Key Concepts: Ischemia, Coronary Syndromes, MI

Question 1

A reduction in flow in the coronaries can be due to?

Answer 1

Stenosis (chronic), VMT (vaso motor tone; acute), spasm, change in microvessels which could be vasoconstriction or
hypertrophy : an example would be an intense, acute stress, mediated by adrenaline, which causes vasoconstriction.

For example in Takotsubo, there is an acute persistent constriction of the microvasculature due to an acute intense stress, with a high peak in adrenaline which will in turn cause myocardial damage.

Question 2

Does ischemia always equal pain?

Answer 2

No. The pain depends on the adenosine spillover, in other words the effort in maintaining the vasodilation. Perception of pain can also be related to the extent and duration of the ischemia, the amount of jeopardizes myocardium and pain threshold.

With the same gating,but with a greater stimulus, pain is perceived. The same stimulus however, in the presence of a greater gating, does not produce pain.

Question 3

How can we verify the extent of myocardial damage?

Answer 3

Through high sensitivity troponin levels. 1 mg of myocardial damage is enough to increase troponin levels.

Question 4

What are the main components that can cause myocardial ischemia?

Answer 4

Artherosclerotic disease, vasospastic disease, micro vascular dysfunction.
Artherosclerotic plaque could be stable if there is a coronary flow reserve but could rupture or cause angina and ischemia during exercise.
Vasospastic disease can be focal, transient or persistent. Transient is also known as prinzmetal angina, persistent can cause MI.
Microvasculature impairment in overcoming reduction of perfusion pressure can contribute to ischemic manifestation of variable degree.

Question 5

Pressure flow relationship for stenosis in coronaries?

Answer 5

The linear path represents the ability to vasodilate in order to meet oxygen demand. A stenosis of 50% or less shows no significant impairment of coronary reserve flow. 50% to 70% shows a significant reduction in the capability to vasodilate. Greater than 70% is considered very severe and over 85/90% there is no flow change.

Question 6

What are collateral vessels?

Answer 6

Some patients during chronic ischemic phase may develop collateral vessels. This explain why a portion of patients do not develop an acute event. The vessels could collapse in case of the opening of the occluded vessel.

Question 7

How can ischemia manifest? What are some factors increasing likelihood of ischemia?

Answer 7

Ischemia may manifest : anginal discomfort, ST segment changes on ECG, neck or jaw pain, nausea vomiting, sweats, fatigue and dyspnea.

Clinical determinants include male sex, smoking, hypertension, diabetes mellitus, hypercholesterolomia.

Question 8

How does angina pectoris manifest?

Answer 8

Chest pain if ischemic is called angina. It will be diffuse pain since it is visceral not somatic. Lasts a few minutes, not seconds not hours as most of the myocardium would be dead leading to other symptoms.
It is frequently associated to arrhythmias and dyspnea. Transition between normal myocardium and ischemic area is not clear, this could lead to a sort of short circuit causing ventricular tachycardia.
Dyspnea can be present as the left ventricle end diastolic pressure increases causing the atrial pressure to increase causing the pulmonary vessel pressure increase. This leads to possible transmutation in the bronchi or alveolar space causing impaired gas exchange. This happens if the capillary pressure is over 18 mmHg.

Question 9

What should we ask patients with chest pain?

Answer 9

When did the pain start? If recently it is a big red flag.
If it has the characteristics of typical angina : substernal chest discomfort (heaviness), provoked by exertion or emotional stress, and relived by rest or nitrates.
Atypical angina would have 2 out of three, non angina chest pain would have one or none.

We should ask is it predominantly in the day because if it occurs during the night with low HR then it is vasospastic, if the patient has good or bad days because the vasomotor tone depends on temperature (bad on cold days), if they can exercise on their good days.

Question 10

What are acute coronary syndromes? What is their cause?

Answer 10

They are caused by an impairment in the amount of oxygen and nutrients the heart receives because of a lack of flow. It is caused by a thrombus following the rupture of an artherosclerotic plaque.Thrombus formation is very fast and can reduce blood flow leading to ischemia and pain, although if is thrombolysed fast the blood flow can be restored with no damage.

Patients with suspected ACS may be diagnosed with MI or UA.
In unstable angina the myocytes are ischemic but not necrosed.
In STEMI and NSTEMI we have cardiac cell death the difference is that with an ST elevation we have transmural damage while in NST there is partial necrosis only.

Question 11

How is chest pain assessed in the context of coronary syndromes?

