Patofisiologi sarangan jantung, disabuik juo sabagai infark miokard, maliputi gangguan aliran darah ka bagian otot jantung, nan manyababkan kamatian sel jantung.
Hal iko biasonyo tajadi dek adonyo sumbatan arteri koroner dek gumpalan darah, nan acok disababkan dek aterosklerosis, suatu kondisi dimano plak batumpuak di arteri.
Plak tadiri dari kolesterol, zat lemak, produk limbah sel, kalsium, jo fibrin.
Katiko plak pacah, dapek mambuek tajadinyo gumpalan darah, nan dapek mamblokir arteri jo mancegah darah nan kayo oksigen mancapai otot jantung.
Laweh karusakan tagantuang pado laweh area nan disadiaan dek arteri nan tasumbek jo wakatu antaro sarangan jo pangobatan.
Gejala sarangan jantuang dapek barupo nyeri atau raso indak nyaman di dada, napas pendek, mual, galok, jo nyeri di tangan, guluang, rahang, atau balakang.
Pangobatan untuak sarangan jantung biasonyo maliputi pamulihan aliran darah ka otot jantung sacapek mungkin, malalui ubek atau prosedur sarupo angioplasti jo stenting atau operasi bypass arteri koroner.
Paralu diingek baso patofisiologi sarangan jantung adolah kompleks jo maliputi banyak faktor, tamasuak faktor genetik, gaya hiduik, jo lingkungan.
Faktor risiko untuak sarangan jantuang tamasuak takanan darah tinggi, kolesterol tinggi, marokok, diabetes, obesitas, kurangnyo aktivitas fisik, jo riwayaik kaluarga nan punyo panyakik jantuang.
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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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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