An Editorial on Complications of Acute Myocardial Infarction in Children and Adolescents

Anurag Bajaj^*
*Correspondence: Anurag Bajaj, Department of Cardiovascular Medicine, Mayo Clinic, Rochester, USA, Email:

Editorial

With a fatality rate more than double that of cancer, cardiovascular disease is the leading cause of death in the United States. More than half of all cardiovascular deaths are caused by acute myocardial infarction. The treatment of patients with acute myocardial infarction during and after treatment is investigated, with a focus on primary and secondary prevention, patient autonomy, and decision-making. A look at the future of treatment for acute myocardial infarction is also included. Despite declines in other age groups, cardiovascular disease continues to be a major source of bad outcomes in young people around the world. This group has a unique risk profile with less conventional cardiovascular risk factors as compared to older populations. Although plaque rupture is still the most prevalent cause of myocardial infarction, unique symptoms including plaque erosion, coronary microvascular dysfunction, spontaneous coronary artery dissection, and coronary spasm linked with drug use are more common in this age group [1].

The diversity in diagnosis and presentation, as well as therapeutic effects, highlights the need to examine the profile of myocardial infarction in young people [3]. We searched PubMed for articles with the terms acute myocardial infarction, young, plaque rupture, plaque erosion, spontaneous coronary artery dissection (SCAD), coronary vasospasm, variant or Prinzmetal angina, druginduced myocardial infarction, myocarditis, coronary embolism, microvascular dysfunction, MINOCA, and myocardial infarction in pregnancy.

To educate readers about the prevalence, risk factors, presentation, and treatment of acute myocardial infarction in young people, as well as specific subgroups with diagnostic and therapeutic issues. We also provide a costeffective method for dealing with these tough cases. Myocardial infarction (MI) is the medical term for a heart attack caused by plaque growth in the inside walls of arteries, which restricts blood flow to the heart and damages cardiac muscles due to a lack of oxygen. Shortness of breath, sweating, nausea, vomiting, irregular heartbeat, anxiety, weariness, weakness, stress, sadness, and other symptoms can all be indicators of MI. Two important treatments for MI are aspirin, which prevents blood clotting, and nitro-glycerin, which relieves chest pain and oxygen shortage [2,3].

Food, fat, cholesterol, salt, smoking, nicotine, alcohol, and medicines, as well as weekly blood pressure monitoring, daily exercise, and weight loss, can all assist to prevent heart attacks. To dissolve arterial blockage, thrombolytic or clot-dissolving drugs such as tumor necrosis factor activator, streptokinase, or urokinase are injected into the bloodstream within 3 hours of the onset of a heart attack [2]. Medications like morphine or meperidine can be used to relieve pain. Nitroglycerin and hypertension drugs such as beta-blockers, ACE inhibitors, and calcium channel blockers may be used to lower blood pressure and improve the heart's oxygen demand [3]. An ECG, coronary angiography, and X-ray of the heart and blood vessels may be performed to observe the narrowing of coronary arteries. This page discusses the causes, symptoms, and treatments for MI.

Acute myocardial infarction (MI) can develop in the absence of rapid atherothrombotic plaque breakdown due to increased myocardial oxygen demand and/or restricted supply, a condition known as type-2 myocardial infarction (T2MI). Clinical evidence of myocardial ischemia is required to make the diagnosis, just as it is for any other MI subtype. This syndrome is becoming more generally recognised as cardiac troponin assays become more sensitive, and it is connected to poor short- and long-term outcomes. There is inadequate evidence to identify optimum management strategies because T2MI is a diverse entity with variable etiologies and triggers [4,5]. As a result, these patients need specific attention. A major stumbling barrier is the lack of a unified definition that can be operationalized with high reproducibility. This page outlines T2MI research to help doctors better understand the disease's pathobiology, when to diagnose it, and how to treat it. It also clarifies the prognosis, identifies information gaps, and offers future recommendations.

References

1. Burns, Jane C., Howaida El-Said, Adriana H. Tremoulet, and Kevin Friedman, et al. "Management of myocardial infarction in children with giant coronary artery aneurysms after Kawasaki disease."  J Pediatr 221 (2020): 230-234.

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2. Tsimikas, Sotirios. "Elevated lipoprotein (a) and the risk of stroke in children, young adults, and the elderly." Eur Heart J 42 (2021): 2197-2200.

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3. YoldaÅ?, Tamer, and Utku Arman Ã?rün. "What is the significance of elevated troponin I in children and adolescents? A diagnostic approach." Pediatr Cardiol 40 (2019): 1638-1644.

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4. Gulati, Rajiv, Atta Behfar, Jagat Narula, and Ardaas Kanwar, et al. "Acute myocardial infarction in young individuals." Mayo Clin Proc  95 (2020): 136-156.

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5. Tunuguntla, Hari, Aamir Jeewa, and Susan W. Denfield. "Acute myocarditis and pericarditis in children." Pediatr Rev 40 (2019): 14-25.

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