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Hypertension in a Young Golfer

Martha I. Pyron, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 30 - NO. 6 - JUNE 2021


In Brief: A collegiate freshman golfer was hypertensive at her preparticipation physical exam (PPE). Further investigation revealed coarctation of the aorta with secondary hypertension that had been asymptomatic. The PPE is a good forum for hypertensive screening because it may be one of the few times an apparently healthy adolescent is seen by any physician. This case emphasizes the need to screen for silent hypertension and discern its cause in adolescents.

Coarctation of the aorta is an uncommon cardiovascular defect that can cause periductal aortic stenosis, upper-extremity hypertension, prelesion aortic dilation, and collateral circulation. Most cases are discovered during infancy, but the preparticipation physical exam (PPE) provides an excellent opportunity to detect anomalies that may have progressed without symptoms. Although it is an uncommon finding, coarctation is a treatable cause of hypertension.

Case Report

During a preseason PPE, an 18-year-old golfer discussed a bicuspid aortic valve (diagnosed at birth) and brought the report from an echocardiogram performed 1 year earlier. She had no history of hypertension, thyroid disease, kidney disease, headaches, visual disturbance, syncope, near-syncope, menstrual irregularity, chest pain, fatigue, or shortness of breath. Her family history was negative for heart disease, sudden death, hypertension, and renal abnormalities. She did not use tobacco, alcohol, steroids, excessive caffeine, or notable over-the-counter medications.

Physical exam. She appeared to be her stated age, and her height and weight were proportional. Her blood pressure was elevated at 150/90 mm Hg, but other vital signs were within normal limits. Her ophthalmic exam was negative, her neck was without thyromegaly or carotid bruits, and her lungs were clear on auscultation.

The cardiac exam was significant for a loud holosystolic murmur, heard best over the upper left sternal border with radiation to the back between the shoulder blades. Otherwise, the cardiac exam showed a regular rate, normal S1 and S2, and absence of an S3 or S4 abnormality, gallop, or rub. The apex was not displaced, and the abdomen was without bruits. Her distal pulses were strong and palpable in all four extremities, but there was a half-second delay between the radial and femoral pulses. Lower-extremity blood pressure was 135/80 mm Hg by thigh cuff measurement.

Diagnostic tests. A chest x-ray revealed no rib notching. An echocardiogram (figure 1) showed a 40-mm-Hg gradient coarctation in the descending aortic arch and a bicuspid aortic valve with an 11-mm-Hg gradient, but no valvular thickening or calcifications.

Diagnosis. She was given a final diagnosis of coarctation of the aorta with hypertension and a bicuspid aortic valve.

Treatment. Surgery was scheduled for the next school break. In the meantime, her blood pressure was monitored regularly. She was withheld from weight training but continued to participate in golf.

Surgical correction of the coarctation with placement of a Dacron graft was performed. She recovered without complications, and a follow-up echocardiogram showed a normal gradient.

Follow-up. This patient has returned to full activity without complications and continues to participate in golf. Her limitations include being withheld from contact sports and high-intensity static exercise for 1 year after surgery, being restricted from power lifting for the rest of her life, and considering cesarean section rather than vaginal delivery if she becomes pregnant. Otherwise, all activity was permitted 6 months after surgery. Her blood pressure remains normal. She will have yearly stress echocardiograms and blood pressure measurements to monitor for complications. Her blood pressure and follow-up exams to date show no complications.

Discussion

Adolescent hypertension is a watershed between children who have lingering, rare, congenital, or genetic abnormalities that cause hypertension and adults who have the more common essential hypertension. The PPE setting is ideal for detecting silent hypertension. Otherwise, an apparently healthy adolescent may not be seen by any physician for many years.

The blood pressure of adolescent patients should be assessed regularly and screened for hypertension. Correlating blood pressure readings with the height and weight of children1 will determine abnormal findings. Serial testing of adolescents can separate those who have an occasional elevated reading from those who are truly hypertensive. Also, eliciting help from school nurses, athletic trainers, or other ancillary healthcare professionals can help discern adolescents with "white coat" hypertension from those with consistent hypertension.2

Children with essential or primary hypertension show significantly higher rates of obesity, familial hypertension, "faulty regimen of living," and other diseases.3 The more severe the hypertension and the earlier it appears, the more likely there is an associated underlying secondary cause.4 The most common causes of hypertension in children 12 to 18 years old are essential hypertension, iatrogenic causes, renal parenchymal disease, renovascular disease, endocrine causes, and coarctation of the aorta. Hypertension may also be caused by easily treatable conditions, such as sleep apnea, anxiety, or supplement misuse.3

