[43092] in Discussion of MIT-community interests
#1 Trick to Prevent Heart Attacks
daemon@ATHENA.MIT.EDU (Heart Attack Fighter OmegaK)
Wed May 20 03:16:00 2015
Date: Wed, 20 May 2015 03:15:58 -0400
To: mit-talk-mtg@charon.mit.edu
From: Heart Attack Fighter OmegaK <heartattackfighteromegak@tuphery.eu>
Reply-to: Heart Attack Fighter OmegaK <heartattackfighteromegak@tuphery.eu>
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, apoptosis, also plays a role in the process of tissue damage following an MI.[55] As a result
, the person's heart will be permanently damaged. This myocardial scarring also puts the person at
risk for potentially life-threatening abnormal heart rhythms (arrhythmias), and may result in the
formation of a ventricular aneurysm that can rupture with catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The differ
ence in conduction velocity between injured and uninjured tissue can trigger den cardiac death. Ho
wever, VT usually results in rapid heart rates that prevent the heart from pumping blood effective
ly. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coron
ary ischemia and extension of the infarct.
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o it where must we go what mz7y must we do? </p>re-entry or a feedback loop that is believe
d to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibril
lation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac
death. Another life-threatening arrhythmia is ventricular tachycardia (V-tach/VT), which can cause sud
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that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coron
ary arteries, it leads to MI (necrosis of downstream myocardium).[50][51] It is estimated that one billion car
diac cells are lost in a typical MI.[54]
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the
heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow ba
ck. A collagen scar forms in their place. Recent studies indicate that another form of cell death
The cardiac defibrillator device was specifically designed to terminate these potentially fatal arrhythmias.
The device works by delivering an electrical shock to the person to depolarize a critical mass of the heart mu
scle, in effect "rebooting" the heart. This therapy is time-dependent, and the odds of successful defibrillati
on decline rapidly after the onset of cardiopulmonary arrest.
Myocardial infarction in the setting of plaque results from underlying atherosclerosis.[18] Inflamm
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