Notes

Mini Problem 3 :Myocardial infarction
1. What is Ms. Nora suffering from?
Familial Combined Hyperlipidemia (FCH)

2. What is familial combined hyperlipidemia?
Also called (Multiple lipoprotein-type hyperlipidemia ) is an inherited condition. Individual with FCH have a high triglyceride level as well as a high cholesterol level. It is more likely it is caused by a combination of genes working individually or together to affect the levels of blood fats. .
3. How common is FCH?
It is the most common genetic cause of hyperlipidemia t is affecting around one person in every hundred People with FCH are at increased risk of cardiovascular disease
4. Name two differences between familial combined hyperlipidemia (FCH) and familial hypercholesterolemia (FH)?
FCH:Although originally described as autosomal dominant, more recent data indicate a more complex inheritance. Several loci with major and minor impacts on risk of FCH, as well as environmental factors, have been demonstrated. The diagnosis of FCH is difficult, An increase in apolipoprotein B, together with elevated numbers of small, dense LDL particles, appears to be a more consistent phenotype for FCH than are total cholesterol and triglycerides, whose levels vary over time
FH: is autosomal dominant and associated with early vascular disease diagnosis based on high LDL-cholesterol levels (usually 250 mg/dl) in untreated adults and frequent tendinous xanthomas.

5. What is the treatment of FCH?
• A healthy diet and lifestyle are a key part of treatment including limiting alcohol and sugary foods ; reducing saturated fats and replacing them with unsaturated fats.
• Medication: depend on the individual’s levels of triglycerides and cholesterol:
Statins, ezetimibe,bile acid-sequestering resins, Fibrates ,Nicotinic acid and a newer class PCSK9 inhibitors

Which type of anti-lipidemic drugs you would chose for patients with FCH?

Clinically there is no specific classes but we must treat them to reduce their cholesterolemia and triglyceridemia to the best goals suggested by the international guidelines ,we can use the previous agents either as monotherapy or in combination then according to the lipid profile we continue or shift to to another agent.

6. WHY THE DOCTOR DID ORDERED ALL CARDIAC BIOMARKERS AND NOT JUST ONE?
• Glycogen phosphorylase isoenzyme BB (GPBB): specific to heart muscle ,so most specific for myocardial infarction
•
Troponin: The most sensitive and specific test for myocardial damage and stay raised for longer time up to 7 days.
•
creatine kinase CK-MB : raised fast and go down fast ,back to normal within 2–3 days..
•


7. What is the mechanism of Niacin action? Niacin affects apolipoprotein B-containing lipoproteins (eg, very-low-density lipoprotein [VLDL], low-density lipoprotein [LDL], lipoprotein[a]) ,increases high-density lipoprotein [HDL])and Inhibit triglycerides (TG) synthesis
8. What are the side effects of Niacin? And what is the second line of drugs that can be used?
Flushing or redness of the skin, especially on the face and neck, tingling , headache, itching, Nausea, , diarrhea, peptic ulceration, runny nose, cough. All are prostaglandin mediated side effects so aspirin will reduce them. Use of aspirin 30 minutes before using nicotinic acid dose reduce their intensity and considerably improves the tolerance to this drug.
They are prostaglandin mediated side effects so aspirin will reduce them

9. What is the action of aspirin in MI?
inhibits platelet generation of thromboxane A2, resulting in an antithrombotic effect.

10. After 3 months therapy with Pravastatin the result of Ms. Nora lipid profile was as follow..

11. Comment on the two result?
Still high

12. What is the rational for using GPBB as biomarker for MI?
It is specific for MI , since it is found only in the heart and brain , but due to blood brain barrier that it can’t pass, so the presence of GPBB would indicate myocardial infarction .

13. What is the type of pain experienced by the patient?
It is visceral pain produced by ischemia
14.Which nerves carry the pain sensation from the heart?
Sympathetic nerve fibers from the sympathetic trunk in the thoracic and cervical trunk

15. Which spinal cord segments are involved in pain transmission?
T1-T4

16.Which coronary artery involved in this type of infarction?
Right coronary artery or may be the circumflex because she has a posterior infarct where the two arteries meet, but in inferior infarct ,the involved one is RCA and LCA if lateral infarct

17.Which part of heart is supplied by the affected artery?
Posterior wall, basal part of the LV, posterior third interventricular septum.

18. Is there any possible that the SA node might be affected by the occlusion of the artery? Why?
Yes, because the right coronary artery supplies right atrium in 60% of cases
19 What are the changes seen in this ECG?what is your diagnosis?
ST segment elevation, Inverted T waves
the diagnosis is posterior MI.

20. What is your assumption from the ECG?
Posterior MI will cause RBBB

14. What are the signs and symptoms of left ventricular failure?
Palpitation, dizziness, orthopnea,paroxysmal nocturnal dyspnea, pulmonary edema, S3-S4


15. What are the risk factors for IHD

Diabetes mellitus, hypertension, hyperlipidaemia, obesity,family history



16. What are the types of IHD and MI?
IHD: Angina, unstable angina, myocardial infarction, and sudden cardiac death, chronic IHD,
MI: transmural infarcts and subendocardial infarcts.

17. How a patient with myocardial infarction is managed?
Transport patient as soon as possible to hospital. Empirical treatment of patients with suspected STEMI with morphine, oxygen, nitroglycerin, and aspirin.

18. What are the different classes of drugs that can be used for management of MI?
• Thrombolytics, analgesics, vasodialators, beta adrenergic blocking agents,anti-arrhythmic, anti-thrombotic.

19. What are the routes of administration of glyceryl trinitrate (GTN)?
Sublingual,oral, transdermal or IV

20. What are the main complications of vasodialators?
Headache, hypotension, allergic dermatitis.

21. What is nitrate tolerance? How can we avoid it?
. Nitrate tolerance develops can develop in as little as 24 hours. It is characterized by loss of hemodynamic and antianginal effects after repeated dosing; higher and higher doses are needed to obtain the same physiologic effect.
we avoid it by using smallest effective dose, use of the long-acting oral nitrates,provide a nitrate-free interval of > 10 hrs/day

22. What are the complications and contraindications of thrombolytics?
• Bleeding complications especially intra-cranial hemorrhage is the most serious
Contraindication: uncontrolled hypertension, history of stroke, dementia, or central nervous system,
head trauma within 3 weeks or brain surgery within 6 months, known intracranial neoplasm, suspected aortic dissection.