Prevalence. Hypertension is the most common cardiovascular condition seen in people who engage in competitive athletics.5 Sinaiko et al6 found the prevalence of significant hypertension (either essential or secondary) to be 2% among 14,000 school children ages 10 to 15. Up to 80% of hypertensive adolescents have essential hypertension7; however, a secondary cause is found in 80% of children younger than 10 years old.8 Adolescents may have a previously undiagnosed secondary cause of hypertension or may be developing adult essential hypertension.9 At least 90% of hypertensive adults have no underlying secondary cause.10

Daniels11 found a 14% prevalence of left ventricular hypertrophy in adolescents who had essential hypertension. Schieken et al12 found that blood pressure was linked to increased left ventricular mass and was lower in girls than boys. The adolescents were repeatedly studied between ages 11 and 17, and researchers found blood pressure readings were equivocal in white and black children until late adolescence, at which point black adolescents demonstrated a higher incidence of hypertension.

Other causes of secondary hypertension include renovascular disorders (12%), endocrine disorders (8%), and a variety of rare conditions (2%) such as coarctation of the aorta. Secondary hypertension usually abates when the underlying disorder is corrected; therefore, every effort should be made to diagnose and treat secondary causes. In this case, the discovery and correction of the coarctation resolved the hypertension.

Coarctation

Coarctation of the aorta occurs in about 2% of all cardiovascular anomalies.8 More than half (56%) of all patients who have coarctation are asymptomatic13; however, symptoms may include chest pain, shortness of breath, easy fatigue, headaches, nosebleeds, signs of congestive heart failure, or claudication (table 1).

TABLE 1. Indications of Coarctation of the Aorta
in the History and Physical Exam

History
Asymptomatic
Headaches
Nose bleeds
Chest pain
Shortness of breath
Lower-extremity claudication (rarely evident because of
    extensive collateral circulation)
Physical Exam
Upper-extremity hypertension
Weak or absent femoral or dorsalis pedis pulse
Low-intensity murmur located at the base of the heart,
    radiating to axilla; may be loudest over the back in left
    infrascapular region
Bruits over intercostal arteries
Bicuspid aortic valve with systolic click; murmur best
    heard over right sternum or supraclavicular notch
Radial-to-femoral pulse delay
Upper-extremity blood pressure greater than lower-
    extremity pressure
Signs of congestive heart failure

Severe obstruction of the aorta from coarctation causes significant upper-extremity hypertension, diminished femoral or dorsalis pedis pulse, a radial-to-femoral pulse delay, left ventricular hypertrophy, turbulent flow across the defect, and a corresponding holosystolic murmur. Collateral circulation, as evidenced by rib notching on an x-ray (figure 2: not shown), is also likely if the condition is long-standing (10 years or more).

If coarctation remains untreated, the patient is at risk for aortic dissection, aortic aneurysm and rupture, cerebrovascular accidents, and left ventricular hypertrophy. More demanding sports tend to produce earlier symptoms and possibly select out those with coarctation.

Bicuspid Valves

The patient in this case also has a bicuspid aortic valve. A bicuspid aortic valve occurs in tandem with coarctation in 25% to 50% of patients.14 When asking for an echocardiogram to confirm a suspected bicuspid valve, one should specify the need to look for both conditons.15 Isolated bicuspid valves can occur and appear to form by a separate developmental process.14,16 The typical ejection click that occurs with a bicuspid valve was not heard on this patient, probably because the murmur was so loud it overshadowed the click.

Bicuspid valves do not necessarily lead to complications, but thickening and calcification can lead to stenosis and/or regurgitation. Antibiotic treatment should be used for endocarditis prophylaxis. Surgery is the recommended treatment for symptomatic patients and for patients who have a pressure gradient greater than 20 mm Hg across the valve. In this case, the gradient was only 11 mm Hg, and the valve appeared without thickening or calcification, so it was not treated.

Serious Sequelae

Hypertension from any cause can lead to end-organ disease. Possible sequelae of uncontrolled hypertension include left ventricular hypertrophy, sudden death, peripheral vascular disease, cerebrovascular disease, retinopathy, and renal dysfunction.11 Evaluation for end-organ dysfunction with an echocardiogram, electrocardiogram, retinal exam, and renal studies is warranted in hypertensive patients of all ages. Further workup with appropriate radiologic studies and laboratory evaluation should be undertaken when necessary, based on the patient's history and physical findings.

Definitive Surgery

Surgery does not always alleviate hypertension, presumably because of permanent changes in aortic compliance. Surgical complications include paralysis of the lower extremities (0.4%), persistent hypertension after surgical correction of stenosis (up to 50%), and mesenteric arteritis.15 Despite these possibilities, surgery is still recommended to avoid the long-standing effects of hypertension.

