Coronary Heart Disease Is Not a Plumbing Problem

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Majid Ali, M.D.

New York  212-873-2444    *    New Jersey . 201-966-0027

 

Two Enemies of the Heart: Conflict and Anger

Conflict cannot be cleared by letting the steam out.

Anger sometimes can be cleared by letting the steam out.

 

Two Paths at the Cross-Road

The cross-road for coronary heart diseases offers two pathways:

  1. The mechanical plumbing way that leads to coronary stents to coronary stents, coronary bypasses to coronary bypasses, then to stents for legs and kidneys, and carotid arteries, and elsewhere;
  2. The way of the science and philosophy of holism in health and healing –  a way of learning, enlightenment, responsibility, and spirituality. This path does not exclude stents or bypasses for emergency situation, but it rejects the science of the plumbing model.

Endo Health for Vascular Health

Oxygen-Insulin Signaling Matrix for Endo Health

Endo Health for Vascular and Heart Health

Disruptions of the Oxygen-Insulin Signaling Matrix Lead to Coronary Heart Attacks and Other Forms of Cardiovascular Diseases

 

Two Enemies of the Heart: Conflict and Anger

Conflict cannot be cleared by letting the steam out.

Anger sometimes can be cleared by letting the steam out.

Clearer the Knowledge,

Better the Cardiovascular Health

Two Critical Links: the More the Coronary Plaques, Fewer the Heart Deaths 

https://majidalimd.me/2012/06/05/the-more-coronary-plaques-fewer-deaths-paradox/

Blood Cells Tell the Full Heart Disease Story

In coronary heart disease, attenuated oxygen signaling and accentuated insulin signaling tell the full story.

Red Blood Cells of a Healthy Person (upper picture) Figure 1

Early Stress on Red Blood Cells (lower picture) Figure 2

Micro-plaque Formation In Uncontrolled Diabetes (both pictures) 

What Is Endothelium?

What Are Good Endo Spices?

What Are Good Endo Herbs

 

What Hurts Endos Most?

Disrupted Oxygen-Insulin Signaling Matrix.

What Disrupts Oxygen-Insulin Signaling Matrix Most? 

Conflict and Anger

 

Crucial Endo Factors

Endothelium Maintains the Vasodilation and Vasoconstriction Balance

inhibition and promotion of the migration and proliferation of smooth muscle cells, fibrinolysis and thrombogenesis as well as prevention and stimulation of the adhesion and aggregation of platelets.

 

What Are Endos?

The vascular endothelium is a multifunctional organ and is critically involved in modulating vascular tone and structure. Endothelial cells produce a wide range of factors that also regulate cellular adhesion, thromboresistance, smooth muscle cell proliferation, and vessel wall inflammation. Thus, endothelial function is important for the homeostasis of the body and its dysfunction is associated with several pathophysiological conditions, including atherosclerosis, hypertension and diabetes. Patients with diabetes invariably show an impairment of endothelium-dependent vasodilation.

Endo Workers

  1.  Reactive Oxygen Species
  2.  Nitric Oxide
  3. Angiotensin II
  4.  EDHF      Endothelium-derived Hyperpolarization Factor
  5. .  Prostacyclin (PGI2
  6.    Antithrombotic (NO and PGI2 both inhibit platelet aggregation) 
  7.   Prothrombotic molecules [von Willebrand factor,
  8.   Plasminogen activator inhibitor-1 (PAI-1)

 

Nitric oxide

NO is a crucial player in vascular homeostasis. NO is synthesized within endothelial cells during conversion of l-arginine to l-citrulline by endothelial nitric oxide synthase (eNOS) [15]. It is released from endothelial cells mainly in response to shear stress elicited by the circulating blood or receptor-operated substances such as acetylcholine, bradykinin, or serotonin [16]. NO diffuses to vascular smooth muscle cells (VSMC) and activates soluble guanylate cyclase (sGC), yielding increased levels of cyclic guanosine-3,5-monophosphate (cGMP) and relaxation of VSMC [1,17]. Additionally, NO also prevents leukocyte adhesion and migration, smooth muscle cell proliferation, platelet adhesion and aggregation, and opposes apoptosis and inflammation having an overall antiatherogenic effect (Fig. 3) [18].

