1. “Managing Hypertension in
Physically Active Patients”
Summary By: Jonathan Noury

2. Risk Factors for HTN in Athletes
• African American
• Elderly
• People who are obese
• Diabetes
• Renal disease
• FHx of HTN
Prevalence:
20-30 yrs: 5-10%
30-60 yrs: 20-25%

3. Secondary HTN
• Develops in fewer than 5% of athletes
– Young patients increased estrogen from
contraception pills.

4. Clinical Evaluation
• Hx of behaviors
– High intake of sodium and saturated fats
– Use of alcohol/drugs
– NSAIDS
– Dietary supplements for “energy” or “weight
control”
• BP measurement
– Referral for blood work

6. Treatment
• Compliance with lifestyle modification
– Reduction in sodium, processed food
– Increase intake of potassium
• Weight loss
– Loss of 10 lbs. can lead to significant reduction in
BP for overweight patients.
– High fiber foods
• Stress management

7. Exercise Modification

8. Pharmacological Tx

10. Calcium Channel Blocker
• Bind to calcium channels located on
the vascular smooth muscle, cardiac
myocytes, and cardiac nodal tissue
• Responsible for regulating the influx
of calcium into muscle cells
stimulates smooth muscle
contraction and cardiac myocyte
contraction

11. ACE Inhibitors
• Produce vasodilation by
inhibiting the formation of
angiotensin II.
• Angiotensin I is then
converted to angiotensin II by
angiotensin converting
enzyme.
• Angiotensin II constricts
arteries and veins by binding
to receptors located on the
smooth muscle.

12. Beta Blockers
• Bind to beta-adrenoceptors and
thereby block the binding of
norepinephrine and epinephrine
• Inhibits normal sympathetic
effects that act through these
receptors.

13. “Sudden Cardiac Death in
Competitive Athletes”
“Hypertrophic Cardiomyopathy: A
Systems Review”
A Summary By: Jonathan Noury

14. Sudden Cardiac Death
• “Unexpected sudden cardiac death that
occurs within 6 hours of a previously normal
state”
Pete Maravich (39)
Congenital Missing
Left Coronary
Artery
Len Bias (23)
Cocaine use Cardiac
arrhythmia

15. Epidemiology
• 1983-1993 (<35 y/o)
– Incidence in males:
7.47:1,000,000
– Incidence in females:
1.33:1,000,000
• Older athletes (>35)
- Estimated incidence:
1:15,000-1:50,000
Majority of deaths occur in basketball and
football players
Even if there was a tool to screen for SCD with 99% sensitivity the
PPV would be 0.05%  1 correct positive out of 2000 (1999 FP)

16. Etiology
• Athletes above 35 years old
– Most common cause of SCD is
atherosclerotic coronary
artery disease
• Athletes below 35 years old
- Aortic aneurism or malignant
and fatal arrhythmia leads to
death

17. Some Causes
• Hypertrophic cardiomyopathy
– Autosomal-dominant congenital disorder
• Congenital coronary anomalies
– Abnormal anatomical variations of coronaries
– Hypoplastic vessels
• Substance abuse
– Leads to arrhythmia
• Wolff-Parkinson-White syndrome
– Congenital extra electrical connection inside heart that acts as a
short circuit resulting in tachycardia

18. What To Look For
• Auscultation
- Arrhythmias, heart sounds-
normal if they disappear with
exercise
• History of:
• Cardiac arrest
• Ventricular Tachycardia
• syncope or near syncope
with exercise
• Chest pain
• Unexpected or
unexplained SOB or
fatigue with exercise
•Past detection of heart
murmur
•Low BP in response to
exercise
•FHx of SCD or relative who
has suffered cardiovascular
disease age< 50
•FHX of hypertrophic
cardiomyopathy, dilated
cardiomyopathy, Marfan’s
syndrome
Detailed cardiovascular history

