Myocardial Infarction in Young Adults: A Case Series and Comprehensive Review of Molecular and Clinical Mechanisms

Figures

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  Figure 1. Mechanisms of myocardial infarction in young adults.

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  Figure 2. Multifactorial mechanisms linking human immunodeficiency viruses to coronary artery disease in young adults.

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  Figure 3. Pathophysiological mechanisms of HIV-related plaque formation and destabilization. ART, antiretroviral therapy; HIV, human immunodeficiency virus.

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  Figure 4. Electrocardiogram with anterior STEMI (red arrows).

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  Figure 5. Coronary angiography of the left coronary system: (a) acute thrombotic occlusion of the left anterior descending artery; (b) subocclusion of the marginal artery.

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  Figure 6. Speckle-tracking echocardiography demonstrating GLS analysis in apical four-chamber (4CH), two-chamber (2CH), and apical long-axis (APLAX) views. The bull’s-eye plot shows segmental strain reduction in the anterior and septal regions, with a calculated GLS of −13.6%.

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  Figure 7. (a) Coronary angiography of the left coronary system (with subocclusive lesion at the left anterior descending artery). (b) Placement of a drug-eluting stent at that level.

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  Figure 8. (a) Coronary angiography of the left coronary system (with SCAD at the left anterior descending artery). (b) Placement of the wire and after that the two drug-eluting stents at that level.

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  Figure 9. Electrocardiogram with postero-infero-lateral STEMI (red arrows).

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  Figure 10. (a) Coronary angiography of the left coronary system. (b) Coronary angiography of the right coronary system. Coronary angiography showed severe three-vessel disease: 90% stenosis of the LAD and first diagonal branch, chronic proximal occlusion of the LCX, and 95% proximal stenosis of the RCA involving the posterior descending artery. A 30% distal stenosis of the LM artery was also noted.