The pioneer of heart transplant surgery , Christian Bernard said “ I have saved the lives of 150 people by heart transplants.If I had focussed on preventive medicine earlier, I might have saved 150 million”
Heart disease is the Leading cause of death worldwide.Although it was almost unknown a century ago it has become so rampant now that the general public is fussing about Cholesterol.
According to the latest NHANES data (2020), an average man is pre-diabetic !!! and possesses a risk factor for developing heart attacks and strokes !!! According to Dr.Kraft , "those with Cardiovascular disease not identified with diabetes are simply undiagnosed” and mostly in the stages of prediabetes ( OGTT ) and pre-prediabetes ( Diabetes in situ - Krafts curve ).There has been a drastic shift in the occurrence of heart disease in the old age to the middle aged and even younger age groups in the last 2 decades because of the increased prevalence of Insulin resistance worldwide which is indicated by the shift towards the left in the Insulin level.
"Epidemics persist only as long as the genuine cause of the disease is not understood and hence preventive and therapeutic measures could not be developed ".
It holds true with respect to Heart disease.
Cholesterol is not well understood even to this day by conventional science. Just because cholesterol numbers are altered and high in heart disease , it is often viewed as the Causation that Cholesterol gets deposited leading to atheroma and thence heart attacks.Correlation is not causation.It could be the greatest error of the century !!!
" Knowledge moves forward not by repeating the known facts but by refuting the false dogmas "
Insulin Resistance is independently associated with two variables which goes hand in hand with each other. 1.Dyslipidemia - characterisation ( increased Triglycerides and small dense LDL , decreased HDL-C ) & 2.Prothrombotic state - its effect .Scientific communities linked LDL-Cholesterol as the causative factor of Heart disease ( Correlation vs Causation confusion).
The discovery of nitric oxide , a Nobel Prize winning science, is a landmark discovery in the field of medicine. The Superman molecule, Nitric oxide is produced by the endothelial cells which causes relaxation of blood vessels , protects against Platelet aggregation, smooth muscle proliferation , monotype adhesion & superoxide radical elaboration preventing oxidative damage of vascular walls. Insulin Resistance causes less Nitric oxide production , thereby losing the protective effect is now prone for the development of Hypertension , Heart disease and Stroke.
Another problem in the understanding of Heart disease is the atherosclerotic plaque vs Thrombosis.
Whereas most of the heart attacks ( 70 % ) arise from soft plaques - vulnerable plaques , Angioplasty and Bypass are more and more focused towards stabilized hard plaques ( could be the reason for stable angina ).
Lp(a) rather than LDL-C is consistently associated with atherosclerotic plaque. Lp(a) has more of a reparative role as a bandaid. Cholesterol lowering drugs like Statins and PCSK9 inhibitors are widely used for Hypercholesterolemia.
Heart attack is literally the infarction of the particular area of the heart that developed over a period of minutes by thrombosis ( which inturn is caused by plaque rupture ) . Angina is all about supply-demand concepts particularly during exertion ( incapacitating because of poor circulation ) .
The true indication of angioplasty is within 3-6 hours of onset of symptoms in heart attacks ( which can account for < 5 % of all the angioplasty done nowadays ) and in the relief of intractable chest pain resistant to medications. Although angioplasty looks fascinating, we are not treating the root cause but rather disturbing the stabilized atherosclerotic plaques.
Atherosclerotic plaque in Coronaries develop over a period of years that the insufficient oxygen demand is compensated by angiogenesis ( formation of new blood vessels bypassing the stenotic plaques ).The very reason why most patients are still normal without incapacitating chestpain even with 90 % or 95 blockage % is collateral circulation. It's the natural bypass which the heart has done for itself without a scalpel !!!! Atherosclerotic plaques are compensated by Collateral circulation for effective functionality of the heart by keeping up the perfusion.
A mystery to be revealed to solve the misery of the present and future.
Heart attacks occur only in humans !! animals don’t. Why ?
Atherosclerotic plaques form in arteries but not in veins.. Why ?
Infarctions occur in the heart but are rare in other organs.. Why ?
A fascinating molecule leads the way to the puzzle of human cardiovascular diseases.
