The left anterior descending artery is the primary source of blood for the anterior wall of the heart. The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left side of the heart.

Option A: The circumflex artery supplies the lateral wall. The circumflex artery, fully titled as the circumflex branch of the left coronary artery, is an artery that branches off from the left coronary artery to supply portions of the heart with oxygenated blood. The circumflex artery itself divides into smaller arterial systems.
Option B: The internal mammary artery supplies the mammary. The internal thoracic artery (ITA), previously commonly known as the internal mammary artery (a name still common among surgeons), is an artery that supplies the anterior chest wall and the breasts.
Option D: The right coronary artery supplies the inferior wall of the heart. The right coronary artery supplies blood to the right ventricle and then supplies the underside (inferior wall) and backside (posterior wall) of the left ventricle.

Although the coronary arteries may receive a minute portion of blood during systole, most of the blood flow to coronary arteries is supplied during diastole.

Option A: Breathing patterns are irrelevant to blood flow. It has been suggested that the diaphragm will preferentially steal blood flow from working locomotor muscles during increased activity (Bradley & Leith, 1978; Musch, 1993). In healthy adults, the cost of breathing is <5% of the total oxygen consumption at low-level exercise but approaches 15% during heavy exercise in young athletes or older fit subjects (Aaron et al. 1992; Dempsey & Johnson, 1992). Further, reflex vasoconstriction of the locomotor muscles is evident when a substantial respiratory load is applied sufficient to elicit diaphragm fatigue
Option C: Expiration is not related to the blood flow. The pulmonary system is intimately linked with the cardiovascular system anatomically and hemodynamically and plays a significant role in exercise intolerance through a number of mechanisms (Olson et al. 2006a,b;).
Option D: There is a little portion of the blood that the coronary arteries receive during systole. During systole, intramuscular blood vessels are compressed and twisted by the contracting heart muscle and blood flow to the left ventricle is at its lowest. The force is greatest in the subendocardial layers where it approximates to intramyocardial pressure.

Coronary artery disease accounts for over 50% of all deaths in the US.

Option A: Cancer accounts for approximately 20%.
Option C: Liver failure accounts for less than 10% of all deaths in the US.
Option D: Less than 10% of all deaths in the US can be attributed to renal failure.

Atherosclerosis, or plaque formation, is the leading cause of CAD.

Option B: DM is a risk factor for CAD but isn’t the most common cause. Near-normal glycemic control for a median of 3.5 to 5 years does not reduce cardiovascular events. Thus, the general goal of HbA1c <7% appears reasonable for the majority of patients. Iatrogenic hypoglycemia is the limiting factor in the glycemic management of diabetes and is an independent cause of excess morbidity and mortality.
Option D: Renal failure doesn’t cause CAD, but the two conditions are related. Chronic kidney disease (CKD) accelerates the course of coronary artery disease, independent of conventional cardiac risk factors. In addition, CKD has been shown to confer inferior clinical outcomes following successful coronary revascularisation, which may be offset by arterial grafting.
Option C: Myocardial infarction is commonly a result of CAD. Myocardial infarction occurs when a coronary artery is so severely blocked that there is a significant reduction or break in the blood supply, causing damage or death to a portion of the myocardium (heart muscle).

Arteries, not veins, supply the coronary arteries with oxygen and other nutrients. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcification.

Option A: Atherosclerosis is a direct result of plaque formation in the artery. Most often, the culprit morphology is plaque rupture with exposure of highly thrombogenic, red cell-rich necrotic core material. The permissive structural requirement for this to occur is an extremely thin fibrous cap, and thus, ruptures occur mainly among lesions defined as thin-cap fibroatheromas.
Option C: Blood clots form inside the vessel wall and impede circulation. Also common are thrombi forming on lesions without rupture (plaque erosion), most often on pathological intimal thickening or fibroatheromas. However, the mechanisms involved in plaque erosion remain largely unknown, although coronary spasm is suspected.
Option D: Hardened vessels can’t dilate properly and, therefore, constrict blood flow. During atherogenesis, the local vessel segment tends to remodel in such a way that the lumen area is usually not compromised until plaques are large (expansive remodeling). Thereafter stenosis formation may occur through continued plaque growth or shrinkage of the local vessel segment (constrictive remodeling) or a combination of the 2 processes.