Microclots in Circulating Blood Part 2 from Majid Ali on Vimeo.

Red Blood Cells of a Healthy Person (upper picture) Figure 1
Early Stress on Red Blood Cells (lower picture) Figure 2

Red Blood Cells in a Micro-clot In Uncontrolled Diabetes (upper Picture) Figure 3

Red Blood Cell Clot Breaking Up (lower Picture) Figure 4

Micro-plaque Formation In Uncontrolled Diabetes (both pictures) Figures 5-6

Figure 7 (top) illustrates severely damaged erythrocytes in a 52-year-old man with persistent atrial fibrillation. Close examination shows some zones of congealing surrounding many damaged red blood cells.
Figure 8 (bottom) illustrates a zone of plasma congealing unaccompanied by any cellular elements of the blood (seemingly a “spontaneous” phenomenon) in a diabetic with IHD. In our view, such congealing represents accelerated oxidative stress on plasma.
Figure 9 (top) shows some needle-like and amorphous granular microclots in a patient with unstable angina.
Figure 10 (bottom) shows a “dirty” blood smear of a man with severe peripheral vascular disease and extensive bilateral leg ulcerations, showing zones of plasma congealing and lumpiness, platelet clumping, and some other zones of plasma congealing unaccompanied by any blood corpuscular elements, representing diffuse changes of AA oxidopathy.
Figure 11 (top) shows a microclot formed by a large aggregate of platelets and congealed plasma in a patient five days after angioplasty.
Figure 12 (bottom) shows another field from the same smear and illustrates how microclots in oxidative coagulopathy grow in size when oxidative stress persists.
Figure 13 (top) and figure 14 (bottom) show two microplaques in a patient who had received three unsuccessful angioplasties for advanced IHD. Photomicrographs were taken the day after a major nosebleed. Note the compaction of necrotic debris and blood elements in microplaques as contrasted with loose structure of microclots in figure 11.

 

of excess excess insulin and acidity in the blood damages blood cell membranes, clumps cells, forms crystals of acids, and weakens immune and hunter cells of the blood. In this article, the blood and its cells tell the diabetes story.
I hope people will study the microscopic pictures at the end of this article, understand their meanings, and then study them again with their children to teach them the dangers of eating excess sugary drinks and foods.
These pictures make it easy to learn and understand how diabetes causes poor circulation, heart attacks, and stroke. —for prevention and reversal—more simply and elegantly than any medical textbook or a doctor. Of course, cells can tell their diabetes story only to those who are willing to listen to them. We cannot understand the “cell-speak” if we keep repeating that diabetes is a sugar problem. Sugar is not a cell nor is diabetes cells. Nor can we communicate with cells if our focus is on excess insulin or insulin resistance.