It may not be necessarily so. Lipoprotein (a) links arteriosclerosis and blood clot clot formation. Lp(a) not LDL binds to fibrin , collagen and endothelial cells and is the primary contributor to the arteriosclerotic plaque. Earlier researchers had missed looking for apo(a) and therefore came to the wrong conclusion that the LDL causes arteriosclerosis. Lipoprotein(a) accumulation parallels the size of the arteriosclerotic plaque.
The atherosclerotic plaque is an initially life saving repair process of the artery wall when it is weakened by long term deficiency in micronutrients. It develops when this repair process goes too far and overcompensates.Lipoprotein (a) is a mobile repair molecule that reaches the sites of tissue repair. The adhesive apoprotein (a) is a substitute for collagen in the vascular wall whenever it is injured or structurally impaired. Lipoprotein (A) is a repair molecule for the vitamin-deficient artery wall.
Conventionally LDL-C has been demonized as bad cholesterol and most of the therapeutic and preventive measures are based on reducing the LDL-C to minimize the cardiovascular risk
The current understanding of cardiovascular diseases
Fat transporting molecules enter the artery wall and deposit their fat content inside this wall ; it occurs at random ; no biological purpose . arteriosclerosis is a fatalistic process and it is essentially irreversible
Lipid molecules are deposited inside the artery walls mainly as intact lipoprotein particles, predominantly lipoprotein (a).It has an important biological purpose of protecting against scorbutic blood loss. Arteriosclerosis is a regulatory process. The formation of arteriosclerosis is reversible by an optimum intake of micronutrients which inturn causes progressive plaque cap thickening and plaque shrinkage.
Understanding the past is the way to the future
Understanding scurvy as the biggest threat to the survival of the human race in the past is the key to the eradication of cardiovascular disease of the future.human lipoprotein(a) is a surrogate for vitamin C in the artery wall.
We cannot redo the delete button in evolution ( lost the ability to synthesis vit C ) !!!
Stable plaques are Fibrous , slowly occlusive & stenotic which can cause stable angina or silent occlusion ; this is compensated by collateral circulation.
Vulnerable plaques are thin capped fibroatheroma or eroded ; typically non-stenotic prior to the event producing unstable angina , acute myocardial infarction and sudden cardiac deaths.
Plaque rupture causes thrombosis
A crack develops in the surface of a tiny plaque and the inner contents come spurting out, acting as a catalyst to cause the blood to clot, forming an occluding thrombus
“The sales pitch” taught to students- an angiogram showing shadows of old plaques. The critical view point which is often missed is that the severity of heart disease is closely related to the absence of flow in the blood vessel supplying the heart and not the degree of stenosis.
Calcium in arteries is the end of inflammation. Calcification is a result of chronic inflammation and is laid down in old scars. The vulnerable plaque is often small and unseen even with an Angiogram or CT-heart scan( CAC).
Both of them are palliative procedures with no survival benefits with the exception of relief of angina.surgically treated blocks are hard like a rock ; bypassed are large stable lesions ( non-lethal). The culprit lesions ( volatile plaques) are left untouched. Surgery treats the hard, fibrous plaques( scars ) which never kill : rupture of tiny volatile plaques kills the heart muscle.Doctors can see and treat large scars. Tiny pustules are unseen with no treatment ( other than diet ). Placement of a bare metal stent to prop open the artery causes cells to proliferate : 40 % of arteries are closed down within a year. Drug eluting stents (DES) dissolve out of the device -medications over the first 4 months , to become bare metal stents,.DES are associated with a reduced risk of closure, but an increased risk of blood clots. Angioplasty breaks up the blockages and dilates the artery.
Unfortunately , products of injury released by fracturing the plaque cause further blood clotting. Half of arteries so treated are completely closed down within 5 months.
12 Randomized , Clinical Trials Enrolling 7182 Participants
Percutaneous Coronary Intervention Versus Optimal Medical Therapy in Stable Coronary Artery Disease
A Systematic Review and Meta-Analysis of Randomized Clinical Trials Conclusion: In this most rigorous and comprehensive analysis in patients with stable CAD, PCI, as compared with OMT, did not reduce the risk of mortality, cardiovascular death, nonfatal myocardial infarction, or revascularization.
