Cardiology Week 8 Summary

Question 36

Who still needs antibiotics prophylaxis as per the latest AHA/ADA guidelines published in 2007?

In 2007, the American Heart Association (AHA) and the American Dental Association (ADA) published the new guidelines on the prevention of infection endocarditis (IE) (1). Prophylactic antibiotics should not be given based on a lifetime risk for infective endocarditis alone, but are recommended for high-risk patients undergoing “procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.”

Such “high-risk” patients, according to the guidelines, include those with the following:

  1. Prior infective endocarditis
  2. Prosthetic cardiac valves
  3. Unrepaired cyanotic congenital heart defects, including palliative shunts and conduits
  4. Congenital heart defects completely repaired with prosthetic material or a device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
  5. Repaired congenital defects with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device
  6. Cardiac transplants and development of cardiac valvulopathy.

The latest document shifted the emphasis away from a focus on a dental procedure and antibiotic prophylaxis toward a greater emphasis on improved access to dental care and oral health among patients who are at highest risk of adverse outcome from IE, and those conditions that predispose to the acquisition of IE.

It is impractical to recommend antibiotic prophylaxis for routine daily activities for those high risk patients, such as chewing food, brushing, flossing, use of toothpicks, and use of water irrigation devices, etc.

The presence of dental disease may increase the risk of bacteremia associated with these routine activities. It is, therefore, even more important to recommend to these patients to have good dental hygiene by having routine dental check ups, as well as good teeth brushing and flossing routines.

Wilson W. et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9;116(15):1736-54

Question 37

When should you screen for abdominal aortic aneurysm (AAA) and how often should you follow the patient with AAA?

Recommendation: AAA screening

  1. Men aged 65-74 (grade 1A)
  2. Women aged 65 with cardiovascular disease and positive family history of AAA (grade 3C)
  3. Men aged 50 and above with a positive family history (grade 3C)

Recommended AAA follow-up based on initial size:

<3.0 cm Repeat ultrasound follow-up in 3-5 years
3.1-3.4 cm Repeat ultrasound in 3 years
3.5-3.9 cm Repeat ultrasound in 2 years
4.0-4.5cm Repeat ultrasound in 1 year
>=4.5cm Referral to vascular surgeon and repeat ultrasound Q6mths
If >1cm growth in 1 year Referral to vascular surgeon for consideration of repair

Question 38

What is the definition and the causes of dilated cardiomyopathy?

Primary myocardial failure in the absence of underlying coronary, valvular, or pericardial disease.

Causes include:

  1. Toxins
    • Ethanol
    • Chemotherapy agents e.g. anthracyclines(adriamycin), cyclophosphamide
    • Heavy metals (cobalt, lead, mercury)
    • Cocaine, Catecholamines
    • Antiretroviral agents
    • Radiation
    • Psychothreapeautic drugs (tricyclic, quadricyclic, phenothiazine)
  2. Metabolic abnormalities
    • Nutritional deficiencies (thiamine, selenium, carnitine, kwashiorkor)
    • Endocrine (hyper/hypothyroidism, acromegaly, Cushing’s, pheochromocytoma, diabetes)
    • Electrolyte abnormalities (Uremia, Hypokalemia, hypomagnesemia, Hypocalcemia/phosphatemia)
  3. Infectious
    • Viral (Coxsackie B, CMV, HIV)
    • Rickettsia
    • Diphtheria
    • Mycobacteria
    • Fungal
    • Parasitic(toxoplasmosis, trichinosis, Chagas’)
  4. Inflammatory
    • Collagen vascular(scleroderma, lupus, dermatomyositis)
    • Hypersensitivity
    • Sarcoidosis
    • Granulomatous disease e.g. Wegener’s granulomatosis
    • Giant cell arteritis
    • Peripartum (1 month before and 5 months after)
  5. Neuromuscular syndromes
    • Duchenne’s
    • Facioscapulohumeral muscular dystrophy
    • Erb’s limb-girdle dystrophy
    • Myotonic dystrophy
    • Friedrich’s ataxia
  6. Familial cardiomyopathies
  7. Neoplasms
  8. CAD with diffuse epicardial coronary-artery disease (if CAD is not excluded as an etiology)

In North America, the most common causes are:

  1. CAD
  2. Post-viral myocarditis
  3. Alcoholic cardiomyopathy

Question 39

What are surgical indications for thoracic aortic aneurysm?

Aortic aneurysm is a permanent localized dilatation of the aorta having a diameter at least 1.5 times that of expected normal diameter of that given aortic segment.

Initially, medical treatment with beta blockers has shown to reduce the rate of expansion and improved in survival (by reducing dp/dt & alter connective tissue metabolism).

Surgical therapy is often recommended prophylactically to prevent the morbidity and mortality associated with aneurysm rupture. However, the optimal timing of surgery for a thoracic aortic aneurysm is uncertain since the natural history is variable, particularly for aneurysms less than 50 mm in size. Many patients die of other cardiovascular causes before the aneurysm ruptures because majority of the patients have concomitant cardiovascular disease that increases the risks associated with surgery.

Indications for surgery include:

  • The presence of symptoms (e.g. chest, back, flank, or abdominal pain, aortic insufficiency leading to heart failure)
  • A diameter of 5 to 6 cm for an ascending aortic aneurysm and 6 to 7 cm for a descending aortic aneurysm
  • Replacement before aortic size index (aortic diameter (cm) divided by body surface area (m2)) for the ascending of aorta is 2.75 cm/m2.
  • Accelerated growth rate (>=1 cm per year) in aneurysms less than 5 cm in diameter
  • Evidence of dissection
  • In patients with aortic regurgitation of any severity and primary disease of the aortic root or ascending aorta (such as Marfan syndrome), the 2006 ACC/AHA valvular disease guidelines recommend aortic valve replacement and aortic root reconstruction when the degree of dilatation is 5 cm. The guidelines note that some have recommended surgery for this group at a lower level of dilatation (4.5 cm) or based on a rate of increase of 0.5 cm per year or greater in surgical centers with established expertise in repair of the aortic root and ascending aorta.

Question 40

For a patient with ST-elevation myocardial infarction (STEMI), how you decide on whether the patient should receive thrombolysis versus primary percutaneous coronary intervention (PCI)?

Prompt restoration of myocardial blood flow is essential to myocardial salvage and mortality reduction after ST-elevation myocardial infarction (STEMI). If high-quality percutaneous coronary intervention (PCI) is available, multiple randomized trials have shown enhanced survival compared to thrombolysis with a lower rate of intracranial hemorrhage and recurrent MI.

If primary PCI is not available on site, rapid transfer to a PCI center can still produce better outcomes than thrombolysis, as long as the door-to-balloon time, including interhospital transport time, is less than 90 minutes. However, this door-to-balloon time is difficult to obtain unless rapid transport protocols and relatively short transport distances are in place.

The 2004 ACC/AHA and ACCP guidelines recommend the use of thrombolytic therapy for patients with STEMI who present to a facility in which the relative delay necessary to perform primary PCI (the expected door-to-balloon time minus the expected door-to-needle time) is greater than one hour.

Antman et al., Management of Patients With STEMI: Executive Summary. J Am Coll Cardiol 2004;44:671-719

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