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Communications to the Editor |

Myocardial Infarction in the Very Young FREE TO VIEW

Basil M. RuDusky, MD, FCCP
Author and Funding Information

Affiliations: Wilkes-Barre, PA,  Gundersen Lutheran Heart Institute, La Crosse, WI

Correspondence to: Basil M. Rudusky, MD, FCCP, 15 Public Square, Suite 208, Wilkes-Barre, PA 18701-1702



Chest. 2002;122(3):1099-1100. doi:10.1378/chest.122.3.1099
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To the Editor:

The report on the well-performed study “Myocardial Infarction in Young Adults With Low-Density Lipoprotein Cholesterol Levels < 100 mg/dL,” which was published in a recent issue of CHEST (December 2001),1 merits additional clinical commentary. The authors correctly pointed out the limitations of the study, especially with regard to the absence of homocysteine levels and lipoprotein subgroup analysis, are being addressed in a study that is presently being performed by their group. The report beckons the attention of the reader toward the less common presentation of acute myocardial infarction in patients who are in the truly young age group of < 20 years old.

One must question the proclamation of young adults in the title of this study, for it is doubtful that clinicians would consider ages 55 to 65 years as young adults, even with the SD of ≤ 8 years that is given by the authors. These patients are basically in middle age in the population profile, with young adults being classified as < 45 years old. The problem is in classifying patients into categories in which the young are truly so (ie, < 30 years old), for then we have children, adolescents, and the younger population beyond the adolescent stage through the teenage years included.

In the study, a total of 6 patients were noted to have “either negative or insignificant levels of residual plaques” among the 79 patients in groups 1 and 2. These were patients who fell into the enigmatic category of acute myocardial infarction with healthy coronary arteries. This situation is the usual finding in very young (ie, teenaged) patients and is even more problematic in the absence of associated risk factors. These risk factors include a host of disease states, metabolic and endocrine disorders, illicit drug use, and coagulopathies. In some of these patients, coronary vasospasm is undoubtedly the mechanism involved in the production of the acute infarct, but this would not explain all cases. As the authors point out, a search for “novel risk factors” is needed, as these may be responsible for the development of premature coronary artery disease in young adults with optimal low-density lipoprotein cholesterol levels. The authors also mention “emerging risk factors such as homocysteine, lipoprotein (a), small dense LDL [low-density lipoprotein] and C-reactive protein.” One must also question the placement of C-reactive protein with this group, for its presence is not considered to be a primary risk factor, but one of a secondary nature that is initiated by some other abnormal state or process, and its “risks” are measured in association with other parameters.

The “gold standard” for the quantification and diagnosis of coronary artery disease remains cardiac catheterization. All patients in the younger age group with acute myocardial infarction, regardless of cause, generally are subjected to this procedure. They then are submitted for echocardiographic study and scintigraphic stress testing. When healthy coronary arteries are found on cardiac catheterization, the dilemma begins. A host of differential diagnoses are considered, and numerous biochemical and metabolic factors are evaluated for coagulopathic disorders, especially if coronary vasospasm was excluded during the emergent cardiac catheterization (an uncommon occurrence under these acute circumstances). These studies should include the following: platelet count; fibrinogen level; activated protein C resistance; protein C activity; protein S activity; antithrombin III activity; lupus anticoagulant level; presence of anticardiolipin antibodies; and the abnormality of a rapid inhibitor of tissue plasminogen activator.2 A test for platelet aggregation will soon become available for more common and practical use.

Duvernoy et al3described two boys, ages 14 and 15 years, who experienced acute myocardial infarcts involving the distribution of the left anterior descending coronary artery with healthy coronary arteries and no known inciting factors. Similar circumstances were presented by Smith and Vieweg4(anterolateral infarct in a patient aged 22 years) and Nizet and Robertson5 (posterior infarct in a 17-year-old boy). One can conclude that the condition of any patient who experiences an acute myocardial infarction without known clinical, genetic, and extraneous risk factors, and who has healthy coronary arteries, is indeed a diagnostic and therapeutic dilemma.

References

Akosah, KO, Cerniglia, RM, Havlik, P, et al (2001) Myocardial infarction in young adults with low density lipoprotein cholesterol levels ≤ 100 mg/dL.Chest120,1953-1958. [PubMed] [CrossRef]
 
Hamsten, A, Wiman, B, deFaire, V, et al Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction.N Engl J Med1985;313,1557-1563. [PubMed]
 
Duvernoy, CS, Bates, ER, Fay, WP, et al Acute myocardial infarction in two adolescent males.Clin Cardiol1998;21,687-690. [PubMed]
 
Smith, DC, Vieweg, VR Acute transmural myocardial infarction: its occurrence in a young man without demonstrable coronary artery disease.JAMA1974;229,811-813. [PubMed]
 
Nizet, PM, Robertson, L Normal coronary arteriogram following myocardial infarction in a 17 year old boy.Am J Cardiol1971;28,715-717. [PubMed]
 
To the Editor:

We thank Dr. RuDusky for his comments. He raises important issues in dealing with young adults, having to do with the lack of a standardized criterion for age inclusion. Family history of premature coronary artery disease is considered positive if it was diagnosed in a first-degree relative at age 55 or younger for men, and age 65 or younger for women. As premature coronary artery disease becomes more appreciated, it will become necessary to have a consistent definition, as Dr. RuDusky suggests.

A second issue concerns the unfortunate presentation of myocardial infarction in the very young. In the very young population that Dr. RuDusky discusses, myocardial infarction may occur in the absence of angiographically proven coronary artery disease. The differential diagnosis may include thromboembolism, metabolic and endocrine disorders, illicit drug use, coagulopathies, or infections. However, there are disease processes separate from coronary artery disease, as angiography fails to reveal underlying atherosclerotic lesions. Our study deals with people with coronary artery disease in whom the clinical presentation occurred at an early age. Traditionally, it has been thought that myocardial infarctions are relatively rare at this age.

Another difference between our population and the population that Dr. RuDusky talks about is that our subjects have high rates of traditional risk factors, including hypertension, smoking, obesity, and a family history of premature coronary artery disease. Our message is that young adults with cardiovascular risk factors are at risk for early presentation of myocardial infarction. Contrary to popular belief, a normal lipoprotein profile in a young adult with risk factors does not imply freedom from coronary artery disease.

Concerning novel risk factors, we believe it is important to understand all contributing causes of coronary artery disease. However, sufficient evidence exists to support the aggressive management of all modifiable risk factors. Ironically, most of these risk factors are preventable in the first place. Yet we do poorly in controlling them.

We must not necessarily wait for new answers to start taking premature coronary heart disease seriously. A good beginning is to translate what is already known into clinical practice, focusing on elimination of all modifiable risk factors.


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References

Akosah, KO, Cerniglia, RM, Havlik, P, et al (2001) Myocardial infarction in young adults with low density lipoprotein cholesterol levels ≤ 100 mg/dL.Chest120,1953-1958. [PubMed] [CrossRef]
 
Hamsten, A, Wiman, B, deFaire, V, et al Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction.N Engl J Med1985;313,1557-1563. [PubMed]
 
Duvernoy, CS, Bates, ER, Fay, WP, et al Acute myocardial infarction in two adolescent males.Clin Cardiol1998;21,687-690. [PubMed]
 
Smith, DC, Vieweg, VR Acute transmural myocardial infarction: its occurrence in a young man without demonstrable coronary artery disease.JAMA1974;229,811-813. [PubMed]
 
Nizet, PM, Robertson, L Normal coronary arteriogram following myocardial infarction in a 17 year old boy.Am J Cardiol1971;28,715-717. [PubMed]
 
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