Biological Science for Practice: Cardiovascular Disease Report

This report analyzes Mr. Scott's case of heart failure, discussing the biological processes involved. It explores the transition of monocytes to foam cells in atherosclerosis, explaining how atrial fibrillation contributes to heart failure and the causes of paroxysmal nocturnal dyspnea. The report also calculates the Number Needed to Treat (NNT) for dabigatran and warfarin in preventing bleeding. It references relevant research papers and textbooks to support the analysis of cardiovascular disease and its management, providing insights into the patient's diagnosis, symptoms, and treatment options. The report emphasizes the importance of understanding the underlying biological mechanisms to effectively manage cardiovascular conditions.

Running Head: Biological Science For Practise
BIOLOGICAL SCIENCE FOR PRACTISE

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Table of Contents
Answer to Question 1.................................................................................................................3
Answer to Question 2.................................................................................................................3
Answer to Question 3.................................................................................................................3
Answer to Question 4.................................................................................................................4
Reference list..............................................................................................................................5

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Answer to Question 1
Circulating monocyte, changes into foam cell and leads to occurrence of atherosclerosis.
Intimal penetration of monocyte indicates that circulating monocytes are responsible for
formation of foam cells. In addition, preferential adherence of monocytes proves that
monocyte helps in creation of foam cells, which leads to occurrence of atherosclerosis.
Monocytes might scavenge dead cells and researches have shown that it can be differentiated
into foam cells for doing this action (Hilgendorf, Swirski & Robbins, 2015). As foam cells
cause fat deposition in blood cells, it can be stated that monocyte plays important role in
occurrence of atherosclerosis.
Answer to Question 2
Mr. Scott has a history of atrial fibrillation. However, this atrial fibrillation (AFib) can lead
to permanent heart failure. This can occur because during atrial fibrillation heart did not
pump enough blood, which can meet need of body (Connolly et al. 2010). AFib leads to heart
failure because beating of heart is fast that prevents in filling of heart chambers with enough
blood for pumping out to body. As a result, blood can back up in pulmonary veins. If heart
doesn't pump blood efficiently then fluid in lungs can cause fatigue and shortness of breath
that Mr. Scott is facing currently.
Answer to Question 3
Paroxysmal nocturnal dyspnoea (PND) generally occur due to depression of respiratory
center when sleeping. This reduces arterial tension of oxygen and it occurs in patients who
have reduced pulmonary compliance (Tortora & Derrickson, 2017). A patient with
congestive heart failure if lies down then left ventricle fails to match output with normally

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functioning right ventricle. This causes pulmonary congestion, which can be decreased if
patient takes an erect position while sleeping. Mr. Scott is facing a problem that may be
considered as a symptom of heart failure. Failure of heart muscles to pump blood throughout
the body can lead to this disease and problem during sleeping can occur.
Answer to Question 4
Calculation of NNT= 1/ARR (Absolute Risk Reduction) (Schulman et al. 2009)
=1/ (CER-EER) [CER=Event rate of Control group, EER=Event rate of Experiment group)
NNT calculation to prevent 1 bleeding (Event),
25 patients administered with dabigatran (150 mg) and 25 patients were treated without
dabigatran. EER observed 15% and CER 65%.
ARR= (0.65-0.15)= 0.5
NTT= 1/0.5=2 for Dabigatran (150 mg)
25 patients administered with Warfarin (150 mg) and 25 patients were treated without
dabigatran. EER observed 40% and CER 65%.
ARR= (0.65-0.4) = 0.25
NTT= 1/0.25=4 for Warfarin (150 mg)
Hence, Dabigatran is more effective than Warfarin in preventing bleeding.

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Reference list
Connolly, S. J., Ezekowitz, M. D., Yusuf, S., Reilly, P. A., & Wallentin, L. (2010). Newly
identified events in the RE-LY trial. New England Journal of Medicine, 363(19),
1875-1876. Retrieved from: https://www.nejm.org/doi/full/10.1056/NEJMc1007378
Hilgendorf, I., Swirski, F. K., & Robbins, C. S. (2015). Monocyte fate in atherosclerosis.
Arteriosclerosis, thrombosis, and vascular biology, 35(2), 272-279. Retrieved on 18th
April 2019, from
https://www.ahajournals.org/doi/full/10.1161/ATVBAHA.114.303565
Schulman, S., Kearon, C., Kakkar, A. K., Mismetti, P., Schellong, S., Eriksson, H., ... &
Goldhaber, S. Z. (2009). Dabigatran versus warfarin in the treatment of acute venous
thromboembolism. New England Journal of Medicine, 361(24), 2342-2352. Retrieved
from: https://www.nejm.org/doi/full/10.1056/nejmoa0906598
Tortora, G. J., & Derrickson, B. (2017). Principles of anatomy & physiology. US: John Wiley
& Sons, Incorporated.