Blood Cells Tell the Cell Membrane Story

Cell membranes exist to separate internal order of cells from their external disorder. They are responsible for cellular cross-talk. So, the health and strength of cells in all parts of the body depend on the the health and strength of their membranes. There are no lab tests available at this time for directly assessing the structural and functional integrity cell membrane in the pancreas (the source of insulin), liver, heart, brain, kidneys, muscles, and other body organs. The state of blood cell membranes, easily evaluated by direct microscopic examination of the blood, provides useful information, albeit indirect, about cell membranes in other body organs. Blood cells tell the story of cell membranes in all organs in the body. body I elaborate this crucial point by presenting the case of insulin and insulin receptor protein embedded in cell membranes.
Red Blood Cells of a Healthy Person (upper picture) Figure 1
Early Stress on Red Blood Cells (lower picture) Figure 2
Red Blood Cells in a Micro-clot In Uncontrolled Diabetes (upper Picture) Figure 3
Red Blood Cell Clot Breaking Up (lower Picture) Figure 4
Micro-plaque Formation In Uncontrolled Diabetes (both pictures) Figures 5-6
Figure 7 (top) illustrates severely damaged erythrocytes in a 52-year-old man with persistent atrial fibrillation. Close examination shows some zones of congealing surrounding many damaged red blood cells.
Figure 8 (bottom) illustrates a zone of plasma congealing unaccompanied by any cellular elements of the blood (seemingly a “spontaneous” phenomenon) in a diabetic with IHD. In our view, such congealing represents accelerated oxidative stress on plasma.
Figure 9 (top) shows some needle-like and amorphous granular microclots in a patient with unstable angina.
Figure 10 (bottom) shows a “dirty” blood smear of a man with severe peripheral vascular disease and extensive bilateral leg ulcerations, showing zones of plasma congealing and lumpiness, platelet clumping, and some other zones of plasma congealing unaccompanied by any blood corpuscular elements, representing diffuse changes of AA oxidopathy.
Figure 11 (top) shows a microclot formed by a large aggregate of platelets and congealed plasma in a patient five days after angioplasty.
Figure 12 (bottom) shows another field from the same smear and illustrates how microclots in oxidative coagulopathy grow in size when oxidative stress persists.
Figure 13 (top) and figure 14 (bottom) show two microplaques in a patient who had received three unsuccessful angioplasties for advanced IHD. Photomicrographs were taken the day after a major nosebleed. Note the compaction of necrotic debris and blood elements in microplaques as contrasted with loose structure of microclots in figure 11.

What Is Endothelium?

What Are Good Endo Spices?

What Are Good Endo Herbs

 

What Hurts Endos Most?

Disrupted Oxygen-Insulin Signaling Matrix.

What Disrupts Oxygen-Insulin Signaling Matrix Most? 

Conflict and Anger

 

Crucial Endo Factors

Endothelium Maintains the Vasodilation and Vasoconstriction Balance

inhibition and promotion of the migration and proliferation of smooth muscle cells, fibrinolysis and thrombogenesis as well as prevention and stimulation of the adhesion and aggregation of platelets.

 

What Are Endos?

The vascular endothelium is a multifunctional organ and is critically involved in modulating vascular tone and structure. Endothelial cells produce a wide range of factors that also regulate cellular adhesion, thromboresistance, smooth muscle cell proliferation, and vessel wall inflammation. Thus, endothelial function is important for the homeostasis of the body and its dysfunction is associated with several pathophysiological conditions, including atherosclerosis, hypertension and diabetes. Patients with diabetes invariably show an impairment of endothelium-dependent vasodilation.

Endo Workers

  1.  Reactive Oxygen Species
  2.  Nitric Oxide
  3. Angiotensin II
  4.  EDHF      Endothelium-derived Hyperpolarization Factor
  5. .  Prostacyclin (PGI2
  6.    Antithrombotic (NO and PGI2 both inhibit platelet aggregation) 
  7.   Prothrombotic molecules [von Willebrand factor,
  8.   Plasminogen activator inhibitor-1 (PAI-1)

 

Nitric oxide

NO is a crucial player in vascular homeostasis. NO is synthesized within endothelial cells during conversion of l-arginine to l-citrulline by endothelial nitric oxide synthase (eNOS) [15]. It is released from endothelial cells mainly in response to shear stress elicited by the circulating blood or receptor-operated substances such as acetylcholine, bradykinin, or serotonin [16]. NO diffuses to vascular smooth muscle cells (VSMC) and activates soluble guanylate cyclase (sGC), yielding increased levels of cyclic guanosine-3,5-monophosphate (cGMP) and relaxation of VSMC [1,17]. Additionally, NO also prevents leukocyte adhesion and migration, smooth muscle cell proliferation, platelet adhesion and aggregation, and opposes apoptosis and inflammation having an overall antiatherogenic effect (Fig. 3) [18].

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