The 10% refers to the heart's ejection fraction (EF). Meaning the heart is pumping into circulation 10% of the filled chamber with each heartbeat. Normal is 55 to 75% and below 29% is considered heart failure (the heart is unable to meet the system's demand for blood/oxygen. With an EF below 29%, sometimes the oxygenated blood backs up into the lungs causing pulmonary edema.
The prognosis depends on the underlying cause for the low EF. At one time five years ago, my EF was 29 to 13%. If your father has hypokinesis (impaired heart muscle) caused by a dilated left ventricle (my condition) and a deficit of blood to a portion of the heart due to blockage there can be a return to normal functioning...the appropriate treatment for relief would be a dilation of the vessels to decrease the heart's workload (size can return to normal) and open vessels to the oxygen/blood deficit area. It is possible the heart cells deficit of oxygen is not dead (necrosis), and supplying blood to the area will revitalize heart cells. Damaged heart cells do not properly contract the heart muscles that enable effective pumping, and that is the cause of the low EF.
If the heart muscle is necrotically impaired (dead), the outlook for normal pumping of blood into circulation is not very good (stem cell therapy required to produce new heart cells). Heart muscle can also be damaged by a virus, drugs, alcohol, etc. and there is not a very good prognosis for that group as well.
Slow or fast acting nitrates (time release) and nitro (fast acting) physiologically dilates/relax coronary vessels.
For system vessels angiotensin-converting enzyme (ACE) inhibitors help relax blood vessels. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance in your body that affects your cardiovascular system by narrowing your blood vessels and releasing hormones that can raise your blood pressure. This narrowing can cause high blood pressure and force your heart to work harder.
Beta blockers also reduce the workload of the heart and thereby the demand of the heart muscle for oxygen. Since the chest pain of angina pectoris occurs when the oxygen demand of the heart exceeds the supply, beta blockers can be useful in treating angina by reducing the need of the heart for oxygen.
....A stent implant mechanically structures an opening and changes the natural anatomy of vessel and disrupts endothelium cells functionality. The endothelium is the thin layer of cells that line the interior surface of blood vessels, forming an interface between circulating blood in the lumen and the rest of the vessel wall.
Endothelial cells are involved in many aspects of vascular biology, including: vasoconstriction and vasodilation, and hence the control of blood pressure
Blood clotting (thrombosis & fibrinolysis) at stent site is probable after a stent implant for up to a year or more.
Also endothelial dysfunction is very common in patients with diabetes mellitus, hypertension or other chronic pathophysiological conditions
Harvested vessels for a bypass is vulnerable as well.
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