Answer 11

It is important to rule out life threatening conditions. We can categorizes chest pain of cardiac and non cardiac origin.
Cardiac origin includes ACS and non coronary syndrome such as acute pericarditis, aortic dissection and pulmonary embolism.
Non cardiac origin includes pneumothorax, gastroesophageal reflux disease, lung cancer, pneumonia etc.
For this reason it is important to take into consideration pain history, quality, severity and migration as it could affect the neck, jaw or arms, also onset, duration and frequency.

Question 12

How do we discriminate true retrosternal chest pain from GERD?

Answer 12

Duration, as GERD is generally long lasting. Whether it happens laying down or after meals. Patients with GERD may also present with a cough or voice changed due to vocal cord damage.

Question 13

What is MI? What are the different types?

Answer 13

MI is cardiac cell death due to prolonged ischemia. It is diagnosed through ECG changes and troponin levels. Can be caused by ACS such as STEMI and NSTEMI MIs.
Type I : spontaneous plaque rupture with resultant intraluminal thrombus, cessation of blood flow and acute necrosis.
Type II : ischemic necrosis due to an increase in myocardial oxygen demand in the absence of acute plaque rupture.
Type III : sudden cardiac death related to coronary arterial thrombosis.
Type IV : MI secondary to percutaneous coronary intervention.
Type V : MI secondary to CABG

Question 14

What can ACS cause? How are they differentiated?

Answer 14

They can cause STEMI, NSTEMI or UA. They are differentiated based on ECG findings and troponin levels.

Question 15

What do we do in the case of new onset of chest pain?

Answer 15

Pre test probability based on age, understand if it is a new onset or chronic condition and asses pain characteristics leading to ACS.
We should give nitrates to eliminate vasospasm, troponins used to distinguish between UA and MI and whether the MI is transmural or subendocardial. ECG findings to see ST elevation and if present try to open artery in CATHLAB or through TPA.

Question 16

What do we do if a patients with chronic condition presents with chest pain?

Answer 16

We asses the patients risk factors such as diabetes, smoking, is he/she correctly taking medications, LDL levels.
Glucose controlling drugs indicated for cardiac patients : GLP-1 receptor antagonists and SLGT2 inhibitors.
Hypertension —> if >130/80 give titrate ACE inhibitors. Take half the medication for 6 months and observe.
Lipid levels should be less than 70 in non diabetic and less than 55 in diabetic patients.
No smoking.

Question 17

What shouldn’t be done in a patent with chronic condition presenting with chest pain?

Answer 17

Troponin levels are non useful in the chronic phase. They are used to describe a patient worsening in an acute phase.
It is also not required to do non invasive stress imaging unless there is a change in the wellbeing of the patient.

Question 18

What are some post MI complications?

Answer 18

HF, hypertrophy, fibrosis, change in conduction, decreased EF, arrhythmias, rupture due to hemorrhage in wall, death bc of arrhythmias, multi organ failure.

Question 19

Classes of drugs used for MIs?

Answer 19

Organic nitrates : mainly venous vasodilators, that can also produce coronary vasodilation and, at higher doses, arterial vasodilation.

Calcium channel blockers : being cardioinhibitory and vasodilators.

Beta blockers : that reduce the oxygen demand by reducing heart’s activity and also have an antihypertensive action. There are drugs that are similar to beta blockers in terms of final effect, that can be given in alternative or on top of them to increase effect.

Question 20

What are nitrates? Mechanism of action?

Answer 20

Nitroglycerine, isosorbide and other drugs aree all characterized by the presence of NO2 that is then converted in NO within the cells which causes relaxation of blood vessels. They act as donors of NO that stimulates cGMP production that, through the action of several enzymes, acts at the level of light chain myosin provoking muscle relaxation.

Nitrates mainly act on veins of large diameter reducing the preload at the level of the heart. At higher doses they can induce also arterial dilation, so they can act beneficially at the level of the coronary vessels.

They are used for angina, HF, acute hypertension, MI.
The most common drug in this class is nitroglycerin, has a fast time to peak but shorter duration than isosorbide for example.

Question 21

What are beta blocker? Mechanism of action?

Answer 21

They reduce myocardial o2 consumption, with no effect on o2 supply and blood flow. They cause : reduction of cardiac output, reduced peripheral resistance, reduced atrial conduction, reduced A-V conduction. They are useful in prevention of an acute ischemic attack, in fact they are not used on patients with signs of cardiogenic shock or HF on presentation.

The most frequently used beta-blockers are :
Carvedilol—> it has some alfa-blocking activity. This can be useful because you can also have hypertensive effect due to the relaxation of arterial vessels.
Nadolol—> long acting beta blocker.