Question

A 58 y/o female visits the Health center due to palpitations.

Medical background:

• H/O myocardial infarction in the past and with left ventricular failure, on the following medication:

o Valsartan 80 mg OD

o Furosemide 40 mg OD

o Spironolactone 25 mg OD

o Isosorbide dinitrate PRN

• History of Dyslipidemia since 10 yrs, on

o Atorvastatin 10 mg OD

• Non- Diabetic

History of present illness:

Present condition started few weeks now with palpitations associated with some giddiness, no associated chest pains, cold sweating nor malaise/fever.

Pertinent On Examination:

BP 105/70mmhg​PR 96/min​RR 21/min​Temp: 36.7 C

No anemia

Cardiac: mild tachycardia, irregular rhythm, no murmur

Lungs: Bibasilar crepitation

No edema

ECHO done Ejection fraction 45% with LA and LV, no clots seen

ECG: atrial fibrillation

IMPRESSION:

IHD (ischemic heart disease), CHF(congestive heart failure) , atrial fibrillation w/ normal ventricular respond

INVESTIGATIONS:

a. CBC/LFT/RFT/TFT/CRP/Lipids/Trop I/CKMB if needed

b. Chest XRAY

c. Echo after 6 months to 1 year

Discharge with additional meds:

1. Digoxin 0.25 mg,1 tab OD

2. Aspirin 81 OD

QUESTIONS

3. What is the clinical significance of doing cardiac enzymes for the patient with MI?

4. List at least two complications of MI and explain how they develop?

Answer 1

Answer:

Clinical Significance of doing cardiac enzymes for patient with Myocardial infarction :

Cardiac enzymes ― also known as cardiac biomarkers ― include myoglobin, troponin and creatine kinase. Historically, lactate dehydrogenase, or LDH, was also used but is non-specific. Cardiac enzymes are released into the circulation when myocardial necrosis occurs, as seen in myocardial infarction.

Myoglobin

Myoglobin is released into circulation with any damage to muscle tissue, including myocardial necrosis. Because skeletal muscle contains myoglobin, this measurement is quite nonspecific for MIs. The benefit in myoglobin is that a detectable increase is seen only 30 minutes after injury occurs, unlike in troponin and creatine kinase, which can take between 3 and 4 hours.

Troponin

The enzymes troponin I and troponin T are normal proteins that are important in the contractile apparatus of the cardiac myocyte. The proteins are released into the circulation between 3 and 4 hours after myocardial infarction and remain detectable for 10 days following. This long half-life allows for the late diagnosis of MI but makes it difficult to detect re-infarction, as can occur in acute stent thrombosis after percutaneous coronary intervention, or PCI. There are a number causes for troponin elevation not related to myocardial infarction; however, troponin elevation is much more sensitive than myoglobin and even creatine kinase.

Creatine kinase (CK)

Creatine kinase ― also known as creatine phosphokinase, or CPK ― is a muscle enzyme that exists as isoenzymes. The MB type is specific to myocardial cells, whereas MM and BB are specific to skeletal muscle and brain tissue, respectively. The CK level increases approximately 3 to 4 hours after MI and remains elevated for 3 to 4 days. This makes it useful for detecting re-infarction in the window of 4 to 10 days after the initial insult; troponin remains elevated for 10 days, making it less useful for this purpose.

The first biomarker used to aid in the diagnosis of acute MI was aspartate aminotransferase (AST).AST increases in the blood 3 to 4 hours after an acute MI, peaks at 15 to 28 hours and returns to baseline within 5 days. In current clinical practice, AST has fallen out of favor for diagnosing acute MI because it is not a specific marker for cardiac myocytes. AST levels in the blood elevate in hepatic disease (e.g., hepatitis, hepatic congestion), pericarditis, pulmonary embolism, and shock and as a result, is not used in the diagnosis of acute MI. (LDH) emerged as another potential biomarker for detecting myocardial ischemia. LDH increases in the blood 6 to 12 hours after an acute MI, peaks within 24 to 72 hours and normalizes within 8 to 14 days.Since it is not a specific marker for cardiac myocytes, and its levels can also increase in many other conditions.

Complications of Myocardial infarction are as follows:

• Cardiogenic shock: One of the life-threatening complications of STEMI is cardiogenic shock during which hypotension is present from low cardiac output. This results in end-organ hypoperfusion and potentially multi-system organ failure and can be fatal. Revascularization by PCI or CABG is recommended in such cases.
• Left ventricular aneurysm: A left ventricular aneurysm can form after a STEMI. Most commonly, the apex of the heart is involved however, the inferior wall can form an aneurysm as well. The four main concerns in patients with left ventricular aneurysm are:

  1. Heart failure: The portion of the heart that contains the aneurysm is not contractile and is frequently “dyskinetic”. This results in overall decrease in heart function and the development of congestive heart failure.

  2. Left ventricular thrombus formation: When blood stagnates in any area of the body, there is a risk of platelet aggregation and thrombus formation. The aneurysmal portion of the LV is no different. Embolization of left ventricular thrombi can lead to embolic stroke or other systemic embolisms.

  3. Ventricular tachycardia: The scar within the left ventricular aneurysm is a focus for ventricular arrhythmias which can lead to sudden cardiac death.

  4. Angina pectoris: The aneurysmal tissue can still cause symptoms of angina, even if revascularized.

  An LV aneurysm can be diagnosed on ECG when there is persistent ST segment elevation occurring 6 weeks after a known transmural MI.

• Ventricular arrhythmia: The most common cause of pre-hospital death during STEMI is ventricular fibrillation.

• Atrial fibrillation: Atrial fibrillation is not a common complication of STEMI, however it can occur when atrial infarction occurs (as indicated by PR depression on the ECG). Rapid control of heart rates is crucial to limit the extent of ischemia. Recall that oxygen demand increases as heart rate increases. Emergent cardioversion and amiodarone therapy is frequently needed in the setting of atrial fibrillation and STEMI.

  Ventricular septal defect: When infarction of the interventricular septum occurs, this area can thin with the remodeling process and on occasion, a complete defect between the right and left ventricles can develop. This results in left to right shunting of blood and can be life-threatening when acute.

• Left ventricular thrombus: After myocardial infarctions (especially anteriorly), the myocardial stunning that occurs can result in blood pooling toward the akinetic segment (frequently the cardiac apex) resulting in thrombus formation. Embolization of this thrombus can cause a stroke.

• Left ventricular free wall rupture: This is a fatal complication of myocardial infarction and occurs when thinning of the left ventricular free wall occurs as a part of remodeling.