Coronary Heart Disease Is Not a Plumbing Problem
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:
- 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;
- 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
- Reactive Oxygen Species
- Nitric Oxide
- Angiotensin II
- EDHF Endothelium-derived Hyperpolarization Factor
- . Prostacyclin (PGI2
- Antithrombotic (NO and PGI2 both inhibit platelet aggregation)
- Prothrombotic molecules [von Willebrand factor,
- 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 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





Blood Cells Tell the Cell Membrane Story







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
- Reactive Oxygen Species
- Nitric Oxide
- Angiotensin II
- EDHF Endothelium-derived Hyperpolarization Factor
- . Prostacyclin (PGI2
- Antithrombotic (NO and PGI2 both inhibit platelet aggregation)
- Prothrombotic molecules [von Willebrand factor,
- 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].