Circulation: Cardiovascular Interventions. 2012 August 1 ; 5:476–490
Study Report | 5 Year Survival Rate Surgical | 5 Year Survival Rate Medical |
| Veteran’s Study | 82 % | 80 % |
| European Study | 93 % | 85 % |
| CASS Study | 95 % | 92% |
Angioplasty with sudden closure of vessel benefits when treated within 90 minutes. Treatment benefits seen when from the first contact to reperfusion therapy is less than 90-120 minutes. The sooner the better.
Cholesterol is the greatest scam of the century based on Diet heart hypothesis.two correlation factors were linked together. Lipid hypothesis that saturated fats causes rise in cholesterol & cholesterol causes heart attacks. Therefore saturated fats cause heart attacks is just a prediction rather than science.
Cholesterol is carried by the lipoproteins which contain triglycerides ( for energy delivery to all the cells of the body ) and cholesterol along with antioxidants like tocopherol, lycopenes, carotenes for cellular repair. The excess cholesterol and the junks are removed by HDL back to the liver which inturn is eliminated by the bile.
We can change the cholesterol numbers within days, simply by changing the major source of fuel i.e carbohydrates or fats. If one's diet is carbohydrate rich , then LDL-C will be low ; if diet is rich in fats , then LDL-C will be high. It is based on the lipid energy model.
Liver meets up to 80 % of cholesterol production, our body needs.is our body so stupid enough to make the demonized molecule , cholesterol just to kill itself ? If the diet is high in cholesterol , then the liver senses it makes less cholesterol and if you don’t take cholesterol in your diet , liver makes more of it. LDLl is essential for host defense, modulation of inflammation, prevention of vascular calcification , receptor functioning and processing , cellular signaling , neurotransmitter signaling, cell repair , muscle function , membrane integrity and Energy delivery.
The answer is yes !!! Only, If you stop the repetitive injury from your fork & spoon and smoking
Since angioplasty nor bypass prolong life, the indication is relief of incapacitating chest pains ( angina ) unrelieved by good medical therapy ( medications and lifestyle changes )
The Big Pharma & Food industry , near 100% of cardiologists ( AMA, AHA, ACC ) would like us to use processed vegan diet and Use cholesterol lowering medications like Statins and PCSK9 inhibitors to keep the LDL to near zero ( greater the reduction , higher the benefit ) giving a false sense of security against cardiovascular diseases.It is worthwhile to note that the cholesterol lowering drugs has no role in primary prevention. In fact, the effect of statins on extending lifespan, even in secondary prevention is merely the difference of only 3-5 days.
THE GREATEST DECEPTION OF ALL TIMES
| All Cause Mortality (ACM) timeline in LDL clinical trials with statins and PCSK9 inhibitors | |||||||
| Outcome | 4S | IDEL | CARDSATOR | ASPENATOR | JUPITER | IMPROVEIT | FOURIER |
| No.of Patients randomised | 4444 | 8888 | 2838 | 2410 | 17802 | 18144 | 27564 |
| LDL % reduction | 25.0% | 23.0% | 33.0% | 30.0% | 50.0% | 24.3% | 59.0% |
| Mortality - Treated | 8.2% | 8.2% | 4.3% | 5.7% | 2.8% | 5.8% | 3.2% |
| Mortality - Placebo | 11.5 | 8.4% | 5.8% | 5.7% | 2.2% | 5.7% | 3.1% |
| Mortality Benefit | 3.3 | 0.2% | 1.5% | 0% | 0.55% | 0.10% | 0.1% (+) |
| Year of Publication | 1994 | 2005 | 2004 | 2006 | 2008 | 2015 | 2017 |
What causes atherosclerosis ?
If not LDL-cholesterol , what else can cause heart disease. It is often an inflammatory disease produced by two major factors (i) Ectopic fat deposition (ii) Direct injury by the oxidizing molecules from processed foods - excess Sugars , Acidic drinks , Refined oils (PUFA) ,Trans-Fats , Smoking & Air pollution.. To repair this damage, the cholesterol kicks in and acts as a bandaid stabilizing the vessel wall.The plaque becomes unresolved & progressive if there is poor collagen formation which is largely due to poor micronutrients( vit C & minerals ).
The old concept : higher the LDL cholesterol = more invasion from lumen, crossing the endothelium and promoting atherogenesis ( Inside Out ).
