You could learn more about cardiology courses with Prof. Sameh Allam by clicking on the courses’ library link here:

Objectives for this course:
1- Master the essentials of a successful complex PCI by using the radial approach
2- Essential questions on radial approach and the use of the specific radial device(s)
3- Clinical case strategy and radial approach limits
4- Anatomical variations in the Radial artery.
5- Master the essential steps of a successful radial procedure.

In this lecture, we will discuss “Why CAD behavior differs?”, coronary microvascular dysfunction, and what is chronic total occlusion (CTO).

The coronary arteries are the blood vessels that carry blood to your heart. Coronary artery disease is the narrowing or blockage of the coronary arteries. This condition is usually caused by atherosclerosis.
Atherosclerosis is the build-up of cholesterol and fatty deposits (called plaques) inside the arteries. These plaques can clog the arteries or damage the arteries, which limits or stops blood flow to the heart muscle.

If the heart does not get enough blood, it cannot get the oxygen and nutrients it needs to work properly. This can cause chest pain (angina) or a heart attack.

During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution.
We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD.
Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder.
The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques.
Revascularization effectively relieves ischemia, but we now recognize the need to attend to non obstructive lesions as well.
Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenosis causes many acute coronary syndromes (ACS).
The disrupted plaque represents a “solid-state” stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the “fluid phase” of the blood can also predispose toward ACS.
Recent results have established the multiplicity of “high-risk” plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease.
Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid “stabilization” of other plaques that may produce recurrent events. The concept of “interventional cardiology” must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.

In the daily practice of cardiology, we confront CAD continually. Despite our quotidian familiarity with its clinical aspects, our views of the pathophysiology of coronary atherosclerosis have changed radically in the past decade.
Our understanding of the anatomy and underlying biology of coronary atherosclerosis will likely continue to evolve, driven by advances both at the laboratory bench and in the clinic. We can now link the biology of the blood vessel, the myocyte, and the inflammatory response to our classic hemodynamic approach to achieve a more profound understanding of clinical CAD.

The revision of our classic views of atherosclerosis has important practical implications for patient care. Our revascularization strategies become ever better and more successful. Insights into the mechanisms of thrombosis, both at sites of intervention and in the more distal microcirculation, furnish a foundation for improved concomitant therapy of patients who undergo acute revascularization to reduce complications and preserve myocardium.

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