dynamic stenosis, proximal coronary artery vasoconstriction would decrease the luminal area, and the decreasing distal resistance would further decrease the luminal area. Additionally, due to such a definitive decrease in luminal area, the coronary blood flow increase would be less than the response observed for rigid stenosis. This patient will only achieve light to moderate work levels, such as jogging. For severe dynamic stenosis, proximal coronary artery vasoconstriction would decrease the luminal area, whereas decreasing distal resistance would further decrease the luminal area. This may cause a paradoxically small flow decrease as compared to rigid stenosis response. Thus, in a patient with severe dynamic stenosis maximal physical activity will be severely decreased and an imbalance in myocardial oxygen demand and coronary blood flow will occur at rest. These patients will also experience rest angina without any physical exertion.

 Table 1. Physiological and biochemical characteristics of large and small coronary arteries. 

Characteristics	Large	Small
Autoregulation Reactive hyperaemia Ischaemia Passive distension Total resistance [%] Adenosine Hypoxia KCN Mitochondria Succinic dehydrogenase	No Slight constriction Constriction Yes 5-20 Constriction No Dilation No Dilation 10/unit 1	Yes Dilation Dilation Yes 95-80 Dilation Dilation Dilation 23/unit 2.6

 Induction of reactive hyperaemia by administering vasodilators like nitrates is essential in performing the cardiovascular cartographic study because it is important to achieve arterial modulation of stenosis as some types of coronary artery disease may go undetected. Modulating and creating a coronary artery steal can unmask some of the disease regions not severely altered under basal conditions.

There are two potential types of coronary artery steals that can occur. Both require stenosis in the large coronary arteries. Type I steal involves only one coronary artery and is caused by a redistribution of flow between the endocardium and epicardium. As maybe known, subendocardium is subjected to greater stress and, thus, needs a higher blood flow. In the presence of a proximal stenosis, the epicardial vessels maybe maximally vasodilated even under resting flow conditions. Distal coronary arteriolar vasodilators result in a greater pressure decrease across the stenosis, resulting in a decrease in distal coronary pressure. This pressure decrease can cause a decrease in flow to the subendocardium. It also partially explains why ST-segment elevation is observed on stress ECG test.

The Type II steal involves a decrease in collateral blood flow, aside from an alteration of the coronary flow reserve [CFR]. With the gradual obstruction of a coronary vessel, collateral vessels develop from the other [donor] coronary vessels. Collaterals are thin-walled anastomotic connections that exist between coronary arteries without an intervening capillary bed. They are anatomically present from early life in the form of native collaterals, but mature only if a need for additional coronary flow exists in certain region/s of the heart.

These collateral vessels supply blood flow to the myocardium normally perfused by the diseased [recipient] vessel. The collateral blood flow maybe adequate to maintain the resting energy requirements of the myocardium. However, the collateral circulation is insufficient to meet the needs of the myocardium during periods of physiological stress. In such a vista, distal coronary arteriolar vasodilatation has been reported to shunt blood flow away from the diseased vessel [coronary artery steal]. Consequently, these vessels do not prevent the development of ischaemic changes in stress ECG or abnormalities of ventricular contraction and performance.

Coronary artery steal only occurs in the presence of proximal resistance in the donor circulation. Steal does not occur without stenosis in the proximal recipient artery. For a proximal rigid stenosis in the recipient circulation, coronary steal is due solely to the decrease in collateral blood flow. Likewise, the magnitude of flow reduction in a rigid stenosis is directly related to the decrease in collateral blood flow. In contrast, for a dynamic stenosis in the recipient circulation, coronary steal is due primarily to a decrease in flow through the diseased vessel. Thus, in dynamic stenosis the largest decrease in flow occurs through the native coronary vessel — a self-steal phenomenon.

During the second phase of cardiovascular cartographic studies, the patient is administered 10 mg sub-lingual nitroglycerine. It is advisable to wait till the patient's