Balloon angioplasty for primary treatment is an alternative, but it is associated with high rates of recurrent stenosis. The earlier the patient has surgical correction, the less likely he or she will have persistent hypertension.

Return to Play

An exercise stress test should be performed after surgical correction to determine the patient's hypertensive response to exercise.17 If the blood pressure remains stable, limited return to sports is possible on a case-by-case basis. Contact sports and high-intensity static exercise are not advised for 1 year after surgery.18 Some activities, such as power lifting, may be restricted for the rest of the patient's life. If hypertension persists after surgery, medication and an exercise program emphasizing aerobic training are advised to control the elevated blood pressure.

Hearing the Unpronounced Clues

This case emphasizes the need to screen for silent hypertension and discern its cause in adolescents. Occasionally, a secondary factor can be identified and treated, thus alleviating the morbidity associated with untreated hypertension. Finally, the PPE may be the only medical evaluation an adolescent has for many years. Taking advantage of this opportunity to detect and treat hypertension may make a lifelong difference.

References

  1. Andriska J, Gombik M, Breyer H, et al: Hypertension in children and adolescents: results of a long-term follow-up study 1975-120215. Clin Exp Hypertens A 120216;8(4-5):567-569
  2. McCann BS, Matthews KA: Influences of potential for hostility, type A behavior, and parental history of hypertension on adolescents' cardiovascular responses during stress. Psychophysiology 120218;25(5):503-511
  3. Pistulkova H, Blaha J, Skodova I: Prevalence of hypertension in children and adolescents. Cor Vasa 1976;18(3):237-240
  4. Brouhard BH: Hypertension in children and adolescents. Cleve Clin J Med 1995;62(1):21-28
  5. American Academy of Pediatrics Committee on Sports Medicine and Fitness: Athletic participation by children and adolescents who have systemic hypertension. Pediatrics 1997;99(4):637-638
  6. Sinaiko AR, Gomez-Martin O, Prineas RJ: Prevalence of 'significant' hypertension in junior-high aged children: the Children and Adolescent Blood Pressure Program. J Pediatr 120219;114(4 Pt 1):664-669
  7. Mahan JD, Turman MA, Mentser MI: Evaluation of hematuria, proteinuria, and hypertension in adolescents. Pediatr Clin North Am 1997;44(6):1573-1589
  8. Brem AS: Practical approach to hypertension in children and adolescents. R I Med 1993;76(5):229-231
  9. Fernandes E, McCrindle BW: Diagnosis and treatment of hypertension in children and adolescents. Can J Cardiol 2021;16(6):801-811
  10. Kaplan NM, Lieberman E: Clinical Hypertension. Baltimore, Williams & Wilkins, 1990, pp 3-5, 17, 138, 149-153, 165-171
  11. Daniels SR: Hypertension-induced cardiac damage in children and adolescents. Blood Press Monit 1999;4(3-4):165-170
  12. Schieken RM, Schwartz PF, Goble MM: Tracking of left ventricular mass in children: race and sex comparisons: the MCV Twin Study. Medical College of Virginia. Circulation 192021;97(19):1901-1906
  13. Fyler DC, Nadas AS: Nadas' Pediatric Cardiology. Philadelphia, Hanley & Belfus, 1992, pp 295-304, 537
  14. Kappetein AP, Gittenberger-de Groot AC, Zwinderman AH, et al: The neural crest as a possible pathogenetic factor in coarctation of the aorta and bicuspid aortic valve. J Thorac Cardiovasc Surg 1991;102(6):830-836
  15. Schlant RC, Alexander RW: The Heart, Arteries and Veins, ed 8. New York City, McGraw-Hill, 1994, pp 309-310, 701-706, 1148, 1432, 2230
  16. Lindsay J Jr: Coarctation of the aorta, bicuspid aortic valve and abnormal ascending aortic wall. Am J Cardiol 120218;61(1):182-184
  17. Kaplan NM, Deveraux RB, Miller HS Jr: 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 4: systemic hypertension. J Am Coll Cardiol 1994;24(4):885-888
  18. Mitchell JH, Maron BJ, Raven PB: 26th Bethesda Conference: recommendation for determining eligibility for competition in athletes with cardiovascular abnormalities. Med Sci Sports Exerc 1994;26(10 Suppl):S223-283


Dr Pyron is an assistant professor of orthopedics at Hershey Medical Center at The Pennsylvania State University in State College, Pennsylvania, and a Penn State team physician. Address correspondence to Martha I. Pyron, MD, 1850 E Park Ave, Suite 112, State College, PA 16803; e-mail to [email protected].

Disclosure information: Dr Pyron discloses no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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