Lakhasly

Cardiovascular disease (CVD) is a major health concern in the United States, with a significant number of individuals affected by various conditions. Hypertension affects 75 million people, while coronary heart disease affects 25.155 million, myocardial infarction 790,000, heart failure 6.5 million, and stroke 7.95 million. These numbers cannot be simply added due to the presence of comorbidities.

The underlying pathology of CVD involves the buildup of plaque within arterial walls, a process known as atherosclerosis. This starts with damage to the endothelial cells, triggering an inflammatory response involving phagocytes and monocytes. These monocytes transform into foam cells, ingesting oxidized cholesterol and forming fatty streaks within the vessels. Intracellular microcalcification then occurs, forming deposits within the vascular smooth muscle cells.

A protective fibrin layer, or atheroma, forms between the fatty deposits and the artery lining. Atheromas produce enzymes that cause the artery to enlarge over time, compensating for the narrowing caused by the plaque buildup. This process, while seemingly beneficial, can lead to further complications.

Types and Incidence of
Cardiovascular Disease in the United States
Hypertension: 75,000,000
Coronary heart disease: 25,155,000
Myocardial infarction: 790,000
Heart failure: 6,500,000
Stroke: 7,950,000
Because of comorbidities, it is not possible to add these numbers
together to reach a total (American Heart Association [AHA], 2010;

blood pressure. The inner lining is a thin layer of endothelial cells (the
endothelium) that in a healthy state is smooth and responsive. The
endothelium functions as a protective barrier between tissues and cir-
culating blood. It facilitates bidirectional passage of macromolecules
and blood gases to and from tissues and blood. Endothelial cells sense
changes in blood flow and respond with the release of bioactive
substances that maintain vascular homeostasis. One such substance is
nitric oxide (NO). NO is a soluble gas continually synthesized from
the amino acid l-arginine in endothelial cells. NO has a wide range of
biologic properties that maintain vascular homeostasis. It appears to
be involved in protection from injurious substances and plays a key
role in vasodilation (Tousoulis et al, 2012). Decreased NO is a factor in
the endothelial cell dysfunction that disrupts vascular balance and can
result in vasoconstriction, platelet activation, leukocyte adherence, and
vascular inflammation.
Pathophysiology
ASCVD involves the accumulation of plaque within the walls of the
arteries. It starts with injury to the endothelial cells with an associated
inflammatory response involving phagocytes and monocytes. Once in
the tissue, monocytes evolve into a specialized type of macrophage
called a foam cell that ingests oxidized cholesterol and becomes fatty
streaks in these vessels. Intracellular microcalcification occurs,
forming deposits within the vascular smooth muscle cells of the sur-
rounding muscular layer (Fig. 32.1).
A protective fibrin layer or atheroma forms between the fatty
deposits and the artery lining. Atheromas produce enzymes that cause
the artery to enlarge over time, thus compensating for the narrowing