Tasnudert n tnefsit n wul, yettwasnen daɣen s yisem n infarctus n wul, d asegdel n uḥemmal n yidammen ɣer yiwen n uḥric n uẓar n wul, yettawin ɣer tmettant n yiɣsan n wul.
Aya yettili-d s umata ɣef lǧal n uḥbas n tgezzayt n tgezzayt s uqabel n yidammen, i d-yettasen s waṭas seg atherosclerosis, d talɣa ideg yettimɣur ukala deg tgezzayin.
Taɣessa tettwaxleq s ukkolestrul, tisentanin timellalin, isufar n tsilunin, akalṣyum d fibrin.
Mi ara yerreẓ uẓeṭṭa, yezmer ad d-yeglu s uqabel n yidammen, izemren ad yergel taẓeḍḍayt u ad yegdel idammen yeččuren d uksijin ad awḍen ɣer uẓar n wul.
D lexṣaṣ-a n uksijin i d-yettaǧǧan tisilunin n yiɣsan n wul ad mmtent, dɣa d ayen i d-yettawin aṭṭan n wul.
Azal n lexṣara icudd ɣer teɣzi n wemkan i d-tettak tgejdit-nni yettwamdel akked wakud yellan gar n tuṭṭfa d usafar.
Isekna n tuṭṭfa n wul zemren ad ilin leqriḥ neɣ uḥulfu n diri deg uεebbuḍ, nnefs wezzilen, aεebbuḍ, tazzla, leqriḥ deg iɣallen, amgerḍ, tafrut neɣ aɛrur.
Asafar n waṭṭan n wul yezga yezga deg tujjya n uḥellu n yidammen ɣer uẓar n wul s tɣawla ma yella wamek, ama s ddwa neɣ s tarrayin am angioplasty d stenting neɣ s temhelt n tgezzayt n tgezzayt n wul.
Yessefk ad nẓer belli tasnudert n tnefsit n wul d tin yemgaraden yerna tettawi-d aṭas n yimgan, gar-asen imgan azayanen, amek yettidir umdan d yimgan.
Imgan n umihi n waṭṭan n wul llan deg-sen tazɣent n yidammen, asbuɣer n cholesterol, akeyyef, aṭṭan n sskeṛ, tuget n lmizan, lexṣaṣ n tuzzya n tfekka, akked umezruy n twacult n waṭṭan n wul.
Asefrek n yimgan-a n umihi yezmer ad d-iwenneε ad yenqes umihi n tuṭṭfa n wul.
Scott J: Pathophysiology and biochemistry of cardiovascular disease. Curr Opin Genet Dev. 2004, 14 (3): 271-9.
Liu Chung Ming C, Sesperez K, Ben-Sefer E, Arpon D, McGrath K, McClements L, Gentile C: Considerations to Model Heart Disease in Women with Preeclampsia and Cardiovascular Disease. Cells. 2021, 10 (4): .
Hansen J, Victor RG: Direct measurement of sympathetic activity: new insights into disordered blood pressure regulation in chronic renal failure. Curr Opin Nephrol Hypertens. 1994, 3 (6): 636-43.
LaMacchia JC, Roth MB: Aquaporins-2 and -4 regulate glycogen metabolism and survival during hyposmotic-anoxic stress in Caenorhabditis elegans. Am J Physiol Cell Physiol. 2015, 309 (2): C92-6.
Tham YK, Bernardo BC, Ooi JY, Weeks KL, McMullen JR: Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Arch Toxicol. 2015, 89 (9): 1401-38.
Lonn E: The clinical relevance of pharmacological blood pressure lowering mechanisms. Can J Cardiol. 2004, 20 Suppl B (): 83B-88B.
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['akked (6) azmul n tfekka neɣ n tuqqna tagensit n bab n yizerfan neɣ n umdan yettwafernen ad yexdem s yisem n bab n yizerfan. ']
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['Ttxil-k azen-aɣ-d imayl ma tesεiḍ asteqsi / asumer.']
What is pathophysiology of heart attack?
The pathophysiology of a heart attack, also known as myocardial infarction, involves the disruption of blood flow to a part of the heart muscle, leading to the death of heart cells.
This typically occurs due to the obstruction of a coronary artery by a blood clot, which is often the result of atherosclerosis, a condition where plaque builds up in the arteries.
The plaque is made up of cholesterol, fatty substances, cellular waste products, calcium, and fibrin.
When a plaque ruptures, it can cause a blood clot to form, which can block the artery and prevent oxygen-rich blood from reaching the heart muscle.
This lack of oxygen causes the heart muscle cells to die, leading to a heart attack.
The extent of the damage depends on the size of the area supplied by the blocked artery and the time between the attack and treatment.
Symptoms of a heart attack can include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and pain in the arms, neck, jaw, or back.
Treatment for a heart attack usually involves restoring blood flow to the heart muscle as quickly as possible, either through medication or procedures such as angioplasty and stenting or coronary artery bypass surgery.
It is important to note that the pathophysiology of a heart attack is complex and involves multiple factors, including genetic, lifestyle, and environmental factors.
Risk factors for heart attack include high blood pressure, high cholesterol, smoking, diabetes, obesity, lack of physical activity, and a family history of heart disease.
Managing these risk factors can help reduce the likelihood of experiencing a heart attack.
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