20. Marfan’s Syndrome
• Skeletal:
– Arm span greater than height
– Chest wall deformities
– Kyphoscoliosis
– High arched palate
– Hyperextensible joints
• Cardiovascular:
– Aortic or mitral regurgitation (murmur)
• Ocular:
– Myopia (near-sightedness)
– Ectopia lentis (dislocated lens)
Isaiah Austin

21. Non-Invasive Techniques
• If there is no significant history there is no
reason to refer for:
– Stress Test
– Echocardiography
– Genetic Testing- Hypertrophic Cardiomyopathy

22. No Guarantee
• After examining an athlete for cardiovascular
abnormalities the athlete should be advised that
he/she is not guaranteed to be free potential
sudden death.
• Study:
– 134 athletes who had suffered SCD
– 115 undergone standard pre-participation screening
– 15 underwent individualized medical evaluation for
heart disease
– Only 8 were accurately diagnosed prior to death

23. Interventions
• There are no published evidence based
studies that show that a prescreen can reduce
the risks of SCD.
• HOWEVER:
– In almost all cases of SCD, the final premorbid
event was Ventricular fibrillation
• Decreases chance of survival by 10% every minute AED
is delayed.
• In cases of V-fib , patient will have no pulse

24. Hypertrophic Cardiomyopathy
• Incidence: 1:500
– Most common genetic cardiovascular disease
• Typically Non-obstructive disease
– Autosomal dominant
• Mutation in 1/10 genes coding for cardiac sarcomeres
– Diagnosis:
• 2-dimensional Echocardiography/ECG
• Heart murmur
• Family history

25. Heart Sounds
Hypertrophic Cardiomyopathy • S1 (LUB)- Tricuspid and mitral closure
(loudest at apex)
• S2 (DUB)- Aortic and pulmonic valve closure
(may hear split)
• S3- Faint sound heard during ventricular
filling.(gallop)
• S4- Heard before S1. may be normal with LV
hypertrophy OR suggests Cardiomyopathy
• S4-S1-S2_S3

26. Diagnosis and Screening
• LV wall thickness as seen on echocardiography
– Normal: <13mm
– Mild: 13-15mm (also in trained athletes)
– Massive: >29mm
– 55% of HCM patients will not demonstrate any
risk factors and it is uncommon for them to die
suddenly

28. Prognosis
• Genetic testing provides most information
regarding favorable or adverse prognosis.
– B-myosin heavy chain and Troponin T mutations
may be associated with higher frequency of
sudden death.
– If adult has gene but no LVH then their condition
is usually benign.
– The less congestive symptoms present the better
the prognosis. (unless you have the other risk
factors)

29. What To Look For
• Auscultation
- Arrhythmias, heart sounds-
normal if they disappear with
exercise
• History of:
• Cardiac arrest
• Ventricular Tachycardia
• syncope or near syncope
with exercise
• Chest pain
• Unexpected or
unexplained SOB or
fatigue with exercise
•Past detection of heart
murmur
•Low BP in response to
exercise
•FHx of SCD or relative who
has suffered cardiovascular
disease age< 50
•FHX of hypertrophic
cardiomyopathy, dilated
cardiomyopathy, Marfan’s
syndrome
Detailed cardiovascular history

30. Prevention
• Anti-arrhythmia medication, Beta Blockers
• Best not to start meds until symptomatic
especially in children due to toxicity risk
• Implantable cardio-verter-defibrillator
– Placed inside chest to prevent arrhythmias
– Based on individual clinical judgment
• Lifestyle modifications

31. Gold Standard
• Ventricular septal myotomy-myectomy for
children and adults with obstructive HCM.
– surgeon removes a small amount of the thickened septal
wall to widen the outflow tract from the left ventricle to
the aorta. This eliminates the obstruction and the mitral
valve regurgitation that occurs with this condition. Patients
often experience rapid relief of symptoms after the
procedure

32. Alternate Tx
• Pacemaker- dual chamber pacing
– More accurately replicates ventricular and atrial
contraction
• Alcohol septal ablation
– Introduce 1-4 mL of 100% concentrated alcohol
(absolute) into coronary artery to infarct that
tissue area to reduce the thickness
• Heart Transplant