A 63-YEAR-OLD-MAN

Introduction
Aged people comprise the fastest growing population in many developed countries.
Unfortunately, the most common cause of death in aged people is cardiovascular disease (CVD).
Lipid-lowering treatment has gained popularity since the last decade. Hypercholesterolemia
increases the risk factors in old people. According to research, the mortality rate among the old
population was high when total cholesterol (TC) was lower. (Petersen, Christensen and
Kragstrup, 2010) There is no straightforward TC optimal level was estimated. Nonetheless, there
is insufficient data to suggest any lipid-lowering treatment in the aged population group.
According to the 2018 health guidelines, people who are less than 20 years of age and encounter
atherosclerotic cardiovascular disease (ASCVD) are treated more promptly. People who are
more than 20 years of age, especially aged people who have a prior non-fasting lipid profile can
repeat the lipid-lowering treatment.

Usually, people can reduce the risks of ASCVD to a minimum by adopting healthier lifestyle
practices. By healthier lifestyle practices, it means controlling calorific intake, saturated fats,
cholesterol, and trans fat. Additionally, the patient can exercise to remain physically active and
fit. Even a moderate amount of workout can reduce the risks of ASCVD significantly. Other than
that, statins are used in lipid-lowering treatments.

Adjusting lipid-lowering treatment

There are three main types of statins namely high intensity, moderate intensity, and low-intensity
statins. High-intensity statins can reduce the LDL-C levels by 50%, while moderate-intensity
stains can do by 30%. There is a full-fledge stepwise approach to maintain cholesterol levels, for
instance, adopting therapies unless and until cholesterol levels are reduced. If statins solely prove
to be ineffective, it can be coupled with other drugs to alleviate CVD and hypercholesterolemia.
For example, adding some doses of ezetimibe or bile acid sequestrant along with statin dosage.
This can reduce cholesterol levels by up to 30 percent. According to one research, adding a
PCSK9 enzyme inhibitor can reduce the risks of up to 64 percent. Aged people must administer
tolerated, yet controlled statins. If the person has diabetes then the risks of CVD increase so
he/she must follow proper guidelines. (Cholesterol Management Guide for healthcare
practitioners, 2020)
Patients with prior cardiovascular incidents must adopt secondary prevention procedures to
reduce the risks of subsequent events. They must reduce the cholesterol threshold to 70 mg/dL
along with PCSK9 enzyme inhibitor and ezetimibe dosage.

After patients have chosen the right type of medical procedures, they must assess and monitor
themselves for at least 4 weeks. For better results, a 12 weeks monitoring is suggested both
fasting and nonfasting monitoring. By comparing your LDL-C percentage reductions, one can
calculate the effectiveness of statin medication they are taking. Initially, it might reduce LDL-C
levels by 1 percent, which reduces CVD risks by 1 percent. However, this is a great baseline for
your cholesterol reduction journey. As per well-furnished reports, a statin dosage of 38.7 mg/dL
can reduce the CVD risks up to 21 percent.

Lipoprotein (a) and apolipoproteins

The chemical composition of Lp(a) is similar to LDL. There is an extra protein base called
apolipoprotein and a disulfide B100 bridge. The similarities between apolipoprotein (a) and
lipoprotein (a) are important to discuss while studying thrombosis and atherosclerosis. Lp(a)
usually interferes with tissue plasminogen activator (tPA) to generate a hypercoagulable state.
Human Lp(a) and 17 Kringle recombinant apo(a) inherit concrete inhibition while working with
cofactors.

Some species of apo(a) lack protease domain but still inherit strong inhibition power, this means
that apo(a) plasminogen’s interaction with apo(a) protease domain neglects the plasminogen
activation. A very strong variant, lysine-binding site on kringle type 10, exhibited a reduced
inhibition rate. Apo(a) that was amino-terminally truncated can use additional sequences to
increase inhibition power. (Hancock et al., 2003)

One of the major factors that increase CVD risks is the atherogenicity of lipoprotein (a). it is an
apoprotein which is similar to plasminogen molecule. As a result, it competes with a
plasminogen molecule for activation and uptake of fibrin on cell surfaces. The presence of
lipoprotein (a) in a reaction reduces the function of plasminogen by 70-80 percent. In some of
the arteries, there is no competition because of the absence of lipoprotein (a). (Smith and
Crosbie, 1991)

References
American Heart Association, 2020. Cholesterol Management Guide for healthcare practitioners.
[online] Available at: <https://www.heart.org/-/media/files/health-
topics/cholesterol/chlstrmngmntgd_181110.pdf> [Accessed 30 June 2020].
Hancock, M., Boffa, M., Marcovina, S., Nesheim, M. and Koschinsky, M., 2003. Inhibition of
Plasminogen Activation by Lipoprotein(a). Journal of Biological Chemistry, [online] 278(26),
pp.23260-23269. Available at: <https://pubmed.ncbi.nlm.nih.gov/12697748/#:~:text=Lp(a)
%20may%20interfere%20with,a%20hypercoagulable%20state%20in%20vivo.&text=Human
%20Lp(a)%20and%20a,strong%20inhibition%20with%20both%20cofactors.> [Accessed 30
June 2020].

Petersen, L., Christensen, K. and Kragstrup, J., 2010. Lipid-lowering treatment to the end? A
review of observational studies and RCTs on cholesterol and mortality in 80+-year olds. Age and
Ageing, 39(6), pp.674-680.

Smith, E. and Crosbie, L., 1991. Does lipoprotein(a) (Lp(a)) compete with plasminogen in
human atherosclerotic lesions and thrombi?. Atherosclerosis, [online] 89(2-3), pp.127-136.
Available at: <https://www.sciencedirect.com/science/article/abs/pii/0021915091900525>
[Accessed 30 June 2020].