The emerging concept : Ectopic fat deposition in the heart ( epicardial / intramyocardial ) elicits inflammatory response.The unresolved inflammatory process calls for the cholesterol rescue !!!! Finally Lp(a) is deposited by the blood vessels supplying the blood vessel - vasa vasorum ( Outside In ).
Statins have multiple side effects Cognitive decline and memory loss , accelerated aging , Myopathy and muscle soreness , cardiomyopathy , increase in the incidence of Diabetes. Yet , Statins are one of the most commonly prescribed drugs !!!!
If heart disease is an inflammatory disease ( fire ) , LDL- Cholesterol in particular Lp(a) is a firefighter which uses up antioxidants it carries,& supplies cholesterol for cellular repair ( band aid ).We have wrongly arrested the firefighters just because of their presence whenever there is any injury to blood vessels.
Insulin resistance is associated with chronic inflammation , Procoagulant state and Dyslipidemia ( Triglyceride/ HDL ratio > 1.3 and VLDL-C > 15. Here, Insulin resistance is the causative factor and all others are associated factors. Because of some association of increased LDL-C with Heart disease , it is mistakenly tagged as Causation or risk factors, and most of the measures are addressed to reduce LDL-Cholesterol !!! Wonder why we are not able to tackle the crisis of cardiovascular diseases.
Total LDL - Cholesterol is not a good indicator of Insulin resistance and hence cardiovascular health. But unfortunately, it is the most celebrated cardiovascular risk factor !!!Large dense LDL-C is neutral ( usually increases with low carb diet & lean mass ) with respect to cardiovascular diseases whereas small dense LDL-C( which increases with Insulin resistance and intake of excessive sugars and refined carbohydrates )is associated with increased cardiovascular risk. It is very important to understand that, LDL-C is only a surrogate marker of heart disease.
A unique but highly underrated entity in which the ECG and CT angiogram would be normal but still the patient continues to suffer from chest pain because of poor microvascular circulation ( multiple capillaries perpetrating the Myocardium of the heart).Coronary MVD is heart disease that affects the heart’s smallest coronary artery blood vessels.
Spasms within the walls of these very small arterial blood vessels cause reduced blood flow to the heart muscle. It could be relieved by augmenting the nitric oxide production by reversing Insulin resistance
Patients who go for master health check ups run through the stress test in a treadmill with constant monitoring of ECG or ECHO. The basic idea is whether the patient develops chest pain on exertion, accompanied by changes in the pattern of ECG or ECHO which likely happens when there is > 50-70% blockage in the coronaries. Around ⅔ of heart attacks occur due to soft plaques which cannot be detected by Treadmill stress. Treadmill or even CT angiogram cannot detect those vulnerable plaques !!!! People who are tested positive are advised for Angiogram warranting unnecessary therapeutic interventions in which the hard, fibrous plaques are treated, instead of treating the vulnerable plaques which typically cause plaque rupture and thrombosis.
CIMT ( Carotid Intima media Thickness ) by Ultrasound is a good surrogate indicator of cardiovascular health. The increased IMT reflects early stages of atherosclerosis and cardiovascular risk. It is cheap and non-invasive. Negative stress echo and stress MPI tests only imply a lack of flow limiting disease; they do not indicate lack of atherosclerotic disease. It is important to remember that when these tests are "negative," the implication is favorable short-term prognosis rather than any implication regarding lack of disease. In contrast, carotid intima-media thickness (CIMT) scanning protocols can detect atherosclerotic disease in early and asymptomatic stages. CIMT may be a more optimal screening and risk-stratifying technology. The CAFES-CAVE study showed that Ultrasound screening of B/L Carotid & Femoral bifurcations may the practical, reliable & cost-effective assessment of progression/regression of subclinical atheromas.
Stents , Statins & Surgical bypass are palliative measures not addressing the roots of cardiovascular health.
The key to cardiac wellness is Reversing Insulin Resistance ,
1.Augmenting nitric oxide production - leafy greens and exercise; . 2. Eliminating Ultra Processed foods - excess sugars , trans fats , PUFA (refined oils) & acidic drinks.
3. Avoidance of smoking and Alcoholism , Psychological Stress and Sedentarism.
