Evidence of Learning #3

Date:​ ​February 23, 2020

Subject:​ ​Myocardial Infarctions
MLA Citation:
Saleh, Moussa, and John A Ambrose. “Understanding Myocardial Infarction.” F1000Research,
F1000 Research Limited, 3 Sept. 2018,
www.ncbi.nlm.nih.gov/pmc/articles/PMC6124376/​.

Analysis

Sometimes in life it’s good to take a step back and take a look at the broader
undercurrents. Thus, through this evidence of learning I aspire to take a step back and delve into
a topic that has the broadest applicability: myocardial infarctions. There are countless stories in
my life and many others revolving around the ramifications of this condition. In that sense, this
assessment is a manifestation of all those stories as I attempt to understand its pathogenesis.
An intriguing aspect of the article is its apt definition of myocardial infarctions as an
imbalance in the supply-demand ratios of oxygen to the cardiac muscle. I felt that this
perspective enabled me to garner a deeper understanding of how abnormal heart rhythms can
induce changes in these supply-demand ratios. Furthermore, the article presents an interesting
distinction between non-ST elevation myocardial infarctions (NSTEMI) and ST elevation
myocardial infarctions (STEMI) in that the latter is defined by the complete occlusion of the
epicardial coronary artery and the former is generally characterized by the occlusion of a small
branch. Thus, the magnitude of the ramifications of an STEMI is relatively greater because of the
potential for reperfusion and collateral blood flow that characterizes NSTEMI. On that account, I
found it interesting that the depression of the ST waves on an ECG is an indication of lack of
necessary necrosis to substantiate ST elevations. Thus, this distinction provides valuable context
in terms of understanding distinctions in treatment administration.
From a pathogenesis perspective, I found the information pertaining to the composition
of atherescleroistic lesions to be enlightening. To expound upon, the progression of the
inflammation to accomodate for the fibrous cap leads to the consistent degeneration of the tunica
intima. In essence, the rupture of the fibrous cap activates a pro-thrombotic material due to its
composition of macrophages and monocytes. Thus, it allowed me to visualize the connection
between endothelial damage and the activation of the coagulation pathway through the
infiltration of monocytes and macrophages. ​However, I was confused by how the auto-immune
function of macrophages related to creation of thrombin material? Is it solely due to the
macrophage role in consumption of oxidized-LDL. Or do the macrophages contribute to rupture
of the cap?
In addition the article’s discussion of the oxidation of LDL helped me better understand a
concept I previously studied involving uncontrollable release of neutrophil proteases and oxygen
derived radicals. In essence the presence of these innate immune response mechanisms creates
blood clots and a pro-thrombotic environment. On that note, I aspire to continue to research the
role of macrophages and oxidized LDL in fostering this environment. Are there any drugs
targeted to inhibit macrophage activity?
Through this evidence of learning, I feel that I have been able to expand upon my prior
knowledge of myocardial infarctions to understand how a coronary thrombus is formed. Thus, in
my future research ​I hope to answer my aforementioned questions pertaining to plaque rupture
and address other mechanisms of thrombosis such as plaque erosion and calcified nodules.​ In
addition, I think that by addressing the ECG classifications of myocardial infarctions, I have
developed context for subsequent distinctions in treatment.